Overview

Syndrome of Inappropriate ADH Secretion (SIADH)

1. Clinical Overview

The Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) represents one of the most important causes of hypotonic hyponatraemia in clinical practice. [1,2] It is characterized by the non-osmotic release of arginine vasopressin (AVP) leading to inappropriate water retention by the kidneys. [1]

Key Facts

Fact	Detail
Definition	Hyponatraemia with euvolaemia due to inappropriate ADH secretion
Most Common Cause	Most common cause of euvolaemic hypotonic hyponatraemia (30-40% of cases)
Prevalence	15-30% of hospitalized patients have hyponatraemia; SIADH accounts for majority
Mortality	Hospital mortality 3× higher in patients with Na less than 125 mmol/L
Key Biochemistry	Plasma osmolality less than 275 mOsm/kg, Urine osmolality more than 100 mOsm/kg
Sodium Threshold	Urine sodium more than 30 mmol/L (typically more than 40 mmol/L)
Volume Status	Euvolaemic (no oedema, no clinical dehydration)
Adrenal/Thyroid	Must exclude hypothyroidism and adrenal insufficiency
Correction Rate	Maximum 10 mmol/L per 24 hours to prevent ODS
Emergency Treatment	3% hypertonic saline for severe symptoms

Clinical Pearls

Pearl 1: SIADH is a diagnosis of exclusion - always exclude hypothyroidism and adrenal insufficiency first, as these can mimic SIADH biochemically.

Pearl 2: The urine is inappropriately concentrated. In true water excess, the kidney should dilute urine to less than 100 mOsm/kg - failure to do so indicates SIADH.

Pearl 3: Check recent medication history - SSRIs, carbamazepine, and PPIs are common culprits. Drug cessation may be curative.

Pearl 4: Small cell lung cancer (SCLC) produces ectopic ADH in 10-15% of cases - always check chest imaging in unexplained SIADH.

Pearl 5: Urine Na more than 130 mmol/L and urine osmolality more than 500 mOsm/kg predict failure of fluid restriction.

2. Epidemiology

Incidence and Prevalence

Population	Hyponatraemia Rate	SIADH Proportion
General hospital admissions	15-30%	30-40% of hyponatraemic cases
ICU patients	30-40%	25-35% of hyponatraemic cases
Elderly (more than 65 years)	7-11%	Higher proportion
Oncology patients	20-40%	Often paraneoplastic
Psychiatric inpatients	10-20%	Often drug-induced
Post-operative patients	20-30%	Pain and stress-related

Demographics

Factor	Association
Age	Increases with age; elderly more susceptible due to impaired renal concentrating ability
Sex	Slight female predominance in drug-induced cases
Comorbidities	Higher in malignancy, CNS disease, pulmonary disease

Risk Factors

Risk Factor	Relative Risk	Mechanism
Small cell lung cancer	RR 5-10	Ectopic ADH production
Brain injury/surgery	RR 3-5	Hypothalamic dysfunction
Pneumonia/pulmonary disease	RR 2-4	Inflammatory cytokines stimulate ADH
SSRIs/SNRIs	RR 2-4	Potentiate ADH effect on collecting duct
Carbamazepine/Oxcarbazepine	RR 3-5	Direct ADH-like effect on V2 receptors
Age more than 65 years	RR 2-3	Impaired water excretion capacity
Thiazide diuretics	RR 2-4	Impede free water excretion
PPIs	RR 1.5-2	Uncertain mechanism
Marathon running	Variable	Volume depletion with hypotonic fluid intake

3. Pathophysiology

Stepwise Mechanism

Step 1: Inappropriate ADH Secretion

Arginine vasopressin (AVP) is secreted from the posterior pituitary
Normal trigger: increased plasma osmolality or decreased blood volume
In SIADH: ADH released despite low plasma osmolality and normal/high blood volume
Sources: pituitary (reset osmostat), ectopic (SCLC), drugs, inflammation

Step 2: Renal Water Retention

ADH binds V2 receptors on collecting duct principal cells
Activates adenylate cyclase via Gs protein coupling
Aquaporin-2 (AQP2) channels inserted into apical membrane
Increased water permeability leads to free water reabsorption
Result: concentrated urine inappropriate for plasma osmolality

Step 3: Plasma Dilution and Hyponatraemia

Retained water expands extracellular fluid volume
Plasma sodium diluted (dilutional hyponatraemia)
Volume expansion triggers natriuresis via ANP/BNP release
Urine sodium paradoxically elevated (more than 30 mmol/L)
Patient remains euvolaemic due to escape from antidiuresis

