27 year old male presents to ED with a 3 day history of vomiting and epigastric pain.

Metabolic alkalosis – pH 7.51 and HCO3 48mmHg

Expected PCO2 = (0.7XHCO3) + 20 = 53.6mmHg

The VBG shows a metabolic alkalosis which appears to be adequately compensated for with an expected PCO2 of 53mmHg.  There is a raised lactate and a moderately raised creatinine. There is derangement of the electrolytes, with a mild to moderately low sodium, potassium and chloride. The corrected Ca is moderately raised. The glucose is within normal limits.

Recall the causes of Metabolic alkalosis – CLEVERPD

C  Contraction (volume Contraction)

L  Liquorice

E  Endocrine (Hyperaldosteronism, Bartters, Cushings, Conns)

V  Vomiting, NG suction (chloride loss)

E  Excess alkali (antacids, dialysis, milk alkali syndrome)

R  Renal HCO3 retention (Hypochloraemia, Hypokalaemia)

P  Post hypercapnia

D  Diuretics

A more clinically based way to look at the causes are as follows:

The most common causes of metabolic alkalosis are vomiting, diuretics and hyperaldosteronism.

Chloride loss – GI (vomiting and NG Suction), Renal (diuretics)

Potassium Loss – Sydromes (Cushings, Conns, Bartters), Secondary increase in aldosterone (as a results of low renal blood flow), Eating disorders, Excessive Liquorice

Excess Base – Antacids, NaHCO3 post dialysis, Citrate post blood transfusion, Post hypercapnoea

In this clinical context the metabolic alkalosis is most likely due to a combination of potassium and chloride loss from vomiting (which results in a hydrogen ion loss at the DCT in exchange for the potassium and chloride), as well as the volume contraction resulting in secondary hyperaldosteronism, which adds to the potassium loss.  The volume contraction is evident by the raised creatinine and lactate.  With the previous history of pancreatitis one would assume this would be the cause of his underlying clinical picture. The common cause of alcohol being the most likely culprit.  However he has not consumed alcohol in 6 months and therefore other causes need to be sought. A calcium level should be done in all patients with pancreatitis, as it can be caused by hypercalcaemia  and can cause hypocalcaemia as a complication of pancreatitis. This patient has moderately high hypercalcaemia, which is made worse by the patients dehydration. An underlying cause of the hypercalcaemia needs to be looked for eg  hyperparathyroidism, malignancy, other endocrine disorders, drugs and sarcoid.

Causes of Pancreatitis

1. Gallstones and Alcohol (>80%)
2. Post ERCP
3. Trauma
4. Drugs (Azathioprine, Sulphonamides, Tetracyclines, Valproic Acid, Methyldopa, Frusemide)
5. Infection
6. Hypercalcaemia
7. Hypertriglycerademia
8. Autoimmune
9. Congenital abnormalities

Management of hypercalcaemia

1. Look for and treat underlying cause
2. Promote urinary excretion (if renal and cardiac stable) – saline diuresis 300 -500ml/hr, replacing fluids and forcing a diuresis. Other electrolytes need to be monitored and replaced. Treatment with Frusemide is controversial and should be avoided.
3. Haemodialysis if renal or cardiovascular unstable
4. Calcitonin and Bisphosphonates- takes 48 hours to start to work