Electrolyte Disorders – GCC Nursing Guide

135–145

mmol/L

Normal Sodium

<125

mmol/L

Symptoms Appear

<120

mmol/L

Seizures / Coma Risk

10–12

mmol/L per 24h

Max Correction Rate

⚠

Osmotic Demyelination Syndrome (Central Pontine Myelinolysis): Correcting sodium too rapidly (>10–12 mmol/L per 24h) risks irreversible demyelination. Symptoms appear 2–6 days after over-correction: dysarthria, dysphagia, quadriplegia, altered consciousness.

Hyponatraemia — Classification by Volume Status

Type	Volume Status	Common Causes	Urine Na	Key Feature
Hypovolaemic	Decreased	Diarrhoea, vomiting, diuretics, burns, dehydration	<20 mmol/L (extra-renal) >20 (renal — diuretics)	Dehydrated, tachycardic, low urine output
Euvolaemic	Normal	SIADH (most common), hypothyroidism, adrenal insufficiency, psychogenic polydipsia	>20 mmol/L (>40 in SIADH)	No oedema, no dehydration
Hypervolaemic	Increased	Heart failure, liver cirrhosis, nephrotic syndrome, CKD	<20 mmol/L	Oedema, ascites, raised JVP

SIADH — Diagnostic Criteria

All 4 criteria must be present

Hypo-osmolar hyponatraemia: serum osmolality <275 mOsm/kg
Concentrated urine: urine osmolality >100 mOsm/kg (usually >300)
Euvolaemic — no dehydration, no oedema
Urine sodium >40 mmol/L (kidneys inappropriately retaining Na)

Causes of SIADH

CNS

SAH / meningitis
Encephalitis
Brain tumour
Head injury

Pulmonary

Pneumonia / TB
SCLC (small cell lung cancer)
Empyema
Positive pressure ventilation

Drugs (high-yield for exams)

SSRIs Carbamazepine Opioids Antipsychotics Cyclophosphamide PPIs NSAIDs

Hyponatraemia Treatment

        Fluid restriction 800–1000 mL/day — first-line for SIADH and hypervolaemic hyponatraemia. Treat the underlying cause.
      

Severity-Based Treatment

Severity	Na Level	Treatment
Mild	125–135	Fluid restriction, treat cause
Moderate	120–125	Fluid restriction + consider oral NaCl / tolvaptan
Severe/Symptomatic	<120 or symptoms	3% NaCl hypertonic saline (ITU/HDU only)

Specific Agents

Tolvaptan (vasopressin V2 receptor antagonist) — SIADH-specific; causes aquaresis without Na loss; start in hospital; avoid in liver disease
3% NaCl — symptomatic severe hyponatraemia only; 100–150 mL bolus IV, repeat if needed; max raise 5 mmol/L in first hour then slow
Demeclocycline — chronic SIADH; causes nephrogenic DI; less commonly used now

⚠

Never use hypertonic saline outside monitored setting. Check serum Na every 2–4h during active correction.

Hypernatraemia (>145 mmol/L)

Always Reflects

Water deficit (most common) — inadequate intake, diabetes insipidus, excessive sweating/fever
Sodium excess — hypertonic saline administration, hyperaldosteronism, Cushing's

Symptoms (correlate with rate of rise)

Thirst (earliest symptom)
Confusion / lethargy / irritability
Muscle weakness
Seizures / coma (severe)
Intracranial haemorrhage (brain shrinkage)

Free Water Deficit Formula

FWD = 0.6 × weight(kg) × [(Na / 140) − 1]

Use 0.5 for women and elderly. Result in litres.

Treatment

Replace free water deficit with oral water or IV 5% dextrose / 0.45% NaCl
Max correction rate: 10–12 mmol/L per 24h
Rapid correction → cerebral oedema risk
If haemodynamically unstable: 0.9% NaCl first to restore perfusion, then switch to hypotonic fluids
Treat underlying cause (DI → desmopressin; diuretic misuse → stop)

⚠

Monitor Na every 4–6h during active replacement. Aim for gradual reduction of no more than 0.5 mmol/L per hour.

