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In the ICU, endocrine emergencies rarely announce themselves clearly. They often sit quietly behind hypotension, altered sensorium, or shock that does not respond the way you expect. For residents, the danger is not lack of knowledge, but doing the right treatment in the wrong order.
These clinical scenarios highlight the decisions that truly matter in real-life ICU practice.
Myxedema Coma: Steroids Always Come First
A 72-year-old woman is brought to the ICU during peak winter after being found unresponsive at home. She has a known history of hypothyroidism but stopped her medications months ago. On examination, she is hypothermic, hypotensive, bradycardic, and drowsy. Her skin is dry and puffy, her reflexes are delayed, and ECG shows sinus bradycardia with low-voltage complexes. Laboratory tests reveal hyponatremia, hypoglycemia, very high TSH, and low free T4.
This presentation fits myxedema coma, a rare but fatal form of decompensated hypothyroidism.
The most important step here is often missed in emergencies:
IV hydrocortisone must be given before thyroid hormone replacement.
Adrenal insufficiency commonly coexists in these patients, especially in autoimmune thyroid disease or pituitary disorders. If thyroid hormone is given without steroid coverage, it can increase metabolic demand and precipitate an adrenal crisis.
Practical approach
- Start IV hydrocortisone 100 mg immediately, then continue every 8 hours
- Follow with IV levothyroxine (loading dose 200–400 µg)
- Avoid T3 boluses due to arrhythmia risk
- Provide supportive care with cautious rewarming, fluids, ventilatory support, and vasopressors if needed
Clinical reminder: Never give thyroid hormone alone in suspected myxedema coma.
Thyroid Storm: Sequence Is Everything
A 36-year-old woman with untreated Graves’ disease presents with high fever, agitation, vomiting, delirium, and severe tachycardia. ECG shows atrial fibrillation with a rapid ventricular response. Her TSH is suppressed, and free T4 is markedly elevated.
This is a classic thyroid storm, and survival depends on correct sequencing of therapy.
The most critical rule:
Iodine should never be given before antithyroid drugs.
Giving iodine too early provides substrate for new hormone synthesis, worsening thyrotoxicosis (Jod-Basedow effect).
Correct treatment order
- Beta-blocker (propranolol) to control adrenergic symptoms
- Propylthiouracil (PTU) to block hormone synthesis and T4-to-T3 conversion
- Iodine solution (only after at least 1 hour of PTU)
- Hydrocortisone for adrenal support and additional T3 suppression
Reversing this order can rapidly worsen the patient’s condition.
Adrenal Crisis in Septic Shock: Treat First, Test Later
A 48-year-old man on long-term oral prednisone is admitted with septic shock due to pneumonia. Despite adequate fluids and high-dose vasopressors, his blood pressure remains low. Random cortisol is low.
This scenario strongly suggests adrenal crisis due to HPA axis suppression.
Waiting for ACTH stimulation tests or repeat cortisol levels is dangerous. These tests are unreliable during critical illness and delay life-saving treatment.
What should be done
- Give IV hydrocortisone 100 mg stat
- Continue with 50 mg every 6 hours or continuous infusion
- Hydrocortisone is preferred because it provides both glucocorticoid and mineralocorticoid effects
Golden ICU rule: Never delay steroids in shock unresponsive to fluids and vasopressors.
Diabetic Ketoacidosis: Fluids Before Insulin
A young woman with type 1 diabetes presents with Kussmaul breathing, abdominal pain, hypotension, and altered mental status. Labs show severe hyperglycemia, metabolic acidosis, and ketonemia.
The instinct to start insulin immediately is common—but incorrect.
The primary problem in DKA is severe dehydration due to osmotic diuresis.
First step
- Give 1 litre of isotonic saline immediately
This restores circulation, improves renal perfusion, and starts correcting hyperglycemia even before insulin.
Only after hemodynamic stabilization should insulin be started. Potassium must always be checked beforehand, as insulin drives potassium intracellularly. Bicarbonate is reserved for extreme acidosis (pH < 6.9) with cardiovascular compromise.
Key takeaway: In DKA, fluids save lives before insulin does.
HHS: Correct Slowly or Pay the Price
An elderly man with type 2 diabetes presents with confusion. His glucose is extremely high, sodium is elevated, osmolality is high, but there are no ketones and pH is near normal.
This is hyperosmolar hyperglycemic state (HHS).
Unlike DKA, mortality in HHS is higher, largely due to cerebral edema or circulatory collapse caused by rapid correction.
Management principle
- Gradual rehydration is the cornerstone
Start with isotonic saline to restore volume, then switch to hypotonic fluids based on corrected sodium and osmolality. Glucose should fall slowly—about 50–75 mg/dL per hour. Insulin is added only after partial volume correction.
Remember: Rapid shifts in osmolality are more dangerous than hyperglycemia itself.
Hypoglycemia in the Sedated ICU Patient
A ventilated patient on sedation and insulin infusion develops hypotension and sluggish pupils. Capillary glucose is found to be dangerously low.
In sedated or paralyzed patients, classic adrenergic signs of hypoglycemia may be absent.
The most reliable early indicator in such cases is a sudden fall in EEG activity, not sweating or tachycardia.
Clinical lesson: Always suspect hypoglycemia in unexplained neurological or hemodynamic deterioration in ICU patients.
Final Words
Endocrine emergencies are about priorities and order, not just diagnosis.
Steroids before thyroid hormone.
PTU before iodine.
Fluids before insulin.
Treatment before testing.
Getting these steps right often makes the difference between recovery and collapse.
