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Case Study: Mrs. Geraldine Dayrit

This case study describes a patient presenting with severe hypernatremia, elevated urea and creatinine, and increased glucose. The biochemical abnormalities indicate reduced fluid intake. The clinical signs of tachycardia and hypotension also reflect decreased extracellular fluid volume. While sodium intake was reduced along with water, homeostatic mechanisms minimized sodium loss. The patient's urine osmolality would be high due to antidiuretic hormone secretion in response to hypovolaemia and hypernatremia, while urinary sodium concentration would be very low due to sodium retention. The patient was given 5% dextrose intravenously initially instead of water alone or saline to correct the primary water deficiency.

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42 views1 page

Case Study: Mrs. Geraldine Dayrit

This case study describes a patient presenting with severe hypernatremia, elevated urea and creatinine, and increased glucose. The biochemical abnormalities indicate reduced fluid intake. The clinical signs of tachycardia and hypotension also reflect decreased extracellular fluid volume. While sodium intake was reduced along with water, homeostatic mechanisms minimized sodium loss. The patient's urine osmolality would be high due to antidiuretic hormone secretion in response to hypovolaemia and hypernatremia, while urinary sodium concentration would be very low due to sodium retention. The patient was given 5% dextrose intravenously initially instead of water alone or saline to correct the primary water deficiency.

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© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Clinical Chemistry 2 Mrs.

Geraldine Dayrit
Case Study

CASE STUDY 1
Member: Francisco, Frances Lorraine R.

answers:

a.
Severe hypernatraemia; urea and creatinine are elevated. These
biochemical abnormalities are frequently seen in clinical scenarios
where fluid intake is reduced or less frequently, when fluid loss is
increased. Glucose is raised but may just reflect insulin resistance
acquired from the stress response, which is associated with
increased concentrations of anti-insulin hormones like cortisol and
adrenaline.

b.
Water status is reduced; the evidence for this is primarily clinical
(tachycardia, hypotension), reflecting reduced extracellular fluid
(ECF) volume, although the greater rise in urea (compared with
creatinine) is also consistent with dehydration. Patients are often
less clinically dry than expected given the severity of the
hypernatraemia. This is because water loss is distributed across all
body compartments. Na+ intake will have been reduced for the
same reason as water intake. However, some of the homeostatic
mechanisms designed to protect blood volume (secondary
hyperaldosteronism) minimise Na+ loss, even as insensible losses
of pure water from respiration continue. Hence the relative loss of
more water than Na+, as evidenced by high serum Na+
concentration.

c.
Urine osmolality will be high (>600 mmol/kg), reflecting urine
concentration due to ADH secretion, stimulated by hypovolaemia
(non-osmotic stimulus) and hypernatraemia (osmotic stimulus).
Urinary Na+ concentration will be very low (<10 mmol/L)
reflecting sodium retention due to secondary hyperaldosteronism,
precipitated again by hypovolaemia.

d.
She needs water and was given 5% dextrose IV (she could not
drink initially). This is isotonic with plasma; pure water would
precipitate intravascular haemolysis because of the osmotic
difference across red cell membranes. Isotonic (0.9%) saline
replaces both Na+ and water and does not correct a primary
water deficiency.

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