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Royal Adelaide Hospital Intensive Care Unit

Medical Manual

2010 Edition

Website: http://icuadelaide.com.au/

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Foreword

Welcome to Intensive Care. This manual has been written to facilitate the daily running of the RAH Intensive Care Unit. It is by no means the definitive answer to all intensive care protocols and procedures, nor is it designed to be a textbook. A standardised approach to management is desirable for optimal patient care and safety, improving communication and understanding between members of the ICU team and associated specialties. This approach provides a common platform for staff who come from different countries and training backgrounds. The manual outlines various Protocols, which represent a standard approach to practice within the Unit. These have been derived from the available literature, clinical experience and where appropriate, cost-effectiveness. Guidelines designed to assist in clinical management are included but patient management will ultimately depend upon the clinical situation. Assistance is always available from the Duty Consultant and senior nursing staff. Use your time in the Unit to get the most out of the large clinical caseload. Ask questions about clinical problems, equipment and procedures with which you are unfamiliar. There are numerous textbooks, journals and references available in the Unit. This manual has undergone numerous changes, with contributions from many of the ICU staff and from other specialty services within the hospital. The contents of this manual are produced from the consensus views of the senior medical staff and were accurate at the time of publication. A/Prof Robert Young Director 2010 11th Edition

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CONTENTS CONTENTS ........................................................................................................................ 3PART 1 - ADMINISTRATION ............................................................................................. 6

A. Staffing - Royal Adelaide Hospital ICU ............................................................... 6B. Rostering and Job Descriptions ............................................................................. 8

Table: Team Duties .............................................................................................. 8Table: Registrar Shifts ....................................................................................... 10

C. Orientation .......................................................................................................... 11D. Weekly Programme ............................................................................................. 12

Table: Weekly Unit Programme ........................................................................ 12E. Admission and Discharge Policies ...................................................................... 13F. Care for Patients Discharged from ICU for Terminal Care. ............................... 15G. Clinical Duties in the ICU ................................................................................... 16H. Documentation .................................................................................................... 19I. Consent in ICU ................................................................................................... 21J. ICU Ward Rounds ............................................................................................... 22K. Clinical Duties Outside of the Intensive Care Unit ............................................. 23L. Hospital Emergencies ......................................................................................... 28M. Research in ICU .................................................................................................. 29N. Information Technology in ICU .......................................................................... 30

PART 2 - CLINICAL PROCEDURES ................................................................................. 31A. Introduction ......................................................................................................... 31B. Procedures ........................................................................................................... 31C. Peripheral IV catheters ........................................................................................ 32D. Arterial Cannulation ............................................................................................ 33E. Central Venous Catheters .................................................................................... 34F. Urinary Catheters ................................................................................................ 36G. Epidural Catheters ............................................................................................... 37H. PICCO Catheters ................................................................................................. 37

Table: PiCCO Values and Decision Tree ........................................................... 38I. Pulmonary Artery Catheters ................................................................................ 39

Table: Standard Haemodynamic Variables ........................................................ 41J. Pleural Drainage .................................................................................................. 42K. Endotracheal Intubation ...................................................................................... 44L. Weaning Guidelines ............................................................................................ 49

Flowchart: Ventilation Weaning Protocol .......................................................... 50M. Extubation ........................................................................................................... 51N. Emergency Surgical Airway Access ................................................................... 52O. Fibreoptic Bronchoscopy .................................................................................... 53P. Tracheostomy ...................................................................................................... 54Q. Pericardiocentesis................................................................................................ 57R. Intra-aortic balloon counterpulsation .................................................................. 58S. Cardiac Pacing .................................................................................................... 61T. Oesophageal Tamponade Tubes ......................................................................... 64

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U. Extracorporeal Membrane Oxygenation .............................................................. 65PART 3 - DRUGS AND INFUSIONS .................................................................................... 66

A. Policy ................................................................................................................... 66B. Principles of drug prescription in Intensive Care ................................................ 67C. Cardiovascular Drugs .......................................................................................... 67

Table: Cardiovascular effects of inotropes ......................................................... 68Table: Inotropic Agents Used in ICU ................................................................. 69Table: Vasopressors ............................................................................................ 70Table: Antihypertensive & Vasodilator Agents .................................................. 71Table: Antiarrhythmic Agents ............................................................................ 74Table: Thrombolytics ......................................................................................... 76Table: Antiplatelet Agents .................................................................................. 77

D. Respiratory Drugs ................................................................................................ 78Table: Bronchodilators ....................................................................................... 79

E. Sedation, Analgesia and Muscle Relaxants ......................................................... 80Table: Sedation Levels ....................................................................................... 80Table: Sedatives / Analgesics ............................................................................. 82Table: Muscle Relaxants .................................................................................... 84

F. Anticoagulation ................................................................................................... 85Table: HITS Probability Score �– �‘4T Score�’ ...................................................... 88Table: Anticoagulants ......................................................................................... 89Table: Heparin Infusion Protocol ....................................................................... 90Table: Lepirudin Infusion Protocol .................................................................... 90Table: Age Adjusted Warfarin Loading Protocol* ............................................. 91

G. Endocrine Drugs .................................................................................................. 92Flowchart: Blood Glucose Management in ICU ................................................ 93Table: Insulin Infusion Protocol ......................................................................... 93Flowchart: Insulin Protocol for Patients Discharged from ICU ......................... 94Table: Steroid Doses / Relative Potencies .......................................................... 96

H. Renal Drugs - Diuretics ..................................................................................... 97Table: Diuretics .................................................................................................. 98

I. Gastrointestinal Drugs ......................................................................................... 99Table: GI Drugs ................................................................................................ 100

J. Antibiotics ......................................................................................................... 101Table: Vancomycin Dosing Schedule .............................................................. 104Table: Antibiotic Infusion Schedules ............................................................... 105Table: Peri-operative Antibiotic Prophylaxis ................................................... 107Table: Perioperative Endocarditis Prophylaxis ................................................. 108Table: Empirical Antibiotics ............................................................................ 109Table: Antibiotics for Specific Organisms ....................................................... 111

PART 4 - FLUIDS AND ELECTROLYTES ........................................................................ 112A. Principles of Fluid Management in Intensive Care............................................ 112B. Nutrition ............................................................................................................ 114

Flowchart: Nutritional Therapy Protocol .......................................................... 116Table: Average daily requirements ................................................................... 118Table: Baxter TPN Solution Options ................................................................ 119

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C. Blood Component Therapy ............................................................................... 120Table: Guidelines for the management of an elevated INR ............................. 126Table: Xigris Dosing Schedule ........................................................................ 129Table: Blood Transfusion Reactions ................................................................ 131

D. Guidelines for the Management of Electrolytes ................................................ 132Table: Classification of Lactic Acidosis .......................................................... 140

PART 5 - CLINICAL MANAGEMENT ............................................................................. 143A. Cardiopulmonary Resuscitation ........................................................................ 144

Flowchart: Basic Life Support ......................................................................... 144Flowchart: Advanced Life Support .................................................................. 145Flowchart: Paediatric Cardiorespiratory Arrest ............................................... 146

B. Induced Hypothermia Post Cardiac Arrest ........................................................ 147C. Failed Intubation Drill ....................................................................................... 148D. Respiratory Therapy .......................................................................................... 150

Table: Oxygen Delivery Devices ...................................................................... 150E. Management of Cardiothoracic Patients ........................................................... 167F. Renal Failure ..................................................................................................... 171

Diagram: CVVHDF Circuit ............................................................................. 177G. Neurosurgical protocols .................................................................................... 180

Flowchart: Cerebral Perfusion Pressure Algorithm .......................................... 183World Federation of Neurosurgeons Classification .......................................... 184

H. Microbiology Protocols ..................................................................................... 189I. Drug overdose ................................................................................................... 197

Flowchart: Approach to the unconscious, undetermined overdose ................... 200Graph: Modified Rumack-Matthew Nomogram .............................................. 202Table: N-Acetylcysteine Administration ......................................................... 203

K. Bites and Envenomation ................................................................................... 211K. Limitation of Therapy ....................................................................................... 211L. Brain Death and Organ Donation ...................................................................... 212

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PART 1 - ADMINISTRATION

A. Staffing - Royal Adelaide Hospital ICU 1. Consultant Medical Staff

Director A/Prof Rob Young Deputy Director Dr Peter Sharley Director of Research A/Prof Marianne Chapman Supervisor of Training Dr Nick Edwards Consultants Dr Stuart Baker Dr David Clayton

Dr Adam Deane Dr David Evans Dr Mark Finnis A/Prof Arthas Flabouris Dr Ken Lee Dr Matt Maiden Dr Stuart Moodie Dr Richard Newman Dr Richard Strickland

Dr Mary White Dr Gerald Wong Dr Alex Wurm

2. Senior Nursing Staff

Nursing Director: Mr Ian Blight Clinical Services Coordinators: Ms Deb Herewane

Ms Ros Acott Ms Tracey Cramey Mr Steve Wills

Nurse Managers: Ms Ali Coventry Ms Heather Pile

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3. Administrative Staff

Administrative Manager Ms Emma Przibilla Team Leader / Roster Manager Ms Sherridan Clark Unit Secretary Ms Kristina Gabell Ward Clerks Ms Ann Kerr Ms Lisa Migliaccio

4. Registrars

a) Three levels of registrars are rostered in the unit: i) Senior Registrars: An advanced trainee in the College of Intensive Care

Medicine program (or equivalent training program) who has completed or near completed training. This person may take first call at night and the position gives experience of responsibility at a consultant level. The Senior Registrars also help manage the registrar roster, coordinate registrar presentations, coordinate simulator sessions and contribute to Unit teaching activities.

ii) Senior Trainees: Usually trainees in the College of Intensive Care Medicine (or equivalent) training program, who are rostered according to seniority and experience.

iii) Junior Trainees/RMOs: Vocational trainees, trainees in other programs (e.g. surgical, physician training, etc) or residents in general rotations.

b) Portfolios are determined by experience and rostering requirements. c) All registrars, except SRs, will rotate through Units A, B and C. d) Training positions at Royal Adelaide Hospital:

i) Intensive Care Positions The College of Intensive Care Medicine (was the Joint Faculty of

Intensive Care Medicine, ANZCA) has accredited the RAH as a C24 Unit for training for the fellowship in intensive care (FCICM).

Registered trainees may undertake their full 24 months of core training, required to complete advanced CICM training, in this ICU.

Registrars not enrolled in the above training scheme but wishing to gain further postgraduate experience in intensive care may apply for these positions. Applications including a current c.v. should be forwarded to Dr Alex Wurm. (alex.wurm@health.sa.gov.au)

Trainees enrolled in formal training programs are given priority of appointment.

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ii) Positions for non-intensive care trainees Rotations of registrars in these positions are made from the respective

specialty based training programs at the RAH. Anaesthesia trainees: 1 position (3 or 6 month term). Physician trainees: 1 position (3 or 6 month term). Surgical trainees: 1 position (3 or 6 month term). Emergency Medicine trainees: 2 positions (3 or 6 month term).

iii) Supervisors of Training at Royal Adelaide Hospital:

Intensive Care: Dr Nick Edwards Medicine: Dr S M Guha Anaesthesia: Dr I Banks Surgery: Mr P G Devitt Emergency Medicine: Dr R Dunn

B. Rostering and Job Descriptions

Table: Team Duties

0800 - 1900

ICU Team A Beds 1-12

Consultant Team A Manages Unit A

Senior Registrar A Manages Unit A, TPN

Registrar A1 (D1) Beds 1-6.

Registrar A2 (D2) Beds 7-12.

ICU Team B Beds 12-24

Consultant Team B Manages Unit B

Senior Registrar B Manages Unit B

Registrar B1 (D3) Beds 13-18

Registrar B2 (D4) Beds 19-24

ICU Team C Beds 25-34

Consultant Team C Manages Unit C

Registrar C1 (D5) Unit C, Beds 25-34.

Registrar C2 (D6)

Duty Intensivist Speed Dial 1650

Bed management, Ward consults

D7 registrar Consults, Code blue, TPN

Teaching Consultant Undergraduate and postgraduate teaching

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1830 - 0830

ICU 1st On-Call Consultant

Attends evening handover round. On-call for any problems overnight.

ICU 2nd On-Call Consultant Backs-up ICU 1st on-call when required.

Night Registrar 1 (N1) Beds 1-12

Night Registrar 2 (N2) Beds 13-24

Night Registrar 3 (N3) Beds 25-34

Night Registrar 4 (N4) Consults, Code blue calls. Oversees beds 1-34, allocates workload

Senior Registrar 1 First Consultant call Wednesday and Saturday

Senior Registrar 2 First Consultant call Thursday and Sunday

NB: The allocation of responsibilities overnight is at the discretion of the registrars present and should be established by mutual agreement between the registrars and consultant on call.

1. Roster Guidelines

a) Rosters are primarily designed to meet training and patient care requirements, taking into account overall staff numbers and skill-mix.

b) In addition, award requirements, occupational health & safety considerations, and individuals�’ preferences and requests are taken into account.

c) The system is not infallible �– if there is a problem with any aspect of the roster, please notify the ICU secretary as soon as possible.

d) Each roster covers a 4 week period, with the working week commencing on a Wednesday.

e) Rosters are usually posted two weeks in advance. f) Where possible you will be rostered more than two days-off following night

duty. g) The rostering system utilises a wide variety of different codes as set out in the

following table:

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Table: Registrar Shifts

Abbr Shift Description Times & Meal Breaks Hrs

SR Senior Registrar 08:00-18:00 1x 30min meal break 9.5

D8 Day shift: report to DI

D1,2 Day shift Unit A

08:00-19:00 1x 30min meal break 10.5

D3,4 Day shift Unit B

D5,6 Day shift Unit C

D7 Day shift: consults & Code blue

N1 Night shift Unit A

18:30-08:30 2x 30min meal breaks 13.0

N2 Night shift Unit B

N3 Night shift Unit C

N4 Night shift: consults & Code blue

A Annual, Study, Exam, Conference leave

@ Request

2. Requesting Shifts

a) Particular shifts or days off can be entered on a �‘request roster sheet�’ that is posted on the pin-up board opposite the medical staff pigeon holes.

b) The request sheet is collected on the date indicated on the top of the sheet. c) Requests should also be discussed with the ICU secretary.

(phone 8222 5325 or email: sherridan.clark@health.sa.gov.au). d) Some things to bear in mind when requesting shifts:

i) Requests can significantly complicate the roster and you should therefore exercise some restraint and not request your entire roster.

ii) If you need to request several shifts please indicate in red, which two are the most important and priority will be given to these requests.

iii) Requests cannot be granted if they disadvantage other staff, compromise skill-mix, or overall staffing numbers necessary for the shift.

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3. Changing/Swapping Shifts

a) If you wish to change a shift after the roster has been posted, you may do so with the following guidelines: i) Once the roster is posted, the onus is on the individual to arrange any shift

swaps and these must occur within the same roster period. ii) You should first endeavour to swap the shift with someone in the same

skill group so that the skill-mix is maintained for the shift. iii) You must speak to the ICU Secretary for approval (phone 82225325 or

email: sherridan.clark@health.sa.gov.au) and then note changes on the rosters posted in the ward and on the medical pin-up board.

4. Annual Leave

a) Annual leave for medical staff is on a �“first come - first served�” basis, so book leave as soon as possible.

b) Only 3 registrars can be on leave at any one time, so before filling in an application form check that leave is available with the ICU secretary.

c) Please contact the ICU Secretary if you have any questions or concerns about your roster at anytime.

d) Leave is in accordance with the SA Salaried Medical Officers�’ Award (5 weeks annual and 1 week study leave) and registrars are required to forward a signed copy of leave requests to the Senior Registrar for rostering purposes.

5. Sick Leave

a) If you are sick and unable to attend work, please contact both: i) The Duty Intensivist by day, or

Senior Registrar at night (SD: 1650), and ii) The Roster Manager - Mon-Fri (09:00-16:00)

b) If you can, predict an expected day or night of return to work. c) Mark your pay sheet accordingly as sick leave

C. Orientation 1. Registrars commencing duty within the unit at the main RMO changeover dates will

undergo a half-day orientation program. 2. This will include sessions from:

a) The Director of ICU (or delegate) b) The Director of Research c) Infectious Diseases / Clinical Microbiology d) The Acute Pain Service

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D. Weekly Programme Table: Weekly Unit Programme

Monday Tuesday Wednesday Thursday Friday 08:00 Handover round Handover round Handover round Handover round Handover round 09:00

Bedside round

Bedside round Bedside round Bedside round

Bedside round 10:00 11:00

ICU Grand Round ICU Grand Round 12:00 ICU X-ray meeting

Consultant meeting 13:00

Bedside round 14:00 Simulator Training Simulator Training

15:00 Audit Journal Club

Clinical Teaching (trainees) Trainee Tutorial

BICMed Course junior registrar

tutorial (non-trainees)

16:00

Registrar tutorial (all registrars)

17:00 18:30 Handover round Handover round Handover round Handover round Handover round

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E. Admission and Discharge Policies 1. Admissions Policy

a) Patients are managed by the ICU staff during their stay in ICU. b) Admission is reserved for patients with actual or potential vital organ system

failures, which appear reversible with the provision of ICU support. c) All admissions, including transfers and retrievals, must be approved by the

Duty Intensivist (SD: 1650). d) Retrievals must be discussed with the Consultant when the SR is on 1st call. e) Resuscitation or admission must not be delayed in imminently life threatening

cases, unless specific advanced directives exist and are clearly documented. f) Such admissions should be discussed with the Duty Intensivist ASAP. g) Patients are admitted to ICU under the �‘bed-card�’ of the original or taking clinic. h) Patients admitted via the retrieval service must be admitted under a parent clinic,

who should be notified of the patient�’s admission to the ICU. i) Clinics requesting elective postoperative surgical beds should book the bed at least

one day in advance and must confirm bed availability with the Duty Intensivist on the day of surgery, prior to anaesthesia commencing.

j) Admission disputes must be referred to the Duty Intensivist.

2. Discharge Policy:

a) All discharges should be: i) Approved by the responsible ICU consultant. ii) Discussed with the parent clinic prior to patient transfer, including any

ongoing or potential problems. iii) Transferred �“In hours�”

i.e. prior to 18:00 - unless specifically approved by a consultant. b) A discharge summary must be completed and a copy filed in the case-notes. c) All patients on insulin protocols should be referred to the Endocrine Unit prior to

discharge (preferably the day before) d) Patients discharged on TPN must be entered in the TPN folder in Unit A. e) Notify the Acute Pain Service of patients discharged under their care. f) Withdrawal or limitation of therapy is a consultant responsibility. g) Treatment limitation/non-escalation directives must be discussed with the patient

or patient�’s family, the parent clinic and clearly documented prior to discharge. h) Referral to the Palliative Care should occur pre-discharge where indicated.

3. Deaths Policy:

a) The duty ICU consultant must be informed of all unexpected deaths. b) The duty ICU registrar must ensure:

i) A death certificate is completed or the Coroner notified ii) The parent clinic or duty intern is notified iii) Referring doctors (i.e. GP�’s, other specialists / hospitals) are notified.

c) Where indicated, consent for a post-mortem should be obtained from relatives as soon as possible.

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d) The Coroner must be notified in all cases where death is:

i) A death in custody, e.g. police, corrections, mental health detention. ii) A death by unusual, unexpected, unnatural, violent or unknown cause. iii) A death during, as a result of or within 24 hours of a surgical, invasive or

diagnostic procedure, including the administration of an anaesthetic for the carrying out of the procedure. The following procedures are excluded:

The giving of an intravenous injection The giving of an intramuscular injection Intravenous therapy The insertion of a line or cannula Artificial ventilation Cardio-pulmonary resuscitation Urethral catheterisation The insertion of a naso-gastric tube Intra-arterial blood gas collection Venipuncture for blood collection for testing Subcutaneous injection or infusion

iv) The term �‘anaesthetic�’ means a local or general anaesthetic and includes a sedative or analgesic.

v) A death within 24 hours of being discharged from a hospital or having sought emergency treatment at a hospital.

vi) A death of a person under a �‘protected person�’ order under the Aged or Infirm Persons�’ Property Act 1940 or the Guardianship and Administration act 1993.

vii) A death in the course or as a result or within 24 hours of a person receiving medical treatment to which consent for that treatment has been given under Part 5 of the Guardianship and Administration act, 1993.

viii) A death of a child subject to a custody or guardianship order under the Children�’s Protection Act 1993.

ix) A death on an aircraft or vessel with a place in South Australia as its place of disembarkation.

x) A patient death in an approved treatment centre under the Mental Health Act 1993.

xi) A resident death in a supported residential facility licensed under the Supported Residential Facilities Act.

xii) A death in a hospital or treatment facility for the treatment for a drug addiction.

xiii) If no certificate as to the cause of death has been given to the Registrar of Births, Deaths and Marriages.

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F. Care for Patients Discharged from ICU for Terminal Care. 1. Preparation for discharge.

a) For the families of dying patients, moving from a familiar environment will add a level of anxiety and uncertainty, even if it will be to a quieter setting.

b) Handover to the ward treating team should be as comprehensive as possible, including a social as well as medical history.

c) Families should be supported to accept that there may still be uncertainty about the patient�’s course and the timing of death.

d) Families should be reassured that the focus will be on maintaining comfort. e) Levels of ongoing active support for the patient, e.g. IV or subcutaneous fluids

should be clarified between ICU staff, the Ward team and family members.

2. Symptom management in terminal care. a) Physical symptoms that should be considered in planning ongoing care are:

i) Pain �– either spontaneous or on movement ii) Agitation, restlessness iii) Respiratory tract secretions iv) In a conscious patient there may be other symptoms

e.g. nausea and vomiting, dyspnoea v) Prevention of seizures may be a relevant issue

b) If the patient is requiring either analgesia or sedation in ICU, these should be continued on discharge to the ward. i) Opioid infusions can be continued as subcutaneous infusions via a pump

(e.g. Graseby or equivalent) ii) If sedation is required, midazolam can be administered via subcutaneous

route as a continuous infusion, with an opioid if already in use. c) If the patient has not required regular opioid or sedation in ICU, the following

PRN orders should be in place prior to discharge: i) For pain:

Opioid naïve patient - e.g. morphine 2.5-5mg s.c. 2 hrly prn Opioid tolerant - dose guided by background usage

ii) For agitation, restlessness: Midazolam 2.5mg - 5mg s.c. 1 hrly prn

iii) For management of secretions: Hyoscine hydrobromide 400 µg s.c. 3-4 hourly prn Atropine 600 µg s.c. 3-4 hourly prn

3. Where appropriate, formal consult and involvement of the Palliative Care Service is

encouraged.

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G. Clinical Duties in the ICU 1. Infection Control in ICU

a) Prevention and containment of nosocomial infection is a fundamental principle of effective medical practice.

b) The critically ill patient is highly vulnerable to nosocomial infection, which results in significant morbidity, prolonged length of hospital stay, increased cost and attributable mortality.

c) It is the responsibility of every member of the health care team to ensure compliance with Hospital and Unit infection control policies. This may include reminding senior colleagues or visiting teams to conform to basic issues such as hand-washing or additional precautions.

d) Hand-hygiene remains the only established method of effective infection control and must be strictly performed by all members of the health care team: i) Aqium hand gel must be used by all staff:

Every time they enter or exit a patient�’s cubicle (defined as the line of the door or curtain of bed space.)

Before wearing gloves Before and after patient contact Before and after contact with a patient�’s environment

ii) Hand wash with soap where: Contact with blood or body fluids Hands are visibly soiled After removing gloves

iii) Hand wash with chlorhexidine: Prior to clinical procedures After contact with patients with multi-resistant organisms

e) Gloves i) Disposable gloves must be worn for all contact with patient�’s bodily fluids,

dressings and wounds. ii) Gloves must be disposed of within the patient cubicle on leaving

f) Plastic aprons are to be worn: i) With gross physical contact with the patient (e.g. patient turns) ii) For �“additional precautions�” (see below)

g) Additional precautions: i) The following patients require additional precautions:

Infection or colonisation with: a. Methicillin Resistant Staph. Aureus b. Vancomycin Resistant Enterococcus c. Multiresistant gram negatives d. Clostridium difficile

Burns Febrile neutropenia Immunosuppressed patients as directed by Infection Control

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ii) Unit C patients who are infective risks will normally be managed in either Unit A or B.

iii) An �“Additional Precautions�” sign is placed outside cubicles of patients identified as infective risks:

Red sign = patient has multi-resistant organism Blue sign = patient is immunocompromised

iv) New disposable gowns and gloves must be used for each person entering the cubicle and disposed of within the cubicle upon leaving.

v) Consumable stock within the cubicle should be kept to a minimum. vi) Notify appropriate staff if patients are transported to theatre, for diagnostic

procedures, or for ambulance transport. vii) Once the patient has been transferred or discharged, the area should remain

vacant until �“terminally cleaned�” in accordance with RAH policy. viii) Environmental swabbing in Intensive Care is conducted as required by

Infection Control staff. h) Aseptic technique

i) Aseptic technique is to be used for all patients undergoing major invasive procedures (refer to procedures section).

ii) This includes: Hand disinfection: surgical scrub with chlorhexidine for >1 minute Sterile barrier: full gown, mask, hat, gloves and sterile drapes. Skin prep with chlorhexidine 2% in 70% alcohol: let the skin dry.

i) Sharps disposal i) The person performing the procedure is responsible for disposal of all

sharps (needles, blades) using the sharp disposal containers. ii) Nursing staff are not responsible for disposal of sharps after a medical

procedure. j) �“Traffic control�”

i) Movement of people through the unit should be kept to a minimum. This applies equally to visiting clinics and large numbers of relatives.

ii) All visitors are expected to conform to the above infection control measures and should be tactfully reminded or instructed when necessary.

k) Nominated isolation/quarantine rooms for highly contagious patients: i) Rooms 3, 4, 5 & 6 - shared air-conditioning ii) Rooms 21 & 22 - sealed, independent, negative pressure A/C units.

2. Guidelines for admission of a new patient to ICU

a) Handover from the referring doctor. Obtain as much information as possible. b) Primary survey:

i) Ensure adequate airway, breathing and place the patient on a FiO2 = 1.0 until a blood gas is done.

ii) Check circulation and venous access. c) Notify the duty consultant. d) Secondary survey: fully examine the patient. e) Document essential orders:

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i) Ventilation ii) Sedation / analgesia iii) Drugs, infusions iv) Fluids

f) Outline the management plan to the nursing staff. g) Secure appropriate basic monitoring/procedures:

i) SpO2 ii) ECG iii) Arterial line iv) IDC, nasogastric tube v) CVC for the majority

h) Basic investigations as indicated: i) Routine biochemistry, blood picture and coagulation studies ii) Group and screen. iii) Septic screen/microbiology. iv) Arterial blood gas v) ECG vi) CXR (after placement of appropriate lines)

i) Advanced investigations: CT, angiography, MRI, etc j) Advanced monitoring where indicated: e.g. PA catheter, ICP, PiCCO. k) Document in case notes. (See below) l) Notify the parent clinics of patients admitted directly to ICU

NB: this applies particularly to patients who have been retrieved. m) Clinic Interns and RMOs should clerk hospital admissions direct to ICU. n) Inform and counsel relatives.

3. Daily management in ICU.

a) Daily investigations: i) Routine blood tests (U&E, LFT, Mg, Hb, WCC, Plts, ABG) are ordered on

the daily flow chart and signed for on the 11:00 am fluid round. ii) Coagulation studies, drug levels or other tests are requested as required and

may also be requested on the daily flow chart. iii) The night duty nurses take the bloods at 06:00 and complete the request form,

which must be signed by the night registrar. iv) Registrars are responsible for taking blood specimens:

When nursing staff request assistance. For blood transfusion - the requesting registrar must ensure that the

labelling of the request form and the specimen matches the patient�’s wristband.

v) Chest x-rays are ordered after the morning handover round via OACIS. Routine daily chest x-rays are not performed in ICU Chest x-rays are performed

a. On admission to ICU (beds 1-24) b. Following invasive procedures:

i. Endotracheal intubation

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ii. Complicated percutaneous tracheostomy iii. CVC placement (subclavian or jugular) iv. Nasogastric or IABP placement

c. Suspected pneumothorax d. At the discretion of the attending doctor

b) Handover ward rounds are at 08:00 and 18:30. These are brief business rounds to handover essential information to the next team (either day or night) and are attended by the duty consultant, team registrars and senior nursing staff.

c) Liaison with parent clinics is essential to ensure continuity of management. Clinics must be informed of significant changes in a patient�’s condition or the requirement for specialist investigations or interventions.

d) Complex investigations (e.g. CT, MRI scans) and procedures should be authorised by the duty consultant and discussed with the parent clinic where appropriate.

H. Documentation The following guidelines are designed to facilitate the recording of clear, relevant information that is essential for continuity of care, audit and medico-legal review. Entries should establish a balance, being concise but still accurately recording all relevant information and events. Specific documentation required by ICU registrars includes:

1. Admission note for all patients admitted to ICU (Units A, B & C) 2. Daily entry in case notes during admission. 3. Handover summary 4. Discharge summary 5. Death certificates.

1. Admission Notes

a) All patients admitted to Units A & B must have a detailed admission summary. i) The admitting clinic must be notified, by the admitting registrar, and

invited to record an admission summary for patients admitted directly to ICU. This is to ensure that clinics are aware when a patient has been admitted under their bedcard.

ii) The admission note should incorporate all relevant aspects of the patient�’s medical history, clinical examination and results of appropriate investigations.

b) Complicated Unit C patients require the same level of detail as Unit A & B patients.

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c) Routine postoperative short stay patients in Unit C do not need detailed admission notes. In these patients record: i) Relevant operative & anaesthetic details ii) Significant comorbidities and history iii) Anticipated problems iv) Procedures e.g. epidural, invasive monitoring, TPN

2. Daily case-note entries

a) A daily entry must be made in the case notes.

i) Notes are most efficiently recorded after the 11:00 ward round so that current results and management plans are recorded

b) Additional notes must be made for the following: i) Significant changes in physical condition necessitating changes in

management, e.g. renal failure requiring dialysis. ii) Invasive procedures, e.g. laparotomy, tracheostomy, PAC/CVC insertion iii) Results of specific investigations or tests, e.g. CT scans, endocrine tests iv) Changes in policy, e.g. non-escalation of treatment, advance directives.

3. Handover summary

a) Due to the large number of complex patients, an ongoing handover summary

should be established for each patient b) This facilitates ease of handover between day and night resident staff and for the

duty consultant staff. c) This is not a formal casenote, nor does it take the place of a thorough review of

each patient and their casenotes. Meant to be an aide-mémoire to be updated each shift.

d) This is stored in a specific ICU database available on the PCs in the ICU.

4. Discharge summary

a) All patients transferred from ICU (Units A/B/C) require a Medical Transfer Summary (MR 42) form completed.

b) This is a single page document outlining all relevant transfer information. c) The original should be filed in the case notes and a photocopy placed in the

marked box in the Unit B station for filing by the secretary. d) The duty registrar on the day of transfer is responsible for completing the form. e) Incomplete or missing summaries will be forwarded to the responsible registrar

for completion. f) Short term Unit C patients do not require detailed discharge summaries, only

pertinent information relating to their stay.

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5. Death certificates

a) The following forms need to be completed: i) RAH Notification and Certification of Death (MR 150.2)

all patients including those reported to the Coroner ii) Death Certificate ("the yellow form")

do not complete this for deaths reported to the Coroner iii) First Medical Certificate

do not complete this for deaths reported to the Coroner b) Deaths notifiable to the Coroner:

i) Contact the Coroner�’s office and provide preliminary demographic details of the deceased.

ii) The Coroner�’s office will then fax the Medical Practitioner�’s Deposition form for you to complete and return by fax.

iii) File the original deposition in the patient�’s case-notes. I. Consent in ICU 1. Competent patients:

a) All competent patients undergoing invasive procedures should have a standard RAH consent form (MR: 60.16) completed and signed by the patient.

2. Incompetent patients (sedation, coma or encephalopathy):

a) Third party consent is not necessary for routine ICU procedures, including: i) endotracheal intubation ii) arterial lines iii) central venous lines iv) pulmonary artery catheters v) transvenous pacing wires vi) underwater seal drains vii) jugular bulb catheters viii) intra-aortic balloon counterpulsation ix) oesophageal tamponade tubes x) bronchoscopy

b) However, relatives should be informed prior to the procedure if present. c) The indications, conduct and complications of the procedure should be

documented in the casenotes. d) Major invasive procedures such as percutaneous tracheostomy, coronary

angiography, permanent pacemaker insertion or major surgical procedures require completion of a consent form: i) Emergency procedures signed by two doctors ii) Non-urgent procedures by third party consent (next-of-kin).

e) Ultimate responsibility for consent lies with the operator performing the procedure. ICU staff are not responsible for consent for procedures performed outside of ICU, e.g. surgical tracheostomy, or PICC lines placed in radiology

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f) A person, not necessarily next-of-kin, who has been nominated by the patient as a medical power of attorney may sign or refuse consent on behalf of the patient.

g) Relatives should always be informed of any non-routine procedures and the consent issue explained, irrespective of the presence or absence of a medical or legal power of attorney.

h) If relatives cannot be contacted, emergency life saving treatment should proceed immediately, with discussion with the Duty Consultant.

J. ICU Ward Rounds 1. Grand rounds held on Mondays and Fridays are an integral feature of the running of

the unit. This is an open, multi-disciplinary meeting to discuss management issues and is a valuable teaching forum. Current x-rays and investigation results are displayed via computer projection.

2. The ward round is attended by: a) Team A, B, C and Duty ICU consultants and all floor registrars b) An infectious diseases consultant c) Senior nursing staff d) Physiotherapists e) A pharmacist f) A dietician g) Invited clinics when appropriate h) Medical students

3. Registrars are expected to present their allocated patients at this round and to actively

participate in the discussion. 4. Presentations at this round should be of a standard suitable for a fellowship

examination: a) Presentation should take no more than 5 minutes. b) Emphasise the relevant and pertinent issues only:

i) Patient details and demographics. ii) State day of ICU admission (e.g. Day 6 ICU). iii) Diagnosis or major problems. iv) Relevant pre-morbid history pertinent to this admission. v) Relevant progress and events in ICU

(deterioration/improvement, procedures, investigations). vi) Current clinical status (system by system). vii) Outline features on daily pathology and radiology. viii) Current plan of management:

Medications Further investigations / procedures Discharge planning & prognosis

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5. Bedside patient rounds

a) Are held daily, including grand-round days, at the discretion of the duty consultant. b) Team consultants and registrars review each patient�’s condition. c) Unit A&B flowcharts are re-written daily and include orders for ventilation,

procedures, medications, infusions and fluid therapy. i) To ensure all aspects of patient care have been considered, the

�“FATDOGS�” algorithm should be considered in all patients: F - Feeding & fluids A - Analgesia & sedation T - Thromboprophylaxis D - Drugs �– therapeutic & usual O - Oxygen & ventilation G - Glucose control S - Sit out of bed

ii) You need to either write up each one of these each day or have a reason why you have not.

d) Printed stickers should be used for routine medications and infusions. e) All orders must be signed by a doctor. f) Requests for routine blood tests are made on the chart. g) Patients transferred to Unit C or to the wards must have the hospital �“blue

folder�” completed. As a general rule, all medication orders are re-written and fluid or nutrition orders for the next 24 hours are prescribed. Patients started on TPN should have their details entered in the �“TPN folder�” kept in Unit A.

h) Similarly, Unit C patients have their charts reviewed, however all medications and fluids are recorded on the hospital blue treatment folders.

K. Clinical Duties Outside of the Intensive Care Unit 1. Policy regarding outside consults:

a) NB: The Unit must not be left unattended at any time to attend outside calls. (i.e. at least one registrar must remain on the floor)

b) The consults and code-blue/trauma pagers are carried by the Consults Registrar (D7) during the day and Night Registrar 4 overnight (this may be modified at the discretion of the 1st on-call consultant / senior registrar).

c) All consults should be addressed as soon as possible. d) If the ICU workload is heavy, refer ward consults to the DI, who will delegate

appropriately. e) Notify the senior nurse and fellow registrar(s) when leaving the floor. f) The following duties accompany the Consults pager (pager no #89 1122*):

i) Ward consults ii) Requests for Total Parenteral Nutrition (refer to DI) iii) Requests for retrieval (refer to MedStar)

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g) The following duties accompany the Emergency pager (#33) i) Code blue calls | ii) Escalated MET calls | *see (4) below. iii) Trauma (P1) resuscitation

Trauma pages are subdivided into levels Attendance by the ICU registrar is only required for Level 1 calls.

h) All consults/MET calls potentially requiring admission to ICU must be discussed with the Duty Intensivist (DI).

2. Ward Calls

a) Consults regarding potential admissions from the general wards, theatre, ED. b) Pre-operative consults for potential or booked surgical patients. c) Advice regarding fluid and electrolyte management, oxygen therapy, sedation and

analgesia (usually referred to APS). d) Review as requested patients in the:

i) Spinal Injuries Unit with potential respiratory failure. ii) Burns Unit for airway / breathing assessment, IV access or resuscitation.

e) Requests for venous access: i) Requests must come from registrar level or above and after reasonable

attempts have been made to obtain IV access. ii) Radiology provide a PICC line service in working hours. iii) CVCs are not to be inserted on ward patients.

f) Requests for TPN.

3. Total Parenteral Nutrition (TPN)

a) ICU provides a TPN service for the hospital. b) Requests for TPN are elective (i.e. Mon to Fri: 0800-1800) and should be made

according to recommended indications. c) Requests are made via the DI or consults registrar. d) The �‘TPN Folder�’ is kept in the Unit A ward station. e) The Team A Senior Registrar and Consultant will manage:

i) Initial consultation with the requesting clinic. ii) Recording TPN patients in the �“TPN Folder�”. iii) Insertion of a PICC catheter. iv) Daily:

Review of electrolytes and fluid balance, Review of the central venous catheter/PICC, Prescription of TPN orders ± vitamins / trace elements, Issue a request form for serum electrolytes. Use pink labels from ICU & leave a spare for labelling of specimen tubes

- this ensures priority in the lab f) The Unit A Senior Registrar is responsible for TPN on the weekends. g) Refer to the section on nutrition in the clinical protocols for indications &

complications.

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4. Code Blue & MET Calls

a) The RAH medical emergency code is �“33#�”. i) Upon dialling 33#, switchboard automatically page the following people:

ICU registrar ICU equipment nurse Medical registrar

b) These calls are divided into: i) Code Blue *all calls must be attended immediately

Cardiac &/or respiratory arrest (actual or impending) Threatened airway Major haemorrhage

ii) MET calls Significant clinical deterioration (see MET criteria) MET calls are not routinely attended by ICU Registrars. The ICU Registrar should remain immediately available if a MET call

has been activated, so that assistance can be provided to the MET team if required (e.g. avoid starting procedures such as CVC insertions if the MET pager has activated).

c) When �“33�” is displayed on the pager: i) Dial �“33#�” on an internal phone. ii) Switchboard will then state the location of the arrest. iii) Clearly state who you are (i.e. ICU registrar) and go to the location.

d) Ensure that the ICU staff know where you are going and that the Unit is not left unattended.

e) At the emergency: i) This hospital follows the Australian Resuscitation Council guidelines for

cardiopulmonary resuscitation (refer to flowcharts for basic and advanced life support in the clinical protocols)

ii) The ICU/resuscitation registrar is responsible for initial assessment, securing the airway and establishing effective ventilation.

iii) Basic life support is done by attending nursing and medical staff and may be directed by either ICU or medical registrar.

iv) Advanced life support is directed by the more senior registrar present. This is usually the ICU registrar.

v) Depending on the outcome of the Code Blue, the patient may be admitted to ICU, CCU or remain on the ward according to standard admission policies.

vi) As a general rule, it is better to admit a patient if previous details are not immediately available than to prematurely abandon resuscitation.

vii) Document your involvement with the resuscitation in the casenotes. viii) The home team should be involved or at least informed of their patient�’s

condition, including when resuscitation is unsuccessful.

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5. Trauma Calls

a) As in cardiac arrest, a �“33#�” call is activated for trauma patients who meet specified trauma criteria. (Refer to trauma directives.)

b) Trauma pages will appear as 2 Levels: i) Level 1: major trauma requiring immediate attendance / airway support ii) Level 2: trauma requiring full assessment in ED/Resus.

c) The following people are paged and the level response detailed on the pager: i) ICU/resuscitation registrar ii) Trauma Service registrar iii) Accident and emergency registrar

d) On receiving a Level 1 call the ICU registrar should proceed directly to Resus in the Emergency Department (ED)

e) Ensure that ICU staff know where you are going and that the Unit is not left unattended.

f) At the trauma resuscitation: i) This hospital follows the Early Management of Severe Trauma (RACS)

guidelines. ii) The team leader is designated by the current Trauma Service Directive (found

on the wall in Resus). iii) Role of the ICU registrar:

Primarily as a backup for acute life threatening situations in the event that sufficiently experienced personnel are not available in Resus.

If anaesthetic staff are present in Resus, there is no requirement for ICU registrars to attend the resuscitation unless specifically requested by these personnel or the Trauma Director.

If anaesthetic staff are not immediately available, the following role is indicated until appropriate personnel arrive: a. Initial airway assessment and management. b. Establishing effective ventilation c. Assistance with vascular access and restoration of circulation. d. Other acute interventions (e.g. UWSD) as required

Once anaesthetic & trauma team members are present and the situation is under control, return to ICU: do not leave ICU unattended for lengthy periods of time.

If prolonged resuscitation is anticipated, call in the ICU or Trauma Consultant and/or delegate to the anaesthetic/resuscitation registrars if necessary.

Transportation of trauma patients to CT scan, angiography etc is the responsibility of the emergency anaesthetic staff.

ICU registrars must not do prolonged intra-hospital transports for trauma patients without approval by the duty ICU consultant.

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iv) General principles: Document your involvement with the resuscitation in the casenotes Once the primary survey is completed, proceed to the secondary survey

and order the appropriate investigations - generally all patients need lateral C-spine, chest and pelvis X-rays, group and cross-match. This is coordinated by the Trauma team leader.

In critically ill patients, ensure that a suitably qualified person (in terms of resuscitative skills) remains with the patient at all times. This is mandatory if the patient is transported from Resus (e.g. to radiology, ICU, theatre).

Notify ICU staff of pending admissions. Demarcation disputes are referred to the duty Trauma Consultant.

6. Retrieval Requests

a) Requests for consultation may originate from a number of sources. Namely,

i) The DI phone (SD: 1650) ii) Other ICU telephones iii) ICU registrar pager iv) Other clinics who have been consulted by outside medical officers.

b) All retrieval requests should be referred immediately to the state retrieval service, MedStar on 82224222.

c) All requests from MedStar for the transfer of patients to the Royal Adelaide Hospital must be referred to the on-call ICU consultant.

7. Intrahospital transportation of Intensive Care patients

a) All transports must be authorised by the duty ICU consultant. b) The transport/investigation must be considered in the best interests of the patient. c) All ventilated and potentially unstable transports need a medical escort. d) Stable, self-ventilating patients may be transported by an ICU RN e) If ICU nursing staff are concerned, then a medical escort is required. f) At no stage must the unit be left uncovered. g) If the Unit is busy, or transports clash with ward rounds, other personnel may be

deployed to do the transport. This is coordinated by the duty ICU consultant. h) As a general rule, ICU staff are responsible for transportation of ICU patients. i) Anaesthesia is responsible for transport of the following ICU patients:

i) Trauma resuscitation patients ii) Patients to and from theatre iii) Patients to and from hyperbaric medicine.

j) The transport of patients undergoing prolonged investigations or treatments, (e.g. MRI, angiographic embolisation, invasive radiological procedures, TIPS) should be discussed with the Duty ICU consultant and Duty Anaesthetist (SD 1175)

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k) Guidelines i) Registrars must familiarise themselves with transport monitors, portable

ventilators and infusion pumps. ii) Inform and discuss the transport with the nursing staff as soon as possible. iii) Patients must be appropriately monitored during the transport and

observations recorded on the flow chart. iv) Document any problems which may occur during transport. v) Ensure that the results of investigations performed (e.g. CT scans etc) are

recorded in the case notes by the appropriate person.

