Clinical Details
 An 85 year old man was admitted with severe abdominal pain and shock. The abdominal pain 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). The 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.

Biochemistry at 1520hrs was Na⁺ 138, K⁺ 4.9, Cl^- 107, Total CO2 20, Glucose 11.2, Urea 12.8, creatinine 0.188 (All results in mmol/l). Anion gap was 11.

A lactate level collected at the same time as the blood gases was 8.3 mmol/l.

Intraoperative findings were of 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.

Assessment
Firstly, initial clinical assessment:
The clinical expectations are:

acute metabolic acidosis (lactic acidosis) due to peripheral circulatory failure

respiratory alkalosis due to pain-induced hyperventilation

As only a couple of hours have passed since onset of symptoms, respiratory compensation for the metabolic acidosis would be at an early stage only. Compensation 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.

Secondly, the acid-base diagnosis:  
1. pH:  This is at the acidaemic end of the reference range (7.36-7.44). It suggests that either no real acid-base disorder is present OR there are 2 disorders present which are have balancing effects on the pH (ie an acidosis & an alkalosis).

2. Pattern:  The low pCO2 & low bicarbonate suggest either a metabolic acidosis OR a respiratory alkalosis. The option of no acid-base disorder is rejected on these results leaving us with the option of balancing disorders. In this case, this means a metabolic acidosis & a respiratory alkalosis. A bicarbonate level of 13.8 by itself indicates the presence of a metabolic acidosis as it is below the limit of compensation (18 mmol/l) for an acute respiratory alkalosis. The limit of compensation for a chronic respiratory alkalosis is lower (12-15) but there is no clinical evidence for such a pre-existing disorder in this patient. (Clinical details of past history are absent so this should perhaps not be totally excluded).

3. Clues:  The anion gap is 11 & the chloride is slightly elevated. The urea & creatinine are elevated but are not high enough to support the idea of an acute renal failure causing an acidosis. The glucose is elevated but there is no urine test results given so we don't know whether ketonuria is present but ketoacidosis as the cause is not supported by the history. The lactate level was quite elevated (at 1738hrs) and this was collected about 2 hours after the biochemistry which showed a normal anion gap. The bicarbonate on the initial biochemistry was 20 but had decreased to 13.8 by the time of the gas collection. This indicates the progressive development of the disorder.

4. Compensation: As we know a metabolic acidosis is present, we will use the 'one & a half plus 8 rule' (rule 5) to check the amount of compensation. Expected pCO2 at maximal compensation = (1.5 x 12.8 + 8) = 27.2mmHg. The actual value of 24 is slightly lower than this and we might conclude that compensation was within the limits for maximal compensation. However, these gases were collected at 4.5 hours after onset of symptoms and this is insufficient time for maximal compensation to be reached. At this time a lesser amount of compensation would be expected, not a bit more as here. So an actual pCO2 must definitely indicate the presence of a second acid-base disorder (as we have suspected initially based on the near return of the pH to the reference range).

5. Formulation: A metabolic acidosis (due to lactic acidosis) and a respiratory alkalosis (due to the severe abdominal pain). 

6. Confirmation: A repeat set of electrolyte results taken at the time of collection of the gases would be expected to show an increase in the anion gap. Such an indirect way to further characterize a metabolic acidosis is not necessary if you directly measure the lactate level. A urinalysis result should be obtained from all patients.

Finally, the Clinical Diagnosis:

Acute mesenteric occlusion causing extensive bowel infarction, shock & a lactic acidosis. The ischaemic bowel would also contribute to the increased lactate production. The mesenteric occlusion and the hypotension would result in failure of hepatic clearance of the lactate from the circulation.

Comments
[1] 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%. 

[2] The clinical information of shock always strongly suggests a lactic acidosis. This is confirmed in this case as the blood lactate is very high: expected mortality based on this information alone is high. The high lactate is due to a combination of:

regional hyperproduction from the ischaemic bowel & by peripheral tissues due to the shock, and

hepatic underutilisation. 

Severely ischaemic gut alone can produce large quantities of lactate.

[3] 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.

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