Course Content
Zambian Paediatric & Obstetrics-Gynecology (OB/GYN) Clinical Mastery

Diabetic Coma 

Description

Diabetic coma is a life-threatening complication of diabetes mellitus resulting in altered consciousness or coma. It can arise from:

  1. Diabetic Ketoacidosis (DKA) – usually in type 1 diabetes

  2. Hyperglycaemic Hyperosmolar State (HHS / Non-Ketotic Hyperosmolar State) – usually in type 2 diabetes

  3. Severe hypoglycaemia – due to insulin or oral hypoglycaemic agents

All forms cause electrolyte imbalance, dehydration, and metabolic derangements leading to altered mental status, seizures, or coma.

Pathophysiology

  • DKA: Insulin deficiency → hyperglycaemia → lipolysis → ketone body formation → metabolic acidosis.

  • HHS: Extreme hyperglycaemia → osmotic diuresis → severe dehydration → hyperosmolarity → altered mental status.

  • Hypoglycaemic coma: Glucose < 2.8 mmol/L → inadequate cerebral glucose → CNS dysfunction, seizures, coma.

Risk Factors

  • Poor diabetes control or missed insulin

  • Infection, trauma, surgery, myocardial infarction

  • Medications: steroids, diuretics

  • Alcohol, dehydration

  • Elderly patients for HHS

Signs and Symptoms

  • General symptoms: Polydipsia, polyuria, weight loss, fatigue, lethargy, nausea, vomiting, abdominal pain

  • DKA-specific: Kussmaul’s respiration (deep, rapid breathing), fruity/acetone breath odor

  • HHS-specific: Severe dehydration, hypotension, neurologic deficits (confusion, seizure, coma)

  • Hypoglycemia-specific: Sweating, tremor, palpitations, intense hunger, confusion, possible convulsions

  • Other findings: Low GCS, hypotension, tachycardia, poor perfusion

Investigations

  • Blood glucose: Random plasma glucose

  • Urinalysis: Ketones, glucose, protein

  • FBC: Evaluate infection, Hb, WBC

  • U&E, Cr: Electrolytes and renal function

  • LFTs: Rule out hepatic involvement

  • ABG: Metabolic acidosis (DKA)

  • Serum osmolality: Important for HHS

  • Glycosylated Hb (HbA1C): Diabetes control

  • CXR / ECG: Rule out infection, cardiac complications

  • Blood cultures / Urine MCS: If infection suspected

  • Electrocardiogram: Detect hypokalemia/hyperkalemia effects

Management

1. ABC Approach

  • Airway: Assess and protect; intubate if GCS < 8

  • Breathing: Oxygen supplementation as needed

  • Circulation: Establish 2 large-bore IV lines; monitor vitals and perfusion

2. Fluid Resuscitation

  • DKA: 0.9% NaCl 15–20 mL/kg in first hour; then 0.45% NaCl if corrected sodium high

  • HHS: Aggressive isotonic saline (0.9% NaCl) to restore perfusion, followed by 5% dextrose when glucose < 14 mmol/L

3. Insulin Therapy

  • DKA: IV insulin infusion: 0.1 U/kg bolus followed by 0.1 U/kg/hr; continue until acidosis resolves

  • HHS: Insulin started after adequate fluid replacement; lower doses 0.05–0.1 U/kg/hr

4. Electrolyte Management

  • Potassium: Start supplementation if K+ < 5.0 mmol/L; monitor serum K+ every 2–4 hours

  • Other electrolytes: Phosphate, magnesium as needed

5. Treat Underlying Cause

  • Infection (antibiotics)

  • Myocardial infarction

  • Trauma or other precipitating factors

6. Monitoring

  • Hourly glucose, vitals, neurological status

  • Urine output via catheter

  • ABG and electrolytes frequently

7. Hypoglycemia Management

  • Mild: Oral glucose

  • Severe or comatose: 50% dextrose 25–50 mL IV or glucagon 1 mg IM/SC

Complications

  • Cerebral edema (more common in children)

  • Hypokalemia-induced arrhythmias

  • Thrombosis and DVT

  • Acute kidney injury

  • Sepsis

  • Multi-organ failure

Key Points

  • Differentiate DKA vs HHS vs hypoglycemia by history, labs, and clinical features

  • Fluid resuscitation is the cornerstone of DKA/HHS management

  • Monitor electrolytes closely to prevent cardiac complications

  • ICU or high dependency admission recommended for severe cases

  • Address precipitating factors to prevent recurrence

 

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