Blunt carotid and vertebral arterial injuries.

Blunt carotid and vertebral arterial injuries are uncommon but have the potential for devastating consequences. The classic presentation is a neurologic deficit unexplained by computed tomographic scan findings. Screening patients based on injury mechanisms and patterns allows the diagnosis and treatment of injuries while they are still asymptomatic, potentially improving neurologic outcomes. The development of a grading scale may help refine treatment guidelines. Accessible grade II, III, and V carotid injuries should be repaired surgically. Anticoagulation should be considered first-line therapy for grade I and IV, and inaccessible grade II and III carotid lesions, and grade I-IV vertebral injuries. Grade V and persistent grade III lesions may be best treated employing endovascular techniques.

Phospholipase A(2)--derived neutral lipids from posthemorrhagic shock mesenteric lymph prime the neutrophil oxidative burst.

BACKGROUND: Our previous work identified posthemorrhagic shock mesenteric lymph (PHSML) lipids as key elements in polymorphonuclear neutrophil (PMN)--provoked acute lung injury. We hypothesize that gut phospholipase A(2) (PLA(2)) is responsible for the generation of proinflammatory lipids in PHSML that primes circulating PMNs for enhanced oxidative burst. METHODS: Mesenteric lymph was collected from rats (n = 5) before (preshock), during the induction of hemorrhagic shock (mean arterial pressure, 40 mm Hg x 30 minutes), and at resuscitation (shed blood + 2x lactated Ringer's solution). PLA(2) inhibition (quinacrine, 10 mg/kg, intravenously) was given before shock was induced. Extracted lipids were separated by normal phase high-pressure liquid chromatography and resuspended in albumin. PMNs were exposed to a 5% vol:vol concentration of eluted lipids and activated with N-formyl-methionyl-leucyl-phenylalanine (1 micromol/L). Superoxide production was assessed by cytochrome C reduction. RESULTS: High-pressure liquid chromatography--extracted neutral lipids of lymph collected before hemorrhagic shock did not prime the PMN oxidase, whereas isolated neutral lipids of postshock lymph primed PMNs 2.6- +/- 0.32-fold above baseline (P <.05). PLA(2) inhibition returned PHSML neutral lipid priming to baseline levels. CONCLUSIONS: PLA(2) inhibition before hemorrhagic shock abrogates the neutrophil priming effects of PHSML through reduction of the accumulation of proinflammatory neutral lipids. Identification of these PLA(2)-dependent lipids provides a mechanistic link that may have therapeutic implications for postshock acute lung injury.

Avoidance of abdominal compartment syndrome in damage-control laparotomy after trauma.

HYPOTHESIS: Abdominal compartment syndrome (ACS) is a morbid complication of damage-control laparotomy. Moreover, the technique of abdominal closure influences the frequency of ACS. DESIGN: Retrospective cohort study. SETTING: Urban level I trauma center. PATIENTS: We studied 52 patients with trauma who required damage-control laparotomy during the 5 years ending December 31, 1999, and who survived longer than 48 hours. MAIN OUTCOME MEASURES: Abdominal compartment syndrome, acute respiratory distress syndrome (ARDS), and multiple organ failure (MOF). RESULTS: Mean (+/- SD) age was 33 +/- 2 years; 38 (73%) were male. Mechanism of injury was blunt in 29 patients (56%), and mean (+/- SD) Injury Severity Score was 28 +/- 2. Development of ARDS and/or MOF was seen in 23 patients (44%); ARDS and MOF increased mortality from 12% (3/26) to 42% (11/26). Abdominal compartment syndrome was a common complication (17/52), and was associated with an increase in ARDS and/or MOF (12 patients [71%] vs 11 patients [31%] without ACS; P =.02, chi(2) test) and death (6 [35%] vs 8 patients [23%] without ACS). Primary fascial closure (n = 10) at the initial laparotomy was associated with ACS in 8 (80%) (P =.001, chi(2) test) and ARDS and/or MOF in 9 (90%) (P =.01, chi(2) test); skin closure (n = 25), with ACS in 6 (24%) and ARDS/MOF in 9 (36%); and Bogotá bag closure (n = 17), with ACS in 3 (18%) and ARDS/MOF in 8 (47%). CONCLUSIONS: Damage-control laparotomy is associated with frequent complications. In particular, ACS is a serious complication that increases ARDS and/or MOF and mortality. Avoiding primary fascial closure at the initial laparotomy can minimize the risk for ACS.

