Myxoedema Coma Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: This is a "can't miss" diagnosis. Although rare, it carries a mortality rate of up to 50%. You will see it in a non-compliant patient with long-standing hypothyroidism who is tipped over by a stressor like sepsis.
High-Yield Definition: "Myxoedema coma is a severe, life-threatening state of decompensated hypothyroidism characterized by an exaggerated form of the typical signs and symptoms of hypothyroidism, including altered mental status, defective thermoregulation, and precipitating illness." (UpToDate, 2024).
Clinical One-Liner: A profoundly hypothyroid patient who is now unconscious, cold, and barely breathing.
II. Etiology & Risk Factors
Etiology: Myxoedema coma is the result of a precipitating event in a patient with severe, untreated or undertreated hypothyroidism. The most common cause of hypothyroidism in Malaysia is post-thyroidectomy or post-radioactive iodine ablation for Grave's disease or thyroid cancer.
Common Precipitants:
Infection: Pneumonia and urosepsis are the most common triggers.
Non-compliance: Abrupt cessation of levothyroxine is a major factor.
Drugs: Sedatives, opioids, lithium, amiodarone.
Systemic Illness: Myocardial infarction, CVA, GI bleed, DKA.
Environmental: Cold exposure.
III. Quick Pathophysiology
The profound lack of thyroid hormone leads to a global metabolic shutdown:
CNS: Decreased cerebral metabolism and blood flow, plus hyponatremia-induced cerebral oedema, leads to progressive lethargy, confusion, and coma.
Cardiovascular: Decreased chronotropy and inotropy cause bradycardia and low cardiac output. Increased systemic vascular resistance occurs initially, but hypotension eventually develops from volume depletion and cardiac failure. Pericardial effusions are common.
Respiratory: Weakness of respiratory muscles and decreased central respiratory drive lead to hypoventilation, hypercapnia, and hypoxia.
Metabolic: Reduced thermogenesis causes profound hypothermia. Hyponatremia (from SIADH-like state) and hypoglycaemia (from impaired gluconeogenesis and possible adrenal insufficiency) are common.
IV. Classification
There is no universally accepted staging system. It is the most severe presentation on the spectrum of hypothyroidism. Diagnosis is clinical, based on the triad of:
Altered mental status (ranging from confusion to coma).
Severe hypothyroidism signs (e.g., hypothermia, bradycardia).
Evidence of a precipitating event.
V. Clinical Assessment
🚩 Red Flags & Immediate Actions
GCS < 8 / Unprotected Airway: Action: Immediate intubation and ventilation. Reason: High risk of aspiration and respiratory arrest.
Systolic BP < 90 mmHg: Action: IV fluid bolus, start vasopressors (Noradrenaline). Reason: Cardiovascular collapse.
Temperature < 32°C: Action: Initiate passive rewarming (warm blankets, warm room). Reason: Severe hypothermia precipitates fatal arrhythmias.
Respiratory Rate < 10 or SpO2 < 90% on high-flow O2: Action: Intubate and ventilate. Reason: Impending respiratory failure.
History (from family/carers)
Key Diagnostic Clues: Known history of hypothyroidism, thyroid surgery, or radioactive iodine treatment. History of non-compliance with levothyroxine is critical. Ask specifically about recent infections, new medications, trauma, or cold exposure.
Preceding Symptoms (chronic history):
Common: Extreme fatigue, weight gain, severe cold intolerance, constipation, cognitive slowing ("brain fog").
Less Common: Hoarseness, hair loss, dry skin, depression.
Physical Examination (OSCE Approach)
General Inspection: Obtunded or comatose. Classic myxoedematous facies: dull, expressionless face, periorbital puffiness, macroglossia, and coarse, sparse hair.
Vitals: The hallmark is the combination of hypothermia, hypotension, bradycardia, and bradypnoea.
Disease-Specific Examination:
Head/Neck: Look for a thyroidectomy scar. Palpate for a goitre.
Cardiovascular: Muffled heart sounds (pericardial effusion), bradycardia.
Respiratory: Slow, shallow respirations. Evidence of pleural effusion (dullness to percussion at bases).
Abdomen: Hypoactive or absent bowel sounds, may suggest paralytic ileus.
Neurological: Depressed level of consciousness. Hyporeflexia with delayed relaxation phase of deep tendon reflexes (Woltman's sign) is classic, but may be absent in coma.
Skin: Cool, pale, dry, and feels "doughy" (non-pitting oedema).
Clinical Pearl: Always check a capillary blood glucose at the bedside. Hypoglycaemia is common and an easily reversible contributor to coma.
VI. Diagnostic Workflow
Differential Diagnosis
Septic Shock:
Points For: Hypotension, altered mental status, hypothermia (can occur in severe sepsis). Often the precipitant.
Points Against: Absence of classic myxoedematous features.
How to Differentiate: Urgent TFT.
Adrenal Crisis:
Points For: Hypotension, hyponatremia, hypoglycaemia, altered mental status.
Points Against: Usually no hypothermia or bradycardia. Look for hyperpigmentation.
How to Differentiate: Random cortisol. Note: We treat empirically for this anyway.
Hypothermic Coma (Environmental):
Points For: Hypothermia, coma, bradycardia.
Points Against: Lack of preceding hypothyroid symptoms or myxoedematous features.
How to Differentiate: History of exposure, normal TFT.
Cerebrovascular Accident (CVA):
Points For: Altered mental status.
