This document discusses diabetic emergencies, specifically diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). It covers the pathophysiology, clinical presentation, diagnosis, treatment priorities of volume repletion, potassium replacement, and insulin administration, as well as complications, disposition, and pitfalls in management. The goal of treatment is to correct dehydration, electrolyte imbalances, and acidosis while gradually lowering blood glucose levels.

1. DIABETIC EMERGENCIES
DR. A. SAJJAD PATHAN MBBS MHA
Department of Accident & Emergency Medicine
Kokilaben Dhirubhai Ambani Hospital & Medical Research Institute

2. ACUTE METABOLIC COMPLICATIONS
 Diabetic Ketoacidosis (DKA)
 Hyperosmolar Hyperglycemic State (HHS)
 Absolute/relative insulin deficiency
 Counter-regulatory hormone execess:
Glucagon, Catecholamines, Steroids, GH
 Precipitating Factors: Infection, Drugs, Stress
 Mortality in HHS much higher than DKA (5 – 20
%)

3. DIABETIC KETOACIDOSIS
 Acute, life threatening complication of DM
 Occurs predominantly in Type 1 DM, but can
be seen in Type 2 DM too

4. PATHOPHYSIOLOGY
 Hyperglycemic Crisis
 Due to absence/decreased Insulin
 Excess Glucogenic hormones
 Leading to Increased Osmolarity & Osmotic diuresis,
loss of HCO3 and other electrolytes
 Cellular Starvation
 Ketosis
 Metabolic Acidosis & Hyperventilation (to
compensate)
 Altered LOC due to elevated S. Osmolality > 320
mOsm/L

6. KETOACIDS
 Acetoacetate, B-(OH)butyrate, acetone
 Acetoacetate + NADH is in equilibrium with
B-(OH)butyrate + NAD
 Acetoacetate is routinely detected with Urine
dipstick (nitroprusside test)

7. CLINICAL PRESENTATION
Symptoms Signs
 Polyuria  Hypothermia
 Polydipsia  Tachycardia
 Weight Loss  Tachypnea
 Weakness  Kussmaul Breathing
 Nausea & Vomiting  Ileus
 Abdominal Pain  Acetone breath
 Altered Sensorium

8. DIAGNOSIS & LAB EVALUATION
When DKA suspected,
Initial Steps
 Blood Sugar Strip (RBS)
 Urine test strip
 EKG
 Venous Blood Gases
 NS infusion

9. DIAGNOSTIC CRITERIA
 BSL > 250 mg %
 HCO3 < 15 (ADA def <18)
 pH < 7.3
 Anion Gap > 10
 For HHS, BSL > 600, HCO > 18, variable
AG, and S Osm >320
(Source: ADA, 2009)

10. POTASSIUM, SODIUM & OSMOLALITY
 Total K is depleted
 Measured K may be normal or elevated
 Na Correction is essential, as hyperglycemia
may artificially reduce Na levels
 Corrected Na = m(Na) + {0.016 x (RBS –
100)}
 Osm = 2 m(Na) + Glu/18

11. DIFFERENTIALS
Basically any of the MUDPILES
Big Ones:
Alcoholic KA
Starvation KA
Lactic acidosis
HHS

12. TREATMENT
 Diagnosis suspected at triage
 2 large bore IV Lines
 1st line IV 0.9 % NS fast
 2nd Line IV 0.45 % NS just to keep line patent
 Do not wait for labs
 Order CBC, BMP, Urine dipstick, EKG, VBG
 Blood Cultures
 Other tests as appropriate: XRC, Cardiac
Enzymes, etc

13. ORDER OF THERAPEUTIC PRIORITIES
 Volume first
 Correction of Potassium deficits
 Lastly, Insulin administration

14. IV FLUIDS
First ½ Hour: Suspect DKA
 # 1 Line: NS wide open (1 Litre atleast)
 # 2 Line: ½ NS to keep patent
 In general, first 2 L in 0 – 2 hours, next 2 L in 2 –
6 hours, next 2 L in 6 – 12 hours
 When BSL is ~ 250 mg % , replace ½ NS with
½ DNS
 Consider monitoring CVP/PCWP in
elderly/cardiac comorbidities

15. K+ REPLACEMENT
 Magic Number 3.3 – 5.3
 If K > 5.3, no supplemental is required before
insulin
 If K 3.3 – 5.3, 20 mEq/L of replacement fluid,
while insulin is initiated alongside (~ 250 ml/hr)
 If K < 3.3, 40 mEq/L of replacement fluid before
insulin is initiated, Check K in an hour and Start
Insulin if K > 3.3, while correcting K (~ 10
mEq/hr)
 Adequate Urine output is essential before
initiating K therapy

16. INSULIN
Low dose, regular insulin, thru infusion
If K > 3.3 (excluding hypokalemia)
 IV Bolus: 0.1 U/kg Body Weight (Optional: Adults)
 IV Maintenance: 0.1 U/kg/hr BW
 HGT Hourly
 If sugars < 250 mg %
IV drip: 0.05 - 0.1 U/kg/hr with a
½ DNS in other line until resolution of ketoacisosis

17. INSULIN
 S/C Insulin can also be used, 0.2 U/kg bolus,
then 0.1 U/kg/hr or 0.3 U/kg Bolus, then 0.2
U/kg/2hr till HGT < 250 mg%
 No response: Commonly due to infection (50
– 75 decrease/hr)  double the infusion
dose
 Insulin to be continued until ketonemia and
AG has normalized
 Transition from IV to SQ insulin to prevent
relapse

18. HCO3 ADMINISTRATION
Routine Use is not recommended
 pH > 7.0: No Bicarbonate
 pH < 7.0, and Bicarbonate < 5mEq/L :
One can give 44.6 mEq in 500 ml ½ NS
over 1 hour until pH > 7.0
 Do Not Give HCO3 IV PUSH
(Source: ADA Position Statement Diabetes Care, 2003)

19. PHOSPHORUS
 Not routinely indicated (atleast not in the ED)
 If serum phosphorus < 1mg %  30 – 40
mmol K- Phos over 24 hours
 Monitor Serum Calcium levels

20. OUTCOMES: COMPLICATIONS RELATED TO
THERAPY/ACUTE DISEASES
 Electrolyte abnormalities
 Hypoglycemia
 ARDS
 CEREBRAL EDEMA (esp in young age/new
onset DM)
 Mortality in DKA results mainly from SEPSIS
or Cardiac (MI) or pulmonary complications
in elderly

21. DISPOSITION
 Majority patients go to the Intensive Care
Units/High dependency units
 Selected group with AG < 25 & no co-
morbidities can be managed in IP Diabetes
Units

22. PITFALLS
 10 % of DKA patients have “euglycemic
DKA”
May continue taking their insulin just before
approaching the ED
 Failure to realize other cause of altered
mental status, Calculate Effective Osmolality
 Elevated/Normal Serum K may still be
hypokalemic
 Abdominal Pain with Raised amylase/lipase
is common in DKA in absence of pancreatitis

23. PITFALLS
 Not all patients with ketoacidosis areDKA
 Look for MUDPILES
 Stopping the inslin infusion when serum
glucose goes below 200 – 250 rather than
adding D5W infusion and continuing the
insulin to treat ketosis (Hyperglycemia is
corrected faster than ketoacidosis)
 Failure to search for precipitating causes