The relative infrequency of blunt carotid artery trauma prompted a multicenter review to determine the spectrum of injuries, treatment strategies, and neurologic outcome. During a six-year period, 60 carotid artery injuries from blunt mechanisms in 49 patients were treated at 11 institutions. There were 11 bilateral injuries. Injury mechanisms were diverse but involved motor vehicles in 35 (72%) patients. In 14 (29%) patients, significant neurologic deficits developed more than 12 hours after a normal admission neurologic examination. The diagnosis was confirmed by angiography in 42 (86%). Duplex ultrasound accurately demonstrated the arterial injury in 12 (86%) of 14 patients. Documented injuries included arterial thrombosis in 20 arteries, arterial dissection alone in 19, dissection with pseudoaneurysm in six, pseudoaneurysm alone in five, frank arterial disruption in seven, and carotid-cavernous fistula in three. Arterial dissection was managed nonsurgically in 15 (79%) of 19 cases, the majority with systemic anticoagulation. Arterial thrombosis was managed with supportive therapy alone for 16 (80%) of 20 arteries; most associated with fixed neurologic deficits. Pseudoaneurysm repair was performed for six (55%) injuries. Carotid-cavernous fistulas were treated in all three instances with balloon occlusion. Overall mortality was 16 of 49 patients (43%). Good neurologic outcome was achieved in 22 (45%) patients. We conclude that: (1) Neurologic symptoms may develop in a delayed fashion; prior clinical suspicion and diagnostic testing are essential; (2) arterial dissection without complete occlusion may effectively be managed by anticoagulation; (3) pseudoaneurysms in accessible anatomic locations can be repaired with good results; and (4) injuries with complete arterial thrombosis are associated with high mortality and poor neurologic outcome in proportion to the initial degree of neurologic impairment.

A multi-center experience with 210 severe liver injuries was reviewed to define postoperative changes in hepatic enzyme levels and body temperature profile. The 129 patients who survived initial operation comprised the data base. Serum glutamic oxaloacetic transaminase (SGOT) and lactate dehydrogenase (LDH) peaked within 24 hours (750 +/- 92 IU/L, 870 +/- 120 IU/L) and decreased rapidly during the first 4 days. Serum bilirubin was maximal at 7 days, while alkaline phosphatase rose slowly throughout 14 days. Hepatic enzyme elevations were more dramatic after blunt trauma, reflecting greater hepatocellular disruption. Maximum daily temperatures exceeding 38.0 degrees C and 39.0 degrees C were recorded for the first 3 postoperative days in 82 (64%) patients and 14 (11%) patients, respectively. No infectious source was evident in 13 (93%) of 14 patients with severe hyperpyrexia, implicating release of inflammatory mediators associated with major hepatic trauma. Convalescence from severe hepatic injury is marked by release of SGOT and LDH, as well as fever, which may be anticipated during the first 4 days postinjury.

The experience of six referral trauma centers with 832 blunt splenic injuries was reviewed to determine the indications, methods, and outcome of nonoperative management. During this 5-year period, 112 splenic injuries were intentionally managed by observation. There were 40 (36%) patients less than 16 years old and 72 adults. The diagnosis was established by computed tomography in 89 (79%) patients, nuclear scan in 23 (21%), ultrasound in four (4%), and arteriography in two (2%). There were 28 Class I, 51 Class II, 31 Class III, two Class IV, and no Class V splenic injuries. Nonoperative management was unsuccessful in one (2%) child and 12 (17%) adults (p less than 0.05). Failure was due to ongoing hemorrhage in 12 patients and delayed recognition of pancreatic injury in one patient. Of the 12 patients ultimately requiring laparotomy for control of hemorrhage, seven (58%) were successfully treated with splenic salvage techniques. Overall mortality was 3%; none of the four deaths was due to splenic or associated abdominal injury. This contemporary multicenter experience suggests that patients with Class I, II, or III splenic injuries after blunt trauma are candidates for nonoperative management if there is: 1) no hemodynamic instability after initial fluid resuscitation; 2) no serious associated abdominal organ injury; and 3) no extra-abdominal condition which precludes assessment of the abdomen. Strict adherence to these principles yielded initial nonoperative success in 98% of children and 83% of adults. Application of standard splenic salvage techniques to treat the patients with persistent hemorrhage resulted in ultimate splenic preservation in 100% of children and 93% of adults.

The indiscriminate application of thoracotomy in the resuscitation of trauma has recently been challenged. Since 1 May 1974 400 consecutive trauma patients have undergone resuscitative thoracotomy in our Emergency Departments (ED). The mechanism of injury was blunt in 195 (49%) patients, gunshot wound in 147 (37%), and stab wound in 58 (14%) Upon arrival in the ED, 352 (88%) patients had no obtainable blood pressure (BP), 334 (84%), fixed pupils, and 315 (798%) failed to exhibit agonal respirations or other waning signs of life. One hundred six (27%) patients reached the operating room and 28 (7%) survived to be admitted to the intensive care unit. Sixteen were eventually discharged from the hospital, but four of these survivors had sustained irreversible cerebral damage. Overall, 12 of 400 (3%) patients survived ED thoracotomy with intact neurologic function. Four factors appeared predictive of poor prognosis. There were no survivors with intact neurologic function among: 150 patients sustaining blunt trauma and arriving in the ED without signs of life (BP, pupil reactivity, respiratory effort); or 87 patients with penetrating torso injuries who had no signs of life at the scene. Following thoracotomy, in the absence of cardiac tamponade, there were no intact survivors of 124 patients without cardiac activity or of aortic occlusion. We believe the above factors should militate against initiating resuscitative thoracotomy in the ED or in deciding to continue heroic measures following thoracotomy.