Step 4: Cellular Adaptation

Brain cells at risk during acute hyponatraemia
Water shifts intracellularly causing cerebral oedema
Neurons expel organic osmolytes (taurine, myoinositol, glutamate)
Adaptation occurs over 24-48 hours
Adapted brain vulnerable to osmotic demyelination if corrected too rapidly

Step 5: Steady State vs Decompensation

Chronic mild SIADH: often asymptomatic or subtle cognitive impairment
Acute severe SIADH: life-threatening cerebral oedema
Decompensation triggers: increased water intake, IV hypotonic fluids
Mortality correlates with severity and acuity of hyponatraemia

Classification of SIADH

Type	Mechanism	Characteristics	Example Causes
Type A	Erratic, autonomous ADH secretion	No correlation with osmolality	SCLC, other malignancies
Type B	Reset osmostat	ADH suppresses at lower threshold	CNS disease, chronic illness
Type C	ADH leak	Continuous low-level basal secretion	Idiopathic, TB
Type D	Gain-of-function V2 receptor	ADH-independent aquaporin activation	Rare genetic variant

Aetiological Classification

Category	Specific Causes
Malignancy	Small cell lung cancer (most common), head and neck cancer, lymphoma, thymoma, GI tumours, prostate cancer
Pulmonary	Pneumonia, TB, aspergillosis, lung abscess, positive pressure ventilation, cystic fibrosis
CNS	Stroke, SAH, meningitis, encephalitis, brain abscess, head trauma, brain tumours, MS, Guillain-Barré
Drugs	SSRIs, SNRIs, TCAs, carbamazepine, oxcarbazepine, sodium valproate, NSAIDs, PPIs, opioids, cyclophosphamide, vincristine, ciprofloxacin, MDMA
Surgery/Anaesthesia	Post-operative pain, nausea, stress response
Other	HIV, acute intermittent porphyria, idiopathic

4. Clinical Presentation

Symptoms by Severity

Severity	Sodium Level	Symptoms
Mild	130-135 mmol/L	Often asymptomatic, subtle cognitive impairment, gait instability
Moderate	125-129 mmol/L	Nausea, headache, confusion, lethargy, malaise
Severe	120-124 mmol/L	Vomiting, drowsiness, disorientation, muscle cramps
Profound	less than 120 mmol/L	Seizures, decreased GCS, respiratory arrest, coma, death

Symptom Frequency

Symptom	Frequency	Notes
Fatigue and lethargy	60-80%	Most common presenting complaint
Nausea and anorexia	50-70%	Often early symptom
Headache	40-60%	Due to cerebral oedema
Cognitive impairment	40-70%	Subtle in chronic cases
Falls and gait instability	30-50%	Important in elderly
Muscle cramps	20-40%	Due to sodium imbalance
Confusion	30-50%	More common in acute cases
Seizures	5-10%	Usually when Na less than 120
Coma	2-5%	Emergency presentation

Atypical Presentations

Presentation	Clinical Context
Unexplained falls in elderly	Chronic mild hyponatraemia impairs gait
Subtle cognitive decline	May be mistaken for dementia
Anorexia and weight loss	Especially in malignancy-associated SIADH
Treatment-resistant depression	SSRI-induced hyponatraemia worsening symptoms
Recurrent seizures	Underlying cause may be occult SIADH

Red Flags

Red Flag	Implication	Action
Na less than 120 mmol/L	Severe hyponatraemia, seizure risk	Urgent assessment, consider ICU
Seizures	Acute symptomatic hyponatraemia	Emergency hypertonic saline
Decreased consciousness	Cerebral oedema	Immediate treatment required
Respiratory distress	Neurogenic pulmonary oedema	ICU admission
Na less than 105 mmol/L	Life-threatening	Emergency hypertonic saline, ICU
Acute decline more than 10 mmol/L in 24h	Acute hyponatraemia	Higher risk of cerebral oedema
Suspected malignancy	Paraneoplastic SIADH	Urgent oncology workup

5. Clinical Examination

Structured Approach

General Inspection

Mental state: alert, confused, drowsy, comatose
Signs of volume depletion: dry mucous membranes, reduced skin turgor, tachycardia (ABSENT in true SIADH)
Signs of volume overload: peripheral oedema, ascites, raised JVP (ABSENT in true SIADH)
Nutritional status: cachexia may suggest malignancy

Volume Assessment (Critical)