L. Hospital Emergencies 1. The emergency number is 33# : state the nature and location of emergency 2. Fire

a) A copy of the hospital emergency procedures (fire, smoke, bomb-threat) is kept in the P4A and P4C nursing stations.

b) The chief fire and emergency officer is the overall controller during a fire or smoke emergency (code red).

c) Become familiar with the location of fire exits, extinguishers and blankets in the Unit. i) Unless a fire is small and easily contained do not attempt to fight the fire

yourself. ii) Remove yourself from the immediate vicinity of the fire, alerting other staff

members as indicated, and position yourself behind the automatic fire doors. iii) The MFS has a 3 minute response time to the RAH. iv) Wait for the arrival of the Fire Chief and assist in any patient

movement/evacuation only as indicated by the Fire Chief. d) Role of medical staff:

i) There is no place for �“heroic�” action. Ensure your own safety first. ii) Wait for the arrival of the MFS. iii) Assist in patient assessment/management under the coordination of the Fire

Chief. iv) In the event of a significant fire / smoke hazard, staff will only re-enter the

danger zone in the immediate company of a MFS fire-fighter, with appropriate breathing apparatus.

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M. Research in ICU 1. Personnel:

a) Director of Research �– A/Prof. Marianne Chapman b) Clinical Research Manager �– Stephanie O�’Connor c) Research nurses �– Justine Rivett, Danila Peake

2. Statistical and computing advice is available through ICU Research from the University of Adelaide (Dept. Public Health).

3. Members of the medical and nursing staff are encouraged to become involved in

research during their stay in the Unit. Registrars are expected at least to obtain consent for ongoing studies as part of their responsibilities within the unit. Knowledge of these studies can be obtained from either the Director of Research or the Clinical Research Manager. Further involvement is encouraged and there are supports within the unit to facilitate research to occur.

4. There are broadly 3 types of research projects occurring in the unit:

a) Drug company sponsored projects b) Locally initiated projects (supported by funding from �‘a�’) c) Studies performed with the ANZICS Clinical Trials Group (see below).

5. Completed research projects should be presented at either a local or interstate

scientific meeting. Some funding is available for both nurses and medical staff who present work at any meeting. a) Applications should be made to the Coordinator of Research. b) Eligible meetings include, but are not limited to:

i) ANZICS / ACCCN Annual Scientific Meeting - held in October. Abstracts must be sent by July. Free papers/posters Prizes are awarded for:

a. Best medical and nursing free papers b. Best medical and nursing reviews c. Best poster d. Best paper by a FCICM trainee (Matt Spence Medal).

ii) CICM ASM: free papers. Annual - June. iii) Thoracic Society of Australia and New Zealand: Annual - March. iv) ICE (Institute of Continuing Education), ACCCN Conference. Annual �–

May. c) Further details can be obtained from the Director of Research and the Clinical

Research Manager.

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6. Most projects require prior RAH Research Ethics Committee approval: a) Submission dates and a pro forma may be obtained from the Clinical Research

Manager. b) If the study involves drug administration then it must first go to the

Investigational Drugs Subcommittee. c) A copy of the ethical approval letter and protocol must be given to the Clinical

Research Manager. The Clinical Research Manager will also keep details of progress of research projects.

7. Further information:

a) Facilities are available in the Adelaide University Department of Anaesthesia and Intensive Care for laboratory work. There is an animal laboratory performing predominantly pharmacokinetic & pharmacodynamic studies. Resource persons: Prof Guy Ludbrook or Dr Matt Maiden.

b) ICU database. We have a database extending back many years containing data on all intensive care patients (excluding Unit C). This includes demographics, illness severity scores and outcomes. We also have access to a national database. We also collect other data locally. Resource person: Dr Mark Finnis.

c) ANZICS Clinical Trials Group. There is a national clinical trials group to facilitate multicentre trials in Australia. The group is open to all interested parties and proposals for multicentre trials can be presented for consideration. Meetings twice per year April and October. Resource person: A/Prof. Marianne Chapman.

N. Information Technology in ICU

a) All consultant and registrar offices and the Registrar Teaching Room are equipped with PCs, connected to the RAH local area network (LAN).

b) Facilities available through the LAN include: i) Intranet e-mail accounts ii) WWW browsing facilities (available on application). iii) Intranet resources, which are being continuously expanded:

UpToDate® An extensive range of electronic text books Internal telephone and Australian business directories Medline via �‘OVID�’ ICU Handover Database

iv) On application registrars will be allocated a username, which will carry with it an �‘Internet�’ e-mail account for the duration of their stay.

c) In addition, many of the consultants have access to the University of Adelaide, including Barr-Smith Library resources.

d) The Unit has an internet presence at http://www.icuadelaide.com.au/ e) NB: Use of hospital computers to access inappropriate material is not tolerated.

RAH guidelines detail appropriate use.

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PART 2 - CLINICAL PROCEDURES A. Introduction 1. Registrars are encouraged to become proficient in all Intensive Care procedures. 2. Invasive procedures should be authorised by a senior registrar or the duty ICU

consultant. 3. Adequate familiarisation and supervision with unfamiliar procedures is essential:

there is always someone available to help. 4. The relative risk vs. benefit of all procedures must be carefully considered. 5. Do not persist if you are having difficulty with the procedure: call for help 6. Consent for procedures: *refer to Administration / Consent

a) Competent patients undergoing invasive procedures should have a standard RAH Consent Form (MR:60.16) completed and signed by the patient

b) Third party consent is not necessary for incompetent patients undergoing routine ICU procedures.

c) Major ICU procedures, such as percutaneous tracheostomy or enterogastrostomy, require third party or two-doctor consent.

7. Indications, conduct and any complications of the procedure should be clearly documented in the case notes, in addition to a consent form if this is completed.

8. Discuss the planned procedure with the attending ICU nursing staff and allow sufficient time for setting up of trays and equipment.

9. Remember: the nursing staff have extensive experience with these procedures. 10. It is the responsibility of the operator to discard all sharps used in the procedure and

to ensure that they are placed in a sharps disposal container. B. Procedures 1. Registrars are expected to become proficient in all routine procedures. 2. Specialised procedures are done either by the Duty Consultant or strictly under

consultant supervision. 3. Guidelines for the listed routine and specialised procedures are outlined in the

following sections.

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Routine ICU procedures

1. Endotracheal intubation 2. Peripheral venous catheterisation 3. Central venous catheterisation / PICC line insertion 4. Arterial cannulation 5. Pulmonary artery catheterisation 6. Urinary catheterisation 7. Lumbar puncture 8. Epidural catheterisation 9. Underwater seal drain insertion 10. Pleurocentesis 11. Peritoneocentesis 12. Nasogastric tube insertion Specialised ICU procedures

1. Percutaneous tracheostomy 2. Fibreoptic bronchoscopy 3. Transvenous pacing 4. Pericardiocentesis 5. Oesophageal tamponade tube insertion 6. Intra-aortic balloon counterpulsation 7. Extracorporeal Membrane Oxygenation C. Peripheral IV catheters 1. Indications:

a) First line IV access for resuscitation, especially blood transfusion b) Stable patients where a CVC is no longer necessary

2. Management protocol: a) Remove/replace all resuscitation lines inserted in unsterile conditions. b) Generally avoid peripheral IV use in ICU patients and remove if not in use. c) Use local anaesthesia in awake patients. d) Aseptic technique:

i) Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%) + gloves

ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) e) Dressing: adhesive occlusive (Opsite® or equivalent) f) Change / remove all peripheral lines after 48 hours. g) Avoid lower-limb placement in patients with vascular disease.

3. Complications a) Infection b) Thrombosis c) Extravasation in tissues

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D. Arterial Cannulation 1. Indications:

a) Routine measurement of systemic blood pressure in ICU b) Multiple blood gas and laboratory analysis c) Measurement of BP during transport of patients in hostile environments

2. Management protocol:

a) Remove and replace lines inserted in unsterile conditions as soon as possible. b) Brachial and femoral arterial lines should be changed as soon as radial or

dorsalis pedis arteries are available. c) Aseptic technique:

i) Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%) + sterile gloves

ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) d) Local anaesthesia in awake patients. e) Cannulae:

i) Arrow® radial or femoral kits (Seldinger technique). ii) 20G Insyte®. iii) Single lumen 20G CVC for femoral arterial lines.

f) Insertion sites �– in order of preference: radial > dorsalis pedis > femoral > brachial

g) The femoral artery may be the sole option in the acutely shocked patient. h) Secure with a StatLock® device. i) There is no optimal time for an arterial line to be removed or changed. j) IA cannulae are changed/removed in the following settings:

i) Invasive IA line is no longer necessary. ii) Distal ischaemia iii) Mechanical failure (overdamped waveform, inability to aspirate blood) iv) Evidence of unexplained systemic infection v) Evidence of local infection

k) Measurement of pressure: i) Transducers should be �‘zeroed�’ each nursing shift ii) Zero reference = the mid-axillary line, 5th intercostal space

l) Maintenance of lumen patency i) Continuous pressurised (Intraflo®) saline flush at 3ml/hr.

3. Complications

a) Infection b) Thrombosis c) Digital ischaemia d) Vessel damage / aneurysm e) Haemorrhage / disconnection

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E. Central Venous Catheters NB: Registrars should be familiar with the interpretation and limitations of haemodynamic variables derived from central catheters (CVC, PICCO and PAC) in critically ill patients. 1. Indications:

a) Standard IV access in ICU patients: i) Vasoactive infusions ii) Fluid administration (including elective transfusion) iii) TPN, hypertonic solutions (amiodarone, nimodipine, etc.)

b) Monitoring of right atrial pressure (CVP) c) Venous access for:

i) Pulmonary artery catheterisation (PAC) ii) Continuous renal replacement therapy (CVVHDF), plasmapheresis. iii) Jugular bulb oximetry. iv) Transvenous pacing.

d) Resuscitation i) Large bore peripheral IV line(s) are 1st line. ii) Standard lumen CVCs are not appropriate for acute volume resuscitation. iii) Consider using a PAC sheath if central access is required and adequate

peripheral access is unobtainable.

2. Management protocol: (applies to all types of CVC): a) Types:

i) The default CVC for all ICU patients is a Cook antimicrobial impregnated (rifampicin/minocycline) 7F 15 or 20cm 3-lumen catheter.

ii) Non-impregnated catheters inserted outside the ICU should be changed to an impregnated catheter according to clinical indication.

iii) Dolphin Protect® catheters are used for CVVHDF and plasmapheresis iv) Pulmonary artery catheter sheath (part of the PAC kit) v) Dress non-impregnated catheters with BioPatch®

b) Sites: i) Subclavian is the preferred site for routine stable patients, followed by

internal jugular. ii) Femoral access is preferable where:

Dolphin Protect® / CVVHDF Limited IV access (burns, multiple previous CVC�’s), A thoracic approach is considered hazardous:

a. Severe respiratory failure from any cause (PaO2/FiO2 < 150) b. Hyper-expanded lung fields (severe asthma, bullous disease) c. Coagulopathy (see below)

Inexperienced staff requiring urgent access, where supervision is not immediately available.

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c) Coagulopathic patients: i) INR > 2.0 or APTT > 50s correct with FFP and/or

prothrombinex ii) INR 1.5-2.0 or APTT 40-50s correct with FFP, or

use IJ or femoral approach iii) Platelets < 50,000 transfuse 1 pack (5U) platelets iv) Failure to increment platelet count after transfusion avoid subclavian v) Uncontrolled coagulopathy femoral approach or PICC vi) Check patient anatomy with ultrasound prior to the procedure.

d) Technique policy i) Use local anaesthesia in awake patients. ii) Strict aseptic technique at insertion:

Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%)

Sterile barrier: gown, sterile gloves, mask, hat sterile drapes (CVC - Patient Cover)

Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) iii) Seldinger technique or ultrasound guided insertion �– Sonosite® iv) U/sound guided insertion is preferred where:

There is an increased complication risk (e.g. bleeding, pneumothorax) Large bore catheter insertion. Distorted patient anatomy.

v) CVC Catheter lengths: 15cm - right subclavian or internal jugular 20cm - left subclavian or internal jugular, either side femoral

vi) Secure all lines with a StatLock® device or suture vii) Dressing: non occlusive dressing viii) Flush all lumens with saline. ix) Transduce pressure ASAP post-insertion to exclude arterial placement. x) Check CXR prior to use, except in urgent circumstances

e) Maintenance i) Routine IV administration set change at 7 days. ii) Daily inspection of the insertion site and clinical examination for infection

irrespective of insertion duration. iii) Catheters remain as long as clinically indicated and are changed when:

Evidence of systemic infection a. New, unexplained fever or WCC b. Deterioration in organ function c. Positive blood culture by venipuncture with likely organisms

(S. epidermidis, candida spp.), and/or Evidence of local infection - inflammation or pus at insertion site.

iv) Guidewire exchanges are actively discouraged. They may be indicated in the following situations, only after discussion with a consultant:

Mechanical problems in a new catheter (leaks or kinks) Difficult or limited central access (e.g. burns).

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v) Maintenance of lumen patency Central venous catheters (pre-printed on the patient flowsheet)

a. Flush unused lumens with 1ml normal saline 8 hourly Vascath: into each lumen 8 hourly (printed sticker)

a. Withdraw 2ml and discard. b. Flush with 2ml normal saline. c. Flush 1.5ml solution (5000U heparin/3ml = 2500U/lumen). d. NB: Each lumen has it�’s internal volume printed on it.

3. Complications:

a) At insertion i) Arterial puncture �– haematoma, thrombosis, embolism ii) Pneumothorax, haemothorax, chylothorax iii) Neural injury (phrenic, brachial plexus, femoral nn.)

b) Passage of wire/catheter i) Arrhythmias ii) Wire embolism - if this occurs, notify senior staff immediately iii) Perforation of SVC / RA - tamponade

c) Presence of catheter i) Catheter infection: rates increase under the following conditions:

Size of catheter - thicker catheters (PAC, Vascaths) Site of catheter - femoral > internal jugular > subclavian sites Number of lumens Nature of fluid through catheters - TPN or dextrose solutions

ii) Thrombosis, HITS secondary to heparin iii) Catheter / Air embolism iv) Knotting of catheters (esp. PAC) v) Pulmonary infarct / arterial rupture (PAC)

NB: Where CVC insertion presents a �“significant risk�” in a non-urgent situation, consider insertion of a PICC line as an alternative.

F. Urinary Catheters

1. Standard in all ICU patients 2. Management protocol:

a) Aseptic technique at insertion. i) Hand disinfection: surgical scrub with chlorhexidine for >1 minute ii) Sterile barrier: gloves and sterile drapes. iii) Skin prep: chlorhexidene 1%

b) Local anaesthesia gel in all patients. c) Only BiocathTM catheters should be inserted in ICU & changed 6 weekly. d) Standard Foley catheters should be changed to a BiocathTM after 14 days. e) Silastic catheters should be changed after 1 month. f) Remove catheters in anuric patients and perform intermittent catheterisation

weekly, or as indicated.

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G. Epidural Catheters 1. Indications

a) Post-operative pain relief (usually placed in theatre) b) Analgesia in chest trauma.

2. Management protocol:

a) Notify the Acute Pain Service of any epidural placed in ICU. b) Epidural cocktails should follow the Acute Pain Service protocols c) Strict aseptic technique at insertion. d) Daily inspection of the insertion site. The catheter should not be routinely

redressed, except under the advice of the APS. e) Leave in for a maximum of 5 days and then remove. f) Remove if:

i) Not in use for > 24 hours, or ii) Clinical evidence of unexplained sepsis, or iii) Positive blood culture by venipuncture with likely organisms

(S. epidermidis, candida). g) Heparin/Warfarin Protocol (also see �‘Acute Pain Service Guidelines for

Anaesthetists�’) 3. Complications

a) Hypotension from sympathetic blockade / relative hypovolaemia i) This usually responds to adequate intravascular volume replacement ii) Occasionally, a low-dose vasopressor infusion is required iii) If this is considered, occult bleeding must be excluded.

b) Pruritis, nausea & vomiting, or urinary retention (opioid effects) c) Post-dural puncture headache d) Infection: epidural abscess e) Pneumothorax (rarely)

4. NB: Further guidelines for the management of epidural catheters can be obtained

from �“The Acute Pain Service Guidelines for Anaesthetists�”. Manuals are stored in each ICU station.

H. PICCO Catheters 1. Introduction

a) PiCCO uses a combination of thermodilution and pulse waveform analysis to provide an estimate of cardiovascular status.

b) Trainees should become familiar with the theory of insertion, indications, interpretation and complications of PiCCO catheters.

c) Indicated in the assessment & response to therapy in shock states.

38

2. Technique a) A normal CVC line can be used. b) The peripheral arterial catheter is inserted into a femoral, brachial or axillary

artery using an aseptic Seldinger technique. c) The pulse waveform analysis of continuous cardiac output is calibrated by

thermodilution according to the device instructions. d) Calibration should be repeated once per nursing shift and as indicated. e) Additional measurements of Global End-diastolic Volume Index (GEDI) and

Extravascular Lung Water Index (ELWI) can be made via thermodilution. 3. Below are the normal values and a suggested decision tree from the manufacturer

which should be used as a guide only:

Table: PiCCO Values and Decision Tree

Variable Abbr. Normal Units Cardiac Index CI 3.0-5.0 l/min/m2 Global End-diastolic Blood Volume Index GEDI 680-800 ml/m2 Intrathoracic Blood Volume Index ITBI 850-1000 ml/m2 Stroke Volume Variation SVV 10 % Extravascular Lung Water Index* ELWI* 3.0-7.0 ml/kg

39

I. Pulmonary Artery Catheters

1. Policy a) Insertion of PA catheters must be authorised by the duty consultant. b) Trainees should become familiar with the theory of insertion, indications,

interpretation and complications of PACs. c) Insertion of a PAC must never delay resuscitation of a shocked patient. d) Allow sufficient time for nursing staff to set up insertion trays and transducers. e) Remove catheters once they are not being routinely used. They may be left in

situ for up to 7 days.

2. Indications: a) Haemodynamic measurements (CO/I, SV/I, SVR/I)

i) Aid to diagnosis and response to therapy of shock states, e.g. cardiogenic, septic or hypovolaemic

b) Measurement of right heart pressures (RAP, PAP): i) Acute pulmonary hypertension ii) Pulmonary embolism iii) Cardiac tamponade

c) Estimation of preload / left heart filling (PAOP) i) Intravascular volume status ii) LVF iii) Response to fluid loading

d) Measurement of intracardiac shunt: (Acute VSD) e) Derivation of oxygen delivery & utilization variables (VO2, DO2)

3. Management protocol: a) Insertion protocol as per CVC, with the following features:

i) Sheath introducer (8.5 Fr) with side port, haemostatic valve and plastic contamination shield.

ii) Shared transducer for RAP (proximal) and PAP (distal) lumens iii) Check competence of balloon and concentric position iv) Ensure all lumens are flushed with heparinised-saline prior to insertion. v) Ensure the system is zeroed and an appropriate scale (0-40mmHg) on the

monitor prior to insertion. vi) Insert the catheter observing changing waveforms (RA RV PA) on the

monitor, with the balloon inflated and locked, until catheter displays pulmonary artery occlusion tracing

Subclavian and left IJ ~ 50cm Right IJ ~ 40cm

vii) Deflate the balloon and ensure an adequate PA trace. Adjust catheter depth until a PAOP trace appears with 1-1.5ml air in balloon.

viii) Suture introducer and attach the contamination shield to the hub. ix) Apply a BioPatch® and non-occlusive dressing.

b) Ensure an adequate PA tracing is on the monitor at all times

40

c) �“Wedged�” tracings must be corrected as soon as possible: i) Flush distal lumen with 2ml N.Saline ii) Withdraw the catheter until a PA trace is visible

d) Measurement of pressures: i) Reference pressures to the mid-axillary line ii) Measure at end-expiration of the respiratory cycle iii) Do not disconnect ventilated patients to measure pressures. iv) Measurement of PAOP:

End expiration: lowest point in ventilated patients, highest point in spontaneously ventilating patients

Use the �“electronic cursor�” on monitors after 2-3 respiratory cycles. Do not use the electronic average of the wedge tracing.

e) Haemodynamic measurements i) These are routinely performed by the nursing staff, however registrars

should become familiar with the procedure. ii) Record all measurements in the flow chart in the results folder. iii) Cardiac outputs:

Injectate: 10ml 5% dextrose @ room temperature Inject at random times in the respiratory cycle Take > 3 measurements and ignore values > 10% from average.

iv) Derived variables: CO/CI and SVR are routinely charted (8 hrly or as indicated). Other variables including PVR(I), SV(I), L(R)VSWI are recorded in

the haemodynamics flowsheet. Mixed venous oxygen levels should be measured on a sample taken

from the distal (yellow) port. Oxygen saturation should be directly measured with co-oximetry.

Derived haemodynamic variables (see table), should be used in conjunction with clinical assessment.

4. Complications

a) Related to CVC cannulation (see CVC section) b) Related to insertion/use of a PAC

i) Cardiac perforation ii) Thromboembolism iii) Pulmonary infarction ~ 0-1.4% (2 persistent wedging) iv) Pulmonary artery rupture ~ 0.06-0.2% (mortality 50%) v) Catheter related sepsis vi) Endocarditis vii) Pulmonary valve insufficiency viii) Catheter knotting ix) Balloon fragmentation / embolism x) Tachyarrhythmias xi) RBBB

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Table: Standard Haemodynamic Variables

Variable Formula Normal range Cardiac index CO/BSACI 2.5-5 l/min/m2

Systemic vascular resistance SVRMAP RAP

CO79 9. 750-1500

dyn.sec/cm5/m2

Systemic vascular resistance index 79.9

CIRAPMAPSVRI 1400-2400

dyn.sec/cm5/m2

Pulmonary vascular resistance index 9.79

CIPAOPPAPmPVRI 150-250

dyn.sec/cm5/m2

Stroke volume index HRCISVI 33- 47 ml/beat/m2

LV stroke work index 0.0136SVIPAOPMAPLVSWI 50-120 g/m2 / beat

RV stroke work index 0.0136SVIPAOPmPAPRVSWI 25-55 g/m2 / beat

Arterial oxygen content CaO Hb SaO PaO2 2 2134 0 003. . 17-20 ml/100ml

Venous oxygen content CvO Hb SvO PvO2 2 2134 0 003. . 12-15 ml/100ml

Oxygen delivery index DO I CI CaO2 2 10 550-750 ml/min/m2

Oxygen consumption index VO I CI CaO CvO2 2 2 10 115-160 ml/min/m2

Oxygen extraction ratio O ERVO IDO I2

2

2 0.24-0.4

Shunt equation 010OvCOcC

CaOOcCQtQs

22

22 5-15%

End capillary oxygen content 0.003PAO1.01.34HbOcC 22 80-100 ml/100ml

Alveolar gas equation PAO FiO PaCO2 2 2760 47 125. 100-650 mmHg

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J. Pleural Drainage 1. Indications:

a) Pneumothorax b) Tension pneumothorax may require urgent needle thoracostomy c) Haemothorax d) Large symptomatic pleural effusion

2. Management protocol:

a) Needle thoracostomy (tension pneumothorax): i) 14 or 16G cannula placed in mid-clavicular line, 2nd intercostal space ii) Always place an UWSD following this procedure

b) Pleurocentesis: (pleural effusion) i) Prior to commencement, ultrasound the chest to confirm the presence of

fluid and indentify/mark an appropriate insertion site. ii) Strict aseptic technique at insertion:

Handwash with AVAGARD® (chlorhexidine 2%) or MEDISPONGE® (chlorhexidine 4%)

Sterile barrier: gown, sterile gloves, mask, hat sterile drape(s)

Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol) iii) Local anaesthesia in conscious patients. iv) Seldinger technique:

Pigtail catheter or ThalQuick® 12F kit. Insert guidewire through needle into pleural space Insert catheter into pleural space over wire Aspirate intermittently with closed system or attach to an UWSD.

v) Record volume removed and send for MC&S, cytology & biochemistry. vi) Check CXR post-procedure.

c) Underwater seal drainage: i) Local anaesthesia in awake patients. ii) Aseptic insertion technique - as above. iii) Site:

Mid-axillary line, 3-5th intercostal space Mid-clavicular line, 2nd intercostal space ( air only) Do not insert drains through old wounds

iv) ICU patients need large drains: 28F catheter or larger v) Use soft Mallinkrodt tubes in preference to the stiffer Argyle tubes vi) Remove the trochar from catheter: do not use the trochar for insertion vii) For the usual lateral ICD, go for the anterior or mid-axillary lines, avoid

the posterior sites as the chest wall is too thick, and there is a danger to neurovascular structures

viii) Make a 2-3cm skin incision parallel to the ribs (#10 or #15 scalpel)

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ix) Instruments & technique: Blunt dissect using short artery forceps, avoid long forceps. Do not plunge into the chest with either instrument. Access to the intercostal space is by careful blunt dissection of the

intercostal muscles above the rib below. The chest wall hole must be 2-3 cm wide in order that a finger can be

inserted into the pleural space to identify possible adhesions. The soft tube should be guided by the intrapleural finger so that the

tube goes in between the finger and chest wall x) Connect to an underwater seal drain apparatus xi) Insert 2 purse string sutures:

1 to fasten the tube 1 (�‘Z�’ or purse-string) to close the skin incision on drain removal.

xii) Dressing: occlusive dressing (Hypafix) xiii) Check CXR. xiv) Maintenance

Remove or replace drains inserted in unsterile conditions as soon as possible.

Leave the drain in situ until: a. Radiological resolution of pleural collection (air/fluid) b. No ongoing air-leak (no drain bubbling) c. Minimal drainage (< 150 ml/24 hrs).

Additionally, in ventilated patients, consider clamping drain for 4 hours and removing if the patient remains stable and/or post CXR.

Surgically placed drains are the responsibility of the surgeon and should only be removed in consultation.

3. Complications

a) NB: minimised using the blunt technique b) Incorrect placement - extrapleural, intrapulmonary, subdiaphragmatic c) Pulmonary laceration - haemorrhage, fistula d) Pneumothorax e) Bleeding

i) local incision, intercostal vessels ii) lung iii) IMA (with anterior placement) iv) Great vessels (rare)

f) Infection i) Soft tissue ii) Empyema

g) Mechanical (kinking, luminal obstruction)

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K. Endotracheal Intubation 1. Policy:

a) Endotracheal intubation in ICU patients is a high risk but vital procedure: i) Usually an emergency procedure, with limited time. ii) Usually indicated for acute respiratory failure, or associated with limited

respiratory reserve iii) Patients may have cardiovascular instability and significant co-morbidities iv) Patients may have cervical spine or oropharyngeal trauma / surgery v) Patients are at risk of vomiting and aspirating vi) Positioning is difficult.

b) Familiarisation with the intubation trolleys, equipment and drugs is essential. c) Intubation should ideally not be done as a sole operator procedure.

Skilled assistance should always be sought. d) If you are alone (i.e. after hours): call for help!

i) Expertise in intubation is always available. ii) Remember emergency anaesthesia staff.

e) The majority of ICU patients mandate rapid sequence induction. 2. Indications

a) Institution of mechanical ventilation b) To maintain an airway

i) Upper airway obstruction Potential e.g. early burns Real e.g. epiglottitis, trauma

ii) Patient transportation c) To protect an airway

i) Patients at risk of aspiration ii) Altered conscious state iii) Loss of glottic reflexes

d) Tracheal toilet 3. Techniques

a) Orotracheal intubation is the standard method of intubation in this unit. b) Nasotracheal intubation may be indicated where:

i) Patients require short-term ventilation and are intolerant of oral ET tubes. ii) Nasal Fibreoptic intubation may be indicated for:

Oro-maxillary surgery and pathology Inability to open the mouth:

e.g. intermaxillary fixation, TMJ trauma, rheumatoid arthritis. Upper airway obstruction and nasal route preferred

iii) Contraindicated in base of skull & LeForte facial fractures c) Methods:

i) Direct laryngoscopy, Airtraq® or Glidescope® after rapid sequence induction ii) Fibreoptic bronchoscopic awake intubation (oral or nasal) iii) Intubating laryngeal mask �– LMA �– Fastrac®

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4. Endotracheal Tubes a) Standard tube:

i) Low pressure, high volume cuff. ii) Males: 8mm secure at 21-23cm to incisors iii) Females: 7-8 mm secure at 19-21cm to incisors iv) Do not cut tubes to less than 26 cm length

b) Double lumen tubes: *rarely indicated in ICU: i) Unilateral lung isolation for bronchopulmonary fistula, abscess or

haemorrhage ii) These tubes should be inserted as a temporary manoeuvre prior to a definitive

procedure iii) Allow differential lung ventilation iv) Males: Left 41F v) Females: Left 39F vi) NB: right bronchial tubes harder to site. vii) Position should be checked with bronchoscope.

c) Intubated patients from theatre may have the following tubes that are not recommended for prolonged intubation. These tubes must be changed if intubation is anticipated > 48 hrs and if safe and feasible. i) Plain PVC tubes - no above cuff suction port ii) Armoured tubes - risk kinking & obstruction iii) RAE tubes - difficulty with suction & malposition

5. Protocol for endotracheal intubation in ICU

a) Personnel: i) Intubation is a 3-4 person procedure - skilled assistance is mandatory ii) The �“top end�” intubator coordinates the procedure iii) One person to administer drugs iv) One person to apply cricoid pressure (CP) post-induction:

This is routine for all emergency intubations CP is considered safe in the presence of suspected spinal injury. CP must be correctly applied - distortion of the larynx and difficulty in

intubation may occur if poorly applied. v) One person to provide in-line cervical spine immobilisation (trauma and

spinal patients only). b) Secure adequate IV access c) Equipment (kept in difficult airway & intubation trolleys in P4-A,B&C).

Ensure the following equipment is available and functional: i) Adequate light ii) Oropharyngeal airways iii) Working suction with a rigid (Yankauer) sucker iv) Self-inflating hand ventilating assembly and mask v) 100% oxygen, i.e. working flowmeter at 15 l/min vi) 2 working laryngoscopes (standard & long blades) vii) Magill forceps viii) Malleable introducer and gum-elastic bougie

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ix) 2 Endotracheal tubes Normal size + 1 size smaller Check cuff competence

x) Access to difficult intubation equipment. Be aware of the Failed Intubation Drill. Glidescope or Airtraq® Intubating Fastrach LMA Cricothyroidotomy equipment

a. Percutaneous kit or b. #15 scalpel & #6.0 cuffed ETT

d) Monitoring (on all patients) : i) SpO2, ETCO2, ECG ii) Invasive BP *desirable but not essential and must not delay intubation

e) Drugs i) Induction agent - propofol, fentanyl, ketamine, midazolam ii) Suxamethonium - 1-2mg/kg is the muscle relaxant of choice.

Contraindicated in: a. Burns > 3 days b. Chronic spinal injuries (i.e. spastic plegia) c. Chronic neuromuscular disease (e.g. GBS, motor neurone disease) d. Hyperkalaemic states. (K+ > 5.5)

Consider Rocuronium (1-2 mg/kg) if Sux. contraindicated iii) Atropine - 0.6-1.2mg available iv) Adrenaline - 10ml 1:10000 solution available

f) Procedure: Rapid sequence induction and orotracheal intubation

i) Pre-oxygenate with 100% oxygen for 3-4 minutes. ii) For patients on mask CPAP/NIV, pre-O2 with the NIV mask iii) Preload with 250-500ml IV crystalloid iv) Inotropes may be necessary after induction/intubation v) Induction agent + suxamethonium vi) Cricoid pressure applied vii) Direct visualisation of vocal cords and tracheal intubation viii) Inflation of cuff until airway sealed ix) Confirmation of ETCO2 x) Chest and gastric auscultation with manual ventilation xi) Cricoid pressure released xii) Secure tube at correct length xiii) Connect patient to ventilator (see default ventilator parameters) xiv) Ensure adequate sedation ± muscle relaxant

47

xv) Consider insertion of a naso/oro-gastric tube. Required by the majority of ICU patients. Insertion will avoid repeating the CXR.

xvi) Chest X-ray xvii) Confirm blood gas analysis and adjust FIO2 accordingly.

g) Sedation post-intubation:

i) None if comatose or haemodynamically unstable ii) Propofol and fentanyl as clinically indicated.

6. Maintenance of endotracheal tubes

a) Securing to face i) Secure ETT with white tape after insertion. ii) Ensure that the loop of tape is snug around back of neck but not too tight to

occlude venous drainage. Should allow 2 fingers under tape. iii) Re-secure with adhesive tape once CXR check done.

b) Cuff checks i) Volumetric (sufficient air to obtain a seal + 1ml) tests are done following

insertion and whenever a leak is detected with a manual hyperinflation once per nursing shift.

ii) Seal is assessed by auscultation over trachea during normal ventilation. iii) Manometric tests are inaccurate and do not correlate with mucosal

pressure. These are an adjunct only if cuff malfunction is suspected. c) Persistent cuff leaks

i) Tubes requiring more than 8ml of air to obtain a seal or if there is a persistent cuff leak must be examined by direct laryngoscopy as soon as possible even if taped at the correct distance at the teeth.

ii) Ensure that: The cuff has not herniated above the cords Tube has not ballooned inside the oral cavity and �“pulled�’ the cuff

above the cords. iii) Patients at high risk for cuff leaks:

Nasal RAE�’s - prone to outward migration Cut tubes - do not cut tubes < 26 cm Facial swelling - burns, facial trauma Patients requiring high airway pressures during ventilation

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7. Endotracheal tube change protocol a) Ensure adequate skilled assistance, equipment, drugs and monitoring as for de

novo intubation. b) Procedure

i) Set the FIO2 = 1.0 and change SV modes to SIMV. ii) Ensure sufficient anaesthesia and muscle relaxation (fentanyl / propofol +

neuromuscular blockade) iii) Perform laryngoscopy and carefully identify:

Patency of upper airway after suction Anatomy of larynx Degree of laryngeal exposure and swelling.

iv) IF clear view of larynx and no or minimal laryngeal swelling: Application of cricoid pressure by assistant and careful, graded

extubation under direct laryngoscopic vision. Maintain laryngoscopy and replace tube under direct vision.

v) IF impaired visualisation of larynx: Re-evaluate the need to change ETT Use gum elastic or ventilating bougie Place bougie through tube under direct vision and insert to a length

that would be just distal to the end of the ETT (approximately 30cm from end of tube)

Have an assistant control the bougie so that it does not move during movement of the endotracheal tube

Application of cricoid pressure by assistant and careful, graded extubation

Maintain laryngoscopy and ensure bougie is through the cords on extubation

Replace tube over bougie and guide through larynx under available vision.

Inflate cuff, check ETCO2, auscultation, expired tidal volume and then release cricoid pressure.

Secure tube with tape.

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L. Weaning Guidelines 1. Weaning may be initiated by medical or senior nursing staff. 2. Weaning is contraindicated with any of the following:

a) Unstable ICP (abort weaning if ICP increases) b) Need for heavy sedation (e.g. upper airway obstruction) c) Haemodynamic instability d) Significant bronchospasm e) High work of breathing.

3. Trial pressure support daily if the patient meets both the following criteria: a) PaO2/FiO2 ratio > 150 b) Patient can take spontaneous breaths if SIMV resp-rate reduced.

4. Weaning protocol: a) See the flow diagram following page. b) Set initial pressure support to maintain adequate VT

i) Start at 10 cmH2O and adjust to: VT 6 ml/kg IBW for patients recovering from ARDS. VT 8 ml/kg IBW for all others. IBW Males = 0.91 x (height [cm] �– 152.4) + 50 IBW Females = 0.91 x (height [cm] �– 152.4) + 45.5

ii) Alternatively, use target VT = 80-100% of set SIMV VT iii) Allowable PS range = 5 - 25 cmH2O

If VT cannot be achieved with 25cmH2O, cease trial c) Assess at 15 and 30 minutes for �“weaning success criteria�” d) Assess each hour for suitability to wean PS e) Once PS has reached minimum (5 cmH2O) then wean PEEP to 5 cmH2O f) If PS & PEEP = 5 cmH2O then asses for extubation.

5. Weaning Success Criteria: i) RR < 30/min ii) SpO2 > 90%

May be set lower with COPD, e.g. >86-88% iii) FIO2 0.5 iv) No respiratory distress as shown by 2 or more of the following:

HR > 120% baseline Accessory muscle use Diaphoresis Paradoxical abdominal movements Marked dyspnoea

50

Flowchart: Ventilation Weaning Protocol

PaO2/FiO2 > 150 &

PEEP < 10 cmH2O

PassFail

NO Weaning Contraindication: Unstable ICP Need for heavy sedation Haemodynamic instability Significant bronchospasm.

AND

�“Start Weaning�” Settings: Reduce patient sedation Reduce SIMV-Rate to 8bpm Adjust initial PS to target VT

8ml/kg IBW, or 6ml/kg IBW if ARDS

Allowed PS range (5-25 cmH2O) PEEP remains on previous setting.

Check each 15 minutes - Weaning Success Criteria: RR < 30/min SpO2 > 90% (*lower in COPD) FIO2 0.5 No respiratory distress as shown by

2 or more of the following: HR > 120% baseline Accessory muscle use Diaphoresis Paradoxical muscle movements Marked dyspnoea

Assess After Each Hour - Set Pressure Support Level: If weaning successful after 1st Hour

cease SIMV If successful on subsequent hours

decrease PS, as per �… If no previous weaning failure

decrease PS by 4 cmH2O If previous episode of failure

decrease PS 1-2 cmH2O If at minimum PS = 5 cmH2O

decrease PEEP by 1-2 cmH2O

Weaning Failure: IF post PS decrease

return to previous settings *note change to PS decrease rate

IF post return to settings set PS to max = 25 cmH2O

IF on maximum PS return to SIMV settings

IF PSMax or SIMV, patient should be

reviewed by SR or Consultant

Weaning Complete: If PS = 5 & PEEP = 5 cmH2O Check ABG Assess for Extubation �– see over.

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M. Extubation 1. The decision to extubate is made by medical staff, in consultation with either the

senior registrar or duty consultant. 2. Extubation is to be performed by medical or senior nursing staff, with airway

competent medical staff immediately available. 3. Criteria to predict successful extubation are helpful, however, ongoing success

should never be assumed: a) FiO2 < 0.5 with PEEP 5 cmH2O b) PaO2 > 70 mmHg ** lower values may be appropriate in

SpO2 > 90% chronically hypoxaemic patients c) RR < 30 with PS 5cmH2O (Dräger) d) pH > 7.2 e) No respiratory distress (see over) f) Patient able to obey commands g) Patient able to protect airway and cough h) Patient able to cope with amount of secretions i) Reason for intubation resolved.

*this may include checking for an air leak with the cuff deflated 4. The Tobin Index may additionally be used to predict extubation failure:

a) Place patient on PS = 2 and PEEP = 5 for 30 mins b) RR/VT > 105 predicts extubation failure

5. Early extubation to NIV may be considered for some patients who present with hypercapnic exacerbation of COPD or pulmonary oedema: a) Performed with close supervision by senior medical staff. b) If no improvement after 1-2 hrs, the patient should be considered for

reintubation. 6. Extubation protocol:

a) Ensure equipment, monitoring and adequate assistance is available, as for intubation

b) Plastic surgical and ENT patients with intermaxillary fixation/wiring require consultation with the Parent Clinic. i) A wire cutter must be present in the room at all times. ii) The parent clinic should be given opportunity to be present during extubation

if the jaws are wired. c) All patients should receive supplemental oxygen post-extubation.

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N. Emergency Surgical Airway Access

1. Policy a) Call for skilled assistance then proceed without delay. b) Difficult airway & failed intubation trolleys are in areas A, B & C c) Cricothyroidotomy and jet ventilation are recommended procedures for urgent

surgical airway access and emergency oxygenation. d) Standard percutaneous tracheostomy is not an emergency procedure.

2. Indications:

a) Refer to the failed intubation drill in the clinical protocols section. b) Inability to establish an effective airway despite:

i) Basic manoeuvres - jaw thrust / chin lift / oral-nasal airways ii) Attempted LMA insertion

c) Inability to ventilate. 3. Cricothyroidotomy

a) Surgical technique i) Equipment

Size 15 scalpel + handle Size 6.0 cuffed endotracheal tube Straight forceps Oxygen delivery circuit: Laerdal bag

ii) Procedure Palpate cricothyroid membrane. 2cm horizontal incision through skin and cricothyroid membrane Insert forceps into wound and open to enlarge the wound Consider insertion of long blue ventilating bougie into trachea Insert endotracheal tube, directly into the trachea or over bougie Remove bougie and connect oxygen circuit Confirm placement with ETCO2, auscultation and CXR Perform catheter suction ASAP after adequate oxygenation Cricothyroidotomy is a temporary airway - arrange a definitive surgical

airway (ENT surgeons) as soon as possible. b) Percutaneous technique

i) Equipment Cook Melker Emergency Cricothyrotomy Catheter kit (cuffed)

ii) Procedure Palpate cricothyroid membrane with neck well extended 1cm horizontal incision through skin Locate tracheal lumen with fluid-filled syringe & needle/cannula Insert wire through cannula, then remove the cannula over the wire. Insert dilator/introducer & tube assembly over wire in single motion Remove wire & introducer leaving the cuffed tube. Inflate cuff & suction prior to ventilation. Confirm endotracheal placement with ETCO2 & CXR.

53

4. Jet Ventilation a) Equipment

i) Cook Jet Ventilation Kit (Enk Oxygen Flow Modulator Set) ii) Oxygen flow meter:

15 lpm �‘standard�’ meter - set to highest flow rate 50 lpm �‘high-flow�’ meter - set at 20-30 lpm

b) Procedure i) Palpate cricoid membrane with neck well extended. ii) Locate tracheal lumen with fluid filled syringe & needle/cannula. iii) Feed cannula off needle down the trachea. iv) Attach oxygen delivery tubing from flow-meter to cannula. v) Occlude lumens in tubing to produce the jet of oxygen

1 sec ON : 4 sec OFF vi) Jet ventilation is a temporary emergency measure,

arrange a definitive surgical airway as soon as possible.

O. Fibreoptic Bronchoscopy

1. Policy: a) This is only to be used by skilled personnel and authorised by the duty consultant. b) Under no circumstances may the bronchoscope be loaned to other clinics. c) Expertise with bronchoscopy takes time. Registrars are encouraged to approach

the Department of Thoracic Medicine to attend bronchoscopy clinics to become familiar with the anatomy of the tracheobronchial tree and use of the flexible fibrescope.

2. Indications: a) Difficult intubation (trained staff only): not used as aid to failed intubation b) Persistent lobar collapse that is refractory to physiotherapy c) Foreign bodies d) Diagnostic bronchoalveolar lavage (BAL)

3. Protocol for fibreoptic intubation a) Indication as per endotracheal intubation b) Procedure

i) All equipment, drugs and monitoring c.f. routine endotracheal intubation ii) Supplemental oxygen must be given via a mask and may also be given via the

suction channel of the bronchoscope. iii) Can be via oral (with bite protection mandatory) or via nasal route iv) Local anaesthesia / preparation of the airway:

Nasal mucosa - topical 10% lignocaine or 2% amethocaine spray. Pharynx - viscous lignocaine gargle Larynx - choice according to operator experience

a. Transtracheal injection and/or direct application through the scope b. Nebulised - 5 mls 4% lignocaine c. Superior laryngeal nerve blockade (2-3ml 1-2% lignocaine).

