Cardiac Arrest After Mesenteric Manipulation in a Patient Undergoing Abdominal Surgery

Circulatory fluctuations coincident with mesenteric manipulation have been described during anesthesia for abdominal surgery [1,2]. In this case report, we describe cardiac arrest after mesenteric manipulation in a patient undergoing rectal surgery. Case Report A 55-yr-old, 72-kg man with both gastric and rectosigmoidal tumors was scheduled for rectosigmoidectomy. He was not taking medication, nor did he have a history of allergic reaction. Preoperative laboratory examinations were normal. After premedication with 3 mg of bromazepam as suppository, anesthesia was induced with thiamylal 200 mg, fentanyl 200 micro g, and vecuronium 8 mg intravenously (IV) and was maintained with sevoflurane and nitrous oxide in oxygen. The surgery proceeded uneventfully, and the tumor was resected. Mesenteric manipulation was performed for abdominal lavage with warm saline at the end of surgery. Just after this procedure, ventricular premature beat appeared, systolic arterial pressure decreased from 102 to 58 mm Hg, and heart rate slowed from 72 to 48 bpm with ST segment elevation by 12 mm on heart monitor (Figure 1). Immediately, 12 mg of ephedrine and 0.5 mg of atropine were given, but cardiac arrest occurred. External cardiac massage and electric countershock resuscitated the patient. When the surgical dressings were removed after surgery, large dermal flares were observed on the trunk and extremities, but there were no respiratory symptoms. Blood samplings were taken to measure serum levels of histamine and mast cell tryptase (Tryptase RIACT kit; Pharmacia, Uppsala, Sweden); their normal ranges are 1.14 +/- 0.40 nmol/L and less than 2.0 U/L, respectively (Figure 2).Figure 1: Serial changes of ST in the electrocardiogram monitor lead 2 at first and second surgery. BI = before induction, MM = mesenteric manipulation, PS = postsurgery.Figure 2: Serial changes in serum levels of histamine and tryptase at first and second surgery. BI = before induction, MM = mesenteric manipulation, PS = postsurgery.To determine whether anaphylactic reaction or mesenteric manipulation was responsible, dermal prick test and in vitro histamine release test were performed (Hollister-Stier, West Haven, CT) using all agents given before cardiac arrest; saline, thiamylal, fentanyl, vecuronium, chlorhexidine, lactated Ringer's solution, and hydroxyethylated starch for dermal prick test and for in vitro histamine release test (lower limit of sensitivity 10 nmol/L), excepting sevoflurane and nitrous oxide. However, neither was negative. Coronary angiography with injections of 60 and 40 micro g of ergonovine into the left and right coronary artery were negative. Gastrectomy was scheduled 8 wk later, with premedication of chlorpheniramine 5 mg, famotidine 20 mg, and hydrocortisone 500 mg. Induction and maintenance of anesthesia were performed as described previously. A continuous infusion of 0.5 micro g [centered dot] kg-1 [centered dot] min-1 of nitroglycerine and 1.0 micro g [centered dot] kg-1 [centered dot] min-1 of diltiazem was given. Surgical resection was performed uneventfully. Mesenteric manipulation for abdominal lavage with warm saline induced facial flushing at the end of surgery without circulatory derangement, showing ST segment elevation of 4 mm on the heart scope (Figure 1). These findings were transient, and the surgery was completed. Serum histamine levels at induction, at ST elevation, and at 3 h after the surgery were 0.9, 46.0, and 4.3 nmol/L, respectively. Serum tryptase levels were within normal ranges. The patient was discharged uneventfully. Discussion Hemodynamic instability and dermal flushing are typical during both anaphylaxis and mesenteric manipulation [2,3]. We measured serum histamine and tryptase levels [4], as anaphylaxis is frequently evidenced by increased level of these substances. Tryptase stored in mast cell granules represents an important alternative to histamine when sampling is delayed in anaphylaxis [5,6]. We therefore were reluctant to conclude that an anaphylactic reaction is responsible for the increased level of tryptase because it could increase whenever mast cells are activated [4]. The in vitro histamine release test used to evaluate drug-mediated anaphylactic reactions was negative [5]; therefore, anaphylactic reaction was ruled out. Allergic shock complicated by coronary spasm has been reported [7,8], and vasoactive mediators have been attributed as the causes. As histamine may play a role in provoking coronary spasm [8], an increased number of histaminergic receptors, augmentation of signal transduction in the coronary artery smooth muscle cell, or both are presumed [9]. Although surgical manipulation stimulates release and produces prostacyclin [1-3], prostanoids are deniable as a primary role in coronary spasm [10]. However, we had to consider that prostacyclin would aggravate coronary hypoperfusion and severe arrhythmias. Histamine may be involved in the pathogenesis of coronary spasm if it is massively released [11], and a significant amount of histamine could be released during surgical manipulation. We estimated that the highest histamine level at the first surgery would exceed the level sufficient to induce coronary vasoconstriction [11]. To investigate organic coronary disease, we performed coronary angiography as a routine study by loading an ordinary dose of ergonovine after informed consent was obtained. However, we failed to obtain significant information on coronary disease. As transient ST segment elevation resolved without evidence of infarction, we considered that the event was due to a prinzmetal-type coronary spasm or variant angina. Because a single dose of ergonovine could not disclose focal spasm during coronary angiography, we considered that the possibility of coronary disease was negligible, and patient consent was not obtained for a further incremental dose of ergonovine up to 0.3 mg [12]. We then suspected that the circulatory derangement was due to mesenteric manipulation increasing tryptase and histamine, which could have induced coronary vasoconstriction, leading to cardiac arrest in this patient.