3.5–5.0

mmol/L

Normal Potassium

3.0–3.5

mmol/L

Mild Hypokalaemia

2.5–3.0

mmol/L

Moderate — Weakness

<2.5

mmol/L

Severe — Life-Threatening

>6.5

mmol/L

Hyperkalaemia Emergency

Hypokalaemia — Causes

Category	Examples
GI Losses	Vomiting, diarrhoea, NG drainage, laxative abuse, fistula
Renal Losses	Loop diuretics (furosemide), thiazides, hyperaldosteronism, RTA
Transcellular Shift	Alkalosis (H+ moves out → K+ moves in), insulin, salbutamol, β2 agonists
Inadequate Intake	Malnutrition, prolonged IV fluids without K+ supplementation
Hypomagnesaemia	Coexists and prevents K+ repletion — always check and correct Mg first

ECG Changes in Hypokalaemia

Progressive changes as K falls

EarlyT-wave flattening / inversion

PathognomonicProminent U wave (after T wave)

ModerateST depression

SevereWidened QRS

Life-ThreateningVT / Torsades / VF

⚠

U waves > T waves in same lead is strongly suggestive of hypokalaemia. Obtain 12-lead ECG for any K+ <3.0.

Symptoms by Severity

3.0–3.5	Usually asymptomatic; mild fatigue
2.5–3.0	Muscle weakness, cramps, constipation, palpitations
<2.5	Paralysis, ileus, respiratory failure, life-threatening arrhythmias

Hypokalaemia Treatment Protocol

Oral Replacement (preferred for mild–moderate)

Potassium chloride (Slow-K): 8 mmol per tablet; typical dose 2–4 tabs TDS
Sando-K effervescent: 12 mmol K + 8 mmol phosphate per tablet
Dietary sources: bananas, oranges, potatoes, spinach
Takes 24–48h to adequately correct levels

Key Principle

          Always check and correct magnesium first. Hypomagnesaemia causes renal K+ wasting — K+ replacement will fail if Mg is not corrected concurrently.
        

IV Replacement (symptomatic / severe / unable to take oral)

⚠

Peripheral line: Max concentration 40 mmol/L (risk of phlebitis/necrosis if higher)
Central line: Can give up to 40 mmol/h with continuous ECG monitoring
Standard rate: 10–20 mmol/h — faster rates require HDU/ICU

Never give KCl by IV bolus — fatal cardiac arrest risk
ECG monitoring required for rates >10 mmol/h
Recheck K+ 2–4h after infusion
Each 10 mmol K+ raises serum K+ by approximately 0.1 mmol/L (variable)
Target K+ >4.0 in cardiac patients

Hyperkalaemia (>5.0 mmol/L)

ECG Changes (progressive)

First signPeaked (tall, narrow) T waves

NextBroad, flat P wave → P wave loss

ThenProlonged PR interval

LateWidened QRS

PreterminalSinusoidal pattern

FatalVF / Asystole

Treatment Steps (in order)

Step	Agent	Dose & Effect
1 — Membrane stabilise	Calcium gluconate 10%	10 mL IV over 2–5 min; onset <3 min; duration 30–60 min; no K lowering
2 — Shift K+ into cells	Insulin + dextrose	10 units Actrapid in 50 mL 50% dextrose; lowers K 0.5–1.2 mmol/L
3 — Shift K+ into cells	Salbutamol nebulised	10–20 mg neb; additive to insulin; lowers K 0.5–1.0 mmol/L
4 — Remove K+ from body	Calcium resonium	15 g oral/rectal; onset hours; GI cation exchange resin
4 — Remove K+ from body	Patiromer / SZC	Newer agents; better tolerated than resonium
5 — Dialysis	Haemodialysis	Definitive treatment for refractory or anuric patient

ℹ

See the AKI guide for detailed hyperkalaemia protocols including Salbutamol dosing, sodium bicarbonate indications, and fluid management in AKI.