Evolution of a multidisciplinary clinical pathway for the management of unstable patients with pelvic fractures.

OBJECTIVE: To determine whether the evolution of the authors' clinical pathway for the treatment of hemodynamically compromised patients with pelvic fractures was associated with improved patient outcome. SUMMARY BACKGROUND DATA: Hemodynamically compromised patients with pelvic fractures present a complex challenge. The multidisciplinary trauma team must control hemorrhage, restore hemodynamics, and rapidly identify and treat associated life-threatening injuries. The authors developed a clinical pathway consisting of five primary elements: immediate trauma attending surgeon's presence in the emergency department, early simultaneous transfusion of blood and coagulation factors, prompt diagnosis and management of associated life-threatening injuries, stabilization of the pelvic girdle, and timely insinuation of pelvic angiography and embolization. The addition of two orthopedic pelvic fracture specialists led to a revision of the pathway, emphasizing immediate emergency department presence of the orthopedic trauma attending to provide joint decision making with the trauma surgeon, closing the pelvic volume in the emergency department, and using alternatives to traditional external fixation devices. METHODS: Using trauma registry and blood bank records, the authors identified pelvic fracture patients receiving blood transfusions in the emergency department. They analyzed patients treated before versus after the May 1998 revision of the clinical pathway. RESULTS: A higher proportion of patients in the late period had blood pressure less than 90 mmHg (52% vs. 35%). In the late period, diagnostic peritoneal lavage was phased out in favor of torso ultrasound as a primary triage tool, and pelvic binding and C-clamp application largely replaced traditional external fixation devices. The overall death rate decreased from 31% in the early period to 15% in the later period, as did the rate of deaths from exsanguination (9% to 1%), multiple organ failure (12% to 1%), and death within 24 hours (16% to 5%). CONCLUSIONS: The evolution of a multidisciplinary clinical pathway, coordinating the resources of a level 1 trauma center and directed by joint decision making between trauma surgeons and orthopedic traumatologists, has resulted in improved patient survival. The primary benefits appear to be in reducing early deaths from exsanguination and late deaths from multiple organ failure.

Plasma from aged stored red blood cells delays neutrophil apoptosis and primes for cytotoxicity: abrogation by poststorage washing but not prestorage leukoreduction.

BACKGROUND: Blood transfusion-particularly that of older stored red blood cells (RBCs)--is an independent risk factor for postinjury multiple organ failure. Immunomodulatory effects of RBC transfusion include neutrophil (PMN) priming for cytotoxicity, an effect exacerbated by longer RBC storage times. We have found that delayed PMN apoptosis in trauma patients is provoked by transfusion, independent of injury severity. We hypothesized that aged stored RBCs delay PMN apoptosis, but that prestorage leukodepletion or poststorage washing could abrogate the effect. METHODS: Healthy volunteers each donated 1 unit of blood. One half was leukodepleted, and RBC units were processed in the usual fashion and stored at 4 degrees C. Aliquots were removed on days 1, 14, 21, and 42 and the plasma fraction isolated. Selected aliquots were washed with normal saline before plasma isolation. PMNs harvested from healthy controls were incubated (5% CO2, 37 degrees C) with unmodified, leukoreduced, or washed RBC plasma (20% plasma/80% RPMI 1640), and apoptosis assessed by morphology after 24 hours. Apoptotic index (apoptotic PMNs/total PMNs) was compared. PMN priming for superoxide release was also assessed after plasma exposure. RESULTS: PMN apoptosis was delayed by RBCs stored for 21 or 42 days. Prestorage leukodepletion did not alter the effect. However, washing 42-day-old RBCs abrogated the effect. PMN priming for superoxide was provoked by stored packed RBCs in an identical pattern to delayed apoptosis. CONCLUSION: Plasma from stored RBCs-even if leukoreduced-delays apoptosis and primes PMNs. The effect becomes evident at 21 days and worsens through product outdate (42 days), but may be prevented by poststorage washing. Inflammatory agents contaminating stored blood likely mediate the effect. Modification of transfusion practices (e.g., giving fresher or washed RBCs or blood substitutes) may attenuate adverse immunomodulatory effects of transfusion in trauma patients.

