History: A 60 year old man was seriously ill on arrival at hospital. The patient told of vomiting several hundred mls of dark brown fluid ‘every hour or two’ for about a day plus several episodes of melaena. Past history was of alcoholism, cirrhosis, portal hypertension and a previous episode of bleeding varices. Sclerotherapy for the varices had been performed several months previously at another hospital.
Examination: He was jaundiced and distressed: sweaty, clammy and tachypnoeic. BP 98/50, pulse 120/min. Air entry was good. Heart sounds dual with a systolic murmur. Peripheries were cool. Abdomen was soft and nontender. Signs of chronic liver disease were present (spider naevi, gynaecomastia, testicular atrophy). Urinalysis: glucose, trace ketones.
Pathology: Na+ 131, Cl- 85 K+ 4.2, "total CO2" 5.1, glucose 52, urea 22.6, creatinine 0.245, lactate 20.3 mmol/l. Hb 62 G/l, WCC 23.8
Arterial Blood Gases
pCO2 13.8 mmHg
pO2 103 mmHg
HCO3 4.1 mmol/l
This man was severely ill with circulatory failure and GI bleeding on a background of known cirrhosis with portal hypertension. Lactic acidosis would be suspected. The respiratory efforts may be due to the distress (ie a respiratory alkalosis) or as a consequence of a metabolic acidosis (ie compensatory). The vomiting could have caused a metabolic alkalosis if there has been sufficient loss of gastric acid along with the blood (haematemesis).
1. pH: The severe acidaemia indicates a severe acidosis.
2. Pattern: The combination of a low pCO2 and a low bicarbonate indicate either a metabolic acidosis or a respiratory alkalosis (or both). As this patient has a severe acidosis, the diagnosis is metabolic acidosis. The co-existence of a respiratory alkalosis will be checked when we assess the compensatory response.
4. Compensation: The expected pCO2 at maximal compensation is 14 mmHg (rule 5). The actual measured value of 13.8 is well within the +/- 2 range. Sufficient time has elapsed for respiratory compensation to have reached maximum. There is no evidence of any respiratory acid-base disorder.
5. Formulation: Severe lactic acidosis with maximal respiratory compensation.
6. Confirmation: No further tests are required to confirm the acid-base diagnosis. Other appropriate investigations include coagulation profile & septic screen.
Cirrhosis & portal hypertension with bleeding varices & ?sepsis resulting in shock, lactic acidosis, acute diabetes, acute anaemia & renal failure.
Followup: Despite aggressive resuscitation and management in ICU, this patient did not survive. Patients with chronic liver disease do not develop lactic acidosis unless additional factors are present which depress hepatic lactate metabolism or increase peripheral lactate production. The typical situation is a patient with cirrhosis who develops sepsis or hypovolaemic shock (esp due gastrointestinal bleeding). The combination of cirrhosis and lactic acidosis predicts a very high mortality.