54

v) Check tube cuff vi) Place a warmed appropriately sized ETT (7mm tube for either sex) into

posterior nasal space. vii) Insert the scope through the tube under direct vision. viii) Identify the vocal cords and advance the scope into the trachea. ix) Advance the ETT over scope into trachea, maintaining view of the tracheal

rings or carina, then remove the scope. x) Confirm ETT placement by ETCO2, auscultation and CXR. xi) NB: Suction at least 500ml water or saline through scope immediately

following use and notify the equipment nurse that the scope has been used ASAP.

4. Protocol for BAL

a) Diagnosis of nosocomial pneumonia in selected patients i) Determination of colonization vs. infection in chronically ventilated patients. ii) These patients should ideally be off antibiotics for 24-48 hours. iii) Sufficient reserve to tolerate procedure:

Ideally PaO2 > 70 and FiO2 < 0.7 BAL will commonly result in a 10% reduction in PaO2 for up to 24 hours

after procedure b) Procedure

i) Ensure sufficient sedation & place patient on 100% oxygen ii) Select lobe to be lavaged from recent CXR iii) Local anaesthetic gel is contra-indicated (interferes with culture media) iv) If possible, do not suction through scope prior to lavage (upper airway

bacterial contamination) v) Pass the scope directly into the selected lobe vi) Wedge the scope as far as possible �– ideally to 3rd generation bronchi vii) Lavage with 4-6 x 20-40 ml aliquots of sterile normal saline viii) Aspirate between aliquots and label aliquots accordingly ix) Send aspirates for quantitative culture and atypical pneumonia screen as

directed. P. Tracheostomy 1. Policy:

a) Percutaneous tracheostomy (PCT) is the preferred procedure in suitable patients. b) This procedure is only to be performed by experienced consultant staff or

advanced vocational trainees under supervision. c) Patients must have the option of surgical tracheostomy cleared by the parent

clinic (either medical or surgical). This is a courtesy. d) The decision to do a PCT is at the discretion of the ICU consultant. e) PCT is an elective procedure and has no place in urgent airway access.

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2. Indications : a) The indications for PCT are the same as surgical tracheostomy: b) Airway maintenance

i) Prolonged intubation, e.g. > 10 days ii) Laryngeal pathology �– this may also be a contraindication to PCT

c) Airway protection i) Delayed return of glottic reflexes ii) Tracheal toilet

3. Contraindications to PCT

a) Lack of consent. b) Coagulopathy

i) Platelets: < 100,000 ii) APTT: > 40 iii) INR: > 1.5

c) Difficult anatomy - e.g. previous neck surgery, short fat neck d) Unstable cervical spine injury e) Grade III or IV intubation (relative �– consider use of Glidescope) f) FIO2 0.6 / PEEP 10cmH2O

4. Procedure: a) Ensure consent has been obtained and documented. b) Equipment, monitoring and drugs as per endotracheal intubation c) Coagulation screen prior to procedure. d) Bedside procedure light essential. e) General anaesthesia - the airway operator must be appropriately trained. f) Ventilate the patient on 100% oxygen. g) Tracheostomy equipment:

i) Standard technique: modified Cook Ciaglia kit using the �“Blue Rhino�” ii) Tracheostomy tubes

EVAC® aspirating tubes are standard for all tracheostomies. a. Includes patients having surgical tracheostomies b. Ensure that an EVAC tube goes with the patient to theatre.

Patients who have non-aspirating tracheostomy tubes in place (e.g. from CTSU or other hospitals) must have these tubes changed to an EVAC tube as soon as safe and feasible. This is usually 4-5 days post-tracheostomy.

Other tubes: a. Foam cuffed tubes: indicated in patients with tracheomalacia or

persistent air leaks b. Uncuffed tube (usually size 6.0) as part of weaning of

tracheostomised patients to facilitate secretion clearance c. Fenestrated tube: these are either cuffed or un-cuffed with a

fenestration to allow patients to talk. d. XLT �– extended length tubes: useful for patients with marked

neck or soft tissue swelling.

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h) Insertion technique:

i) Aseptic technique. ii) Goggles are essential for both the operator and anaesthetist iii) Local anaesthetic infiltration (2% lignocaine + 1:200000 adrenaline) over

the pretracheal rings. iv) Check the tube cuff, lubricate and insert the dilator into the tube. v) 2cm horizontal incision over 1st or 2nd tracheal ring vi) Pretracheal tissue blunt dissection down to fascia

*look for anterior jugular vein and ligate if identified. vii) Insert a 14G IV cannula mounted on a syringe with saline into trachea and

aspirate through saline/water to confirm intratracheal placement. viii) Removal the stylet and reconfirm intratracheal placement by aspirating air

via the IV cannula ix) Insert the guide-wire through the IV cannula and remove the cannula. x) Insert a small dilator over the wire into the trachea and make a hole large

enough to accommodate the main dilating instrument. xi) Blue Rhino® graduated 1-step dilator:

Lubricate with water, not gel Place the dilator and guide cannula (white) over the wire, noting:

a. The black marker on the guide at the proximal end of the Rhino b. The silver marker on the wire at the proximal end of the guide

Slowly insert to the required ETT size, ensuring that both markers (wire and guide) remain in alignment at the proximal end.

xii) Remove the dilator leaving the white guide cannula on the wire and insert the tracheostomy tube & dilator over the wire/guide into the trachea

xiii) Remove the dilator and wire, inflate the cuff and suction the trachea xiv) Ventilate and confirm ETCO2 - self-inflating bag or ventilator xv) Secure tracheostomy tube with tapes. xvi) Obtain a CXR post procedure. xvii) Document the procedure in the case notes and complete a separate

operation note.

5. Complications (of tracheostomy) a) Bleeding b) False passage c) Loss of the airway: immediately re-intubate the patient orally d) Pneumothorax e) Cricoid cartilage fracture f) Laryngeal dysfunction g) Tracheal stenosis h) Infection

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6. Prolonged care of tracheostomy a) Cuff checks

i) Volumetric (sufficient air to obtain a seal) tests are done following insertion and whenever a leak is detected with a manual hyperinflation once per nursing shift.

ii) Manometric tests are inaccurate and do not correlate with mucosal pressure. These are an adjunct only if cuff malfunction is suspected.

b) Tube changes i) Routine change at 28 days.

c) Aspirate EVAC tube 2 hourly or more frequently if > 10ml supraglottic secretion per hour.

Q. Pericardiocentesis

1. Policy a) This procedure must be authorised by the duty ICU consultant and performed

by consultant staff, trainees under supervision, or cardiology. b) Confirmation of pericardial effusion or tamponade with echocardiography is

required prior to the procedure, except in peri-arrest situations. c) Liaison with cardiology is essential.

2. Indications

a) Symptomatic pericardial effusion (tamponade). b) Although advocated in EMST (ATLS), this procedure has limited utility in

traumatic pericardial tamponade. 3. Procedure

a) Strict aseptic technique. b) Local anaesthetic infiltration in an awake patient. c) This procedure should be performed under ultrasound guidance. d) Technique: Seldinger technique and insertion of a pigtail catheter

i) Insert needle on syringe at 45° from the horizontal axis and aim for tip of left shoulder

ii) Advance slowly and aspirate until confirmation by aspirating blood or serous fluid

iii) Insert catheter using Seldinger technique over guidewire. iv) Confirm placement by aspiration and/or echocardiography v) Check CXR (pneumothorax) vi) Suture and occlusive dressing if leaving for > 24 hours.

4. Complications

a) Arrhythmias b) Cardiac tamponade! c) Myocardial laceration d) Pneumothorax, pneumopericardium e) Liver laceration

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R. Intra-aortic balloon counterpulsation 1. Policy:

a) The ICU consultant should be involved in the decision to insert an IABP b) Only to be performed by a consultant or advanced vocational trainee under

supervision. c) Become familiar with the theory of insertion, indications, interpretation and

complications of IABP.

2. Indications : a) As a mechanical bridge prior to, and/or following myocardial revascularization

or transplantation: b) Ischaemic heart disease

i) Low cardiac output states following cardiac surgery ii) Cardiogenic shock: in association with angiography and revascularization

(PTCA, stent or CAVG) iii) Acute mitral incompetence (papillary muscle rupture) or VSD following

AMI pending operative repair. c) Myocardial disease

i) Severe myocardial contusion ii) Severe myocarditis iii) Cardiomyopathy iv) Severe blocker overdose.

3. Contra-indications:

a) Aortic regurgitation b) Aortic dissection c) Severe peripheral vascular disease d) Tachyarrhythmias (relative) e) Coagulopathy (relative)

4. Procedure protocol

a) Strict aseptic technique b) Check IABP function prior to insertion:

i) Adequate helium cylinder volume ii) Arterial pressure manifold: referenced to mid-axillary line and correctly

zeroed iii) Dedicated 5 lead ECG connected to IABP iv) Turn on and leave in standby mode v) Initial settings:

ECG sense: 1:3 ratio Augmentation: minimum (pre-insertion only) Inflate and deflate times: zero

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c) Insertion procedure: i) Local anaesthesia in awake patients ii) Scrubbed assistant recommended iii) Select size (by patient�’s height) < 165cm : 34ml balloon

> 165cm : 40ml balloon iv) Femoral artery, Seldinger technique, insertion of a 12F introducer. v) Check the length for balloon catheter insertion, using the angle of Louis

(level of T4) as the surface landmark, prior to insertion. vi) Insert the balloon to the level of T4. The double black marker on the

balloon catheter must be visible �– this indicates that the balloon has fully exited the sheath.

vii) Connect to pressure transducer and pump. viii) Press the [IAB fill] button to fill the balloon & wait for completion. ix) Press the [assist/standby] button to start the pump. x) Start on minimal augmentation and increase to maximum.

NB: subsequent augmentation should not be set below 50% xi) Suture in place and cover with an occlusive dressing. xii) Set timing:

Check balloon inflation against pressure wave: set to peak of dicrotic notch.

Check balloon deflation against ECG: prior to QRS complex and observe decrease in end diastolic pressure.

Check diastolic augmentation on pressure wave. Select augmentation ratio: *standard = 1:1

d) Maintenance i) Check CXR post insertion:

tip of IABP below T4 (carina) & origin of the left subclavian artery ii) Neurovascular obs of insertion site, lower limbs and left arm hourly. iii) Nurse at < 30° elevation. iv) Document pump timing (ratio) and adequacy of augmentation. v) Assess haemodynamic response: CI, MAP, SVR, filling pressures, CXR. vi) Ensure clear balloon tubing is exposed:

Monitor condensation (due to rapid helium shuttling), or Blood in tubing (balloon rupture).

e) Timing during arrhythmias i) Ectopics: keep on ECG trigger, system will automatically deflate on

ectopic ii) Tachycardia > 160/min :

Reduce augmentation (equal to patient systole) Decrease ratio to 1:2 if reducing augmentation is not adequate

iii) Atrial fibrillation: move deflate slide to extreme right to deflate on R wave (not required on newer pumps)

iv) VT or VF: defibrillate or cardiovert as required, the IABP is isolated

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v) Cardiac arrest (no output) start ECM Effective output: set on pressure trigger to synchronise balloon

inflation with ECM No output: set internal mode for a fixed rate of 40 bpm + 20ml

augmentation f) Weaning:

i) Commence when patient�’s haemodynamics have improved. ii) Methods:

Reducing ratio from 1:1 to 1:2 to 1:3 and / or Reduce augmentation. NB: minimum balloon inflation 50%

g) Removal of catheter i) Notify cardiac / vascular surgeons ii) Cease heparin infusion 3 hours prior to removal iii) Disconnect IABP tubing: do not aspirate the balloon iv) Withdraw balloon up to (but not into) the introducer sheath. Even empty

the used balloon will not fit into the sheath, and may rupture if attempted. v) Remove the sheath and balloon as single unit, applying pressure

immediately. vi) Use Femostop® local pressure during catheter removal:

Remove IABP catheter with Femostop at 60-80mmHg Inflate dome to 20mmHg above systolic as catheter is fully withdrawn Reduce pressure by 15mmHg at 10-15 min intervals If bleeding occurs, reinflate the Femostop to the previously effective

pressure and recommence cyclic pressure reduction Remove Femostop and apply a firm dressing

vii) 10-20% may require surgical repair to the artery.

5. Complications: a) Limb ischaemia �– thrombotic or embolic b) Bleeding at the insertion site or systemically c) Infection d) Aortic dissection e) Occlusion of origins of aortic arch vessels if too high f) Occlusion of renal/splanchnic vessels if too low g) Thrombocytopaenia h) Balloon rupture: gas embolism i) Femoral artery aneurysm

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S. Cardiac Pacing 1. Policy:

a) ICU consultant should be involved in decision to insert cardiac pacing wire. b) If inserted by ICU staff, the procedure is only to be performed by consultant

staff or advanced vocational trainees under supervision. c) Become familiar with the theory of insertion, indications, interpretation and

complications of TVP.

2. Indications: a) Medical pacing with adrenaline or transthoracic pacing may be adequate to treat

many symptomatic bradycardias. Note: this is particularly relevant for retrievals and has obviated the need for prophylactic pacing in some high-risk patients.

b) Any sustained symptomatic bradycardia which does not respond to medical treatment, or predisposes to a malignant ventricular arrhythmia. Note: pacing is indicated by the haemodynamic consequences of the rhythm, not the arrhythmia per se.

c) Ventricular tachycardias (especially polyphasic) may respond to overdrive suppression pacing.

d) Following cardiac surgery in high-risk patients (epicardial leads): i) Valve replacement / repair: especially mitral. ii) VSD repair / papillary muscle rupture. iii) Acute myocardial infarction.

3. Types:

a) Semi-rigid, bipolar pacing lead (VVI): insert under image intensification (standard TVP at RAH)

b) Paceport PA catheters - standard at RAH c) Balloon flotation leads - ECG or pressure guided catheters d) Epicardial leads

i) Placed during cardiac surgery in high risk patients ii) Usually unipolar ventricular, but may be bipolar, atrial or ventricular:

check the operative note and liaise with the surgeon. 4. Paceport PA protocol

a) VVI mode only b) Ensure a ventricular demand pacemaker box is available c) Insert the Paceport PA catheter using standard technique (see PAC section) d) A pressure transducer should be attached to the RV as well as the distal port e) The RV port should be 1 to 2cm distal to the tricuspid valve

i) In some patients the catheter may wedge before the RV port is in the RV in these cases an alternate technique should be used

f) Attach the adapter to the RV port g) Insert probe to the reference mark

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h) Attach ECG monitoring and advance until ST elevation indicates contact with the epicardium

i) Secure the probe and connect side port to a saline flush j) Commence pacing k) Check adequate capture and sensing (see next section)

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5. Semi-rigid Wire protocol: (VVI lead) a) Strict aseptic technique b) Image intensification c) Local anaesthesia where appropriate d) Insertion protocol:

i) 6F peel away sheath or PAC introducer ii) Right IJ vein is the preferred route, then left subclavian.

NB: if permanent pacing is likely then avoid subclavian placement. iii) Under I-I control, feed the wire until the tip just stops on the RV wall iv) Connect to the control box (switched off) v) Set output and sense to their minimum value, and rate 20bpm faster than

the patient's own rate (or 70bpm, whichever is greater). vi) Turn the generator on and gradually increase the output while watching the

ECG for capture. vii) If there is no capture or a high output is required:

Place on demand mode Turn output right down, advance or reposition the wire slightly Try to capture again. An ideal capture setting is ~ 2 mA Ensure wires are not exposed and tape both sides

viii) Suture the wire and apply an occlusive dressing ix) Arrange a post-insertion CXR. x) Always be aware of the risk of tamponade even when pacing has been

unsuccessful. e) Daily check:

i) Battery strength ii) Capture: set the output 2x higher than threshold for safety.

6. Flotation Catheter Insertion

a) These may be inserted either �“blind�”, under ECG guidance (standard recommendation), or via pressure guidance for catheters having an infusion lumen (c.f. PA catheter insertion).

b) Aseptic technique & local anaesthesia where appropriate c) Insertion protocol:

i) 6F peel away sheath, do not use a PAC introducer as these will leak ii) Attach V5 lead of an ECG to the distal electrode of catheter & monitor iii) Note P then QRS wave-form changes as the catheter advances to the RV iv) Advance catheter another 2cm, deflate the balloon & advance 1cm v) Connect to the pulse generator (switched off) vi) Set output and sense to their minimum value, and rate 20 bpm faster than

the patient's own rate. vii) Turn the generator on and gradually increase output while watching the

ECG for capture. viii) If there is no capture or a high output is required - see (5.d.vii) above ix) Suture the wire and apply an occlusive dressing x) Arrange a post-insertion CXR.

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T. Oesophageal Tamponade Tubes

1. Policy: a) All patients with tamponade tubes should be intubated prior to insertion and

managed in ICU. b) The ICU consultant should be involved in the decision to insert an oesophageal

tamponade tube. c) Become familiar with the theory of insertion, indications, and complications. d) Routine placement in ICU is performed by the GE Unit.

2. Indications :

a) Variceal haemorrhage: i) Where endoscopy cannot be done due to bleeding ii) Failure of sclerotherapy, banding and/or octreotide infusion.

3. Types of tubes:

a) Minnesota: oesophageal and gastric balloons and 2x aspirating ports b) Sengstaken: oesophageal and gastric balloons and gastric aspirating port c) Linton: gastric balloon and aspirating port

4. Procedure:

a) Preferrably use a bulk & frame bed. b) Prior to insertion:

i) Check both balloons for leaks ii) Inflate the gastric balloon with 300ml of air and check pressure reading. iii) Deflate all balloons completely and lubricate the tube

c) Estimate insertion length = (bridge of nose to earlobe) + (nose to xiphoid process)

d) Insert under direct vision using a laryngoscope then x-ray to ensure the tube is not folded up in the oesophagus. NB: inflating the gastric balloon in the oesophagus is virtually 100% fatal!

e) Inflate the gastric balloon in 50ml increments up to 300ml while monitoring the balloon pressure. NB: If the balloon pressure exceeds 5mmHg above the pre-insertion pressure then incorrect (oesophageal) placement is probable and this mandates deflation of the balloon and reinsertion of the tube.

f) Pull back until resistance is felt as the balloon rests against the gastric fundus. g) Note the measurement at the lips, and fix securely with gentle traction:

i) Rope and pulley system with 500ml bag of fluid, or ii) Adhesive tape to face.

h) Inflation of the oesophageal balloon is usually not required. It should only be inflated in consultation with ICU consultant. If required, connect a pressure gauge to the oesophageal balloon, and inflate to a pressure of 40 mmHg

i) Recheck position on x-ray. j) After 12-24 hours, the balloons should be let down and if bleeding does not

recur the tube may be removed. k) Sclerotherapy is usually performed: ( 50% patients will otherwise re-bleed)

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U. Extracorporeal Membrane Oxygenation 1. Extra Corporeal Membrane Oxygenation (ECMO) is a method of providing

oxygenation to the blood in cases of overwhelming respiratory failure (veno-venous ECMO) or temporary circulatory support in reversible cases of refractory overwhelming cardio-respiratory failure (veno-arterial ECMO).

2. The ECMO service started in 2009 in the RAH ICU, and continues to be developed

further. 3. Any cases of potential ECMO support will be discussed in detail prior to initiation,

and will be supervised closely by ICU consultants. 4. If caring for a patient on ECMO all relevant protocols and contact details will be

made available. Care of the patient on ECMO includes specific requirements. 5. The ECMO circuit and equipment must not be altered without the ICU consultant

and/or perfusionist supervision.

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PART 3 - DRUGS AND INFUSIONS A. Policy 1. Patients admitted to the ICU must have a complete drug history documented:

a) Premorbid and current medications. b) Previous adverse drug reactions and allergies. c) Note potential drug interactions.

2. Charting of drugs and infusions is to be done by ICU medical staff. a) Parent clinics must not write on the ICU flowchart. b) Therapeutic changes suggested by the home team must be communicated to the

appropriate ICU medical staff. 3. All changes or additions to drug and fluid orders must be written and signed for on the

flowchart. a) Nursing staff must be notified of such changes. b) Verbal orders alone are neither sufficient nor legal.

4. All drugs, infusions and fluids are reviewed and transcribed at least daily. 5. Printed �‘sticky�’ labels for the commonly used infusions and drugs should be used

where possible. 6. Standardisation of infusion concentrations is essential for the prevention of drug

errors. Infusion concentrations should not be changed (e.g. �‘double strength�’) from the protocols outlined below.

7. Vasoactive or hypertonic infusions (e.g. TPN) must be administered through a dedicated lumen of a CVC or PICC.

8. Vasoactive infusions must not be used in the general wards, other than for patients en route to ICU and who are being continuously monitored.

9. All antibiotics written on the ICU flowchart must also have an indication of date started and due date for review and/or completion.

10. Patients cleared for discharge from ICU must have all appropriate drugs, infusions and fluids prescribed on the standard hospital forms, prior to discharge. Where appropriate, old drug charts should be re-written.

11. Patients discharged on TPN must have their details entered in the TPN folder (stored in the Unit A office area).

12. Any changes to acute pain drug regimens in patients under the care of the Acute Pain Service should be done in consultation with the Acute Pain Service.

13. Any proposed changes to specialty type drugs, e.g. immunosuppressives, anticoagulants, antiplatelet agents, etc should be discussed with home teams.

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B. Principles of drug prescription in Intensive Care 1. Ideally, drugs should only be prescribed where proven benefit has been demonstrated. 2. Drugs should be prescribed according to Unit protocols and guidelines. 3. Ensure that the drug doses are correct: seek advice if unsure. 4. The risks and benefits of starting any drug must be carefully considered. 5. Critically ill patients have altered pharmacokinetics and pharmacodynamics, with the

potential for toxicity and drug interactions. 6. Where possible:

a) Use drugs that can be titrated or prescribed to an easily measured endpoint. b) Use drugs that can be measured to monitor therapeutic drug levels. c) Avoid drugs with narrow therapeutic indices (e.g. digoxin, theophylline),

particularly in patients with associated hepatic or renal dysfunction. d) Cease a drug if there is no apparent benefit. e) If two drugs are of equal efficacy, choose the cheaper drug as the cost of drugs in

ICU is significant. C. Cardiovascular Drugs 1. Inotropes Inotropes (specifically catecholamines) are frequently used in ICU. There are varied prescription practices and preferences for these drugs, mostly based upon the reported pharmacological effects of the different agents.

a) General principles: i) Defence of blood pressure in critically ill patients forms the basis of

haemodynamic resuscitation and organ perfusion. This must be interpreted in the context of the patient�’s pre-morbid BP, particularly for those patients with renovascular hypertension or cerebrovascular disease.

ii) Hypovolaemia is the most common cause of hypotension and low cardiac output in ICU and must be assiduously monitored and corrected.

iii) The main indications for the use of inotropes are to increase myocardial contractility, heart rate and/or vascular tone.

iv) The use of inotropes requires regular haemodynamic monitoring (arterial line and CVC) and, where indicated, a PA catheter or PiCCO or Edwards Vigileo cardiac output system.

v) No single inotrope (or mixture of inotropes) has been shown to be superior to another.

vi) There is marked inter-individual variation in the response to inotropes. This is partly due to pre-existing chronic illness, genetic variation, co-administration of other drugs, dynamic qualitative and quantitative changes in adrenergic receptor kinetics.

vii) Prolonged exposure to catecholamine infusions can produce adrenergic receptor down-regulation. The clinical implications are:

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b) Catecholamines i) Receptor effects may be unpredictable, however, in general:

-adrenergic effects predominate at low doses, and -adrenergic effects at higher doses.

ii) It is impossible to predict the dose range for an individual patient. iii) Prescription on a body weight basis (µg/kg/min) is of little clinical utility. iv) Infusions should be started at a low rate (3-5 µg/min) and titrated to a set

clinical response, e.g. MAP (not systolic) v) There is no well established maximal dose vi) The use of �“renal protection�” dose dopamine is no longer indicated vii) Regular assessment should be made of both global (pH, lactate) and

regional effects (urine output/creatinine clearance, limb perfusion). c) Phosphodiesterase inhibitors (milrinone)

i) Inhibition of PDE3 increases intracellular cAMP and calcium, causing: an increase in myocardial contractility systemic and pulmonary vasodilatation, and improved diastolic relaxation (lusitropy)

ii) Any resultant hypotension (due to systemic vasodilatation) is usually treated with a vasopressor (e.g. noradrenaline).

iii) Phosphodiesterase inhibitors have longer half-lifes than catecholamines, are less titratable and their half-life is prolonged with renal failure.

Table: Cardiovascular effects of inotropes

Agent

1 effects 2 effects 1 effects 2 effects

Chronotropy Dromotropy Inotropy

Inotropy Vasodilatation Bronchodilatation

glucose/lactate

Inotropy Vasoconstriction

Inotropy Vasoconstriction

Adrenaline Noradrenaline Dopamine

effects predominate at low dose

effects predominate at high dose

Dobutamine + + (+) -

Isoprenaline + (+) - -

+ = strong effect (+) mild effect - = no effect

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Table: Inotropic Agents Used in ICU

Agent Standard Infusion Uses Noradrenaline 6 mg / 100 ml 5% dextrose

(ml/hr = µg/min) First line drug in septic shock Maintenance of cerebral perfusion pressure

Adrenaline 6 mg / 100 ml 5% dextrose (ml/hr = µg/min)

Cardiopulmonary resuscitation Acute severe asthma Anaphylaxis Cardiogenic shock Second line drug in septic shock after noradrenaline Medical pacing

Dobutamine 500 mg / 100 ml 5% dextrose (ml/hr approx µg/kg/min)

Primarily a vasodilator, weak inotropic action Traditionally used in cardiogenic shock or low

output, high afterload states or when filling pressures high

Often used in combination with noradrenaline Dopamine 400 mg / 100ml 5% dextrose

(ml/hr approx µg/kg/min) No advantage over adrenaline/noradrenaline �“Renal dose�” dopamine is not used Endocrine side effects

Isoprenaline 6 mg / 100 ml 5% dextrose (ml/hr = µg/min)

Vasodilator, chronotrope (rarely used) Medical pacing

Levosimendan 12.5 mg / 250 mL 5% dextrose Loading dose: 12-24µg/kg/10min Dose rate: 5-15 ml/hr. NB: Loading dose may cause marked hypotension, may be omitted.

Calcium sensitizer Increases myocardial contractility in an oxygen

efficient manner and dilates coronary and systemic vessels

Role in Intensive Care not established

Milrinone 10mg / 100 ml 5% dextrose Loading dose: 50µg/kg/20 min Dose rate: 0.5 µg/kg/min*

Cardiogenic shock due to diastolic failure Pulmonary hypertension following valve

replacement Catecholamine induced down regulation

*Standard milrinone prescription for 70 kg patient: Loading dose: 3500 µg = 35 ml over 20 minutes Maintenance: 2100 µg/hr = 20 ml/hr.

2. Vasopressor agents

a) General principles i) Vasopressors usually act directly on the peripheral vasculature and are

primarily used to acutely elevate blood pressure ii) The catecholamines have variable effects on the peripheral vasculature. iii) The most common cause of hypotension in ICU patients is hypovolaemia. iv) Pressor agents should not be used as an alternative to fluid resuscitation.

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b) Indications (in ICU) i) Tissue infiltration with local anaesthesia ii) Topically prior to nasal intubation iii) Hypotension following sympathetic block (e.g. epidural anaesthesia) iv) Hypotension refractory to large doses of catecholamines (vasoplegia):

Consider relative hypoadrenalism Consider use of vasopressin

c) Complications i) Rebound hypertension ii) Vagal reflex bradycardia iii) Tachyphylaxis

Table: Vasopressors

Agent Standard Infusion / Dose Uses Metaraminol 10mg / 10ml 5% dex: titrate Potent short acting vasoconstrictor

Ephedrine 30mg / 10ml 5% dex: titrate Synthetic indirect sympathomimetic. Commonly used in anaesthesia, little

benefit over adrenaline.

Vasopressin 20units/20ml 5%dex: 1.8mls/hrs (0.03u/min)

Noradrenaline resistant hypotension. May be useful in septic shock

Phenylephrine Not available in Australia

Methoxamine 3. Antihypertensive agents

a) General principles i) The most common cause of hypertension in ICU patients is sympathetic

drive due to pain, agitation or delirium. These should be treated with adequate sedation and analgesia.

ii) Patients in the recovery phase of acute renal failure are often hypertensive. This usually represents the resetting of endogenous neurohumoral mechanisms and as such does not routinely require treatment.

iii) Hypertension following an intracranial event (haemorrhagic or ischaemic) is common and the underlying mechanism dictates therapy. A high BP may be tolerated in ischaemic stroke, c.f. the setting of SAH with an unclipped aneurysm, where treatment would be paramount.

iv) Target therapy should be titrated against the patient�’s premorbid BP. v) In the absence of adverse effects, the maximal therapeutic dose of a

selected agent should be used prior to commencing a second or third agent.

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b) Indications i) Acute

Acute perioperative control of hypertension post-cardiac, carotid, or cerebrovascular surgery, or for patients with critical myocardial ischaemia.

Hypertensive crisis (malignant hypertension) Pre-eclampsia / eclampsia Phaeochromocytoma Untreated aneurysm or vascular injury,

e.g. intracranial aneurysm, ruptured/dissected aorta ii) Other indications for vasodilators

Reduction of afterload in cardiac ischaemia and CCF Adjunct to passive warming in hypothermia

iii) Chronic Sustained essential hypertension Ischaemic heart disease Cerebrovascular disease

c) Complications �– are many, but in relation to ICU patients: i) First-dose effect / hypotension

especially in hypovolaemic patients ii) Reflex tachycardia iii) Tachyphylaxis iv) Pulmonary vasodilatation causing shunt and hypoxaemia v) Cyanide toxicity (SNP) vi) Angioedema �– especially ACEI vii) Deterioration in renal function viii) Electrolyte disturbances

Table: Antihypertensive & Vasodilator Agents

Agent Infusion & Dose Uses Glyceryl trinitrate (GTN)

30mg / 100ml 5%D (non PVC bottle and giving set) Range 2-25 ml/hr First line drug in RAH ICU Can be given topically.

Mainly venodilation: Useful in cardiac ischaemia Less predictable control of BP than SNP Tachyphylaxis develops within 24-48hr

will need additional agents for persistent BP

Sodium nitroprusside (SNP)

50mg / 250 ml 5%D Range 3-40 ml/hr

Rapid control of hypertensive crises. Tachyphylaxis and metabolic acidosis may imply

cyanide toxicity (total dose > 1.5mg/kg/24 hrs)

Phentolamine 10mg / 10ml 5%D: titrate Pure -blockade, short acting antihypertensive

Hydralazine 5-10 mg as bolus 20-40 mg 6-8 hourly

Short to medium term IV agent. Often use with -blockers to control reflex tachycardia Useful in renovascular hypertension

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Amlodipine 5-10mg oral bd Long acting oral Ca++ antagonist. Caution in renal impairment

Captopril Start low dose ~ 5-6.25mg up to 50mg orally 8 hrly

Syrup: 5mg/ml or tablets Acute hypertension: 5-25mg sublingually prn

Treatment of hypertension Left ventricular dysfunction, esp post-MI Left ventricular failure Diabetic nephropathy Caution in renovascular disease and renal failure

Perindopril Start 2.5mg daily up to 10mg daily orally

Phenoxy-benzamine Oral : 10mg/day and increase until postural hypotension IV : 1mg/kg/day dilute to 200-500ml 1/3 dose over 1/24 2/3 dose over 1/24

Long acting blocker Preoperative preparation of phaeochromcytoma Idiosyncratic hypotension may occur

Prazosin Start with 0.5mg, and increase up to 5mg tds orally

-blocker Potent antihypertensive agent Beware first dose effect, esp if under-filled

Metoprolol Oral: 25-100mg bd IV: 1-2mg bolus every 2-3 minutes up to 10 mg.

High sympathetic drive states: neurogenic BP All grades of hypertension, inc renovascular Cardiac ischaemia Control of reflex tachycardia with vasodilators Thyroid crisis Caution in poor LV function, asthma Mainly eliminated by hepatic metabolism

Esmolol Loading dose 0.5 mg/kg Infuse 100mg/10ml and titrate

Ultra-short acting -blocker Useful as trial for patients with poor LV function. Adjunct to vasodilators post cardiac surgery

Clonidine 25µg boluses of up to 150µg/24hrs Oral: 75µg bd up to 150-300µg tds.

Acute, centrally mediated hypertension Useful post cardiac surgery Withdrawal states Care with hepatic or renal dysfunction Rebound hypertension with chronic use Sedation, especially 1st dose

Dexmedetomidine 400 µg in 40mls load 1µg/kg over 20min infuse 1-5ml/hr

Selective alpha-2-agonist Acute, centrally mediated hypertension Not a first line drug. Selected use by senior medical staff only Sedation

MgS04 5-10 mmol loading Infuse at 4-12 mmol/hr Target plasma [Mg] ~ 1.5-2 mmol/L

Pre-eclampsia / eclampsia Phaeochromocytoma Sympathetic overdrive in tetanus

73

4. Antiarrhythmics

a) General principles i) Prior to administration of antiarrhythmic agents, optimise correction of the

following: Hypovolaemia Metabolic abnormalities

a. K+, Mg++, HPO4=, alkalosis

b. Hypoxaemia, hypo/hyper-carbia Myocardial ischaemia or cardiac failure (especially post-cardiac

surgery) Sepsis Pain and agitation.

ii) All antiarrhythmic drugs are potentially arrhythmogenic. iii) Virtually all depress myocardial contractility. iv) Antiarrhythmics drugs are indicated where:

The arrhythmia causes haemodynamic compromise (hypotension or prolonged tachycardia >120-130/min) or

Susceptible patients with myocardial ischaemia. v) Consider anticoagulation if AF > 48 hours

b) Indications i) Termination of an acute arrhythmia ii) Prophylaxis against recurrence iii) Rate control

74

Table: Antiarrhythmic Agents

Agent Infusion & Dose Uses Amiodarone Acute use:

900mg / 250ml 5%D: Load 100ml / 1 hr (5mg/kg) Infuse 10 ml/h for 24-48 hrs (15mg/kg/day) Bolus Dose 150-300mg Chronic: 200-400 mg IV/oral daily

Rapid AF / flutter or MAT Monomorphic ventricular tachycardia Generally does not suppress contractility Can cause acute hypotension if given too rapidly Less proarrhythmic than most other drugs Causes QTc, but rarely Torsade de pointes Renal excretion is minimal �– no need to change dose

in renal failure Long term side-effects rare in short-term use. Interference with digoxin kinetics and assay. Interference with thyroid function tests.

Magnesium 5-10 mmol IV slow bolus Infuse at 2-5 mmol/hr. 2.4g MgSO4 = 10mmol Mg++

Acts principally as a calcium blocker Useful in AF and Torsade de pointes

Verapamil 5-10 mg IV slow bolus Conversion atrial flutter SR SVT �– 2nd line to Adenosine

Digoxin Loading dose: 0.5-1 mg IV. Maintenance: 62.5-250 µg IV/day Levels: 0.6�–1.0 mmol/l

Ventricular rate control in rapid AF (usually 2nd line to amiodarone in critically ill)

Narrow therapeutic index esp in renal failure and metabolic abnormalities ( K+, Mg, PO4, alkalosis)

Proarrhythmic potential high in critically ill patients Minimal inotropic effect in critically ill patients Hypokalaemia potentiates effects

Metoprolol 1-2mg IV bolus (up to 10 mg) 25-100mg oral bd

Used in high sympathetic drive states : neurogenic hypertension

Control of reflex tachycardia with vasodilators Caution in poor LV function, asthma Mainly hepatic metabolism

Sotolol 10-80 mg IV slow bolus (10-15 min)

Class III and -blocking actions Supraventricular tachyarrhythmias

Conversion AF/flutter SR Low pro-arrhythmic potential

Adenosine 6-12 mg rapid IV push Diagnosis / conversion of SVT

Lignocaine 0.4% solution = 4mg/ml : 60ml/hr (4mg/min) for 1-2 hrs 45ml/hr for 2-4 hrs 30ml/hr for 2-4 hrs

2nd line drug after amiodarone Sustained, recurrent VT No longer routinely used for prophylaxis for VT VF resistant to defibrillation (now questioned) Potent negative inotrope, pro-convulsant

Phenytoin 15mg/kg loading / 1 hr 300 mg/day (level 40-80 mmol/l)

Digoxin toxicity Tricyclic induced malignant arrhythmias

75

5. Thrombolytic Therapy

NB: All patients with acute myocardial infarction should be considered as potential candidates for primary angioplasty. The Cardiology cover must be notified of all patients with an acute MI, as early as possible. The duty cardiologist will decide between primary angioplasty, thrombolysis, and expectant management.

a) Indications

i) Acute myocardial infarction Thrombolytic therapy is standard in the management of AMI,

wherever primary angioplasty is not performed. Administered in consultation with the duty cardiologist. The patient should be advised of the potential risks and benefits. Patient criteria

a. No specific age limit �– discuss with Cardiology b. Ischaemic chest pain > 30 min & < 12 hrs

i. Benefit is inversely proportional to delay in thrombolysis, therapy should be considered a �“medical emergency�”

ii. Late therapy may be inappropriate for �“small�” infarcts. c. ECG evidence of acute infarction:

i. ST segment 2mm in two (or more) chest leads, or ii. ST segment 1mm in two adjacent limb leads, or iii. New LBBB iv. Posterior infarction ( R in V1 + ST in V2)

d. No benefit has been demonstrated for patients with ST-depression, T-wave inversion, or a normal ECG.

ii) Haemodynamically significant pulmonary embolism. An unequivocal diagnosis is necessary prior to thrombolysis (spiral CT

or angiogram). Tenecteplase is preferred in life threatening pulmonary embolism

iii) Ischaemic Cerebrovascular Accident Within 4.5 hrs of onset of symptoms CT head: confirming CVA and excluding intracranial haemorrhage Oedema on initial CT head is associated with a higher incidence of

bleeding In consultation with a neurologist according to RAH protocol.

b) Contraindications:

i) Absolute: Active internal bleeding. Recent head trauma, major trauma or surgery within 3 weeks. CVA within 6 months. Refractory hypertension (> 200/100 mmHg)

76

ii) Relative: Lack of verbal informed consent. Known bleeding diathesis Current use of anticoagulants (warfarin) Active peptic ulceration or other GI bleeding within 6 months. Prolonged CPR (> 10 mins) and/or traumatic resuscitation Pregnancy. Diabetic proliferative retinopathy. Non-compressible vascular puncture/injury.

iii) Each of these relative CIs should be considered in view of the potential clinical benefit and risk to each patient.

c) Complications i) Bleeding (incidence of cerebral haemorrhage is ~ 0.5%) ii) Anaphylaxis/anaphylactoid reactions: hypotension, rash, bronchospasm iii) Reperfusion arrhythmias

d) Routine follow-up i) ECG at 1 and 4 hours post TNK ii) Cardiac enzymes 6, 12 and 24 hours post infusion iii) If ST-elevation persists 1 hr post-TNK,

contact cardiology regarding �“rescue angioplasty�”.

Table: Thrombolytics

Drug Dose Protocol

Tenecteplase TNK

Single dose: 1. 0.5 mg/kg over 10 sec 2. non-glucose containing line 3. flush line with N.Sal pre & post

Maximum dose = 50mg (=10,000U)

Aspirin 150mg pre-Rx, then daily Enoxaparin 30mg IV prior to TNK Enoxaparin 1mg/kg sc bd

(if renal function normal) If renal impairment consider heparin IV

instead of enoxaparin.

Alteplase

Dose = 0.9 mg/kg. Give 10% of dose as bolus over 1 minute. Give remainder of dose over 60 mins via syringe pump. Maximum total dose 90 mg. Refer to RAH protocol.

Observe vital signs and neurological observations every 30 minutes for the first 6 hours post infusion then hourly for the next 16 hours

Repeat BP more frequently if elevated Keep BP <180/105

Tenecteplase - PTE

As Above Heparin 5000U IV pre-TNK Heparin infusion: APTT > 50-80 secs

Bleeding protocol:

Monitor: APTT PT / INR Fibrinogen level Euglobulin clot lysis time

Apply local pressure (if possible) Reverse heparin with protamine Cryoprecipitate 10 units + FFP 2 units Defibrination or intracranial bleed:

tranexamic acid 10 mg/kg over 20 minutes then 1mg/kg/hr infusion

77

6. Antiplatelet Agents

Table: Antiplatelet Agents

Agent Usual dose Indications/Comments

Aspirin 75-150 mg Post acute coronary syndrome Other thrombotic cardiac event Post TIA / stroke

Clopidogrel 75mg orally daily 300mg oral loading dose pre-PTCA (then 75mg daily)

Irreversibly modifies platelet ADP receptor, inhibiting aggregation

Uses: prevention of vascular ischaemic events e.g. MI, CVA, PTCA

ReoPro (abciximab)

Bolus: 0.25mg/kg IV over 1 min, 10mins before PTCA Infusion: 0.125µg/kg/min IV for 12hrs. (max rate = 10µg/min)

Only to be ordered by Cardiology Binds to platelet glycoprotein IIb/IIIa receptor,

inhibiting platelet aggregation and thrombus formation

Primarily used with PTCA Used with aspirin and heparin

(target ACT >200sec) Increased risk of major bleeding and

thrombocytopaenia

Tirofiban (aggrastat)

Bolus: 0.4 µg/kg/min for 30 mins Maintenance: 0.1 µg /kg/min for at least 48hrs NB: reduce doses by 50% with severe renal insuff. (e.g. creat clearance <30ml/min)

Only to be ordered by Cardiology Blocks glycoprotein IIb/IIIa receptor Short half-life (1.4-1.8 hrs) Uses: unstable angina, non-Q wave MI Use with heparin and aspirin Continue through angiography, and for 12-24hrs

post-PTCA Check platelet count 6hrs post-bolus, then at

least daily. If <90,000 cease and contact cardiology

SEs: bleeding (major 1.4%), thrombocytopenia, fever

78

D. Respiratory Drugs 1. Inhaled bronchodilators

a) General Principles: i) Treatment of bronchospasm in ICU (including acute severe asthma). ii) They are not routinely used in all ventilated patients. iii) Once commenced, they must be reviewed frequently regarding efficacy:

Audible wheeze, respiratory rate Subjective and objective work of breathing Lung compliance Blood gases.

b) Indications: i) Pre-existing asthma / chronic obstructive pulmonary disease (COPD) ii) Acute severe asthma or exacerbation of COPD iii) Bronchospasm 2° to infection, aspiration or during mechanical ventilation,

not primarily due to airway secretions iv) For the treatment of hyperkalaemia (nebulised salbutamol only)

c) Metered dose inhalers: i) MDIs are the default therapy for ICU patients ii) Indications for nebulisers are:

Inadequate response to 10 puffs of MDI Status Asthmaticus

2. Parenteral therapy

a) Indications: i) Adjunctive therapy for patients with acute severe asthma or COPD not

responding to nebulised agents ii) Selected patients who are difficult to wean from ventilation

(usually due to COPD) iii) Maintenance therapy in patients with COPD

b) Complications i) Hypokalaemia, metabolic alkalosis ii) Arrhythmias - 2-agonists, theophylline iii) Intercurrent infection - steroids iv) Polyneuropathy - steroids v) Increased lactate - 2-agonists vi) Metabolic acidosis - 2-agonists

79

Table: Bronchodilators

Drug Infusion/ dose Clinical uses

Salbutamol MDI 4 puffs every 4 to 6 hrs Max 10 puffs 4 hrly if needed

First line bronchodilator Default method of administration

Salbutamol (nebulised) Nebulised in N.Saline (1ml:1ml) continuously, 2 or 4 hrly

Bronchospasm refractory to MDI Severe hyperkalaemia

Ipratropium MDI 4 puffs every 6 hrs Max 10 puffs 6 hrly if needed

Chronic obstructive pulmonary disease Bronchorrhoea Ipratroprium bromide Nebulised in addition to salbutamol

(1ml:1ml)

Budesonide (nebulised steroid)

Nebulised 1 mg b.d. Steroid dependent COPD Acute exacerbation of COPD

Beclomethasone MDI 2-4 puffs b.d. Use 4 puffs with a wet circuit

Fluticasone MDI 2-4 puffs twice daily Use 4 puffs for a wet circuit For patients on Seretide® Inhaler

(Salmeterol & Fluticasone) use Fluticasone MDI

For patients on Symbicort® Turbuhaler (Eformoterol & Budesonide)

use Fluticasone or Beclomethasone MDI

Adrenaline (IV) 6 mg / 100 ml 5%D (ml/hr = µg/min)

Acute severe asthma Rapid onset and offset of action Titrate until clinical pressor response

(may require up to 100 µg/min)

Salbutamol (IV) 6 mg / 100 ml 5%D (ml/hr = µg/min)

Acute severe asthma Longer duration of action

Hydrocortisone 100 mg IV 4-8 hourly All patients with acute severe asthma Wean over 48-72 hrs once asthma begins to

resolve Acute exacerbation of COPD

Theophylline 1000mg / 100ml 5%D Loading 5-7mg/kg, Infuse 2-4ml/hr (1gm/day) Levels: 55-110 mol/l

Second line, adjuvant drug. May improve respiratory drive in COPD Narrow therapeutic index: proarrhythmic

Prostacyclin (inhaled)

500µg + 10ml diluent (50µg/ml) Add to 40ml NSal, infuse with syringe driver into nebuliser (set at 8l/min flow rate) at 2-4 ml/hr.

