A 26 year old male presents with nausea, vomiting and confusion. The following blood gas is obtained on admission
pH 7.24 (7.35-7.45)
pCO2 27 (35-45)
paO2 91 (80-100)
HCO3 11 (22-26)
Cl 110 (95-105)
sodium 142 (138-146)
potassium 4.1 (3.5-4.0)
lactate 7 (0-2)
glucose 2.1 (4-8)
Questions
Q1. Describe the blood gas
- The first step: is the patient acidaemic or alkalaemic?
- There is significant acidaemia
- There is a severe metabolic acidosis
- The estimated expected CO2 is 1.5xHCO3 + 8 i.e. expected CO2 is 24 (so similar to actual CO2 of 27)
- The anion gap is elevated at 25 [(Na+ K+) - (Cl-+HCO3-)]
- The anion gap is 11 above normal while the the bicarbonate is 13 below normal. There is a minor contribution to the acidosis due to a normal anion gap acidosis. In this case, the normal anion gap acidosis is hyperchloraemic (chloride is elevated).
- There is a severe raised anion gap metabolic acidosis which is predominantly due to raised lactate. Of note, there is a raised lactate associated with a low glucose.
Q2. Name three causes of raised lactate associated with low glucose?
- overwhelming sepsis
- liver failure
- beta blocker overdose
The biochemistry reveals the following:
Bilirubin 63 (4-22)
ALP 184 (36-100)
ALT 5003 (12-48)
Protein 47 (66-83)
Albumin 27 (38-48)
Q3. What is the diagnosis?
Fulminant hepatic failure
Q4. What are the causes of acute hepatitis?
- paracetamol overdose
- idiosyncratic drug reactions
- hepatitis A
- hepatitis B
- ischaemic hepatitis
- autoimmune hepatitis
- Wilson’s disease
- Budd Chiari syndrome
- Acute fatty liver of pregnancy
Q5. What is the difference between acute severe liver failure and fulminant hepatic failure?
Acute hepatitis with jaundice and coagulopathy without hepatic encephalopathy is referred to as severe acute hepatitis. Fulminant hepatic failure is defined as the appearance of hepatic encephalopathy in a patient with acute deterioration of liver function with no previous history of liver disease.
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