Anesth Analg 2000;91:561-562
© 2000 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Injury to the Abdominal Aorta During Laparoscopic Surgery: An Unusual Presentation
Anna Mases, MD,
Antonio Montes, MD,
Rocio Ramos, MD,
Lourdes Trillo, MD, and
Margarita M. Puig, MD, PhD
Department of Anesthesiology, Hospital Universitario del Mar, Universitat Autonoma de Barcelona, Barcelona, Spain
Address correspondence and reprint requests to Anna Mases, MD, Servicio de Anestesiología y Reanimacion, Hospital, del Mar, Passeig Marítim, 25-29, 08003 Barcelona, Spain. Address e-mail to 30858amf{at}comb.es
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Abstract
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Implications: Laparoscopic cholecystectomy is a very common surgical procedure, and vascular injuries account for one third of major complications during this surgery. We describe an unusual presentation of an abdominal aorta injury.
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Introduction
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Laparoscopic surgery has many advantages, but sometimes life-threatening complications can occur, such as hemodynamic and ventilatory disturbances, complications caused by systemic absorption of intraperitoneal CO2, and traumatic lesions with trocar insertion (1–2). Traumatic complications include gastrointestinal tract perforations, viscera lacerations, abdominal wall hematomas, and vascular injuries.
We report a case of damage to the abdominal aorta during laparoscopic cholecystectomy with an unusual onset with hypertension and a sudden decrease in the ETCO2.
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Case Report
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A 49-yr-old woman, with a weight of 45 kg and height of 165 cm (body mass index, 16.5 kg/m2), was scheduled for an emergency cholecystectomy because of acute cholecystitis. Six years previously, the patient had surgery and radiotherapy for a carcinoma of the uterine cervix. Preoperative laboratory data were within normal limits, except the serum creatinine (4.1 mg/dL). The electrocardiogram and chest radiograph were also normal. During surgery, the following variables were monitored: electrocardiogram with ST analysis (Marquette Tramscope 12c®; Marquette Medical Systems, Milwaukee, WI), noninvasive arterial blood pressure, pulse oximetry, urine output, ETCO2, and inspired and expired gas concentration by mass spectrometry. On arrival to the operating room, her blood pressure was 130/80 mm Hg, her heart rate was 110 bpm, she had an oxygen saturation of 96%. Anesthesia was induced with IV thiopental and fentanyl, and orotracheal intubation was facilitated with a defasciculating dose of atracurium and IV succinylcholine. Anesthesia was maintained with fentanyl and isoflurane (1%–2%) in oxygen/air. Pneumoperitoneum was induced by insufflation of CO2 reaching intraabdominal tensions up to 12 mm Hg. The patient was placed at 30° with a head-up tilt. Thirty-five minutes after the incision and during gall bladder dissection, arterial hypertension (200/120 mm Hg), sinus tachycardia (160 bpm), and a sudden decrease in ETCO2 (from 28 to 9 mm Hg) were observed. Immediately afterward, the patient developed bradycardia resistant to atropine with subsequent cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated and sinus rhythm restored after 12 min; during this period, ETCO2 also increased–an indication of the adequacy of the resuscitative efforts (Figure 1). During CPR, no intraperitoneal bleeding was observed; however, hemoglobin was 3.7 g/dL, and conversion to an open technique revealed a retroperitoneal hematoma secondary to an infrarenal lesion of the aorta. During laparotomy, the patient had a second cardiac arrest that did not respond to CPR, and she died 60 min. afterward. The surgeon requested consent for an autopsy, which was denied by the family.
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Figure 1. Hemodynamic and ETCO2 changes during the procedure. The arrow in the circle shows the point where hypertension, together with an abrupt decrease in the ETCO2, was noticed. HR = heart rate, MAP = mean arterial pressure.
