Identifying the asymptomatic patient with blunt carotid arterial injury.
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Biomechanical Phenomena↗
Biomedical subjects
E E Moore
Publications and source records attributed to E E Moore.
Postinjury suppression of human neutrophil cytokine production results from the stabilization of inhibitory kappaB.
UNLABELLED: Postinjury neutrophil (PMN) dysfunction is a well recognized event that may be responsible for increased infections. PMN cytokine production is an important component of their bactericidal capacity. When PMNs are stimulated, inhibitory factor kappaB (IkappaB) is degraded, allowing nuclear factor kappaB (NFkappaB) to translocate to the nucleus and promotes genes for the transcription of the interleukin-8 (IL-8) and tumor necrosis factor (TNF) genes. We hypothesize that similar to their late postinjury depressed superoxide production, postinjury PMNs manifest suppressed cytokine production, which is mediated by stabilization of IkappaB levels. METHODS: Twelve severely injured patients with an injury severity score (ISS) of 24 (+/-4.6) were studied as well as 10 elective surgical patients as a control. PMNs were isolated and incubated for 24 h in RPMI. PMNs were stimulated with lipopolysaccharide (LPS; 100 ng) or PAF (200 nm) and fMLP (1 microM) and release of IL-8, TNF, and interleukin-1 receptor antagonist (IL-1ra) were measured. Postinjury PMNs were also stimulated with LPS (100 ng), and IkappaB breakdown was measured at 0, 30, and 60 min using gel electrophoresis. RESULTS: Postinjury PMNs displayed a significant suppression of both IL-8 and TNF on postinjury Days 1-3, while the release of IL-1ra was preserved throughout the entire study period. In contrast, elective surgical patients demonstrated no decrease in IL-8 or TNF. Furthermore, IkappaB levels were preserved in the postinjury PMNs as compared with normal control PMNs. CONCLUSION: Postinjury PMNs have a suppressed release of both IL-8 and TNF following injury that did not occur in elective surgical patients. Furthermore, the NFkappaB/IkappaB-independent IL-1ra did not show suppression of release. In addition, stabilization of IkappaB following severe injury leads to decreased PMN IL-8 and TNF production. This genetic reprogramming may help explain PMN dysfunction and subsequent infections seen in severely injured patients.
Adult↗
Can chest CT be used to exclude aortic injury?
PURPOSE: To determine whether chest computed tomography (CT) can be used to exclude aortic injury. MATERIALS AND METHODS: Patients in whom there was very high suspicion of traumatic aortic injury were examined with aortography only. Other patients were examined with contrast material-enhanced CT. Follow-up aortography was performed in all patients with moderate to high suspicion of traumatic aortic injury and in all patients with CT scans that were positive for traumatic aortic injury. CT scans were regarded as positive when they showed mediastinal hematoma or direct findings of aortic injury. During a 4 1/2-year period, 1,009 patients (263 female, 746 male; age range, 3-90 years) were evaluated for possible traumatic aortic injury. RESULTS: Of the 207 patients who underwent aortography directly without CT, 10 had traumatic aortic injury. Of the 802 patients who were examined with CT, 382 underwent follow-up aortography. In this group, there were 10 true-positive and no false-negative CT scans. CT had 100% sensitivity and a 100% negative predictive value for the detection of traumatic aortic injury.
Adolescent↗
Damage control surgery.
The triad of hypothermia, acidosis, and coagulopathy during initial operative and resuscitation efforts has been recognized as a significant cause of death in patients with traumatic injuries. A staged surgical approach with a brief initial laparotomy, subsequent intensive care unit resuscitation, and a planned reoperation is an emerging technique used in trauma surgery, with application to a variety of other surgical challenges. Successful damage control therapy requires a coordinated multidisciplinary team effort by a trauma team experienced in the process of damage control operations, intensive care unit priorities, and potential complications of this innovative surgical approach.
Acidosis↗
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.
Adolescent↗
New mechanisms by which secretory phospholipase A2 stimulates neutrophils to provoke the release of cytotoxic agents.
