Acute Medicine: Electrolytes, acid–base, AKI and metabolic emergencies

• Acid–base: Metabolic Acidosis and the Anion Gap | Metabolic Alkalosis | Working Through Acid–base Problems
• Electrolytes: Hyperkalaemia | Hypokalaemia | Hyponatraemia | Hypernatraemia | Hypercalcaemia | Hypocalcaemia | Magnesium and Phosphate
• Kidneys: Acute Kidney Injury -Definition and Causes | Managing AKI | Rhabdomyolysis
• Metabolic emergencies: Diabetic Ketoacidosis | Hyperosmolar Hyperglycaemic State | Adrenal and Thyroid Emergencies
• Revision: Metabolic Emergencies at a Glance | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🩺 Electrolytes, acid–base, AKI and metabolic emergencies -page 6 of the Acute Medicine and Resuscitation chapter. Abnormal blood results are among the commonest reasons junior doctors are called. Most can wait for the morning -but severe hyperkalaemia, hyponatraemia with seizures, DKA and AKI need action now. Knowing which results are dangerous, how fast to correct them, and how to find the cause is core acute medicine. Detailed physiology is in the Renal and Endocrinology Anatomy, Physiology and Pharmacology chapters; this page covers the acute approach.
Your four questions for every abnormal result: Is it real (haemolysis, drip arm, wrong patient)? Is it dangerous right now -what does the ECG or the patient show? What is the cause (drugs are common)? How fast is it safe to correct?

Metabolic Acidosis and the Anion Gap

• Metabolic acidosis -low pH with low bicarbonate (and negative base excess); compensation by hyperventilation (low PaCO₂ -Kussmaul breathing).
• Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻) -normal about 8–16 mmol/L (some labs include potassium -about 10–20); low albumin lowers the gap (adjust).
• Raised anion gap (extra unmeasured acids):
  • Lactic acidosis -shock, sepsis, hypoxia, ischaemic bowel, seizures, metformin, liver failure, cyanide, CO.
  • Ketoacidosis -DKA, alcoholic ketoacidosis, starvation ketoacidosis, SGLT2 inhibitor-associated (euglycaemic) DKA.
  • Kidney failure (uraemia).
  • Toxins -methanol, ethylene glycol, salicylate, paracetamol (massive -pyroglutamic acid in malnourished), iron, isoniazid.
  • Mnemonic -"MUDPILES" or "GOLDMARK" (Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis).
• Normal anion gap (hyperchloraemic) -loss of bicarbonate or gain of chloride:
  • GI losses -diarrhoea, high-output ileostomy, pancreatic fistula, ureterosigmoidostomy.
  • Renal tubular acidosis (types 1, 2, 4), acetazolamide.
  • Excess 0.9% sodium chloride infusion.
  • Addison's disease (type 4 RTA pattern -high potassium).
• Treatment -treat the cause (fluids, insulin, antibiotics, dialysis, antidotes); sodium bicarbonate only in specific situations (severe acidosis with AKI, certain poisonings, hyperkalaemia, normal anion gap acidosis with bicarbonate loss).

Metabolic Alkalosis

• Metabolic alkalosis -high pH with high bicarbonate; compensation by hypoventilation (raised PaCO₂ -limited).
• Causes:
  • Loss of acid -vomiting, nasogastric suction (hypochloraemic, hypokalaemic alkalosis -e.g. pyloric stenosis in infants).
  • Diuretics (loop and thiazide) -"contraction alkalosis" with hypokalaemia.
  • Mineralocorticoid excess -Conn's syndrome, Cushing's syndrome, liquorice (hypertension, hypokalaemia).
  • Severe hypokalaemia.
  • Bartter and Gitelman syndromes; milk-alkali syndrome (calcium and antacids); excess bicarbonate.
  • Post-hypercapnic -after rapid correction of chronic CO₂ retention (ventilation in COPD).
• Urine chloride helps -low (under 20 mmol/L) in vomiting and past diuretic use (chloride-responsive -give saline and potassium); high in mineralocorticoid excess and current diuretics.
• Features -often none; severe -confusion, arrhythmias, tetany (low ionised calcium), hypoventilation.
• Treatment -treat the cause; 0.9% sodium chloride with potassium for volume and chloride depletion; stop diuretics; potassium-sparing diuretics or treatment of the cause in mineralocorticoid excess.

