Sepsis

Question 1

How do you workup a patient with hyponatraemia?

Answer 1

First thing measure evaluating a patient with hyponatraemia is serum osmolality
- The serum osmolality will normally be low - which will prompt the usual workup
- If it is normal or high
○ Think hyperglycaemia, hyperlipidaemia.

Measure volume status.

ECF low
- Test urine sodium
- Determine urine sodium
○ If urine sodium is low
§ This is an appropriate response thus patient is dry from fluid losses - diarrhoea, vomiting, third spacing etc.
○ If urine sodium is high
§ This is not an appropriate response i.e. there is something wrong with the kidneys
§ Renal losses from diuretics
§ Renal failure.

ECF normal
- Test urine osmolality
○ If urine osmolality high (i.e. concentrated (greater than serum)
§ This is inappropriate
§ SIADH
§ Hypothyroidism
§ Adrenal insufficiency.
○ If urine osmolality low i.e. dilute (less than serum)
§ This is appropriate
§ Primary polydipsia.
§ Low salt intake

ECF high
- Test urine sodium
- Low urine sodium
○ Heart failure (RAAS system is activated to conserve sodium)
○ Cirrhosis (RAAS systemc is activated to conserve sodium)
- High urine sodium
- Renal failure.

Question 2

Treatment for hyponatraemia?

Answer 2

Treatment of hypovolemic hyponatraemia
* Isotonic saline (Normal saline/0.9%)
* Limit to correction of <10mmol in the first 24 hours.
* If patient is unwell and symptomatic
○ Can consider hypertonic saline 3%

Treatment of euvolemic hyponatraemia
* Fluid restrict.

Treatment of hypervolemic hyponatraemia
- Diuresis

Question 3

What derangements occur with a gastric outlet obstruction?

Answer 3

○ Dehydration
§ Leads to activation of ADH from posterior pituitary with conservation of water in the renal tubules and collecting system. Also activation of RAA pathway as below.
○ Hypokalaemia
§ Dehydration causes activation of renin-angiotensin-aldosterone pathway. Aldosterone conserves sodium in the kidney tubules, while wasting potassium in the urine, with the Na-K ATP transporter pump.
○ Hypochloraemia
§ Vomiting causes loss of hydrochloric acid from the stomach, therefore depleting chloride from the body.
○ Metabolic alkalosis with paradoxical aciduria
§ Vomiting causes loss of hydrochloric acid, depleting H+ leading to alkalosis. Conservation of sodium due to dehydration leads to loss of H+ in the kidneys with further alkalosis and production of acid urine.
○ Catabolic state
§ Hypoglycaemia and reduction in nutrition leads to activation of catabolic pathways. Insulin is reduced and glucagon is secreted from the pancreas. Glucose is mobilised from liver by glycogenolysis and mobilised from liver and muscles from protein by gluconeogenesis and proteolysis.
§ Fats are broken down by lipolysis leading to ketones and free fatty acids which are utilised as energy source.
§ Catabolism of adipose tissue and muscle leads to weight loss.
Basal metabolic rate is lower with reduction of ATP production.