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Description
A man in his 60s was admitted to the high dependency unit (HDU) following an elective instrumental fixation of T12-L5 for symptomatic spinal stenosis. He had a medical history of hypertension and sickle cell trait. His surgery was performed in the prone position and lasted 7 hours. He had approximately 1.5 L of blood loss. Brief periods of intraoperative and postoperative hypotension were managed with a combination of intravenous fluids, vasopressors and blood products. There was no period where the mean arterial blood pressure was less than 60 mm Hg. Postoperatively, he was successfully extubated and weaned off of vasopressors.
On day 0 on HDU, he began to develop an unexplained and progressive lactic acidosis with a raised anion gap of 24 mmol/L. Clinical examination was unremarkable. His haemodynamic parameters were within normal range, his thromboelastogram was normal, his urine output was between 1 mL/kg/hour and 2 mL/kg/hour and bedside echocardiography demonstrated that he was fluid replete with no features of tamponade. His lactate however continued to rise and peaked at 9.10 mmol/L (table 1).
Trend in arterial blood gases
Concerns were raised about the possibility of a retroperitoneal haematoma as a likely differential in view of the surgical approach that was taken. A CT scan was therefore performed of his abdomen and pelvis. This showed ischaemia in segments VI and VIII of the liver (figure 1).
CT scan of the abdomen showing ischaemia of segments VI and VIII of the liver.
Subsequent blood tests corroborated these findings with aspartate aminotransferase (AST) of 436 U/L, alanine aminotransferase (ALT) of 479 U/L, international normalised ratio of 1.5 and normal bilirubin (table 2). A liver screen for other possible aetiologies was negative.
Trend in biochemical blood tests
He was managed conservatively with intravenous fluids, N-acetylcysteine and empirical antimicrobials, following input from the liver specialist team. Within 24 hours, his lactic acidosis resolved and after 5 days his liver function tests normalised. He was subsequently discharged from the hospital with no concerns raised at his outpatient follow-up clinics.
This case highlights the importance of broad thinking when approaching lactic acidosis.1 There are many ways of classifying this but one simple framework for the postoperative surgical patient can be seen in table 3.
Causes of lactic acidosis in the postoperative surgical patient
In this particular case, the transient periods of intraoperative and postoperative hypotension were most likely responsible for the development of hepatic centrilobular necrosis and ischaemic hepatitis. This resulted in reduced lactate clearance and lactic acidosis.
The pathogenesis of this condition occurs as a result of a ‘two-hit’ mechanism where a vulnerable liver is exposed to systemic hypoperfusion and ischaemia.2 This leads to cellular hypoxia and a marked but transient elevation in AST and ALT (figure 2). The mortality is high and is dependent largely on the underlying cause of hypotension. Treatment is directed at the underlying cause of haemodynamic disturbance.
The pathophysiology of ischaemic hepatitis as a result of hypoperfusion (created by Dr Muzzammil Ali).
Learning points
Lactate can be elevated for many reasons. While tissue hypoperfusion may be the most common cause of elevation, many other aetiologies exist. Clinicians need to be aware of the many potential causes of lactate elevation as the clinical and prognostic importance of an elevated lactate level varies widely by disease state. Moreover, specific therapy may need to be tailored to the underlying cause of the elevation.
Ischaemic hepatitis is a clinical syndrome frequently encountered in critically ill patients that represents a complication of underlying cardiac, circulatory or respiratory failure. The pathogenesis of ischaemic hepatitis appears to occur as a result of a ‘two-hit’ mechanism where cellular hypoxia plays a central role. The mortality is high and is dependent largely on the underlying cause of hypotension. Treatment is directed at the underlying cause of the haemodynamic disturbance.
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Patient consent for publication
Footnotes
Contributors HN and MA gained consent, gathered the clinical information for the case, were involved in the diagnostic process and assisted with the write up of the case. TT critically reviewed the article for intellectual content and assisted with the write up of the case. MA and JK were involved with the conception and design of the manuscript, image creation and review of the literature.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.