Selected patients with ARDS with pulmonary HT and severe hypoxia.

Consultant authorisation mandatory.

80

E. Sedation, Analgesia and Muscle Relaxants 1. Sedatives and analgesics

a) Adequate analgesia and anxiolysis are primary goals in the management of the critically ill patient.

b) Pain and anxiety are associated with significant adverse effects: i) Hypertension, tachycardia ii) Increased myocardial and cerebral oxygen consumption iii) Gastric erosions iv) Intracranial hypertension v) Persistent catabolism

c) Sedatives and analgesics are also associated with adverse effects: i) Respiratory depression ii) Prolonged ventilation and associated complications (e.g. nosocomial

infections) iii) Emergence delirium and sympathetic overdrive. iv) Hypotension due to unmasked hypovolaemia. v) Gastroparesis, ileus and resultant feed intolerance vi) Increased cost, ventilator days

d) Sedation protocol for ICU patients: i) It is important, although often difficult, to obtain a reasonable balance

between the awake, distressed patient and the patient that is over-sedated. ii) Sedation should be given by infusion to maintain constant levels, with

boluses as required for discrete interventions. iii) Titrate infusions to clinical effect: there is marked inter-individual variability

and absolute doses are meaningless iv) Patients with renal, hepatic or associated encephalopathy may require lower

doses (or no sedation at all) v) Prescribe the desired sedation level by circling the box on the flow chart:

Table: Sedation Levels

Light: default

eyes open to speech, easily roused purposeful responses usually spontaneous or partial support ventilation nocturnal sedation

Moderate: eyes closed rouses to tactile or painful stimuli, usually partially or fully ventilated

Heavy: no motor response to stimulus weak cough on suction fully ventilated paralysis

81

vii) Nurse controlled sedation protocol Titrate sedation to prescribed level (as above) If the patient becomes over-sedated

a. Hold the infusion until the patient becomes responsive b. If ongoing sedation is required, recommence the infusion at half the

previous rate. If the patient is under-sedated

a. Use a bolus of sedation/analgesia and increase rate according to dose range prescribed.

b. If insufficient repeat until a satisfactory sedation level is attained. Sequential increases in infusion rate, without the use of a bolus dose,

increases the risk of over-sedation as the infusion approaches steady-state (5 half-lives)

Remember, the half-life for fentanyl increases with the duration of infusion, so time to steady-state may be greatly prolonged �– see context sensitive graph below.

Grimacing alone is not a reliable sign and may only indicate awareness or reflex activity.

Infusions should not be titrated to responses during high-intensity stimuli, e.g. suction. In this situation, bolus sedation may be required.

viii) NB: In the absence of a specific contraindication, sedation should be held daily from 0800 for all patients, except those prescribed �‘deep sedation�’.

ix) PCA or epidurals are considered when the patients are awake. Notify the Acute Pain Service of these patients (see next section)

2

50

100

150

200

250

300

4 6 8 10 12 14

Fentanyl

Propofol

Infusion Duration (Hrs)

Con

text

-Sen

sitiv

e H

alf-T

ime

(min

s)

82

Table: Sedatives / Analgesics

Drug Infusion/dose Clinical uses Propofol 10mg/ml (neat solution),

Start at 3ml/hr and titrate against effect Maximum 20ml/hr

Short term sedation where extubation is expected within 24-48 hrs

Do not use where prolonged ventilation is anticipated, except where repeated neurological assessment is required (e.g. CHI), or in the presence of hepatic or renal failure.

Anaesthesia for minor procedures where prompt return of consciousness is required (e.g. tracheostomy, CVC)

Potent myocardial depressant/vasodilator No analgesic effect.

Fentanyl 100-200 µg IV bolus Infusion: 50-200 µg/hr (neat solution)

Haemodynamic stability Potent medium acting narcotic Useful for ICU procedures.

Morphine and Midazolam

morphine 60mg + midazolam 30mg per 50ml 5% dextrose Rate: 1-30 ml/hr

Review rate/sedation at least daily Effects prolonged in renal failure

Morphine 1-5 mg IV, sc prn, or PCA per protocol

First line analgesic Caution in renal failure

Diazepam IV: 2-10 mg prn Orally: 5-10mg bd-qid*

First line anticonvulsant (IV) First line anxiolytic esp in delirium Larger doses may be required in acute alcohol

withdrawal* Epidural cocktail (APS protocol)

Fentanyl 5µg/ml and Bupivacaine 0.1% or Ropivacaine

Standard epidural analgesic regimen Plain bupivacaine may be used (0.25%) Maximal duration 4 days unless indicated Rate: age related doses (per APS)

Dexmedetomidine 400 µg in 40mls load 1µg/kg over 20min infuse 1-5ml/hr

Selective alpha-2-agonist Short term sedation / weaning from ventilation /

withdrawal states Not a first line drug. Selected use by senior medical staff only

Haloperidol 0.5-2 mg IV prn First line major tranquilliser Delirium, agitation Esp. in opioid / benzodiazepine withdrawal. blocker : may cause hypotension

Chlorpromazine 2.5-5 mg IV prn As for haloperidol; 2nd line tranquilliser More sedating, unpredictable & longer acting Vasodilator

83 2. Analgesia in Awake Patients �– See APS Intranet Guidelines

ACUTE PAIN SERVICE �– 2010 SC AND ORAL OPIOIDS �– INITIAL DOSES

Age (yrs)

SC morphine/oxycodone (mg)

Oral oxycodone* (mg)

15 �– 39 7.5 �– 12.5 15.0 �– 25.0 40 �– 59 5.0 �– 10.0 10.0 �– 20.0 60 �– 69 2.5 �– 7.5 5.0 �– 15.0 70 �– 85 2.5 �– 5.0 5.0 �– 10.0

> 85 2.0 �– 3.0 2.5 �– 5.0

Recommended dose interval: 2 hourly prn * if pain not severe

Acute Pain Service (APS) contact numbers

Mon-Fri: 0830-1730 pager 22556

After 1730 hrs SD 1175

W/E & Pub Hol via Switch

Notes: Suggest start in middle of dose range; upper limit of dose range can be

increased if analgesia is inadequate, sedation score is less than 2 and resp rate > 8 /min (first check that doses are correct/ have been given as ordered)

Sedation score 2 = constantly drowsy, still easy to rouse but unable to stay awake once woken

Simple analgesia: Unless contraindicated, paracetamol is best ordered for all patients and on a

regular rather than prn basis

Dose equiv. SC (mg) Oral (mg)

Morphine 10 30

Oxycodone 10 20

Fentanyl 150 microgram -

Buprenorphine 400 microgram (patch) 800 microgram (SL)

84

3. Muscle relaxants

a) General principles i) These agents have a limited role in ICU and must not be used unless the

patient is adequately sedated (heavy sedation). ii) Non-depolarising agents (except rocuronium) should not be used for

emergency (rapid sequence induction) endotracheal intubation. b) Indications

i) Depolarising: suxamethonium First line relaxant for emergency endotracheal intubation (see section on

intubation) ii) Non-depolarising: rocuronium, vecuronium, atracurium

Acute control of ventilation post-intubation Patient transport / retrieval on Oxylog ventilator who cannot be

managed by other means Selected patients with poor lung compliance who are difficult to

ventilate following �“heavy�” sedation With anaesthesia for procedures: tracheostomy, bronchoscopy

c) Complications i) Hyperkalaemia, bradycardia (suxamethonium) ii) Sympathetic overdrive, particularly in under-sedated patients iii) Adverse outcome in head injury when used as a measure to control ICP iv) Use of non-depolarising relaxants may be associated with increased risk of

critical illness polyneuropathy, especially with concomitant use of steroids.

Table: Muscle Relaxants

Relaxant Dose Comment

Suxamethonium 100-200 mg or 1-2 mg/kg

1st line agent in Rapid Sequence Induction (RSI) Consider pre-treatment with atropine (0.6-1.2mg) if

potential bradycardia Contraindicated in burns (>3 days), chronic spinal and

neuromuscular disease, hyperkalaemic states (K+ > 5.5) Caution in any patient with any central or peripheral

muscle weakness including critical illness related weakness

Rocuronium 0.6 mg/kg 1.0 mg/kg for RSI

First line non-depolarising agent in ICU Rapid onset (60secs) 2nd line agent in RSI = alternative to suxamethonium Duration of action : 30-40 minutes

Vecuronium 6-10mg IV prn 2nd line non-depolarising agent in ICU Duration similar to rocuronium

85

F. Anticoagulation 6. General principles

a) All patients on systemic anticoagulation must have an APTT, INR and CBP performed daily.

7. Indications

a) Acute systemic anticoagulation: i) As a general rule, heparin infusions titrated to a therapeutic APTT are used

in critically ill patients. This allows monitoring and the provision for reversal if indicated (e.g. procedures, bleeding complications).

ii) Therapeutic enoxaparin is effective but potentially more difficult to use in critically ill patients, due to inability to easily monitor activity, dose variation in renal disease and inability to reverse effect.

iii) Indications: Proven venous or arterial thromboembolism Acute coronary syndromes: as sole therapy or following TNK Prosthetic heart valves:

a. Prior to commencement of oral anticoagulants b. During an acute illness, where oral anticoagulation is relatively

contraindicated. AF in patients complicated by emboli < 70 years. AF for more than 48 hours, in which cardioversion is being considered Extracorporeal circuits e.g. CVVHDF, ECMO IABP

iv) RAH Heparin Protocol �– see below b) Partial anticoagulation (low dose IV heparin (500 u/hr), IV prostacyclin) c) Oral anticoagulants (warfarin)

i) The kinetics of warfarin are highly variable in the critically ill. ii) Normally only used in stable long term patients iii) Prosthetic valves (mitral > aortic valves) iv) Previous thromboembolism v) Maintenance of thromboprophylaxis in high risk patients (# pelvis)

8. Protocol for DVT/VTE prophylaxis

a) All patients must have a documented plan for DVT prophylaxis b) TED stockings

i) All patients except those with: Significant PVD Significant lower limb trauma, cellulitis, dermatitis or oedema Peripheral venous or arterial access on lower limb(s) For most of the above patients, a single TED should be used on the

unaffected limb ii) TED stockings can be used in patients with proven DVT to decrease the

incidence of post DVT thrombophlebitis iii) Continue until the patient can mobilise effectively

86

c) Prophylaxis with sequential calf compression devices (SCCD�’s) i) SCCD�’s have an additive preventative effect to other forms of DVT

prophylaxis ii) There are a limited number of devices available and priority is given to

patients who are unable to use chemoprophylaxis or are at high risk iii) If a patient has had a prolonged period of time (greater than 24 hours)

without DVT prophylaxis consideration should be given to a lower limb ultrasound to exclude DVT prior to application of SCCD�’s

d) Enoxaparin 40 mg s/c daily i) LMWH of choice, all patients unless contraindicated ii) Start on day 1 or as early as possible especially in high risk patients,

including those with: Previous/family history of DVT or PE Significant trauma involving pelvis and lower limb fractures Vasopressor therapy Post hip or knee replacement surgery Prolonged femoral venous catheters Prolonged immobility, neuromuscular wasting

e.g. Guillain Barré, polyneuropathy, spinal injury End stage renal disease (consider UF heparin)

e) Enoxaparin 60 mg s/c daily (20mg mane + 40mg nocte) i) Should be considered for high risk patients:

Pelvic or long bone fractures Significant spinal injury or paralysis Previous PTE/DVT

ii) Routine monitoring is not necessary. If required, measure anti-Xa activity iii) Continue enoxaparin throughout ICU stay

f) Cease enoxaparin for: i) Significant bleeding ii) Suspected HITS - see below iii) Active and mobile patients who have a short ICU stay and no risk factors

for DVT as outlined above g) Absolute and relative contraindications for enoxaparin:

i) Significant active haemorrhage ii) High risk of bleeding

Coagulopathy - DIC, thrombocytopenia, liver failure, etc. Post-surgical - neuro, spinal, eyes Major trauma - TBI with parenchymal lesions, liver/spleen injury

iii) Known or suspected adverse reaction to heparin Documented or suspected HITS, known heparin allergy

iv) Patients already on therapeutic anticoagulation v) Renal failure

h) Unfractionated (UF) Heparin i) Second line agent for DVT prophylaxis ii) 5000U s/c b.d.-t.d.s. generally has lower efficacy and similar risk of

bleeding in high risk patients compared to enoxaparin

87

iii) Considered in patients with a high risk of bleeding or renal failure, due to its relatively shorter duration of action and ease of reversal.

i) For patients with a high risk of bleeding, communication with the relevant surgical teams (neurosurgery, spinal, ophthalmology, etc) is essential.

j) NB: No other DVT prophylaxis protocols are to be used i) Except for patients post - pelvic surgery ii) The adjusted dose heparin protocol may be used,

see �“VTE Prophylaxis in Orthopaedics�” on the RAH Intranet 9. High risk trauma patients - must have an active plan for VTE prophylaxis 10. Perioperative anticoagulation in patients on Warfarin

a) Heparin infusion remains the first choice in ICU, as the effect is more readily monitored and reversed.

b) Where heparin is contraindicated, consider danaparoid or consult haematology.

11. Protocol for Heparin Induced Thrombocytopaenia Syndrome (HITS) a) General principles

i) HITS is a prothrombotic drug reaction caused by platelet-activating antibodies

ii) It is an intense hypercoagulable state that is often complicated by venous and arterial thrombosis

iii) Risk factors Duration of therapy *see 4T table Type of Heparin UFH > LMWH Type of patient postsurgical > medical > pregnancy

b) Diagnosis i) The 4T Score �‘pre-test probability�’ of HITS

Points - 0, 1, or 2 for each of 4 categories (see table) Maximum possible score = 8

a. High risk 6-8 points b. Intermediate risk 4-5 points c. Low risk 0-3 points

If probability is intermediate or high do a HIT screen for antibodies. If high probability cease heparin immediately pending test results

ii) HIT Screen ELISA detects antibodies against heparin and PF4. Also detects other non-HIT heparin-Ab, therefore lower specificity If ELISA positive then test further with a "functional assay",

serotonin release assay (SRA) iii) Lower limb doppler U/S

88

Table: HITS Probability Score �– �‘4T Score�’

Risk Factor 2 Points 1 Point 0 Points

Thrombocytopenia Platelet fall > 50% Nadir > 20

Platelet fall 30-50% or >50% fall due to surgery or nadir 10-19

Platelet fall < 30% Nadir < 10

Timing of onset of platelet fall (or other sequelae of HITS)

Day 5-10 or Day 1 with heparin in last 30 days

> Day 10 or timing unclear or < Day 1 with heparin in last 31-100 days

< Day 4 No recent heparin

Thrombosis or other sequelae

Proven new thrombosis, skin necrosis or Anaphylactoid reaction after IV heparin bolus

Progressive or recurrent thrombosis, erythematous skin lesions, suspected thrombosis, asymptomatic upper limb DVT

None

OTher cause of platelet fall

None Possible Definite

Pretest probability score: High (6-8) | Intermediate (4-5) | Low (0-3)

d) Treatment principles i) Two Do�’s

Do stop all heparin (including flushes, LMWH, etc ) Do start an alternative non-heparin anticoagulant in therapeutic doses.

a. Lepirudin - difficult to use, or b. Danaproid - may cross react c. Discuss with haematology

ii) Two Don�’ts Don�’t administer warfarin acutely and if warfarin has already been

administered, give vitamin K Don�’t give prophylactic platelet transfusions

iii) Two Diagnostics Test for HIT antibodies Investigate for lower limb DVT

89

7. Anticoagulants

Table: Anticoagulants

Drug Infusion / Dose

Warfarin Variable dose INR See age-adjusted Warfarin loading protocol below Daily INR

Heparin (infusion) 25000u/50ml = 500u/ml See below: titrate against APTT: Cease 4-6 hours prior to surgical procedures

Heparin (subcut) 5000 u subcut bd <70 kg 5000 u subcut 8 hrly >70 kg or high risk DVT

Enoxaparin (Clexane®)

Prophylaxis: 40mg subcut daily 20mg subcut daily if Creat clearance < 30ml/min

�“High risk�” 20mg mane 40mg nocte Treatment:

1mg/kg subcut bd - lean body mass 1mg/kg subcut once daily if Creat clearance <30ml/min

Prostacyclin (infusion) Dose: 0.2-0.6 µg/kg/hr 500µg (+10ml diluent): add to 40ml NSal = 10µg/ml solution Start at 2ml/hr and monitor platelet count May cause hypotension

Danaparoid sodium (Orgaran®) Infusion

IV loading dose: < 60kg 1500 U 60-75 kg 2250 U 75-90 kg 3000 U > 90 kg 3750 U

Infusion: 2250U of danaparoid in 250ml 5% dextrose: 44 ml/hr (400 U/hr) x 4 hours 33 ml/hr (300 U/hr) x 4 hours 22 ml/hr (200 U/hr)

Adjust dose to anti-Xa levels (target 0.5-0.8 anti-Xa U/ml) Long half life (25 hrs): cease early if changing to oral anticoagulants

Danaparoid (subcut) 750 U 8-12 hourly

Lepirudin Complex see below

90

Table: Heparin Infusion Protocol

Weight (kg) 45-55 56-65 66-75 76-85 86-95 >95

Bolus (U) 3,500 4,200 4,900 5,600 6,300 7,000 Infusion (U/hr) 900 1,100 1,250 1,400 1,600 1,800 Infusion adjustment

APTT IV bolus Stop Infusion Rate Change Repeat APTT

< 37 5,000 units 400u/hr 6 hrs 38-64 200u/hr 6 hrs 65-110 No change Daily 111-130 50u/hr 6 hrs 131-140 30 min 100u/hr 6 hrs 141-150 60 min 150u/hr 6 hrs

>150 120 min or APTT < 150 200u/hr 2 hrs

Note: Infusion: 25,000 units in 50ml syringe = 500U/ml Check first APTT 6 hrs after bolus dose

8. Lepirudin

a) Recombinant direct thrombin inhibitor b) Dose range varies by a factor of 20x

i) Care must be used in determining the precise dose ii) Renally excreted and must be carefully monitored in the critically ill

c) NB: bolus is only used if patient has life threatening thrombus

Table: Lepirudin Infusion Protocol

CrCl (ml/min) Bolus Dose Maintenance Infusion

mg/kg/hr % original dose

> 60 0.4 mg/kg (max 44mg) 0.1 (max 11mg/hr) 100%

45-60 0.2 mg/kg 0.05 50%

30-44

None

0.025 25%

15-29 0.01 10%

< 15 0.005 5%

CVVHDF 0.01 10%

91

Table: Age Adjusted Warfarin Loading Protocol*

Day INR Dose (mg) according to age (yrs)

50 yrs 51�–65 yrs 66�–80 yrs 80 yrs

1 1.4 10 9 7.5 6

2 (16hrs after 1st dose) 1.5 10 9 7.5 6

1.6 0.5 0.5 0.5 0.5

3 (16hrs after 2nd dose)

1.7 10 9 7.5 6

1.8�–2.3 5 4.5 4 3

2.4�–2.7 4 3.5 3 2

2.8�–3.1 3 2.5 2 1

3.2�–3.3 2 2 1.5 1

3.4 1.5 1.5 1 1

3.5 1 1 1 0.5

3.6�–4.0 0.5 0.5 0.5 0.5

4 0 0 0 0

4 (16hrs after 3rd dose)

1.5 10�–15 9�–14 7.5�–11 6�–9

1.6 8 7 6 5

1.7�–1.8 7 6 5 4

1.9 6 5 4.5 3.5

2.0�–2.6 5 4.5 4 3

2.7�–3.0 4 3.5 3 2.5

3.1�–3.5 3.5 3 2.5 2

3.6�–4.0 3 2.5 2 1.5

4.1�–4.5 Omit next dose, then

1�–2 0.5�–1.5 0.5�–1.5 0.5�–1

4.5 Nil. Hold dose.

*Roberts GW, Gallus AS, Druskeit T et al. Comparison of an age adjusted warfarin loading protocol with empirical dosing and Fennerty�’s protocol. Aust NZ J Med. 1999; 29: 731-6.

NB. This table is meant only as a guide, and was developed for non-critically ill patients, whose pharmacodynamics may differ significantly from the intensive care population. INR must be checked daily.

92

G. Endocrine Drugs 1. Insulin

a) Indications: i) Diabetic emergencies �– DKA and hyperosmolar coma ii) Treatment of hyperkalaemia

50% dextrose 50ml, plus Actrapid 10U iii) Perioperative diabetic patients (both insulin and non-insulin dependent) iv) General ICU patients

Hyperglycaemia 10 mmol/l or glycosuria in acute illness: a. Maintaining BGL 10mmol/l using an insulin infusion is

recommended for all critically ill patients. b. Majority of ICU patients will require insulin using this protocol. c. NB: This protocol is not designed for patients with diabetic

ketoacidosis and is a guideline only. d. Some patients will require individual manipulation of dose.

Subcutaneous sliding scale insulin: a. No longer recommended by the RAH Endocrine Unit. b. May be used in a small number of less critically ill patients with a

limited need for insulin and for recovering patients in whom IV access is not available

c. A regular dose of subcutaneous insulin, adjusted according to BGL is also suitable in ICU patients.

b) ICU Insulin Protocol �– see following page.

i) Target BGL = 5-10mmol/l ii) Take BGL from arterial line, substituted every 4hrs by finger prick for

patients on insulin infusions iii) Protocol Precautions:

If insulin rate 8 U/hr and the BGL remains high, measurement may be erroneous take a sample from another site and send it to the lab for BGL check.

Consider holding the infusion if feed or glucose infusions are stopped. Potassium level

a. Administration of insulin reduces K+ levels. b. Check K+ on ABG specimen at least twice daily and more often if

the insulin infusion rate is high or changing acutely. c. If [K+] < 3.5 mmol/l

KCl ~ 30 mmol over 1h via a pump.

93

Flowchart: Blood Glucose Management in ICU Table: Insulin Infusion Protocol

BGL Bolus Starting infusion Subsequent infusion Repeat BGL

mmol/l Units IV Units/hr Units/hour Hours

>15 2 2 Increase by 1 1

10.1-14.9 1 1 Increase by 1 1

8-10 0 0 If BGL dropping continue current rate. If static or rising increase by 0.5 1

5-7.9 0 0 Continue current rate If BGL dropping for 2 consecutive hrs decrease rate by 0.5.

1 (2hrly if BGL stable for 6 hrs)

3.5-4.9 0 0 Cease 1 (4hrly if off insulin>6hrs)

<3.5 Call MO 0 Cease 1

c) Discharge Management: i) See �“Insulin Protocol for Patients Discharged from ICU�” below. ii) Pre-discharge, cease insulin infusion for at least 4 hours and check BGL iii) Order BGL to be checked 8 hourly on the ward iv) See �‘Diabetes Management Guidelines�’ on the RAH intranet.

Target BGL = 5-10mmol/l Perform BGL on Admission

BGL = 5-10mmol/l

BGL > 10 mmol/l Commence Protocol Perform BGL 4hrly

94

Flowchart: Insulin Protocol for Patients Discharged from ICU

*See Diabetes Management Guidelines on the RAH Intranet

95

2. Diabetes insipidus: protocol for DDAVP a) Diabetes insipidus may occur in the following situations:

i) Post ablative pituitary surgery ii) Severe head injury, esp. anterior cranial fossa #, trauma iii) Evolving brain death iv) Lithium administration

b) Indications for DDAVP i) Acute perioperative management (24-48hrs) of DI following pituitary

surgery is usually fluid based. Use of DDAVP is rarely indicated. ii) In the above situations:

Persistent polyuria in the absence of diuretics a. > 300ml/hr for > 3-4hrs b. Ensure you document/inform the nurse that you want to be

notified if this occurs, as can quickly get behind Altered conscious state, inability to detect thirst or take oral fluids Low urine osmolality in the presence of high plasma osmolality Pre-existing hyperosmolar state or predisposition to pre-renal failure

where persistent polyuria may exacerbate this. c) Maintenance fluids should be prescribed in the usual manner, according to

volume status, renal function and osmolality. d) DDAVP Prescription

i) Dose 1-2 µg s.c. bd as required. (4µg is excessive) ii) Adjust maintenance fluids according to the response

e) In patients with brain death, DI should be treated promptly as a delay can result in significant electrolyte abnormalities.

3. Steroids

a) Indications i) Pre-existing steroid therapy:

Wide variety of indications, doses and durations of therapy. The need to continue steroids, with or without dose adjustment, should

be assessed. ii) A number of conditions present within the ICU where steroid therapy may

be beneficial. In the majority of these supporting data is variable and the decision to administer steroids should be made on a case-by-case basis:

Adult meningitis - esp. pneumococcal & prior to antibiotics Septic shock - non-responders to a SST ARDS - fibro-proliferative phase + negative cultures Anaphylaxis Post-extubation laryngeal oedema / stridor

b) Contra-indications / non-indications i) Active infection ii) ARDS except as above iii) Acute head injury iv) Guillain-Barré syndrome v) Fat embolism syndrome

96

c) Relative drug potencies

Table: Steroid Doses / Relative Potencies

Drug Equivalent dose (mg)

Glucocorticoid activity

Mineralocorticoid activity

Hydrocortisone 100 1 1 Prednisone 25 4 0.3 Methylprednisolone 20 4 0 Dexamethasone 4 30 0 Cortisone acetate 125 0.8 0.8 Fludrocortisone 1 10 250

d) Short synacthen test (SST) i) Indication:

Suspicion of hypoadrenalism Hyperkalaemia, hyponatraemia, hypoglycaemia, refractory acidosis May be in association with septic shock (incidence is 75%):

a. Refractory hypotension despite aggressive inotropes/IVT b. Relative hypothermia

ii) Test: Semi-quantitative adrenal response to extrinsic ACTH Baseline serum cortisol Synacthen 250 µg IV Serum cortisol level at 30 and 60 minutes

iii) Interpretation: Normal (septic): baseline > 250 nmol/l, increment > 250 nmol/l Hypoadrenalism: baseline < 200 nmol/l, no response to ACTH Intermediate: baseline 200-1000 nmol/l

may or may not increment > 250 nmol/l Note:

a. Hydrocortisone will interfere if given pre-test (false neg). b. Dexamethasone won�’t but has less mineralocorticoid (thus

haemodynamic) benefit c. Aim to perform the test and use hydrocortisone ASAP

iv) Increment < 250 nmol/l may warrant steroid replacement therapy: Hydrocortisone 50 mg qid iv Can be started post-SST and stopped if SST normal Fludrocortisone 50 µg daily NG can also be given.

97

H. Renal Drugs - Diuretics 1. General principles

a) Oliguria in acutely ill patients is frequently a manifestation of: i) Hypovolaemia �– relative or absolute ii) Decreased cardiac output iii) Direct renal toxicity, or iv) A combination of these factors.

b) Therapy should be directed toward causative factors and not maintenance of urine output by the administration of a diuretic agent.

c) Urine output, in the absence of diuretic use, represents one of the best markers of end-organ perfusion and is a useful guide to clinical management.

d) Diuretics should never be used to treat oligo/anuria, they are only a treatment for fluid overload

2. Indications a) Symptomatic fluid overload

i) Pulmonary oedema ii) Congestive cardiac failure: cor pulmonale

b) Hyperaldosterone states: ascites c) Clinical fluid overload d) Chronic renal failure (maintenance)

3. Contraindications

a) Hypovolaemic and/or Na+-depleted states b) Known drug hypersensitivity (esp. sulphonamide group)

4. Complications

a) Hypovolaemia b) Hyperosmolal states due to inappropriate diuresis in hypovolaemia c) Potentiation of renal failure - 2° to hypovolaemia d) Electrolyte disturbance especially K+, Mg, PO4, metabolic alkalosis e) Natriuresis and kaliuresis will alter urine electrolytes and osmolality for 24-48

hrs post dose.

98

Table: Diuretics

Drug Infusion/dose Clinical uses

Frusemide 40-250 mg/day IV / oral

First line, potent loop diuretic Doses may be increased in diuretic dependence K+, Mg, PO4, metabolic alkalosis common

Acetazolamide 250-500 mg IV tds Carbonic anhydrase inhibitor Alkaline diuresis with HCO3- excretion Used for severe metabolic alkalosis after

correction of hypovolaemia: K+, Mg, PO4 May be useful in weaning COPD from ventilation

with post hypercapnic alkalosis

Spironolactone 25-100 mg oral bd Potassium sparring diuretic Often given with loop and thiazide diuretics Indicated as part of diuretic treatment regime for

left ventricular failure Use in ascites especially if secondary

hyperaldosteronism

Mannitol 20% solution / 200 mg/ml Dose 100 ml prn (20g) (0.5g/kg is too much!!)

Potent osmotic diuretic May cause initial hypervolaemia, then late

hypovolaemia and hyperosmolal states. Causes an osmolal gap

(measured-calculated osmolality). Maintain measured osmolality < 300 mosmol/l Limited role in suspected acute life-threatening

intracranial hypertension as a bridge to definitive surgical therapy.

Limited (unproven) roles in rhabdomyolysis, transfusion reactions, myoglobinuria for renal protection

99

I. Gastrointestinal Drugs 1. Stress ulcer prophylaxis

a) Routine stress ulcer prophylaxis is not indicated. i) Low prevalence of clinically significant bleeding due to stress ulceration ii) No evidence of survival benefit iii) Possible increased incidence of VAP

b) High risk stress-ulcer patients i) Prophylaxis - ranitidine 50mg iv tds ii) Reduce dose in renal compromise

c) Patients on pre-existing therapy (with PPIs or H2-blockers) should be continued d) Patients with known or clinically suspected GI bleeding should commence on a

PPI e) Enteral feeding should be commenced as soon as possible

2. Acute GI bleeding a) Definition

i) Overt bleeding Blood in the NGT Haematemesis or malaena

ii) Plus either: MAP > 20 mmHg Hb 20 g/L in 24 hours Required 2+ units blood transfusion in 24 hrs

iii) Blood in the NG tube is frequently due to local erosion and by itself does not constitute clinically significant GI bleeding.

b) Management i) Resuscitation - ABC ii) Correct coagulopathy iii) Cease heparin / anticoagulants iv) Commence PPI - pantoprazole 40 mg bd/tds. v) Endoscopy sclerotherapy vi) If the source is not identified and with ongoing bleeding, consider:

Labelled red cell scan Angiography (+/-embolisation) or Colonoscopy.

100

3. GI drugs

Table: GI Drugs

Drug Dose Clinical uses

Metoclopromide 10 mg IV 6 hrly, prn Persistent vomiting, nausea Large gastric aspirates

(in combination with erythromycin)

Erythromycin 100 mg IV bd Large gastric aspirates (in combination with metoclopramide)

Droperidol 0.625 mg IV prn Potent, effective antiemetic Minimal side effects

Tropisetron 2 mg IV / oral daily Third line antiemetic after metoclopramide and droperidol

Use if anticholinergic side effects are to be avoided.

Ondansetron 4 mg IV prn / 12 hrly Second line, antiemetic (not available at RAH)

Ranitidine 50 mg 8hrly IV 150-300 mg daily po

Peptic ulcer disease First-line stress ulcer prophylaxis Does not prevent acute rebleeding Reduce dose in renal failure.

Pantoprazole Acute RX: 40 mg IV bd/tds Maint. RX: 40 mg daily

Refractory peptic ulcer, ulcerative oesophagitis First line RX for peptic ulceration Z-E syndrome Upper GI bleeding

Octreotide Bolus: 50 g IV Varices: 50 g / hr Fistulae: 100-200 IV / sc 8-hrly

Variceal bleeding (as effective as sclerotherapy)

Enteric, pancreatic fistulae Sulphonylurea overdose Severe secretory diarrhoea, e.g. post-chemo

101

J. Antibiotics 1. Policy

a) Prescription of antibiotics must conform to RAH guidelines. b) The over-prescription and irrational use of antibiotics is associated with the

development of bacterial resistance, nosocomial infection and drug related morbidity

c) All antibiotics must be reviewed daily and where appropriate, discussed with Infectious Diseases or Clinical Microbiology.

d) Record the day and expected course of antibiotics in the left-hand margin of the drug chart, e.g. �‘D4/7�’ = day 4 of a 7 day course.

e) Record date, test and results (including sensitivities) in the �“results folder�”. 2. Principles of antibiotic prescription

a) The treatment of infection consists of (in order of priority) i) Adequate resuscitation ii) Surgical drainage of infected collections where indicated iii) Relevant samples for microbiological and/or histological analysis iv) Standard cultures:

Blood - 2 sets at different times from venous stabs Urine Sputum Any other suspicious site

v) Rational prescription of empiric antibiotics vi) Prompt administration of culture-directed antibiotics vii) NB: time to effective ABx treatment affects outcome.

b) General indications for antibiotics:

i) Prophylaxis for invasive procedures and operations Proven indications

a. Abdominal surgery which involves a breach of the colonic mucosa (traumatic or elective), or draining an infected cavity

b. Selected obstetrical and gynaecological procedures: i. Caesarean section with ruptured foetal membranes ii. Vaginal hysterectomy

c. Insertion of a prosthetic device d. Compound fractures e. Amputation of gangrenous limb

Unproven but recommended a. Lacerations penetrating into periosteum or into joint cavities b. Crush injuries c. Insertion of a neurosurgical shunt d. Cardiac valve replacement e. Arterial prosthesis

102

ii) Empirical antibiotics where infection is likely prior to definitive bacteriological diagnosis:

Obtain as many cultures as possible before antibiotics commenced. In sick patients "best guess" antibiotics should be commenced prior to

results When gram stain or culture results return, antibiotic cover should be

rationalised to specific treatment for isolated organisms. iii) Specific infections where the organisms is known

c) Complications of antibiotics

i) Antibiotic effect related Bacterial resistance Nosocomial infection Pseudomembranous colitis

ii) Systemic reactions Skin rashes Anaphylactoid / anaphylactic reactions

iii) Specific organ toxicities, e.g. Interstitial nephritis, ATN Seizures Marrow suppression, thrombocytopaenia QT prolongation

iv) Cost

d) Gentamicin i) Pharmacodynamic properties

Concentration-dependent killing peak:MIC ~ 10:1 Significant post-antibiotic effect

ii) Toxicity Nephrotoxicity - non-oliguric renal failure Ototoxicity - permanent, vestibular or auditory

iii) Dosing All dosing for gentamicin is by Lean Body Weight (LBW) Estimate lean body mass:

a. Male: 50kg + 0.9kg/cm height > 150cm b. Female: 45kg + 0.9kg/cm height > 150cm

Initial Dose: 5-7 mg/kg *irrespective of renal function Measure level 6-10 hrs post-dose:

a. See target levels on following graph, or b. Liaise with ICU Pharmacist (Pg: 22916) or

Drug Information (Ext: 25546) re further dose requirements. Synergistic gentamicin, e.g. tds dosing in endocarditis

a. Measure pre-dose trough levels b. Aim for < 1.0 mg/L to avoid toxicity.

103

e) Vancomycin i) Pharmacodynamic properties

Time-dependent killing max 24h-AUC:MIC ratio Moderate post-antibiotic effect

ii) Toxicity Ototoxicity < 2% Nephrotoxicity

a. Very rare (20 case reports 1956-84) b. Probably non-existent with current preparations

�‘Red-man�’ syndrome rate of IV administration. iii) Preference in ICU is for continuous infusion, c.f. interval dosing.

Moderately irritant to veins If given via a peripheral line,

infusion volume should be 250ml solution @ 10ml/hr iv) Renally cleared. Plasma t½ = 4-6 hrs v) NB: assessment of renal function by serum creatinine is sub-optimal.

Elderly patients and those with low muscle mass may have a significantly impaired GFR in the setting of a �“high-normal�” creatinine

Do NOT use if CrCl < 60 ml/min

104

Table: Vancomycin Dosing Schedule

Renal Function CrCl > 50 ml/min

CrCl 10-50ml/min

CrCl < 10 ml/min CRRT

Initia

l Dos

ing Loading dose IV

1.0g or 15 mg/kg if wt >80kg, or 25 mg/kg if �‘critically unwell�’ slow infusion (1/24) in All Patients

Infusion Rate 2.0g / 24 hrs 1.0g / 24 hrs Not indicated

Subsequent Dosing 1.0g IV 12 hrly 500mg IV 12 hrly Per levels

Level Monitoring 1hr pre-dose #6 (usually day 3) Daily

Infu

sion

Dose

Ad

justm

ent

Target Level �– Infusion: 20-25 mg/L

[Vanc] < 15mg/L Dose 1g/day max = 4g/day Dose 0.5g/day

Not indicated [Vanc] = 20-25mg/L Cont. Cont.

[Vanc] > 30mg/L Hold 24 hrs Recheck Level

Hold 24 hrs Recheck Level

Inte

rval

Dose

Ad

justm

ent

Target Level - Interval [Trough]: 15-20 mg/L

[Vanc] < 10mg/L Dose 1g/day max = 4g/day Dose 0.5g/day

Dose & Interval Per

Daily Levels

[Vanc] = 10-15mg/L Dose 0.5g/day Dose 0.25g/day

[Vanc] = 20-25mg/L Dose 0.5g/day Dose 0.5g/day

[Vanc] > 25mg/L Hold 24 hrs Recheck Level

Hold 24 hrs Recheck Level

105

Table: Antibiotic Infusion Schedules

Antibiotic IV Loading All Patients

Max Hrs Stability

1Standard Infusion Dose (per 24 hrs) Renal Function CrCl > 50 ml/min CrCl ~ 10-50ml/min CrCl < 10 ml/min CRRT

Vancomycin2 1.0-2.0g 24 2.0-4.0g 1.0g Not indicated

Penicillin G 1.2-1.8g 12 4.8-14.4g 4.8-9.6g 2.4g 4.8-9.6g

Amoxycillin 1.0-2.0g 6 4.0-12.0g 4.0-6.0g 2.0g 4.0-12.0g

Flucloxacillin 1.0-2.0g 24 4.0-12.0g 4.0g 4.0-12.0g

Piperacillin 4.0g 24 12.0-16.0g 8.0g 12.0-16.0g

Tazocin 4.5g 24 13.5g 9.0g 13.5g

Ceftriaxone 1.0g 24 1.0-4.0g

Ceftazidime 1.0-2.0g 24 3.0-6.0g 2.0-4.0g 1.0-2.0g 2.0-4.0g

Meropenem 1.0-2.0g 8 3.0-6.0g 1.0-2.0g 0.5g 2.0g

1 Standard Infusion Orders: 24 Hrs Dose in 100ml {N.Saline | 5%Dext.} @ 4ml/hr (per Max Hrs Stability) 12 Hrs (Dose / 2) in 100ml {N.Saline | 5%Dext.} @ 8ml/hr 8 Hrs (Dose / 3) in 100ml {N.Saline | 5%Dext.} @ 12ml/hr 6 Hrs (Dose / 4) in 100ml {N.Saline | 5%Dext.} @ 16ml/hr 2 Vancomycin should be diluted into 250mls if given via a peripheral line. Loading dose over at least 60 mins, or 10mg/min.

*NB: Add the reconstituted solutions to a 100mL bag of compatible fluid, having first removed an equivalent volume of solution, i.e. so the final total volume of the bag remains 100ml, then administer over the required interval.

106

3. Ventilator associated pneumonia (VAP) a) Significant cause of mortality and morbidity in ICU b) Clinical diagnosis based on combination of some of the following

i) New CXR infiltrates (hard to see in patients with ARDS) ii) New clinical chest signs iii) Increasing oxygen requirement iv) Increased purulent sputum v) Indications of systemic sepsis

Increased WCC Fever Hypotension

c) Treatment i) Sputum culture ii) Commence antibiotics immediately

Tazocin 13.5g/24hrs (or 3 divided doses) & Gentamicin 5mg/kg on day 1, then as per levels

If gentamicin contraindicated, ciprofloxacin 200-400mg b.d. In patients with known MRSA or ICU stay > 5days

a. Add vancomycin b. Stop if no gram positive organisms seen on micro

iii) Review sputum culture If no organism and not on ABx consider another diagnosis De-escalate to narrow spectrum therapy ASAP Normal treatment 5-7 days except pseudomonas sp. then 10-14 days

4. Antibiotic prophylaxis

a) Peri-operative (Table) i) Ongoing prophylactic therapy is required for selected post-operative

patients in ICU. ii) Refer to individual protocols for recommendations on pre-operative

antibiotic prophylaxis.

107

Table: Peri-operative Antibiotic Prophylaxis

Specialty Procedure Antibiotics

Orthopaedics Elective cases Cefazolin 1g IV 8h x 3 doses

Traumatic wounds Involving bone or joint

compound fractures

Cefazolin 1g IV 8h x 2 days

+ severe tissue damage + myonecrosis + vascular injury

Cefazolin 1g IV 8h x 2 days + Gentamicin 5 mg/kg IV daily x 2 days + Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days

Abdominal Surgery Colorectal Cefazolin 1 gm ± gentamicin 3 mg/kg + Metronidazole 500mg IV single doses

Biliary surgery Gentamicin 3 mg/kg x 1 dose, or cefazolin 1g x 1 dose

Vascular surgery Elective cases + severe bowel injury + myonecrosis or

vascular injury Amputation

Cefazolin 1g IV 8h x 3 doses + Gentamicin 5 mg/kg LBW IV daily x 2 days

+ Metronidazole 500 mg IV bd x 2 days + Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days

Cefazolin 1g IV 8h x 3 doses + Metronidazole 500 mg IV bd x 2 doses

Neurosurgery CSF leak / # Skull base None: treat only if signs of meningitis

Craniotomy / ICP insertion Cefazolin 1g IV at induction

Head & neck, thoracic

Craniofacial with breach of nasal or oral mucosa

Cefazolin 1g IV 8h x 3 doses + Metronidazole 500 mg IV bd x 2 doses

Cardiac Surgery CABG CABG + Penicillin allergy

Cefazolin 1g IV 8h x 3 doses Vancomycin 1g (over 1 hr)

+ Gentamicin 240mg at induction

Cardiac valve surgery Vancomycin 1g + 500mg 12 hrs later + Gentamicin 240mg at induction

108

Table: Perioperative Endocarditis Prophylaxis

109

Table: Empirical Antibiotics

Infection Type / Comment Antibiotics

Pneumonia

Community acquired Immunocompetent Admitted to ICU / HDU

(i.e. respiratory failure)

Azithromycin 500mg IV daily, plus *Ceftriaxone 1 IV daily

For treatment failure, consider Moxifloxacin 400mg IV daily ± Flucloxacillin 1g 6h (if high suspicion of S.aureus)

*Default ICU therapy differs from the RAH standard protocol (penicillin + gentamicin) due to the wide variability in renal function in ICU patients and the inability to use baseline creatinine as a marker of renal function.