Resuscitation with a blood substitute abrogates pathologic postinjury neutrophil cytotoxic function.

BACKGROUND: Resuscitation with oxygen-carrying fluids is critically important in the patient with hemorrhagic shock caused by trauma. However, it is clear that a number of biologic mediators present in stored blood (packed red blood cells [PRBCs]) have the potential to exacerbate early postinjury hyperinflammation and multiple organ failure through priming of circulating neutrophils (PMNs). PolyHeme (Northfield Laboratories, Evanston, IL), a hemoglobin-based substitute that is free of priming agents, provides an alternative. We hypothesized that PMN priming would be attenuated in patients resuscitated with PolyHeme in lieu of stored blood. METHODS: Injured patients requiring urgent transfusion were given either PolyHeme (up to 20 units) or PRBCs. Early postinjury PMN priming was measured via beta-2 integrin expression, superoxide production, and elastase release. RESULTS: Treatment groups were comparable with respect to extent of injury and early physiologic compromise. PMNs from patients resuscitated with PRBCs showed priming in the early postinjury period by all three measures. No such priming was evident in patients resuscitated with PolyHeme. CONCLUSION: The use of a blood substitute in the early postinjury period avoids PMN priming and may thereby provide an avenue to decrease the incidence or severity of postinjury multiple organ failure.

The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery.

BACKGROUND: The abdominal compartment syndrome (ACS) is a recognized complication of damage control surgery (DCS). The purposes of this study were to (1) determine the effect of ACS on outcome after DCS, (2) identify patients at high risk for the development of ACS, and (3) determine whether ACS can be prevented by preemptive intravenous bag closure during DCS. METHODS: Patients requiring postinjury DCS at our institution from January 1996 to June 2000 were divided into groups depending on whether or not they developed ACS. ACS was defined as an intra-abdominal pressure (IAP) greater than 20 mm Hg in association with increased airway pressure or impaired renal function. RESULTS: ACS developed in 36% of the 77 patients who underwent DCS with a mean IAP prior to decompression of 26 +/- 1 mm Hg. The ACS versus non-ACS groups were not significantly different in patient demographics, Injury Severity Score, emergency department vital signs, or intensive care unit admission indices (blood pressure, temperature, base deficit, cardiac index, lactate, international normalized ratio, partial thromboplastin time, and 24-hour fluid). The initial peak airway pressure after DCS was higher in those patients who went on to develop ACS. The development of ACS after DCS was associated with increased ICU stays, days of ventilation, complications, multiorgan failure, and mortality. CONCLUSIONS: ACS after postinjury DCS worsens outcome. With the exception of early elevation in peak airway pressure, we could not identify patients at higher risk for ACS; moreover, preemptive abdominal bag closure during initial DCS did not prevent this highly morbid complication.

Secondary abdominal compartment syndrome is a highly lethal event.