0.7–1.0

mmol/L

Normal Magnesium

0.8–1.4

mmol/L

Normal Phosphate

>3.0

mmol/L Mg

Loss of DTRs

>5.0

mmol/L Mg

Respiratory Depression

Hypomagnesaemia (<0.7 mmol/L)

Causes

Diarrhoea / malabsorption
Long-term PPI use — reduces Mg absorption (OMEPRAZOLE — high-yield exam point)
Alcohol excess (most common in Western settings)
Loop and thiazide diuretics
Cisplatin chemotherapy
Amphotericin B
Calcineurin inhibitors (tacrolimus/cyclosporin)
Refeeding syndrome

Clinical Effects

Neuromuscular: tremor, muscle cramps, tetany, seizures, positive Chvostek/Trousseau
Cardiac: Torsades de Pointes (polymorphic VT — long QT + low Mg)
Metabolic: causes refractory hypokalaemia AND hypocalcaemia — correct Mg first or K/Ca will not respond

⚠

If K+ is not rising despite replacement — check Mg. Hypomagnesaemia prevents renal K+ conservation.

Magnesium Treatment

IV Replacement (symptomatic / severe <0.4 / arrhythmia)

        10–20 mmol MgSO4 IV over 10–30 min (symptomatic/emergency)

        40 mmol MgSO4 over 24h (maintenance/moderate)

        1g MgSO4 = 4 mmol magnesium

Torsades de Pointes: 2g (8 mmol) MgSO4 IV over 10–15 min (ACLS protocol)
Monitor reflexes (loss of patellar reflex = early toxicity)
Monitor respiratory rate (give calcium gluconate as antidote if toxicity)
Repeat Mg levels 4–6h post-infusion

Oral Replacement (mild, asymptomatic)

Magnesium glycerophosphate — better absorbed, less diarrhoea than oxide
Magnesium oxide — less bioavailable, causes diarrhoea (avoid in GI loss aetiology)
Stop precipitating drug (PPI → switch or reduce dose)

Hypermagnesaemia (>1.0 mmol/L)

Causes: Eclampsia treatment overdose, Mg-containing antacids in renal failure
>3 mmol/L: loss of deep tendon reflexes (first clinical sign)
>5 mmol/L: respiratory depression (monitor RR closely)
>7 mmol/L: cardiac arrest
Treatment: Stop Mg; IV calcium gluconate 10 mL 10% (antagonist); IV fluids; dialysis if severe/renal failure

Phosphate Disorders

Hypophosphataemia (<0.8 mmol/L)

Refeeding syndrome — most important cause in hospital; phosphate shifts intracellularly when glucose/insulin administered after starvation; can be life-threatening (see nutrition guide)
DKA treatment — insulin drives phosphate into cells
Alcohol excess and malnutrition
Malabsorption syndromes
Hyperparathyroidism (PTH increases renal phosphate excretion)
Vitamin D deficiency

Severity & Effects

0.3–0.8	Mild: weakness, fatigue
<0.3	Severe: respiratory muscle weakness (wean failure), haemolytic anaemia, rhabdomyolysis, cardiac failure, confusion

Treatment

Oral: Phosphate-Sandoz (16 mmol phosphate per tablet) — preferred for mild–moderate
IV: Potassium or sodium phosphate infusion — severe/unable to take oral; give over 6–12h
Recheck phosphate 4–6h post-replacement

Hyperphosphataemia (>1.4 mmol/L)

CKD — most common cause; kidneys fail to excrete phosphate
Hypoparathyroidism (PTH deficiency → reduced renal excretion)
Rhabdomyolysis
Tumour lysis syndrome

ℹ

In CKD, hyperphosphataemia drives calcium-phosphate deposition, worsens renal osteodystrophy, and increases cardiovascular mortality.

