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Overview of inpatient management of the adult trauma patient

Overview of inpatient management of the adult trauma patient
Literature review current through: Jan 2024.
This topic last updated: Oct 25, 2022.

INTRODUCTION — Trauma remains the leading cause of death in those less than 44 years of age in the United States, and for those older than 45, trauma is one of the top five causes of death. The management of patients with traumatic injuries presents a variety of challenges. Patients require multidisciplinary evaluation, securing the airway and breathing, hemorrhage control, resuscitation, and stabilization in the emergency department and possible operative intervention prior to inpatient admission. For the combined burn/trauma patient, the immediate management priority is stabilization and resuscitation of the patient from a trauma/management of injury perspective [1]. Management of the burn wounds is a secondary priority.

Patients remain at risk for complications due to unrecognized injuries or related to initial or ongoing management.

The general care and management of injured patients who require hospital admission is reviewed here. Initial evaluation and treatment in the emergency department is discussed separately. Specific injuries are discussed in separate topic reviews. (See "Initial evaluation and management of blunt abdominal trauma in adults" and "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial evaluation and management of abdominal gunshot wounds in adults" and "Initial evaluation and management of abdominal stab wounds in adults" and "Initial evaluation and management of penetrating thoracic trauma in adults".)

DAMAGE CONTROL AND RESUSCITATION — Damage control surgery, which has become a common approach to the treatment of the severely injured patient, involves immediate operative control of hemorrhage and contamination (ie, bowel injury) followed by transfer to the intensive care unit for ongoing resuscitation. Damage control surgery has been shown to reduce mortality in severely and multiply injured patients [2-4]. (See "Overview of damage control surgery and resuscitation in patients sustaining severe injury".)

Upon arrival to the intensive care unit, acidosis, hypothermia, and coagulopathy are corrected with ongoing fluid resuscitation and component transfusion therapy. Once the patient is stabilized, definitive treatment of the patient's injuries can be undertaken. Damage control and the management of specific injuries are discussed in separate topic reviews.  

Brain injury (see "Management of acute moderate and severe traumatic brain injury")

Spinal injury (see "Acute traumatic spinal cord injury")

Cardiac injury (see "Initial evaluation and management of blunt cardiac injury" and "Management of cardiac injury in severely injured patients")

Splenic injury (see "Surgical management of splenic injury in the adult trauma patient")

Liver injury (see "Management of hepatic trauma in adults")

Duodenal and pancreatic injury (see "Management of duodenal trauma in adults" and "Management of pancreatic trauma in adults")

Vascular injury (see "Clinical features and diagnosis of blunt thoracic aortic injury" and "Management of blunt thoracic aortic injury" and "Overview of blunt and penetrating thoracic vascular injury in adults" and "Abdominal vascular injury")

Small bowel and colon injury (see "Traumatic gastrointestinal injury in the adult patient")

Chest wall injury (see "Inpatient management of traumatic rib fractures and flail chest in adults")

Retroperitoneal injury (see "Overview of the diagnosis and initial management of traumatic retroperitoneal injury")

Kidney injury (see "Overview of traumatic upper genitourinary tract injuries in adults" and "Management of blunt and penetrating renal trauma")

Ureteral injury (see "Overview of traumatic and iatrogenic ureteral injury")

Bladder/urethral injury (see "Overview of traumatic lower genitourinary tract injury" and "Traumatic and iatrogenic bladder injury" and "Posterior urethral injuries and management")

Female reproductive tract injury (see "Evaluation and management of female lower genital tract trauma")

Male reproductive tract injury (see "Traumatic injury to the male anterior urethra, scrotum, and penis")

Extremity injury (see "Severe upper extremity injury in the adult patient" and "Surgical management of severe upper extremity injury" and "Severe lower extremity injury in the adult patient" and "Surgical management of severe lower extremity injury")

PATIENT ASSESSMENT — Ongoing inpatient assessment and monitoring is critical to managing injured patients. This is particularly true in patients who have undergone damage control surgery or those with injuries that are being managed nonoperatively, such as blunt splenic, hepatic, duodenal, or pancreatic injury. Recognition of the full extent of traumatic injury requires an accurate history, skillful physical examination, and timely and judicious use of diagnostic studies.

Obtain a complete history — Patients with serious traumatic injuries often are unable to give details of their past medical history upon presentation to the emergency department, and collateral sources of information (eg, family or other caregivers, friends) may not be available initially. It is therefore incumbent upon the admitting clinician to obtain additional information about past medical history, outpatient medications, allergies, and any history of drug or alcohol use.