Working Through Acid–base Problems

Hyperkalaemia

• Severity (UK Kidney Association) -mild 5.5–5.9, moderate 6.0–6.4, severe 6.5 mmol/L or more (or any level with ECG changes).
• Exclude pseudohyperkalaemia -haemolysed sample, delayed processing, very high platelets or white cells, drip arm, fist clenching -repeat urgently (but treat if ECG changes or high risk).
• Causes -AKI and CKD, drugs (ACE inhibitors, ARBs, spironolactone, amiloride, trimethoprim, NSAIDs, potassium supplements, heparin, ciclosporin, digoxin toxicity), acidosis (DKA), tissue breakdown (rhabdomyolysis, tumour lysis, haemolysis, burns, GI bleeding), Addison's disease, missed dialysis.
• ECG changes (may be absent even with severe hyperkalaemia) -tall tented T waves → flattened or absent P waves, prolonged PR → broad QRS → "sine wave" → VF or asystole; also bradycardia and heart block.
• Treatment (severe or ECG changes):
  1. Protect the heart -IV calcium -10% calcium gluconate 30 mL (or 10% calcium chloride 10 mL) over 5–10 minutes; repeat if ECG changes persist (works in minutes; lasts 30–60 minutes; doesn't lower potassium).
  2. Shift potassium into cells -10 units soluble insulin (Actrapid) with 25 g glucose (e.g. 50 mL of 50% or 250 mL of 10%) over 15 minutes -lowers potassium by about 1 mmol/L within 30–60 minutes; monitor glucose for 6 hours (hypoglycaemia is common -give a glucose infusion if pre-treatment glucose is low); nebulised salbutamol 10–20 mg as an adjunct.
  3. Remove potassium from the body -sodium zirconium cyclosilicate or patiromer (potassium binders); treat the cause; dialysis for refractory hyperkalaemia, especially with AKI or ESRD.
  4. Stop contributing drugs; continuous cardiac monitoring; recheck potassium at 1, 2, 4, 6 and 24 hours.
• Sodium bicarbonate -consider only with severe metabolic acidosis (specialist).
• Calcium in digoxin toxicity -traditionally avoided; use DigiFab for digoxin-induced hyperkalaemia.

Hypokalaemia

• Severity -mild 3.0–3.4, moderate 2.5–2.9, severe under 2.5 mmol/L (or symptomatic).
• Causes:
  • GI losses -diarrhoea, vomiting (also via alkalosis), laxative abuse, high-output stoma, villous adenoma.
  • Renal losses -loop and thiazide diuretics (commonest), mineralocorticoid excess (Conn's, Cushing's, liquorice, steroids), hypomagnesaemia, RTA (types 1 and 2), Bartter and Gitelman syndromes, DKA treatment.
  • Shift into cells -insulin, salbutamol (high doses), theophylline, alkalosis, refeeding, thyrotoxic periodic paralysis.
  • Poor intake (with other factors).
• Features -weakness, cramps, constipation and ileus, palpitations and arrhythmias (worse with digoxin and heart disease), rhabdomyolysis (severe).
• ECG -flattened T waves, ST depression, U waves, prolonged QT, arrhythmias (VT, torsades).
• Treatment:
  • Mild -oral potassium (e.g. Sando-K 2 tablets 2–3 times daily) and treat the cause; consider potassium-sparing diuretics.
  • Severe or symptomatic -IV potassium in pre-mixed bags (e.g. 40 mmol KCl in 1 L 0.9% sodium chloride), no faster than 10 mmol/hour peripherally (higher rates only with cardiac monitoring per local policy).
  • Check and replace magnesium -hypokalaemia won't correct until magnesium is normal.
  • Monitor potassium regularly (daily or more often).
• Hypokalaemia with hypertension -think primary hyperaldosteronism (Conn's) -aldosterone/renin ratio.

Hyponatraemia

• The commonest electrolyte disorder in hospital -sodium under 135 mmol/L; severe under 125, or with severe symptoms at any level.
• Symptoms depend on speed and level -nausea, headache, confusion, falls, gait problems (chronic mild); severe -vomiting, seizures, reduced consciousness, cardiorespiratory arrest (acute or very low).
• Assessment:
  1. Exclude pseudohyponatraemia (high lipids or protein) and hyperglycaemia (shifts water -corrected sodium).
  2. Serum osmolality -true hypotonic hyponatraemia under 275 mOsm/kg.
  3. Volume status -hypovolaemic, euvolaemic or hypervolaemic.
  4. Urine osmolality and urine sodium (paired, before treatment if possible).
• Causes:

