Renal - Electrolyte and acid base disturbances Flashcards
What are disorders of sodium balance?
When sodium balance is disturbed, as a result of imbalance between intake and excretion, any tendency for plasma sodium concentration to change is usually corrected by the osmoregulatory mechanism (increased sodium intake increases plasma osmolality, detected by osmoreceptors in supra optic and paraventricular nuclei —> stimulates ADH release from posterior pituitary –> water reabsorption in distal nephron –> decreases plasma osmolality at expense of a greater ECF)
Because of this, disorders of sodium balance usually present as altered ECF volume rather than altered sodium concentration
Causes of sodium depletion
Inadequate intake
GI sodium loss: vomiting, diarrhoea, external fistulae
Skin sodium loss: excess sweating, burns
Renal sodium loss: diuretics, mineralocorticoid deficiency
Internal sequestration: bowel obstruction, pancreatitis
Clinical features of sodium depletion
Symptoms and signs of hypovolaemia:
- thirst
- dizziness on standing
- weakness
- low JVP
- postural hypotension
- tachycardia
- dry mucous membranes
- confusion
- weight loss
Biochemistry may also show: low plasma sodium, high urea, high urine osmolality, low urine sodium (pre renal AKI)
How should sodium and water depletion be managed?
1) Treat the cause where possible, to stop ongoing salt and water loss
2) Replacement of salt and water deficits, provide ongoing maintenance fluids, by i.v. fusion if depletion is severe
Typical adult requires 2.5-3L of water, 100-140mmol of sodium and 70-100mmol of potassium per day
Causes of sodium excess
If the heart and kidneys are functioning normally, an excessive intake of salt and water is unlikely to lead to clinically obvious features of hypervolaemia
Causes of sodium and water excess include:
- impaired renal function: primary renal disease
- primary hyperaldosteronism: Conn’s syndrome
- secondary hyperaldosteronism: CCF, cirrhotic liver disease, nephrotic syndrome
Peripheral oedema is the most common physical sign associated with these conditions, although it is not usually a feature of Conn’s syndrome
Management of sodium excess
Management of ECF volume overload involves:
- specific treatment directed at the cause - e.g. ACEi in heart failure, corticosteroids in minimal change nephropathy
- restrict dietary sodium to 50-80mmol/day
- diuretics (loop or thiazide)
The osmoregulatory mechanism means that ECV is altered to normalise plasma osmolality when sodium intake is altered. How is the ECV returned to normal once osmolality has been corrected?
ECV effects reabsorption in the proximal convoluted tubule
Reabsorbed water is added to the venous compartment first, not the arterial one. This ECF volume expansion decreases peritubular capillary protein concentration and plasma oncotic pressure falls. At the same time, capillary hydrostatic pressure increases. These change the Starlings forces causing a decrease in reabsorption and increased delivery of Na to the distal nephron
If water is lost, ECF volume contraction increases reabsorption. Volume contraction increases peritubular capillary oncotic pressure (plasma proteins become concentrated) and capillary hydrostatic pressure falls. These factors increase PCT reabsorption, which returns the ECV back to normal
How do disorders of water balance present?
(in the absence of changes in sodium balance) disturbances of water balance affect plasma sodium concentration, which changes plasma osmolality. The main consequence of changes in plasma osmolality, especially when rapid, is altered cerebral function. This is because, when extracellular osmolality changes abruptly, water flows rapidly across cell membranes, with resultant cell swelling (during hypo-osmolality) or shrinkage (during hyper-osmolality). Cerebral function is very sensitive to such volume changes, particularly during cell swelling, when an increase in intracerebral pressure causes reduced cerebral perfusion.
Hyponatraemia
Plasma Na <135mmol/L
If gradual - asymptomatic
Rapid changes in plasma osmolality and plasma sodium are associated with: anorexia, nausea, vomiting, confusion, lethargy, seizures , coma
Causes of hyponatraemia
Hyponatramia is always associated with a decrease in plasma osmolality, and as a result water shifts INTO the intracellular fluid compartment.
Causes of hyponatraemia are classified based on the volume status of the patient - into hypervolaemic, euvolaemic, and hypovolaemic hyponatraemia
What causes hypovolaemic hyponatraemia?
= net loss of sodium in excess of water (i.e. more sodium is lost than water), hypertonic loss of sodium
Plasma osmolality is decreased and water shifts into the intracellular compartment causing hypovolaemia in the vascular compartment; ECF volume contracts, ICF volume expands
- signs of volume depletion are present
Causes:
- loop diuretics
- Addison’s disease (loss of mineralocorticoids)
- 21 hydroxylase deficiency (loss of mineralocorticoids)
Causes of euvolaemic hyponatraemia
= gain of pure water
Plasma osmolality and serum sodium are decreased, but there is expansion of BOTH the ICF and ECF
Normal skin turgor, because total body Na is normal
Causes:
- SIADH
- psychogenic polydipsia
- primary polydipsia
What causes hypervolaemic hyponatraemia?
= hypotonic gain of sodium, net gain of water in excess of sodium (i.e. more water is gained than sodium)
Plasma osmolality and serum sodium decrease
Expansion of both compartments
Produces pitting oedema states
Causes:
- RHF with an increase in venous hydrostatic pressure
- Cirrhosis and nephrotic syndrome with a decrease in plasma oncotic pressure (former from a decrease in albumin and the latter from a loss of albumin in the urine)
What investigations should be performed in hyponatraemia?
