Hyperkalaemia = K⁺ > 5.5 mEq/L (mild 5.5–6.0; moderate 6.0–6.5; severe > 6.5 → life-threatening ). K⁺ is predominantly intracellular → small changes in serum K⁺ reflect large total body shifts.

• Causes: ↓ Renal excretion (CKD/AKI #1; drugs — ACEi/ARB, spironolactone, NSAIDs, trimethoprim; Addison's ); Shift from ICF to ECF (metabolic acidosis; DKA; beta-blockers; rhabdomyolysis; haemolysis; tumour lysis syndrome ); ↑ intake (IV K⁺ rapid infusion; massive blood transfusion)
• ECG changes (in order of severity): Tall peaked T-waves (first sign) → ↑ PR interval → wide QRS → sine wave pattern → VF → asystole

• Causes in full: decreased renal excretion (AKI, CKD, Addisons disease, type IV RTA, drugs: ACE-i, ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, heparin); shift out of cells (acidosis, rhabdomyolysis, massive haemolysis, insulin deficiency, beta-blockade, succinylcholine); excess intake (rarely alone, usually with reduced excretion).
• Clinical features: muscle weakness (ascending, can lead to flaccid paralysis); palpitations; ECG changes in order - peaked T waves, widening PR, wide QRS, sine wave pattern, ventricular fibrillation; hyperkalaemia itself causes few symptoms until levels are very high.
• Monitoring response: repeat ECG and electrolytes 1 h after treatment; recheck potassium every 2-4 h; treat underlying cause to prevent recurrence; restrict dietary potassium and review drugs.

Hypokalaemia = K⁺ < 3.5 mEq/L (mild 3.0–3.5; moderate 2.5–3.0; severe < 2.5 mEq/L).

• Causes: GI losses — vomiting (metabolic alkalosis + ↓ Cl⁻ → ↑ aldosterone → ↑ K⁺ loss in urine); diarrhoea (#1 cause globally; K⁺ lost in stool); laxatives; NG suction. Renal losses — Diuretics (thiazide + loop diuretics most common drug cause ); Conn's syndrome; Cushing's; RTA type 1 and 2; Bartter's/Gitelman's syndrome; Hypomagnesaemia (↑ K⁺ excretion; correct Mg before K⁺ ). ECF→ICF shift: Insulin; alkalosis; beta-2 agonists; refeeding syndrome; thyrotoxic periodic paralysis
• Clinical: Muscle weakness (proximal; ascending; respiratory failure in severe ); Paralytic ileus (gut smooth muscle); cramps; ECG changes: flat/inverted T-waves + U-waves (hallmark) + ST depression + QTc prolongation → VF risk; nephrogenic DI (polyuria, polydipsia); metabolic alkalosis (K⁺ shifts into cells, H⁺ leaves cells)

▶ Oral KCl — 40–100 mEq/day in divided doses (Slow-K; Syrup KCl); first-line if oral route available

▶ IV KCl — for moderate-severe or unable to take oral; max rate 10–20 mEq/hr (faster causes cardiac arrhythmia ); never undiluted IV bolus (cardiac arrest); central line for > 40 mEq/L concentrations; continuous ECG monitoring

• Correct hypomagnesaemia FIRST — without adequate Mg²⁺, K⁺ replacement is ineffective (Mg²⁺ needed for K⁺ repletion)
• ECG changes: flattening and inversion of T waves, prominent U wave (after T wave in precordial leads, particularly V2-V3), PR prolongation, ST depression; severe hypokalaemia can cause ventricular tachycardia and torsades de pointes.
• Special situations: Conn syndrome (primary hyperaldosteronism) - hypokalaemia with HTN and suppressed renin; Bartter/Gitelman syndrome - hypokalaemia with metabolic alkalosis and normal BP; diarrhoea - hypokalaemia with metabolic acidosis and low urine potassium.
• Monitoring: check potassium 4-6 h after replacement; recheck magnesium; ECG monitoring when IV replacement at rates > 10 mEq/h; never use peripheral IV for concentrations > 40 mEq/L.