Finding	Hypovolaemia	Euvolaemia (SIADH)	Hypervolaemia
JVP	Low	Normal	Elevated
Skin turgor	Reduced	Normal	Normal
Mucous membranes	Dry	Moist	Moist
Peripheral oedema	Absent	Absent	Present
Postural BP drop	Yes	No	No
Urine Na	less than 20	more than 30	Variable

Systems Examination

System	Findings to Seek	Significance
Respiratory	Consolidation, effusion, masses	Pneumonia, TB, lung cancer
Neurological	Focal deficits, meningism, papilloedema	CNS cause
Lymph nodes	Lymphadenopathy	Malignancy
Thyroid	Goitre, hypothyroid features	Hypothyroidism mimics SIADH
Skin	Hyperpigmentation	Adrenal insufficiency mimics SIADH

Special Tests

Test	Method	Interpretation
Fluid challenge	1-2L 0.9% saline over 6-12h	SIADH: Na unchanged or falls further
Water restriction test	500-750 mL/day for 48-72h	Improves if SIADH; failure suggests severe disease
Short Synacthen test	250 mcg IV, cortisol at 0, 30 min	Rule out adrenal insufficiency
GCS assessment	Serial monitoring	Track worsening encephalopathy

6. Investigations

Laboratory Investigations

Investigation	Expected Finding in SIADH	Notes
Serum sodium	less than 135 mmol/L (usually less than 130)	Define severity
Serum osmolality	less than 275 mOsm/kg	Confirms hypotonic hyponatraemia
Urine osmolality	more than 100 mOsm/kg (often more than 300)	Inappropriately concentrated urine
Urine sodium	more than 30 mmol/L (usually more than 40)	High despite hyponatraemia
Serum uric acid	Low (less than 0.24 mmol/L)	Due to increased clearance
Serum urea	Low-normal	Due to dilution
TFTs	Normal (exclude hypothyroidism)	Essential before diagnosing SIADH
9am cortisol	more than 450 nmol/L or Synacthen normal	Exclude adrenal insufficiency
Glucose	Normal	Exclude pseudohyponatraemia
Lipid profile	Normal	Exclude pseudohyponatraemia

Diagnostic Criteria for SIADH (Bartter and Schwartz)

Criterion	Requirement
Serum osmolality	less than 275 mOsm/kg
Urine osmolality	more than 100 mOsm/kg (inappropriately concentrated)
Clinical euvolaemia	No signs of dehydration or oedema
Urine sodium	more than 30 mmol/L on normal salt/water intake
Normal thyroid function	TSH and fT4 within normal range
Normal adrenal function	Short Synacthen test normal or adequate cortisol
No diuretic use	Within preceding week
No severe renal disease	eGFR more than 30 mL/min/1.73m²

Additional Investigations

Investigation	Indication
CXR	Exclude lung pathology (pneumonia, SCLC)
CT chest	If CXR abnormal or high suspicion of malignancy
CT/MRI brain	CNS symptoms, suspected intracranial pathology
Lumbar puncture	Meningitis, SAH suspected
CT CAP	Malignancy workup if no cause identified
Plasma copeptin	Research tool - stable surrogate for AVP

7. Management

Management Algorithm

     SIADH SUSPECTED (Na less than 135, euvolaemic)
                        ↓
┌─────────────────────────────────────────────────────┐
│           CONFIRM DIAGNOSIS                          │
│  - Serum osmolality less than 275 mOsm/kg           │
│  - Urine osmolality more than 100 mOsm/kg           │
│  - Urine Na more than 30 mmol/L                     │
│  - Euvolaemic on examination                        │
│  - TFTs normal, cortisol normal                     │
└─────────────────────────────────────────────────────┘
                        ↓
┌─────────────────────────────────────────────────────┐
│            ASSESS SEVERITY                           │
├─────────────────────────────────────────────────────┤
│  SEVERE (Na less than 120 OR symptoms)              │
│  → Seizures, confusion, coma                        │
│  → EMERGENCY: 3% Hypertonic Saline                  │
├─────────────────────────────────────────────────────┤
│  MODERATE (Na 120-129)                              │
│  → Symptomatic: Consider hypertonic saline          │
│  → Asymptomatic: Fluid restriction                  │
├─────────────────────────────────────────────────────┤
│  MILD (Na 130-135)                                  │
│  → Fluid restriction, treat cause                   │
└─────────────────────────────────────────────────────┘
                        ↓
┌─────────────────────────────────────────────────────┐
│     EMERGENCY TREATMENT (Severe/Symptomatic)        │
│  - 150 mL 3% NaCl over 20 min IV                   │
│  - Check Na+ after 20 min                           │
│  - Repeat bolus x2 if needed                        │
│  - Target: 5 mmol/L rise in first hour              │
│  - MAX: 10 mmol/L in 24 hours                       │
└─────────────────────────────────────────────────────┘
                        ↓
┌─────────────────────────────────────────────────────┐
│          ONGOING MANAGEMENT                          │
│  FIRST-LINE: Fluid restriction 750-1000 mL/day      │
│  + Treat underlying cause                           │
│                                                     │
│  IF FLUID RESTRICTION FAILS:                        │
│  SECOND-LINE OPTIONS:                               │
│  • Oral urea 30-60g/day                            │
│  • Tolvaptan 15mg OD (initiate in hospital)        │
│  • Demeclocycline 300mg BD-TDS                     │
│  • Salt tablets + loop diuretic                     │
└─────────────────────────────────────────────────────┘
                        ↓
┌─────────────────────────────────────────────────────┐
│              MONITORING                              │
│  - Check Na+ 4-6 hourly during acute treatment     │
│  - Daily Na+ once stable                            │
│  - Watch for overcorrection                         │
│  - If overcorrection: desmopressin 2 mcg IV        │
└─────────────────────────────────────────────────────┘

