Blog

---

Read Also : Pitfalls in the Management of Diabetic Ketoacidosis (DKA)

---

Presentation

• 3Ps – Polyuria, Polydipsia, Polyphagia

• Non-specific symptoms:
  • Weakness, vomiting, abdominal pain, blurry vision

• Physical Exam:
  • Acetone smell
  • Dehydration / tachycardia / hypotension / shock
  • Kussmaul’s respiration (deep/labored breathing secondary to acidosis)

Diagnosis

• DKA diagnostic criteria:
  • Hyperglycemia: serum glucose >250 mg/d
  • Acidosis: arterial pH <7.3, anion gap >10, serum bicarbonate <18 mEq/l
  • Ketosis: ketonuria or ketonemia
    • Serum beta-OH-butyrate is the preferred method for measuring ketonemia

DKA Diagnosis

□ D-Diabetes, Blood Sugar > 250
□ K-Ketones in urine/serum
□ A-Acidosis-pH<7.3, HCO3<18

Causes

• Infection (UTI, pneumonia, gastroenteritis, pancreatitis) in 40-50%
• Infarction (ACS, MI)
• Infraction (patient noncompliance with therapy)
• Infant (pregnancy)
• Ischemic (CVA)
• Illegal (alcohol, drug abuse/cocaine abuse)
• Iatrogenic (prescription drug interactions, e.g. steroids)
• Idiopathic (new onset type 1 diabetes or other cause)

Treatment

Initial Resuscitation

• Altered sensorium based on level of combination of hyperosmolarity and acidosis (Diabetes Care 2010;33:1837–1839)
• Start with 2L IV Normal Saline empiric before labs

IV Fluids

• Start with 2L IV Normal Saline bolus
• Fluid deficit about 100ml/kg (7-8L deficit) secondary to glucose osmotic diuresis
• Can decrease glucose to 300 with IV fluids

Sodium

• Falsely lowered level (hyponatremia) secondary to hyperglycemia
• Correction: Add 1.6 to Na for every 100 over 100 in glucose level
• Corrects with IV Fluids
• 1/2 Normal Saline: Switch to 1/2 NS when Na normalizes

Insulin

• Mechanism of Action: Stops ketogenesis and breakdown of fatty acids

• Caution: Hypokalemia
  • Prevalence 5.6% (3 out of 54 patients with hypokalemia) (Am J Emerg Med. 2012;30(3): 481)
  • Do not start insulin until you check potassium → if patient hypokalemic, can drop K even more → arrhythmia
  • Hold insulin until K>3.3

• Dose: Start 0.1 U/kg/h gtt
  • Do not need bolus → insulin bolus not associated with any benefit to patients (J Emerg Med 2010;38(4):422)
  • Priming dose of insulin unnecessary if dosing adequately (Diabetes Care 2008;31(11):2081)
  • Bolus option dosing: bolus 0.1 U/kg; gtt: 0.1 U/kg/h

• Monitor
  • If glucose not decrease by 50mg/dl in first hour → double rate or SQ insulin bolus
  • If Glucose >1000 mg/dl, rapid correction puts patient at risk for cerebral edema
  • Glucose reaches 200mg/dl:
    • i. Reduce Insulin gtt to 0.02-0.05 U/kg/hr or
    • ii. Rapid acting insulin 0.1 U/kg SC every 2 hours
  • Anion gap closed
    • i. Goal: Resolution of acidosis/ketosis (not euglycemia) → do not stop insulin until anion gap closed
    • ii. Transition dose SQ insulin (5 Units per 50 over 150-max 20)
    • iii. D/C insulin gtt one hour after SQ dose

• Dextrose: When glucose is < 200 mg/dl, add D5 to replacement fluids
  • Allows continued insulin administration until ketonemia is controlled while at the same time avoiding hypoglycemia

Potassium

• Total body potassium deficit (average deficit 3-5 meq/kg)
• May see relative hyperkalemia because of acidosis
• Repletion: PO (if able to tolerate) and IV
• Do not start insulin until potassium is > 3.3

HCO3 (Bicarbonate)

• Controversial, recommended by ADA for pH<7.0
• Retrospective studies show no improvement in outcome (Crit Care Med 1999;27:2690)
• No prospective randomized studies concerning the use of bicarbonate in DKA with pH values <6.9 have been reported (Diabetes Care 2002;25:2113–2114)

Other Electrolytes

• Magnesium → depleted secondary to osmotic diuresis, ok to replete
• Phosphorus → may precipitously drop with treatment of DKA, must replete

Monitoring

• Glucose q 1 hour
• pH and electrolytes q 2-4h
  • ABG not needed, VBG is adequate for monitoring (Emerg Med J 2006;23(8):622)

Complications

• Hypoglycemia – overzealous DKA treatment

• Hyperglycemia – undertreatment

• Hypokalemia
  • Caused by insulin tx, correction of acidosis and volume expansion

• Return of DKA (Must bridge with SQ insulin dose)

• Hyperchloremia

• Cerebral Edema
  • Prognosis: mortality (20-50%), 1/3 survivors in vegetative state
  • Risk factors: age < 5, new onset DM
  • Symptoms: Depressed LOC/AMS (Altered Mental Status), pupillary changes, seizures
  • Treatment
    • Mannitol 1-2 gm/kg
    • Consider: Intubation, Dexamethasone, hypertonic saline (5-10ml/kg)

---

Read Also : Pitfalls in the Management of Diabetic Ketoacidosis (DKA)

---

References

• Hyperglycemic crises in adult patients with diabetes . (https://pubmed.ncbi.nlm.nih.gov/19564476/)
• Acidosis: the prime determinant of depressed sensorium in diabetic ketoacidosis. https://pubmed.ncbi.nlm.nih.gov/20484127/
• Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. https://pubmed.ncbi.nlm.nih.gov/21316179/
• Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. https://pubmed.ncbi.nlm.nih.gov/18514472/
• Is a Priming Dose of Insulin Necessary in a Low-Dose Insulin Protocol for the Treatment of Diabetic Ketoacidosis? https://pubmed.ncbi.nlm.nih.gov/18694978/
• Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? https://pubmed.ncbi.nlm.nih.gov/10628611/
• The use of alkali therapy in severe diabetic ketoacidosis. https://pubmed.ncbi.nlm.nih.gov/12401775/
• Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate. https://pubmed.ncbi.nlm.nih.gov/16858095/