Case Management:Acute Respiratory Failure

Santos, Jennifer JoySantos, Ma. Socorro

Tiongson, Denver

Y.d.

• 57 year old• Female• Widow• Born Again Christian• Right-handed• from Baclaran, Paranaque

Patient Profile• Chief Complaint : Dyspnea• Non-hypertensive, non-diabetic,

non-asthmatic• No history of PTB• With a finding of an intracranial mass

(temporal lobe) in CT scan c/o PGH (2005)

History of present illness

5 yrsPTA

•Patient noted a polyp in the Left nostril

•(+) rhinitis. No associated anosmia, bleeding, headache

•Consult at PGH – OPD. CT scan done.

•A > Small intracranial mass, Right temporal lobe

•Advised surgery but deferred due to fear of surgery

•On regular follow-up c/o PGH-NSS

•Dexamethasone 4 mg BID, taken with good compliance

•In the interim, patient was able to do daily activities with no symptoms

History of present illness

2 yrsPTA

•Gradual onset weakness of extremities, LE>UE

•Numbness of left hemifacial and circumoral area

•Gradual slurring of speech described as ”parang lasing”

•Still able to do daily activities of selling, although at a slower rate

•(+) anterior neck mass, (+) palpitations, (+) weight loss. No heat intolerance, AUB, changes in bowel movements.

•Consulted at PGH-ORL for A> DTG. On Levothyroxine for succeeding 2 years with good compliance.

•Never followed-up with NSS during visits in PGH.

History of present illness

8mosPTA

•Gradual but progressive weight loss

•(+) numbness , Left hemifacial area

•(+) weakness, Left UE and LE, requiring assistance in daily activities

•Last follow-up with PGH-ORL.

•Never followed up with NSS.

History of present illness

4mosPTA

•(+) Fall episode

•Patient was admitted at PGH ER

•MRI and CT scan was done, where intracranial mass was found to be “larger” and patient was advised surgery

•Patient agreed and decked for scheduling c/o NSS.

•Discharged after 3 days. Awaiting schedule from NSS.

History of present illness

2weeks

PTA

•Patient cannot rise from bed and was dependent on ADL’s (feeding, combing, transfers).

•Patient was in bed all the time, wears diaper, and fed in bed

•Youngest child was her caregiver.

•(+) productive cough with yellowish sputum.

•(+) post-nasal drip and nasal congestion

•(-) fever, dyspnea, tachypnea, loss of consciousness

•No consults done. No medications taken.

History of present illness

1weekPTA

•Severe dyspnea, with associated tachypnea.

•(+) productive cough

•No fever, headache, change in sensorium, blurring of vision, seizure like episode.

•(+) 50 % weight loss, (+) anorexia

•Prompted consult at PGH.

•Admission

Review of Systems

(-) fever(+) weight loss (50%)

(+) anorexia(-)LOC

(-) headache(-) BOV

(-) epistaxis(-) hearing loss

(-) colds(-) hemoptysis(-)chest pain

(+) palpitations(-) orthopnea

(-) abdominal pain(-)nausea

(-) vomiting(-)melena(-)dysuria

(-) constipation(-) diarrhea

(-) hematuria

paST MEDICAL HISTORY

(+) Allegedly diagnosed with Diffuse Toxic Goiter - 2004, presented with palpitations and anterior neck masss/p RAI, (PGH, 2008)(+) Intracranial mass, Left temporal lobe (2005)

(-) Hypertension(-) Diabetes Mellitus(-) Bronchial asthma(-) Heart disease(-) Stroke(- )Pulmonary Tuberculosis(+) Allergy to unrecalled antibiotic given at PGH-ER

Family history

• (+) HPN- mother• (+) CVD- siblings• (+) MI- brother• (-) known Cancer of any type• (-) PTB, DM

Personal /social history

• Non-smoker• Non alcoholic beverages• Denies illicit drug use• Works in buy and sell business• Church worship leader• High school graduate• Lives with youngest daughter aged 16 y/o in their

old house, while the other 2 daughters are now living with their respective families

Course at the emergency room

3/10/2010, DEM

BP 110/70 HR 120

RR 28 T 38.4(+) crackles Bilateral LF(-) murmurs

A> t/c CAP HREncephalopathy,

probably secondary to

metastasisRight temporal

lobe mass

CeftazidimeAzithromycin

3/10 InterpretationHgb 83 LowHct 0.317 NormalWBC 9.5 HighRBC 2.4 LowLymphocytes 0.837Monocytes 0.014Platelets 176 NormalReticulocytes 0.029MCV 93.1 NormalMCH 31.0 NormalMCHC 333 NormalRDW 17.2 High

PBS: normocytic, hypochromic (++), (+) toxic granulation in PMNs. Reticulocytes adequate.