Emergency Treatment (Severe Symptomatic Hyponatraemia)

Step	Action	Notes
1	150 mL 3% NaCl IV over 20 minutes	Bolus approach preferred
2	Check serum Na+ after 20 minutes	Monitor response
3	Repeat bolus if Na+ risen less than 5 mmol/L	Maximum 3 boluses
4	Target 5 mmol/L rise in first 1 hour	To reduce cerebral oedema
5	Maximum 10 mmol/L in first 24 hours	Prevent ODS
6	Maximum 8 mmol/L per 24 hours thereafter	Until Na+ reaches 130

Conservative Management

Measure	Dose/Target	Evidence
Fluid restriction	750-1000 mL/day (500-750 if severe)	First-line; effective in ~50%
Identify and treat cause	Stop offending drugs, treat infections	May be curative
Salt intake	6-9g sodium chloride daily	Increases solute excretion

Second-Line Pharmacotherapy

Drug	Dose	Mechanism	Notes
Urea (oral)	30-60g/day in divided doses	Osmotic diuresis, solute loading	European guideline preference; poor palatability
Tolvaptan	15mg OD, titrate to 60mg OD	V2 receptor antagonist (vaptan)	Start in hospital; risk of overcorrection; monitor LFTs
Demeclocycline	300mg BD-TDS	Induces nephrogenic DI	Nephrotoxic; avoid in liver disease
Salt tablets + furosemide	3-9g NaCl + 20-40mg furosemide	Increases solute and free water excretion	Combination therapy

Correction Rate Guidelines

Scenario	Maximum Correction Rate	Rationale
General	10 mmol/L in 24 hours	Prevent ODS
High-risk patients*	8 mmol/L in 24 hours	Higher ODS risk
First few hours (symptomatic)	5 mmol/L in first 1-2 hours	To control symptoms
Subsequent days	8 mmol/L per 24 hours	Until Na+ reaches 130

*High-risk: alcoholism, malnutrition, liver disease, hypokalemia, Na+ less than 105 mmol/L

Managing Overcorrection

Situation	Action
Na+ risen more than 10 mmol/L in 24h	Re-lower Na+ with desmopressin
Desmopressin dose	2 mcg IV or 4 mcg SC every 8 hours
Co-administration	5% dextrose IV to lower Na+ back
Target	Bring Na+ back to safe correction limits

8. Complications

Immediate Complications

Complication	Incidence	Mechanism	Management
Cerebral oedema	5-10% of severe cases	Water shifts into brain cells	Hypertonic saline
Seizures	5-10% when Na less than 120	Neuronal dysfunction	IV lorazepam + hypertonic saline
Coma	2-5%	Severe cerebral oedema	ICU, intubation if needed
Respiratory arrest	Rare	Brainstem compression	Emergency airway management

Early Complications (Days 1-7)

Complication	Notes
Overcorrection	May lead to ODS
Fluid restriction intolerance	Thirst, poor compliance
Drug side effects	Tolvaptan: hepatotoxicity; Demeclocycline: nephrotoxicity
Failure to respond	Consider second-line agents