Plasma and urine electrolytes and osmolality help classify
Urine Na >20mmol/L Sodium depletion, renal loss (patient often hypovolaemic) - diuretics - Addison's - diuretic stage of acute renal failure
If patient euvolaemic = SIADH (urine osmolality >500), hypothyroidism
Urine Na <20mmol/L
Sodium depletion, extra renal losses
- diarrhoea, vomiting, sweating
- burns
Water excess (patient often hypovolaemic and oedematous)
- secondary hyperaldosteronism: heart failure, cirrhosis
- redued GFR: renal failure
- IV dextrose, psychogenic polydipsia
Treatment of hypovolaemia
Rx depends on how quickly hyponatraemia develops and the underlying cause.
If hyponatraemia develops rapidly (over hours to days) and there are signs of cerebral oedema (patient is obtunded or convulsing) sodium levels should be rapidly restored to normal by infusion of hypertonic (3%) sodium chloride solution
Rapid correction of hypovolaemia that has developed slowly (i.e. over weeks and months) may lead to central pontine myelinolysis, which may cause permanent structural and functional cerebral changes and is generally fatal. The rate of plasma sodium correction in chronic asymptomatic hyponatraemia should not exceed 10mmol/day
Specific treatments should be directed at the underlying cause
What causes SIADH?
Tumours - esp small cell lung cancer
CNS disorders: stroke, trauma, infection, psychosis
Pulmonary disorders: pneumonia, TB
Drugs: anticonvulsants, psychotropics, antidepressants, cytotoxics, oral hypoglycaemics, opiates
Idiopathic
Hypernatraemia
Plasma sodium >148mmol/L, reflects the kidneys inability to concentrate urine in the face of unrestricted water intake
Patients with high sodium generally have reduced cerebral function and cerebral dehydration. This triggers thirst and drinking, and if adequate water is obtained, is self limiting. If adequate water is not obtained, dizziness, confusion, weakness and ultimately coma and death can result.
Causes of hypernatraemia
Hypernatraemia can also be classified based on the volume status of the patient. High sodium increases plasma osmolality creating an osmotic gradient. Water shifts from the ICF (contracts) into the ECF (expands).
What causes hypovolaemic hypernatraemia?
= hypotonic loss of Na+ (net loss of water in excess of Na)
- both POsm and serum Na+ are increased
- both compartments contract
- signs of volume depletion are present
Causes:
- sweating
- osmotic diuresis
- diarrhoea (osmotic type - laxatives)
- vomiting
Euvolaemic hypernatraemia
= loss of pure water
- both POsm and serum Na+ are increased
- both compartments contract, but ECF contraction is mild because no sodium is lost
Causes:
- diabetes insipidus
- insensible water loss (e.g. fever, where water evaporates from the warm skin surface)
What causes hypervolaemic hypernatraemia?
= hypertonic gain of Na+ (net gain in sodium in excess of water, i.e. more sodium is gained than water)
- both POsm and plasma Na increase
- ECF compartment expands; ICF contracts
Causes:
- infusion of sodium bicarbonate or Na+ containing antibiotics
- oral salt administration
- chronic kidney disease (during water restriction)
Management of hypernatraemia
Depends on both the rate and the underlying cause
If condition has developed quickly, correct with appropriate volumes of IV hypotonic fluid
In older patients, it is more likely the disorder has developed slowly and extreme caution should be taken in lowering plasma Na (correct at a rate of 0.5mmol/hr) to avoid the risk of cerebral oedema
Hypovolaemia = isotonic saline if hypotension present then switch to oral replacement or more hypotonic Na+ containing i.v. fluid
Euvolaemic = water replacement
Hypervolaemic = restrict sodium/ remove exogenous cause
Symptoms of hypokalaemia
Asymptomatic if mild (3-3.3 mmol/L). larger reductions cause:
- muscle weakness, tiredeness
- cardiac effects: ventricular ectopics or more serious arrhythmias, potentiation of adverse effects of digoxin
- functional bowel obstruction due to paralytic ileus
- long standing can cause damage to renal tubules (hypokalaemic nephropathy) and interference with the tubular response to ADH (acquired nephrogenic diabetes insipidus) –> polyuria and polydipsia
Causes of hypokalamia
1) Decreased intake - elderly, diet, i.v. therapy
2) Transcellular shift (intracellular)
- Alkalosis: vomiting, loop diuretics, hyperventilation
- Drugs enhancing Na+/K+ ATPase: insulin, salbutamol
3) GI losses - diarrhoea, laxatives, vomiting
4) Renal loss
- loop/ thiazide diuretics (MCC), excessive exchange of Na for K+ in DCT
- osmotic diuresis
- mineralocorticoid excess: primary aldosteronism, 11-hydroxylase deficiency, Cushing’s syndrome, secondary aldosteronism (cirrhosis, congestive heart failure, nephrotic syndrome; decreased CO decreases blood flow and activates RAAS)
Hypokalaemia and hypertension
This relates to renal loss of potassium and mineralocorticoid excess:
Primary (Conn’s)/ secondary hyperaldosteronism
Cushing’s syndrome
Steroids
Ectopic ACTH
11 beta hydroxylase deficiency
Hypokalamia and normal/low BP
Diuretics RTA (type 1 and 2) Post obstructive diuresis Recovery after acute tubular necrosis Inherited tubular disorders (Barters syndrome, Gitelman's syndrome)
ECG features of hypokalaemia
Moderate - flattened T wave
Severe - ST depression, U wave
