Episode 5: Hyponatremia Schema and SIADH

CHECK OUT THIS CPSOLVERS LINK FOR AN AWESOME HYPONATREMIA SCHEMA: https://clinicalproblemsolving.com/dx-schema-hyponatremia/

SIADH

What is SIADH?

Unsuppressed release of ADH characterized by water excretion impairment

Etiology

Central nervous system disturbances= trauma, stroke, hemorrhage, infection, trauma, mental illness/psychosis
Malignancy= Small Cell Lung Cancer (formation of ectopic ADH)
Drugs= carbamazepine, oxacarbazepine, chlorpropamide, cyclophosphamide, and SSRIs (the drug either increases ADH release, mimcs ADH to agonize the receptors, or increases V2 receptors)
Iatrogenic= think CNS surgery like removal of pituitary adenoma
Pulmonary diseases= pneumonia
Exogenous Hormone Administration= desmopressin for treatment of VWD hemophilia, or platelet dysfunction, vasopressin to control GI bleeds, or oxytocin during L/D (why? They all increase V2 receptors)

Normal Physiology

ADH= antidiuretic hormone (anti-loss of water hormone)
Main function of ADH is osmoregulation, or maintaining plasma tonicity and electrolye balance in the body
It is formed in the hypothalamus and released by the posterior pituitary cells
ADH is released when there is increased tonicity in the plasma/hypovolemia--à acts on V2 receptors in the renal collecting ducts
Result of ADH action= formation of aquaporin-2 water channels in the tubular cells that reabsorb water via concentration gradient action
ADH also acts on vascular smooth muscle via V receptor agonistà vascular constrictionà increased systemic vascular resistance (a good way to maintain blood pressure in a hypovolemic state)

Pathophysiology

Too much ADH? Leads to excessive water reabsorption-->dilution hyponatremia
Euvolemia… But why? Even though ADH is pulling in a lot of water, the body has other ways to get rid of water… by removing excess salts and creating a gradient for the water to follow… but now getting rid of salts will worsen the hyponatremia
Cerebral edema is the main source of signs/symptoms and the severity of condition is based on degree of cerebral edema
Hyponatremia= decreased ECF osmolality (hypotonic solution outside of the cells)=water will move along its concentration gradient into cells= cellular edema in the brain!

Signs and Symptoms

Mild hyponatremia (>130mmol/L)= nausea, malaise, may even by asymptomatic
Moderate hyponatremia (125-130mmol/L)= vomiting, headache, anorexia
Altered Mental status worsens from 115-125mmol/L = confusion, agitation, hallucination, incontinence
Severe (<115mmol/L)= seizures, obtundation, coma, respiratory arrest (death)
NOTE: A case of chronic SIADH will have less severe symptoms because of cerebral adaptation over time
An interesting pearl: asymptomatic patients with chronic hyponatremia have increased risk of falling, as well as increased risk of fracture with fall… Check out this article to learn more: https://cdn.mdedge.com/files/s3fs-public/pdfs/journals/1932_ftp.pdf

Diagnosis

Tests to order: BMP, Serum osmolality, Urine sodium concentration and osmolality, BUN and Creatinine, Thyroid profile, Random Blood Glucose, Serum Cortisol, Fasting Lipid Profile, LFTs .......WHY ALL THESE TESTS: confirm our suspicions and rule out hypothyroidism, adrenal insufficiency, and other causes of hyponatremia
The Schwartz and Bartter Clinical Criterion give us a way to diagnose SIADH because there isn’t any single confirmatory test (SEE IMAGE BELOW)

Let’s Talk About Why We See These Test Results

Posm < 275 mOsm/Kg H2O = Hypoosmolar serum is due to dilution of serum by all the water that ADH is telling the kidney to reabsorb

Uosm >100 mOsm/kg H2O = Hyperosmolar urine because the body is compensating for the influx of water by trying to get rid of all the salt

Clinical euvolemia= we do not see a hypervolemic state because the body is still able to compensate for the water influx

Elevated urinary sodium excretion while on a normal salt and water intake= the body is compensating for the influx of water by trying to get rid of all the salt, this means loss of sodium.

Abnormal water load test, absence of correction of serum sodium with volume expansion but improvement after fluid restriction= again, makes sense, ADH is soaking up the water and the body is compensating by pushing out more and more salt. But if we restrict water, we are not adding more water PO to the equation and we are essentially starving out the available water for ADH to get to, so there will be a slight improvement in sodium levels as volume contracts in the vascular space

Treatment

2 treatment goals: CORRECT HYPONATREMIA and CORRECT UNDERLYING CAUSES
The Choice of treatment depends on the severity of symptoms at presentation
Mild/moderate sx= fluid restriction <800ml/day and oral salt tablets +/- loop diuretics
Severe sx= we need to correct Na faster than fluid restriction can; 100ml bolus of 3% NS and repeat measurements to monitor rise in Na
In order to correct hyponatremia with fluids, the sodium level must be greater than the urine osmolality (urine osmolality is very high!!) This means 3% NS
Long term treatment= Vasopressin receptor anatagonists (tolvaptan) prevent ADH action by antagonizing V2 receptors

A CRITICAL PEARL WHEN IT COMES TO CORRECTING ANY SODIUM LEVELS!!!!

Rate of correction is extremely important; if you correct hyponatremia too quickly, you can cause osmotic demyelination syndrome… this is LETHAL… check it out and understand why

Safe rate of sodium correction= no more than 8 mEq/L per 24 hours or 0.5-1mEq/L per hour