3/10 3/10HDL 0.16 (6) LowTriglycerides 292 HighLDL 1.8 (69.4) NormalFBS 6.02 113.9 HighRBS 6.33 NormalBUN 4.99 NormalCrea 55 46 NormalCholesterol 3.52 NormalNa 135 NormalK 4.0 NormalCl 98 NormalAlbumin 14 LowAST 42 NormalALT 48 NormalCa 1.78 (2.3) NormalMg 0.71 LowP 1.8 (69.4) Normal

abG3/10

pH 7.448

pCO2 39.5

PO2 79.4

HCO3 27.3

BE 3.4

O2 sats 95.5

Interpretation normal

PTB extensive disease with possible cavitationPneumonia with consolidationSubsegmental atelectasis, L

WAT IS OUR aditional READING of this XRAY?-Elevated Right diaphragm can mean pulmonary contraction-- cardiac reading?

Course at the emergency room 3/10/2010, POD

Awake,coherent, in mild respiratory

distressCXR: Bilateral

infiltrates(+) opacity at apex

(+) cavity formation(+) subsegmental

atelectasis

A> CAP HR t/c aspiration component

Temporal mass, RDTG s/p RAI, 2008

PTB suspectStress hyperglycemia

Anemia prob. Secondary to chronic

disease

ClindamycinAnti-Koch’s

Course at the emergency room

3/10/2010, Gen Med

Awake,coherent, in mild respiratory

distressDxtics:

sputum GS/CSAFBTSH

A> CAP HR t/c aspiration

componentTemporal mass, RDTG s/p RAI, 2008

PTB suspectStress hyperglycemia

Anemia prob. Secondary to chronic

disease

ClindamycinHold Anti-Koch’s

Course at the emergency room

3/10/2010, Day MHAPOD

decreased sensorium, in cardiorespiratory

distress with subcostal retractions

O2 sat 82.5%, (+) crackles Bilateral

LFgood air entry

A> CAP HR t/c aspiration component

Temporal mass, RDTG s/p RAI, 2008

PTB suspectStress hyperglycemia

Anemia prob. Secondary to chronic

disease

Intubated ET 7.5 L20, with yellow secretions. ET 7.5 L 18 from L 26

Other pertinent laboratory results

3/11 • ETA GS: 0-2 gram (-) bacilli; 0-2 yeast cells• KAYA KAYA NATING MAHANAP YUNG CULTURE

STUDIES NYA PARA MALAMAN UNG ETIOLOGIC AGENT? =)

Eventually admitted at Ward 1

Physical examination on admission• Awake, conscious, responsive, intubated @ET 7.5 L18, NICRD• BP= 120/80 HR=120 RR=40sT=37.6• HEENT: pale palpebral conjunctivae, anicteric sclerae, pupils 2mm

EBRTL, (+) NVE, (+) Anterior neck mass 3x4 cm firm, nodular, movable. (-) CLAD

• Chest: Equal chest expansion, harsh breath sounds, (+) crackles bilateral LF mid to base, (-) wheezes.• Heart: DHS, tachycardic, regular rhythm, apex beat at 5th ICS

anterior axillary line. (-) murmurs.• Abdomen: soft, flabby, normoactive bowel sounds, (-)

masses/tenderness• Extremities: pink nailbeds, full and equal pulses, CRT<2 sec. (-)

edema/cyanosis, (+) grade I sacral ulcer, Right

• Acute Respiratory Failure type I, secondary to CAP, High Risk

• Community Acquired Pneumonia, High Risk• Pulmonary Tuberculosis, Category I• Intracranial mass, Right temporal lobe (2005)• Diffuse Toxic Goiter, not in storm (2004) s/p

RAI (2008)• Impaired Fasting Glucose• Dyslipidemia• Anemia, severe. considerations:

• Chronic disease• Occult GI bleed• IDA, multifactorial

Working impression on admission

managementOrders

• Mech vent settings: AC mode, FiO2 100%, TV 400, IFR 60, PEEP 5, BUR 16

• Diet: TCR 1800 kcal/day• CHO 250 g/day• CHON 60 g/day• Fats-rest

Medications

• Pip-Tazo 4.5 g IV OD• HRZE 4 tabs OD• NAC 200 mg/sachet in 50

cc H2O q12• Combivent neb q6• Paracetamol 50 mg/tab

q4• Dexamethasone 40

mg/tab TID• Simvastatin 40 mg ODHS• Omeprazole 40 mg OD

pre-breakfast

Course at the ward3/11/2010, 2 AM

Conscious, coherent, follows commands, GCS 13 (E4V3iM6)

BP 120/80 HR 120s, irregular RR 24 MV O2 sats 95% CBG 256

T 37.8PPC, AS, pupils 2/2 BRTL,

(+) NVEECE, good air entry, (+) crackles L LLF

(-) rhonchi/wheezes, (-) heaves/ thrills/murmurs,

tachycardic, irregular rhythmSoft flabby abdomen, (-)

masses/tendernessFEP, good CRT, PNB, (-) edema

WARD AdmissionContinue present

medications

LabsReferred for tachycardia

Interventions done

3/11 3/11

pH 7.47 7.46

pCO2 42.2 48.6

PO2 44.6 100.6

HCO3 31.2 34.9

BE 7.4 10.9

O2 sats 83.5 97.8

Interpretation metabolic alkalosis metabolic alkalosis

Other pertinent laboratory findings

3/12• CKMB 23.5• CK total 42

Rules out ACS

Course at the ward3/11/2010, 4 AM

Conscious, coherent, follows commands, GCS 13 (E4V3iM6)

BP 120/80 HR 180s, irregular RR 26 MV O2 sats 75% CBG 256

T 37.8PPC, AS, pupils 2/2 BRTL,

(+) NVEECE, good air entry, (+) crackles L

LLF (-) rhonchi/wheezes, (+) coffee ground materials per NGT

(-) heaves/ thrills/murmurs, tachycardic, irregular rhythm

Soft flabby abdomen, (-) masses/tenderness

Stat ECG- AF in RVR, NA, NSSSTWC

Shifted to CAB w/o improvement in O2 sats.

Shifted back to MV. Suctioning and

nebulization done. ET in place.

A> Acute AF in RVR prob extracardiac due to sepsis.

r/o ACS (NSTEMI)

Digoxin 0.5 mg/amp 1 amp IV at 3:30 am

(HR 160-180, BP 120/80)

Verapamil 2.5 mg/amp IV at 5: 30 am

(HR 140-150, BP 100/60)

Course in the ward3/11/2010, 9 AM

noted BP 70/50

A> ARDS 2’ CAP HRSepsis secondary to CAP HRPTB cat IIntracranial mass, R lobeDTG in storm, s/p RAIIFGDyslipidemiaAnemia prob secondary to chronic disease.

Dopamine drip started

Course in the ward : 3/12/2010

Revived after 9 minutes. BP=weak, HR=88

Eventually had BP=0 HR=0. CODE called

Epinephrine given x 3 dosesWeak pulses

inotropes were continued, dopa max 20 mcg/kg/min

LabsAfter first code called

3/12

pH 7.312

pCO2 69.9

PO2 62.6

HCO3 35.1

BE 86.4

O2 sats 89.4

Interpretation Respiratory Acidosis

3/12 : 12-L ECG: MFAT, normal axis, non-specific ST-T wave changes

Course in the ward

3:06 pm- pronounced dead after a total of 26 minutes of code

During code, (+) Atrial Fibrillation noted on Cardiac monitor

Defibrillation was done (biphasic 200 joules)Another code called after 15 minutes

Epinephrine given 7x

Sinus tachycardia, normal axis, low voltage complexes, NSSTTWC

Discussion

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

ARDS• Severe dyspnea of acute onset (< 2 weeks)• Hypoxemia• Diffuse bilateral pulmonary infiltrate on CXR• PaO2/FiO2 < 200 mmHg• No elevated left atrial pressure (PCWP <18

mm Hg)

Respiratory Failure

CausesDirect Injury Indirect Injury

Pneumonia (30% overall)Toxic inhalation

Aspiration of gastric contentsPulmonary contusion

Sepsis and bacterial pneumonia (40-50%develop ARDS)

Head traumaMultiple bone fractures

Flail chestBurns

Drug overdosePancreatitis

Near drowningMultiple blood transfusions

Acute Lung Injury (ALI) less severe disorder but has the potential to evolve into ARDSALI: PaO2/FIO2 200 – 300 mmHg ARDS: PaO2/FIO2 <200 mmHg

