Thirst axis
Renin- angiotensin aldosterone (RAA) axis
Hypothalamic-Pituitary -ADH axis
Two hormones are involved with the regulation intravascular volume
Aldosterone :Reabsorbs salt and water in isotonic proportions
ADH :
Reabsorbs water only
In the presence of volume depletion 2 mechanisms come into play.
The juxtaglomerular cells secrete renin which promotes the conversion of angiotensinogen (inactive form ) produced by the liver to angiotensin 1.
Angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzyme. Angiotensin 2 promotes the secretion of Aldosterone by the adrenal cortex which promotes reabsorption of Na and Water thereby restoring volume status back to normal.
Hyponatremia
- Severe <120 meq/L
- Moderate 120 to 129 meq/L
- Mild 130-135 meq/L
May be classified according to (3)
- SERUM OSMOLALITY
- VOLUME STATUS ( Hypervolaemic, Euvolaemic, Hypovolaemic) judged clinically
- ADH LEVELS (not usually done)
Investigations (3)
- Urine sodium
- Urine osmolality
- Serum osmolality (not usually done) ( Normal 275 – 290)
Classification by serum osmolality (3)
In all of the above the hyponatremia is associated with low serum osmolality - Hypotonic hyponatremia ie. the serum osmolality is <275 ( Normal 275 – 290)
Hypertonic Hyponatremia
- Hyperglycemia
- Mannitol
Isotonic Hyponatremia
- Severe hyperlipidemia
- Severe hyperprotinaemia
(pseudohyponatraemia)
Classifying true hyponatremia according to volume status (3)
With volume depletion
True volume depletion
- Vomiting
- Diarrhea-
- Diuretic use
- Cerebral salt wasting syndrome
- Adrenal insufficiency
Effective volume depletion (could be classified under hypovolemic also)
- Cardiac failure-
- Liver failure with hypoalbuminaemia
With normal volume
- Primary polydipsia –(Excessive Beer intake ---Tea and toast diet)
- Hypothyroidism
- Syndrome of Inappropriate secretion of ADH
With increased volume
- Advanced renal failure
Classify further with urine sodium, urine osmolality & ADH levels
Symptoms of hyonatraemia
- Severe
disorientation, delirium, seizures, low GCS , coma
- Moderate
muscle weakness dizziness, gait disturbances, forgetfulness, confusion, and lethargy, dysarthria
- Mild
Confusion, and/or lethargy
Management
- If volume depletion is present
Correct by infusion of N Saline
- If volume depletion is not present
Restrict water intake +/- diuretics
MORE AGGRESIVE
- Increase oral salt intake
- Infusion of hypertonic saline
- Administration of a vasopressin receptor antagonist ( in patients with normal volume)
What does the rate of correction depend on?
- Degree of hyponatremia
- Whether the patient is symptomatic
- Whether the syndrome is acute (<48 hours) or chronic
- Urine osmolality and creatinine clearance
Things to keep in mind in rate of correction?
- serum sodium to be raised by no more than 6 meq/L any 24-hour period.
- rate of infusion of hypertonic saline of20-30 ml/h
- Rapid correction can give rise to
osmotic demyelination syndrome (formerly called central pontine myelinolysis)
- Check Na levels every 2-6 hours
Hypernatremia (usually carries a poor prognosis)
- Serum Na> 145
Causes? (5)
- Poor access to water
Mental or physical impairment
- Increased loss of water
GI loss Diarrhea Vomiting
- Diabetes insipidus
- Osmotic diuresis
Diabetes Mannitol
- Lactulose
Diagnostic evaluation?
History
Investigations
- Urine Osmolality < 300 mos/l Diabetes insipidus
- Urine Osmolality >600 Impaired thirst or access to water
300 – 600 Osmotic diuresis DM
- IF DI is suspected Trial of Desmopressin
Correction of hypernatremia?
- Too rapid correction causes Cerebral oedema ( rate of correction not more than 0.5 m mol/ h0ur: 10mmo/day
- Primary therapy water
- Fluid
- Oral Water
- Infusion ½ N saline
- 5% Dextrose
- Rate - ref protocol
- Duration - refer protocol
- If concurrent volume depletion correct volume depletion with
NS/ ½ NS first
Diabetes Insipidus
Central
- idiopathic
- Trauma
- Infiltrative disorders
- Malignancies
- CNS infections
Nephrogenic
- Medications Lithium (40%)
- Chronic hypercalaemia
- Chronic hypokalaemia
- Renal disorders- Amyloidosis MM, Sjogren’s Sy
Symptoms?
