SIADH Flashcards

1
Q

SIADH

A

The syndrome of inappropriate ADH secretion (SIADH) is characterised by hyponatraemia secondary to the dilutional effects of excessive water retention.

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2
Q

Causes of SIADH

A

Causes of SIADH

Malignancy:
small cell lung cancer
also: pancreas, prostate

Neurological:
stroke
subarachnoid haemorrhage
subdural haemorrhage
meningitis/encephalitis/abscess

Infections:
tuberculosis
pneumonia

Drugs:	
sulfonylureas*
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide
MDMA/Ecstasy
*the BNF states this has been reported with glimepiride and glipizide.

Other causes
positive end-expiratory pressure (PEEP)
porphyrias

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3
Q

SIADH - Mx

A

Management
correction must be done slowly to avoid precipitating central pontine myelinolysis
fluid restriction
demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
ADH (vasopressin) receptor antagonists have been developed

NB: The initial treatment option for SIADH is by fluid restriction which, under most circumstances, will correct the biochemical abnormalities in almost every case.

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4
Q

SIADH Diagnosis: Example Question

A

A 58-year-old patient who has a history of hypertension is operated on by the neurosurgeons for an intracranial haemorrhage.

Over the next few days his serum sodium level progressively declines and by the third day has fallen to 118 mmol/l despite fluid restriction to 1L per day. Urine osmolarity is 700 mOsmo/l and urinary sodium is raised at 80 mmol/l.

What is the most likely diagnosis?

	Addisonian crisis
	> Secretion of inappropriate antidiuretic hormone
	Cranial diabetes insipidus
	Hypovolaemia
	Fluid overload

The hyponatraemia and hypotonic blood plasma, coupled with the raised urine osmolality and raised urinary sodium excretion indicates a diagnosis of syndrome of inappropriate ADH secretion. This is a condition that can occur after head trauma, a central nervous system infection and intracranial haemorrhage.

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5
Q

SIADH vs Cerebral Salt Wasting Syndrome : Example Question

A

A 72-year-old woman is recovering on the neurosurgical unit following a subdural haemorrhage. Four days earlier she underwent Burr hole surgery. You are asked to see her due to a persistently low sodium for the past three days. You note the following investigations:

Day 2 post-surgery
Serum Na+ 116 mmol/l

Day 3 post-surgery
Serum Na+ 117 mmol/l

Day 4 post-surgery
Serum Na+ 115 mmol/l
Urinary Na+ 25 mmol/l
Serum osmolality 280 mmol/l

Examination of the patient demonstrates dry mucous membranes and delayed capillary refill time.

What is the most likely diagnosis?

	SIADH
	Diabetes insipidus
	> Cerebral salt wasting syndrome
	Renal tubular acidosis type IV
	Sheehan's syndrome

Diabetes insipidus is classically associated with hypernatraemia. Sheehan’s syndrome refers to the specific situation of pituitary necrosis following childbirth. The cardinal feature of renal tubular acidosis type IV is hyperkalaemia.

This leaves SIADH and cerebral salt wasting syndrome. The hydration status in this patient can be considered hypovolaemic making SIADH unlikely (typically euvolaemic). Additionally, this diagnosis should only be made in the absence of hypothyroidism and adrenal dysfunction.

Cerebral salt wasting syndrome can occur following neurosurgery. It occurs due to sodium wasting in the urine. Comparatively, it is treated with replacing fluid and sodium losses.