Hyponatraemia = Na⁺ < 135 mEq/L (mild 130–135; moderate 125–130; severe < 125 mEq/L). Most common electrolyte disorder.

• Symptoms: Mild (nausea, headache); moderate (confusion, lethargy); severe (seizures, coma, respiratory arrest) — correlate with rapidity of fall more than absolute level
• OSMOTIC DEMYELINATION SYNDROME (ODS/CPM) — most feared complication of TREATMENT; occurs if chronic hyponatraemia (> 48 hrs) corrected too rapidly → pontine + extrapontine demyelination → locked-in syndrome, quadriplegia, death ; prevent by correcting Na at < 8–10 mEq/L per 24 hours (< 10–12 mEq/L per 24 hrs for severe chronic)

▶ Acute severe (< 48 hrs) with symptoms: IV 3% NaCl 100 mL over 10 min → repeat × 2 if needed → target 5 mEq/L rise in Na over 1 hr (for seizures/coma) → then slow correction < 10 mEq/L per 24 hrs

▶ Chronic hyponatraemia: Fluid restriction (SIADH — 500–800 mL/day); Tolvaptan (V2-receptor antagonist; aquaretic; for SIADH/CCF/cirrhosis); 0.9% NaCl + furosemide (for SIADH); Treat underlying cause

• Pathophysiology of SIADH: euvolaemic hyponatraemia from inappropriately high ADH secretion despite low osmolality; causes - CNS disease (stroke, SAH, meningitis, head injury), pulmonary (pneumonia, TB, mechanical ventilation), drugs (carbamazepine, SSRIs, antipsychotics, cyclophosphamide, vincristine), ectopic ADH (SCLC - most common malignant cause).
• Diagnostic criteria for SIADH: low serum osmolality (< 275 mOsm/kg), concentrated urine (osmolality > 100, usually > 300 mOsm/kg), urine sodium > 40 mEq/L, clinically euvolaemic, normal thyroid and adrenal function, no diuretics.
• ODS prevention: in chronic hyponatraemia (> 48 h), correct Na by no more than 8-10 mEq/L in 24 h; if sodium rises too fast, give 5% dextrose and DDAVP to re-lower it.

• Metabolic acidosis: pH < 7.35 + HCO3- < 22 mEq/L; compensation: ↓ PaCO2 (Kussmaul breathing )
• Anion gap (AG) = Na - (Cl + HCO3) ; normal 8–12 mEq/L
• High AG causes (MUDPILES ): Methanol; Uraemia; DKA; Propylene glycol; INH; Lactic acidosis; Ethylene glycol; Salicylates
• Normal AG (hyperchloraemic) causes (HARDUP ): Diarrhoea (#1 in India); RTA; Acetazolamide; Ureteral diversion
• Delta-delta ratio: (AG-12)/(24-HCO3); if > 2 = pure high AG with metabolic alkalosis; < 1 = mixed high AG + normal AG metabolic acidosis
• Compensation: Winters formula - expected PaCO2 = 1.5 x HCO3 + 8 ± 2; if actual PaCO2 is lower than expected, there is an additional respiratory alkalosis; if higher, there is an additional respiratory acidosis.
• Clinical approach: calculate anion gap; if high, use the delta-delta ratio to find mixed disorders; check urine anion gap (positive in RTA, negative in diarrhoea) for normal anion gap metabolic acidosis.
• Key causes with treatment: DKA - insulin and fluids; lactic acidosis - treat the underlying cause (restore perfusion); salicylate poisoning - urinary alkalinisation and haemodialysis; methanol/ethylene glycol - fomepizole; uraemia - haemodialysis.
• Recognising mixed disorders: if a patient has a high AG acidosis but the bicarbonate is not as low as expected from the AG rise, there is a co-existing metabolic alkalosis (e.g. vomiting + DKA); if the bicarbonate is much lower than expected, there is a co-existing normal AG acidosis; use the delta-delta ratio to identify these.
• Lactic acidosis: type A (tissue hypoperfusion - shock, severe sepsis, cardiac arrest) is most common; treat by restoring oxygen delivery; type B (no hypoperfusion - metformin especially in AKI, thiamine deficiency, nucleoside analogues, liver failure, malignancy); lactate > 10 mmol/L carries high mortality.

