Severe Non-Occlusive Mesenteric Ischemia without Lactate Elevation

Case Presentation

Austin Dig Syst. 2017; 2(1): 1007.

Severe Non-Occlusive Mesenteric Ischemia without Lactate Elevation

Paparoupa M¹* and Schuppert F²

¹Department of Pulmonary Diseases, Infectious Diseases, Gastroenterology, Nephrology and Intensive Care Unit, University Hospital of Giessen, Germany

²Department of Gastroenterology, Hepatology, Endocrinology, Diabetology, Infectious Diseases and General Medicine, Klinikum Kassel, Kassel School of Medicine, Germany

*Corresponding author: Maria Paparoupa, Department of Pulmonary Diseases, Infectious Diseases, Gastroenterology, Nephrology and Intensive Care Unit, University Hospital of Giessen, Germany

Received: March 30, 2017; Accepted: April 27, 2017; Published: May 04, 2017

Abstract

Non-occlusive mesenteric ischemia is frequent in critically ill patients with hemodynamic instability. Plasma Lactate is a marker of tissue hypoperfusion and its diagnostic significance in the setting of mesenteric ischemia remains controversial. We present a case of severe non-occlusive mesenteric ischemia without lactate elevation over normal values although extended intestinal necrosis requiring right hemicolectomy and total ileoectomy was present. Serial lactate concentration measurements were insufficient to detect intestinal hypoperfusion and predict the length of bowel necrosis.The pre-and postoperative clinical monitoring was subsequently guided by vasoactive medication demand.

Keywords: Non-occlusive mesenteric ischemia; Intestinal necrosis; Lactate; Lactate acidosis

Introduction

Acute Mesenteric Ischemia (AMI) is a life-threatening reduction of the intestinal perfusion observed after arterial or venous occlusion or non-occlusive arterial infarction secondary to vasospasm more often in critically ill patients with hemodynamic instability under vasoconstrictive medication. Plasma lactate has been tested as a marker of mortality [1] and Irreversible Transmural Intestinal Necrosis (ITIN) [2] in the setting of acute mesenteric ischemia. Although lactate concentration several hours before death or surgical interventionwas recognized as independent risk factor predicting the severity of AMI [1-3] its role in the diagnosis of this condition in early stageremains controversial. Lactate is an unspecific marker of organ hypoperfusion and becomes elevated only after significant tissue damage [4]. Plasma D-lactate was initially introduced as a more specific alternative to routinely measured stereoisomer L-lactate in the sense of its anaerobic bacterial origin [5]. However experimental studies put the significance of D-lactate under question [6] and novel markers of gut mucosal damage like intestinal fatty acid-binding protein were recommended [4,7]. According to many observations lactate remains a reliable marker of mesenteric ischemia detection secondary to acute aortic dissection [8,9]. We present a case of a severe non-occlusive mesenteric ischemia with gut necrosis requiring right hemicolectomy and total ileoectomywithout lactate elevation over normal values.

Case Presentation

The 76-year-old man with unremarkable medical history was treated in our intensive care unit with Acute Respiratory Distress Syndrom (ARDS) by eosinophilic pneumonia, occurred without a detectable pathogen and by missing underlying immunologic insufficiency. During the clinical course hypoxemia secondary to lung failure ensued and support of Veno Venous Extra Corporeal Membrane Oxygenation (VV ECMO) was required. The patient received treatment with steroids and broad spectrum antibiotics. Having recovered, VV ECMO was removed and weaning from sedation was initiatedunder mechanical ventilation. 48 hours after sedative withdrawal, respiratory effort was observed and assisted ventilation was started. A sinus tachycardia (110-120 beats/min) and elevated body temperature (37.5-37.8°C) were evaluated as cardiovascular reaction during the recovery phase. 12 hours later acute arterial hypotension occurred, requiring vasoconstriction with Nor-adrenalin, as application of crystalloids was insufficient. Because of the simultaneous appearance of respiratoryinstability with progressive hypoxemia, a new sepsis course with lung focus as a result of the weaning phase was supposed. Considering the Central Lineassociated Bloodstream Infection all lines and catheters were changed. Echocardiography excluded cardiogenic shock. Physical examination revealed meteorismus with hypoactive abdominal sounds but abdominal Ultrasonography was at the time point unremarkable. We initiated osmotic and stimulant laxatives as by intensive careassociated constipation and decided to wait and observe. 4 hours later abdominal circumference increased manifestly and abdominal Ultrasonography revealed aerobilia, which was a peculiar finding, as the patient had no history of a biliary system intervention. Because of the severe clinical deterioration, we decided to perform a contrastenhanced whole-body computed tomography in order to expand our diagnostic panel. The computed angiography excluded pulmonary embolism as a cause ofrespiratory and cardiovascular instability. An extended acute mesenteric ischemia occurring in the blood supply region of the superior mesenteric artery with hepatic portal venous gas and pneumatosisintestinaliswas diagnosed (Figure 1) and the patient underwent an emergency laparotomy with right hemicolectomy and ileoectomy because of irreversible bowel necrosis. An atherosclerotic disease or thrombotic occlusion of the abdominal aorta and its mesenteric branches was not present and we presumed an acute nonocclusive mesenteric ischemia due to vasospasmus. The postoperative course was unremarkable and clinical recovery was achieved eight weeks later (Figure 2).