BACKGROUND: Recent reports have described resuscitation-induced, "secondary" abdominal compartment syndrome (ACS) in trauma patients without intra-abdominal injuries. We have diagnosed secondary ACS in a variety of nontrauma as well as trauma patients. The purpose of this review is to characterize patients who develop secondary ACS. METHODS: Our prospective ACS database was reviewed for cases of secondary ACS. Physiologic parameters and outcomes were recorded. Data are expressed as mean +/- SEM. RESULTS: Fourteen patients (13 male, aged 45 +/- 5 years) developed ACS 11.6 +/- 2.2 hours following resuscitation from shock. Eleven (79%) had required vasopressors; the worst base deficit was 14.1 +/- 1.9. Resuscitation included 16.7 +/- 3.0 L crystalloid and 13.3 +/- 2.9 red blood cell units. Decompressive laparotomy improved intra-abdominal, systolic, and peak airway pressures, as well as urine output; however, mortality was 38% among trauma and 100% among nontrauma patients. CONCLUSIONS: Secondary ACS may be encountered by general surgeons in a variety of clinical scenarios; resuscitation from severe shock appears to be the critical factor. Early identification and abdominal decompression are essential. Unfortunately, in our experience, this is a highly lethal event.

Single-layer continuous versus two-layer interrupted intestinal anastomosis: a prospective randomized trial.

OBJECTIVE: To determine the suitability of a single-layer continuous technique for intestinal anastomosis in a surgical training program. SUMMARY BACKGROUND DATA: Several recent reports have advocated the use of a continuous single-layer technique for intestinal anastomosis. Purported advantages include shorter time for construction, lower cost, and perhaps a lower rate of anastomotic leakage. The authors hypothesized that the single-layer continuous anastomosis could be safely introduced into a surgical training program and that it could be performed in less time and at a lower cost than the two-layer interrupted anastomosis. METHODS: The study was conducted during a 3-year period ending September 1999. All adult patients requiring intestinal anastomosis were considered eligible. Patients who required anastomosis to the stomach, duodenum, and rectum were excluded. Patients were also excluded if the surgeon did not believe either technique could be used. Patients were randomly assigned to one- or two-layer techniques. Single-layer anastomoses were performed with a continuous 3-0 polypropylene suture. Two-layer anastomoses were constructed using interrupted 3-0 silk Lembert sutures for the outer layer and a continuous 3-0 polyglycolic acid suture for the inner layer. The time for anastomosis began with the placement of the first stitch and ended when the last stitch was cut. Anastomotic leak was defined as radiographic demonstration of a fistula or nonabsorbable material draining from a wound after oral administration, or visible disruption of the suture line during reexploration. RESULTS: Sixty-five single-layer and 67 two-layer anastomoses were performed. The groups were evenly matched according to age, sex, diagnosis, and location of the anastomosis. Two leaks (3.1%) occurred in the single-layer group and one (1.5%) in the two-layer group. Two abscesses (3.0%) occurred in each group. A mean of 20.8 minutes was required to construct a single-layer anastomosis versus 30.7 minutes for the two-layer technique. Mean length of stay was 7.9 days for single-layer patients and 9.9 days for two-layer patients; this difference did not quite reach statistical significance. Cost of materials was $4.61 for the single-layer technique and $35.38 for the two-layer method. CONCLUSIONS: A single-layer continuous anastomosis can be constructed in significantly less time and with a similar rate of complications compared with the two-layer technique. It also costs less than any other method and can be incorporated into a surgical training program without a significant increase in complications.

The devastating potential of blunt vertebral arterial injuries.

OBJECTIVE: To formulate management guidelines for blunt vertebral arterial injury (BVI). SUMMARY BACKGROUND DATA: Compared with carotid arterial injuries, BVIs have been considered innocuous. Although screening for BVI has been advocated, particularly in patients with cervical spine injuries, the appropriate therapy of lesions is controversial. METHODS: In 1996 an aggressive arteriographic screening protocol for blunt cerebrovascular injuries was initiated. A prospective database of all screened patients has been maintained. Analysis of injury mechanisms and patterns, BVI grades, treatment, and outcomes was performed. RESULTS: Thirty-eight patients (0.53% of blunt trauma admissions) were diagnosed with 47 BVIs during a 3.5-year period. Motor vehicle crash was the most common mechanism, and associated injuries were common. Cervical spine injuries were present in 71% of patients, but there was no predilection for cervical vertebral level or fracture pattern. The incidence of posterior circulation stroke was 24%, and the BVI-attributable death rate was 8%. Stroke incidence and neurologic outcome were independent of BVI injury grade. In patients treated with systemic heparin, fewer overall had a poor neurologic outcome, and fewer had a poor outcome after stroke. Trends associated with heparin therapy included fewer injuries progressing to a higher injury grade, fewer patients in whom stroke developed, and fewer patients deteriorating neurologically from diagnosis to discharge. CONCLUSIONS: Blunt vertebral arterial injuries are more common than previously reported. Screening patients based on injury mechanisms and patterns will diagnose asymptomatic injuries, allowing the institution of therapy before stroke. Systemic anticoagulation appears to be effective therapy: it is associated with improved neurologic outcome in patients with and without stroke, and it appears to prevent progression to a higher injury grade, stroke, and deterioration in neurologic status.