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6
Q

Causes of SIADH

A

The causes of SIADH are as follows

1. Tumours
Small cell CA of the lung
Prostate
Thymus
Pancreas
Lymphoma
  1. Pulmonary Lesions
    Pneumonia
    Tuberculosis
    Lung abscess
3. CNS Causes
Meningitis
Tumours
Head injury
Subdural haematoma
Cerebral abscess
SLE
Vasculitis
  1. Metabolic Causes
    Alcohol withdrawal
    Porphyrias
5. Drugs
Carbamazepine
Chlorpropamide
Cyclophosphamide
Vincristine
Phenothiazines
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7
Q

SIADH 2dry to Carbamazepine Treatment: Example Question

A

A 28-year-old male with a history of epilepsy, for which he is taking carbamazepine and has not had any seizures for the last two years, presents with irritability and nausea for the last 2 weeks. His girlfriend says that he is often confused and seems to be lost most of the time. He takes alcohol occasionally and smokes ten to twelve cigarettes per day.

On examination, he is irritable but conscious and alert. Clinical examination revealed eczema over the face, shins and extensor surfaces of the forearms and a tattoo on the right shoulder. There was no evidence of any peripheral oedema.

Lab reports were as follows:

Hb	150 g/l
MCV	81 fl
MCH	31 pg
WBC	9 * 109/l
Plt	250 * 109/l
Urea	3.2 mmol/l
Creatinine	75 µmol/l
9:00 am Cortisol	345 nmol/l	(170 700 nmol/l)
TSH	2.4 mU/l
Total T4	102 nmol/l	(68 174 nmol/l)
Na+	119 mmol/l
K+	4.2 mmol/l

Which of the following would be the most appropriate initial management option?

	> Fluid restriction to 500 - 1000 ml daily
	Demeclocycline 600 - 1200 mg daily
	IV hypertonic saline
	Intranasal desmopressin twice daily
	Hydrochlorothiazide 12.5 mg daily

The diagnosis in the scenario described above is SIADH secondary to carbamazepine treatment. The findings of eczema are coincidental and have no bearing on the diagnosis. However, in the management the presence of skin lesions such as eczema may pose difficulty in opting for the use of demeclocycline which may cause photosensitive rashes.

The initial treatment option for SIADH is by fluid restriction which, under most circumstances, will correct the biochemical abnormalities in almost every case.

Demeclocycline is indicated if fluid restriction is poorly tolerated or ineffective.

Hypertonic saline is indicated only when the syndrome is very severe, acute and symptomatic.

Intranasal desmopressin is used for the management of diabetes insipidus, and thiazide diuretics are only rarely used as alternative agents in diabetes insipidus.

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8
Q

Correction of Hyponatraemia - Cx:

A

Hyponatraemia: correction

Central pontine myelinolysis
demyelination syndrome caused by rapid correction of chronic hyponatraemia
may lead to quadriparesis and bulbar palsy
diagnosis: MRI brain

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9
Q

SIADH - Diagnosis: Example Question

A

A 70-year-old man with a history of smoking 15 cigarettes/day presents with drowsiness, weight loss and a persistent cough. His investigations show:

Na+ 115 mmol/l (135-145 mmol/l)
K+ 5.1 mmol/l (3.5 - 5.0 mmol/l)
Urea 3 mmol/l (2.0-7 mmol/l)
Creatinine 74 µmol/l (55-120 µmol/l)

Plasma osmolality
270 mOsm/kg (285-295 mOsm/kg)
Urine osmolality 1210 (500 - 800 mOsm/kg)

What is the most likely diagnosis?

	> Small cell lung cancer
	Hypothyroidism
	Encephalitis
	Congestive cardiac failure
	Squamous cell carcinoma

Hyponatraemia, reduced plasma osmolality and increased urine osmolality are suggestive of syndrome of inappropriate ADH secretion (SIADH).

The increase in ADH causes more aquaporin utilisation in the collecting duct system of the kidney. This causes more water to be retained, diluting the electrolytes in the blood and making the electrolytes in the urine more concentrated.

Small cell lung cancer is a common cause of SIADH and is the most likely diagnosis in this man with an extensive smoking history, cough and weight loss.