Three Phases

ExudativePhase

Diffuse alveolar and endothelial damage Alveolar edema, PMN infiltration, Hyaline membrane formation

ProliferativePhase

Interstitial inflammation and Fibrotic changes (lung repair, increase type II pneumocytes which produce new surfactants)

Recovery

Fibrotic Phase Exudates become alveolar duct and interstitial fibrosis and bullae formation leading to pulmonary hypertension

0 7 14 21 6 mos

Exudative Proliferative FibroticRecovery

Increase pulmonary vascular permeability

Alveolar edemaPMN infiltration of lungs

Hyaline membrane formation

Inactivation of surfactant due to exudates

Accumulation in dependent portions

Atelectasis

Atelectasis and increase work of breathing:

DyspneaTachypneaHypoxemia

Microvascular occlusion, pulmonary hypertension, increase in dead space:

Hypercapnia

Diffuse alveolar and endothelial damage

Proliferative Phase

• Time of Lung repair• Layering of exudates• Lymphocytic infiltration• Type II pneumocytes reproduce

surfactant

Fibrotic Phase

• Fibrosis• Emphysema like changes (bullae)• Vascular occlusion

Complications:o Pulmonary Hypertensiono Pneumothoraxo Increase in dead space

Mechanical Ventilation• Augments the increase in work of breathing• But can aggravate lung injury via repeated Alveolar

Overdistention and Recurrent Alveolar Collapse• Set MV at lower tidal volumes– 6 ml/kgBW ( vs standard 12ml/kgBW)

• Optimal PEEP for alveolar recruitment : – 12-15 cmHg

• Target RR < 35• ARDS net protocol: Low volume, High frequency

ventilation

Management

• Manage Respiratory Acidosis• Fluid restriction and diuretic – to reduce left atrial filling pressure–Dry Lungs are Happy Lungs!

• Steroids –anti-inflammatory No role!

Mortality

• 41-65%• Mostly from non-pulmonary causes

(Sepsis, organ failure)• Recovery of lung function within 6

months

ACUTE RESPIRATORY FAILURE

• Inability of the lung to meet the metabolic demands of the body

• Dysfunction in lung’s main function:–Oxygenation–Carbon Dioxide elimination

• PaO2 <60 mmHg

• PaCO2 >50 mmHg• Develops 4-48 hours

Signs• Tachypnea• Exaggerated use of accessory muscles• Intercostal, supraclavicular and subcostal

retractions• Neuromuscular disease: signs of respiratory

distress may not be obvious• CNS disease: bradypnea + shallow breathing

Respiratory Tract•CNS (medulla) •Peripheral nervous system (phrenic nerve) •Respiratory muscles •Chest wall •Lung •Upper airway •Bronchial tree •Alveoli •Pulmonary vasculature

Type 1: Hypoxemic rf

HEPoxemicHemorrhage

Edema and exudatespneumonia

Alveolar Flooding

Ventilation perfusion mismatch and

Intrapulmonary shunting

Hypoxemic RF• SaO2 < 90% despite

FiO2 > 0.6• Interference with O2 exchange, but overall

ventilation is maintained• Goal of MV: provide adequate SaO2 to improve

VP matching and reduce IP shunt• Most common

Causes of hypoxemic ARF

1. FiO2

2. Hypoventilation ( PaCO2)

3. V/Q mismatch (eg.COPD)4. Diffusion limitation 5. Intrapulmonary shunt -

Pneumonia - Atelectasis - CHF (high pressure pulmonary edema) - ARDS (low pressure pulmonary edema)

• Focal infiltrates on CXRAtelectasis

Pneumonia

• Diffuse infiltrates on CXRCardiogenic Pulmonary EdemaNon cardiogenic pulmonary edema (ARDS)Interstitial pneumonitis or fibrosisInfections

Hypoxemic respiratory failure The major problem is PaO2.