Maximal human neutrophil priming for superoxide production and elastase release requires p38 mitogen-activated protein kinase activation.

HYPOTHESIS: Neutrophil priming has been implicated in the development of multiple organ failure, although the precise intracellular mechanisms that regulate neutrophil priming remain unclear. Our previous work characterized platelet-activating factor (PAF) priming of human neutrophils for concordant superoxide anion (O2-) generation and elastase degranulation. The p38 mitogen-activated protein kinase (MAPK) is activated by PAF stimulation. We hypothesized that PAF-induced human neutrophil priming for O2- and elastase release is mediated via the p38 MAPK pathway. DESIGN: Isolated neutrophils from 6 human donors were preincubated with the specific p38 MAPK inhibitor SB 203580 (1 micromol/L) or buffer (control) for 30 minutes. Cells were then primed with PAF (200 nmol/L), followed by receptor-dependent (N-formyl-methionyl-leucyl-phenylalanine, 1 micromol/L) or receptor-independent phorbol myristate acetate (PMA, 100 ng/mL) activation. SETTING: Urban trauma research laboratory. PATIENTS: Healthy volunteer donors of neutrophils. MAIN OUTCOME MEASURES: Maximal rate of O2- generation was measured by superoxide dismutase-inhibitable reduction of cytochrome c and elastase release by the cleavage of N-methoxysuccinyl-Ala-Ala-Pro-Val-p-nitroanilide. RESULTS: SB 203580 significantly attenuated the generation of O2- and release of elastase from neutrophils activated with N-formyl-methionyl-leucyl-phenylalanine but not with PMA. Independent of the activator receptor status, SB 203580 almost completely blocked the exaggerated neutrophil cytotoxic response due to PAF priming. CONCLUSIONS: The p38 MAPK pathway is required for maximal PAF-induced neutrophil priming for O2- production and elastase degranulation. Therefore, the MAPK signaling cascade may offer a potential therapeutic strategy to preempt global neutrophil hyperactivity rather than attempt to nullify the end products independently.

Optimal management of complicated empyema.

BACKGROUND: Despite continued improvement in medical therapy, empyema remains a challenging problem for the surgeon. Multiple treatment options are available; however, the optimal therapeutic management has not been elucidated. METHODS: A retrospective review was performed of all adult patients admitted to Denver Health Medical Center between January 1, 1993, and December 31, 1998, with the diagnosis of empyema. Data tabulated included patient demographics, presentation, chest computed tomography (CT) findings, treatment, and outcome. RESULTS: Empyema was diagnosed in 58 patients, 45 cases of which were multiloculated at the time of presentation. Empyema was secondary to pneumonia is 41 patients and posttraumatic in 15. In addition to antibiotic therapy, initial treatment included chest tube drainage alone (n = 6), chest tube drainage with primary operation (n = 19), and chest tube drainage with intrapleural fibrinolytic therapy (n = 33). In 15 patients (45%), fibrinolytic therapy failed. Initial chest CT revealed a pleural peel in 5 patients treated with fibrinolytics and all failed. Multiloculation, however, was not a factor in failure of fibrinolysis. Moreover, chest CT missed the presence of a pleural peel in 17 of 31 patients documented to have a significant peel at the time of thoracotomy. CONCLUSION: Multiple therapeutic options are available for the management of empyema. Multiloculation is not a contraindication to an initial trial of chest tube drainage or fibrinolytic therapy. In contrast, CT evidence of a pleural peel uniformly predicted failure of nonoperative treatment.