CKD Phosphate Management

Dietary restriction: limit high-phosphate foods (dairy, nuts, processed foods)
Calcium carbonate — phosphate binder with meals; also provides Ca; avoid if hypercalcaemia
Sevelamer — non-calcium binder; preferred if hypercalcaemia; also lowers LDL
Lanthanum carbonate — chewable tablet with meals
Dialysis removes some phosphate but often insufficient alone

          Phosphate × Calcium product >4.4 mmol²/L² increases risk of vascular calcification and should be avoided in CKD patients.
        

2.2–2.6

mmol/L

Normal Adj. Calcium

>2.6

mmol/L

Hypercalcaemia

<2.2

mmol/L

Hypocalcaemia

    Adjusted Calcium Formula: Adjusted Ca = Measured Ca + 0.02 × (40 − albumin g/L). Always correct for albumin before interpreting calcium. Low albumin falsely lowers measured calcium. If ionised calcium available, use that instead.
  

Hypercalcaemia — Causes

Most Common (80–90% of cases)

Cause	Mechanism	PTH
Malignancy	PTHrP secretion (humoral), bone metastases, local osteolysis	Low/suppressed
Primary hyperparathyroidism	Parathyroid adenoma (85%) — most common outpatient cause; autonomous PTH secretion	Elevated (inappropriate)
Sarcoidosis / granulomas	Extrarenal 1α-hydroxylase in macrophages → excess Vit D3 activation	Low
Familial hypocalciuric hypercalcaemia (FHH)	CaSR mutation — benign; low urine Ca:Cr ratio <0.01	Normal/slightly high
Vit D toxicity / excess	Excessive supplementation	Low
Thiazide diuretics	Reduce renal Ca excretion	Low

Symptoms Mnemonic: "Bones, Stones, Groans, Thrones, Moans"

Bones
Bone pain, pathological fractures, osteitis fibrosa cystica

Stones
Renal calculi (calcium oxalate/phosphate), nephrocalcinosis

Groans
Nausea, vomiting, constipation, pancreatitis, peptic ulcer

Thrones
Polyuria, polydipsia (nephrogenic DI effect)

Moans
Depression, fatigue, confusion, lethargy, coma

Hypercalcaemia Treatment

Severity-Based Approach

Level	Severity	Priority
<3.0 mmol/L	Mild	Outpatient management, treat cause
3.0–3.5 mmol/L	Moderate	Admit, IV fluids, bisphosphonate
>3.5 mmol/L	Severe (crisis)	Emergency management

Treatment Steps

IV 0.9% NaCl 3–4 L/24h — first line; volume expands and promotes renal Ca excretion; must assess fluid status first
Zoledronic acid 4 mg IV (bisphosphonate) — over 15–30 min; onset 48–72h; preferred for malignancy-related; avoid if eGFR <30; check dentistry before (osteonecrosis of jaw)
Pamidronate 60–90 mg IV — alternative bisphosphonate
Calcitonin 4 IU/kg SC/IM q12h — rapid onset (4–6h); short-lived effect (tachyphylaxis <48h); useful as bridge to bisphosphonate
Denosumab — RANK-L inhibitor; useful if bisphosphonate contraindicated (renal failure)
Corticosteroids — for granulomatous disease (sarcoidosis) and haematological malignancies (myeloma, lymphoma)
Dialysis — severe refractory hypercalcaemia or renal failure

Hypocalcaemia (<2.2 mmol/L)

Causes

Hypoparathyroidism — post-thyroidectomy or parathyroid surgery (most common surgical cause); check Ca daily post-op
Vitamin D deficiency — extremely common in GCC (indoor lifestyle, clothing, high prevalence); treat with cholecalciferol (Vit D3)
Hypomagnesaemia — causes functional hypoparathyroidism; correct Mg first
Acute pancreatitis — Ca binds to necrotic fat (saponification)
Hungry bone syndrome — post-parathyroidectomy; bones avidly absorb Ca; severe hypocalcaemia
CKD — reduced 1α-hydroxylase activity, hyperphosphataemia
Rhabdomyolysis (acute), massive blood transfusion (citrate chelates Ca)

