diabetic emergencies
TRANSCRIPT
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DIABETIC EMERGENCIESDR. A. SAJJAD PATHAN MBBS MHADepartment of Accident & Emergency MedicineKokilaben Dhirubhai Ambani Hospital & Medical Research Institute
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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 %)
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DIABETIC KETOACIDOSIS
Acute, life threatening complication of DM
Occurs predominantly in Type 1 DM, but can be seen in Type 2 DM too
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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
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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)
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CLINICAL PRESENTATION
Symptoms Polyuria Polydipsia Weight Loss Weakness Nausea & Vomiting Abdominal Pain
Signs Hypothermia Tachycardia Tachypnea Kussmaul Breathing Ileus Acetone breath Altered Sensorium
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DIAGNOSIS & LAB EVALUATION
When DKA suspected, Initial Steps Blood Sugar Strip (RBS) Urine test strip EKG Venous Blood Gases NS infusion
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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)
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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
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DIFFERENTIALS
Basically any of the MUDPILESBig Ones:Alcoholic KAStarvation KALactic acidosisHHS
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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
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ORDER OF THERAPEUTIC PRIORITIES
Volume first Correction of Potassium deficits Lastly, Insulin administration
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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
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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
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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
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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
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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)
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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
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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
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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
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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
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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