A51-18 When Lactic Lies

Lactic acidosis is classically associated with tissue hypoxia and ischemia. An elevated lactate often raises concern for catastrophic intra-abdominal processes such as bowel ischemia or perforation. However, lactate may not always reflect the trust extent of injury. We present two contrasting cases in which reliance on serum lactate influenced clinical decision making in suspected bowel perforation. A 38 year old male with month long history of severe constipation developed shock requiring vasopressors and abdominal compartment syndrome causing renal failure (anuric) due to extrinsic compression. Peak pressure on mechanical ventilation was 47. CT imaging revealed portal venous gas concerning for bowel perforation. Despite these findings, ex-lap was deferred due to normal serum lactate. Q4H lactic acid checks did not cross over 2.6 u/L. Upon transfer, emergent surgery revealed feculent peritonitis, severe colonic dilation and extensive ischemia of the ascending, transverse and proximal descending colon. Notably, peak ventilator pressures dropped significantly after peritoneal decompression. The normal lactate may falsely reassure clinicians even in the setting of advanced ischemic injury. The second case was a 46 year old female patient with acute pancreatitis complicated by distribute shock developed imaging evidence of bowel perforation. Lipase levels peaked at 7800. Her physical exam revealed a profoundly distended and tense abdomen. Ex-lap was initially deferred due to a normal lactate and pH. Upon trending the serum lactic acid, the levels did not cross over 2.3 u/L. Abdominal imaging revealed diffuse peritoneal gas extending throughout the small bowel and cecum. Vasopressor requirements continued to increase which ultimately led to exploratory laparotomy which confirmed widespread ischemia and perforation. In this case, early reliance on lactate delayed definitive intervention despite clinical and radiographic signs of perforation. Both cases highlight the limitations of using lactate as a decisive marker for bowel ischemia. Normal lactic levels may occur early as compensatory mechanisms maintain perfusion. Additionally, if bowel cells have been compromised and dead for an extended time, they will no longer produce lactic acid. Serum lactic acid therefore should not be the sole determinant for surgical exploration as a comprehensive assessment including imaging and clinical trajectory remain essential. This abstract is funded by: None