Hyponatraemia Flashcards
Hyponatraemia may be caused by-?
Water excess or sodium depletion
Causes of pseudohyponatraemia
-
High blood lipid or protein >>>
- Hyperlipidaemia (raised serum volume)
- Hyperproteinaemia (as in myeloma)
- Taking blood from a drip arm
Why is it important to diagnose pseudohyponatraemia?
Because, As the plasma osmolality is normal >>> no treatment is required
Diagnostic tests of hyponatraemia
- Urinary sodium
- Plasma osmolarity level
Relation between Na (sodium) level and blood glucose level
Hyperglycaemia causes hyponatraemia
100mg/dL increase of blood glucose >>> Lower Na level as much as 1.6mEq
Relation between Na salt and blood pressure
Adding 6g NaCl salt per day >>> Adds 10mmHg systolic BP
(As such, cutting down 6g NaCl salt/day >>> Lowers systolic BP by 10mmHg)
Normal plasma osmolality (isotonic)
275 to 290 mOsm/L (= mOsm/Kg = mmol/Kg)
Hypertonic plasma osmolality
>290mOsm/L (= mOsm/Kg = mmol/Kg)
Hypotonic plasma osmolality level
<275 mOsm/L (= mOsm/Kg = mmol/Kg)
Classification of hyponatraemia
Classification of hyponatraemia (Na <135mmol/L)
By plasma (=serum) osmolality
- Hypertonic (plasma osmolality >290)
- Isotonic (plasma osmolality 275 to 290)
-
Hypotonic (plasma osmolality <275) (Most common)
- High volume
- Normal volume
- Low volume
By urinary sodium (Na)
-
Urinary sodium >20mmol/L
- Na depletion, renal loss (patient often hypovolaemic)
- Patient often euvolaemic
-
Urinary sodium <20mmol/L
- Na depletion, extra-renal loss
- Water excess (patient often hypervolaemic and oedematous)
Hypertonic hyponatraemia >>> Causes
(Na <135mmol/L + plasma osmolality >290mOsm/L)
-
Severe hyperglycaemia
- DKA
- HHS
- Hypertonic mannitol
Isotonic hyponatraemia >>> Causes
(Na <135mmol/L + plasma osmolality 275-290mOsm/L)
-
Pseudohyponatraemia
- Hyperlipidaemia (raised serum volume)
- Taking blood from a drip arm
-
Na free irrigant solutes
- Hysterectomy
- TURP (Trans-urethral resection of prostate)
Hypotonic hyponatraemia >>> Classification
(Na <135mmol/L + plasma osmolality <275mOsm/L) >>> Classification
- High volume
- Normal volume
- Low volume
Hypotonic hyponatraemia + high ECF volume >>> Causes
(Na <135mmol/L + Plasma osmolality <275mOsm/L + high ECF volume) >>> Causes
Includes interstitial fluid shift
- CCF (Congestive cardiac failure) >>> oedema
- Liver Cirrhosis >>> oedema
- Nephrotic syndrome >>> oedema
- Renal failure (ARF or CRF) >>> oedema
- Sepsis
- Anaphylaxis
- Pregnancy
Hypotonic hyponatraemia + normal ECF volume >>> Causes
(Na <135mmol/L + Plasma osmolality <275mOsm/L + normal ECF volume) >>> Causes
Limited interstitial fluid shift
-
SIADH (following are the causes of SIADH)
-
Malignancy (Mass lesions)
- Small cell lung cancer (SCLC)
- Pancreatic cancer, prostatic cancer
-
CNS disorders/Neurological (all relate to bleeding)
- Stroke
- Haemorrhage (subarachnoid, subdural)
- Meningitis, Encephalitis, Abscess
- Surgery
- Trauma
-
Pulmonary infections
- TB
- Pneumonia
-
Other pulmonary causes
- Acute respiratory failure
- Positive-pressure ventilation
-
Drugs
- Sulfonylureas (e.g. Chlorpropamide)
-
SSRIs
- Citalopram,Escitalopram,Fluoxetine,Paroxetine,Sertraline
- TCA, antipsychotics, neuroleptics
- Carbamazepine, Na-valproate
- Cyclophosphamide
- Cisplatin
- Vinca alkaloids (Vincristine, Vinblastine)
- Ecstasy (MDMA)
- Desmopressin (A Tx of DI)
- Others: Porphyrias (e.g. AIP)
-
Malignancy (Mass lesions)
- Hypothyroidism
- Secondary adrenal insufficiency
- Carcinomas
-
Decreased intake of solutes
- Beer potomania
- Tea-and-toast diet
- Primary polydipsia
Hypotonic hyponatraemia + Low ECF volume >>> Causes
(Na <135mmol/L + Plasma osmolality <275mOsm/L + low ECF volume) >>> Causes
-
Cerebral salt wasting
- Haemorrhage
- Surgery
- Trauma
- Hypokalaemia (K <3.5mmol/L)
-
Renal Na loss (Urinary Na>20mmol/L)
- Diuretic agents: Loop diuretics, Thiazides, Indapamide, Amiloride etc.
