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Successful Management of Cold-Induced Urticaria During Hypothermic Circulatory Arrest

2013; Elsevier BV; Volume: 96; Issue: 5 Linguagem: Inglês

10.1016/j.athoracsur.2013.03.030

1552-6259

Anne K. Ellis, Tarit Saha, Ramiro Arellano, Andrew Zajac, Darrin Payne,

Food Allergy and Anaphylaxis Research

Cold-induced urticaria (CIU) is a potentially life-threatening immunologic disorder characterized by swelling and edema of exposed tissue in response to a cold stimulus. We describe the successful management of a patient with a history of severe CIU who required coronary bypass and repair of an ascending aortic aneurysm using hypothermic circulatory arrest. Cold-induced urticaria (CIU) is a potentially life-threatening immunologic disorder characterized by swelling and edema of exposed tissue in response to a cold stimulus. We describe the successful management of a patient with a history of severe CIU who required coronary bypass and repair of an ascending aortic aneurysm using hypothermic circulatory arrest. Cold-induced urticaria (CIU) is a potentially life-threatening immunologic disorder characterized by swelling and edema of exposed tissue in response to a cold stimulus. Severe cases are associated with hypotension and cardiovascular collapse. We describe the successful management of a 70-year-old man with a previous history of CIU who required coronary bypass and repair of an ascending aortic aneurysm using hypothermic circulatory arrest. An 81-kg, 70-year-old man presented with symptoms of crescendo angina. Coronary angiography revealed a 90% left main coronary artery lesion and an 80% lesion in a dominant right coronary artery. Thoracic computed tomography revealed an ascending aortic aneurysm measuring 56 mm in maximal diameter, tapering to 40 mm at the takeoff of the innominate artery and 35 mm in the arch. The aortic root was not enlarged. Echocardiography revealed preserved left ventricular function with a normally functioning aortic valve. In addition to a history of hypertension and a history of previous smoking, the patient had cold-induced urticaria (CIU) with earlier life-threatening reactions to cold, having had an anaphylactic reaction secondary to river water emersion. Circulatory arrest was deemed essential to perform an adequate repair of his ascending aortic aneurysm. Allergy and clinical immunology colleagues were consulted, and the patient was prescribed a 3-day treatment schedule of cetirizine 10 mg orally twice daily (BID) and ranitidine 150 mg orally BID. This degree of histamine receptor antagonism produced a partial suppression of his ice test result. The ice test involves applying a frozen solid 1-cm glass vial (containing a diluent negative control for standard skin testing) to the volar surface of the patient's forearm and observing for the development of a wheal and flare response. At 7 days preoperatively, this regimen was expanded to cetirizine 20 mg BID, ranitidine 150 mg BID, and montelukast 10 mg once daily. This was further expanded 5 days preoperatively to include prednisone 25 mg BID, which was continued until the day of operation. The patient's metoprolol was replaced with amlodipine. We used an extensive perioperative and intraoperative regimen consisting of combinations of methylprednisolone, ranitidine, and diphenhydramine. An hour before the patient was transferred to the operating room, he was given intravenous methylprednisolone 2 g, ranitidine 50 mg, and diphenhydramine 100 mg. Intravenous methylprednisolone 125 mg and diphenhydramine 100 mg were given 1 hour before starting cardiopulmonary bypass. Before rewarming, we administered intravenous methylprednisolone 60 mg, ranitidine 50 mg, and diphenhydramine 100 mg. The patient also received methylprednisolone 60 mg, ranitidine 50 mg, and diphenhydramine 50 mg intravenously 6 hours postoperatively. Intraoperatively and postoperatively we sampled serial serum tryptase and plasma histamine levels. Arterial cannulation was accomplished through the right axillary artery with an 8-mm Dacron graft. We used a 2-stage right atrial venous cannula. Cardioplegia was delivered using initial antegrade doses through the root with subsequent retrograde administration through the coronary sinus. Intraoperatively, the patient was cooled to a core temperature of 28°C. Distal bypass grafting was performed while the patient was cooling. At 28°C, circulatory arrest was commenced using selective antegrade cerebral perfusion (delivered at 28°C) through the right axillary artery. Total circulatory arrest time was 11 minutes. Total cardiopulmonary bypass time was 159 minutes with 78 minutes of cross-clamping. The patient proved difficult to rewarm, requiring more than an hour to attain normothermia. Systemic hypotension, managed with inotropic and pressor support, was an issue throughout the rewarming period. Once warm, the patient required only a low-dose epinephrine infusion. He experienced a brief but impressive lactic acidosis postoperatively (Fig 1). Pressor support was weaned several hours after the operation, and the acidosis resolved by the following morning. Serum histamine and tryptase levels were determined at baseline, at the onset of bypass, once the patient was cooled to 28°C, after completion of circulatory arrest, once rewarming was completed, and at 2, 4, and 6 hours after rewarming. Baseline serum histamine levels measured 7 nmol/L and tryptase levels were 1.3 μg/L. Serum histamine levels peaked at 8 nmol/L measured at the onset of bypass and remained at 5 nmol/L and less for all subsequent measurements. Serum tryptase levels ranged from 2.3 to 3.4 μg/L, with peak levels occurring 6 hours after rewarming (Fig 2). The patient recovered uneventfully and was discharged home on postoperative day 6.Fig 2Preoperative, intraoperative, and postoperative serum histamine and tryptase levels. (DHCA = deep hypothermic circulatory arrest; X-clamp = cross-clamp.)View Large Image Figure ViewerDownload (PPT) CIU is an uncommon albeit well-described phenomenon resulting from mast cell degranulation with subsequent release of inflammatory mediators after cold exposure. Histamine appears to mediate most of the clinical manifestations. Its release is greatest on withdrawal of the cold stimulus. Avoidance of short-term and prolonged exposures to cold stimuli is central to the management of these individuals. Although patients with CIU requiring cardiac operations have been reported [1Booth K. Parissis H. Management of cold-induced urticaria during cardiac surgery.J Card Surg. 2011; 26: 158-159Crossref PubMed Scopus (9) Google Scholar, 2Bakay C. Onan B. Onan I.S. Ozkara A. Coronary artery bypass grafting in cold- induced urticaria.Ann Thorac Surg. 2010; 89: 949-951Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar, 3Johnston W.E. Moss J. Philbin D.M. et al.Management of cold urticaria during hypothermic cardiopulmonary bypass.N Engl J Med. 1986; 306: 219-220Crossref Scopus (27) Google Scholar, 4Lancey R.A. Schaefer O.P. McCormick M.J. Coronary artery bypass grafting and aortic valve replacement with cold cardioplegia in a patient with cold-induced urticaria.Ann Allergy Asthma Immunol. 2004; 92: 273-275Abstract Full Text PDF PubMed Scopus (12) Google Scholar], this remains an unusual clinical entity for cardiac surgeons. Booth and Parissis [1Booth K. Parissis H. Management of cold-induced urticaria during cardiac surgery.J Card Surg. 2011; 26: 158-159Crossref PubMed Scopus (9) Google Scholar] reported on a patient with known CIU requiring coronary artery bypass grafting (CABG). They administered a combination of hydrocortisone, ranitidine, and chlorphenamine immediately before induction of anesthesia. This patient was kept normothermic throughout the case. Bakay and Onan [2Bakay C. Onan B. Onan I.S. Ozkara A. Coronary artery bypass grafting in cold- induced urticaria.Ann Thorac Surg. 2010; 89: 949-951Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar] reported a similar patient with CIU who underwent CABG; they maintained the patient at or near 37°C. They administered 1 mg/kg methylprednisolone 12 hours preoperatively, with another 1 mg/kg methylprednisolone and a single dose of an antihistamine (pheniramine maleate, 45 mg) given intravenously before induction. Postoperatively the patient was given a 3-day tapering regimen of intravenous methylprednisolone. Johnston and colleagues [3Johnston W.E. Moss J. Philbin D.M. et al.Management of cold urticaria during hypothermic cardiopulmonary bypass.N Engl J Med. 1986; 306: 219-220Crossref Scopus (27) Google Scholar] reported a patient with known CIU who required a coronary operation. He was administered diazepam, scopolamine, morphine, and hydrocortisone before entering the operating room; he also received intravenous administration of cimetidine (300 mg), diphenhydramine (90 mg), and hydrocortisone (100 mg) before induction of anesthesia. This patient was cooled to 31°C. Before rewarming, he was given 300 mg cimetidine and 90 mg diphenhydramine. Intraoperatively they observed a significant rise in serum histamine levels; however, the patient remained clinically stable. Lancey and associates [4Lancey R.A. Schaefer O.P. McCormick M.J. Coronary artery bypass grafting and aortic valve replacement with cold cardioplegia in a patient with cold-induced urticaria.Ann Allergy Asthma Immunol. 2004; 92: 273-275Abstract Full Text PDF PubMed Scopus (12) Google Scholar] reported a case of combined aortic valve replacement and CABG in a patient with CIU. This patient was cooled to 32°C for the procedure. An extensive regimen of fexofenadine, ranitidine, methylprednisolone, and diphenhydramine was used beginning 5 days preoperatively and continuing into the postoperative course. To our knowledge, this is the first reported case of a patient with CIU undergoing hypothermic circulatory arrest. Similar to Lancey and colleagues, we used an extensive preoperative, intraoperative, and postoperative regimen to blunt the CIU response. Antegrade cerebral perfusion throughout the period of circulatory arrest allowed us to cool the patient to no lower than 28°C. Others have shown an increase in plasma histamine levels with rewarming during cardiopulmonary bypass [3Johnston W.E. Moss J. Philbin D.M. et al.Management of cold urticaria during hypothermic cardiopulmonary bypass.N Engl J Med. 1986; 306: 219-220Crossref Scopus (27) Google Scholar]. To blunt this response we used an extensive pharmacologic regimen initiated well in advance of the operative date. The lack of an observed rise in tryptase levels suggests that we successfully achieved mast cell stabilization. Our patient required transient low-level inotropic support for a few hours postoperatively. He also experienced significant lactic acidosis, with serum lactate levels peaking at 25 mmol/L 2 hours postoperatively. There was no clinical evidence of organ malperfusion or ischemia, and he remained clinically stable. Although the cause of the lactic acidosis remains unclear, we believe it to be due to "washout" from peripheral tissue beds. Although not known to be characteristic of CIU, perhaps this patient had a pronounced peripheral arterial vasoconstriction in response to cold stimuli. If this patient had effectively reduced flow to peripheral tissue beds during cooling, this would explain the accumulation of lactic acid and the subsequent spike we observed after reperfusion. This could also help explain the time it took and the difficulty we had rewarming the patient. In conclusion, this case suggests that patients with CIU complicated by anaphylaxis can successfully undergo cardiac bypass operations using deep hypothermic circulatory arrest. We would recommend using an aggressive preoperative, intraoperative, and postoperative pharmacologic strategy.