Ventilator associated Hospital acquired

Tazocin 4.5g IV 8 hrly or 13.5g/day + Gentamicin 5 mg/kg IV daily

Consider Vancomycin 1g b.d. IV See above

Immunocompromised host Contact ID

Aspiration No antibiotics without evidence of proven infection.

With proven infection Benzyl penicillin 1.2g IV 6 hrly, plus metronidazole 500 mg IV 12 hrly

Exacerbation of COPD No clinical signs of pneumonia Treat as community acquired pneumonia

Epiglottitis Usually H. influenzae Ceftriaxone 1 g IV daily

Meningitis/ encephalitis

Suspected bacterial Usually: meningococcus

pneumococcus, or H. influenzae

Ceftriaxone 2g IV 12 hrly, plus Penicillin 1.8g to 2.4g IV 4 hrly

Dexamethazone 10mg IV before or with the first dose of antibiotic then 6hrly for 4 days

Not definitely bacterial Consider Acyclovir 10mg/kg IV 8hrly

Urinary tract infection

Without systemic sepsis in patients with a urinary catheter

No treatment. Remove / change catheter

With systemic sepsis Amoxycillin 2g IV 6 hrly, plus gentamicin 5mg/kg IV daily, or

Ceftriaxone 1gm IV daily if unable to tolerate gentamicin

Intra-abdominal sepsis

Faecal peritonitis Perforated viscus

Amoxycillin 2 gm IV 6 hrly + Gentamicin 5 mg/kg IV daily + Metronidazole 500 mg IV bd x 7 days

Recurring intra-abdominal sepsis or failed Rx with above

Consult ID/Clinical Microbiology

Pancreatitis No CT evidence of necrosis No antibiotics Significant CT necrosis Tazocin 4.5g IV 8 hrly

Biliary sepsis

Acute cholecystitis Ascending cholangitis

Amoxycillin 1 g IV 6 h + Gentamicin 5 mg/kg/d IV x 7 days

Amoxycillin 2 gm IV 6 h + Gentamicin 5 mg/kg/d IV

Previous biliary tract surgery or known biliary obstruction

add Metronidazole 500mg IV BD x 7 days

110

Gynae sepsis

Septicaemia secondary to PID Amoxycillin 2g IV 6 h + Gentamicin 5 mg/kg IV dly + Metronidazole 500 mg IV bd x 5 days

Suspected S. aureus infection Lincomycin 1.2g IV bd + Gentamicin 5 mg/kg IV dly x 7 days

Suspected Bacterial Endocarditis

Community acquired Benzyl penicillin 1.8 g IV 4 h + Gentamicin 1 mg/kg IV tds ± Flucloxacillin 2g IV qid

Hospital acquired Prosthetic valve, or Penicillin allergic

Vancomycin 1g IV bd + Gentamicin 1 mg/kg IV tds

3 sets of blood cultures, and review at 48 hrs Manage pre-dose trough levels for gentamicin <1 mg/L to avoid toxicity

Fungal Septicaemia

Suspected candidiasis Amphotericin 0.5-1 mg/kg/day, or Fluconazole 400 mg IV daily

(in non-neutropaenic patients) Suspected aspergillosis Voriconazole IV/oral 6mg/kg BD loading for 24

hours, then 4mg/kg BD or

Caspofungin 70mg IV daily loading for 24 hours, then 50mg daily

1. Consult ID for all proven fungaemias 2. Remove all potential sources of infection (lines, catheters, etc) 3. Monitor renal / hepatic function during the course of antifungal therapy. 4. Adjust the amphotericin dose in renal insufficiency, or consider the use of fluconazole if

appropriate 5. Voriconazole levels can be monitored for toxicity and clinical responses. 6. IV voriconazole is contraindicated in patients with CrCl < 30mL/min due to accumulation

of the excipient Burns No antibiotics without evidence of bacterial infection

Cutaneous infections

Wound infection + signs of systemic sepsis

Benzylpenicillin 1.8 g IV 4 h + Flucloxacillin 1-2 g IV 6 h or

Cefazolin 1g IV 8h Synergistic gangrene Necrotising fasciitis

In addition to surgery

± hyperbaric oxygen

Meropenem plus

Lincomycin 600 mg IV 8 hrly, or Clindamycin 600 mg IV 8 hrly

Consider IV-Ig 2.0g/kg total dose (3 days) Severe oral infections Penicillin 1.2 g IV 4-6 hourly

+ Metronidazole 500 mg IV bd

Line sepsis

Patient not overtly septic Remove unnecessary, old or clinically suspect lines & send for culture.

Blood cultures by venipuncture No antibiotics

Patient overtly septic Prosthetic valve / arterial graft High risk patient

Vancomycin 1 g IV BD until blood culture results available

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Table: Antibiotics for Specific Organisms

Organism 1st choice 2nd choice Pneumococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1 IV dly

Staphylococcus aureus Flucloxacillin 2 gm IV 6 h Vancomycin 1gm IV bd or Cefazolin 1-2g IV 8h

Meningococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1g IV dly

Meningococcus contacts Ciprofloxacin 500mg po x 1dose Rifampicin 600mg po bd x 2 days

MRSA Vancomycin 1g IV bd Consult ID

Enterococcus Amoxycillin 1-2 g IV 6 h (+ Gentamicin 5 mg/kg if SBE)

Vancomycin 1g IV dly (+ Gentamicin 5mg/kg if SBE)

Gp A Strep. With Shock

Benzylpenicillin 1.8g 4 hrly IV + Lincomycin 1.2g IV bd + Intragam 2.0g/kg total dose (3 days)

Consult ID Cease IG when pt. improves

Haemophilus influenzae Ceftriaxone 1g IV daily Amoxycillin 1-2 g IV 6 h (if sensitive)

H. influenzae contacts (meningitis) Rifampicin 600 mg oral bd x 4 days Ceftriaxone 1g IM dly x 2 doses

E. Coli Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly

Enterobacter Gentamicin 5 mg/kg IV dly Meropenem 500mg IV 8h

Klebsiella Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly Pseudomonas aeruginosa Piperacillin 4 g IV 8 hrly

+ Gentamicin 5-7 mg/kg IV dly

Choice based on sensitivity results: Ceftazidime 2g IV 8hrly or Tazocin 4.5g IV 8hrly PLUS Gentamicin 5-7 mg/kg IV daily or Ciprofloxacin 400mg IV bd

Legionella spp. Moxifloxacin 400mg IV daily Azithromycin 500mg IV daily

Mycoplasma pneumoniae Erythromycin 1g IV 6h Pneumocystis jurovecii Co-trimoxazole 15-20 ml IV 6 h

+ methylpred 40mg bd x 5d, methylpred 40mg die x 5d, methylpred 20mg die x 11d,

Pentamidine isethionate 4 mg/kg/day IV + methylprednisolone 40mg 6 hrly x 7days

Clostridium difficile: 1. Mild / moderate 2. Severe, or relapse post RX

Cease antibiotics 1. Metronidazole 400 mg o tds

(or 500mg IV if npo) x 7-10 days

2. Repeat above

Consult ID or Clinical Micro. Treatment options are: Bacitracin 25,000U 6hrly 7-10d or Vancomycin 125mg po 6hrly 7-10d

Clostridial infection (Polymicrobial Infection)

Benzylpenicillin 1.8g IV 4 hrly + Gentamicin 5 mg/kg IV dly + Metronidazole 500 mg IV bd + surgical debridement hyperbaric oxygen

Lincomycin 600 mg IV 8 hrly + Gentamicin 5 mg/kg IV daily

NB: Dose for Ceftriaxone is 1.0g IV daily, except where the site of infection is meningitis or endocarditis, or the infection is life-threatening

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PART 4 - FLUIDS AND ELECTROLYTES A. Principles of Fluid Management in Intensive Care 1. All fluids, infusions are reviewed daily and

a) Rewritten on the ICU flowchart (Units A & B), or b) In the IV Fluid chart in the ward folder (Unit C).

2. Assessment of volume status and fluid balance involves all of the following: a) Clinical markers

i) Skin turgor, mucous membranes, capillary refill, peripheral perfusion ii) HR, BP, Urine output iii) CVP, PAOP iv) PiCCO catheter - GEDI, ELWI, stroke volume variability. v) CXR, interstitial oedema vi) Echo �– IVC distensibility index, LVOT- VTI variability

b) Biochemical markers i) Serum Na+, Cl-, osmolality ii) Urea / creatinine (± ratio) iii) Bicarbonate iv) Haematocrit

c) Charted fluid balance (notoriously inaccurate!) i) Total intake including drug/infusion volumes ii) Total output including urine output, drains, NG losses, blood loss iii) Insensible losses due to pyrexia, transcellular shifts, etc.

(NB: usually impossible to quantify accurately) 3. Fluids should be considered in two components:

a) Maintenance fluids i) Usually crystalloids:

4% dextrose + 1/5 N.Saline 5% dextrose / N.Saline Hartmann�’s

ii) Usual volumes: 25-30 ml/kg/day 80-120 ml/hr iii) TPN (refer to guidelines)

b) Replacement / resuscitation fluids i) N.saline should be used for most fluid resuscitation.

Equivalent to 4% albumin for resuscitation Better for patients with head trauma.

ii) Colloid (4% albumin, gelofusine) may be considered for fluid resuscitation in selected patients. Greater cost, no demonstrable advantage.

iii) Blood and blood component therapy as indicated and according to NH&MRC guidelines.

iv) Crystalloid replacement is usually used for excessive renal, enteric and burns losses (see below).

v) Hyperchloraemia may be harmful so consider the use of fluids with other anions, e.g. Hartmann�’s.

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4. Composition of commonly used fluids (1000ml solution):

Solution Na+ K+ Cl- Ca++ Lact. Gluc. Osm. Prot. N Saline 150 150 300 N/2 Saline 75 75 150 N/5 Sal. + 4% Dex. 30 30 40 g 282 5% Dextrose 50 g 278 Hartmann�’s 131 5.0 111 2 29 280 Gelofusine (500ml) 77 60 274 20g Albuminex 4% (500ml) 70 62.5 25g

5. Fluid management in burns patients

a) The RAH Burns Unit uses the modified Parkland regimen. b) This is a guide - other clinical markers such as urine output, heart rate, blood

pressure, CVP, serum sodium and osmolality, and haematocrit must be taken into account.

c) As a result, both solution composition and administration rate may have to be modified in order to maintain the above parameters within normal ranges.

d) Protocol: i) Assess the patient�’s % burn surface area (%BSA) using an accurate chart. ii) Assess patient weight (kg). iii) Formula:

First 24 hours = total fluid (as Hartmann�’s solution): Wt. x %BSA burn x 4.0 ml a. give ½ the total fluid during first 8 hours post-burn b. give ½ the total during the subsequent 16 hours

Second 24 hours fluid is given as Albuminex 4% Wt x %BSA burn x 0.5 ml

Other maintenance fluid is given according to the above physiological parameters

The primary endpoint of fluid resuscitation is generally accepted to be urine output 0.5-1 ml/kg/hr

Catecholamines: a. Should be commenced only when adequate volume replacement is

unable to maintain a satisfactory urine output, or there is associated myocardial failure.

b. The duty consultant or SR should be consulted prior to use. iv) Commence enteral feeding as soon as possible, per protocol.

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B. Nutrition 1. Enteral nutrition

a) Enteric feeding is the preferred mode of nutritional support and must be considered in all patients as soon as possible after admission to ICU.

b) Advantages i) Early EN in trauma patients has been associated with improved outcome. ii) Use of the gut decreases mucosal atrophy, which may reduce bacterial

translocation thereby reducing the incidence and duration of sepsis. iii) The incidence and severity of gastric erosions and stress ulceration may be

reduced. iv) Cheaper than TPN v) Complications of central vascular access (especially infection) are reduced

or avoided. c) Disadvantages

i) Regurgitation / aspiration ii) Nosocomial pneumonia iii) Diarrhoea (other causes are more likely than enteral feed)

d) Indications i) As soon as possible in all intubated / tracheostomised patients, where

admission and duration of intubation is expected to be > 24-48 hours. ii) Patients with an operative jejunostomy may commence feeding within 6

hours of placement. e) Contraindications

i) Gastrointestinal (including oesophageal) perforation, gastrointestinal fistulae, bowel obstruction, ileus.

ii) Recent bowel anastomosis is not a contraindication �– however, discussion with the surgical team is essential.

iii) Absent bowel sounds is not a contraindication. f) Protocol (see feeding protocol at bedside)

i) Liaise with the dietician (who will order feeds) during the fluid round. ii) Outline any problems: e.g. hyperkalaemia, renal failure, osmolality iii) Place a 12F or larger nasogastric tube (to allow reliable aspiration) iv) Use orogastric tubes in patients with anterior and middle cranial fossa # v) Check the position of the feeding tube with x-ray prior to use. vi) Nurse the patient at 30-45° head up. vii) Commence feed at 80 ml/hr continuously according to the protocol. viii) Aspirate the tube 6 hrly

Including all NG tubes and PEGs. Do not aspirate jejunostomies, naso-duodenal/jejunal tubes or PEJs

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ix) Flush jejunostomy/gastrostomy tubes with 20ml N.saline 6hrly. Aspirate < 250 ml:

a. Return aspirate to stomach b. If rate < max, then increase rate by 20 ml/hr c. Repeat aspiration at 6hrs and

if < 250 ml then to max rate (usually 80-100 ml/hr) Aspirate > 250 ml:

a. Return 250ml b. Halve the feed rate (not less than 20 ml/hr) c. Continue to aspirate 6 hrly d. Consider prokinetics:

i. Metoclopramide 10 mg IV 6 hrly, plus Erythromycin 100 mg IV bd

ii. Continue until tolerating feed for > 72hrs, then cease and observe

iii. Recommence as needed e. Reduce narcotic administration if possible.

If aspirates > 250 ml while receiving prokinetics consider: a. Post-pyloric feeding tube

(either using Cortrak® device or endoscopically by the GI Unit) b. Feeding jejunostomy c. Nasogastric naloxone 4-8mg tds d. TPN.

x) Consider a PEG, PEJ or feeding jejunostomy in long term patients e.g. Guillain Barré or severe head injury

xi) Cease feeds 4 hrs prior to extubation, tracheostomy, ET tube change. xii) There is no requirement to cease feeds until immediately prior to going to

theatre, unless: Surgical procedure on the GIT Planned for tracheostomy or ETT change.

xiii) Remember to modify insulin dose when feeds are reduced or ceased. 2. Enteral Protocol

a) See over page.

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Flowchart: Nutritional Therapy Protocol

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3. Post-pyloric feeding protocol:

a) Commence feed at 1ml/kg/hr, up to a maximum 80 ml/h. b) No need to cease feed for any procedures. c) Consider placement of a NG tube to aspirate and ensure an empty stomach.

4. Parenteral Nutrition

a) General principles i) TPN may be harmful in critically ill patients. ii) Enteral nutrition is preferred and TPN should only be considered for patients

in whom this is not possible. iii) Supplementing EN with TPN is not beneficial and should be avoided. iv) Refer to �‘Clinical Duties Outside ICU�’, regarding the responsibilities and

management of ward patients receiving TPN. v) TPN is usually ordered by the Unit A Senior Registrar, under the supervision

of the Unit A consultant. vi) IV access may be via a CVC or PICC line, with the latter being preferred. vii) TPN for ICU patients is prescribed during the midday fluid round. viii) Patient being discharged from ICU on TPN must be entered into the TPN

folder in Unit A.

b) Indications for TPN in the patient who cannot be fed enterally are: i) GIT Failure > 7-10 days and expected duration of support > 5-7 days.

Prolonged post operative ileus Enteric fistulae

ii) Short GIT syndrome following major intestinal resection.

c) Complications of TPN: i) Depression of immune function, esp. in cancer patients ii) Gut villous atrophy iii) Metabolic imbalance

Electrolyte disturbances ( K+, HPO4=, Mg++)

Glucose intolerance: hyperglycaemia and glycosuria Hyperosmolar dehydration syndrome Rebound hypoglycaemia on cessation of TPN Hyperbilirubinaemia CO2 production, esp. in COPD patients

iv) Fluid imbalance v) Trace element and vitamin deficiencies vi) Central venous access complications

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d) Protocol i) On commencement:

Add the following orders to the patient's drug folder: a. Cernevit MV 1 ampoule IV daily. b. Trace elements 1 ampoule daily c. Vitamin K 10 mg IV weekly d. Commence insulin:

i. Initial dose = 5U s.c. qid *hold if BGL < 10 ii. Check BGL qid iii. Adjust the dose on subsequent days guided by BGLs iv. �“Sliding Scale�” regimens are no longer used.

Commence TPN solution at a lower rate (40ml/hr) in �“starved�” patients a. Potential movement of K+ / HPO4

= into cells with refeeding b. May cause acute severe hypokalemia and hypophosphataemia.

Slowly increase to desired rate, usually 60-80 ml/hr. Dietician will provide a calculated energy requirement as a guide

ii) Daily: Review the patient, CVC site, biochem, BGL chart and fluid balance. Prescribe TPN selecting the most appropriate �“option�” from the

following table. These bags are pre-prepared and must not be altered, i.e. no further

additives. Patients requiring K+, PO4 and fluids etc. above the quantities provided must receive these in a separate line/infusion.

iii) Intralipid Commence TPN with lipid-free solutions (#3, #4) Lipid is indicated if the period of malnutrition > 4 weeks or if the patient

is hyperglycaemic.

Table: Average daily requirements Water 30-40 ml/kg/day

Calories 30-40 kcal/kg/day 1. Glucose: 2g/kg/day @ 4.1 kcal/g 2. Fat: 2g/kg/day @ 9 kcal/gram

Protein 0.5-1.0 g/kg/day 1. 2:5 essential:total amino acids 2. 150:1 kcal:g N2 (non-nitrogen kcal)

Sodium 1.0 mmol/kg/day

Potassium 1.0 mmol/kg/day Dependent on renal function

Phosphate 0.2 mmol/kg/day Dependent on renal function

Vitamins B groups daily B12, Folate, A, D, E, K weekly Trace elements as required.

Replacement solutions

1. Urine 2. Nasogastric/ileostomy 3. Pancreatic/biliary fistulae

1. ½ Normal saline ± KCl 10 ml/L 2. ½ Normal saline ± KCl 10 ml/L 3. Hartmann�’s solution

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Table: Baxter TPN Solution Options

Composition Baxter Option 1

With Lipid With Potassium

Baxter Option 2 With Lipid

No Potassium

Baxter Option 3 No lipid

With Potassium

Baxter Option 4 No Lipid

No Potassium Total Volume (ml) 2000 2100 2000 2100 Glucose (gm) 250 250 500 500 Lipids (gm) 100 100 0 0 Energy (kcal) 2270 2270 2300 2300 Protein (gm) 100 100 100 100 Nitrogen (gm) 16.5 16.5 16.5 16.5 Na+ (mmol) 73 73 73 73 K+ (mmol) 60 0 60 0 Mg++ (mmol) 5 5 5 5 HPO4= (mmol) 37.5 7.5 30 0 Cl- (mmol) 70 110 70 110 Acetate (mmol) 150 82 150 82 Solution shelf life 12 mths room T 6 mths room T 12 mths room T 6 mths room T 1. Lipid source is Clinoleic 20% which comprises olive oil 80% and soya oil 20%. 2. Multivitamin and trace elements to be given separately from TPN. 3. Nothing may be added to TPN bags. 4. All solutions come in triple phase bag and have light protection cover.

NB: Specialised prescription TPN can be ordered via pharmacy, e.g. when large daily potassium requirements are not feasibly administered by 10mmol/100ml bags and the standard 60mmol/2L TPN.

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C. Blood Component Therapy 1. Indications

a) Blood component therapy should only be given if benefit outweighs the risk b) Potential risks including

i) Mis-identification / acute transfusion reaction ii) Transfusion associated acute lung injury iii) Bacterial / viral infection iv) Immune modulation

c) The best way to reduce the risk of blood component therapy is to reduce requirements i) Minimise unnecessary blood sampling ii) Minimise blood loss during procedures iii) Consider nutritional and iron stores state

2. Red Blood Cells

a) Elective *as per NHMRC / ASBT guidelines. i) Haemoglobin < 70g/L ii) Haemoglobin 70-100g/L, plus any of the following:

Ongoing bleeding. Dyspnoea, tiredness/weakness, angina, syncope. Cardiac ischaemia or cardiac failure due to anaemia.

iii) Blood sent for �“type & screen�” is held for 10 days for compatibility testing. However, if the patient requires transfusion, a new specimen is needed for cross-match every 72 hours.

b) Resuscitation i) Abnormal bleeding is usually surgical and requires urgent surgical and/or

radiological intervention. ii) A full cross-match takes 30 minutes if marked urgent (not including the

time for transfer of blood); this should be performed if possible while volume is replaced with crystalloid or colloid.

iii) If blood is required faster than this the request �“Time Required�” box should be marked:

�“Desperate�” group O Rh(D)-ve blood is issued immediately (see massive transfusion protocol)

�“10 minutes�” group-specific (ABO/Rh-D) but without full compatibility testing

�“30 minutes�” urgently processed, fully crossmatched blood iv) NB: The requesting MO accepts full responsibility for (a) or (b) v) Blood replacement should start immediately with:

Rapid blood loss leading to hypovolaemia and shock. Blood loss is estimated or anticipated to exceed 20-25% of blood

volume, i.e. 1000-1500 ml in a normal adult.

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Procedure Comments Laboratory investigations

CBE, INR, APTT, fibrinogen; Samples to Blood Bank for T&S; Biochemical profile, blood gases etc.

Repeat CBE, INR, APTT, fibrinogen after blood component infusion, or every 4 hr until stable.

Take samples at earliest opportunity as results may be affected by colloid infusion.

Mis-identification is commonest transfusion risk.

May need to give components before results available.

Use �“Massive Transfusion�–Priority Processing�” labels with �‘Red bag�’ to alert lab for speedy processing.

Suitable red cells Un-crossmatched group O Rh(D) negative in extreme emergency until blood group known, then group-specific.

Then fully crossmatched blood when time permits.

To prevent hypothermia by the use of blood warmer and/or rapid infusion device.

Employ intra-op blood salvage if available and appropriate.

Rh(D) positive is acceptable if patient is male or post-menopausal female.

Laboratory will complete compatibility testing after issue.

Further compatibility test not required after replacement of 1 blood volume (8�–10 units).

Blood-warmer indicated if flow rate >50 ml/kg/hr in adult.

Salvage contraindicated if wound heavily contaminated.

Platelets Anticipate platelet count <50x109/L after 2 x blood volume replacement.

Target platelet count: >100x109/L for multiple/CNS trauma or if platelet function abnormal.

Target >50x109/L for other situations.

FFP (10�–15 ml/kg �– 1 litre or 4 units for an adult)

Aim for INR <1.5 and APTT <40 secs. Allow for 30 min thawing time.

INR >1.5 and APTT >40 secs correlates with increased surgical bleeding.

Keep Ca++>1.13mmol/L

Cryoprecipitate (2-4 units)

Replace fibrinogen. Aim for fibrinogen >1.0 g/L. Allow for 30 min thawing time.

Fibrinogen <0.5 strongly associated with microvascular bleeding.

Fresh whole blood Request hospital Blood Bank to contact ARCBS on-call MO.

Anticipated major blood loss in elective patients with platelet or coagulation abnormalities. Continued significant bleeding even after use of conventional component therapy. Role in haemostasis controversial.

Recombinant FVIIa (Novoseven) ~90 g/Kg

Obtain approval from consultation with senior Surgeons / Anaesthetists / Intensivists and Haematologists / ARCBS on-call MO.

May be considered when the patient�’s condition continues to deteriorate to likely haemorrhagic death, usually as a desperate effort after all other measures fail.

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3. Massive transfusion Protocol a) Definition:

i) Loss of one blood volume within a 24 hr period. ii) Alternative, more practical definitions:

50% blood volume loss within 3 hr, or 150 ml/min rate of loss.

b) The RAH has a massive transfusion protocol which should be activated as soon as the need is identified

c) Correction of critical bleeding requires simultaneous approach to: i) Control the source of bleeding ii) Contact key personnel required for haemorrhage control iii) Maintain blood volume iv) Prevent hypothermia and acidosis

d) Principles i) Trauma patients with critical bleeding are coagulopathic on presentation ii) Prevention of further coagulopathy with aggressive management is much

more effective than delayed treatment iii) Acidosis worsens coagulopathy iv) Hypothermia worsens coagulopathy

e) On identification i) Take blood for:

Group and match CBE Extended coags and place in red bags

ii) Notify transfusion medicine on 47* iii) Dispatch blood samples ASAP iv) Transfusion will provide products in �“Massive Transfusion Packs�” v) Notify transfusion when bleeding controlled

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4. Platelets a) Prophylactic transfusion before surgery or other �“at risk�” procedures:

i) Platelet count < 50 × 109/L ii) Platelet count > 50 × 109/L

with evidence of (inherited or drug-induced) platelet dysfunction. b) Prophylactic transfusion in marrow failure:

i) Platelet count < 10 × 109/L, or ii) Higher levels with clinical evidence of bleeding

c) Therapeutic transfusion for uncontrolled haemorrhage: i) Platelet count < 100 × 109/L

and/or evidence of platelet dysfunction. d) ITP: Only if life-threatening bleeding is present. e) Platelet dysfunction can contribute to bleeding with a normal platelet count

5. Fresh Frozen Plasma (FFP)

a) Prophylactic transfusion before surgery or other invasive procedure that could result in significant bleeding: i) Urgent correction of prolonged INR or APTT in warfarin overdose or

vitamin K deficiency (see below) ii) Correction of prolonged INR or APTT in liver disease iii) Correction of inherited coagulation factor deficiencies where specific

coagulation factor concentrates are not available b) Therapeutic transfusion for uncontrolled haemorrhage in:

i) Warfarin overdose ii) Liver disease iii) Vitamin K deficiency iv) Inherited coagulation factor deficiencies where specific coagulation factor

concentrates are not available v) DIC

c) Plasma exchange in TTP & related syndromes d) Post massive transfusion with coagulopathy:

i) Indicated if the INR (prothrombin time) > 1.5, or ii) APTT (activated partial thromboplastin time) > 40 seconds

6. Extended Life Plasma a) Recent regulatory changes allow transfusion laboratories to used thawed FFP

for up to 5 days. b) By using thawed FFP the product can now be provided immediately, c.f. the

standard 20-30 minute delay normally involved in thawing. c) Five day thawed FFP will be labelled �‘Extended Life Plasma�’

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Table: Guidelines for the management of an elevated INR

Clinical setting Action

INR < 5.0 Bleeding absent

Lower the dose or omit the next dose of warfarin. Resume therapy at a lower dose when the INR approaches therapeutic range. If the INR is only minimally above therapeutic range (up to 10%), dose reduction

may not be necessary.

INR ~ 5.0�–9.0* Bleeding absent

Cease warfarin; consider reasons for INR and patient-specific factors. If bleeding risk is high, give vitamin K1 (1.0�–2.0mg orally or 0.5�–1.0mg IV) �†. Measure INR within 24 hrs, resume warfarin at a reduced dose once INR is in

therapeutic range.

INR > 9.0 Bleeding absent

Where there is a low risk of bleeding Cease warfarin, give 2.5�–5.0mg vitamin K1 orally or 1.0mg IV Measure INR in 6-12 hrs & resume warfarin at a reduced dose once INR < 5.0. Where there is high risk of bleeding�‡ Cease warfarin, give 1.0mg vitamin K1 IV. Consider Prothrombinex-HT (25�–50 IU/kg) and FFP (150�–300mL) Measure INR in 6-12 hrs, resume warfarin at a reduced dose once INR < 5.0.

Any clinically significant bleeding where warfarin induced coagulopathy is considered a contributing factor

Cease warfarin therapy, give 5.0�–10.0mg vitamin K1 intravenously, as well as Prothrombinex-HT (25�–50 IU/kg) and fresh frozen plasma (150�–300mL), assess patient continuously until INR < 5.0, and bleeding stops.§ or

If fresh frozen plasma is unavailable, cease warfarin therapy, give 5.0�–10.0mg vitamin K1 intravenously, and Prothrombinex-HT (25�–50 IU/kg), assess patient continuously until INR < 5.0, and bleeding stops.§ or

If Prothrombinex-HT is unavailable, cease warfarin therapy, give 5.0�–10.0mg vitamin K1 intravenously, and 10�–15mL/kg of fresh frozen plasma, assess patient continuously until INR < 5.0, and bleeding stops.§

* Bleeding risk increases exponentially from INR 5 to 9, INR 6 should be monitored closely. �† Vitamin K effect on INR can be expected within 6-12 hours. �‡ Examples of patients with a high bleeding risk:

active gastrointestinal disorders (such as peptic ulcer or inflammatory bowel disease) those receiving concomitant antiplatelet therapy those who underwent a major surgical procedure within the preceding two weeks, and those with a low platelet count.

§ In all situations carefully reassess the need for ongoing warfarin therapy.

From consensus guidelines Australian Society of Thrombosis and Haemostasis 2004

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6. Cryoprecipitate a) Bleeding and fibrinogen < 1.0 g/L in:

i) DIC. ii) Massive transfusion. iii) Hereditary hypofibrinogenaemia.

b) 10U of cryoprecipitate will plasma fibrinogen by ~ 1.0g/l c) Standard dose = 8U for hypofibrinogenaemia.

7. DDAVP

a) Standard dose = 0.3-0.4µg/kg intravenously over 30 mins b) Increases factors VIII:C, VIII:vWF and platelet adhesion. c) Indications: actual, or significant risk of bleeding with,

i) Haemophilia A ii) type I von Willebrand's disease iii) Post cardio-pulmonary bypass iv) Clinical scenarios where platelet dysfunction is likely

Uraemia Drugs - aspirin, clopidogrel

8. Recombinant activated factor VII (rFVIIa, NovoSeven)

a) TGA approved indications i) Haemophilia patients with antibodies to factor VIII ii) Glanzmann's thrombasthenia with antibodies to GPIIb-IIIa and/or HLA,

and who have past or present refractoriness to platelet transfusions iii) Patients with congenital factor VII deficiency

b) Effective in improving coagulopathies associated with trauma, major surgery, and organ transplantation = �‘off-label�’ indications.

c) No risk of virus transmission and contains no human protein d) Binds to tissue factor (TF) activating both factors IX and X.

i) High doses activate factor X on the surface of activated platelets ii) Has both TF-dependent and TF-independent effects

e) Recommended dose for the treatment of a severe coagulopathy is 50µg/kg f) Acts within a few minutes and has a half-life of about 2.5 hours. g) Requires consultant approval because of high cost and absence of current TGA

approval for these indications. 9. Disseminated intravascular coagulation (DIC)

a) Definition i) DIC occurs when the balance of the haemostatic and fibrinolytic systems

becomes disordered. It occurs in response to severe pathophysiological stimuli and is a part of multisystem organ dysfunction (often associated with ARDS and acute renal failure). It is characterised by:

Microthrombi formation causing microvascular obstruction Consumption of platelets and clotting factors Abnormal fibrinolysis

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b) DIC screen: i) Complete blood picture

microangiopathic haemolytic anaemia with red cell fragmentation haemolysis thrombocytopenia

ii) Extended coagulation screen: prolongation of TCT, APTT, PT hypofibrinogenaemia low factor VIII excess fibrinolysis with elevated FDPs

iii) Liver and renal function tests c) Treatment

i) Treatment of the underlying cause ii) Replacement of blood components in the bleeding patient

FFP - based on INR/APTT cryoprecipitate - for marked fibrinogen deficiency

iii) Controversial therapies (following consultant approval only) heparin, fibrinolytics (tPA) anti-fibrinolytics (EACA)

10. Activated Protein C - Drotrecogin alfa (activated)

a) The role of Activate Protein C (APC) in ICU practice is unclear: i) Not currently used in routine practice in the RAH. ii) RAH is involved in an ongoing trial with APC at the time of writing this

manual b) Xigris® is a recombinant form of human Activated Protein C c) Pharmacological effects

i) Antithrombotic effect by inhibiting Factors Va and VIIIa. ii) Indirect profibrinolytic activity by:

inhibiting plasminogen activator inhibitor-1 (PAI-1), and limiting activation of thrombin-activatable-fibrinolysis-inhibitor.

iii) APC may exert an anti-inflammatory effects: inhibiting TNF production by monocytes blocking leukocyte adhesion to selectins, and limiting thrombin-induced inflammatory responses within the

microvascular endothelium. d) Indications are severe sepsis and at least 2 organ failures which could include:

i) Cardiovascular - inotropes despite adequate filling ii) Respiratory - PaO2/FiO2 < 250 iii) Renal - poor urine output < 0.5ml/kg/h iv) Haematology - platelets < 80,000 v) Metabolic - lactic acidosis, pH < 7.3 & lactate > 5.

e) APC infusions should be ceased 1-2 hours before and restarted 12 hours after major surgical procedures, or sooner after minor procedures.

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f) Full anticoagulation should not be given in addition to APC but DVT prophylaxis can be administered. APC cannot be monitored but may affect APTT slightly

g) Increased bleeding risk with a low platelet counts (<30,000) even if platelets are administered.

h) Administration of APC for severe sepsis requires approval of the Duty Consultant and hospital administration due to the high cost of the drug.

i) Prescribed by a RAH ICU consultant after: i) Completing the patient assessment criteria with a second ICU consultant ii) Completed and signed �‘RAH Checklist�’ is faxed to pharmacy - ext 25891

j) Dose: 24 µg/kg/hr given as a continuous infusion for 96 hours i) Dose is based on actual body weight ii) No dose adjustment for hepatic or renal impairment, or sepsis severity iii) Calculate the dose & infusion rate from the table below iv) Diluted to 50mls with normal saline & administered via a syringe pump v) The resulting infusion solution must be used within 12 hours

Table: Xigris Dosing Schedule Patient wt

(kg) Dose of Xigris

diluted to 50ml NS Final conc�’n

(µg/mL) Infusion rate

(mL/hr) 40 10 mg 200 4.8 45 10 mg 200 5.4 50 10 mg 200 6.0 55 15 mg 300 4.4 60 15 mg 300 4.8 65 15 mg 300 5.2 70 20 mg 400 4.2 75 20 mg 400 4.5 80 20 mg 400 4.8 85 20 mg 400 5.1 90 25 mg 500 4.3 95 25 mg 500 4.6 100 25 mg 500 4.8 105 30 mg 600 4.2 110 30 mg 600 4.4 115 30 mg 600 4.6 120 30 mg 600 4.8 125 35 mg 700 4.3 130 35 mg 700 4.5 135 35 mg 700 4.6 140 40 mg 800 4.2

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11. Blood transfusion reaction protocol a) Plasma can cause reactions ranging from mild pruritus, erythema and urticaria

through to severe flushing, hypotension, fever, angioedema, bronchospasm and fulminant anaphylaxis.

b) Suspected Reaction Protocol i) Stop the transfusion immediately �– do not disconnect the IV line. ii) Recheck the patient identification on the blood product pack label against

the patient�’s wristband and verbally with the patient if possible. iii) If there is an unexplained discrepancy, discontinue the transfusion and

treat as per (iv, v below) iv) Mild Reactions

Temp. < 1.5º C Mild or no hives or rash. Action - slow the rate and continue transfusing the same unit of blood.

v) Severe Reactions Severe hives and/or a rash. Temp. > 1.5°C and is the only clinical sign or symptom Action

a. Consider an antihistamine and antipyretic b. Cease and then restart transfusing the same unit of blood after

approximately 20 minutes. If there are further signs & symptoms of a reaction

discontinue & order a transfusion reaction investigation If there is a sudden and acute change in the patient�’s condition, e.g.

cyanosis, bad headache, backache, or significant change in pulse or blood pressure for no apparent clinical reason

discontinue & order a transfusion reaction investigation vi) Investigation of a transfusion reaction:

A transfusion reaction investigation form (IMVS 224) should be completed and sent to Transfusion Medical Unit (TMU) with: a. A description of the relevant clinical findings and vital signs b. A post-reaction 10ml EDTA blood specimen, preferably from a

vein other than that used for transfusion c. Any used or unused blood packs and the attached IV set(s).

If there is a major reaction, it is also recommended that the first urine specimen voided after reaction is saved, and patient�’s urine output over the next few hours is recorded.

Further blood samples for biochemical assays, coagulation tests, and cultures will be needed.

Administration of incompatible blood constitutes a sentinel event. vii) Haemovigilance

The IMVS and RAH are participating in the �‘Blood Safe�’ haemovigilance scheme, an adverse incident reporting system aimed at the quality and safety improvement of transfusion practices.

Contact the Transfusion Safety RN (Pager: 1575, Tel: 22975)

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Table: Blood Transfusion Reactions

Type Signs & Symptoms Treatment Prevention Febrile non-haemolytic transfusion reaction (FNHTR)

Pyrexia (> 1°C rise) Rigors/chills Anxiety

Withhold transfusion. Mild fever without other symptoms may be treated by slowing infusion. An antipyretic may be helpful. Investigate as for suspected HTR if the reaction is significant.

Consider use of leucodepleted red cells or platelets if a recurrent problem.

Circulatory Overload Distended cervical veins. Pulmonary oedema Dyspnoea. Headache. Heaviness in limbs.

Discontinue. Institute treatment for fluid overload, e.g. diuretic

Give all fluids slowly to patients with compromised cardiac or renal status. Use red cell concentrates. If anticipated, give diuretic.

Allergic Flushing Urticaria, itchy hives Facial oedema

Slow rate of flow. Consider anti-histamine. Watch for laryngeal oedema and development of anaphylaxis.

When anticipated, use prophylactic antihistamines.

Anaphylaxis Dyspnoea from laryngeal oedema or bronchospasm, sometimes cyanosis and collapse

Discontinue transfusion immediately. Institute treatment for anaphylaxis, e.g. Adrenalin, steroids

Use of Medi-Alert wristband in proven IgA deficient patients.

Acute Haemolytic Transfusion Reaction (HTR)

Pyrexia Rigors/chills Lumbar pain Pain along vein Jaundice Haemoglobinuria Oliguria �– later uraemia

Discontinue transfusion immediately. Get expert advice immediately. Save all used packs, blood samples. Save all urine. Collect fresh blood samples.

Extreme care in collecting the correct blood sample for T&S. Careful compatibility testing by laboratory. Careful method for storing & labelling blood. Careful identification of the correct recipient.

Infected blood Bacterial sepsis with hyperpyrexia Pain in limb & chest Headache Pallor Burning pain along vein Low blood pressure Rapid pulse Profound collapse & shock

Discontinue transfusion immediately. Acute medical emergency �– get advice immediately. Save used packs, all blood samples, with labels. Save all urine. Anti-shock treatment and antibiotics.

Storage at correct temp. Do not remove from refrigerator until immediately before transfusion

Non-cardiogenic pulmonary oedema. Transfusion related acute lung injury (TRALI): rare

Dyspnoea ARDS picture within 6 hours after transfusion.

Maintain blood pressure & cardiac output with fluid support. May require ventilatory support.

Difficult, usually in the setting of multiparous blood donor with anti-recipient-WBC antibodies.

NB: See RAH Intranet, Transfusion Medicine (http://rahadm05v.had.sa.gov.au/)

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D. Guidelines for the Management of Electrolytes 1. General principles

a) Total body water (60% total body weight): i) intracellular fluid : predominant ions : K+, PO4

2- ii) extracellular fluid:

75% interstitial fluid: predominant ions : Na+, Cl- 25% plasma volume (PV)

b) Osmotic equilibrium is maintained by Na+/K+ pump i) ECF ions therefore reflect total osmolality:

Calculated osmolality = 2xNa+ + urea + glucose ii) Magnesium is a cofactor for this pump

c) Most electrolyte disturbances in critically ill patients relate to changes in the

distribution and concentrations of the predominant ECF and ICF ions. d) As a general rule, changes in one ion will be reflected in the associated cation or

anion. e) Electrolyte disturbances should be considered in terms of the following groups:

i) Erroneous results Lab error Bloods taken from a drip arm Haemolysed specimen - traumatic (old IA lines), delayed samples Osmolar agents

ii) Decreased or increased losses: usually Renal Extra renal: GIT, skin losses

iii) Transcellular shifts. iv) Decreased or increased intake

Plasma - Interstitium

ECF ICF

ATPMg++

Na+

K+

HPOProteinMg

4=

=

++

ClHCO

-

-3

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f) Treatment should be directed at the underlying cause. g) Rapid correction of electrolyte disturbances may be deleterious. h) One electrolyte disturbance may be predictive of another electrolyte disturbance

e.g. K+ often associated with Mg+ i) The following paragraphs outline the common electrolyte disturbances.

2. Hyponatraemia: Na+ < 130 mmol/l

a) Aetiology / classification i) Misleading result

Isotonic - Hyperlipidaemia - Hyperproteinaemia

Hypertonic - Hyperglcaemia - Mannitol, glycerol, glycine or sorbitol excess

ii) Water Retention Renal Failure Hepatic Failure Cardiac Failure SIADH Drugs Psychogenic polydipsia

iii) Water retention and salt depletion Post-operative, post-trauma Patients with excess fluid losses given inappropriate replacement Adrenocortical failure Diuretic excess

b) Diagnosis & Management:

i) Factitious: ignore and manage underlying condition then recheck Na+ ii) Misleading:

Hyperglycaemia: BGL 10 mmol/l [Na+] 3 mmol/l a. Hyponatraemia per se is real, but treatment is directed at the

underlying cause, where correction of the hyperglycaemia will correct the plasma [Na+]

b. NB: Total body Na+ deficit may co-exist with diuresis in DKA Mannitol:

a. [Na+] early, then diuresis & late [Na+] are more problematic b. Maintain adequate plasma volume with N.saline initially

Alcohols: permeate solutes, [Na+] less problematic iii) Hypovolaemic states:

Restore volume with colloid or normal saline according to clinical markers: urine output, plasma [Na+], RAP

Aim for slow Na+ correction: 2 mmol/l/hr, unless seizures. Urine Na+ is uninterpretable after diuretics or catecholamines for 24hrs

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iv) Hypervolaemic states: *most common clinically Fluid restriction < 15 ml/kg/day

a. �“Water Excess�” ~ (140 - Na+ )/140 x (Wt x 0.6) e.g., 70kg patient with plasma [Na+] = 120 mmol/l: = (140 - 120)/140 x (70kg x 0.6) = 6 litres

b. Will slowly correct excess - ADH group & �“reset osmostat�” c. Treat the underlying cause - CCF, nephrotic synd., ascites

v) SIADH Causes

a. Ectopic ADH production by tumours e.g. small cell bronchogenic tumour

b. CNS disorders e.g. tumour, abscess, trauma, SAH etc

c. Pulmonary diseases e.g. TB, pneumonia, abscess etc

Diagnosis a. Hypo-osmolar hyponatraemia b. Urine osmo > plasma osmo c. Urine Na+ > 40 mosm/l d. Normal endocrine, renal, hepatic, cardiac function e. No diuretics or drugs affecting ADH secretion f. Corrected by water restriction alone

Management: fluid restriction vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness

Resuscitation / ABC Consider anticonvulsants - phenytoin benzodiazepines Hypertonic saline (3%) may be indicated

a. Always discuss use with the Duty Consultant b. Correct [Na+] rapidly only to ~ 120mmol/l

Thereafter, slow correction with N.saline over 24-36hrs ( 2 mmol/l/hr) Treat the underlying cause.