Clinical Signs

Perioral / fingertip paraesthesia — earliest symptom
Chvostek's sign — tap CN VII (facial nerve) anterior to tragus → ipsilateral facial twitch
Trousseau's sign — inflate BP cuff above systolic for 3 min → carpal spasm (more specific than Chvostek)
Tetany — involuntary muscle spasms
Laryngospasm — medical emergency
Seizures
QTc prolongation on ECG → Torsades de Pointes risk
Cataracts (chronic)

Treatment

⚠

Symptomatic hypocalcaemia = medical emergency. Laryngospasm or seizures require immediate IV calcium.

IV Calcium gluconate 10% — 10 mL (2.25 mmol Ca) IV over 10 min for symptomatic/acute; repeat if symptoms persist
Calcium gluconate infusion: 10 ampoules (100 mL) in 1 L 0.9% NaCl over 24h — maintenance post acute treatment
Oral calcium carbonate — 1–3 g/day elemental calcium for maintenance/mild
Alfacalcidol (1α-hydroxyvitamin D3) — for hypoparathyroidism and CKD (bypasses kidney activation step)
Cholecalciferol (Vit D3) — for Vit D deficiency (requires hepatic and renal activation)

          Do not use IV calcium chloride peripherally — highly caustic, causes tissue necrosis. Use calcium gluconate for peripheral IV access.
        

Monitoring

Recheck adjusted Ca 4–6h post-IV replacement
Check Mg and phosphate concurrently
ECG for QTc in symptomatic patients
Post-thyroidectomy: check Ca at 6h, 12h, 24h, and discharge

7.35–7.45

Normal pH

4.7–6.0

kPa

Normal PaCO2

22–26

mmol/L

Normal HCO3

8–12

mmol/L

Normal Anion Gap

Systematic ABG Interpretation

1.pH: <7.35 = acidosis; >7.45 = alkalosis
2.Primary process: PaCO2 drives → respiratory; HCO3 drives → metabolic
3.Compensation: expected vs actual (if different → mixed disorder)
4.Anion gap: if metabolic acidosis present
5.Delta ratio: if high AG acidosis — screen for mixed disorder

Compensation Rules

Disorder	Expected Compensation	Speed
Metabolic acidosis	PaCO2 = (1.5 × HCO3) + 8 ± 2 (Winter's formula)	Minutes–hours
Metabolic alkalosis	PaCO2 rises 0.7 mmHg per 1 mmol/L HCO3 rise	Hours
Respiratory acidosis (acute)	HCO3 rises 1 mmol/L per 10 mmHg PaCO2 rise	Minutes
Respiratory acidosis (chronic)	HCO3 rises 3.5 mmol/L per 10 mmHg PaCO2 rise	3–5 days
Respiratory alkalosis (acute)	HCO3 falls 2 mmol/L per 10 mmHg PaCO2 fall	Minutes
Respiratory alkalosis (chronic)	HCO3 falls 5 mmol/L per 10 mmHg PaCO2 fall	3–5 days

Anion Gap & MUDPILES

Anion Gap = Na − (Cl + HCO3) = 8–12 mmol/L

High AG Metabolic Acidosis — MUDPILES

M — Methanol

U — Uraemia (CKD/AKI)

D — Diabetic ketoacidosis

P — Propylene glycol

I — Isoniazid / Iron / Infection (sepsis)

L — Lactic acidosis (type A/B)

E — Ethylene glycol

S — Salicylates

Normal AG Metabolic Acidosis (HARDUPS)

Hyperchloraemic — excess NaCl administration
Addison's disease (adrenal insufficiency)
RTA (renal tubular acidosis)
Diarrhoea — bicarbonate loss
Ureteral diversion
Pancreatic fistula
Saline infusion excess

Delta Ratio

Delta ratio = (AG − 12) / (24 − HCO3)

<0.4	Normal AG metabolic acidosis only (no high AG component)
0.4–1.0	Combined high AG + normal AG metabolic acidosis
1.0–2.0	Pure high AG metabolic acidosis
>2.0	High AG acidosis + concurrent metabolic alkalosis

