Hypophosphataemia

Also known as: Hypophosphatemia, Low phosphate

Hypophosphataemia is a low serum phosphate, and matters because phosphate is essential for ATP generation and for 2,3-DPG in red cells.

Severe depletion therefore impairs energy metabolism across every tissue, with the clinical consequences concentrated in muscle — including respiratory and cardiac muscle.

Causes group into redistribution into cells (refeeding syndrome, treatment of diabetic ketoacidosis with insulin, respiratory alkalosis, recovery phase of severe illness), reduced intestinal absorption (malnutrition, malabsorption, chronic alcohol use, phosphate binders, vitamin D deficiency), and renal loss (hyperparathyroidism, Fanconi syndrome, diuretics, post-transplant, and tumour-induced osteomalacia).

Serum phosphate falls predictably during treatment of diabetic ketoacidosis and during refeeding, which makes these settings ones where hypophosphataemia should be anticipated and monitored rather than discovered.

Most hypophosphataemia is mild and asymptomatic. Features appear with severe depletion, generally below about 0.32 mmol/L.

Muscle weakness, which is the dominant feature, including respiratory muscle weakness causing failure to wean from ventilation — a classic and easily missed contributor in intensive care
Rhabdomyolysis, particularly in chronic alcohol use where muscle phosphate is already depleted
Cardiac: impaired contractility, cardiomyopathy and arrhythmia
Neurological: irritability, confusion, paraesthesia, seizures and coma in profound depletion
Haematological: haemolysis, impaired leucocyte and platelet function, and impaired oxygen delivery from reduced 2,3-DPG
Chronic depletion causes osteomalacia and bone pain

The combination of unexplained weakness, difficulty weaning, and a recent period of nutritional repletion or diabetic ketoacidosis treatment should prompt a phosphate check.

Anticipate and monitor rather than react: check phosphate before and daily during refeeding, and during treatment of diabetic ketoacidosis

Mild to moderate, asymptomatic:

Oral phosphate supplementation, with diarrhoea as the dose-limiting side effect
Increase dietary phosphate (dairy products, meat, nuts)
Address the underlying cause

Severe (<0.32 mmol/L) or symptomatic:

Intravenous phosphate replacement, given slowly over several hours, since rapid infusion causes hypocalcaemia through calcium-phosphate precipitation, and can also cause hyperkalaemia or hypernatraemia depending on the salt used
Potassium phosphate or sodium phosphate is chosen according to the patient's potassium and sodium status, and the accompanying cation load must be accounted for
Monitor calcium, magnesium and potassium alongside phosphate during replacement
Reduce the dose in renal impairment, where accumulation and consequent hyperphosphataemia are real risks
Recheck phosphate after each replacement dose rather than giving repeated empirical doses

Alongside:

Replace magnesium, which is frequently deficient in the same patients and impairs correction
In refeeding syndrome, give thiamine before and during nutrition, start feeding at a low rate and increase slowly, and correct phosphate, potassium and magnesium as they fall
Review contributing drugs, particularly phosphate binders and diuretics

Referral: nephrology for persistent renal phosphate wasting; endocrinology if tumour-induced osteomalacia or hereditary hypophosphataemia is suspected; nutrition support team for refeeding management.

Severe Dehydration

Also known as: Hypovolaemia, Volume depletion

A significant deficit of total body water and electrolytes, most commonly from gastrointestinal losses, but also from inadequate intake, excessive sweating, burns, diabetic emergencies, or renal losses. Severe dehydration is a medical emergency given the risk of hypovolemic shock, electrolyte derangement, and end-organ hypoperfusion.

Classified by degree (WHO clinical assessment):

No dehydration: <5% body weight fluid loss
Some/moderate dehydration: 5-10% fluid loss
Severe dehydration: >10% fluid loss

Also classified by tonicity, which is relevant to correction rate: isotonic (proportionate water and sodium loss, most common), hypotonic (sodium loss exceeds water loss; greater risk of shock at a given deficit), hypertonic (water loss exceeds sodium loss ; risk of cerebral injury if corrected too rapidly).

