Describe and interpret this venous blood gas:
History: 55-year-old man presents with epigastric pain after drinking alcohol.
|pH 7.48||Na 128 mmol/L|
|pCO2 50 mmHg||K 4.1 mmol/L|
|HCO3 36 mmol/L||Cl 79 mmol/L|
|Lactate 2.2 mmol/L||Glucose 36 mmol/L|
What is the pH?
7.48 = alkalaemia
What is the primary process?
HCO3 36 = primary metabolic alkalosis
Is there compensation?
Metabolic Alkalosis: 0.7 plus 20 rule
Expected pCO2 = 0.7 x HCO3 + 20 (+/-5)
= 0.7 x 36 + 20
Actual pCO2 is 50, therefore there is complete respiratory compensation.
Are there other clues to diagnosis?
Corrected sodium = Na + (glucose – 5)/3
= 128 + (36 – 5)/3
Therefore corrected sodium is within normal limits.
Potassium is normal.
Chloride is markedly low.
Lactate is mildly elevated.
Glucose is markedly elevated.
Description: This VBG shows a completely compensated, hypochloraemic, metabolic alkalosis with overall mild alkalaemia. There is marked hyperglycaemia and pseudohyponatraemia which corrects into the normal range when glucose is accounted for. Potassium is normal and lactate is mildly elevated.
Interpretation: In this clinical situation, the metabolic alkalosis is likely to be secondary to volume contraction from hyperglycaemia, or vomiting secondary to abdominal pathology. Endocrine causes (hyperaldosteronism, Cushing’s syndrome, Conn’s syndrome) should also be considered, although the relatively normal sodium and potassium results would argue against this. The severe hyperglycaemia is likely to be secondary to diabetes mellitus without ketoacidosis or coma. This may be type 2 diabetes, but could also be type 1 due to pancreatic failure from chronic alcoholic pancreatitis (in view of epigastric pain). Management will include assessment of volume status, rehydration with normal saline and administration of insulin.
Additional information: Alcoholic gastritis with dehydration, resolved with IV fluid supplementation. First presentation of diabetes secondary to chronic pancreatic failure from alcoholism.