Weight loss, generalized weakness, cognitive dysfunction, lethargy, obtundation, confusion, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks
Dehydration or clinical signs of volume depletion Orthostatic blood pressure changes, tachycardia, oliguria, dry oral mucosa, abnormal skin turgor, dry axillae
Medications that cause nephrogenic diabetes insipidus?
- Lithium (40% of patients)
- Amphotericin B
Demeclocycline
- Dopamine
*IF DI is suspected Trial of Desmopressin
Hyperkalaemia
- Mild Hyperkalaemia is defined as a potassium level > 5.5 mEq/L
- Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L
- Severe hyperkalaemia is a serum potassium > 7.0 mE/L
Causes of hyperkalaemia
Impaired renal excretion
- Sever renal impairment
- Low aldosterone (3)
Hyporeninaemic- diabetic nephropathy, NSAID use
Normoreninaemic - ACE inhibitor therapy, Chronic heparin use. Primary adrenal insufficiency, critical illness,
Aldosterone resistance- Aldosterone antagonists spironolactone, inherited disorders of the aldosterone receptor
Release of K from cells
- Tumor lysis
- Massive hemolysis
- Rhabdomyolysis
- Medication
- Acidosis
- Exercise
- Hyperkalemic periodic paralysis
Clinical manifestations? (2)
- Muscle weakness
- Cardiac conduction abnormalities
Cardiac abnormalities associated with hyperkalaemia?
Mild Hyperkalaemia is defined as a potassium level > 5.5 mEq/L
Peaked T waves
Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L
- P wave widens and flattens
- Any conduction block: AV Block/ BBB
- QRS widens PR segment lengthens
- P waves eventually disappear
Severe hyperkalaemia is a serum potassium > 7.0 mE/L
- Bizarre QRS morphology
Development of a sine wave appearance (a pre-terminal rhythm)
MANAGEMENT
- 1 Evaluate renal function.
- 3 Evaluate medication list
- 2 Evaluate for –aldosterone and renin, (renin aldosterone ratio) , cortisol
- 4 Treat underlying cause
- 5 Rapidly acting transient therapies
IV calcium ( 10 cc of 10% Ca gluconate over 10 min)
Insulin and glucose
Beta 2 agonists
6 Removing K from body
K exchange resins
Adverse effect -Intestinal necrosis
- Diuretics
mild to moderate hyperkalemia
renal function nor severely impaired
If other indication for use of diuretics are present: HTN, hypervolaemia
- 7 Dialysis
End stage renal disease
Severe ECG changes
Cardiac arrhythmia
HYPOKALAEMIA
Clinical manisfestation
- Muscles Weakness Cramps ileus Rhabdomyolysis
- Cardiac : AF, VT and Tosade
ECG changes
- ST depression
- T wave inversion
- Prominent U waves
Etiology? (6)
4 ways transmembrance shift of K into cells occurs?
- Insulin
- Alkalosis
- Catecholamines
- Hypoklaemic periodic paralysis
Diagnostic evaluations/ investigation?
How to replace K?
- Oral
KCl tablets
- IV
Rate of infusion 10 meq /hr
- Rate of rise of serum
K 0.1 meq / 10 meq of infused K
- Check Serum Mg levels
- Correct if deficient
SIADH
Other findings?
e
- A low serum osmolality
- An inappropriately elevated urine osmolality (above 100 mosmol/kg and usually above 300 mosmol/kg)
- A urine sodium concentration usually above 40 meq/L
- Lowblood urea nitrogen and serum uric acid concentration
- A relatively normal serum creatinine concentration
- Normal acid-base and potassium balance
- Normal adrenal and thyroid function
Causes of SIADH?
- Malignancy ( small cell Carcinoma )
- CNS pathology ( strokes Haemorrahge )
- Pulmonary pathology ( pneumonia COPD exacerbation )
- Drugs ( Carbamazepine SSRI)
Investigations?
- Smoking history
- Detailed neurological examination
- Medications list
- X ray of Chest
- Head CT
Examples for ADH receptor antagonists?
- Blocks action of ADH
- Pure water diuresis
- Tolvaptan oral
- Conivaptan IV
- Extremly expensive