Hypercalcaemia = serum Ca > 2.65 mmol/L (10.5 mg/dL) (correct for albumin: add 0.2 mmol/L for every 10 g/L fall in albumin below 40 g/L ).

• Causes (90% from hyperPTH + malignancy): Primary hyperparathyroidism (#1 cause outpatients — solitary parathyroid adenoma 85%); Malignancy (#1 cause inpatients — PTHrP [humoral hypercalcaemia of malignancy — squamous lung, breast, renal]; lytic bone mets [MM, breast]); Sarcoidosis (↑ 1-OH of vit D by macrophages); Vit D toxicity; Granulomas (TB ); Milk-alkali syndrome; Thiazide diuretics; Lithium; Immobilisation
• Clinical — 'Bones, Stones, Groans, Psychic Moans':

• Bones: Osteitis fibrosa cystica; subperiosteal resorption; Brown tumours; bone pain
• Stones: Renal calculi (Ca oxalate); nephrocalcinosis; polyuria (nephrogenic DI)
• Groans: Nausea; vomiting; constipation; anorexia; peptic ulcer; pancreatitis
• Psychic moans: Depression; confusion; drowsiness; coma (severe > 3.5 mmol/L)

• ECG: Short QTc (shortened ST segment); bradycardia; heart block

▶ Acute severe hypercalcaemia (> 3.0 mmol/L):
IV 0.9% NaCl 200–500 mL/hr (volume expansion + ↑ renal Ca excretion — FIRST )
IV Furosemide 40 mg (ONLY after adequate rehydration — ↑ calciuresis)
IV Zoledronic acid 4 mg over 15 min (bisphosphonate — inhibits osteoclasts; onset 48–72 hrs; sustained effect; drug of choice for malignancy-related )
IV Pamidronate 60–90 mg if zolendronate unavailable
Calcitonin 4 units/kg SC q12h (rapid onset — 4 hrs; tachyphylaxis after 24–48 hrs )
Dialysis (refractory/severe + CKD)

• Investigations: corrected calcium, albumin, PTH (high in hyperparathyroidism, suppressed in malignancy), PTHrP (raised in humoral hypercalcaemia of malignancy), 25-OH and 1,25-OH vitamin D, ACE level (sarcoidosis), serum and urine protein electrophoresis (myeloma), ECG (short QT).
• Management detail: IV saline 200-500 mL/h to promote calciuresis (IV fluids alone often bring calcium down significantly); bisphosphonate (zoledronic acid or pamidronate) acts within 2-4 days and is the cornerstone for malignancy-related hypercalcaemia; cinacalcet for hyperparathyroidism if surgery not possible; steroids for sarcoidosis/vitamin D toxicity.

Hypocalcaemia = corrected serum Ca < 2.12 mmol/L (8.5 mg/dL) . Ionised Ca < 1.17 mmol/L.

• Causes: Hypoparathyroidism (#1 — post-thyroidectomy/parathyroidectomy; autoimmune; rare congenital); Vitamin D deficiency (most common globally — dietary/sunlight/malabsorption); Hypomagnesaemia (impairs PTH secretion + action); CKD/ESRD (↓ 1-OH of vit D + ↑ phosphate); Hungry bone syndrome (post-parathyroidectomy — bones rapidly remineralise after surgery → severe hypocalcaemia ); Acute pancreatitis (saponification); Rhabdomyolysis; Sepsis; ↑ phosphate
• Clinical: Tetany (Trousseau's + Chvostek's ); circumoral/acral paraesthesia; laryngospasm (life-threatening); bronchospasm; seizures; Prolonged QTc → TdP/VF ; papilloedema; cataracts (chronic hypoparathyroidism ); basal ganglia calcification (Fahr's disease in chronic )
• ECG: Prolonged QT → Torsades de Pointes (potentially fatal) — MOST IMPORTANT COMPLICATION

