Endocrine Emergencies

By Clare Di Bona Acknowledgement to Yusef Mamoojee (Lab Case 46, 47) & Tony Lourensen

(DKA Guideline, HHS Guideline)

Interpretation

 1) ph shows severe acidaemia  2) Primary disorder severe metabolic

acidosis given HC03 8   Anion gap (Na+K)-(HC03+Cl)=31   HAGMA likely contributors: ketones,

raised lactate, renal dysfunction

Interpretation

 3) Compensation  Expected pC02 can be calculated

from Winter’s formula   1.5xHC03+8   =1.5X8+8=20   But the measured pC02 was 30!

Therefore there is either inadequate compensation or an additional respiratory acidosis

Interpretation

 4) p02 65mmHg   Patient is breathing with Fi02 80% (15L

NRBM) therefore expected p02 5X80=300mmHg

  Perhaps even a healthy person could not get up to 300 even so 65 is VERY HYPOXIC!

  5) Lets calculate the A-a gradient and see if there is VQ mismatch

Interpretation

  A-a gradient=   Alveolar Pa02-Arterial Pa02   Arterial Pa02 is given as 65mmHg   Alveolar Pa02 needs to be calculated from

Alveolar gas equation   =(760-47)xFi02-(1.25xpC02)   =533-65=468   Normal=Age/4 + 4   There is a significant VQ mismatch!  Given High WCC and CRP likely LRTI

Interpretation-Other

 Hyperkalaemia   Contributors: dehydration,

hyperglycaemia/insulin deficiency/renal failure

 Na   likely pseudohyponatraemia given high

BSL   Corrected Na=glucose/3 +Na

Interpretation-Other

 Glucose 42  Osmolality 2xNa+urea+glucose=303

(285=295)  Ketones >7  Ph 7.03

 This fits the criteria for DIABETIC KETOACIDOSIS

Management

 Now what do I do?..........

 Follow the JEDO Guidelines on DKA

 Part of the Management is knowing what to do the other part is making sure it gets done in a timely manner!!

Diagnosis

 Venous ketones >3mmol/L AND  BSL >11mmol/L AND  Ph <7.3 and/or HC03 <15

Diagnosis

 Pitfall!

 Note if there is considerable hyperglycaemia (>30mmol/L) WITHOUT significant ketones or acidosis AND

 Osmolality >320 mosm/kg (2xNa + urea + BSL)

 PROCEED TO HHS GUIDELINE

Causes/Precipitants

  First Presentation Type 1 diabetic (DKA) HHS usually Type II

  Viral infection   Bacterial infection ie UTI, pneumonia, cellulitis   Acute major illness: MI, CVA, pancreatitis, sepsis   Alcohol/drugs ie cocaine   Poor lifestyle ie non-compliance   Pump system failure ie blockage or leakage   Drugs that increase glucose, decrease insulin ie

atypical antipsychotics (clozapine, olanzapine), propranolol, phenytoin, Ca channel blockers, corticosteroids, diuretics (thiazides)

Pathophysiology

 Low insulin to glucagon ratio leads to   Breakdown of glycogen in liver and

muscle   Gluconeogenesis in liver   AA breakdown in muscle   Lipolysis in adipose tissue   Formation of ketone bodies in

mitochondria of liver

Management Principles

  Fluid Resuscitation   Insulin Infusion  Monitoring of biochemical parameters (Ph,

ketones, bicarb)  Making adjustments as needed ie

  K replacement needed when using insulin   Dextrose infusion needed if ongoing insulin

requirement and BSL <15   Increase insulin infusion is patient not

responding to treatment ie ph, ketones, bicarb not shifting

Management Principles

  Be efficient in initiating treatment!  Get a senior doctor   Need to go to resus   Ideally two nurses   At least two large IV lines (one line for

blood sampling)   Its one thing to write down the treatment its

another to make sure it gets done!

Management principles

 Follow the JEDO DKA guideline to write up fluids and insulin infusion

Rehydration

Resuscitation fluids may be needed. Give 250ml boluses of normal saline until good perfusion (SBP >90, peripheral perfusion) usually no more than 1.5L needed

K Replacement

Insulin Infusion

Monitoring

Record Sheet-Very Important!!