Male gender is a risk factor for major infections after surgery.

BACKGROUND: Accumulating clinical and epidemiological evidence suggests significant gender differences in the incidence of and outcome following major infection. In a rodent model of hemorrhagic shock, investigators have shown that males manifest depressed cell-mediated immunity that is reversed by castration or pharmacologic testosterone receptor blockade. Female rats, in contrast, show enhanced immune function that is reduced to male levels by testosterone administration. This sexual dimorphism is believed responsible for the improved outcome in female mice following septic challenge. HYPOTHESIS: Male gender is a risk factor for major infections following severe injury. DESIGN: Five-year prospective cohort study ending October 1998. SETTING: Urban level I regional trauma center. PATIENTS AND METHODS: A total of 545 trauma patients older than 15 years with an Injury Severity Score greater than 15 and survival more than 48 hours were prospectively identified and studied. Collected data included age, injury mechanism, and Injury Severity Score. Major infections, defined as pneumonia, abdominal and pelvic abscess, wound infection requiring operative debridement, and meningitis, were tabulated. The occurrence of major infections in males and females was compared using multiple logistic regression analysis. MAIN OUTCOME MEASURE: Postinjury major infectious complications. RESULTS: Of the 545 patients, 135 (24.8%) were female and 410 (75.2%) were male. Major infections occurred in 219 (40.2%) patients. Logistic regression confirmed that male gender is an independent risk factor for major infections (P=.04) after controlling for age and Injury Severity Score. Males had a 58% greater risk of developing a major infection (odds ratio, 1.58; 95% confidence interval, 1.01-2.48). CONCLUSIONS: Male gender is associated with a dramatically increased risk of major infections following trauma. This effect is most significant following injuries of moderate severity (Injury Severity Score 16-25) and persists in all age groups.

Neutrophils are primed for cytotoxicity and resist apoptosis in injured patients at risk for multiple organ failure.

BACKGROUND: Postinjury multiple organ failure (MOF) is the result of a dysregulated systemic inflammatory response in which primed neutrophils (PMNs) are sequestered in tissues, vulnerable to activation through secondary insults. Apoptosis is critical to the normal clearance of these sequestered PMNs. Conversely, dysfunctional apoptosis prolongs the PMN functional life span, potentially exacerbating PMN-mediated tissue injury and the development of MOF. We hypothesized that severe trauma, in addition to priming PMNs, provokes dysfunctional PMN apoptosis. METHODS: Neutrophils were harvested daily from 12 severely injured patients at high risk for MOF, cultured for 24 hours, and assessed for apoptosis with use of acridine orange-ethidium bromide staining and fluorescence microscopy. Priming for elastase release was measured in freshly isolated patient PMNs. Plasma from patients was assessed for its ability to delay apoptosis of normal PMNs. RESULTS: Four patients (33%) had MOF. Neutrophil apoptosis was profoundly delayed in severely injured patients throughout the 5-day study period. Priming for elastase release was augmented concomitantly. Patients' plasma delayed apoptosis of normal PMNs. CONCLUSION: In patients at high risk for postinjury MOF, PMNs are not only primed for cytotoxicity but also resist apoptosis. The dysfunctional apoptosis is attributed, at least in part, to a plasma-borne mediator. The net effect may facilitate hyperinflammatory organ injury.

Optimizing screening for blunt cerebrovascular injuries.