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10
Q

SIADH and CAP - Example Question

A

An elderly male presents with a 2 week history of breathlessness. His past medical history includes diet-controlled type 2 diabetes, ischaemic heart disease, hypothyroidism and depression. His medication list includes levothyroxine, aspirin, simvastatin, ramipril, bisoprolol and citalopram. Observations on presentation to Emergency Department are as follows: respiratory rate 26/min, saturations 94% (on 4 litres oxygen via Venturi), heart rate 80 beats per minute, blood pressure 156/82 mmHg. Auscultation demonstrates crackles at the left base with no wheeze. The abdomen is soft and non-tender. There is no oedema peripherally.

Blood results on admission are provided below:

Hb	134 g/l
Platelets	172 * 109/l
WBC	13.3 * 109/l
Na+	128 mmol/l
K+	5.1 mmol/l
Urea	13 mmol/l
Creatinine	178 µmol/l
Serum osmolality	220 mosm/kg
Urinary sodium	50 mEq//l

What is the most likely cause of hyponatraemia?

	Hypothyroidism
	Chronic kidney disease
	Addison's disease
	Salt-losing nephropathy
	> Syndrome of inappropriate antidiuretic hormone (SIADH)

This question demonstrates a common scenario in clinical practice. Management of hyponatraemia first requires clarification of fluid status (clinical hypovolaemia, euvolaemia or hypervolaemia), as differentials are influenced by this. This patient’s history, examination findings and haemodynamic parameters are consistent with clinical euvolaemia.

Differentials for euvolaemic hyponatraemia would include hypothyroidism and SiADH. There are no clinical features suggestive of the former. Findings are consistent with community-acquired pneumonia with associated SiADH. This is confirmed by the presence of reduced serum osmolality and high urinary sodium. Measurement of urinary sodium concentration is an useful adjunct in helping to differentiate between hyponatraemia secondary to hypovolaemia and SiADH. With SiADH (and salt-wasting syndrome), the urinary sodium is high. With hypovolaemia, the urinary sodium is typically low.

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11
Q

ADH

A

ADH is secreted from the posterior pituitary gland - promotes water reabsorption in collecting ducts of kidneys by insertion of aquaporin-2-channels

SOURCE = synthesised in supraoptic nuclei of the hypothalamus, released by pituitary

FUNCTION = Conserves body water! Promotes water reabsorption in the collecting ducts of the kidneys by insertion of aquaporin-2-channels

Regulation:
INCREASES SECRETION OF ADH
- ECF osmolality increase
- volume decrease
- pressure decrease
- angiotensin II

DECREASES SECRETION OF ADH

  • ECF osmolality decrease
  • volume increase
  • temperature decrease

NB Diabetes insipidus is either a deficiency of ADH (Cranial) or an insensitivity to ADH (Nephrogenic)

Cranial DI can therefore be treated with ADH analogue! = Desmopressin

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12
Q

SIADH Mx

A

The initial treatment option for SIADH is by fluid restriction which, under most circumstances, will correct the biochemical abnormalities in almost every case.

Demeclocycline (reduced responsiveness of collecting tubule cells to ADH) is indicated if fluid restriction is poorly tolerated or ineffective.

Hypertonic saline is indicated only when the syndrome is very severe, acute and symptomatic.

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13
Q

Cerebral Salt Wasting Syndrome vs SIADH

A
Both can occur after Neurosurgery
Both = Hyponatraemia
BUT
SIADH= Euvolaemic
Cerebral Salt wasting syndrome = Hypovolaemic

Cerebral salt wasting syndrome can occur following neurosurgery. It occurs due to sodium wasting in the urine. Comparatively to SIADH which is managed with fluid restriction, it is treated with replacing fluid and sodium losses.

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14
Q

THINK SIADH IF:

A

EUVOLAEMIC
HYPONATRAEMIC
HIGH URINE OSMOLALITY
REDUCED PLASMA OSMOLALITY

Increase in ADH = more aquaporin utilisation in the collecting duct system of the kidney = more water retained = dilutes the electrolytes in the blood making the electrolytes in the urine more concentrated.

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