Targets

• If you are not meeting the targets increase insulin by 1 unit/hr=1ml/hr

• Add in 10% dextrose at 125ml/hr in addition to rehydration fluid if BSL dropping and insulin still required

Other

Resolution

Investigations

DKA Versus HHS

DKA HHS

Ph <7.3 Ph>7.3

Younger <65yrs Older >65yrs

Significant ketones/acidaemia No significant ketones/acidaemia

Normal osmolality <320mosmol/kg

High osmolality >320 mosm/kg

BSL <44mmol/L usually (19-27)

BSL >56mmol/L

Lower glucose as earlier symptoms (ketones) Also younger patients with higher GFR

Occurs less frequently and has higher mortality

HHS

 Usually occurs in type II diabetic with concomitant illness and dehydration

 Not as common  Occurs more in the elderly  Higher mortality than DKA 10-20%  Most present dehydration and focal or

global neurological deficits

HHS

  In HHS the person has a pre-existing lack/resistance to insulin plus a stress (acute illness) further reduction in insulin

  Hyperglycaemia and hyperosmolarity lead to a fluid shift into the intravascular space and further intracellular dehydration and osmotic diuresis

  But why aren’t there ketones? Reason largely unknown.   Theory that there’s just enough insulin to

prevent ketones   Theory that hyperosmolarity decreases lipolysis

Diagnosis HHS

 Hypovolaemia  Hyperglycaemia >30mmol/L

WITHOUT significant ketones or acidaemia

 Osmolality >320mosm/kg

Clinical Symptoms/Signs HHS

  Age >65yrs   Insidious onset initially no symptoms then

polyuria, polydipsia, weight loss   Followed by lethargy   Neurological signs/symptoms common

  especially osmolality >320   Obtundation &coma   Focal neurology ie hemiparesis, hemianopsia   Seizures

Clinical signs/symptoms

 Most cases of DKA in comparison present hyperventilation and abdominal pain

 Signs of dehydration are common to both

Management Principles

 Rehydration  Electrolyte replacement   Insulin infusion If needed

Management Principles

 Treatment is based on gradual lowering of BSL and frequent calculations of osmolality

 HHS is VERY insulin sensitive to avoid rapid BSL shifts insulin is started at half the rate compared to DKA

Fluids

 Give 1L over 1hr   Then continue at 500ml-1000ml/hr

(decreased if signs of fluid overload)   Catheter is very important   Aim for U/O of 0.5ml.kg/hr and adjust fluids

to achieve this as long as pt tolerates  Goal

  decrease osmolality 3-8mosmol/kg/hr   Positive balance 2-3L by 6hrs   Positive balance 3-6L by 12hrs

Electrolyte Replacement

Insulin Infusion

Other

Goals of Therapy

Record Keeping is Very Important!

References   Mamoojee, Y. Emergucate: Lab Case 47 [internet]. 2015 [updated 2015 Feb 23; cited

2015 March 9]. Available from: http://www.emergucate.com/2015/02/23/lab-case-47/   Mamoojee Y. Emergucate: Lab Case 46 [Internet]. 2015 [updated 2015 Feb 10; cited

2015 Feb 17]. Available from: http://www.emergucate.com/2015/02/10/lab-case-46/

  Lourensen A. Hyperosmolar Hyperglycaemic State (HHS) Management Guideline-Adults [Internet] 2012 [updated 2015 Jan; cited 2015 March 10]. Available from:

  www.jhced.org   Lourensen, A, McQuillan C. Diabetic Ketoacidosis (DKA) Management Guideline-

Adults. [Internet]. 2012 [updated 2014 Dec; cited 2015 March 9]. Available from: www.jhced.org

  Kitabchi A, Hirsch I, Emmett M. Diabetic ketoacidosis and hyperosmolar hyperglycaemic state in adults: Epidemiology and pathogenesis [Internet]. 2014 [updated 2014 Jul; cited 2015 March 9]. Available from: www.uptodate.com

  Kitabchi A, Hirsch I, Emmett M. Diabetic ketoacidosis and hyperosmolar hyperglycaemic state in adults: Clinical features, evaluation and diagnosis [Internet] 2014 [updated 2014 Jul; cited 2015 March 9]. Available from:

www.uptodate.com