  Volume	Causes	Urine sodium
  Hypovolaemic	Diuretics (thiazides), vomiting, diarrhoea, Addison's disease, cerebral salt wasting	High (renal losses) or low under 20 (GI losses)
  Euvolaemic	SIADH (pneumonia, lung cancer, CNS disease, pain, nausea, drugs -SSRIs, carbamazepine, PPIs, opioids, cyclophosphamide), hypothyroidism, glucocorticoid deficiency, low solute intake ("tea and toast"), primary polydipsia, beer potomania, MDMA	Usually high (over 30) in SIADH; low in polydipsia and low solute
  Hypervolaemic	Heart failure, cirrhosis, nephrotic syndrome, advanced CKD	Low (unless on diuretics)

• Severe symptoms (seizures, coma, vomiting) -hypertonic saline: 150 mL of 2.7% or 3% sodium chloride over 20 minutes, repeat up to 2–3 times (checking sodium) to raise sodium by about 5 mmol/L -in HDU or ICU with frequent monitoring (European guideline).
• Correction limits -no more than 10 mmol/L in the first 24 hours (and 8 mmol/L in each subsequent 24 hours); 8 mmol/L in 24 hours in high-risk patients (alcohol excess, malnutrition, hypokalaemia, liver disease, sodium under 120) -risk of osmotic demyelination syndrome (dysarthria, dysphagia, quadriparesis, locked-in -days later). If over-correction occurs -relower with 5% glucose and/or desmopressin (specialist).
• Treatment by cause -hypovolaemic: 0.9% sodium chloride (watch for rapid rise as ADH switches off); SIADH: fluid restriction (e.g. 0.5–1 L/day), stop drugs, treat cause, tolvaptan or urea (specialist); hypervolaemic: fluid restriction, treat heart or liver failure; adrenal or thyroid replacement where needed.

Hypernatraemia

• Sodium over 145 mmol/L -almost always a water deficit (losing water or not drinking enough), rarely sodium excess.
• Who -older, frail, confused or immobile people who can't access water; infants; ICU patients; people with diabetes insipidus.
• Causes:
  • Inadequate intake -dementia, delirium, stroke, care home residents, nil by mouth.
  • Water losses -fever, sweating, burns, diarrhoea, osmotic diuresis (hyperglycaemia -HHS), diabetes insipidus (cranial -head injury, pituitary surgery; nephrogenic -lithium, hypercalcaemia, hypokalaemia).
  • Sodium gain (rare) -hypertonic saline or sodium bicarbonate, salt ingestion.
• Features -thirst (if able), confusion, drowsiness, irritability, seizures, coma; high mortality in older inpatients.
• Treatment -replace water -oral water if possible; otherwise IV 5% glucose (or 0.45% saline if also volume-depleted -0.9% saline first if shocked); correct slowly -no more than about 10 mmol/L in 24 hours in chronic hypernatraemia (risk of cerebral oedema); monitor sodium every 4–6 hours initially; treat the cause (desmopressin for cranial DI).

Hypercalcaemia

• Adjusted calcium over 2.6 mmol/L; severe over 3.0–3.5 or symptomatic.
• Causes -primary hyperparathyroidism (commonest in the community; PTH normal or raised) and malignancy (commonest in hospital; PTH suppressed) -together about 90%:
  • Malignancy -PTHrP (squamous cell lung, breast, kidney), bone metastases, myeloma, lymphoma (vitamin D).
  • Others -vitamin D excess, sarcoidosis and granulomatous disease, thiazides, lithium, milk-alkali syndrome, thyrotoxicosis, immobilisation, Addison's disease, familial hypocalciuric hypercalcaemia.
• Features -"bones, stones, groans, thrones and psychiatric overtones" -bone pain, kidney stones, abdominal pain, constipation, nausea, pancreatitis, polyuria and thirst (dehydration), confusion, low mood, drowsiness; short QT, arrhythmias.
• Investigations -PTH (key), U&E, phosphate, ALP, vitamin D, protein electrophoresis, chest X-ray, myeloma screen, PTHrP, imaging for malignancy.
• Acute treatment (severe or symptomatic):
  • IV fluids -0.9% sodium chloride (e.g. 3–4 L over 24 hours, adjusted for heart and kidney function) -the most important step.
  • IV bisphosphonate after rehydration -zoledronic acid 4 mg (or pamidronate) -works over 2–4 days; adjust in kidney impairment.
  • Stop thiazides, calcium and vitamin D supplements, lithium.
  • Others -denosumab (refractory or kidney failure), calcitonin (short-term), steroids (granulomatous disease, lymphoma, vitamin D toxicity), cinacalcet (parathyroid causes), dialysis (severe with kidney failure).