▶ Symptomatic/acute: IV Calcium gluconate 10% 10–20 mL (2.25–4.5 mmol Ca) over 10 min; cardiac monitoring (may cause arrhythmia if too fast); then IV Ca infusion (10% calcium gluconate 50 mL + 500 mL 5% dextrose × 6–12 hrs) until oral Ca tolerated

▶ Maintenance/chronic: Oral calcium carbonate 1–2 g elemental Ca/day + Alfacalcidol/Calcitriol (1-OH or 1,25-(OH)₂ vit D — bypasses absent PTH-mediated 1-hydroxylation in hypoparathyroidism ); correct hypomagnesaemia first

• Investigations: corrected serum calcium, albumin, phosphate, magnesium, PTH, vitamin D (25-OH and 1,25-OH), renal function, ECG (prolonged QT).
• Causes in detail: hypoparathyroidism (post-surgical - most common, autoimmune, familial); vitamin D deficiency (dietary, malabsorption, lack of sunlight, CKD); hypomagnesaemia (prevents PTH secretion and action); pancreatitis (saponification); blood transfusion with citrate; hungry bone syndrome after parathyroidectomy.
• Complications: prolonged QT leading to torsades de pointes, laryngospasm, seizures and neuropsychiatric symptoms; long-term - cataracts and basal ganglia calcification in chronic hypoparathyroidism.

Shock = state of acute circulatory failure resulting in inadequate tissue perfusion and oxygenation → cellular hypoxia → organ dysfunction. NOT simply hypotension.

• Pathophysiology: all shock types share a final common pathway of cellular hypoxia; compensatory mechanisms (tachycardia, vasoconstriction, redistribution) initially maintain MAP but eventually fail; cellular hypoxia leads to anaerobic metabolism, lactic acidosis and multi-organ failure.
• Recognition: tachycardia, hypotension (MAP < 65), oliguria (< 0.5 mL/kg/h), altered consciousness, raised lactate (> 2 mmol/L in septic shock); SOFA score assesses organ dysfunction.
• Septic shock management: Surviving Sepsis Campaign bundles - within 1 hour: blood cultures (before antibiotics), broad-spectrum antibiotics, 30 mL/kg IV crystalloid for hypoperfusion, vasopressors (noradrenaline, target MAP >= 65), check lactate; reassess fluid responsiveness with dynamic measures.

• Enteral vs parenteral: enteral nutrition (EN) via the gut is always preferred; maintains gut mucosal integrity and prevents bacterial translocation; check tube position before each feed; complications of EN include aspiration pneumonia (most common), diarrhoea, and tube displacement.
• Micronutrient deficiencies: thiamine deficiency (Wernicke encephalopathy - always give thiamine before glucose), vitamin B12 (subacute combined degeneration), vitamin C (scurvy - perifollicular haemorrhages, bleeding gums, corkscrew hairs), vitamin K (bleeding, prolonged PT), zinc (poor wound healing, dysgeusia, skin rash).

ENTERAL NUTRITION

• Enteral nutrition (EN) = delivery of nutrients via GI tract (oral/NGT/PEG/PEJ) — ALWAYS preferred over parenteral (maintains gut mucosa integrity; prevents bacterial translocation; cheaper; safer; more physiological)
• Indications: Patients with functional GI tract who cannot eat adequately: coma/neurological (stroke ); head/neck cancer; burns; sepsis (early EN within 48 hrs of ICU admission improves outcomes); post-surgical malnutrition; Crohn's disease (remission induction in children )
• Nasogastric tube (NGT) — for short-term (< 4–6 weeks ); nasojejunal (NJ) if gastroparesis/aspiration risk; PEG (Percutaneous Endoscopic Gastrostomy) for long-term (> 4–6 weeks )
• Complications of EN: Aspiration pneumonia (most common) → confirm tube position before feeding; elevate head 30–45°; diarrhoea (osmotic; infection; formula intolerance); electrolyte disturbances; refeeding syndrome (with malnourished patients)