Late Complications

Complication	Timing	Features
Osmotic Demyelination Syndrome (ODS)	2-6 days after correction	See below
Chronic cognitive impairment	Months-years	Persistent subtle deficits
Recurrent hyponatraemia	Variable	If cause not addressed
Falls and fractures	Ongoing	Gait instability increases fracture risk 4×

Osmotic Demyelination Syndrome (ODS)

Feature	Detail
Previous name	Central Pontine Myelinolysis (CPM)
Pathophysiology	Rapid correction depletes brain organic osmolytes → myelin damage
Location	Pons (central) or extrapontine (basal ganglia, thalamus)
Timing	2-6 days after overcorrection
Symptoms	Dysarthria, dysphagia, quadriparesis, locked-in syndrome
Imaging	MRI: T2 hyperintense pontine lesions (may be delayed)
Prognosis	50% mortality if severe; survivors often have permanent disability
Prevention	Strict adherence to correction limits

9. Prognosis and Outcomes

Natural History

Scenario	Outcome
Drug-induced SIADH	Usually resolves 2-4 weeks after drug cessation
Malignancy-associated	Depends on underlying cancer prognosis
CNS-associated	May be transient or persistent
Idiopathic	May require long-term management

Mortality Data

Sodium Level	In-Hospital Mortality
Na more than 135	1-2%
Na 130-135	2-4%
Na 125-129	5-10%
Na less than 125	15-25%
Na less than 120	25-50%

Long-Term Outcomes

Outcome	Data
30-day mortality (severe hyponatraemia)	10-15%
1-year mortality (cancer-associated SIADH)	60-80%
Falls risk	4× increased in chronic hyponatraemia
Cognitive recovery	Most recover, but subtle deficits may persist
ODS recovery	Variable; 50% mortality, survivors often disabled

10. Evidence and Guidelines

Major Guidelines

Guideline	Year	Key Recommendations
European Clinical Practice Guidelines	2014	Comprehensive hyponatraemia management; 150 mL 3% NaCl boluses; urea as second-line; max 10 mmol/L/24h
US Expert Panel Recommendations	2013	Similar principles; emphasizes 4-8 mmol/L/day for safety
NICE Clinical Knowledge Summaries	2022	Diagnosis and initial management pathway

Landmark Trials

Trial	Year	N	Key Finding	PMID
SALT-1 and SALT-2	2006	448	Tolvaptan significantly increased serum Na+ vs placebo in SIADH, heart failure, cirrhosis	17105757
INSIGHT	2015	57	Fluid restriction combined with salt tablets effective	25870972
EVEREST	2007	4133	Tolvaptan improved Na+ but no mortality benefit in heart failure	17384437
Urea meta-analysis	2018	343	Urea effective and safe for chronic SIADH	29556453

Evidence Levels

Intervention	Evidence Level	Strength
Fluid restriction	Low-Moderate	First-line despite limited RCT data
Hypertonic saline (severe)	Moderate	Observational data; guideline consensus
Tolvaptan	High	RCT evidence (SALT trials)
Urea	Moderate	Observational + meta-analysis
Demeclocycline	Low	Older studies; limited modern data

11. Patient Explanation

Simple Explanation

What is SIADH? SIADH stands for "Syndrome of Inappropriate Antidiuretic Hormone." Normally, a hormone called ADH tells your kidneys when to hold onto water and when to release it. In SIADH, your body makes too much of this hormone when it shouldn't, causing your kidneys to hold onto too much water. This dilutes the sodium in your blood, which can make you feel unwell.

What causes it? Common causes include:

Some medicines (especially antidepressants and anti-seizure drugs)
Lung infections like pneumonia
Brain conditions like stroke or infection
Some cancers, especially lung cancer
Sometimes we can't find a cause

What are the symptoms?

Feeling very tired or weak
Feeling sick (nausea)
Headaches
Confusion
If severe: fits (seizures) or becoming unconscious

How is it treated?

Limit your fluids: We usually ask you to drink less (often less than 1 litre per day). This helps your body get rid of the extra water.
Find the cause: If a medicine is causing it, we may stop that medicine. If there's an infection, we treat it.
Medicines: If fluid restriction doesn't work, we might use other tablets to help.
Emergency treatment: If your sodium is very low and you're having fits, we give you a strong salt solution through a drip.

What do I need to watch for?