Hypocalcaemia

• Adjusted calcium under 2.2 mmol/L; severe under 1.9 or symptomatic. Check albumin (adjusted calcium) or ionised calcium on a blood gas.
• Causes -vitamin D deficiency, CKD, hypoparathyroidism (after thyroid or parathyroid surgery, autoimmune, hungry bone syndrome), hypomagnesaemia (PPIs, alcohol, diuretics), acute pancreatitis, rhabdomyolysis, tumour lysis, massive transfusion (citrate), drugs (bisphosphonates, denosumab, cinacalcet, foscarnet), sepsis, alkalosis (low ionised calcium).
• Features -perioral and peripheral tingling, muscle cramps, tetany, Trousseau's sign (carpal spasm with BP cuff), Chvostek's sign (facial twitch), laryngospasm, seizures, prolonged QT, arrhythmias, heart failure; chronic -cataracts, basal ganglia calcification.
• Treatment:
  • Severe or symptomatic -IV calcium gluconate 10% -10–20 mL in 50–100 mL of 5% glucose over 10 minutes with ECG monitoring, then an infusion (e.g. 100 mL of 10% calcium gluconate in 1 L over 24 hours, adjusted to levels) (Society for Endocrinology).
  • Correct magnesium first or at the same time (PTH needs magnesium).
  • Mild -oral calcium and vitamin D (colecalciferol for deficiency; alfacalcidol or calcitriol in hypoparathyroidism and CKD).
  • Avoid IV calcium extravasation (tissue necrosis) -use a large vein; don't mix with bicarbonate (precipitates).

Magnesium and Phosphate

• Hypomagnesaemia (under 0.7 mmol/L; severe under 0.4):
  • Causes -PPIs (long-term), diuretics, alcohol, diarrhoea, high-output stoma, malnutrition, refeeding, aminoglycosides, ciclosporin and tacrolimus, cisplatin.
  • Features -tremor, tetany, seizures, arrhythmias (torsades), refractory hypokalaemia and hypocalcaemia.
  • Treatment -oral magnesium (diarrhoea) for mild; IV magnesium sulfate (e.g. 20 mmol over 4–12 hours; 8 mmol (2 g) over 10–15 minutes for torsades or seizures); stop or switch PPI.
• Hypermagnesaemia -usually kidney failure plus magnesium-containing laxatives or antacids, or magnesium treatment in pre-eclampsia -loss of reflexes, weakness, hypotension, respiratory depression, heart block -stop magnesium; IV calcium gluconate; dialysis.
• Hypophosphataemia (under 0.8; severe under 0.3):
  • Causes -refeeding syndrome, alcohol, DKA treatment, malnutrition, vitamin D deficiency, hyperparathyroidism, IV iron (ferric carboxymaltose), respiratory alkalosis.
  • Features -weakness (including respiratory muscles -failure to wean), confusion, haemolysis, heart failure, rhabdomyolysis.
  • Treatment -oral (Phosphate Sandoz) or IV phosphate for severe or symptomatic (careful in kidney impairment); prevent refeeding syndrome (slow feeding, thiamine, monitor).
• Hyperphosphataemia -CKD, tumour lysis, rhabdomyolysis -phosphate binders; dialysis.

Acute Kidney Injury -Definition and Causes

• AKI -a rapid fall in kidney function (KDIGO):

  Stage	Serum creatinine	Urine output
  1	Rise of 26.5 µmol/L or more within 48 hours, or 1.5–1.9 times baseline (within 7 days)	Under 0.5 mL/kg/hour for 6–12 hours
  2	2.0–2.9 times baseline	Under 0.5 mL/kg/hour for 12 hours or more
  3	3 times baseline or more, or creatinine 354 µmol/L or more, or starting renal replacement therapy	Under 0.3 mL/kg/hour for 24 hours or more, or anuria for 12 hours

• Causes:
  • Pre-renal (commonest) -hypovolaemia (dehydration, bleeding), sepsis, hypotension, heart failure, cirrhosis (hepatorenal), drugs (NSAIDs, ACE inhibitors, ARBs, diuretics).
  • Intrinsic (renal) -acute tubular necrosis (prolonged hypoperfusion, sepsis, nephrotoxins -aminoglycosides, contrast, rhabdomyolysis), glomerulonephritis (vasculitis, anti-GBM, lupus -blood and protein on dipstick), acute interstitial nephritis (drugs -PPIs, NSAIDs, antibiotics), myeloma, thrombotic microangiopathy (HUS, TTP), malignant hypertension.
  • Post-renal (obstruction) -prostatic enlargement, urinary retention (anticholinergics, constipation), stones, pelvic tumours, retroperitoneal fibrosis, blocked catheter.
• Risk factors -older age, CKD, diabetes, heart failure, liver disease, sepsis, nephrotoxic drugs, contrast, major surgery.

