An 85 year old man was admitted with severe abdominal pain and shock. The abdominal pain had started about 1500hrs and quickly became quite severe. There was no radiation to the back. The patient was known to have an abdominal aortic aneurysm (AAA). On arrival at hospital, the patient was shocked with peripheral circulatory failure and hypotension (BP 70-80 systolic). His abdomen was guarded and quite tender. He was distressed but able to talk and could understand instructions. Past history was of hypertension (on metoprolol and prazosin) and angina (on Isordil). Prior to this event, the patient was mobile and independent.
A ruptured AAA was diagnosed clinically and he was transferred to theatre for emergency laparotomy. On arrival in theatre, BP was 120 systolic. The patient was talking but distressed by pain with rapid respirations at a rate of 30/min. It was noted that neck veins were very distended. An external jugular triple lumen central line and a brachial arterial line were placed before the surgical team had arrived in theatre. CVP was +40 mmHg. The blood gases were collected from an arterial line during preoxygenation with 100% oxygen at 1738 hrs (i.e. about 4.5 hours after onset of symptoms).
Investigations: Biochemistry at 1520hrs was Na+ 138, K+ 4.9, Cl- 107, Bicarbonate 20, Glucose 11.2, Urea 12.8, creatinine 0.188, lactate 8.3 (all results in mmol/l). Haemoglobin 133 G/l.
The clinical expectation was an acute metabolic acidosis (lactic acidosis) due to peripheral circulatory failure, and respiratory alkalosis due to pain-induced hyperventilation.
Respiratory compensation for the metabolic acidosis would be at an early stage only as such compensation (i.e. hyperventilation) takes 12 to 24 hours to reach maximum. The clinical details given do not give sufficient detail about previous medical conditions (eg history of chronic airways disease) or any medication history - such details are important.
Acute mesenteric occlusion causing extensive bowel infarction, shock and lactic acidosis. The ischaemic bowel contributes to increased lactate production. The mesenteric occlusion and the hypotension results in failure of hepatic clearance of the lactate from the circulation.
Intraoperative findings were almost total infarction of the small bowel and part of the stomach due to acute mesenteric vascular obstruction. The AAA was unruptured. The surgical assessment was that the situation was inoperable and not survivable. The patient arrested and died on the table at 1805hrs.
A significant shunt is indicated by a pO2 of only 182mmHg despite 100% O2. On Nunn's Isoshunt Diagram, this would be a shunt of about 25%.
Clinical shock always suggests lactic acidosis, and there is a correlation between blood lactate and mortality. Expected mortality for a lactate of 8mmol/l due to shock is 90% (e.g. see fig 5 in Mizock and Falk). This relationship depends on context; some conditions (e.g. prolonged fitting) can result in high but transient lactate levels which do not carry the same bad prognosis as in shocked or critically ill patients. The high lactate is due to a combination of regional hyperproduction from the ischaemic bowel, and by peripheral tissues due to the shock, and decreased uptake by the liver. Severely ischaemic gut alone can produce large quantities of lactate.
Continued marked hyperventilation is required following intubation to keep the pCO2 low and prevent marked deterioration in pH. End-tidal pCO2 would be an unreliable guide to arterial pCO2 in this patient because significant alveolar dead space would cause a large difference between them. Serial blood gases will be required.