BACKGROUND: The recognition that early diagnosis and intervention, prior to ischemic neurologic injury, has the potential to improve outcome following blunt cerebrovascular injuries (BCVI), led to a policy of aggressive screening for these injuries. The resultant epidemic of BCVI has created a dilemma, as widespread screening is impractical. We sought to identify independent predictors of BCVI, to focus resources. METHODS: Cerebral arteriography was performed based on signs or symptoms of BCVI, or in asymptomatic patients with high-risk mechanisms (hyperextension, hyperflexion, direct blow) or injury patterns. Logistic regression analysis identified independent predictors. RESULTS: A total of 249 patients underwent arteriography; 85 (34%) had injuries. Independent predictors of carotid arterial injury were Glasgow coma score < or =6, petrous bone fracture, diffuse axonal brain injury, and LeFort II or III fracture. Having one of these factors in the setting of a high-risk mechanism was associated with 41% risk of injury. Of patients with cervical spine fracture, 39% had vertebral arterial injury. CONCLUSIONS: Patients sustaining high-risk injury mechanisms or patterns should be screened for BCVI. In the face of limited resources, screening efforts should be focused on those with high-risk predictors.

Age of transfused blood is an independent risk factor for postinjury multiple organ failure.

BACKGROUND: Blood transfusion has repeatedly been demonstrated to be an independent risk factor for postinjury multiple organ failure (MOF). Previously believed to represent a surrogate for shock, packed red blood cell (PRBC) transfusion has recently been shown to result in neutrophil priming and pulmonary endothelial cell activation. We have previously observed that the generation of inflammatory mediators is related to the length of PRBC unit storage. The purpose of this study was to determine if age of transfused PRBC is a risk factor for the development of postinjury MOF. METHODS: Using our prospective database of trauma patients at risk for developing MOF, we identified patients who developed MOF (MOF+) and received 6 to 20 units of PRBCs in the first 12 hours following injury. A similar cohort of patients, matched for ISS and transfusion requirement, who did not develop MOF (MOF-) were also identified. The age of each unit of PRBC transfused in the first 6 hours was determined. Multiple logistic regression was performed to determine if age of transfused blood is an independent risk factor. RESULTS: Sixty-three patients were identified, 23 of whom were MOF+. There was no difference in ISS and transfusion requirement between MOF+ and MOF- groups. MOF+ patients, however, were significantly older (46+/-4.7 years versus 33+/-2.3 years). Moreover, mean age of transfused blood was greater in the MOF+ patients (30.5+/-1.6 days versus 24+/-0.5 days). Similarly, the mean number of units older than 14 and 21 days old were greater in the MOF+ patients. Multivariate analysis identified mean age of blood, number of units older than 14 days, and number of units older than 21 days as independent risk factors for MOF. CONCLUSION: The age of transfused PRBCs transfused in the first 6 hours is an independent risk factor for postinjury MOF. This suggests that current blood bank processing and storage technique should be reexamined. Moreover, fresh blood may be more appropriate for the initial resuscitation of trauma patients requiring transfusion.

Staged physiologic restoration and damage control surgery.

The fundamental objective of staged laparotomy is to accomplish definitive operative management in a calculated, stepwise fashion based on the patient's physiologic tolerance. This important concept has emerged from collective experience with massive acute abdominal injuries but clearly extends to elective operative procedures and surgical challenges in other torso compartments. Whereas the inability to achieve hemostasis is due most frequently to a recalcitrant coagulopathy following trauma, other scenarios include inaccessible venous injuries, coexisting extraperitoneal life-threatening injuries, uncertain viability of abdominal contents, and the inability to reapproximate abdominal fascia due to reperfusion-induced visceral edema. There are five critical decision-making phases of staged laparotomy: I, patient selection; II, intraoperative reassessment; III, physiologic restoration in the surgical intensive care unit; IV, return to the operating room for definitive procedures; and V, abdominal wall reconstruction. The abdominal compartment syndrome (ACS) is a common, often insidious complication of staged laparotomy. In fact, during phases II and III there is often a delicate balance between effective pressure tamponade of capillary bleeding and the untoward effects of the ACS. During phases IV and V a frequent dilemma is how to enclose the abdominal contents to reduce protein loss and facilitate patient mobilization.

The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome.