Managing AKI

• Assess (NICE NG148):
  • Volume status (dehydrated, euvolaemic, overloaded), BP, urine output (catheter in severe AKI).
  • Drug review -stop nephrotoxins and drugs that accumulate (see the Clinical Pharmacology chapter).
  • Urine dipstick -blood and protein suggest glomerular disease (send urine PCR, consider ANCA, anti-GBM, ANA, complement, immunoglobulins -urgent nephrology).
  • Bloods -U&E, potassium, bicarbonate (blood gas), calcium, phosphate, FBC, CK (rhabdomyolysis), LFTs.
  • Renal tract ultrasound within 24 hours if obstruction is suspected, or the cause is unclear (within 6 hours if infected obstructed kidney suspected -pyonephrosis).
• Treat:
  • Fluids if hypovolaemic (500 mL boluses with reassessment); avoid overload.
  • Treat sepsis and the cause.
  • Relieve obstruction -catheter (watch for post-obstructive diuresis), nephrostomy or stent.
  • Manage complications -hyperkalaemia, acidosis, fluid overload.
  • Monitor -daily U&E, fluid balance, weights.
• Indications for urgent renal replacement therapy (dialysis or haemofiltration) -"AEIOU":
  • Acidosis -severe metabolic acidosis (pH under 7.15–7.2) not responding to treatment.
  • Electrolytes -refractory hyperkalaemia.
  • Intoxication -dialysable poisons (lithium, methanol, ethylene glycol, salicylate).
  • Overload -fluid overload (pulmonary oedema) not responding to diuretics.
  • Uraemia -encephalopathy, pericarditis, bleeding.
• Refer to nephrology -stage 3 AKI, suspected glomerular disease or intrinsic cause, AKI not responding to treatment, complications, kidney transplant or CKD stage 4–5.
• After AKI -follow up kidney function (risk of CKD), restart withheld drugs carefully, sick day rule advice.

Rhabdomyolysis

• Muscle breakdown releasing myoglobin, potassium, phosphate and CK.
• Causes -long lie after falls, crush injury, prolonged seizures, extreme exercise, hyperthermia (heat stroke, NMS, serotonin syndrome, MDMA), drugs and toxins (statins -especially with fibrates or clarithromycin, cocaine, amphetamines, alcohol, antipsychotics), infections (influenza), hypokalaemia and hypophosphataemia, compartment syndrome, inherited myopathies.
• Features -muscle pain, weakness, swelling, dark ("cola") urine; may be asymptomatic.
• Tests -CK (over 5 times normal; often over 10,000 in significant cases), urine dipstick positive for blood without red cells on microscopy (myoglobin), U&E (AKI), potassium (high), phosphate (high), calcium (low early, high in recovery), LFTs.
• Complications -AKI, hyperkalaemia (arrhythmias), compartment syndrome, DIC.
• Treatment -aggressive IV fluids (crystalloid) aiming for a high urine output (e.g. 200–300 mL/hour -over 1–2 mL/kg/hour) while avoiding overload; treat hyperkalaemia; avoid nephrotoxins; stop causative drugs; check compartments (fasciotomy); dialysis if severe AKI. Bicarbonate and mannitol are not routinely recommended.