Mixed Disorders & GCC-Specific Patterns

Common Mixed Disorder Combinations

Combination	Clinical Scenario
Metabolic acidosis + Respiratory acidosis	COPD + septic shock; severe asthma with fatigue; cardiac arrest
Metabolic alkalosis + Respiratory alkalosis	Liver failure with vomiting; hyperventilating anxiety patient on diuretics
Metabolic acidosis + Respiratory alkalosis	Salicylate poisoning (directly stimulates respiratory centre); sepsis early phase
Metabolic alkalosis + Respiratory acidosis	COPD on long-term diuretics; post-hypercapnic correction

GCC-Specific Acid-Base Patterns

          DKA — most common high AG metabolic acidosis in GCC (high diabetes prevalence). Expect: low pH, low HCO3, high AG, ketonaemia, hyperglycaemia. K+ may be high initially (transcellular shift) but total body K+ depleted — replace carefully with insulin.
        

          Heat exhaustion — isotonic dehydration; normal sodium; normal acid-base initially. Treat with IV 0.9% NaCl and cooling.
        

          Heat stroke — hyperthermia + CNS dysfunction. Lactic acidosis from hypoperfusion + rhabdomyolysis. Risk of AKI, DIC, multi-organ failure. Aggressive cooling + organ support.
        

GCC-Specific Clinical Context

High Prevalence Conditions in GCC

Type 2 diabetes — DKA most common cause of high AG metabolic acidosis; hypokalaemia common during DKA treatment
Summer heat (extreme temperatures) — severe dehydration causes Na and K losses; heat stroke causes lactic acidosis
Vitamin D deficiency — hypocalcaemia very common; indoor lifestyle, cultural clothing; screen all patients
CKD — high diabetes + hypertension prevalence; hyperphosphataemia, hyperkalaemia, metabolic acidosis
SIADH from drugs — high SSRI/antipsychotic use in Gulf; PPIs nearly ubiquitous → Mg depletion

Ramadan-Specific Electrolyte Considerations

          Dehydration during Ramadan: 12–18h fasting without fluid in extreme summer heat. Na and K losses through sweat. Breaking fast rapidly with large volumes of plain water (without electrolytes) → dilutional hyponatraemia. Educate patients to break fast gradually with electrolyte-containing fluids.
        

          Diabetic patients on SGLT2 inhibitors + Ramadan: Increased DKA risk, especially euglycaemic DKA. Monitor electrolytes closely. Discuss medication adjustments with physician before Ramadan.
        

DHA / DOH / SCFHS High-Yield Exam Topics

        SIADH Diagnosis

        Serum Osm <275 + Urine Osm >100 + Euvolaemic + Urine Na >40. Most common cause = CNS/pulmonary/drugs.

        Correction Rate — Na

        Max 10–12 mmol/L per 24h. Faster → osmotic demyelination. Hypernatraemia correction also max 10–12 mmol/L per 24h → cerebral oedema.

        Hypokalaemia ECG

        U waves (hallmark), T-wave flattening, ST depression, widened QRS, VT. Check and correct Mg first.

        Hypercalcaemia of Malignancy

        PTHrP-mediated. Treat with IV 0.9% NaCl + zoledronic acid. PTH suppressed (contrast with primary hyperPTH).

        Torsades de Pointes

        Treat with 2g MgSO4 IV. Long QT + low Mg/K. Check electrolytes for every prolonged QTc.

        Winter's Formula

        Expected PaCO2 = (1.5 × HCO3) + 8 ± 2. If actual PaCO2 higher = additional respiratory acidosis. If lower = additional respiratory alkalosis.

MCQ Practice — Electrolyte Disorders

Electrolyte Quick Reference Checker

Enter an electrolyte value and patient context to receive instant clinical guidance, GCC-specific causes, treatment protocol, and monitoring frequency.

Electrolyte

Value (mmol/L)

Patient Context