- Osmotic diuretics: Mannitol, urea, glucose etc.
- Addison’s disease (Primary adrenal insufficiency)
- Salt wasting neprhopathy
- Lithium
- Bicarbonaturia
- Ketonuria
-
Extra-renal Na loss (Urinary Na<20mmol/L)
- Diarrhoea
- Vomiting
- Blood loss
- Excessive sweating
-
Fluid sequestration ‘3rd space’
- Bowel obstruction
- Peritonitis
- Pancreatitis
- Muscle trauma
- Burns
Hyponatraemia (Serum Na <135mmol/L) + Urinary Na >20mmol/L
Na depletion, renal loss (patient often hypovolaemic)/ dehydrated
- Diuretic agents: Loop diuretics, Thiazides, Indapamide, Amiloride etc.
- Osmotic diuretics: Mannitol, glucose, urea etc.
- Diuretic stage of renal failure
- Acute tubular necrosis of ARF (urinary Na >40mmol/L)
- Addison’s disease (Adrenal insufficiency)
Patient often euvolaemic
- SIADH (urine osmolarity >100mOsm/L or mmol/Kg (often >500) > with all its causes
- Hypothyroidism
Hyponatreamia (Serum Na <135mmol/L) + Urinary Na <20mmol/L >>> Causes
Na depletion, extra-renal cause
- Dirrhoea
- Vomiting
- Sweating
- Burns
- Adenoma of rectum
Water excess (patient is often hypervolaemic + oedematous)
-
Secondary hyperaldosteronism
- CCF, Cirrhosis (both >> oedema)
- Liver cirrhosis
- Nephrotic syndrome
- Low GFR: Renal failure + volume overload (=oedema)
- IV dextrose
- Psychogenic polydipsia
Pre-renal uraemia of ARF has urine Na <20mmol/L
Hyponatraemia >>> Approach to diagnosis (finding the cause)
- In hyponatraemia >>> check urinary Na
-
If urinary Na >20mmol/L >>>
- Check if hypovolaemic or Na depletion by renal loss (See relevent causes)
- OR euvolaemia (See relevent causes)
-
If urinay Na <20mmol/L >>>
- Check if hypovolaemic or Na depletion by extra-renal loss (See relevent causes)
- OR hypervolaemia (See relevent causes)
SIADH is characterised by - ?
Hyponatraemia secondary to the dilutional effects of excessive water retention
SIADH >>> Mechanism
Due to inappropriate ADH secretion >>> excessive water retention >>> dilutional effects >>> hyponatraemia (low Na conc.) >>> low plasma osmolality + high urine osmolality + elevated urine sodium (above 20 mmol/L)
(Free water excretion is likely to be reduced)
SIADH >>> Findings
- Na conc. in blood: <135mmol/L
- Urine Na: >20 mmol/L
- Plasma osmolarity: <275 mOsm/kg
- Urine osmolarity: >100 mOsm/kg (often >500mmol/kg)
SIADH >>> Causes
-
Malignancy (Mass lesions)
- Small cell lung cancer (SCLC)
- Pancreatic cancer, prostatic cancer
-
CNS disorders/Neurological (all relate to bleeding)
- Stroke
- Haemorrhage (subarachnoid, subdural)
- Meningitis, Encephalitis, Abscess
- Surgery
- Trauma
-
Pulmonary infections
- TB
- Pneumonia
-
Other pulmonary causes
- Acute respiratory failure
- Positive-pressure ventilation (PPV)
-
Drugs
- Sulfonylureas (e.g. Chlorpropamide)
- SSRIs
- Citalopram, Escitalopram, Fluoxetine, Paroxetine, Sertraline
- TCA, antipsychotics, neuroleptics
- Carbamazepine, Na-valproate
- Cyclophosphamide
- Cisplatin
- Vinca alkaloids (Vincristine, Vinblastine)
- Ecstasy (MDMA)
- Desmopressin (A Tx of DI)
- Others: Porphyrias (e.g. AIP)
SIADH >>> Dx Criteria
- Hyponatraemia (Na <135mEq/L)
- Urine Na >20mEq/L
- Plasma/serum osmolarity is decreased (<270mOsm/kg)
- Urine osmolarity is greater than that of serum osmolarity (inappropriately high urine osmolarity >100mOsm/L)
- No clinical evidence of oedema (fluid overload) or dehydration [Patient is euvolaemic]
- Normal adrenal, normal renal, normal thyroid function [adrenal insufficiency, renal failure, and thyroid disorder are excluded]
SIADH >>> other diagnosting points
(also to check these, after main Dx criteria)
- Suppression of RAS (Renin Angiotensin System)
- No equal concentration of ANP (atrial natriuretic peptide)
- Maintained hypervolemia
- Normal serum creatinine
- Normal acid base and K balance
- ↓BUN
- ↓Uric acid
- ↓Albumin
SIADH >>> Association
AIP (Acute intermittent Porphyria)
SIADH >>> Management
- Fluid restriction
-
Slow correction of Na
- Rapid correction >>> precipitates central pontine myelinolysis
-
DOC: Demeclocycline
- M/A: reduces the responsiveness of the collecting tubule cells to ADH
- S/E: Nephrogenic DI
- ADH (vasopressin) receptor antagonists (have been developed recently);
Also Lithium can do so >> so, sometimes used as a treatment of SIADH >>> S/E: Nephrogenic DI
Why do we need to slowly correct the hyponatraemia in SIADH management?
