Patrick J. Offner

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.

Blunt carotid arterial injuries : implications of a new grading scale

BACKGROUND Blunt carotid arterial injuries (BCI) have the potential for devastating outcomes. A paucity of literature and the absence of a formal BCI grading scale have been major impediments to the formulation of sound practice guidelines. We reviewed our experience with 109 BCI and developed a grading scale with prognostic and therapeutic implications. METHODS Patients admitted to a Level I trauma center were evaluated with cerebral arteriography if they exhibited signs or symptoms of BCI or met criteria for screening. Patients with BCI were treated with heparin unless they had contraindications, and follow-up arteriography was performed at 7 to 10 days. Endovascular stents were deployed selectively. A prospective database was used to track the patients. RESULTS A total of 76 patients were diagnosed with 109 BCI. Two-thirds of mild intimal injuries (grade I) healed, regardless of therapy. Dissections or hematomas with luminal stenosis (grade II) progressed, despite heparin therapy in 70% of cases. Only 8% of pseudoaneurysms (grade III) healed with heparin, but 89% resolved after endovascular stent placement. Occlusions (grade IV) did not recanalize in the early postinjury period. Grade V injuries (transections) were lethal and refractory to intervention. Stroke risk increased with injury grade. Severe head injuries (Glasgow Coma Scale score < or =6) were found in 46% of patients and confounded evaluation of neurologic outcomes. CONCLUSION This BCI grading scale has prognostic and therapeutic implications. Nonoperative treatment options for grade I BCI should be evaluated in prospective, randomized trials. Accessible grade II, III, IV, and V lesions should be surgically repaired. Inaccessible grade II, III, and IV injuries should be treated with systemic anticoagulation. Endovascular techniques may be the only recourse in high grade V injuries and warrant controlled evaluation in the treatment of grade III BCI.

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.

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 authors 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.

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

ObjectiveTo 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 DataHemodynamically 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. MethodsUsing 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. ResultsA 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%). ConclusionsThe 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.

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.

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.

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.

Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients.

Hypothermia in critically ill patients can be difficult to treat with standard rewarming (SR) techniques. We developed a rewarming method that is significantly faster than SR. Percutaneously placed femoral arterial and venous catheters were connected to the inflow and outflow side of a countercurrent fluid warmer to create a fistula through the heating mechanism (CAVR). Over a 10-month period 34 hypothermic (temperature less than 35 degrees C) patients were treated. Eighteen received SR only; CAVR was added to SR in the remaining 16 patients. Both groups were similar in APACHE II, Injury Severity, and Acute Physiology scores, prewarming blood and fluid requirements, and incidence of coagulopathy. Hypothermia resolved in 39 minutes with CAVR vs. 3.23 hours with SR (p less than 0.001). This was associated with an improved survival after moderately severe injury (p = 0.04), and a significant reduction in blood and fluid requirements, organ failures, and length of ICU stay.

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.