DIABETIC EMERGENCIESDR. A. SAJJAD PATHAN MBBS MHADepartment of Accident & Emergency MedicineKokilaben Dhirubhai Ambani Hospital & Medical Research Institute

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 %)

DIABETIC KETOACIDOSIS

Acute, life threatening complication of DM

Occurs predominantly in Type 1 DM, but can be seen in Type 2 DM too

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

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)

CLINICAL PRESENTATION

Symptoms Polyuria Polydipsia Weight Loss Weakness Nausea & Vomiting Abdominal Pain

Signs Hypothermia Tachycardia Tachypnea Kussmaul Breathing Ileus Acetone breath Altered Sensorium

DIAGNOSIS & LAB EVALUATION

When DKA suspected, Initial Steps Blood Sugar Strip (RBS) Urine test strip EKG Venous Blood Gases NS infusion

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)

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

DIFFERENTIALS

Basically any of the MUDPILESBig Ones:Alcoholic KAStarvation KALactic acidosisHHS

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

ORDER OF THERAPEUTIC PRIORITIES

Volume first Correction of Potassium deficits Lastly, Insulin administration

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

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

INSULIN

Low dose, regular insulin, thru infusionIf 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 a½ DNS in other line until resolution of

ketoacisosis

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

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)

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

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

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

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

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