If you feel more confused or drowsy
If you have a seizure
Severe headache or vomiting

12. References

Ellison DH, Berl T. Clinical practice. The syndrome of inappropriate antidiuresis. N Engl J Med. 2007;356(20):2064-2072. doi:10.1056/NEJMcp066837. PMID: 17507705
Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-42. doi:10.1016/j.amjmed.2013.07.006. PMID: 24074529
Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014;170(3):G1-47. doi:10.1530/EJE-13-1020. PMID: 24569125
Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355(20):2099-2112. doi:10.1056/NEJMoa065181. PMID: 17105757
Decaux G, Andres C, Gankam Kengne F, Soupart A. Treatment of euvolemic hyponatremia in the intensive care unit by urea. Crit Care. 2010;14(5):R184. doi:10.1186/cc9292. PMID: 20946652
Fenske W, Störk S, Koschker AC, et al. Value of fractional uric acid excretion in differential diagnosis of hyponatremic patients on diuretics. J Clin Endocrinol Metab. 2008;93(8):2991-2997. doi:10.1210/jc.2008-0330. PMID: 18456574
Sterns RH. Disorders of plasma sodium--causes, consequences, and correction. N Engl J Med. 2015;372(1):55-65. doi:10.1056/NEJMra1404489. PMID: 25551526
Bartter FC, Schwartz WB. The syndrome of inappropriate secretion of antidiuretic hormone. Am J Med. 1967;42(5):790-806. doi:10.1016/0002-9343(67)90096-4. PMID: 5337379
Liamis G, Mitrogianni Z, Liberopoulos EN, Tsimihodimos V, Elisaf M. Electrolyte disturbances in patients with hyponatremia. Intern Med. 2007;46(11):685-690. doi:10.2169/internalmedicine.46.6223. PMID: 17541221
Sahay M, Sahay R. Hyponatremia: A practical approach. Indian J Endocrinol Metab. 2014;18(6):760-771. doi:10.4103/2230-8210.141320. PMID: 25364669
Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol. 2009;29(3):282-299. doi:10.1016/j.semnephrol.2009.03.002. PMID: 19523575
NICE. Hyponatraemia - NICE CKS. 2022. Available at: https://cks.nice.org.uk/topics/hyponatraemia/
European Society of Endocrinology Clinical Guideline: Understanding hyponatraemia. 2014. PMID: 24569125
Konstam MA, Gheorghiade M, Burnett JC Jr, et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. JAMA. 2007;297(12):1319-1331. doi:10.1001/jama.297.12.1319. PMID: 17384437
Rondon-Berrios H, Berl T. Vasopressin receptor antagonists: characteristics and clinical role. Best Pract Res Clin Endocrinol Metab. 2016;30(2):289-303. doi:10.1016/j.beem.2016.02.004. PMID: 27156765

13. Examination Focus

Common Exam Questions

Question Type	Example
MCQ	A 68-year-old on sertraline presents with Na+ 118 mmol/L, plasma osmolality 265, urine osmolality 420. What is the most likely diagnosis?
SAQ	Describe the diagnostic criteria for SIADH and outline first-line management.
OSCE	Counsel a patient about fluid restriction for SIADH.
Viva	Discuss the causes and emergency management of severe hyponatraemia.

High-Yield Viva Points

Topic	Key Points
Diagnosis	Low serum osm, high urine osm (more than 100), urine Na more than 30, euvolaemic, exclude thyroid/adrenal
Causes	Malignancy (SCLC), drugs (SSRIs, carbamazepine), CNS, pulmonary
Emergency treatment	3% NaCl 150 mL over 20 min; target 5 mmol/L rise in 1h; max 10 mmol/L/24h
ODS	Occurs 2-6 days after overcorrection; pontine demyelination; dysarthria, quadriparesis
Second-line	Urea, tolvaptan, demeclocycline, salt + loop diuretic

Common Mistakes

Mistake	Correct Approach
Diagnosing without excluding thyroid/adrenal disease	Always check TFTs and cortisol
Correcting Na+ too fast	Maximum 10 mmol/L in 24 hours
Using 0.9% saline in SIADH	May worsen hyponatraemia due to ADH effect
Missing drug cause	Review all medications, especially SSRIs
Ignoring chronic symptoms	Even mild hyponatraemia causes cognitive and gait issues

Examination Cheat Sheet

Parameter	Value
Serum osmolality	less than 275 mOsm/kg
Urine osmolality	more than 100 mOsm/kg
Urine sodium	more than 30 mmol/L
Volume status	Euvolaemic
Emergency Na threshold	less than 120 mmol/L or symptomatic
Hypertonic saline dose	150 mL 3% NaCl over 20 min
Maximum correction	10 mmol/L in 24 hours
ODS timing	2-6 days post-correction