Severe dehydration: lethargy or reduced consciousness, markedly sunken eyes, inability to drink or drinking poorly, very slow skin pinch return (>2 seconds), dry mucous membranes, absent tears, tachycardia progressing to bradycardia (pre-terminal), weak or absent peripheral pulses, prolonged capillary refill (>3 seconds), hypotension (a late sign ; significant volume is already lost by the time BP drops), cool or mottled extremities, minimal or absent urine output
Infants: sunken fontanelle, absence of tears when crying, marked irritability or lethargy
Assess underlying cause: fever and diarrhea (infectious), polyuria and polydipsia preceding (diabetic emergency), burns history, poor oral intake (elderly, disability, neglect)
Complications: acute kidney injury (pre-renal), hypovolemic shock, electrolyte derangement, seizures (especially with hypernatremic or hyponatremic dehydration), metabolic acidosis

Primarily clinical assessment of severity: do not delay treatment awaiting lab results in clinically severe cases
U&E/creatinine: electrolyte derangement, renal function (urea rising disproportionately to creatinine in a pre-renal pattern)
Glucose: exclude or identify a diabetic emergency as the cause
Venous blood gas: metabolic acidosis, lactate as a tissue hypoperfusion marker
FBC: hemoconcentration
Urinalysis: specific gravity, ketones if relevant
Identify the underlying cause: stool studies if diarrheal, blood cultures if septic, medication review (diuretics)

Differentials for the underlying presentation: sepsis or septic shock (which frequently coexists with and compounds dehydration rather than being mutually exclusive), diabetic ketoacidosis or HHS, adrenal insufficiency, heat illness.

Severe dehydration is an emergency, obtain IV access immediately, considering intraosseous access if IV cannot be obtained rapidly in a critically unwell child.

IV fluid resuscitation:

Adults: initial bolus 500mL-1L isotonic crystalloid (Ringer's lactate or 0.9% saline) over 15-30 minutes if shocked, reassess and repeat as needed; then calculate ongoing deficit replacement (weight × %deficit) plus maintenance plus ongoing losses, typically over 24 hours
Children (WHO severe dehydration protocol, if not shocked): 100mL/kg total: infants <12 months, 30mL/kg over 1 hour then 70mL/kg over 5 hours; older children, 30mL/kg over 30 min then 70mL/kg over 2.5 hours; reassess frequently and switch to oral or NG ORS as soon as able to drink
If shocked (any age): rapid bolus 10-20mL/kg crystalloid, reassess, repeat as needed, escalate to senior or ICU review if not responding after 40-60mL/kg

Tonicity-specific correction:

Hypernatremic dehydration (Na >150mmol/L): correct SLOWLY ; rapid correction risks cerebral edema. Aim to reduce serum sodium by no more than 0.5mmol/L/hour (10-12mmol/L per 24 hours), replacing the deficit over 48 rather than 24 hours
Hyponatremic dehydration: correct cautiously if severe or symptomatic ; risk of osmotic demyelination syndrome with overly rapid correction; general limit <8-10mmol/L rise per 24 hours

Other:

Potassium replacement once urine output is established and hyperkalemia excluded ; dehydration with acidosis causes a transcellular shift that masks a total body deficit
Monitor: vital signs, urine output (target ≥0.5mL/kg/hr adults, ≥1mL/kg/hr children), mental status, repeat electrolytes every 4-6 hours during aggressive correction, fluid balance chart
Treat the underlying cause concurrently
Transition to oral rehydration as soon as tolerated, continuing to replace ongoing losses

Admission/escalation: any severe dehydration, hemodynamic instability, altered consciousness, significant electrolyte derangement, inability to tolerate oral rehydration, complicating comorbidity, or extremes of age.

Hypophosphataemia

Overview

Clinical Features

Management

Overview

Clinical Features

Diagnosis

Management