If due to low V/Q mismatch: O2 therapy If due to pulmonary intra-parenchymal shunts

(ARDS): Assisted ventilation with PEEP If due to intracardiac R-L shunt: Surgical

Type 2 : hypercarbic rf

1. Decrease minute ventilation

2. Increase physiologic dead space

Alveolar Hypoventilation

Inability to eliminate CO2 effectively

PaCO2 > 50 mm Hg and arterial pH< 7.3

Hypercarbic RF

• Hypoxemia is always present• pH depends on level of HCO3

• HCO3 depends on duration of hypercapnia• Renal response occurs over days to

weeks

Hypercarbic RF: Causes• Impaired CNS central drive :

– Dug overdose, Brainstem injury, Sleep-disordered breathing, Hypothyroidism

• Impaired neuromuscular transmission – MG, GBS, Phrenic injury

• Respiratory muscle weakness and fatigue• Increase load in respiratory system

– Increase resistive load/bronchospasm ie Asthma and COPD• Reduced lung compliance

– Atelectasis, Edema • Reduced chest wall compliance

– Pneumothorax, Pleural effusion, Abdominal distention• Increase minute ventilation

– Pulmomary Embolus with incr dead space, Sepsis

Acute Hypercarbic RF• Arterial pH is < 7.35 •Acute on Chronic:• This occurs in patients with chronic CO2

retention who worsen and have rising CO2 and low pH.• Mechanism: respiratory muscle fatigue

Hypercarbic RF• Goal: Normalize arterial pH through CO2 elimination• Respiratory muscle fatigue ssx: – Inability to speak full sentences– Use of accessory muscle– Paradoxical abdominal muscle activity– Extreme tachypnea (>40bpm)– Decrease RR despite increase in drive to breath

• Tx must be directed at reversing cause of ventilatory failure: NIPPV

• Contraindications: hemodynamic instability, inability to protect airway, respiratory arrest

Hypercapnic Respiratory failure

To MechVent or Not to MechVent ? In Acute respiratory acidosis: Mechanical

ventilation! Chronic Respiratory acidosis: Close monitoring,

mechanical ventilation is rarely required. In acute-on-chronic respiratory failure, the

trend of acidosis over time is a crucial factor.

Lung atelectasis A.k.a Perioperative RF

Type III RF

General Anesthesia

Decrease FRC(functional

residual capacity)Atelectasis

Type III RF : Tx• frequent change in position• chest physiotherapy• upright positioning• aggressive control of postop pain• NIPPV

Type IV RF• Systemic hypoperfusion• Occurs in Shock (pulmonary edema, lactic

acidosis, anemia)• Normally, muscles consume < 5% total CO and

O2 delivery 40% CO• Tx: Intubation and MV– to allow redistribution of CO away from

respiratory muscles and into vital organs

Diagnostics• ABG • PaO2

• PaCO2

• Compute Alveolar-Arterial PO2 Gradient

P(A-a)O2 Gradient = PIO2 – PaCO2 / Rwhere PiO2 = partial pressure of inspired air, R = 0.8

Normal range: 5-10 mm of Hg

• Hyperoxia Test – Give 100% O2 and assess improvement

CASE - SPECIFIC MANAGEMENT AND DISCUSSION

Subjective / objective / problems

Diagnosis Management

intracranial mass predisposing to weakness and bedridden state, poor care, elderlySevere dyspnea of acute onset, tachypnea at 40, O2 sat < 85%, subclavicular retractions(+) productive coughcrackles bilateral lung fieldnormal ABG (consistent in acute state)

CXR: diffuse lung infiltrate with subsegmental atelectasis on Left

Acute Respiratory Failure 2’ Community Acquired Pneumonia, High Risk

CeftazidimeAzithromycin

shifted to…

Clindamycin

Shifted to

Pip-tazo 4.5 g IV

CAP 2010 Guideline

• CAP HR criteria• CAP HR treatment options• Risk factors for Pseudomonas• Risk factors for Anaerobes• Ceftazidime– With gram negative and anti-pseudomonas coverage

Clindamycin Covers for anaerobes

• Pip-Tazo

Subjective / objective / problems

Diagnosis Management

CXR : PTB extensive disease with possible cavitation

PTB category I HRZE

low HDL, high TG, high FBS, high CBG -- stress hyperglycemiahypoalbuminemiahypomagnesemia

Dyslipidemia simvastatinNo correction for Mg

RBC 2.4 Anemia, severe. considerations:Chronic diseaseOccult GI bleedIDA, multifactorial

Mechanical Ventilation: Indications

1. PaO2< 55 mm Hg or PaCO2 > 60 mm Hg despite 100% oxygen therapy.

2. Deteriorating respiratory status despite O2 and Nebulization

3. Anxious patient with deteriorating mental status.

4. Respiratory fatigue: for relief of metabolic stress of the work of breathing