BACKGROUND: Secretory phospholipase A2 (sPLA2) is a potent proinflammatory enzyme that stimulates inflammation through the production of reactive lipids. However, enzymatic inhibitors have been disappointing in their effectiveness in halting hyperinflammation. OBJECTIVE: To determine whether sPLA2 acts directly on neutrophil plasma membrane lipids or via a nonenzymatic mechanism. DESIGN: Isolated neutrophils (PMNs) were incubated with 3 types of sPLA2, and elastase and superoxide release from PMNs was measured. Ethyleneglycotetraacetic acid was used as a selective enzymatic inhibitor. The PMNs were exposed to sPLA2 in the presence and absence of ethyleneglycotetraacetic acid and the release of elastase was measured. SETTING: Urban trauma research laboratory. PATIENTS: Normal healthy donors of PMNs. MAIN OUTCOME MEASURES: Stimulated release of superoxide and elastase. RESULTS: The sPLA2 acted directly on plasma membrane lipids to stimulate the PMN to produce superoxide and release elastase. This mechanism is blocked with enzymatic inhibition of sPLA2. The sPLA2 also provokes elastase release from PMNs independently of its enzymatic function. This mechanism is not blocked with traditional enzymatic inhibitors. CONCLUSIONS: These data indicate that the sPLA2 can act directly on PMNs to stimulate the release of inflammatory mediators via enzymatic degradation of plasma membrane lipids. In addition, sPLA2 can act as a ligand and stimulate the PMN independently of its enzymatic activity.
Animals↗
Interleukin-6 augments neutrophil cytotoxic potential via selective enhancement of elastase release.
BACKGROUND: Interleukin-6 (IL-6) appears to be a reliable marker of disease severity in critically ill patients at risk for inflammatory organ injury such as ARDS and MOF. Debate continues, however, as to whether this pleiotropic cytokine acts principally as a proinflammatory or counterregulatory mediator. Because the polymorphonuclear leukocyte (PMN) is a central effector of inflammatory injury, defining the effects of IL-6 on mechanisms of PMN cytotoxicity may be revealing. Previous investigations of PMN release of reactive oxygen species demonstrate that IL-6 in concert with other mediators may augment cytotoxicity. We hypothesized that IL-6 alone increases PMN cytotoxic potential through selective enhancement of elastase release. MATERIALS AND METHODS: Isolated human PMNs were incubated with IL-6 in the physiologic range observed in critically ill patients (0.1 to 100 ng/ml) for 10 to 30 min. Selected cells were then activated with fMLP (1 microM). Elastase release was measured by specific cleavage of AAPV-pNA and compared to untreated cells and cells activated with formyl-Met-Leu-Phe (fMLP; 1 microM) alone. To determine if changes in elastase release might be due to IL-6 induced generation of PAF, WEB 2347 (50 microM) was preincubated with selected cells for 20 min. Surface expression of beta 2 integrins was measured by flow cytometry after incubating with labeled antibodies to CD11b and CD18. RESULTS: IL-6 alone at 100 ng/ml augmented basal elastase release by 116 +/- 41% within 10 min. Doses as low as 0.1 ng/ml stimulated elastase release when the incubation time was increased to 30 min. After 30 min of incubation, IL-6 at all doses examined augmented the elastase release of fMLP-activated cells (increases of 33 to 45%). WEB 2347 preincubation did not block augmentation of elastase release by IL-6 at 10 ng/ml. IL-6 had no effect on surface expression of beta 2 integrins at 10 ng/ml. CONCLUSIONS: IL-6 alone enhances both basal and fMLP-stimulated elastase release by PMNs. This proinflammatory action on PMNs may help explain the observed correlation between circulating IL-6 levels and inflammatory organ injury.
CD18 Antigens↗
Primed neutrophils require phosphatidic acid for maximal receptor-activated elastase release.
