Diabetic Emergencies. Diabetic Ketoacidosis -Type 1 DM -+ve ketones + art. pH < 7.30 + bicarb. -
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Transcript of Diabetic emergencies
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