3. Hypernatraemia: Na+ > 145 mmol/l

a) Hypernatraemia is always a hyperosmolar state b) Most body fluids have a [Na

+] < plasma net water loss

c) Aetiology / classification: i) Water depletion / inadequate replacement

Renal a. Diuretics, glycosuria b. ARF/CRF, partial obstruction c. Central diabetes insipidus

i. Post traumatic head injury or surgery ii. CNS infection, tumour, granulomatous disease, GBS

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d. Nephrogenic diabetes insipidus: i. 1° : congenital renal resistance to ADH ii. 2° : hypokalaemia, hypercalcaemia, lithium, multiple

myeloma, sickle cell anaemia, nephrocalcinosis, amyloid GIT losses - diarrhoea, vomiting, fistulae, SBO Respiratory - IPPV with dry gases Skin losses

a. Fever, high ambient temperature b. Vasodilatory states c. Exfoliative skin disorders, burns d. Thyrotoxicosis

Unconsciousness �“Reset osmostat�”

ii) Salt gain - Na+ gain > H2O gain Iatrogenic

a. Most common cause b. Excess �“normal saline�” ~ 150 mmol/l [Na+] c. NaHCO3, feeding formulae, TPN

Mineralocorticoid excess: a. Conn's, Cushing's syndromes b. Steroid excess

d) Management i) Hypovolaemic states

Restore volume according to clinical markers: BP, HR, urine output, RAP a. Hartmann�’s solution - slightly hypo-osmolar b. Colloid: initial resuscitation, severe hypovolaemic states

ii) Slow Na+ correction: 2 mmol/l/hr Water deficit: ~ (Na+ - 140)/140 x (B.Wt x 0.6)

e.g. 70 kg patient, with plasma [Na+] = 160 mmol/l ~ (160-140)/140 x (70 x 0.6) ~ 6.0 litres 1 litre water replacement will reduce [Na+] ~ 3-4 mmol/l

In addition to basal fluid requirements & ongoing losses Replace over a 24-48 hr period with 5% dextrose Monitor [Na+] regularly Manage aetiological causes Cease causal drugs and inappropriate IVT DDAVP for central DI only ~ 1-2 µg s.c.

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4. Hypokalaemia: K+ < 3.0 mmol/l plasma K+ < 3.5 mmol/l serum

a) Aetiology / classification: i) Compartmental / transcellular shift

Alkalaemia pH ~ 0.1 [K+]pl ~ 0.5 mmol/l Catecholamines / salbutamol Insulin / anabolism - refeeding effect Hypomagnesaemia - ICF K+ depletion Toxic / poisoning - barium, toluene Familial periodic paralysis Hypothermia

ii) Reduced intake - urine [K+] < 20 mmol/L Starvation TPN

iii) Increased clearance/losses Renal - urine [K+] > 20 mmol/L

a. Diuretics distal tubular flow i. Loop agents - frusemide, bumetanide ii. PT agents - acetazolamide, mannitol iii. Early DT - thiazides

b. Steroids / Mineralocorticoid excess i. Conn�’s, Cushing�’s, Bartter�’s syndrome ii. Ectopic ACTH - Small cell Ca lung

- Pancreatic, thymus carcinoma iii. Exogenous steroids

c. Drugs i. Anionic drugs - antibiotics (penicillins, amphotericin) ii. High dose gentamicin iii. Lithium

d. Hypomagnesaemia, Hypocalcaemia e. RTA I, II

GIT losses a. Villous adenoma b. Ureterosigmoidostomy c. Fistulae, malabsorption syndromes d. Diarrhoea, Laxatives

Skin losses

b) Management: i) Treat underlying cause ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis

and hypokalaemia iii) Always add Mg++

normomagnesaemia is essential for correction of hypokalaemia iv) Look for and treat concurrent hypophosphataemia

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v) Potassium preparations KCl: 10 ml = 10 mmol/l KH2PO4: 10 ml = 10 mmol/l K-acetate: 5 ml at 5 mmol/ml

25 mmol K+ + 25 mmol acetate (bicarbonate)

5. Hyperkalaemia: K+ > 5.0 mmol/l serum K+ > 4.5 mmol/l plasma

a) Aetiology / classification: i) Artefactual

Drip arm specimen Tourniquet / Haemolysed specimen (extravascular) Thrombocytosis > 750,000

Leukocytosis > 50,000 ii) Compartmental / transcellular shift

Acidosis pH ~ 0.1 [K+] ~ 0.5 mmol/l Insulin deficiency: DKA

NB: normo- or hypo-kalaemia in the presence of severe DKA is associated with a marked total body K+ deficit, which must be addressed prior to correction of the acidaemia.

Familial periodic paralysis Suxamethonium Digoxin, -blocker overdose Fluoride poisoning ECF tonicity

a. Water moves from cells [K+]ICF and passive diffusion b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg) c. Hyperkalaemia of DKA is due to this in addition to the acidaemia

& insulin deficiency iii) Cellular disruption / death

Tissue breakdown Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion Severe burns Tumour lysis syndrome, leukaemia

iv) Increased intake - rarely a problem unless impaired renal function Massive transfusion Direct IV/oral Drugs (penicillins)

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v) Reduced clearance Acute renal failure

a. Any cause for distal tubular flow, or distal NaCl delivery b. Hypoaldosteronism

i. Mineralocorticoid deficiency, Addison�’s ii. K+ is multifactorial - K+

ICF K+ECF

- distal tubular flow - DT aldosterone effect

Type IV RTA ACE Inhibitors Potassium sparing diuretics

a. aldosterone antagonists - spironolactone b. distal Na+ channel inhibitors - amiloride, triamterene

b) Management:

i) The clinical scenario will dictate treatment ii) Acute K+ > 6.0 mmol/l is a medical emergency iii) Associated with acute ECG changes, or haemodynamic compromise:

In following order (not mixed together), CaCl2 10 ml IV stat NaHCO3 50-100 ml IV stat Glucose 50% 50g + Insulin 20 units Salbutamol nebs continuously

iv) Refractory or persistent: CVVHDF intermittent dialysis

v) Chronic K+ or slow rate of rise or no ECG changes: Resonium 30g oral / PR 8 hourly

vi) Address aetiological factors vii) Normalise renal function / volume status

6. Acid base disturbances

a) Acid base disturbances in ICU are frequently mixed disorders b) Correction of these should be directed at the underlying cause and maintenance

of cardiopulmonary homeostasis. c) Primary correction of an acid base disturbance with acid or alkali is seldom

required.

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7. �“Rules of thumb�” *these are approximations only a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO2

i) Met Acid to min 7.10 e.g. pH 7.25 PaCO2 25 mmHg ii) Met alkalosis to max 7.60 e.g. pH 7.57 PaCO2 57 mmHg

b) Primary respiratory acidosis: i) HCO3 ~ 1mmol/l per 10mmHg PaCO2 above 40 to max 30

c) Primary respiratory alkalosis i) HCO3 ~ 2.5mmol/l per 10mmHg PaCO2 below 40 to min 18

d) Chronic respiratory acidosis HCO3 ~ 4mmol/l per 10mmHg PaCO2 above 40 to max 36

8. Metabolic acidosis

a) Assessment of metabolic acidosis must include the anion gap:

Anion Gap = [Na+ + K+] - [Cl- + HCO3-] ~ 12-17 mmol/l

Unmeasured cations Unmeasured anions

Mg++ ~ 1.2 mmol/l Albumin ~ 15 mEq/l Ca++ ~ 2.2 mmol/l H2PO4- ~ 2 mmol/l IgG Small HSO4- ~ 1 mmol/l

Organic ~ 5 mEq/l ~ 7.0 mEq/l ~ 23 mEq/l

b) This allows sub-classification of metabolic acidosis into raised or normal anion

gap acidoses. i) Beware a low [Alb] in critically ill lowering the measured AG ii) Measurement of chloride in the lab is highly variable iii) Assessment of the AG must be viewed within the clinical context.

c) Aetiology of raised anion gap: i) Renal failure - H2PO4

- , HSO4- (rarely AG > 23)

ii) Lactic acidosis - types A&B * normal AG does not exclude a lactic acidosis

iii) Ketoacids - -OH-butyrate, acetoacetate - diabetes mellitus, starvation, alcohol

iv) Rhabdomyolysis - organic acids v) Drugs / poisons:

Aspirin - salicylate, lactate, ketones Paracetamol - lactate, pyroglutamate Ethanol - acetoacetate, lactate Methanol - formate (formaldehyde), lactate Paraldehyde - formate, acetate, lactate, pyruvate Ethylene glycol - oxalate Xylitol, Sorbitol - lactate Fructose - lactate

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Table: Classification of Lactic Acidosis

Type A Type B Drug induced Hereditary

Severe exercise Seizures Cardiac arrest Shock Hypoxia Anaemia

Thiamine deficiency Diabetes Hepatic failure Renal failure Infection Leukaemia, lymphoma Pancreatitis Short bowel syndrome

Phenformin Metformin Ethanol Methanol Salicylates IV fructose Xylitol Sorbitol

G6PD deficiency Fructose-1,6-DP-deficiency

d) Aetiology of low or normal anion gap:

i) Hyperchloraemic metabolic acidosis Resolving renal failure Resolving DKA Renal tubular acidosis / carbonic anhydrase inhibitors Mineralocorticoid deficiency Pancreatic, enteric fistulae Ureterosigmoidostomy IV HCl, NH4Cl, Arginine

ii) Metabolic alkalosis due to HCO3- gain

iii) Hypoalbuminaemia iv) Myeloma - IgG has positive charge, 's AG v) Increased Mg++ or Ca++ (rarely) vi) Artefactually elevated Cl- vii) ? Hyperlipidaemia

e) Management i) High anion gap

Treat the underlying cause No indication for NaHCO3

ii) Normal anion gap Treat the underlying cause. Replace HCO3 serum level and losses

a. Approx. deficit = (24 - [HCO3]) x (Wt. x 0.6) mmol/l e.g. for a 70kg patient with a [HCO3] = 4 mmol/l deficit = (24 - 4) x (70 x 0.6) = 840 mmol (= ml of standard bicarb solution)

b. Replace 1/3-1/2 of this amount then remeasure blood gases.

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9. Metabolic alkalosis a) Aetiology / classification

i) Common causes: Diuretics Vomiting Post-hypercapnia > 48 hours Commonly associated with hypovolaemia and/or hypokalaemia

however, actual causation by these is debated ii) Increased proton losses: acid loss is either renal or GIT

Renal a. Na+ reabsorption (hypovolaemia, dehydration, etc.) b. Cushing's syndrome, exogenous steroids c. Hyperaldosteronism 1° / 2° d. Bartter's syndrome (JGA hyperplasia) e. Liddle's syndrome f. Hypercalcaemia / hypomagnesaemia nephrogenic DI g. Drugs: steroids, diuretics, carbenoxolone

GIT a. N/G suctioning, protracted vomiting b. Diarrhoea

iii) Increased bases Administration of NaHCO3 Metabolism of exogenous acid anions - citrate, lactate, acetate Milk/alkali syndrome Renal conservation of HCO3

- - acidosis, hypercarbia iv) Factors tending to maintain an alkalosis

Any fluid loss replaced with insufficient Na+ H+ excretion (contraction alkalosis)

Hypovolaemia Hypokalaemia, hypochloraemia, hypomagnesaemia Chronic hypercapnia Mild chronic renal failure

b) Management i) Correct hypovolaemia

*normal ECF volume is essential for the correction of alkalosis ii) Inotropic support of cardiac output and GFR iii) Correct K+, Mg++, HPO4

= iv) Consider acetazolamide if the alkalosis is persistent - provided the above

are corrected.

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10. Respiratory acidosis a) Aetiology

i) Any cause of hypoventilation respiratory failure (see diag.) A. Respiratory centre / CNS B. Upper motor neuron / spinal cord C. Anterior horn cell D. Lower motor neuron E. Neuro-muscular junction F. Respiratory muscles G. Elasticity/compliance of lungs/chest wall H. Structural integrity of chest wall & pleural cavity I. Increased airways resistance �– intra/extrathoracic

ii) May be acute or chronic

b) Management i) Restore ventilation / manage underlying cause(s) ii) No indication for HCO3

2. Respiratory alkalosis

b) Aetiology i) Early hypoxia, shock or hypotension ii) Anxiety, hysteria, neurogenic hyperventilation iii) PTE iv) Hepatic failure v) Prescribed hyperventilation (rarely indicated)

c) Management i) Treat underlying cause ii) Neurogenic hyperventilation is a marker of severity of head injury

143

PART 5 - CLINICAL MANAGEMENT The following clinical protocols are designed to facilitate clinical management of patients in the Intensive Care. These protocols may vary from other ICUs and do not represent the sole means of patient management. However, they do represent the standardised approach that this ICU has evolved over the years. Each clinical scenario is managed according to the particular situation and individual patient - it is neither practical nor appropriate to apply rigid policies to clinical situations. However, as clinical medicine is more of an art than a science, these protocols are designed to assist in areas that are unfamiliar and to standardise approaches by all staff members of the Unit. The following protocols are outlined. A. Cardiopulmonary resuscitation

B. Failed intubation drill

C. Respiratory therapy

D. Management of cardiothoracic patients

E. Renal failure

F. Neurosurgical protocols

G. Microbiology protocols

H. Drug overdose

I. Withdrawal of therapy

J. Organ donation and brain death

144

A. Cardiopulmonary Resuscitation Flowchart: Basic Life Support

145

Flowchart: Advanced Life Support

146

Flowchart: Paediatric Cardiorespiratory Arrest

147

B. Induced Hypothermia Post Cardiac Arrest 1. Aim: To improve CNS outcome by actively cooling TCore to ~ 33°C 2. Inclusion Criteria

a) Non-traumatic cardiac arrest with return of spontaneous circulation a) Unconscious, intubated and ventilated b) Absence of an immediately correctable cause for coma c) TCore > 34.5°C

4. Exclusion Criteria a) Cardiac arrest related to trauma or intracranial injury b) Ongoing CPR and/or persistent cardiovascular instability c) Cardiology consultation need for intervention d) Criteria that preclude 40mls/kg of cold Hartmann�’s solution,

e.g. acute pulmonary oedema, T < 34.5°C e) Time from cardiac arrest to ED > 12 hrs f) Pregnancy �– relative C/I

5. Procedure - Initial Treatment Protocol a) ECG and routine blood tests as indicated b) Record core temperature: rectal, oesophageal or bladder catheter c) Ensure adequate IV access (1x 16G) d) Document neurological function, specifically:

i) Pupillary responses to light ii) Response to painful stimuli (all limbs), vocalization iii) Reflexes �– gag, conjunctival, lash, tendon & plantar

e) Hartmann�’s (at 4°C): Bolus = 40mls/kg @ 100mls/min f) Maintain MAP ~ 80-100mmHg (note premorbid BP) g) Maintain K+ ~ 4-5mmol/L and Mg++ between 0.8-1.2mmol/L h) If temp > 35°C after 1 hour, add surface cooling (cooling blanket / packs) i) If patient is shivering and/or temp > 33°C:

i) Midazolam (0.05mg/kg bolus, repeat 5min as required) ii) Midazolam infusion of 1-5mg/hr iii) If sedation ineffective, consider a non-depolarizing muscle relaxant

j) Aim for core temp. ~ 32-33°C 6. Observations

a) Maintain temp ~ 32-34°C for 24 hrs from the time of first temp 33°C b) To increase temp (T < 31.5°C), use heated air blanket until 33°C c) To decrease temp (T > 34.5°C), use cold packs, cooling blanket, sedation and

then consider using non-depolarizing muscle relaxants 7. Complications

a) Arrythmia b) Reduced cardiac index / increased systemic vascular resistance c) Hyperglycaemia

8. Aftercare a) At 24 hrs cease all active cooling and allow passive rewarming. b) If temp increases < 1°C per 4 hours then rewarm actively to temp > 36°C c) Once temp > 35°C, cease sedation and no further muscle relaxants

148

C. Failed Intubation Drill

Oxygenate/ventilate

Committed to Intubation

Best Attempt Laryngoscopy

ILMA +/- Bronchoscope

Failure to Ventilate

Crico- Thyroidotomy

FURTHER ATTEMPTS USING

ADVANCED DEVICE McCoy / Flextip Glidescope Airtraq Bronchoscope

Intubate

Intubate

Call for help

No CALL

EMERGENCY

Failure or SpO2 < 88%

Yes

149

Failed Intubation Drill - Notes: 1. Good anaesthetic algorithms for managing the difficult airway (ASA, DAS) have

limited application in ICU patients where our �‘hand�’ is usually forced. Allowing the patient to wake-up in the event of a failed intubation is rarely practical.

2. Risk of failed intubation in ICU is unquantified but certainly higher than the 0.5-

1% incidence of the general anaesthetic population. 3. Following rapid sequence induction we are generally committed to securing the

airway somehow.

4. Time is of the essence. ICU patients have limited O2 reserves and desaturate quickly. If an intubation technique fails, move on quickly to an alternative.

5. If intubation attempts fail, or the patient desaturates significantly:

a) Refocus efforts toward oxygenating the patient. b) Failure to achieve manual ventilation is an absolute emergency

(incidence in anaesthesia 0.001-0.002%).

6. The intubating laryngeal mask (ILMA or Fastrach) a) Shown in many studies to be easy to insert (~ 100% success after 3 attempts) b) Provides an adequate airway for ventilation in 96% of surgical patients. c) Default airway device for the �“can�’t intubate/can�’t ventilate�” scenario.

7. All of the equipment in the algorithm is available on the RAH ICU difficult intubation trolley. Become familiar with it, and practice using examples kept in the registrar teaching room.

8. Before intubating, ensure you have a contingency plan for a difficult airway/failed

intubation tailored to suit your skill mix and experience.

9. Always have the difficult intubation trolley at hand during intubations.

150

D. Respiratory Therapy 1. Respiratory failure

a) Definition: failure of efficient gaseous exchange and/or effective ventilation: i) Hypoxaemia: PaO2/FiO2 ratio < 300 mmHg ii) Hypercarbia: PaCO2 > 50 mmHg, with a pH < 7.35

2. Oxygen delivery capacities of available oxygen circuits.

Table: Oxygen Delivery Devices

Apparatus/Device Oxygen flow (l/min) Approximate FIO2 (%)

Nasal catheters 2 4 6

28 35 45

Semi - rigid masks (e.g. Hudson, CIG)

5 6 8 10 12

35 50 55 60 65

Venturi type mask (e.g. Ventimask, Accurox) 2 - 8 24 - 50

(per manufacturer)

Nasal High Flow (humidified circuit) 30-50 l/min 21 - 95

Reservoir plastic masks (Non-rebreathing mask) 6 - 15 FiO2 = 21% + 4% per l/min

Non Invasive or Invasive positive pressure mechanical respiratory support

Variable 21 - 100

Oxylog 1000 and 2000 Oxylog 3000

Variable

Variable

Airmix : 60 No airmix : 100

40 - 100

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3. Humidification

a) All intubated patients must have adequate humidification of inspired gases for optimal mucociliary function and conservation of temperature.

b) Optimal humidification requires the following i) Delivery of gas to the trachea at a constant temperature (32-36ºC) ii) Relative humidity 75-100% saturation iii) No increase in circuit resistance iv) No increase in circuit dead space v) Applicable to spontaneous and controlled ventilation vi) Sterile inspired gas

c) Types of humidifiers available i) Heat/moisture exchangers (HME)

Effective for most patients: first line humidification Incorporates a bacterial and viral filter Cannot be used with nebulised drugs Change to wet circuit (FP) in patients with bronchorrhoea or mucous

inspissation. Secretions increase resistance and reduce HME efficacy. Single use & change every 48 hrs, or as required

ii) Fisher Paykel (FP) evaporative humidifier (wet circuit) Indications

a. Bronchorrhoea or mucous inspissation b. Hypothermic or heat-loss susceptible patients (e.g. burns) c. Hypernatraemic patients

Set chamber to 40°C Set chamber control to �“Auto�” / �“Mask/Tube�”

iii) Inspiron (aerosolised T-piece) Relatively inefficient humidification Allows variable FiO2 : 0.21-0.7

4. MDI bronchodilators

a) MDI + Spacer = preferred method of administration. b) Can be used in ventilated patients, but requires dose adjustment. c) Each patient has their own canister. d) MDI adapter must be present in circuit:

i) Inspiratory limb of Fisher Paykel wet vent circuit ii) Dry circuits need a separate adapter between HME and stress reliever.

e) Shake MDI well f) Should be �“puffed�” with single puff dose during inspiration. g) Standard MDI Doses:

i) Salbutamol: 4 puffs 4-6 hrly max = 10 puffs 4 hrly. ii) Ipratropium: 4 puffs 6 hrly max = 10 puffs 6 hrly. iii) Steroids: 2-4 puffs BD (beclomethasone or fluticasone)

152

5. Nebulised bronchodilators

a) See section on respiratory drugs. b) These agents are the mainstay of treatment of bronchospasm in Intensive Care

(including acute severe asthma). c) They are not to be routinely used in all ventilated patients. d) Once commenced, they must be reviewed daily regarding efficacy. This is

assessed by improvements in audible wheeze, lung compliance, respiratory rate and blood gases.

e) Indications: i) Pre-existing asthma / chronic obstruction pulmonary disease (COPD) ii) Acute severe asthma iii) Acute bronchospasm 2° to infection, aspiration or during IPPV iv) Acute exacerbation of COPD v) Acute hyperkalaemia

f) All patients admitted to ICU for acute severe asthma: i) Continue routine prophylactic/preventative agents ii) Additional bronchodilators for episodes of bronchospasm iii) Should not be routinely started on empiric antibiotics, unless there is clinical

evidence of infection (also applies to exacerbation of COPD). Clinical evidence of infection may be

a. New onset fever, WCC b. Change in quantity/quality of sputum c. New radiological infiltrate d. Bacteria, positive viral PCR or WCC in a sterile fluid

iv) Should be reviewed by the Thoracic Medicine Unit. 6. Mechanical ventilation

a) Mechanical ventilation is one of the mainstays of intensive care medicine. b) An understanding of the indications, complications, practical aspects of mechanical

ventilators and respiratory failure is essential. c) Standardisation of default ventilation modes and settings is essential for patient

safety, particularly in a large unit with large numbers of staff. d) Registrars should familiarise themselves with the ventilators, understand the

default settings and common modes of ventilation. e) The nurse educators and senior CCRN�’s are useful resource people to aid in

troubleshooting and assistance with the ICU ventilators. f) All changes to ventilation orders must be recorded on the flowchart. g) Also, notify the bedside nurse of any prescribed ventilation changes. h) All ventilator alarms must be addressed as soon as possible: patient disconnection

or barotrauma are potentially lethal. i) Upon initiation of ventilation, the default FiO2 = 1.0 (100%). This should be

titrated down as soon as possible based upon SpO2 and PaO2.

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j) Indications for mechanical ventilation i) Respiratory Failure ii) Maintenance of cardiopulmonary homeostasis

Following cardiac arrest Post operative support in high risk surgical patients Control of intracranial pressure.

iii) Relaxant anaesthesia iv) Need for tracheal intubation, other than for respiratory failure

k) Parameters for institution of ventilation i) Clinical assessment is the most sensitive assessment of respiratory failure. ii) Do not delay the initiation of ventilatory support pending results, blood gases

or mechanical measurements where clinically indicated, e.g. Threatened airway Fatigue / exhaustion Failure of secretion clearance Overt respiratory failure Speech impairment due to dyspnoea Reduced GCS in the absence of other causes

iii) Objective measurements are adjuncts to clinical assessment and must be used in the clinical context, e.g.

Respiratory Rate: RR > 35 bpm Vital capacity: VC < 15 ml/kg Oxygenation: PaO2/FiO2 < 300 Ventilation: PaCO2 > 60 mmHg *with a pH < 7.2

l) Principles in optimising ventilation in ICU patients i) Optimise oxygenation:

Use the lowest FiO2 to achieve an �‘adequate�’ SpO2 / PaO2 a. Default: SpO2 > 95% and/or PaO2 > 80 mmHg b. Lower values may be appropriate with chronic lung disease

PEEP = 5-15 cmH2O ii) Optimise PaCO2:

Adjust relative to premorbid PaCO2 Permissive hypercapnia in patients with poor lung compliance

iii) Optimise patient-ventilator interface: Reduce work of breathing through the ETT and ventilator circuit

a. Pressure support (10-20 cmH2O) in all patients b. Automatic Tube Compensation (ATC), if available

Prevent gas trapping: measurement and manipulation of auto-PEEP Patient positioning

iv) Optimise sedation and analgesia Review the need for sedation daily and cease where appropriate.

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v) Minimise volutrauma (barotrauma) A modified ARDSNet Ventilation Protocol is used at the RAH (see

following section #6). This protocol is not the default setting for ventilation of patients on

arrival in the ICU, rather this protocol should be prescribed for patients at risk of barotrauma and acute lung injury, where no contraindication exists (e.g. acute CHI, severe asthma).

m) Modes of mechanical ventilation used in ICU

i) Synchronised intermittent mandatory ventilation (SIMV) + PEEP + Pressure Support + Pressure limited to 40 cmH2O:

Default ventilation setting at RAH Features:

a. Prescribed tidal volume / variable airway pressure b. Baseline / intermediate ventilation mode to begin weaning c. Mean airway pressure < 25-30 cmH2O

Complications a. Patient ventilator dyssynchrony, gas trapping b. Barotrauma / volutrauma

ii) Pressure control ventilation (PCV) + PEEP: Features

a. Requirement for full ventilation: i.e. not a weaning mode b. Mean airway pressure > 25-30 cmH2O c. Prescribed peak pressure, variable tidal volume

Complications a. High sedation requirements, occasional use of muscle relaxants b. Patient ventilator dyssynchrony, gas trapping

iii) Pressure Support Ventilation (PSV) + PEEP Indications

a. Stand alone mode of ventilation in patients with adequate respiratory drive and mechanics

b. Weaning from ventilation c. Patients with gas trapping, high auto-PEEP and high work of

breathing (e.g. COPD) Complications

a. Increased patient respiratory effort compared with other �“mandatory�” modes of ventilation

b. May precipitate incipient or overt cardio-respiratory failure or fatigue during weaning

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n) Complications of mechanical ventilation i) Haemodynamic

Reduced preload Increased RV afterload unmasked hypovolaemia

ii) Respiratory Altered V/Q ratios Nosocomial and/or aspiration pneumonia Volutrauma / Barotrauma Ventilator associated lung injury Patient ventilator dyssynchrony

iii) Metabolic Post-hypercapnoeic metabolic alkalosis SIADH

iv) Raised intracranial and intraocular pressure v) Global

Need for sedation Reduced patient mobility (DVT, pressure sores, muscle deconditioning,

reduced joint movement.) Critical illness weakness

vi) Local Pressure effects from intubation, tracheostomy or face masks

o) ICU ventilators:

i) Dräger EVITA 2 Dura ventilator The Evita 2 are the default ventilator at the RAH.

a. Modes: - SIMV, PCV, Pressure Support, CPAP, APRV. b. Non-invasive ventilation modes are also available.

Specific features: a. Auto flow: automated adjusted inspiratory flow according to lung

mechanics during controlled ventilation b. Rise time: manual adjustment in all modes c. Automated estimation of auto-PEEP and occlusion pressure (P0.1) d. 100% O2 suction button: delivers 100% oxygen for 3 minutes e. Programmable default parameters f. Flow and Pressure - Volume loops g. Preset emergency and apnoea ventilation parameters h. Automatic tube compensation to assist weaning i. Automated respiratory mechanics module:

i. static and dynamic compliance ii. inspiratory airway resistance iii. negative inspiratory pressure iv. vital capacity

j. Nitric oxide delivery system

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Default settings: SIMV: 600 x 12 | PS = 5 | PEEP = 5 | FiO2 = 1.0 a. Press �“Mode setting�” button b. Select the desired parameter via the respective button. Adjust the

displayed value via the rotating knob, then press to select the desired value.

c. Select mode: SIMV i. FiO2: 1.0 ii. Select tidal volume: 0.6 l iii. Select respiratory rate: 12 bpm iv. Pressure support: 5 cmH2O v. PEEP: 5 cmH2O vi. Rise time: 0.2 secs vii. Adjust TInsp. so that I:E ratio is 1:2 (default 1.7 secs)

d. �“Extra settings�” mode: i. Flow trigger: 5 l/min ii. Backup ventilation (CMV) : off

PC (Pressure control) + PEEP PSV a. The actual settings that are set on the ventilator must be

prescribed. b. Default settings:

PInsp = 30 x 12 | PEEP = 5 | FiO2 = 1.0 | I:E=1:2 c. Select mode: PCV+ d. Settings:

i. Select total inspired level of pressure (Pinsp) which includes PEEP: Default: 30 cmH2O

ii. Select desired rate: 12 iii. Adjust TInsp. so that I:E ratio is 1:2 (default 1.7 secs) iv. Rise time: 0.2 secs v. Pressure support: 5 cmH2O vi. Select PEEP: 5 cmH2O vii. FiO2: 1.0

e. Alarms / limits unchanged from default f. Do not exceed total inspired pressure > 40 cmH2O g. Tidal volume is determined by the patients compliance h. I:E ratio = 1:2

*alteration of the I:E ratio is potentially hazardous and should only be done following discussion with the duty consultant.

Measurement of auto-PEEP a. Measurement of intrinsic PEEP at end expiration + closed airway b. Not accurate in SV modes or with patient effort, patients should be

well sedated. c. If I:E ratio or RR are altered:

i. Expiratory time is reduced ii. Auto-PEEP may be affected and should be measured

d. Press the [Special Procedure] button & select [PEEPi]

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i. Press [Start] to begin the automatic 7sec manoeuvre ii. Read off the PEEPi and trapped gas volume (Vtrap) iii. The value displayed includes applied PEEP, so:

auto-PEEP = PEEPi - applied PEEP Measurement of occlusion pressure (P0.1)

a. Measurement of the negative airway pressure generated in the first 100msec of inspiration against an occluded airway.

b. Reflects diaphragmatic effort and neuromuscular drive c. Normal value = 3-4 mbar d. Higher values > 6 mbar reflect fatigue e. Press [Special Procedure] button

i. Select P0.1 and press �“start�” to begin ii. Read off P0.1

Always examine the flow, pressure and volume vs time graphs, e.g. a. Flow does not return to baseline prior to next breath may indicate

dynamic hyperinflation. b. Pressure that does not return to set PEEP may also indicate dynamic

hyperinflation. c. Sudden reversal of flow pressure which does not trigger a breath may

indicate wasted patient effort. d. Inspiratory hold and observing the peak-plateau pressure gradient

can give an indication of airflow resistance. Examine P-V loops for clinical patterns of:

a. Upper/lower airway obstruction b. Recruitable lung c. Dynamic hyperinflation.

PS (pressure support) + PEEP a. Settings described above for use with SIMV, PCV b. Note �– total inspiratory pressure, when using PS on the Evita, is the

dialed value plus dialed PEEP value c. Stand alone settings:

i. Select mode: CPAP ii. Rise time: 0.2 secs iii. Pressure support: 10 cmH2O iv. PEEP: 5 cmH2O v. FiO2: 1.0

CPAP a. As above for PS but with PS = 0 / PEEP = 5cmH2O.

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7. RAH - �“ARDSNet�” Ventilation Protocol

a) Initial Ventilator Set-up and Adjustments (Dräger) i) Mode: SIMV + PS = 5 cmH2O ii) Resp. Rate: 18 bpm iii) Inspiratory Flow Rate: Autoflow iv) Tidal Volume: 6 ml/kg IBW

b) Tidal Volume Settings are determined by calculated Ideal Body Weight

i) Males = 0.91 x (height [cm] �– 152.4) + 50 ii) Females = 0.91 x (height [cm] �– 152.4) + 45.5 iii) Calculate IBW and Vt = 6 x IBW

c) Maintenance / Management

i) Adjust RR to achieve the pH goals according to ABG�’s. (see below). ii) Adjust Vt according to plateau pressure goals.

NB: Observe spontaneous tidal volumes and adjust PS downwards if volumes generated are higher than the calculated goal Vt.

iii) Adjust FIO2 according to SpO2 and PaO2 iv) Check and adjust I:E ratio.

d) Goal pH pH = 7.20 �– 7.45

i) Acidosis management: pH < 7.20 RR until pH > 7.20 or PaCO2 < 25mmHg

a. max RR = 35bpm If pH < 7.20 and RR = 35, then

a. Vt by 1 ml/kg IBW steps until pH > 7.20 b. Pplat. goal may be exceeded

ii) Alkalosis management: pH > 7.45 Decrease RR if possible

e) Goal Plateau Pressure: Pplat < 30 cmH2O

i) Check inspiratory plateau pressure with a 0.5sec inspiratory pause every 4 hrs and after each change in PEEP or Vt.

ii) Method (Dräger): go into measurements + press inspiratory hold for 0.5sec Pplat will appear on the screen next to Pplateau for 1 second.

iii) Pplat > 30 cmH2O Vt by 1 ml/kg IBW steps min Vt = 4ml/kg IBW

iv) Pplat < 25 cmH2O and Vt < 6ml/kg IBW Vt by 1ml/kg IBW

until Pplat >25 cmH2O or Vt = 6ml/kg IBW.

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FiO2 PEEP0.3 50.4 50.4 80.5 80.5 100.6 100.7 100.7 120.7 140.8 140.9 140.9 160.9 161 16

f) Goal Arterial Oxygenation: PaO2 = 55-80 mmHg or SpO2 88-95% i) If SpO2 or PaO2 are outside goal range, use the table

(right) to adjust FiO2 / PEEP combinations for the PaO2 range required.

ii) Take ABG�’s only as clinically indicated, changes can be made according to SpO2.

iii) Examples: If a patient is on FiO2 0.4 and a PEEP of 5 and the

PaO2 = 54 mmHg the next step would be to increase the PEEP to 8 cmH2O.

If a patient was on FiO2 = 0.9 / PEEP = 14 and the SpO2 = 99% the next step would be to decrease the FiO2 to 0.8.

g) Goal I:E Ratio = 1:1.0 �– 1:3.0 i) After any RR change, check the I:E ratio and modify

the TInsp ii) Do not inverse the I:E ratio with this protocol

risk of breath stacking and hypotension. 8. Extra-Corporeal Membrane Oxygenation (ECMO)

a) ECMO can be used to provide either: i) Oxygenation in cases of overwhelming respiratory failure (veno-venous

ECMO) or, ii) Circulatory support in reversible cases of refractory overwhelming cardio-

respiratory failure (veno-arterial ECMO). b) ECMO services commenced at the RAH in 2009, and continue to evolve. c) Any cases for potential ECMO support will be discussed in detail prior to

initiation, and will be supervised closely by duty ICU-ECMO consultant. d) If caring for a patient on ECMO all relevant protocols and contact details will

be made available. e) Care of the patient on ECMO includes specific requirements. f) The ECMO circuit and equipment must not be altered without the ICU

consultant and/or perfusionist supervision. g) NB: The policies, protocols and procedures for ECMO are contained in a

stand-alone manual which is attached to the ECMO machine.

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9. Non-invasive ventilation

a) Definition: Mechanical positive pressure respiratory support in the absence of tracheal intubation (e.g. via a face mask, nasal mask, head piece/box)

b) Modes

i) Continuous positive airway pressure (CPAP) ii) Bi-level positive airway pressure (BiPAP).

c) Indications

i) As an adjunct to weaning from ventilation, e.g. extubation to NIV ii) Incipient respiratory failure with high work of breathing in selected diseases:

Acute exacerbations of COPD Cardiogenic pulmonary oedema Obstructive sleep apnoea Acute quadriplegia Post-extubation hypoxia due to pulmonary oedema or atelectasis Cystic fibrosis Febrile neutropaenia with pulmonary infiltrates Pneumonia As a bridge where:

a. Appropriate airway assistance is sought or resuscitation is undertaken, prior to induction and safe intubation, or

b. Appropriateness of invasive ventilatory support is being considered.

d) Prerequisites i) Adequate glottic reflexes should be present to protect from aspiration:

moribund patients require intubation where appropriate ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B. iii) Unit C patients requiring NIV should be considered for transfer. iv) Selected patients may be managed in Unit C:

Tracheostomised patients with isolated PEEP dependency - i.e. slow weaning

Rapidly resolving respiratory failure with face mask CPAP/BiPAP a. Diuresing pulmonary oedema b. Resolving stridor c. Stable COPD during hospitalisation for exacerbation d. Patients with OSA, with and without their own machines

e) Complications

i) Aerophagia, gastric distension, aspiration ii) Claustrophobia and mask intolerance iii) Pressure necrosis of nasal bridge iv) Dry secretions v) Barotrauma vi) Reduced preload and hypotension vii) Raised intracranial and intraocular pressure

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f) Ventilators

i) Dräger CPAP circuit. Adjust flow rate to maintain desired CPAP level (typically > 40 l/min) Select CPAP (cmH2O) on external PEEP valve Select FiO2 (air / oxygen mix with two rotameters) Always use with wet humidified circuits (Fisher-Paykel)

ii) BiPAP® Vision / Harmony ventilators spontaneously ventilating, non-intubated patients

Select IPAP = Inspiratory positive airway pressure Select EPAP = Expiratory positive airway pressure (PEEP) Pressure support = IPAP - EPAP

iii) CPAP via Dräger EVITA® Select non-invasive mode Select CPAP in [OtherModes] Set CPAP/PEEP and FiO2 Adjusting Press Support and Press Rise Time will add assisted breaths to

CPAP. See ASV.

g) Assisted Spontaneous Ventilation i) The Dräger Evita is best configured to achieve ASV by Pressure Support.

The same settings as CPAP on Evita Select non-invasive mode Adjust Press Support and Rise Time to provide the assisted breaths Default settings:

a. Pressure support 10 cmH2O (above PEEP) b. PEEP 5 cmH2O c. Inspiratory time 4 sec d. Trigger 5 l/min

ii) Vision® BiPAP Microprocessor controlled spontaneous breathing assist ventilator in

either CPAP or spontaneous/timed breathing mode (S/T). Mixes pipeline oxygen with ambient air via an internal pump Monitors machine pressure against proximal airway (mask pressure) to

ensure effective delivery of pressure despite circuit leaks. Uses internal algorithm for respiratory cycling and leak adjustment. Nasal, face & full head masks can be used. Liquid crystal displays

a. IPAP, EPAP, rate, oxygen b. Vt, Vmin, PIP, insp. time/total cycle time. c. Leak (patient & total), % patient triggered breaths d. Graphical display of pressure, volume & flow.

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Need to calibrate for tubing and mask. Operation �– machine starts up in mode previously used.

a. Press [Mode] hard key to display CPAP or S/T mode b. Select soft key parameters displayed & turn adjustment knob

accordingly c. Press [Activate New Mode] soft key to select the new mode. d. The ventilator will continue in the old mode until �‘activated�’

CPAP Mode a. Default setting: CPAP 5cmH2O, FiO2 1.0 b. Only CPAP setting & FiO2 soft keys are active.

S/T Mode a. Default setting: IPAP 15cmH2O, EPAP 5cmH2O, Rate 12, Timed

insp 1 sec, FiO2 1.0, IPAP rise time 0.1 sec b. Adjust settings accordingly

Setting modification a. Press [Parameter] hard key b. Select soft key & turn adjustment knob. c. Press [Monitoring] hard key to return to monitoring screen

Alarm limits a. High Pressure 30 cmH20 b. Low Pressure 5 cmH20 c. Low Min Vol 0 l/min d. High resp rate 30 b/min e. Low resp rate 6 b/min f. Low press delay 20 sec

10. Weaning from ventilation

a) General principles i) No mode of weaning has been demonstrated to be superior to another ii) Short-term patients with acute resolution of respiratory failure (e.g. post-

operative, drug overdose, trauma) may be rapidly weaned to extubated. iii) Long-term patients with multiple intercurrent problems take longer and

effectively �“go at their own pace�”. iv) It is important to balance over-sedation and prolonged ventilation against

rapid weaning, patient exhaustion and failed weaning or extubation. v) See �– Flowchart: Ventilation Weaning Protocol, p50.

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b) Clinically important determinants for weaning from ventilation: i) Resolution of the process requiring ventilation ii) No new CXR abnormality iii) Completion of therapeutic options that require ventilation

(e.g. debridements, operations) iv) Appropriate conscious state; cooperative patient v) Appropriate peripheral motor function vi) Adequate analgesia vii) Haemodynamic stability viii) Metabolic, acid-base stability

c) Methods

i) Spontaneous effort is required for the patient to be weaned ii) SIMV with reducing rate and tidal volume in conjunction with PSV and

PEEP is standard iii) Use PSV + PEEP alone once the patient�’s spontaneous rate is sufficient to

prevent a respiratory acidosis at pH < 7.3 iv) Intubated CPAP v) T-piece weaning: intermittent T-piece and positive pressure (PSV / CPAP /

SIMV). vi) Non-invasive bi-level ventilation

d) �“Objective�” measurements

i) Adjuncts to the assessment of weaning success. ii) These are not specific and must be interpreted in the clinical context. iii) Respiratory rate and tidal volume are the most sensitive:

Rate (f): < 30/min Tidal volume: > 5 ml/kg f/VT: < 100 (rapid shallow breathing index) PaO2/FiO2: > 200 and PEEP < 10 cmH2O PaCO2 < 60 mmHg

11. Extubation protocol

a) Ensure equipment, monitoring and adequate assistance, in case of re-intubation. b) Extubation is preferentially done during daylight hours and is a medical

responsibility.

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c) Extubation criteria: i) Return of adequate conscious state to maintain adequate protective laryngeal

reflexes and secretion clearance. ii) Adequate pulmonary reserve (see objective measures above) iii) In patients with upper airway surgery or swelling the demonstration of an

adequate air leak around the deflated endotracheal tube cuff and assessment with pre-extubation laryngoscopy.

iv) Plastic surgery and ENT patients require consultation with the Parent Clinic. Those patients with intermaxillary fixation and wiring must have a person from the Parent Clinic familiar with the placement of the wires and a wire cutter present during extubation.

d) All patients must receive supplemental oxygen post extubation.

12. Protocol for ventilation in the prone position

a) General principles i) This technique may improve oxygenation in up to 60% of patients with

severe ARDS. This may �“buy time�”, however no mortality benefit has been demonstrated to date.

ii) Prone ventilation in critically ill patients is potentially hazardous: Difficult airway and patient access Increased risk of endotracheal tube dislodgment or malpositioning Difficulty in tracheal suction Pressure necrosis �– particularly involving the face and eyes. High incidence of facial oedema Labour intensity Difficulty in performing CPR

iii) The decision to ventilate a patient prone is made by the Duty Consultant. iv) Patients must only be turned if adequate numbers of staff are available,

ideally during working hours, in discussion with senior nursing staff.

b) Indications i) Local or anatomical factors, e.g. posterior burns ii) Severe ARDS

Rationale of improved oxygenation in prone ventilation in ARDS: a. Improvement in FRC by alveolar recruitment b. Preferential redistribution of pulmonary blood flow

improved V/Q ratios c. Uniform distribution of lung water and exudate d. Reduction in intrapleural pressures e. Non-restriction of abdominal contents f. Reduction of diaphragmatic splinting and improved movement of

the posterior diaphragm.

