Answers:

Question 1:

PH = 7.49 (> 7.45) so we have alkalaemia
HCO3 = 41 (> 24) so we have metabolic alkalosis. Next we look at compensation,
Expected PCO2 for metabolic alkalosis = 0.7 x HCO3 + 20 (range: +/- 5).
Accordingly, expected PCO2 = 0.7 x 41 +20 = 48.7 (+/- 5) So we have pure metabolic Alkalosis.
Other findings:

Ionised calcium level is elevated, that is moderate hypercalcemia (1.5 – 1.7 mmol/L).
Creatinine is elevated, SO we have impaired kidney function.
Lactate level is mildly elevated/ Mild hyperlactataemia.

Next, using the useful mnemonic – CLEVER PD, we will narrow the differential diagnosis:
C – contraction (dehydration) – possible, patient is dehydrated.
L – liquorice (diuretic), laxative abuse. Patient denied taking both
E – endocrine (Conn’s, Cushing’s), unlikely
V – vomiting, GI loss (villous adenoma), Patient denied.
E – excess alkali (antacids), This patient was taking gaviscon for his GORD.
R – renal (Bartter’s), severe K depletion. Unlikely as K level is with in normal range
P – post hypercapnia, very unlikely. Usually post BiPAP treatment.
D – diuretics. Patient denied taking any.

The combination of Metabolic alkalosis, hypercalcemia and renal impairment should make us suspicious of Milk Alkali Syndrome. The milk-alkali syndrome is triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with the ingestion of large amounts of calcium and alkali.

This patient was taking large doses of Gaviscon for his GORD, Gaviscon contains Ca carbonate and Sodium bicarb.

Alkalosis is caused by combination of excessive alkaline intake and the contraction alkalosis caused by hypercalcemia.

Question 2:

Milk-alkali syndrome is now the third leading cause after hyperparathyroidism and malignancy.

Causes of hypercalcemia can be remembered by the mnemonic “CHIMPANZEES”
C – Calcium supplementation
H – Hydrochlorothiazide
I – Iatrogenic, immobilization
M – Multiple myeloma, milk-alkali syndrome, medication (e.g Lithium)
P – Parathyroid hyperplasia or adenoma
A – Alcohol
N – Neoplasm (e.g breast cancer, lung cancer)
Z – Zollinger Ellison syndrome
E – Excessive vitamin D
E – Excessive vitamin A
S – Sarcoidosis.

For further evaluation of hypercalcemia 1st we need to stop the offending agent if it exists. If no cause was found on history taking, then we need to measure the parathyroid hormone level. if PTH is suppressed then we need to look for malignancy.
If PTH is normal or high, then we need to measure 24-hour urinary calcium level. If low, then it is familial hypocalciuric hypercalcemia. If normal or high, then it is parathyroid disease.

Question 3:

Treatment of hypercalcemia

HYDRATION AND DIURESIS
In patients with mild hypercalcemia, adequate hydration should be encouraged and immobilization discouraged.
In patients with severe hypercalcemia, the most important part of treatment is aggressive intravenous rehydration. Normal saline should be used to achieve a urine output of 200 mL per hour. Only when the intravascular volume is restored then a loop diuretic can be used in low dose (frusemide, 10 to 20 mg) to further lower the serum calcium level if necessary.
In malignancy-associated hypercalcemia, intravenous pamidronate, 60 to 90 mg, can be given by four-hour infusion.
DIALYSIS, In cases of resistant, life-threatening hypercalcemia.
And lastly, treatment of the cause.