BACKGROUND: Priming of neutrophils (PMNs) for protease release is believed to be central to the pathogenesis of PMN-mediated tissue injury observed in ARDS/MOF. Defining the intracellular signaling pathways involved with this excessive protease release may aid in establishing future therapies for ARDS. Phospholipase D (PLD) production of phosphatidic acid (PA) is thought to be pivotal in reactive oxygen species generation but its role in degranulation (i. e., protease release) remains unclear. Our hypothesis was that primed neutrophils require PLD production of PA for maximal activated release of elastase. METHODS: Isolated human PMNs were incubated with a well described antagonist of PA production, ethanol (ETOH, 100-1000 mg/dL), and then primed (PAF, 200 nM) followed by activation (fMLP, 1 microM). To mimic fMLP receptor-dependent activation, PMNs were primed and then directly activated with exogenous dioctanoyl l-alpha-phosphatidic acid (PA8, 0.5-200 microM). To confirm the importance of PA in elastase release, PA8 was given to primed-activated PMNs after ethanol pretreatment in an attempt to recover the maximal response. Elastase release was measured by the cleavage of AAPV-pNA. RESULTS: PA blockade with ETOH attenuated PAF-primed/fMLP-activated PMN elastase release in a dose-dependent manner. Exogenous PA8 reproduced maximally primed-activated PMN elastase release, and furthermore, PA8 was able to restore maximal elastase release following ethanol attenuation. CONCLUSIONS: Elastase release from PAF-primed/ fMLP-activated neutrophils is dependent on PA production. Thus, PA production appears to be involved in both oxidant-dependent and independent mechanisms of neutrophil cytotoxicity and may be a potential therapeutic target in the treatment of hyperinflammatory diseases such as ARDS/MOF.
Humans↗
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.
Abdominal Injuries↗
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.
Adult↗
Driveway crush injuries in young children: a highly lethal, devastating, and potentially preventable event.
BACKGROUND/PURPOSE: The aim of this study was to investigate driveway-related injuries in children, identify associated risk factors, and evaluate outcome compared with other mechanisms of blunt trauma. METHODS: A 6-year review (1991 to 1996) of pediatric (age less than 18 years) pedestrian injuries treated at two urban trauma centers was conducted: one regional pediatric trauma center and one level I trauma center with pediatric commitment. Five hundred twenty-seven children injured in pedestrian accidents were identified from the trauma registry; 51 children (10%) sustained traumatic injuries as a result of being struck in their driveway. Data are reported as mean +/- SEM. RESULTS: Children less than 5 years of age (n = 41) had an injury severity score (ISS) of 12.3+/-2.3, 15 (37%) sustained closed head injury, 13 (37%) had torso trauma, 19 (46%) skeletal trauma, and eight (20%) died. Children > or = 5 years old (n = 10) had an ISS of 10.7+/-2.4, three (30%) sustained closed head injury, four (40%) torso trauma, six (60%) skeletal trauma, and none died. In contrast, all other pediatric pedestrian accidents analyzed over the same time period had a mortality rate of only 2% (11 of 476). CONCLUSIONS: Pediatric driveway trauma carries a significant risk of head injury and a 10-fold increase in mortality in children under 5 years of age when compared with all other pediatric pedestrian accidents. More emphasis must be placed on injury prevention and public education to prevent this devastating mechanism of injury in these young, vulnerable children.
Accidents, Home↗
The first randomized trial of human polymerized hemoglobin as a blood substitute in acute trauma and emergent surgery.