NUTRITIONAL POLYNEUROPATHY

• B12 deficiency causes: Pernicious anaemia (anti-IF Ab; autoimmune); veganism (dietary); gastrectomy; terminal ileal disease (Crohn's, ileal resection); metformin; bacterial overgrowth; SIBO
• Clinical: Megaloblastic anaemia + neurological (SACD ) + psychiatric; glossitis
• Subacute combined degeneration (SACD): demyelination of the dorsal columns (proprioception, vibration) and lateral corticospinal tracts (UMN signs); the combination of sensory ataxia (positive Romberg) with spastic weakness and extensor plantars is characteristic; peripheral neuropathy may also be present.
• Investigations: low serum B12 (< 200 pg/mL), raised MCV, hypersegmented neutrophils, raised LDH and indirect bilirubin (intramedullary haemolysis); anti-intrinsic factor and anti-parietal-cell antibodies for pernicious anaemia; Schilling test (now rarely used) distinguished absorption from dietary deficiency.
• Treatment: hydroxocobalamin 1 mg IM daily for 7 days then every 3 months (lifelong if pernicious anaemia or ileal disease); oral cyanocobalamin 1000 mcg daily is effective for dietary deficiency; ALWAYS give B12 before folate if both are low.
• Schilling test: now rarely performed but historically important; measures B12 absorption; stage 1 - oral radiolabelled B12 given with IM unlabelled B12 (flushing dose to saturate body stores); collect 24-h urine; excretion < 10% = malabsorption; stage 2 - repeat with oral intrinsic factor; correction with IF = pernicious anaemia; no correction = ileal disease or bacterial overgrowth.
• Schilling Test: Stage 1 = oral ⁵⁷Co-B12 without IF + IM 'flushing' dose → ↓ urine excretion (< 10%) = B12 malabsorption; Stage 2 = repeat with IF → excretion corrects = pernicious anaemia; Stage 3 = antibiotics → corrects = bacterial overgrowth; Stage 4 = pancreatin → corrects = pancreatic insufficiency

Refeeding syndrome = severe hypophosphataemia (+ hypomagnesaemia + hypokalaemia + fluid shifts) occurring when malnourished patients receive sudden aggressive nutrition (enteral or parenteral) → insulin surge → massive intracellular shift of phosphate (for ATP synthesis) + K⁺ + Mg²⁺ → life-threatening deficiencies.

• At-risk patients: Severe malnutrition (anorexia nervosa; cancer cachexia; prolonged starvation); chronic alcoholism; prolonged nil-by-mouth; bariatric surgery; oncology patients during chemotherapy
• Consequences of hypophosphataemia: Cardiac failure (most dangerous — phosphate needed for cardiac ATP); respiratory failure (diaphragm weakness); haemolysis; rhabdomyolysis; seizures; neurological dysfunction; leucocyte dysfunction (→ infections)

• Pathophysiology: during starvation, cells adapt to using fat and protein; on refeeding, insulin surges with carbohydrate, driving glucose, phosphate, potassium and magnesium into cells; the resulting hypophosphataemia causes failure of ATP-dependent cellular processes, particularly in cardiac and respiratory muscle.
• Clinical features: hypophosphataemia (< 0.5 mmol/L) causing heart failure, respiratory failure and respiratory muscle weakness, seizures, haemolytic anaemia, rhabdomyolysis; also hypokalaemia, hypomagnesaemia and thiamine deficiency.
• Management: identify at-risk patients; check and replace electrolytes BEFORE starting nutrition; start feeds at 10 kcal/kg/day (50% of requirements) and increase slowly over 4-7 days; give thiamine before and during refeeding; monitor electrolytes daily; restrict sodium and fluid.