Because rapid correction precipitates central pontine myelinolysis
Demeclocycline >>> Mechanism
It reduces the responsiveness of the collecting tubule cells to ADH
Demeclocycline >>> Side effect
Nephrogenic Diabetes insipidus
How are SIADH & Diabetes insipidus related regarding cause & treatment?
- Lithium & Demeclocyline cause nephrogenic DI ; But they treat SIADH
- Desmopression treat Nephrogenic DI ; But it causes SIADH
- Diabetes insipidus itself is a cause of “hypernatraemia”
Drug causes of SIADH
- Sulfonylureas (e.g. Chlorpropamide)
-
SSRIs
- Citalopram, Escitalopram, Fluoxetine, Paroxetine, Sertraline
- TCA, antipsychotics, neuroleptics
- Carbamazepine, Na-valproate
- Cyclophosphamide
- Cisplatin
- Vinca alkaloids (Vincristine, Vinblastine)
- Ecstasy (MDMA)
- Desmopressin (A Tx of DI)
Drug causes of hyponatraemia
By the mechanism of SIADH + reduced urinary Na reabsorption + high urinary Na excretion >20mmol/L + normovolaemia (normal ECF volume)
- Sulfonylureas (e.g. Chlorpropamide)
-
SSRIs
- Citalopram, Escitalopram, Fluoxetine, Paroxetine, Sertraline
- TCA, antipsychotics, neuroleptics
- Carbamazepine, Na-valproate
- Cyclophosphamide
- Cisplatin
- Vinca alkaloids (Vincristine, Vinblastine)
- Ecstasy (MDMA)
- Desmopressin (A Tx of DI)
NOT by mechanism of SIADH + BUT by reduced urinary Na reabsorption + high urinary Na excretion >20mmol/L + hypovolaemia (low ECF volume)
- Diuretic agents: Loop diuretics, Thiazides, Indapamide, Amiloride etc.
- Osmotic diuretics: Mannitol, glucose, urea etc.
- Lithium
What is Beer potomania?
- A recognized cause of hyponatraemia in alcohol misusers
- Findings: “osmolar gap” due to presence of osmotically active “ethanol” in the blood
- Tx: the electrolyte imbalance normally corrects itself with cessation of alcohol.
Ascites and hyponatraemia - any relation?
- Patients with CLD and ascites >>> often “hyponatraemia” (difficult to manage)
- Diuretic therapy for the management of ascites often contributes to the hyponatraemia.
Patient with ascites (CLD) with hyponatraemia >>> Management?
British society of gastroenterology guidelines suggest >>>
-
If serum Na ≤120 mmol/L >>>
- Stop diuretic therapy
- Volume expansion (with colloid or normal saline)
-
If serum Na 121 to 125 mmol/L >>>
- Check Sr. creatinine >>> if normal >>> may continue diuretic therapy (but reduce the dose) (so that > if necessary, we can stop it)
-
If serum Na 126-135 mmol/L >>>
- No specific intervention
- Only careful monitoring
-
If serum Na is normal + but sr. creatinine is rising (high) >>>
- Stop diuretic therapy
- Volume expansion (with colloid or normal saline)
-
When to give fluid restriction >>>
-
Only in them who are >>>
- Clinically euvolaemic + not on diuretics + severe hyponatraemia + normal serum creatinine
-
Only in them who are >>>
ADH >>> chemical nature
A nona-peptide (nona = 9)
ADH is manufactured in - ?
Supra-optic (SO) and paraventricular (PV) nuclei of the hypothalamus
ADH is released (secreted) from - ?
Posterior pituitary
ADH: Mechanism of action
- It acts on the collecting ducts >>> improves water permeability >>> hence, water retention
- It inserts aquaporin-2 channels in the collecting ducts of the kidneys >>> promotes water reabsorption
ADH >>> site of action
collecting ducts
ADH secretion is potentiated (increased) by - ?
- Sulfonylureas (e.g. Chlorpropamide)
-
SSRIs
- Citalopram, Escitalopram, Fluoxetine, Paroxetine, Sertraline
- TCA, antipsychotics, neuroleptics
- Carbamazepine, Na-valproate
- Cyclophosphamide
- Cisplatin
- Vinca alkaloids (Vincristine, Vinblastine)
- Ecstasy (MDMA)
- Desmopressin (A Tx of DI)
(All the drug causes of SIADH)
ADH secretion is inhibited by - ?
Ethanol