It is also important to obtain information about the circumstances that led to the injury since falls from a height or motor vehicle collisions may have been precipitated by medical causes such as cardiac dysrhythmia, hypoglycemia, or stroke and injuries from assault may be a result of domestic violence. In addition, self-inflicted injuries may be a manifestation of a psychological disorder that needs to be identified and treated.

In addition to its value in optimizing medical management, accurate information about the medical history can be valuable in estimating prognosis. The patient's baseline health status also affects the length of stay. One study of over 27,000 trauma admissions found that the probability of a trauma patient remaining hospitalized for more than three weeks nearly doubles with the presence of at least one significant underlying medical condition, such as end-stage kidney disease, chronic obstructive pulmonary disease, or malignancy [5]. (See 'Outcomes' below.)

In one study, ongoing drug or alcohol use disorder was present in over 30 percent of individuals admitted for trauma [6]. These individuals had increased risk of complications during hospitalization, particularly those related to pneumonia and other infections. These patients are at risk for withdrawal syndromes, which may be difficult to recognize in the setting of obtundation, intubation, or closed-head injury [7,8]. The possibility of an intentional drug overdose prior to injury should also be considered. (See 'Alcohol/drug screening' below and "Identification and management of unhealthy alcohol use in the perioperative period" and "General approach to drug poisoning in adults".)

Repeat the physical examination and tertiary survey — The injured patient admitted from the emergency department or operating room warrants full reassessment by the receiving team in accordance with advanced trauma life support (ATLS) guidelines. Missed injuries are more likely to occur in the patient with polytrauma who requires emergent surgical intervention. Performing a repeat trauma survey (tertiary survey) on all patients decreases the frequency of missed injuries [9]. A review of observational studies that included over 12,000 trauma patients found a significantly increased risk of missed injury for trauma patients who did not have a tertiary survey compared with those who did (odds ratio 2.65, 95% CI 1.40-5.01) [10]. (See 'Consider other potential injuries' below.)

Immediate attention should be given to the ABCs (ie, airway, breathing, and circulation) [11,12]:

Breath sounds should be evaluated, and, if the patient is intubated, the position of the endotracheal tube should be assessed to ensure that it has not become dislodged during transport. (See 'Review diagnostic studies' below and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients".)

The patient's cardiovascular status should be evaluated, the patency of peripheral and central intravascular catheters confirmed, and the total volume of intravenous fluids and blood products administered since presentation established. (See 'Fluid therapy and nutrition support' below.)

A complete neurologic examination should be repeated and documented. Sedatives may need to be withheld to obtain an accurate assessment.

A complete vascular examination should be repeated and documented. Patients with extremity injury should have ankle pressures taken bilaterally and each compared with their systolic brachial pressure. (See "Noninvasive diagnosis of upper and lower extremity arterial disease", section on 'Ankle-brachial index'.)

The patient should be examined completely, from head to toe, and front to back, to evaluate for unidentified external injuries and to note and confirm the correct positioning of any catheters, chest tubes, or drains that have been placed.

The secondary survey of burn wounds should include examination of the hands, extremities, and chest for increased edema formation and increased tissue pressures under a relatively nonyielding eschar. (See "Emergency care of moderate and severe thermal burns in adults", section on 'Escharotomy'.)

Review diagnostic studies — Each of the diagnostic studies the patient has previously undergone, including plain films and computed tomography (CT) studies, should be reviewed and the final radiology report obtained. Plans should be made to obtain follow-up studies for injuries that have been identified, when indicated. Incidental findings not related to trauma should be reported to the patient and the patient's primary care provider [13].

Repeat chest radiograph should be ordered upon patient arrival to verify accurate endotracheal tube position, if present, and reassess the status of the lungs. The correct internal positioning of any chest tubes or central lines should also be verified, particularly those that may have been placed emergently (in the emergency department or operating room). (See 'Catheters, tubes, drains, and lines' below.)

Particular attention should be given to any films that may have been performed in the operating room as a result of an incomplete sponge count. Patients who have undergone damage control surgery are at high risk for retained surgical foreign body, and misinterpretation of films obtained in the operating room is not uncommon. (See "Retained surgical sponge (gossypiboma) and other retained surgical items: Prevention and management".)

Consider other potential injuries — In spite of diagnostic guidelines for the initial evaluation in trauma, the reported incidence of missed injuries ranges from 1.3 to 39 percent [14-16]. The true incidence of missed injuries and delayed diagnoses is difficult to determine, in part because of the variability in the definition of what constitutes a missed injury. Missed injuries have been shown to increase morbidity, prolong hospital stay, and increase mortality [17-19].