BACKGROUND: Human polymerized hemoglobin (PolyHeme) is a universally compatible, disease-free, oxygen-carrying resuscitative fluid. This is the first prospective, randomized trial to compare directly the therapeutic benefit of PolyHeme with that of allogeneic red blood cells (RBCs) in the treatment of acute blood loss. STUDY DESIGN: Forty-four trauma patients (33 male, 11 female) aged 19-75 years with an average Injury Severity Score (ISS) score of 21+/-10 were randomized to receive red cells (n = 23) or up to 6 U (300 g) of PolyHeme (n = 21) as their initial blood replacement after trauma and during emergent operations. RESULTS: There were no serious or unexpected adverse events related to PolyHeme. The PolyHeme infusion of 4.4+/-2.0 units (mean +/- SD) resulted in a plasma [Hb] of 3.9+/-1.3 g/dL, which accounted for 40% of the total circulating [Hb]. There was no difference in total [Hb] between the groups before infusion (10.4+/-2.3 g/dL control vs. 9.4+/-1.9 g/dL experimental). At end-infusion the experimental RBC [Hb] fell to 5.8+/-2.8 g/dL vs. 10.6+/-1.8 g/dL (p < 0.05) in the control, although the total [Hb] was not different between the groups or from pre-infusion. The total number of allogeneic red cell transfusions for the control and experimental groups was 10.4+/-4.2 units vs. 6.8+/-3.9 units (p < 0.05) through day 1, and 11.3+/-4.1 units vs. 7.8 +/-4.2 units (p = 0.06) through day 3. CONCLUSIONS: PolyHeme is safe in acute blood loss, maintains total [Hb] in lieu of red cells despite the marked fall in RBC [Hb], and reduces the use of allogeneic blood. PolyHeme appears to be a clinically useful blood substitute.
Adult↗
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.
Adolescent↗
Synergy of bone fractures, soft tissue disruption, and hemorrhagic shock in the genesis of postinjury immunochaos: the pathway to multiple organ failure.
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Animals↗
Clinically relevant concentrations of ethanol attenuate primed neutrophil bactericidal activity.
BACKGROUND: Acute alcohol intoxication is associated with an increased risk of infection in the injured patient. The impact of clinically relevant levels of ethanol (ETOH) on neutrophil (PMN) bactericidal activity remains ill-defined. PMN priming optimizes microbicidal activity by enhancing oxygen radical production, degranulation, and adhesion molecule up-regulation. We hypothesized that clinically relevant levels of ETOH attenuate these primed PMN responses critical to eradicate infection. METHODS: After incubation with ETOH (0-1.0%), isolated human PMNs were primed with beta-acetyl-gamma-O-alkyl and activated with N-formyl-methionyl-leucyl-phenylalanine. Superoxide generation was measured by cytochrome c reduction, elastase release was measured by cleavage of methoxysuccinyl-ala-ala-pro-val-p-nitroanilide, and CD11b was measured by fluorescent monoclonal antibody staining. Bactericidal activity was assessed by Staphylococcus aureus killing. RESULTS: ETOH attenuated superoxide production dose-dependently with significance at 0.3% ETOH. Elastase release was attenuated starting at 0.2% ETOH, and CD11b expression was reduced starting at 0.4% ETOH. S. aureus killing was impaired dose-dependently with significance at 0.3% ETOH. CONCLUSION: Clinically relevant concentrations of ETOH attenuate PMN functions critical in host defense against invading pathogens. These results provide direct in vitro evidence consistent with previous in vivo data that acute alcohol intoxication is important in the pathogenesis of trauma-related infections.
Alcoholic Intoxication↗
Hypertonic saline activates lipid-primed human neutrophils for enhanced elastase release.
BACKGROUND: Ongoing clinical trials have revived interest in hypertonic saline (HTS) for postinjury resuscitation; these studies have documented serum Na+ concentrations > or = 170 mmol/L. Recent animal studies have shown that HTS enhances T-cell and monocyte function, but effects on the polymorphonuclear neutrophil (PMN) remain unclear. The postinjury lipid mediators platelet-activating factor (PAF) and leukotriene B4 (LTB4) have been implicated in PMN priming for cytotoxicity, which is believed to be important in the pathogenesis of multiple organ failure. We hypothesized that HTS would stimulate PMN superoxide (O2-) and elastase release from PAF- and LTB4-primed PMNs. METHODS: Isolated PMNs from five donors were primed for 5 minutes with 200 nmol/L PAF or 1 micromol/L LTB4 in Kreb's-Ringer's phosphate with dextrose at a Na+ concentration of 140 mmol/L (normal serum Na+ concentration), pelleted, and resuspended in Kreb's-Ringer's phosphate with dextrose for 10 minutes at a Na+ concentration of 130 to 170 mmol/L. O2- generation was measured by superoxide dismutase-inhibitable reduction of cytochrome c and elastase release by cleavage of N-methoxysuccinyl-Ala-Ala-Pro-Val p-nitroanilide. RESULTS: HTS with Na+ concentration up to 170 mmol/L had no significant effect on O2- production or elastase release from quiescent cells. Na+ concentration of 160 and 170 mmol/L, however, activated PAF- and LTB4-primed PMNs for enhanced elastase release with no effect on O2- production. CONCLUSION: In clinically relevant concentrations, elevated Na+ activates lipid-primed neutrophils for enhanced elastase degranulation. Consequently, the administration of HTS in the early postinjury resuscitation period, when PMNs are maximally primed, may activate PMN elastase release and thereby promote the development of multiple organ failure.