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Timing a. Severe ARDS with PaO2:FiO2 ratio < 100 b. Pulmonary hypertension : MPAP > 35 mmHg c. Non-response to standard supportive care

i. Optimisation of fluid balance ii. Treatment of infection iii. Circulatory support

c) Contraindications

i) Absolute Inadequate staff or insufficient staff familiarity Spinal injury Pelvic fracture �– unstable Orthopaedic traction Open abdomen

ii) Relative Anterior UWSD Patients on CVVHDF or with an IABP Morbid obesity Patients unable to lie flat Closed head injury

d) Procedure

i) Staff required More than one intensive care doctor Minimum of four nurses

ii) Essential monitoring / equipment Electrocardiograph (ECG) electrodes placed on the back Arterial line Pulse-oximetry End-tidal carbon dioxide monitor Intubation /resuscitation trolleys Closed suction device in situ 2 secure IV accesses.

iii) Safety check before turn Check ETT position on CXR prior to turn ETT should be secured with cotton tape and adhesive tape Check security of tracheostomy tapes Secure all invasive lines and drains. Ensure patency, accessibility and sufficient slack for the turn Recirculate/hold dialysis if in progress Deflate air mattress Ensure the patient is heavily sedated Consider the use of neuromuscular blocking drugs Apply lubricant to the eyes and close with tape or plastic film

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Replace head pillow with a small foam gel pad. Ensure sufficient padding

iv) Procedure Explanation to patient and relatives where appropriate Ensure adequate sedation and or analgesia The doctor must take control of the head and airway and coordinate

the turn Place the patient flat on their back with arms by the side Lift the patient (on a draw sheet) to side of the bed away from the

ventilator, i.e. turn towards the ventilator. Place a firm pillow or foam support under the hips and shoulders Tuck lower hand under hip Slowly roll the patient onto the pillows/foam taking care of lower the

arm & shoulder Place the head to one side, check the eyes are shut Check the airway, oxygen saturation, ventilation, invasive lines

(position and access to them) and haemodynamic response Place the arms in an anatomical position: check a/c and elbow joints Check all potential skin pressure points Re-inflate the air mattress Take an arterial blood for gas analysis.

v) Maintenance Routine ICU observations Hourly face pressure care and head repositioning Monitor plantar flexion, neck hyperextension and facial oedema Continuous ETCO2 monitoring whilst prone ABG as soon as the patient is stabilised. CXR can be conducted whilst patient is prone (ensure that CXR

request clearly states patient is prone) vi) Duration

If there is a major deterioration in the arterial oxygenation, the patient must be turned supine as soon as possible.

If the oxygenation is unchanged or improved, leave prone for up to 12 hrs. Some patients may show gradual improvement over this period.

Repeat rotations once per shift according to clinical progress / response.

In general, patients should not be turned at night. Ensure all safety issues are followed in reverse when return patient to

supine position.

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E. Management of Cardiothoracic Patients 1. General Principles

a) The following guidelines apply to elective post-cardiac surgical patients. 2. Respiratory

a) Following surgery commence all patients on default ventilator settings: SIMV + PS 20cmH2O + PEEP 5cmH2O + FIO2 = 1.0

b) After the first ABG, adjust the FIO2 to maintain a PaO2 > 80mmHg c) Wean from ventilation according to past history, surgery performed and current

clinical status d) Extubation criteria:

i) Temperature > 36 C ii) Awake, able to obey commands iii) Adequate analgesia iv) Cardiovascular stability on minimal inotropes

(< 10µg/min noradrenaline or adrenaline) v) Adequate gaseous exchange: PaO2 > 80 mmHg on FIO2 0.5, PEEP 5cm vi) Bleeding: drain losses < 100 ml/hr

e) Respiratory failure post-op secondary to collapse / consolidation is common. i) Ensure good analgesia and frequent, effective physiotherapy ii) CPAP may be required in the first 48 hours.

f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to extubation failure and may benefit from the use of ACE inhibitors, inodilators or a trial of spontaneous ventilation prior to extubation.

3. Management of bleeding

a) Notify the surgical team. b) Perform appropriate investigations: ACT, APTT/INR, Hb, Plts, fibrinogen. c) Treat abnormalities of above:

i) Protamine 50mg slow IV if ACT > 125 sec or APTT > 60 sec ii) FFP if INR > 1.5 iii) Give platelets if count below 80,000 or as below.

d) If bleeding continues or is brisk or > 1500mls in first 12 hours. i) Platelet transfusion of one adult pack, irrespective of platelet count. ii) Perform CXR and/or echocardiogram to exclude tamponade iii) Initiate review by cardiothoracic surgeons

e) Consider re-opening if: i) Bleeding > 200 ml/hr for 3-4 hrs, or ii) Total loss > 1500-2000 ml. iii) If no evidence of tamponade re-open in OT.

If evidence of tamponade consider re-opening in ICU

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4. Hypotension a) Hypovolaemia

i) Return any remaining pump blood as soon as possible ii) Correct fluid/blood losses as appropriate

maintain Hb > 80 g/L and CVP ~ 6-10 mmHg iii) Check ECG

b) Myocardial failure i) Noradrenaline, often with low dose dobutamine (to improve regional blood

flow to splanchnic/renal vascular beds), is the first choice inotrope combination. Adrenaline is used for severely impaired ventricles.

ii) If required inotropes > 10µg/min and the patient is euvolaemic, consider: PA catheter insertion Pulse contour CO measurement e.g. PiCCO or Edwards Vigileo. Echo to exclude tamponade, AMI, papillary muscle rupture, or VSD.

iii) Consider pacing (either epicardial or transvenous) if hypotension is rate related (HR < 60). A-V sequential pacing is the ideal mode (DDD)

iv) Consider IABP if hypotension persists despite inotropes. v) Consider milrinone for patients with predominantly diastolic cardiac

failure or pulmonary hypertension. vi) Levosimendan may have a role in patients with poor LV function, both

prophylactically during surgery and post-operatively c) Vasodilatation

i) Noradrenaline is the 1st line agent for persistent vasodilatation and hypotension.

ii) Consider vasopressin ~ 0.02-0.04 µg/min iii) Consider insertion of a PA catheter or PiCCO/Vigileo system to determine

CO, SVR and SV to aid in management. d) Tamponade

i) This is a medical emergency. If suspected, the cardiothoracic surgeon and duty consultant must be notified immediately.

ii) Diagnosis: Refractory hypotension despite adequate volume replacement and

inotropic support Cessation / reduction of blood coming from drains Globular heart shadow on CXR and muffled heart sounds may be

present but are unreliable signs Diastolic equalisation of right-sided pressures on PA catheter insertion Echocardiographic evidence of tamponade.

iii) Treatment Support MAP with aggressive volume and inotropic support. Ensure sufficient blood is cross-matched ( 6 units) If stable, reopening in theatre is the definitive treatment In emergent situations the chest may need to be opened in ICU.

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5. Hypertension a) MAP should be kept at approximately 70 mmHg for the first 24-36 hrs. b) This may vary according to the patient�’s pre-morbid BP. c) Management:

i) Ensure adequate analgesia ii) Nitroprusside 50 mg in 250 ml 5% dextrose:

titrate to maintain MAP ~ 70 mmHg. iii) If nitroprusside infusion > 40-50 ml/hr (2 µg/kg/min), consider:

-blocker: metoprolol 1-2 mg IV, (if no contraindication) Clonidine: 25-50 µg IV (up to 300µg/24 hrs) Hydralazine: 10-20 mg IV Captopril: 6.25-12.5mg 2 hourly PRN (up to 150mg/24 hrs)

6. Sedation/Analgesia

a) Generally as per general ICU sedation protocols b) In patients difficult to sedate and expected to be extubated within 24 hrs,

consider dexmedetomidine (Precedex): i) 2: 1 -agonist activity ~ 1600:1, providing both sedation and analgesia ii) Loading dose: 0.5-1.0 µg/kg/min over 10 mins iii) Infusion: 0.2-0.7 µg/kg/hr iv) Patients coming from theatre should not require a loading dose v) Complications: hypotension, bradycardia.

c) Morphine IV 1-2mg boluses PRN while on ventilator d) Morphine subcutaneously post-extubation e) Paracetamol IV or po 4/24 PRN for first day then 6/24 if no contraindication f) Oxycodone po 4/24 PRN in appropriate dose from second postoperative day

7. Anticoagulation a) All patients receive subcutaneous heparin

i) < 70 kg 5000U 12 hrly ii) > 70 kg 7500U 12 hrly

b) All patients with coronary artery graft should receive aspirin 300mg po daily post-extubation, or via a NGT if extubation is delayed.

c) Commence patients with mechanical valve replacements on warfarin (5mg nocte) from the second post-operative day if extubated.

d) Patients with a mitral valve replacement ventilated > 48hrs may require heparinisation as will patients in AF for > 48hrs.

e) For antiplatelet drugs see �“drugs and infusions�’ subsection �“thrombolysis�” 8. Antibiotic prophylaxis

a) See guidelines in antibiotic section in Drugs.

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9. Other Drugs a) Calcium Channel Blockers

i) Patients receiving radial artery grafts generally receive diltiazem 30mg po tds from first postoperative day

b) Stress ulcer prophylaxis is not routinely indicated unless the patient has pre-existing peptic ulcer disease.

c) Insulin is managed as per the general ICU protocol. 10. Management of Minimally Invasive Mitral Valve Repairs

a) These are performed through a right sided mini-thoracotomy with the patient on femoro-femoral bypass

b) Patients generally have a �“pain buster�” placed perioperatively for analgesia c) Management as for other cardiothoracic patients. d) Clarify with surgeon whether warfarinisation is required postop. This may vary

with exact type of repair, use of annuloplasty ring, heart rhythm etc.

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F. Renal Failure 1. Background

a) The mortality from acute renal failure remains high: from 8% in isolation to 70% when associated with other organ or system failures.

b) Patients who die with acute renal failure, usually die from the underlying cause rather than ARF itself.

c) There is a spectrum of renal dysfunction with variable definitions of what constitutes �“Renal Failure�”.

d) Bellomo has proposed the following definitions:

Creat Creat Urea Urea UO Normal 15-70 2-6 >800 Acute Renal Impairment > 120 > +60 > 8 > +4 <800 Acute Renal Failure > 240 > +120 > 12 > +8 <400

e) Approx. 30% of ICU patients have pre-existing renal impairment. f) Patients at high risk of developing ARF are those with:

i) Pre-existing renal impairment (creatinine > 120). ii) Severe sepsis iii) Hypertension iv) Diabetes v) Arteriovascular disease vi) Heart failure vii) Large contrast media loads

g) The minimum urine output required to excrete the obligatory solute load is ~ 0.5 ml/kg/hr.

h) ARF can be �“oliguric�” or �“non-oliguric�”. Non-oliguric renal failure has a better prognosis.

i) Duration of ARF is variable and depends upon resolution of the underlying injury, severity of the injury and pre-morbid renal function.

j) Consequences of ARF: i) Fluid overload. ii) Uraemia �– encephalopathy, platelet dysfunction, pericardial effusions. iii) Acidaemia. iv) Electrolyte derangements �– K+, PO4

=, HCO3-

v) Accumulation of pro-inflammatory cytokines (theoretical)

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2. Pathogenesis �– ARF in critically ill patients is usually multifactorial.

a) Pre-Renal i) The most common cause of renal failure in ICU. ii) Aetiologies:

Low cardiac output states Hypovolaemia. Vasodilation - sepsis, vasodilators Renal vasoconstriction - NSAIDs Renal artery obstruction - stenosis, embolus, post-surgical

iii) Reduced renal blood flow GFR and renal function angiotensin-II and glomerular efferent arteriolar constriction blood flow to the renal medulla If maintained, then ischaemic renal injury occurs (e.g. ATN).

b) Renal i) Acute Tubular Necrosis.

Ischaemic - see above Nephrotoxic - drugs, contrast, myoglobin, sepsis

ii) Interstitial Nephritis - infections, drugs iii) Vascular disease - renal vein occlusion, HUS, vasculitis iv) Glomerulonephritis

c) Post-Renal i) Obstruction of the renal collecting system leads to GFR. ii) Must be considered in unexplained renal failure. iii) Cannot be reliably ruled out clinically and hence requires imaging. iv) Ensure a bladder catheter is inserted and draining freely. v) Aetiologies:

Drugs - opiates, anticholinergics Pelvic neoplasms. Retroperitoneal collections (e.g. blood, pus, fibrosis). Pregnancy. Prostatic Obstruction Renal calculi

d) Specific Renal Failure Syndromes i) Increased intra-abdominal pressure (IAP)

Effects at all levels - pre-renal, renal and post-renal May consider decompression when IAP > 20 mmHg with ARF.

ii) Hepato-Renal Syndrome - predominantly a pre-renal albumin, vasodilatation, splanchnic shunting diuretics for oedema, lactulose, diarrhoea, intra-abdo pressure

iii) Rhabdomyolysis - pre-renal, renal and post-renal iv) Ineffective plasma volume

e.g. nephrotic syndrome, liver failure, cardiac failure.

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3. Renal Investigations

a) Blood tests i) Creatinine

Logarithmic (inverse) relationship with GFR. Can lose up to 60% renal function and still maintain a �“normal�”

creatinine. Conversely in severe renal failure, a small decrease in renal function can cause large rises in serum creatinine.

Lags behind the evolution of renal injury. Insensitive where muscle mass is low �– elderly, wasting diseases

ii) Creatinine clearance (ClCr) ClCr slightly overestimates GFR due to tubular secretion Estimated on IMVS biochemistry (eGFR) from single specimen

creatinine, thus has same inaccuracies as creatinine Measured ClCr requires min 8 hour urine collection

iii) Urea Less accurate indicator of GFR than creatinine Modified by diet, catabolic state, GIT blood, liver disease

iv) Electrolytes - Na+, K+, HPO42-, ABGs.

v) GN screen - ESR, C3, C4, ANA, RhF, ANCA, anti-GBM. vi) Haemolysis screen - RBC frags, LDH, haptoglobins, bilirubinaemia.

b) Urine i) M,C& S - infection must always be excluded ii) Myoglobin iii) Urinary electrolytes - impossible to interpret in the presence of diuretics or

natriuretic agents (e.g. catecholamines). iv) Urinary sediment

Epithelial cell casts - ATN RBC / WBC casts - GN Eosinophils - interstitial nephritis Crystals - oxalate (e.g. ethylene glycol)

- urate (e.g. tumour lysis) c) Imaging

i) Ultrasound Exclude urinary tract obstruction. Doppler studies can assess renal artery and venous flows

ii) CT Renal Tract (non-contrast) �– highlights renal stones and masses. iii) IVP - rarely required given availability of U/S and CT. iv) DMSA scan - a static radionuclide scan to reveal kidney structure. v) MAG3 scan - a dynamic radionuclide scan

- renal function, collecting system obstruction, ATN. d) Biopsy

i) Glomerulonephritis ii) Interstitial nephritis iii) Infiltration

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4. Renal protection

a) Established renal protection strategies i) Fluid resuscitation to maintain circulating blood volume. ii) Haemodynamic support of blood pressure and cardiac output using inotropes

(adrenaline, noradrenaline, dobutamine). iii) Exclusion of post-renal obstruction (check IDUC, renal tract U/S,

nephrostomy). iv) Avoidance / close monitoring of nephrotoxic drugs

aminoglycosides, amphotericin contrast agents ACE inhibitors NSAIDs

v) Prompt detection & treatment of urinary infection. b) Unproven strategies for renal protection

i) Frusemide infusion / high dose ii) Mannitol infusion / intermittent iii) Aminophylline infusion iv) N-acetyl cysteine v) Calcium channel blockers vi) Clonidine vii) HCO3

- for rhabdomyolysis. c) Contrast Prophylaxis

i) Best evidence is to use HCO3-

ii) Add 150ml 8.4% NaHCO3 to 850ml 5% Dextrose. iii) Run at 3ml/kg the hour prior to contrast administration,

then continue at 1ml/kg/hr for 6 hours d) Low Dose Dopamine

i) May temporarily increase urine output ii) Does not reduce the incidence of dialysis dependent renal failure or

mortality. (ANZICS CTG).

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5. Indications for renal replacement therapy

a) Symptomatic or refractory: i) Acidosis ii) Hyperkalaemia iii) Fluid overload - e.g. pulmonary oedema iv) Uraemia - urea > 35 mmol/l or symptomatic

b) Severe sepsis i) Developing oliguric renal failure ii) Removal of cytokines / inflammatory mediators (unclear benefit)

High ultrafiltration rates increase clearance The clinical significance is currently being studied.

c) Diuretic resistant pulmonary oedema. d) Drug removal.

i) Salicylate ii) Methanol iii) Theophylline iv) Ethylene glycol v) Lithium vi) Other drugs (water-soluble drugs that are not highly protein bound).

e) The decision to commence RRT should be discussed with the duty consultant. f) Generally, RRT is initiated early in the course of ARF, before serious

complications develop. g) The choice of RRT modality depends on patient�’s type and severity of illness,

equipment availability and local expertise. h) The renal unit should be notified �“early�” of patients who are potential long-term

dialysis candidates.

6. Renal Replacement Therapy Principles

a) Haemofiltration. i) Convective solute and fluid removal down a hydrostatic pressure gradient

to form an ultrafiltrate (UF). ii) Clears middle molecules (>500 D) and fluid. iii) UF formation is dependent on the pressure gradient and membrane

characteristics (effective pore size & surface area). iv) Predilution replacement of ultrafiltrate with balanced salt solution

increases the availability of urea for convective transfer by favouring its movement from red cells.

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b) Haemodialysis. i) Diffusion of solute down a concentration gradient across a semi-permeable

membrane, running dialysate fluid counter-current to blood flow ii) Clears urea, creatinine, electrolytes (i.e. small molecules). iii) Solute clearance is adjusted by changing the dialysate fluid solute

concentration, blood and dialysate flow rates. iv) Intermittent HD (IHD)

Utilised if the patient is stable and requires longer-term dialysis. Takes 3-5 hours using higher blood flows of 300 ml/min Fluid removal occurs quickly, not tolerated in unstable patients. Performed by the Renal Unit.

v) Sustained Low Efficiency Dialysis (SLED) Similar to standard IHD but occurs over 8-12 hours Lower blood and dialysate flow rates. Well tolerated by the critically ill. Used in some ICUs (not the RAH) for nursing and cost reasons. Although better tolerated than IHD in the critically ill, there is little

evidence to confirm equipoise with CVVHD/F in terms of outcomes.

c) Continuous veno-venous haemodiafiltration (CVVHDF). i) Standard form of continuous renal replacement therapy in this Unit. ii) The combination of ultrafiltration and dialysis improves solute clearance. iii) Advantages of CVVHDF over conventional intermittent haemodialysis:

d) Effective and more flexible control over fluid balance. e) Greater cardiovascular stability. f) Does not require attendance of Renal Unit staff. g) May have a role in modification of the septic response. h) Some trials suggest improved patient mortality (not proven). i) Allows patients to receive continuous protein rich diet.

7. Complications of CVVHDF

a) Hypothermia. b) Prolonged exposure to heparin: incidence of HITS, bleeding c) Prolonged venous access: infection, thrombosis. d) Air embolism. e) Increased nursing workload. f) Catheter flow disruption (�“high access pressures�”).

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Diagram: CVVHDF Circuit

Heparin

UltrafiltrateReplacement

To Patient

DialysateSolutionEffluent

DeaerationChamber

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8. CVVHDF Equipment

a) Dialysis catheters i) Priority of site placement and optimal catheter length:

Femoral R.IJ L.IJ R.SC L.SC 25cm 15cm 20cm 15cm 20cm

ii) Use Dolphin Protect® high flow catheter guided as above iii) Heparin lock all catheter lumens 8 hourly when not in use

5000U in 3 mls, divided equally into both lumens. b) Filters

i) Older filters were made from cellulose and would often initiate an inflammatory response (i.e. �“membrane reaction�”).

ii) Membranes are now synthetic (polycarbonate, polyacrylonitrile) iii) These are more permeable and biocompatible iv) We use Prisma® AN69 filters:

Membrane = acrylonitrile Membrane thickness = 50 m. Surface area = 1m2

(larger filters 1.2�–2m2 allow blood flow and clearance) Blood volume in set = 150ml

c) Dialysis machine settings i) The PrismaFlex® is the standard dialysis machine at the RAH ii) Older �“Prisma�” machines are still in use but are being phased out.

d) For patients on ECMO, CVVHDF can be performed via the ECMO circuit without additional Vas-Cath placement. i) Must be discussed with ICU consultant supervising ECMO

9. Prescribing CVVHDF

a) Orders for the PrismaFlex or Prisma® should be written on a standard sticker. b) The following variables require assessment/prescription for CVVHDF. c) Haemofiltration solution (�“replacement�”)

i) Gambro® Hemosol B-zero solution - bicarbonate buffered, 5L bag ii) Flow rate = 1000-2000 ml/hr (higher rates in catabolic patients) iii) Ultrafiltration rates of 35 ml/kg/hr may improve survival. iv) Standard is to deliver replacement post-filter, but may be given pre-filter if

required (e.g. short filter life problem, or for intracellular urea clearance) v) If given pre-filter on the PrismaFlex®, still require at least 100ml/hr

replacement post-filter for the deaeration chamber to function properly. d) Dialysis solution

i) Gambro® Hemosol B-zero solution - bicarbonate buffered, 5L bag ii) Rate = 500-2000 ml/hr (higher rates if marked electrolyte abnormalities)

e) Blood flow rate i) When commencing CVVHDF, gradually increase blood flow as tolerated

by patient haemodynamics ii) Target rate = 250ml/min - limited by machine/access pressures.

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f) Anticoagulation i) Blood passing through the filter activates the clotting cascade.

Anticoagulation is often required to prolong �“filter life�” ii) Circuit is primed with heparin 5,000U iii) No ongoing anticoagulation is required for patients with coagulopathy iv) Systemic anticoagulation (if no contra-indications to anticoagulation)

Heparin 5000 units stat, then continue at 1,000 units/hr Heparin is infused into the circuit pre-filter Check APTT after 6 hrs and then daily if stable End-point is �“filter life�” rather than a therapeutic APTT (i.e. if filter is

working and APTT < 45sec, there is no need to increase heparin dose) v) Regional anticoagulation

Utilised when: a. Maintenance of filter life is problematic. b. There is a contra-indication to systemic anticoagulation c. No contraindication to heparin administration.

The circuit still needs to be primed with heparin Heparin is administered pre-filter as above Protamine 5-10 mg/hr post-filter

vi) Check APTT 6 hourly after any dose changes. vii) For patients with heparin induced thrombocytopenia (HIT) consider

Citrate (see citrate protocol) Prostacyclin 5 ng/kg/min (see protocol) Danaparoid (given systemically, not into circuit �– see protocol)

g) Fluid removal i) Determine how much fluid should be removed from the patient. Consider

its effects on patient haemodynamics ii) The amount of fluid removed is the difference between the effluent and the

dialysate plus replacement fluid volumes h) Potassium

i) Gambro® Haemosol B-zero solution contains no potassium. ii) Supplementary K+:

Required for all patients, except in the initial management phase of marked hyperkalaemia

Should to be added to both the replacement & dialysate bags iii) Target [K+] = 3-4mmol/L, dose = KCl 15-20 mmol per 5L bag iv) K-Acetate can be used in severe acidosis:

Acetate is effectively metabolised to HCO3- via the liver

Vial = 25mmol/5ml, dose = 3-4mls per 5L bag i) Drug prescription

i) Consult Antibiotic Guidelines / Pharmacy regarding antibiotic dosing e.g. meropenem, ciprofloxacin, fluconazole

ii) Monitor drugs that are renally cleared and potentially toxic e.g. gentamicin, vancomycin, digoxin

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G. Neurosurgical protocols 1. Neurotrauma in ICU

a) Close liaison and communication with the neurosurgeons is essential for the coordinated management of acute head injuries.

b) ICU management of the neurotrauma patient includes: i) Acute trauma resuscitation ii) Liaison and coordination with other clinics in the multi-trauma patient. iii) Cardiopulmonary / renal / metabolic homeostasis. iv) Maintenance of cerebral homeostasis

NB: refer to cerebral perfusion pressure (CPP) algorithm v) Transport for imaging

c) Principles of ICU management:

i) Ventilation Maintain normoxia: PaO2 > 80 mmHg Ventilation to normocapnia: PaCO2 = 35-40 mmHg

ii) Haemodynamics: Fluid maintenance

a. Maintain euvolaemia b. Crystalloid depending upon Na+ and measured osmolality c. Avoid dehydration if patients become polyuric (DI / mannitol)

Maintain cerebral perfusion pressure: a. CPP ~ 60�–70 mmHg

i. A lower threshold may be tolerable in some patients ii. Must be discussed with the ICU Consultant

b. MAP ~ 80 mmHg in the absence of ICP measurement c. NB: use inotropes if required once euvolaemic

Avoid interference with cerebral venous return a. Nurse patients at 30° head-up elevation b. Neutral head position c. Avoid circumferential ETT ties, etc.

ICP control �– Mannitol (osmotherapy): a. Patient must be euvolaemic and normotensive (relative to pre-

morbid BP) before the administration of mannitol b. The indications for mannitol prior to ICP monitoring are:

i. Unequivocal signs of intracranial hypertension prior to imaging or evacuation of an intracranial mass lesion

ii. Threatened transtentorial/brainstem herniation, or iii. Progressive neurological deterioration not due to systemic

pathology. c. Measured osmolality should not exceed 320mosmol/l

i. Mannitol and alcohol cause an osmolal gap ii. calculated measured osmolality

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d. Standard dose = 0.25g/kg i. 1.25ml/kg of 20% mannitol ii. Duration of action is variable (90min �– 6hrs)

e. A urinary catheter is essential. Hypertonic saline is a reasonable alternative to mannitol.

a. Standard dose is 20ml of 20%NaCl b. Slow IV push through a CVC

Hyperosmolar infusions are to be discussed with the ICU Consultant iii) Seizure prophylaxis - indications:

Closed head injury with structural damage (intracerebral or paraxial haematomas)

Penetrating head injuries Depressed skull fracture Pre-existing epilepsy Phenytoin prescription:

a. 15 mg/kg loading over 30 minutes b. 300 mg iv daily or 400mg NG x 7 days only c. Monitor levels: therapeutic 40-80 mol/l

iv) Antibiotics - indications: Insertion of ICP monitoring catheters: cefazolin 1g stat Base of skull fractures: antibiotics are not indicated in the absence of

signs of meningitis Nosocomial infections: as per infectious diseases guidelines.

v) Sedation: Consider the use of propofol in patients where regular review of CNS

status is required (majority of patients) Control large sympathetic swings with morphine / midazolam,

fentanyl boluses (100-200µg IV) Many opioids have been demonstrated to increase ICP and should not

be used as sole therapy to control intracranial hypertension. The use of muscle relaxants is relatively contraindicated. Infusions of

muscle relaxant must be discussed with the ICU Consultant. Consider -blockade or clonidine in labile neurogenic hypertension.

vi) Nutrition: Establish enteral feeding as soon as feasible Maintain BGL in the normal range: hyperglycaemia is common in the

acute phase and may precipitate a hyperosmolar state with resultant polyuria. Use insulin infusions if necessary.

vii) Stress ulcer prophylaxis is not routinely indicated (see protocol) viii) Thromboprophylaxis:

All patients should have TED stockings and sequential calf compression devices applied within 8hrs of admission unless contra-indicated.

Pharmacological thromboprophylaxis is relatively contraindicated in the first 72 hrs after injury or surgery or if there is ongoing bleeding.

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Thromboprophylaxis may be commenced when indicated following discussion with Neurosurgery

In patients at high risk of VTE or with contra-indications to mechanical prophylaxis, consideration should be given to early insertion of a caval filter

ix) Avoid hyperthermia. d) Monitoring of head injured patients:

i) Cardiorespiratory: In addition to routine ICU monitoring ETCO2 is recommended

a. Interpret with caution & calibrate with PaCO2 when, i. Change in ventilation ii. Sudden rise in ICP

b. Adjust ETCO2 to PaCO2 = 35-40 mmHg ii) Neurological:

ICP monitoring a. At the RAH ICP monitors are inserted by neurosurgeons b. Indications:

i. Severe CHI (GCS < 8) and an abnormal CT scan, or ii. GCS < 8 and two of

Age > 40 yrs Focal motor signs Hypotension after volume resuscitation

iii. Brain swelling following evacuation of intracranial haematoma

iv. Intracerebral haematomas where the decision to operate will depend on ICP

v. Polytrauma patients in whom cerebral status cannot be adequately assessed (e.g. patients requiring ventilation)

vi. Rarely in non-traumatic raised ICP Meningitis / encephalitis Hepatic failure.

Ventricular drain and external pressure monitor: a. Closed system b. CSF for M,C&S as clinically indicated c. Set height for drainage according to neurosurgical consultation. d. Preferred for ICP monitoring in CHI

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Flowchart: Cerebral Perfusion Pressure Algorithm

THERAPY FAILURE: ICP > 20 mmHg for > 10min or CPP < 60 mmHg 1. Ensure accurate MAP, ICP and where relevant, SjO2 readings 2. Immediately correct hypovolaemia and hypoxia 3. Check PaCO2 and ensure normocarbia PaCO235-40 mmHg 4. Ensure adequate sedation 5. Consider drainage 2-5ml CSF if intraventricular catheter in situ 6. Exclude contributing factors

Neck position / venous obstruction 30º head-up position Fever, Seizures

7. Commence osmotherapy with Hypertonic saline or mannitol and notify ICU Consultant

8. Consider short-term hyperventilation whilst arranging urgent CT 9. Consider neuromuscular blockade 10. Notify neurosurgeon on-call

Non-Surgical Lesion 1. Attempt to maintain CPP > 60 mmHg with fluids / inotropes 2. Consider additional therapies after discussion with Duty ICU

Consultant: Propofol / barbiturate coma Hypothermia

Initial Therapy to Optimise CPP 1. Maintain euvolaemia with IV fluids 2. Ensure appropriate sedation 3. Commence inotropes to maintain CPP 60 - 70 mmHg (MAP �– ICP) 4. Maintain normocarbia, PaCO2 35-40 mmHg

URGENT

CT Head Scan

Surgical Lesion Immediate

Neurosurgical Consultation

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2. Aneurysmal Subarachnoid Haemorrhage

a) Principles of ICU management: i) Admission to ICU/HDU:

Acutely prior to angiography or surgery Post-operatively

ii) Priorities: Monitoring of airway and adequacy of ventilation Maintenance of adequate cerebral perfusion

maintain appropriate MAP (relative to premorbid BP) Monitoring of conscious state (GCS) Early diagnosis and treatment of causes of reduced GCS

a. Rebleed from aneurysm (notify neurosurgeon) b. Hydrocephalus (notify neurosurgeon) c. Vasospasm d. Seizure

iii) Monitoring: ECG, SpO2, Invasive BP ICP in patients with a ventricular drain in situ:

a. May be set at a level (usually 10 cm) above head and/or b. Connected to monitor transducer c. CSF culture as clinically indicated

b) Prevention and treatment of vasospasm

i) Specific drug therapy: Nimodipine:

a. Indications i. CT proven SAH ii. IV preferably through central line (2 mg/hr)

*may be given through a peripheral IV iii. Change to oral as soon as possible (60mg 4hrly)

b. Complications: hypotension (may require cessation of nimodipine) Statins:

a. Statins may reduce the incidence of radiological vasospasm and improve outcomes following SAH.

World Federation of Neurosurgeons Classification

Grade GCS Motor Deficit I 15 Absent II 13-14 Absent III 13-14 Present IV 7-12 Present or absent V 3-6 Present or absent

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b. In the absence of a contra-indication patients should be commenced on simvastatin 80mg daily.

ii) Triple H therapy (hypertension / hypervolaemia / haemodilution): Has no role in the prevention of vasospasm

prophylactic HHH therapy may be harmful It is imperative to avoid hypotension and hypovolaemia. Patients should have fluid therapy targeted at maintaining euvolaemia.

iii) Euvolaemic hypertension May be indicated in selected patients with proven vasospasm post-

aneurysmal clipping / coiling. Induced hypertension must be titrated to a mean arterial pressure:

systolic BP is not an accurate indicator of cerebral perfusion pressure. Principles:

a. Discuss with ICU consultant prior to initiating therapy b. Intra-arterial pressure monitoring is mandatory c. Maintain IV volume

i. Continue IV filling until clinically euvolaemic ii. Avoid volume overload (pulmonary congestion/oedema) iii. Monitor electrolytes 8 hrly normal osmolality and [K+].

d. Commence noradrenaline titrated to: i. MAP > 90mmHg, or ii. MAP > 10mmHg above premorbid baseline

(for known hypertensive patients) iii. Reset target MAP if high doses (> 10 g/min) are required, or

if polyuria, arrhythmias or other complications ensue. Complications:

a. Pulmonary oedema, hypoxia b. Cardiac arrhythmias, myocardial ischaemia c. Polyuria, electrolyte disturbances

iv) Chemical (papaverine / verapamil) or balloon angioplasty Limited role in angiographically proven vasospasm Requires transport for angiography and may be performed on

consecutive days. v) Operative therapy:

Early (within 48 hrs): currently recommended at RAH a. Advantages (proposed): prevention of rebleeding, reduction of

vasospasm, prevention of ischaemia b. Disadvantages: high intraoperative risk of rupture, difficult

dissection Late (after 11 days)

a. Advantages: easier procedure, opportunity to monitor. b. Disadvantages: re-rupture, prolonged risk of vasospasm

vi) Anticonvulsants: as clinically indicated vii) Steroids not indicated

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2. Status epilepticus a) Definition:

i) More than 30 minutes of: Continuous seizure activity Two or more sequential seizures without full recovery of

consciousness between seizures b) Principles of ICU management

i) Assessment of airway and adequacy of ventilation Intubate and ventilate if appropriate Avoid muscle relaxants after intubation

ii) IV access iii) Control of seizures:

Midazolam: 1-10 mg/hr via infusion, or Diazepam: 10-20 mg IV prn

Phenytoin: 18 mg/kg load, then 300 mg daily check for previous administration therapeutic 40-80 mol/l

If refractory: (liaise with neurologists) a. Clonazepam 1-2 mg IV prn or by infusion 0.5-2 mg/hr b. Consider Valproate 200-500mg po/IV 8 hrly c. Nasogastric Levetiracetam d. Thiopentone infusion

i. Loading dose: 5mg/kg of 25mg/ml solution (2500mg / 100ml N.sal)

ii. Infusion: 1-3 mg/kg/hr (~ 150 mg/hr or 6 ml/hr)

e. Obtain EEG and consider EEG monitoring iv) Look for a cause and treat appropriately: CT scan with contrast if unclear

Previous epilepsy / poor compliance Intracranial pathology:

a. Vascular (haemorrhage, thrombosis), spasm b. Infection (consider LP if no evidence of raised ICP on CT) c. Tumour

Extracranial pathology: a. Metabolic: exclude hypoglycaemia, thiamine deficiency b. Check electrolytes: especially Na+, Ca++, Mg++, K+, PO4

= Infection Severe hypertension

c) Maintenance of homeostasis / seek and treat complications i) Ensure adequate hydration: maintenance fluids according to

creatinine/urea, Na+ and osmolality ii) Ensure adequate urine output: prolonged seizures may be associated with

rhabdomyolysis iii) Evaluate for joint dislocations and occult fractures

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4. Exclusion of acute cervical spinal injury following trauma a) Safe practices are vital to prevent secondary damage to the cord b) Spinal immobilisation should be practiced in all patients with;

i) significant distracting injury or injury above the clavicles ii) altered conscious state for any reason (head injury, alcohol, drugs etc) iii) neck pain or tenderness iv) abnormal neurological signs or symptoms v) NB:

Hard collars allow up to 73% of normal flexion and extension �– and so still need appropriate spinal care even if in place.

Soft collars do not provide effective C-spine immobilisation. c) Clinically clearing the C-spine requires all of the following criteria to be

fulfilled; i) normal conscious state, with no drugs or alcohol onboard ii) no neck pain or tenderness iii) no abnormal neurological signs or symptoms iv) no significant distracting injury, or significant injury above the clavicles

and then, v) normal head control (unassisted) vi) pain-free movement

d) If all of these are confirmed, the hard-collar can be removed, and the C-spine cleared.

e) If the C-spine cannot be clinically cleared for any reason, radiology needs to be performed (the majority of patients seen in Trauma Resus)

f) Virtually all patients presenting to Trauma Resus require a trauma series of adequate AP, lateral, and odontoid C-spine plain views

g) A complete series of 3 plain views will still miss up to 7% of C-spine injuries �– hence the importance of clinically clearing (if possible) the C-spine even if the Xrays appear normal.

h) If the C-spine cannot be clinically cleared following normal plain films, maintain spinal precautions and liaise with the Trauma Registrar.

i) Clearing the C-spine in the patient with altered conscious state: i) If drugs, alcohol or minor closed head injury are the problem, they are

often resolved within 12 hours �– maintain spinal precautions until that stage, and then assess clinically

ii) If the patient is unlikely to become clinically assessable and clearable within 12-24 hours (most intubated patients):

Perform a complete plain Xray series in ED, and: Perform a limited CT;

a. C0-2 in all, during first visit to scanner b. CT any suspicious areas on the plain films c. CT may be required to visualise cervicothoracic junction

or d. CT entire cervical spine with 3-D reconstructions (the current

recommendation)

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If these films are all documented normal, the collar may be removed and the C-spine cleared �‘as per RAH protocol�’.

Any ongoing concerns are referred to the Trauma and/or Spinal Registrar

j) Flexion-extension views of the C-spine must not be performed, unless ordered by the Spinal Unit, with the Spinal Fellow in attendance

k) As with the C-spine, the thoracolumbar spine should be imaged in all patients in whom it can not be clinically assessed. This should be done prior to arriving in ICU. If CT chest and abdomen have been performed, these images can be used to assess and clear the thoracic and lumbar spines.

l) 25% with a spinal injury at one level will have a second non-contiguous injury. Therefore, if a fracture is found anywhere in the spine, the entire spine should be Xrayed

m) Spinal Xrays should ideally be performed in an Xray area (Trauma Resus Room or Xray Dept) prior to ICU admission. Quality of spinal Xrays performed in ICU is usually very poor

n) The Trauma Registrar must document the status of spinal clearance on the Trauma Form

o) Steroid use in acute spinal cord injury is not currently recommended by the Spinal Injuries Unit.

p) The RAH Trauma Service Procedures, Practices and Guidelines (TSPPG) on �‘Acute Spinal Injury Management�’ is available on the RAH Intranet and contains more detail.

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H. Microbiology Protocols 1. Policy

a) The prompt diagnosis and treatment of infection in critically ill patients is both important and difficult.

b) Sepsis is the most common cause of death in critically ill patients. It must be aggressively sought and promptly treated with surgical drainage (where indicated) and appropriate antibiotics.

c) Simple preventative measures are the most important factors in the containment of nosocomial infection and minimisation of bacterial resistance: i) Compulsory hand washing and/or use of alcohol hand-gel by all staff ii) Attention to aseptic technique for invasive procedures iii) Attention to invasive procedure protocols as outlined in this manual iv) Avoidance of over-prescription of antibiotics

d) Regular routine microbiological examination in critical care patients is not cost effective. Investigations should only be ordered on specific indications.

e) Septic screens must follow the guidelines below.

2. Definitions a) Systemic Inflammatory Response Syndrome (SIRS)

i) Describes the inflammatory process that occurs in response to a variety of clinical insults resulting in a clinical picture suggestive of �“sepsis�”

ii) The syndrome includes at least 2 of the following: temperature > 38° or < 36° C heart rate > 90 bpm respiratory rate > 20 bpm, or

PaCO2 < 32 mmHg WCC > 12,000/mm3, or

< 4,000/mm3, or > 10% immature (banded) neutrophils

iii) SIRS is non-specific and may be due to non-infectious causes: Trauma, Post-operatively after major surgery Haemorrhagic shock, post blood transfusion Pancreatitis Burns Drug reactions Intracranial pathology, esp. intraventricular or thalamic blood

b) Sepsis: the presence of SIRS 2° to infection c) Septic shock: decreased vital organ perfusion/function 2° to sepsis d) Nosocomial infection is defined as infection that occurs during hospitalisation

that was neither present, nor incubating on admission. e) Colonisation is defined as the presence of microorganisms that do not elicit an

inflammatory response.

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3. Septic screen a) Routine, performed only on the clinical suspicion of sepsis:

i) New pyrexia ii) WCC, WCC, or Platelets iii) Deterioration in gaseous exchange or pH iv) Cardiovascular instability

Hypotension / relative hypovolaemia Increased or new inotrope requirement

v) Oliguria or increased creatinine b) Screen:

i) Urine - C&S ii) Tracheal aspirate - urgent gram stain, C&S iii) Blood culture x2 iv) Any other drainage fluid as indicated, e.g. wound, pleural etc.

c) Other i) Fungal cultures ii) Pleural fluid, CSF iii) Sinus x-rays iv) Bronchoscopy specimens (BAL)

d) Urine: i) UTI in a catheterised patient is defined as:

> 105 bacteria + positive culture of organisms, plus > 500 WBC/HPF.

ii) Bacteria and white cells are a normal finding in a catheterised patient iii) Treatment with antibiotics will not result in clearance of colonisation and

is only indicated for systemic involvement. iv) The only effective treatment is catheter removal. v) Bladder wash-out may reduce bacterial load / infective risk.

e) Tracheal aspirate: i) Cultures often grow mixed colonising oral flora:

Gram positive cocci - S. aureus and S. pnuemoniae Gram negative bacilli - H. influenzae Yeast - Candida sp.

ii) Antibiotics will not result in a clearance of colonisation and are only indicated for invasive (local or systemic) infection.

f) Blood cultures: i) May be contaminated by skin organisms: requires careful technique:

Clean the skin with an alcohol or betadine swab Clean the top of culture medium bottle with an alcohol swab:

allow to completely dry before injecting. Use a sterile needle and aseptic technique during venipuncture Inject blood immediately into bottle with same needle - do not touch

the needle. ii) Blood cultures are best taken by clean venipuncture. iii) Skin organisms grown from a single bottle are usually considered a

contaminant but must be interpreted in the context of the patient.

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4. Investigation of pneumonia

a) Community acquired pneumonia: i) Usual organisms: S. pneumoniae, H. influenzae ii) Less commonly:

Bacterial: Legionella sp., Gram neg bacilli, S. aureus Viral: Influenza A, B, Parainfluenza, Adenovirus, RSV Other : Mycoplasma pneumoniae,

Chlamydia psittaci (birds), Coxiella burnetti (sheep or cattle), TB, Chlamydia pneumoniae

iii) Investigations Haematology - High (> 15000) or Low (< 3000) WCC

- coagulopathy Biochemistry - note renal function and LFTs CXR ABGs Microbiology: * prior to antibiotic Rx where possible

a. Blood cultures x 2 b. Endotracheal aspirate

i. M,C&S + urgent gram stain ii. Legionella culture iii. Respiratory viral Ag (PCR) & culture

NB: If not intubated, then collect a nasopharyngeal aspirate for respiratory viruses

c. Urine - L. pneumoniae 1 Ag * only where high index of suspicion or outbreak

d. Pleural fluid - M,C&S b) Community acquired pneumonia �– Immunosuppressed Host:

i) Possible organisms As above plus

a. Bacterial: Nocardia b. Viral: CMV, HSV, varicella zoster c. Fungal: candida, cryptococcus, aspergillus d. Protozoal: pneumocystis jirovecii (PCP)

Consider non-infective causes of a similar picture e.g. ARDS ii) Investigations: * As per above, plus

Sputum or tracheal aspirate - limited value, need BAL! a. Pneumocystis stain

HIV patients only �– all others require BAL b. Acid fast bacilli

Viral studies, request CMV, HSV. Consider BAL if initial cultures negative

a. PCP staining on BAL only for HIV(-) patients HIV serology

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iii) Treatment prior to microbiological diagnosis: refer to antibiotic guidelines & discuss with ID.

c) Nosocomial pneumonia in ICU

i) Principles: Accurate diagnosis and treatment are important but difficult. Incidence: 20% of all ICU patients

70% of patients with ARDS major cause of death in patients with ARDS

Clinically indistinguishable from pulmonary fibrosis, alveolar haemorrhage, atelectasis and other causes of lung infiltrates

Clinical diagnosis, including use of tracheal aspirate, has poor sensitivity and specificity

Appropriate antibiotics do improve outcome Empiric broad-spectrum antibiotics are potentially harmful.

ii) Consider nosocomial pneumonia when: New and persistent CXR changes Tachycardia, tachypnoea Fever or hypothermia - temperature >37.5 or <35.5 Leucocytosis or leucopaenia - WCC: >10 or < 4 x 109/l Purulent sputum Deterioration in lung function

iii) Confirmation of pulmonary infection: Tracheal aspirate MC&S Preliminary results to direct therapy may be obtained on gram stain Consideration should be given to obtaining pulmonary samples by

bronchoalveolar lavage (or open lung biopsy) for patients with: a. Persistent signs of pneumonia b. Inadequate response to antibiotics c. Inabililty to obtain adequate tracheal aspirates, or d. To exclude non-infectious causes of respiratory failure

e.g. interstitial fibrosis or alveolar haemorrhage Septic screen including blood cultures should also be performed.