Diabetic Ketoacidosis

• Diagnosis (JBDS):
  • Ketonaemia -blood ketones 3.0 mmol/L or more (or urine ketones 2+ or more).
  • Blood glucose over 11 mmol/L or known diabetes (euglycaemic DKA occurs with SGLT2 inhibitors, pregnancy, starvation).
  • Acidosis -venous pH under 7.3 and/or bicarbonate under 15 mmol/L.
• Triggers -new type 1 diabetes, missed insulin, infection, MI, surgery, pancreatitis, SGLT2 inhibitors, steroids, alcohol, pregnancy.
• Features -polyuria, thirst, vomiting, abdominal pain, Kussmaul breathing, ketotic breath, dehydration, drowsiness.
• Treatment (follow local DKA protocol):
  • Fluids -0.9% sodium chloride (e.g. 1 L in the first hour, then reducing rates; 500 mL bolus if systolic under 90); care in young adults, older people, pregnancy, heart or kidney failure.
  • Fixed-rate IV insulin infusion -0.1 units/kg/hour (soluble insulin); continue long-acting basal insulin.
  • Potassium -add to fluids according to levels (none if over 5.5; 40 mmol/L if 3.5–5.5; senior review if under 3.5 -insulin will lower potassium).
  • Add 10% glucose (e.g. at 125 mL/hour) when glucose falls below 14 mmol/L, continuing insulin until ketones clear.
  • Monitor -hourly glucose and ketones; venous gas (pH, bicarbonate, potassium) at 1, 2 and 4 hours, then every 4 hours; aim for ketones to fall by at least 0.5 mmol/L/hour.
  • Resolution -ketones under 0.6 and pH over 7.3 -switch to subcutaneous insulin with a meal (stop IV 30–60 minutes after).
• Complications -hypokalaemia, hypoglycaemia, cerebral oedema (children and young adults -headache, falling GCS), aspiration, VTE, ARDS.
• Severe DKA (ketones over 6, pH under 7.0, bicarbonate under 5, potassium abnormal, GCS under 12, hypotension) -HDU or ICU.
• Involve the diabetes team; education before discharge (sick day rules, ketone testing).

Hyperosmolar Hyperglycaemic State

• HHS -severe hyperglycaemia and dehydration without significant ketoacidosis, usually in older people with type 2 diabetes (may be the first presentation); develops over days; higher mortality than DKA.
• Features (JBDS) -marked hyperglycaemia (30 mmol/L or more), hypovolaemia, high osmolality (320 mOsm/kg or more -calculated as 2Na + glucose + urea), ketones under 3, pH over 7.3; confusion, drowsiness, seizures, focal signs.
• Triggers -infection, MI, stroke, drugs (steroids, thiazides), poor fluid intake.
• Treatment:
  • IV 0.9% sodium chloride -the main treatment -replace fluid gradually over 24–48 hours (fluid deficits are large -100–200 mL/kg).
  • Insulin only if ketones are raised (over 1) or glucose stops falling with fluids -low-dose fixed-rate insulin 0.05 units/kg/hour.
  • Aim for slow falls -glucose by up to 5 mmol/L/hour; sodium by no more than 10 mmol/L in 24 hours; osmolality by 3–8 mOsm/kg/hour.
  • VTE prophylaxis (high thrombosis risk), foot care, monitor potassium and kidney function, treat the cause.
• Sodium may rise initially as glucose falls -acceptable if osmolality is falling.

Adrenal and Thyroid Emergencies

• Adrenal crisis:
  • In people with Addison's disease, hypopituitarism, or long-term steroid use (stopped suddenly, missed doses, or intercurrent illness without dose increase).
  • Features -vomiting, abdominal pain, weakness, confusion, hypotension and shock, hyponatraemia, hyperkalaemia (primary), hypoglycaemia.
  • Treatment -IV or IM hydrocortisone 100 mg immediately, then 200 mg over 24 hours (continuous infusion or 50 mg 6-hourly); IV 0.9% sodium chloride (1 L over the first hour); glucose; treat the trigger; don't delay treatment for tests (take a cortisol sample first if possible).
• Thyroid storm (thyrotoxic crisis):
  • Triggered by infection, surgery, iodine, stopping antithyroid drugs, childbirth.
  • Fever, tachycardia (AF), heart failure, agitation, delirium, vomiting and diarrhoea, jaundice.
  • Treatment -propranolol (or esmolol), propylthiouracil or carbimazole, Lugol's iodine (at least 1 hour after the antithyroid drug), hydrocortisone, supportive care (cooling, fluids), treat the trigger; critical care.
• Myxoedema coma (severe hypothyroidism):
  • Older people, often triggered by infection, cold, sedatives -hypothermia, bradycardia, hypotension, hypoventilation, hyponatraemia, hypoglycaemia, reduced consciousness.
  • Treatment -IV hydrocortisone first (possible coexisting adrenal insufficiency), then thyroid hormone (IV liothyronine or levothyroxine, cautiously), passive rewarming, ventilatory support, treat infection.
• Pituitary apoplexy -sudden headache, visual loss, ophthalmoplegia -hydrocortisone, neurosurgery (see page 5).
• See the Endocrinology Emergencies chapter for detail.

Metabolic Emergencies at a Glance