Humans↗
Secretory phospholipase A2 cleavage of intravasated bone marrow primes human neutrophils.
BACKGROUND: Recent clinical reports suggest that early femoral intramedullary rod (IMR) fixation in patients with multiple injuries increases the risk of adult respiratory distress syndrome (ARDS). We have shown that lipid-mediated neutrophil (PMN) priming and elevated circulating levels of secretory phospholipase A2 (sPLA2) within the first 24 hours after injury correlate with the development of ARDS. We thus hypothesized that circulating lipid products, generated by sPLA2 cleavage of intravasated bone marrow, prime PMNs for enhanced superoxide anion (O2-) production. METHODS: Isolated PMNs from healthy volunteers were incubated for 5 minutes with buffer or sPLA2-lysed bone marrow (100 U/mL) collected from trauma patients. After formyl-methionyleucylphenylalanine (fMLP) activation, O2- production was quantified by the superoxide dismutase-inhibitable reduction of cytochrome c. Blood samples were also drawn from five injured patients before and 24 hours after femoral IMR fixation. PMNs were isolated and assessed for in vivo priming. RESULTS: PMNs incubated with sPLA2-lysed bone marrow were primed for more than 3.5 times greater fMLP-induced O2- production. Furthermore, in patients with femoral fractures, PMN O2- release in response to fMLP after IMR fixation was more than 2.5 times higher than before fixation. CONCLUSION: Collectively, the findings suggest that bone marrow released from acute fracture sites may become a lipid substrate for the elevated sPLA2 levels found in injured patients. The resultant priming of PMNs may thus render the injured patient at risk for ARDS. Although clearly hypothetical at present, we submit that these observations warrant further investigation because of their clinical implications.
Adolescent↗
Ultrasound is an effective triage tool to evaluate blunt abdominal trauma in the pediatric population.
BACKGROUND: Although computed tomography has been considered the diagnostic modality of choice for pediatric patients with blunt abdominal trauma (BAT), it is costly, time-consuming, requires sedation, and may be associated with complications in young children. Abdominal ultrasonography (US) is a promising modality in the evaluation of BAT that is quick, noninvasive, repeatable, and cost-effective. We hypothesized that emergency department US, performed by trauma surgeons, is a useful triage tool for pediatric BAT that reduces the need for computed tomography. METHODS: The 230 children (<18 years old) with suspected BAT were initially evaluated with US in the emergency department by surgeons. Subsequent computed tomographic scan or exploratory laparotomy was performed as indicated by the key clinical pathway. RESULTS: Twelve children (5.2%) had documented intra-abdominal injuries. All five injured children with significant intraperitoneal fluid were identified by US. Of the seven patients who had intra-abdominal injury not detected by US, six sustained solid organ injuries that were managed nonoperatively. Extrapolated reductions in hospital charges due to the decreased number of computed tomographic scans total $130,000. CONCLUSIONS: Using US as a triage tool may dramatically reduce the cost of pediatric BAT evaluation while being able to quickly identify significant intraperitoneal fluid that requires further evaluation and possible laparotomy.
Abdominal Injuries↗