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5. Vascular catheter sepsis a) Refer to the invasive procedures section b) Suspect line sepsis when:

i) Evidence of systemic infection New, unexplained fever Unexplained or in WCC Deterioration in organ function Positive blood culture by venipuncture with likely organisms

(coagulase negative staph, candida), and/or ii) Evidence of local infection - inflammation or pus at the insertion site iii) The following patients are more susceptible to line infections:

Prolonged vascular access (> 7-10 days) exponential increase in line infection after 4 days.

Endovascular infection (SBE, prosthetic graft infection) Cutaneous infection Burns Severe intra-abdominal infection (pancreatitis) Deep-seated infections (empyema / abscess)

iv) The incidence of line sepsis with the antibiotic impregnated lines is around 1% and most of these are due to Candida spp.

c) Protocol i) Take blood cultures from a peripheral vein ii) Positive blood cultures from the line may only indicate colonisation so

blood culture bottles must be carefully labelled as to site of sampling Common organisms in line sepsis are normal skin flora

e.g. Staph spp., C. albicans In ICU gram negative organisms can also be involved

iii) On suspicion of line sepsis the line should be removed iv) The tip of the catheter should be sent for culture

Avoid contamination of the catheter tip with skin organisms Skin should be cleaned thoroughly with alcohol, allowing at least one

minute drying time, before removing the catheter v) Catheter related bloodstream infection is defined as infection where the

same organism is grown from the blood and from the catheter tip d) Treatment

i) Removal of the line will usually clear low-virulence organism bacteraemias, e.g. S. epidermidis

ii) Antibiotics are indicated if: The patient is high risk - e.g. joint or endovascular prosthesis Infection with a virulent organism, e.g. S. aureus Signs of sepsis continue after catheter removal

iii) If ongoing sepsis occurs, additional blood cultures should be taken prior to starting antibiotics

iv) Refer to antibiotic guidelines.

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e) Further venous access: i) Reassess the need for ongoing central access, consider PICC line ii) Whenever possible:

Wait 24 hours before reinsertion Select a different insertion site

iii) Guidewire exchanges are not performed unless: Mechanical problems in a new catheter (leaks/kink & < 4 days old) Difficult or limited central access (e.g. burns)

6. Bacterial Meningitis a) Steroids should be started before antibiotics in all patients with a high

probability of bacterial meningitis. i) No demonstrated benefit given post-antibiotics. ii) Should occur in A&E / pre-retrieval - check on admission

b) Dose: dexamethasone 10mg 6 hrly for 4 days c) Antibiotics are as per ID guidelines

7. Fungal infections a) General principles

i) The incidence of systemic fungal infections in ICU patients has increased: Increased numbers of immunosuppressed patients admitted to ICU The use of broad-spectrum antibiotics, and Prolonged use of intravascular catheters

ii) Fungaemia is an indication to commence antifungal therapy. iii) Whilst candidaemia is associated with significant mortality, systemic

infections can occur with negative blood cultures. b) Risk factors for candidaemia and disseminated candidiasis:

i) Neutopaenia ii) Long term CVC use iii) Candida colonization iv) Broad spectrum antibiotics v) Haemodialysis vi) Immunosuppressants

c) Antifungal prophylaxis i) Systemic prophylaxis is not recommended for general ICU patients ii) Solid organ transplant patients do not require prophylaxis iii) Posaconazole prophylaxis is effective and tolerated in bone marrow

transplant and neutropaenic cancer patients d) Indications for antifungal therapy

i) Candiduria in high risk patients with deteriorating clinical status ii) Single positive blood culture in a high-risk patient iii) Isolation of candida from any sterile body site (except urine) iv) Positive microscopy for yeast from a sterile specimen v) Histological evidence of yeast or mycelial forms in tissue from high-risk

patients

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e) Specific antifungal therapy *always seek ID opinion i) Fluconazole

Proven candidaemia Dose: 400 mg IV daily

ii) Voriconazole Suspected or confirmed aspergillosis, or resistant candida Loading Dose: 6 mg/kg IV bd x1 day, then

4 mg/kg IV bd x3 days *do not continue IV past 24 hrs if CrCl < 30 ml/min

Maintenance: 200-300mg po bd iii) Caspofungin

Second line agent to voriconazole or in presence of renal failure Loading Dose: 70 mg/day Maintenance: 50 mg/day

iv) Amphotericin B / Ambisome Rarely indicated due to potential nephrotoxicity.

8. Protocol for patients with necrotising soft tissue infections

a) General principles i) This is a generic group of patients with life threatening infections

involving combinations of mucocutaneous, fascial and myofascial planes ii) These infections represent a medical emergency: patients may present with

severe septic shock and rapidly developing multiple organ failure iii) In rapidly progressive infections, local signs of inflammation may

underestimate the degree of underlying tissue necrosis iv) Usually due to one or more of the following organisms:

Anaerobes - clostridium spp, bacteroides Gram positives - group A streptococcus, staphylococcus Gram negatives - enteric organisms

b) Management protocol: i) Appropriately trained personnel, familiar with the severity of the patient's

condition and with appropriate resuscitative equipment, must accompany these patients during all phases of their management

ii) The hallmarks of management involve a detailed multidisciplinary approach coordinated by the duty Intensive Care consultant and involving the following:

The duty ID consultant must be notified as soon as possible. Prompt and effective resuscitation, restoration of vital organ perfusion

and control of metabolic emergencies (e.g. hyperkalaemia, hypoglycaemia, coagulopathy). This is coordinated by the Intensive Care team and must not significantly delay surgery.

Early, aggressive and repeated surgical debridement. a. Patients with necrotising soft tissue infections must be reviewed

by a plastic surgical consultant (not trainee) ASAP. b. The Duty Anaesthetist must be notified as soon as surgery is

planned.

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Prompt identification of organisms with early prescription of appropriate empirical, then specific antibiotics as required (refer empirical and specific antibiotics section).

Immune Globulin (IVIg) a. Clearest evidence in Gp A Strep infections. b. Should be used in conjunction with clindamycin c. Liaise with ID in all cases & confirm if to be used d. Standard regimen over 3 days:

i. 1.0g/kg Day1 ii. 0.5g/kg Days 2&3

e. �“Rescue Therapy�” i. May be considered in cases where surgery would prove

devastating, or where surgery is unduly delayed ii. Dose: 2.0g/kg as single bolus over 3-6hrs.

NB: This may be > 3000ml IVIg Hyperbaric oxygen is an adjunctive therapy in selected patients:

a. HBO must not delay debridement and resuscitation must be maintained during treatments.

b. Indications for hyperbaric oxygen: i. Progressive bacterial (clostridial) gas gangrene. ii. Selected patients with severe multisystemic disease not

responding to resuscitation, antibiotics and surgery. c. The number of HBO treatments on a given day will depend on the

stability of the patient, availability of staff and timing of surgery. d. As a general rule, patients undergoing surgical debridement will

return to ICU following surgery for stabilisation and assessment prior to subsequent transfers for HBO. This will be co-ordinated by the duty Intensive Care and hyperbaric medicine consultants.

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I. Drug overdose These guidelines have been influenced by and modeled on an excellent text: Murray L, Daly F, Little M, Cadogan M. Toxicology Handbook. Elsevier 2007. 1. General principles

a) The majority of drug overdoses are poly-pharmaceutical and respond to general supportive measures.

b) Overall, early mortality is low and usually relates to cardiorespiratory arrest. c) Following admission, morbidity relates primarily to aspiration pneumonitis, or a

delay in definitive respiratory care. d) There is a poor correlation between depth of coma and preservation of glottic

reflexes. Accordingly, if there is any doubt the patient should be intubated. e) Antidotes such as naloxone or flumazenil:

i) Should generally not be used as alternatives to supportive measures ii) Are not to be used to facilitate gastric lavage or charcoal administration iii) The main utility is in aiding diagnosis of the underlying cause of coma

- small doses only are required iv) Usefulness in treatment is limited by their short half-lives v) Continuous infusion is required where ongoing therapy is contemplated vi) Both agents may initiate a withdrawal syndrome or unmask to the toxicity

of co-ingestants. In the case of flumazenil these effects may be life threatening.

f) ICU/HDU admission criteria following an overdose: i) Intubated patients ii) Reduced GCS with potential airway compromise iii) Uncontrolled seizures iv) Persistent hypotension v) ECG criteria:

Ventricular or supraventricular tachyarrhythmias Sinus tachycardia > 140/min with tricyclics or thyroxine AV block 2nd or 3rd degree QTC interval > 0.5s QRS interval 0.12s Acute RBBB

vi) Metabolic disturbance requiring HDU-level of care vii) Requirement for extracorporeal elimination

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2. Gastrointestinal Decontamination

a) A variety of approaches have been used historically in an attempt to reduce the dose absorbed following an oral ingestion.

b) There is minimal evidence for improved survival or shortened duration of toxicity, particularly when applied to unselected patients.

c) The decision to use decontamination requires individual patient risk-benefit analysis. Appropriate patients and modalities should be selected, and gastrointestinal decontamination should never proceed to the detriment of resuscitative and supportive care.

d) Gastric lavage i) Largely historical ii) Formal lavage (large bore tube placement, water instillation and aspiration)

should not be performed. iii) For intubated patients, an orogastric or nasogastric tube of appropriate

(standard) size should be inserted, and any gastric content aspirated iv) No additional fluid should be instilled via the tube.

e) Charcoal i) Charcoal aspiration has a high morbidity and mortality:

Adequate airway reflexes must be present, or If there is any doubt the patient should be intubated

ii) For appropriate ingestions administer: 1g/kg body weight (to a maximum of 100g) stat 25g 4 hourly x 3 doses - slow release medications

- drugs with enterohepatic circulation Cease administration should an ileus develop.

iii) Indications: Presentation < 1hr from ingestion

a. Compound bound by charcoal b. Ingestion expected to cause significant morbidity or mortality.

Presentation > 1hr, consider administration for: a. Salicylates b. Slow release or enteric coated preparations c. Agents which delay gastric emptying, and d. Drugs with enterohepatic circulation.

iv) Charcoal ineffective for: Elemental metals and their salts Hydrocarbons and alcohols Acids or alkalis

v) With multiple dose charcoal administration, constipation is likely and the addition of sorbitol may be considered.

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f) Whole bowel irrigation i) Use of polyethylene glycol solution to decontaminate the bowel. ii) Use restricted to life threatening overdoses where:

The agent is a slow release or enteric coated preparation The agent is not expected to be bound by charcoal. A good outcome is not expected with supportive care and antidote

administration alone. The patient presents before the advent of severe toxicity

iii) May be potentially useful following: Iron overdose > 60mg/kg Slow release potassium chloride > 2.5mmol/kg Major slow release verapamil or diltiazem ingestion Symptomatic arsenic trioxide ingestion Lead ingestion Body packers (heroine)

iv) Contraindications Good outcome expected with standard care Uncooperative patient Uncontrollable vomiting Reduced GCS or seizures expected in subsequent 4 hours Ileus or bowel obstruction Intubated patients (relative)

v) Technique Polyethylene glycol solution (standard endoscopy bowel prep.) Administer via correctly placed nasogastric tube at 2L/hour

(25ml/kg/hr in children) To minimize vomiting start at a slower rate & titrate up as tolerated Administer metoclopramide to enhance gastric emptying Be prepared for explosive diarrhoea

- sit on commode or place effluent tube for example Continue until rectal effluent is clear or an ileus/abdominal distension

occurs.

3. Osmolal Gap

a) OG = Measured �– calculated osmolality b) Calculated Osmo = 2 x (Na + K) + Gluc + Urea + ethanol c) Baseline osmolar gaps are highly variable in the normal population. d) Evaluation of potential toxic alcohol ingestion requires serial assessments over

time looking for a characteristic pattern with worsening acidaemia, increasing anion gap and decreasing osmolar gap.

e) Single measurements may confirm an ingestion but are not reliable in excluding it.

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Flowchart: Approach to the unconscious, undetermined overdose

RESUSCITATION (ABCDEFG) 1. Airway 2. Breathing 3. Circulation 4. Don�’t Ever Forget Glucose

Consider: 1. Glucose 50% 2. Naloxone 3. Thiamine

History: 1. Patient 2. Relatives 3. SAAS Crew

Examination: 1. Clinical toxidromes 2. Trauma 3. Nerve palsies 4. Pressure areas 5. Preganacy?

Investigation: Blood Urine Biochem:

Electrolytes Glucose Renal LFTs Coags

Urine drug screens rarely influence management and should be used sparingly

Drug levels: Paracetamol routinely Others as indicated only

Other ECG ABG Measured osmolality

NO Metabolic Acidosis 1. Sedatives 2. Hypnotics 3. Paracetamol 4. Theoplylline 5. Anticholinergics 6. Antihistamines 7. Antipsychotics 8. Antidepressants 9. Anticonvulsants 10. Lithium 11. Organophosphates

Metabolic Acidosis

Normal Anion Gap 1. Acid ingestion 2. Toluene sniffing 3. Bicarbonate loss

Raised Anion Gap +

Osmolal Gap§

OG < 10 Salicylates Cyanide Carbon monoxide Lactic acidosis

OG > 10 Methanol Other alcohols

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4. Specific therapies / protocols

a) Paracetamol: Acute overdose i) Defined as a single ingestion, or staggered ingestion occurring over 8

hours or less. ii) If the time of ingestion can be defined risk assessment and the decision to

treat may be based upon the Rumack-Matthew nomogram (use the initial ingestion time as the assumed total ingestion time when plotting staggered ingestions occurring over < 8hrs).

iii) Where the nomogram cannot be used (repeated supratherapeutic ingestions, sustained release preparations) the decision to treat is based upon the dose/kg ingested, a serum level, and aminotransferase levels

iv) Potentially hepatotoxic dose in a fit adult is > 200 mg/kg (or > 10g) v) Markedly less in high risk individuals:

Chronic alcoholics and the malnourished Pre-existing liver disease Those taking cytochrome P450 inducing medications

vi) The risk of hepatic injury without NAC (N-acetylcysteine) is predicted by plotting a level taken 4-15 post ingestion on the Rumack-Matthew nomogram.

vii) The probability, with a 4hr drug level, is: 1-2% < 1320 µmol/L (200mg/L) 30% ~ 1320-1980 µmol/L (200-300mg/L) 90% > 1980 µmol/L (> 300mg/L)

viii) The risk of hepatic impairment with NAC is determined primarily by the time from overdose to commencement of NAC:

Survival is 100% where NAC is commenced within 8 hours Benefit is reduced if NAC commenced at 8-24 hours Benefit is not confirmed if commenced beyond 24 hours, except in the

setting of hepatic failure. ix) The administration of NAC is indicated in the following settings:

Patients who present within 8 hours of ingestion and have a 4-8 hour level falling above the treatment line

All patients presenting 8-24 hours post-ingestion *may be ceased if the subsequent level is non-toxic and transaminases are normal

Patients presenting beyond 24 hours post-ingestion with detectable paracetamol and elevated transaminases

Unknown time of ingestion with detectable paracetamol *may be ceased if subsequent history allows for plotting of a demonstrably non-toxic level on the nomogram

Late presenters with clinical or biochemical evidence of hepatic injury

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x) NAC may be ceased in the following settings: Patients in whom NAC was commenced < 8 hours post-ingestion who

are clinically well and without hepatic tenderness at the completion of the 20 hour infusion (no further investigation required)

Patients in whom NAC was commenced > 8 hours post-ingestion who are clinically well and have normal transaminases at the completion of the 20 hour infusion. Those whose transaminases are abnormal at this time should continue an infusion at 100mg/kg/16 hrs until transaminases and INR (tested 12-24 hourly) are falling.

xi) Consultation with liver transplant services (FMC) for consideration of transplant should commence with any of the following high risk criteria:

INR > 3.0 at 48 hours or > 4.5 at any time Oliguria or creatinine > 200 µmol/L Acidosis with pH < 7.3 after resuscitation Ongoing hypotension with systolic BP < 80mmHg Hypoglycaemia Severe thrombocytopenia Encephalopathy (any degree)

xii) The above guidelines do not apply to: Sustained release paracetamol preparations Repeated supra-therapeutic ingestions Toxicological advice should be sought in these settings. The default position, if in doubt, should be to treat with NAC.

Graph: Modified Rumack-Matthew Nomogram

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Table: N-Acetylcysteine Administration

NAC 150mg/kg in 200mls of 5% dextrose over 30 minutes NAC 50 mg/kg in 500mls of 5% dextrose over 4 hours NAC 100mg/kg in 100mls of 5% dextrose over 16 hours

b) Lithium - Acute overdose i) Generally produces significant GIT symptoms with nausea, vomiting,

abdominal pain and diarrhoea. ii) Ingestion < 25g in the setting of normal renal function is benign iii) Ingestion > 25g may cause more significant GIT toxicity iv) Neurotoxicity is rare with good supportive care and hydration v) Renal impairment, dehydration and sodium depletion cause a reduction in

renal lithium excretion and increase the risk of delayed neurotoxicity vi) Patients presenting late with established neurotoxicity should be managed

as for chronic toxicity, and have similar long term morbidity vii) Lithium levels > 5mmol/L 4-8 hrs post ingestion are not uncommon viii) Treatment

Normal saline rehydration Maintenance of urine output > 1ml/kg/hr

ix) Haemodialysis is reserved for: Those with established or worsening renal failure, and Those presenting late with established neurotoxicity

c) Lithium - Chronic poisoning:

i) The clinical features of chronic toxicity are primarily neurological ii) Develops when renal lithium excretion is impaired for any reason iii) Serum lithium levels correlate poorly with clinical toxicity iv) Neurotoxicity may persist well after lithium levels return to normal. v) The Hansen-Amdisen classification may be used to grade severity:

Grade 1 (mild): tremor, weakness, ataxia, hyperreflexia Grade 2 (moderate): stupor, rigidity, hypertonia, hypotension Grade 3 (severe): myoclonus, convulsions, coma

vi) Lithium levels Confirm a diagnosis but should not be used to grade severity Are useful serially to monitor response to therapy

vii) Principles of therapy Careful correction of fluid and sodium balance Cease lithium and any medications that may impair excretion Monitor urine output, renal function, electrolytes and lithium levels

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viii) Indications for haemodialysis Neurotoxicity and a serum level > 2.5 mmol/L Grade 3 neurotoxicity regardless of level Pre-existing renal or cardiac disease preventing the achievement of an

adequate urine output with hydration alone Repeated haemodialysis treatments may be required

d) Opioids

i) Produce CNS and respiratory depression, frequently at just above analgesic doses

ii) Death is due to respiratory failure, either primary effect or compounded by aspiration, and good supportive care ensures survival

iii) Some opioids may possess additional cardiac and neurologic toxicity - e.g. dextropropoxyphene, tramadol, pethidine

iv) Controlled release preparations may cause delayed and prolonged toxicity v) Treatment is generally supportive vi) Naloxone (50 to 100µg IV repeated as needed)

Useful for diagnostic purposes Can assist in the management of airway and breathing May result in a withdrawal syndrome

vii) If repeated naloxone boluses are required to ensure a protected airway, intubation is the preferred method of ongoing management

viii) If a naloxone infusion is established: Initial hourly requirement is generally half the effective dose used over

the preceding hour, i.e. that required to achieve airway protection and adequate tidal volumes

Infusions require constant observation/assessment Hospital deaths have occurred due to inadequate observation

e) Carbon monoxide

i) CO is a common cause of poisoning death and most occur pre-hospital. ii) Those that arrive at hospital alive should survive, and in-hospital

management involves supportive care and identification of those at risk of long term neuropsychiatric sequelae

iii) Acute effects are due to tissue hypoxia iv) Delayed neurological effects are secondary to unrelated and incompletely

understood mechanisms v) HbF binds CO more avidly than HbA, and the foetus is at particular risk vi) Deliberate self poisonings involve high concentration, short term

exposures, and are associated with fewer long-term sequelae than industrial and domestic exposures (low concentration, prolonged exposures)

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vii) High risk features for delayed neurological sequelae: Loss of consciousness or coma Persisting neurological deficit (e.g. confusion) Cerebellar signs Metabolic acidosis Myocardial ischaemia Age > 55yrs

viii) Treatment options Normobaric oxygen at high flow via non rebreather mask

a. Continue until all symptoms resolve b. Pregnant women to continue for 24 hours with concomitant foetal

assessment Hyperbaric oxygen

a. May be indicated in patients with 1 or more high risk factors b. Indications and effectiveness are controversial

f) Cyanide i) Acute cyanide poisoning is rare, dramatic and lethal ii) Removal from the source of exposure, good resuscitative care and selective

antidote use provide the best chances of survival iii) Most deaths will occur pre-hospital, and those who arrive alive in hospital

post-inhalational exposure are likely to survive with supportive care. iv) Risks to those involved in care delivery are negligible. v) Decontamination should involve removal of clothes and washing of skin

with soap and water. vi) Cyanide levels are not available in a timely manner and do not aid

management vii) Serum lactate levels parallel cyanide levels and may be used as a proxy

marker of exposure viii) A lactate level > 10 mmol/L correlates with a toxic cyanide level

(in the absence of an alternative cause for elevation) ix) Management should proceed along normal resuscitative lines with the

delivery of 100% oxygen x) Consider using an antidote in the following settings:

Altered mental state Seizures Hypotension Significant and persisting metabolic acidosis (lactic)

xi) Antidote choice and administration 100% oxygen in all cases Hydroxocobalamin (1st line)

a. 5g in 200mls of 5% dextrose over 30 minutes b. Repeat in 15 minutes if no improvement

Sodium thiosulphate (adjunct to Hydroxocobalamin, or 2nd line) a. 12.5g IV b. Repeat dose at 30 minutes if acidosis persists

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Sodium nitrite a. 300mg IV over 3 minutes b. Follow immediately with sodium thiosulphate c. Half dose may be repeated in 30 minutes if required d. Monitor methaemoglobin (must not exceed 40%)

g) Toxic alcohols

i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are used as industrial solvents, cleaning agents and reactants.

ii) Accidental ingestions are rarely of sufficient volume to cause toxicity iii) Deliberate ingestion is associated with severe metabolic acidosis,

multiorgan dysfunction and potentially death. iv) Cause an initial �“ethanol like�” intoxication followed by a progressive

metabolic acidosis and compound specific end organ toxicities which may include:

Retinal toxicity/blindness (methanol) Acute renal failure (multiple agents) Seizures (multiple agents) Refractory hypotension (multiple agents) Delayed neurological sequelae (diethylene glycol)

v) Diagnosis is based upon a history of suggestive ingestion and a characteristic evolution of metabolic acidosis

Initially: osmolar gap (OG) + normal pH and anion gap (AG) Evolution of acidosis with pH, OG and AG Variability in osmolar gap amongst the normal population is such that

a single assessment of acid-base, AG and OG is insufficient to exclude significant exposure (although it may confirm it)

vi) Specific treatment Ethanol

a. Commence ASAP, regardless of symptomatology, in all with: i. Acidosis, or ii. An elevated OG (with or without acidosis),

b. Check baseline BAL, if > 0.1g/dl a loading dose is not required c. Titrate to BAL to 0.1g/dl to 0.2g/dL while on dialysis d. May be given orally (via NGT) or by IV infusion e. Oral protocol *not used in ICU

i. Loading dose of 1.8ml/kg of 43% ethanol (4 x 30ml vodka shots for a 70 kg adult)

ii. Maintenance infusion of 0.2-0.4 ml/kg/hr (1 x 40ml vodka shot per hour)

f. Intravenous protocol i. Loading dose: 8ml/kg of 10% ethanol ii. Maintenance: 1-2ml/kg/hr of 10% ethanol

g. Actual requirements vary widely between individuals, and serial blood alcohol assessments are required to ensure a level within the target range

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h. If on CVVHDF, then safer to dialyse against desired [ETOH] i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement) ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag

Haemodialysis (HD) a. Significantly more efficient at clearing alcohols than CVVHD b. Indications

i. Serum pH < 7.3 ii. Serum bicarb < 20 mEq/L iii. Worsening acidosis or vital signs despite supportive care and

ethanol infusion Folate 50mg IV QID Thiamine 300mg IV daily

h) Organophosphorous agents i) Includes the organophosphates (OP) and carbamates (CM) ii) Similar initial presentation iii) Most deaths occur as a consequence of respiratory failure iv) OPs as a group have greater lethality

Form a covalent bond with serine esterase enzymes In contrast to the competitive bond formed by CM.

v) There is great variability amongst the OPs in terms of enzyme aging, toxicity profiles, and pralidoxime responsiveness

vi) High quality supportive care and aggressive use of antidotes is necessary to ensure survival.

vii) The diagnosis is essentially clinical: Muscarinic features - diarrhoea, emesis, urination

- miosis, lacrimation, salivation - bronchorrhoea, bronchospasm - bradycardia, hypotension

Nicotinic features - fasciculation, tremor, weakness - respiratory muscle paralysis - tachycardia, hypertension

CNS features - agitation, seizures, coma - delayed neuropsychiatric effects

viii) Cholinesterase levels: Plasma cholinesterase levels fall more rapidly and recover more

quickly than RBC cholinesterase levels, they are useful in confirming exposure but do not correlate with toxicity.

RBC cholinesterase levels correlate better with toxicity and response to therapy, but take longer to perform (limiting their clinical utility)

ix) Decontamination These agents do not vapourise at atmospheric pressure There is no risk to care providers from inhalational exposure The characteristic odour is due to a hydrocarbon solvent, which may

cause headaches & eye irritation, but is otherwise harmless Staff should wear impermeable gowns, gloves, glasses and facemasks

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Care should be delivered in a well ventilated setting The patient�’s clothing should be removed and the skin washed with

soap and water x) Treatment

Ventilatory and CVS support as indicated Atropine

a. Reverses muscarinic effects only �– will not reverse paralysis! b. Titrate 0.6-2.4 mg at 3-5 min intervals until signs of successful

atropinisation are noted i. Drying of secretions ii. Breathing less laboured iii. Reduction of ventilatory resistance

c. Over 10-20 mg, or infusions of up to 5 mg/hr may be required in severe poisoning

d. NB: HR and pupil size are not useful for clinical monitoring after nerve agent exposure

Diazepam IV a. Treatment of seizures b. Reduces the incidence of neuropsychiatric sequelae c. Regular dosing is recommended.

Pralidoxime Iodide a. Efficacy is unclear and is likely to be compound specific b. Default is to give ASAP c. Not required for documented carbamate ingestion (although not

contraindicated) i. 1g IV over 30 minutes ii. 500 mg/hr for 24 hours iii. May be ceased at 24 hours in the absence of nicotinic or

muscarinic features. The benefit of continuing beyond 24 hours is unclear and warrants specialist consultation.

i) Calcium Channel Blockers

i) Of the common slow release formulations, verapamil and diltiazem frequently cause profound CVS collapse 4-16 hrs post-ingestion.

ii) Other agents within the class rarely cause major toxicity iii) Onset of toxicity may be delayed:

Up to 2 hours post-ingestion of the standard preparation, and Up to 16 hours after ingestion of the SR formulation

iv) Ingestion of > 10 tablets of verapamil SR or diltiazem SR may cause serious toxicity

v) The key issues in management are: Identification of patients at risk Judicious use of the pre-toxicity window of stability Consideration of GIT decontamination options

(including whole bowel irrigation), and A graduated approach to developing or established toxicity

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vi) Risk of serious toxicity is significantly increased by: Co-ingestion of other cardiac medications, and Underlying cardiac disease or advancing age

vii) Graduated response to hypotension: failure to achieve stability at each step should prompt immediate initiation of the next

Fluid load with 10-20 ml/kg isotonic crystalloid (avoid overload) Calcium load

a. Calcium gluconate - 60ml of 10% solution, or b. Calcium chloride - 20ml of 10% solution c. Commence an infusion to keep calcium levels > 2.0mEq/L

Atropine to a total of 1.8mg Catecholamine infusion effects are variable in terms of:

a. Central - negative inotropic & chrontropic effects - Adrenaline is an appropriate 1st line agent

b. Peripheral - reduced vascular tone -Noradrenaline 1st line agent

High dose insulin & dextrose / euglycaemia a. Most effective when used early b. Do not persist with escalating inotrope doses in the setting of

continued instability c. Seek guidance from Clinical Toxicologist (via switchboard or

Poisons Information Centre) or ICU consultant staff regarding protocol

Cardiopulmonary bypass, ECMO and intra-aortic balloon pumps have been used successfully as extraordinary manoeuvres

j) Beta Blockers

i) Overdoses generally result in minimal toxicity and require only simple supportive care.

ii) By contrast overdoses of sotalol or propranolol may be life threatening iii) In addition to class 1 and 2 effects (bradycardia, conduction blocks and

hypotension) Propranolol

a. Na+ channel blocking effects wide complex arrhythmias b. Highly lipid soluble enters the CNS (causing coma and

seizures) Sotalol

a. Blocks cardiac K+-channels b. Causing QT prolongation and Torsades

iv) The clinical response to overdose is highly variable, but the threshold for severe toxicity from propranolol may be as low as 1g

v) With the exception of sotalol and slow release preparations, toxicity is usually apparent within a few hours post-ingestion

vi) PR prolongation in the absence of bradycardia is an early marker of toxicity

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vii) Approach to immediate life threatening symptoms: Bradycardia and hypotension

a. Atropine b. Adrenaline c. Noradrenaline d. Glucagon 5-10mg bolus & 1-5mg/hr infusion, or e. High dose insulin dextrose euglycaemia

(targeting impaired contractility) Wide QRS

a. Sodium bicarbonate bolus 1-2 mEq/kg b. Repeat as required c. Intubate and hyperventilate targeting serum pH = 7.5 to 7.55

Torsades de pointes a. Isoprenaline b. Magnesium c. Overdrive pacing

k) Tricyclic Antidepressants (TCAs)

i) Tricyclic antidepressant use has escalated after an initial reduction secondary to SSRI introduction

ii) TCAs remain a significant cause of toxicological morbidity and mortality iii) Self poisoning is associated with rapid onset CNS and CVS toxicity that is

expected to peak between 4 and 6 hours post ingestion: Dose > 10mg/kg is potentially life threatening Dose > 30mg/kg is expected to cause severe cardiotoxicity and coma. Prompt intubation, hyperventilation and sodium bicarb administration

at the onset of major toxicity is life saving. iv) The investigation of choice is the 12 lead ECG, with diagnostic and

prognostic features including: Prolongation of the PR and QRS intervals Terminal R wave in aVR Increased R/S ratio (>0.7) in aVR QRS > 100 ms is predictive of seizures QRS > 160 ms is predictive of ventricular tachycardia

v) The approach to resuscitative management includes the following: Prompt intubation and hyperventilation (to serum pH 7.5-7.55) at the

onset of CNS depression Ventricular arrhythmias are unlikely to respond to defibrillation:

a. NaHCO3 ~ 2 mmol/kg IV every 2 minutes until perfusing rhythm restored

b. Lignocaine is a 2nd line agent if arrhythmias persist despite pH. Hypotension is managed with crystalloid and alkalinisation followed

by noradrenaline Seizures are managed with benzodiazepines (*avoid phenytoin)

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K. Bites and Envenomation 1. Up to date and detailed information on envenomation may be found at the

toxinology website http://www.toxinology.com/ managed by the Women�’s & Children�’s Hospital

2. Medical advice for doctors can be sought by contacting the clinical toxinologist, A/Prof Julian White via the WCH switchboard (Ph: 81617000)

3. Emergency cases are seen through the Emergency Departments of major hospitals, while less urgent cases are seen after discussion with the treating doctor.

K. Limitation of Therapy

a) Limitation may involve either withholding and/or withdrawal of life supporting

therapies. There is no ethical or legal distinction between these processes. b) Limitation of therapy involves potentially challenging ethical and legal issues;

however, in patients with no realistic chance of survival or meaningful recovery, decisions to limit life-sustaining therapies are both clinically and ethically indicated.

c) Assisted suicide and euthanasia are medically and ethically distinct from limitation of therapy, are illegal in SA and should never occur.

d) The administration of medication to relieve the suffering of a dying patient is imperative, even though a side-effect may be to hasten the onset of the patient�’s death. Such therapy is legally distinct from euthanasia.

e) At the RAH, approximately 70% of all ICU deaths involve some limitation of therapy.

f) Absolute requirements for limitation of therapy are: i) Medical consensus, including the treating ICU and admitting clinical teams ii) Clear and open discussion with the patient, family, or next of kin, regarding

this consensus medical opinion; and, an �‘absence of objection�’ to this proposed management direction.

iii) Clear documentation in the patient�’s case-notes, along with a description of the process by which the decision was made.

g) Counselling patients and families in limitation of therapy requires clarity and sensitivity to ensure that all parties understand and accept the plan of management. The concerns and wishes of the patient and family are important considerations.

h) The overriding goal is to provide the best care possible for the patient. This may be to concentrate on palliation, rather than life sustaining therapies.

i) The decision to limit treatment is a consultant responsibility.

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L. Brain Death and Organ Donation 1. Reference: ANZICS Statement on Death and Organ Donation - Third Edition 2008 2. For further information, trainees should liaise with the �‘Organ Donation Hospital

Medical Directors�’: a) Dr David Evans b) Dr Stewart Moodie c) Dr Peter Sharley d) Dr Alex Wurm

3. Declaration of brain death a) This is an absolute requirement prior to �‘beating-heart�’ organ donation b) Declaration must be made by two members of the ICU staff:

i) The Duty ICU consultant, and ii) Another ICU doctor (more than 5yrs qualified with appropriate experience).

c) The declaration of brain death may be by either clinical or imaging certification. 4. Clinical certification of brain death

a) The procedure is completed on a Certification of Brain Death form (MR150.0) and documented in the case notes.

b) Record the time of onset of coma i) Last time the patient showed response such as breathing, pupil reaction or

coughed on suction. ii) This can be determined from the nursing observations

c) Pre-conditions: i) A recognised irreversible cause of coma must be identified. ii) Potentially reversible causes of unresponsiveness and coma have to be

excluded, including the effects of: Hypotension Hypothermia *core temp must be > 35ºC Drugs or poisons. Neuromuscular blocking drugs Metabolic or endocrine disturbance including:

a. Deranged renal or hepatic function b. Hyperglycaemia, hypoglycaemia, thyroid function c. Electrolyte disturbances

iii) Ability to perform examination of Cranial nerves Apnoea testing (e.g. not severely hypoxaemia or high cervical injury)

d) Clinical confirmation of absent brain stem function:

This procedure is performed separately by 2 doctors, with the first test at least 4 hours after the onset of coma (longer in the case of hypoxaemic/ischaemic injuries).

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i) Absent pupillary responses to light, both direct and consensual ii) Absent corneal reflexes iii) Absent vestibulo-ocular reflex

No nystagmus on injection of 20ml iced water into the ear Check tympanic membranes prior to this procedure Occulo-cephalic reflexes are often tested, but are not formally required

iv) Absent gag / cough reflex v) Absent response to pain in the cranial nerve distribution. vi) Apnoea following disconnection from the ventilator:

Pre-oxygenate patient with 100% oxygen Disconnect ventilator and connect to bag with 100% oxygen insufflation

at low flow (1-2 l/min) Wait until PaCO2 > 60 mmHg and pH < 7.30

a. Confirm this by blood-gas analysis b. Ensure PaO2 > 60mmHg

Continuously look for apnoea clinically e) The following are compatible with Brain Death

i) Spinal reflexes ii) Sweating, blushing and tachycardia iii) Normal BP without pharmacological support iv) Absence of Diabetes Insipidus

f) The 2 practitioners may choose to be present at each examination, however, each must perform and be responsible for one of the 2 examinations

g) From the onset of coma until the second set of testing, there should be a continuous period of observation by nursing staff

h) Families may benefit from witnessing the clinical testing for brain death i) The time of death is the time when certification of brain death is completed �– i.e.

on completion of the second examination and documentation in the case notes. j) There is no legal requirement for certification of persons not considered for

organ donation, however this is encouraged as it can assist in counselling relatives and the subsequent cessation of inappropriate medical intervention.

5. Imaging (Non-clinical) certification of brain death

a) Clinical examination is �“consistent with�” brain death, however, the preconditions (2c) for clinical certification cannot be met.

b) Demonstrated absence of cerebral blood flow is therefore required. c) Ideally there should be a period of observation of 4 hours to increase the likelihood

that no flow will be demonstrated. d) Absence of cerebral blood flow may be established by either:

i) Radionuclide cerebral perfusion scan (Tc99 HMPAO). ii) 4 vessel cerebral angiography (rarely performed at the RAH)

e) Certification of brain death is by 2 clinicians, (not including the doctor who performed the imaging investigation) who have considered the onset and cause of coma, the clinical examination and the results of the investigation performed.

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6. Organ donation a) General principles

i) Any patient who is, or may become brain dead is a potential donor. There are no automatic exclusion criteria.

ii) Identifying potential organ donors involves all Intensive Care staff. iii) All potential donors should be offered the opportunity to donate iv) Notify the Donor Coordinator from the South Australian Organ Donation

Agency (Ph: 82077117) when a potential donor is identified. b) Criteria for brain dead organ donation

i) The patient has been declared brain dead (for donation after cardiac death see below)

ii) All brain dead patients should be discussed with the Donor Coordinator, regardless of these listed relative contraindications.

iii) Usually, no patient history of: HIV IV drug abuse Untreated bacterial, fungal or viral infection. Malignancies other than primary brain tumours and minor skin lesions. Treatment with hormones of human pituitary origin. Dementia (or family history of dementia). Disease of the donor organ

c) Procedure: i) Organ donation should not be discussed with the family until brain death has

been certified and the family informed. ii) Counselling families with regard to brain death and organ donation requires

considerable compassion, knowledge, skill and time. While this is primarily a consultant responsibility, advanced trainees are encouraged to participate in the process.

iii) Family approaches regarding donation prior to death should be referred to the consultant

iv) The wishes of the patient and family are paramount. v) A �“donor kit�” is kept in the cupboard in P4A which contains a check-list, plus

all the forms and specimen bottles required. vi) Following consent for organ donation, blood should be sent for:

HTLV-1, HIV 1 + 2 HBsAg, HBsAb, HBcAb, HCV CMV-IgG, EBV, RPR Group and X-match Tissue typing �– volume of blood varies according to blood group Mark the request forms: �“Urgent �– Organ Donor, Copy to: SAODA�”

vii) Coronial approval will be sought by the Donor Coordinator where required. viii) The RAH Designated Officer may give permission for donation if all efforts

to find relatives have failed. ix) Notification of the recipient and procuring teams (which may come from

interstate) and coordination of operating theatre time, collation of results and investigations are dealt with by the Donor Coordinator(s)

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x) Donor coordinators may seek assistance from ICU staff with ordering investigations.

xi) The following investigations are normally required: Recent ECG Recent CXR Echocardiography ABG

d) Management of the organ donor: i) The situation is time critical as it is not possible to stabilise a brain dead

patient indefinitely. ii) Aim to ensure perfusion and protection of all organs for donation to achieve

the optimal outcome for all recipients iii) Avoid focused management strategies aimed at single organ systems iv) Ventilation:

Adequate oxygenation (PaO2 > 60 mmHg ; FIO2 < 0.5 is preferred) PaCO2 ~ 35-45 mmHg

v) Cardiovascular instability: Common around the time of cerebral herniation (coning). Hypertensive episodes should be treated with short acting agents. Maintain MAP > 70 mmHg with fluid or inotropes. Ensure adequate volume loading before using high doses of inotropes High dose inotropic support may reduce organ viability.

vi) Aim for a urine output > 0.5ml/kg/hr vii) Maintain normothermia:

Established hypothermia can be difficult to manage. Prevention is preferred, using active warming devices if necessary.

viii) Check biochemistry and maintain normal electrolytes. ix) Diabetes insipidus is a common problem and treatment should commence on

clinical suspicion and not be delayed for confirmatory results. Immediate treatment with fluid replacement and DDAVP (1-2 µg IV bd)

x) Hypernatraemia in the donor adversely affects liver transplant outcomes. xi) Evidence for hormonal resuscitation is conflicting. Steroids and vasopressin

may be considered. xii) Consider non-depolarising muscle relaxants if spinal reflexes persist, as these

may be disconcerting for relatives and attending carers. 7. Tissue Donation

a) Patients who die in the ICU may also become tissue donors b) Tissues donated include

i) Corneas ii) Heart valves iii) Bones

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8. Donation after Cardiac Death (DCD) (Draft protocol)

a) The National DCD protocol is still under development and local protocols may change. (Refer to the national guidelines)

b) DCD may be an option in patient where: i) There is a clear decision to withdraw therapy ii) The period between withdrawal and death is likely to be short iii) There is a desire for organ donation

c) Organ donation should not be discussed with family before discussion about withdrawal of therapy (unless raised by the family)

d) Brain death organ donation is preferable to DCD e) If treatment is futile and the patient is likely to progress to brain death, consider

discussion with the family about allowing this to occur. f) Kidneys, liver and lungs may be donated g) Patient eligibility

i) Family supportive of DCD organ donation ii) Age < 65 iii) Adequate organ function iv) Withdrawal of therapy is planned due to futility of ongoing treatment v) Patient expected to die within 60 minutes of therapy withdrawal.

h) Process i) Identify any potential DCD donor & refer to the duty ICU consultant. ii) Discuss futility of treatment/withdrawal of therapy with the family. In certain

circumstances a 2nd ICU consultant may become involved to avoid any perceived conflict of interest.

iii) Discuss the subject of organ donation with the family. The Australian Organ Donation Register records may assist with family discussions.

iv) The Organ Donation Hospital Medical Director(s) should be involved. v) Enlist the help of the Organ Donation Coordinator early. vi) Withdrawal is best done as planned event in working hours and the ODC will

normally organize a team meeting of all those involved vii) Coordination is required between ICU theatre and retrieval teams viii) The organ retrieval teams should not be involved in patient care before death ix) The role and validity of ante-mortem interventions, such as heparin, are still

under debate and senior advice should be sought. x) Withdrawal may occur either in the ICU or the theatre viewing room. xi) Certification of death needs to be done by an ICU consultant or a Senior

Registrar of more than 5 years experience. If an arterial line is present this is the preferred method looking for absent cardiac output

xii) A following the loss of cardiac output the patient is observed for a period of time (currently 2 minutes) to ensure auto-resuscitation does not occur

xiii) The time interval from death to the operating theatre should be minimized. i) Other considerations

i) DCD is difficult therefore the family must be strongly supportive of organ donation and have an understanding that progression to actual donation will rely on time to death post withdrawal of therapy.

ii) Theatre and ICU resource issues may impact on this process

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