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Discussion
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Vascular injuries account for one third of major complications in laparoscopic surgery (1). Their real incidence is unknown because many of these cases are not reported, but it is approximately 0.05% to 2% (3–6). In a French review of 103,852 laparoscopies, the vessels more frequently involved were iliac (n = 16 cases), epiploic (n = 10), inferior vena cava (n = 6), aorta (n = 5), superior mesenteric vein (n = 3), pelvic (n = 3), and lumbar (n = 2) (6). The incidence of major retroperitoneal vascular lesions in laparoscopic cholecystectomy is 0.05% (7), and the most commonly affected vessels are the aorta, the iliac vessels, and the inferior vena cava.
Vascular injuries are usually induced by the insertion of the Veress needle or the first trocar, because both are usually introduced blindly. The insertion of the secondary trocars has a lesser risk, because they are placed under direct vision (8). Vascular lesions with the dissectors are much less frequent.
Factors that increase the likelihood of vascular injury include surgeon inexperience, incorrect raising of the abdominal wall, inadequate pneumoperitoneum, anomalous anatomical references, and skeletal deformities (9). Extreme thinness (10) and previous abdominal surgery have also been implicated (6).
Although vascular injury is usually diagnosed by direct view of bleeding in the abdominal cavity, the absence of free intraperitoneal blood caused by retroperitoneal bleeding may delay the diagnosis, because blood is not observed through the laparoscope (11). Clinical signs of hemodynamic instability (tachycardia, hypotension), shortly after needle insertion, suggest a vascular lesion. However, the high intraabdominal pressure secondary to pneumoperitoneum is associated with a decrease in venous return, which in turn, can reduce arterial bleeding (11). Furthermore, a retroperitoneal hematoma can decrease a vessel leak, restraining the bleeding.
In our case, the onset of clinical signs was unusual, because the patient presented with hypertension, tachycardia, and an abrupt decrease of the ETCO2, 35 minutes after pneumoperitoneum insufflation. There are two possible explanations for this anomalous presentation: The Veress needle may have produced a small tear in the aorta’s wall, developing a retroperitoneal hematoma that would tamponade the aortic flow (11). Our patient had previous radiotherapy, which could induce the retroperitoneal space to become less compliant in the presence of a sudden distension. Our second hypothesis is that the Veress needle could have induced a tear in the intima, developing a dissecting hematoma, which finally would limit or contain the aortic flow. Both hypotheses would explain the increase in arterial blood pressure in the upper limbs (where blood pressure was monitored) and the decrease in the ETCO2 caused by a reduced venous return and decreased cardiac output. In the presence of competent carotid and aortic baroreflexes, an increase in sympathetic nervous system activity would occur and would counteract the reduction in cardiac output. This mechanism, together with the increase in systemic vascular resistance induced by the tamponade of the aortic flow by the retroperitoneal hematoma, could have contributed to the hypertension observed in our patient. At the time of surgery, the patient was not taking any medication that could have altered the cardiovascular response. She had no hypertension, nor did she have any cardiovascular disease that could have modified the physiologic responses.
Although, in the presence of a sudden decrease in ETCO2 during laparoscopic surgery, we should suspect a pulmonary embolism, and especially a CO2 embolism, we quickly rejected this possibility. In this situation, we would have seen hypotension and hypoxemia (no decrease in pulse oximetry was observed), and in CO2 embolism, the decrease in ETCO2 would have been preceded by an increase (1).
Despite our efforts, the patient suffered a second cardiac arrest as a consequence of a hypovolemic shock refractory to treatment. This fatal outcome may have been avoided if we had suspected the lesion earlier, because critical time was probably wasted.
Although a tear in the aorta’s wall was observed during the laparotomy, to obtain a definite diagnosis it would have been essential to perform an autopsy, but the family refused. From our experience, we would like to point out that, during laparoscopic surgery, we should be aware of vascular injury, not only when hypotension and tachycardia are observed but also in the presence of hypertension associated to an abrupt decrease in the ETCO2.
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References
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Accepted for publication May 11, 2000.
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Abstract
Introduction