Points Against: Usually presents with focal neurological deficits.
How to Differentiate: Urgent CT Brain.
Investigations Plan
Bedside / Initial (First 15 Mins):
ECG: Sinus bradycardia, low voltage QRS complexes, prolonged QT interval, T-wave inversions.
ABG: Hypoxia, hypercapnia (respiratory acidosis), metabolic acidosis.
CBG: Check for hypoglycaemia.
First-Line Labs & Imaging:
Thyroid Function Test (TFT): The key diagnostic test. Expect very high TSH and very low free T4 and T3.
Random Serum Cortisol: Crucial to rule out concurrent primary adrenal insufficiency (Schmidt's syndrome). Send this before giving steroids if possible, but do not delay treatment.
Renal Profile: Hyponatremia, raised creatinine (AKI).
FBC, CK: Anaemia is common. CK is often markedly elevated.
Septic Workup: FBC with differential, blood and urine cultures, CRP.
CXR: May show cardiomegaly (pericardial effusion), pleural effusions, or signs of pneumonia.
Confirmatory: The diagnosis is clinical, supported by TFT results. There is no single "gold standard" test beyond this.
VIII. Management Plan
Admit to ICU. Management is threefold: supportive care, hormone replacement, and treating the precipitant.
A. Principle of Management: Aggressive resuscitation, immediate glucocorticoid and thyroid hormone replacement, and treatment of the underlying cause.
B. Immediate Stabilisation (The ABCDE Plan)
A - Airway: Intubate if GCS ≤ 8 or signs of airway compromise.
B - Breathing: Mechanical ventilation is often required for hypoventilation and respiratory failure.
C - Circulation:
Hypotension: Cautious IV Normal Saline 0.9%. Avoid fluid overload. If refractory, start vasopressors (Noradrenaline).
Bradycardia: Usually responds to thyroxine replacement. Atropine is often ineffective.
D - Disability:
Hypoglycaemia: Correct with IV Dextrose 50%.
Coma: Manage as per standard ICU protocol.
E - Exposure/Environment:
Hypothermia: Use passive rewarming (e.g., warm blankets). Active rewarming can cause peripheral vasodilation and worsen hypotension.
C. Definitive Treatment (The Ward Round Plan)
Glucocorticoids (Give FIRST or concurrently):
Why: To prevent precipitating an adrenal crisis in patients with concurrent adrenal insufficiency.
Dose: IV Hydrocortisone 100 mg STAT, then 100 mg IV every 8 hours.
Thyroid Hormone Replacement:
IV levothyroxine is the ideal formulation but is not readily available in most Malaysian hospitals.
Pragmatic Approach (NG Tube):
Loading Dose: Levothyroxine 200-400 mcg via NG tube STAT.
Maintenance Dose: Levothyroxine 50-100 mcg via NG tube once daily. Start at the lower end in elderly patients or those with known ischemic heart disease.
Treat the Precipitating Cause:
Start empirical broad-spectrum IV antibiotics (e.g., Ceftriaxone) after taking cultures if sepsis is suspected.
D. Long-Term & Discharge Plan
Once the patient is haemodynamically stable and conscious, transition to oral levothyroxine.
Intensive patient and family education on the critical importance of lifelong medication compliance.
Referral to an endocrinologist for long-term follow-up.
IX. Complications
Immediate: Respiratory arrest, cardiovascular collapse, arrhythmias (VT/VF). Action: ICU resuscitation.
Short-Term: Adrenal crisis (if steroids are missed), seizures (from hyponatremia), paralytic ileus, aspiration pneumonia. Action: Monitor electrolytes, neuro-observations, continue supportive care.
Long-Term: Anoxic brain injury and persistent cognitive deficits if coma was prolonged. Action: Early involvement of rehabilitation medicine.
X. Prognosis
Poor. Mortality remains high at 25-50%, even with intensive care.
Negative Prognostic Factors: Advanced age, persistent hypothermia, severity of coma (low GCS on admission), presence of sepsis or concurrent MI.
XI. How to Present to Your Senior
Use the SBAR format. Be clear and concise.
"Dr. [Senior's Name], I am calling from the Emergency Department about Puan [Patient's Name], a 65-year-old female.
(S)ituation: I am concerned she is in myxoedema coma. She presented with a GCS of 6, is hypotensive at 80/50 mmHg, bradycardic at 35 bpm, and her core temperature is 31.5°C.
(B)ackground: She has a history of a total thyroidectomy and is known to be non-compliant with her levothyroxine. Her family reports a 3-day history of productive cough and fever.
(A)ssessment: Her vitals are unstable. Bedside ABG shows acute-on-chronic respiratory acidosis. CBG is 3.1 mmol/L. ECG shows sinus bradycardia with low voltages.
(R)ecommendation: I have initiated resuscitation and have sent urgent TFT, cortisol, and septic workup. I have given IV Hydrocortisone 100 mg. I am preparing to intubate her. I require your urgent review for ICU admission and to proceed with Levothyroxine loading via NG tube."
XII. Summary & Further Reading
Top 3 Takeaways:
Suspect myxoedema coma in any comatose patient who is also bradycardic and hypothermic.
Management priorities are ABCs, IV Hydrocortisone first, then Levothyroxine.
Actively search for and treat the precipitating illness, most commonly sepsis.
Key Resources:
UpToDate: Myxedema coma
Amboss: Myxedema coma
StatPearls: Myxedema Crisis