OBJECTIVE: To determine the benefit of screening for blunt carotid arterial injuries (BCI) in patients who are asymptomatic. SUMMARY BACKGROUND DATA: Blunt carotid arterial injuries have the potential for devastating complications. Published studies report 23% to 28% mortality rates, with 48% to 58% of survivors having permanent severe neurologic deficits. Most patients have neurologic deficits when the injury is diagnosed. The authors hypothesized that screening patients who are asymptomatic and instituting early therapy would improve neurologic outcome. METHODS: The Trauma Registry of the author's Level I Trauma Center identified patients with BCI from 1990 through 1997. Beginning in August 1996, the authors implemented a screening for BCI. Arteriography was used for diagnosis. Patients without specific contraindications were anticoagulated. Endovascular stents were deployed in the setting of pseudoaneurysms. RESULTS: Thirty-seven patients with BCI were identified among 15,331 blunt-trauma victims (0.24%). During the screening period, 25 patients were diagnosed with BCI among 2902 admissions (0.86%); 13 (52%) were asymptomatic. Overall, eight patients died, and seven of the survivors had permanent severe neurologic deficits. Excluding those dying of massive brain injury and patients admitted with coma and brain injury, mortality associated with BCI was 15%, with severe neurologic morbidity in 16% of survivors. The patients who were asymptomatic at diagnosis had a better neurologic outcome than those who were symptomatic. Symptomatic patients who were anticoagulated showed a trend toward greater neurologic improvement at the time of discharge than those who were not anticoagulated. CONCLUSIONS: Screening allows the identification of asymptomatic BCI and thereby facilitates early systemic anticoagulation, which is associated with improved neurologic outcome. The role of endovascular stents in the treatment of blunt traumatic pseudoaneurysms remains to be defined.

Resuscitation of the injured patient with polymerized stroma-free hemoglobin does not produce systemic or pulmonary hypertension.

BACKGROUND: Hemoglobin-based blood substitutes appear poised to deliver the promise of a universally compatible, disease-free alternative to banked blood. However, vasoconstriction following administration of tetrameric hemoglobins has been problematic, likely because of nitric oxide binding. Polymerized hemoglobin is effectively excluded from the abluminal space because of its size, and is thus less likely to perturb vasorelaxation. We therefore hypothesized that hemodynamic responses would be no different in injured patients receiving polymerized hemoglobin versus banked blood. METHODS: Injured patients requiring urgent transfusion were randomized to receive either polymerized hemoglobin or banked blood. Systemic arterial pressure, pulmonary arterial pressure, cardiac index, pulmonary capillary wedge pressure, systemic vascular resistance, and pulmonary vascular resistance were measured serially. RESULTS: There was no difference in any of the measured hemodynamic parameters between patients resuscitated with polymerized hemoglobin versus blood. CONCLUSIONS: Polymerized hemoglobin given in large doses to injured patients lacks the vasoconstrictive effects reported in the use of other hemoglobin-based blood substitutes. This supports the continued investigation of polymerized hemoglobin in injured patients requiring urgent transfusion.

Selective management of penetrating neck trauma based on cervical level of injury.

BACKGROUND: Selective surgical exploration of penetrating neck wounds is now the standard of care, but the safety and cost effectiveness of selective diagnostic testing remains controversial. We herein review our 18-year prospective evaluation of a progressively selective approach. PATIENTS AND METHODS: Since 1979, 312 patients sustained penetrating trauma to the anterior neck; 75% were stabbed and 24% were shot. Zone I was penetrated in 13%, zone II in 67%, and zone III in 20%. RESULTS: In all, 105 (34%) of the patients had early exploration (16% were nontherapeutic). Of the 207 (66%) observed, 1 (0.5%) required delayed exploration. Length of stay was 8.0 days following exploration, 5.1 days following negative exploration, and 1.5 days following observation. In the last 6 years, 40% have had adjunctive testing: 69% of zone I, 15% of zone II, and 50% of zone III injuries. CONCLUSION: Selective management of penetrating neck injuries is safe and does not mandate routine diagnostic testing for asymptomatic patients with injuries in zones II and III.