Missed injuries are more commonly associated with an abbreviated injury scale (AIS) >3, but missed injuries that are life-threatening are uncommon [14]. Reasons cited for missed diagnoses include assessment errors, misinterpretation of radiographs, and, for musculoskeletal injuries, lack of radiographs of the specific area of injury. A review of 1124 patients admitted to a level I trauma center identified missed injuries in 8 percent of patients [15]. The missed injury involved an extremity in 68 percent of patients. Significant factors associated with missed injury were injury severity score (ISS) ≥16 and Glasgow coma scale <8. Of the 122 missed injuries, 72 were missed in spite of a tertiary survey. In another review in which the missed injury rate was 15 percent, higher ISS, higher maximum AIS of the thorax, and nonsurgeon trauma team leader status were significant predictors of missed injuries [16].

Injuries can also be missed during emergent exploratory laparotomy. In a database review from two level I trauma centers, 19 of 90 patients who underwent emergent exploratory laparotomy for penetrating (n = 66) or blunt (n = 25) trauma had additional injuries within the surgical field that were not identified intraoperatively but were diagnosed on postoperative abdominopelvic CT [20]. The injuries included mostly solid organ injuries but also unexpected active bleeding, a diaphragmatic injury, spine injury, colonic injury, and arteriovenous fistula. Eight of the injuries (8.9 percent of the entire cohort) were severe enough to require additional treatment (surgery or angioembolization). Undiagnosed fractures were also identified. Rates of unsuspected injuries within the surgical field were similar for patients who were empirically imaged compared with those with specific indications for CT (20.9 versus 21.4 percent). However, those with a specific indication for CT had a higher rate of intervention (14.2 versus 6.5 percent). These retrospective findings suggest that when clinical suspicion is present (unknown trajectory of penetrating missile or unexplored regions following blunt trauma), postoperative CT imaging can be useful to elucidate additional injuries, but whether empiric imaging is useful is not clear.

A concerted effort should be made to identify potentially life-threatening injuries that can be missed so that they may be properly treated. These are discussed briefly below.

Intra-abdominal injury — A missed or delayed diagnosis of intra-abdominal injury constitutes an important cause of preventable death in injured patients, particularly in the setting of blunt trauma [21-23].

A review of 607 abdominal trauma patients reported that 2 percent of patients had injuries that were missed on initial evaluation or at first surgery [24]. Missed diagnoses were attributed to clinical inexperience, overlooked or atypical radiographic findings, and an unclear history of trauma.

A missed intra-abdominal injury should be suspected in patients with blunt or penetrating trauma who have evidence of ongoing acidosis, persistent tachycardia, need for ongoing fluid resuscitation or transfusion, abdominal sepsis, and systemic inflammatory response syndrome (SIRS). Abdominal sepsis is a late finding, whereas the other clinical signs usually manifest within 24 to 36 hours of injury.

Tests to diagnose intra-abdominal injury include computed tomography, ultrasound, magnetic resonance cholangiopancreatography, endoscopic retrograde cholangiopancreatography, and diagnostic peritoneal lavage. However, exploratory laparotomy remains the gold standard and should be performed in any patient for whom a significant operable injury is suspected but that cannot be determined by abdominal examination (eg, intubated, spinal cord injury) along with available diagnostic studies. Diagnostic laparoscopy may represent a less invasive means to directly examine the peritoneal cavity and its contents but may miss small intestinal injuries.

Diaphragm injury — Diaphragm injuries, particularly related to penetrating trauma, are often difficult to detect. A high index of suspicion should be maintained in patients with injury mechanisms that are associated with diaphragm rupture, such as simultaneous injuries above and below the diaphragm, and liver and spleen injuries, among others. The clinical evaluation and diagnosis of diaphragm injury in adults is discussed in detail elsewhere. (See "Recognition and management of diaphragmatic injury in adults".)

Pulmonary contusion — Pulmonary contusion, which is injury to the parenchyma of the lung, is the most common lung injury identified in the setting of blunt chest trauma, occurring in 17 percent of multiple trauma patients. The associated mortality rate ranges from 6 to 25 percent, often due to a superimposed pneumonia or acute respiratory distress syndrome [25,26]. Common mechanisms of pulmonary contusion include rapid deceleration in high-speed motor vehicle collisions, falls, assault, penetrating injury, and blast injury (often combined blunt and penetrating trauma) [26].

Pulmonary contusion is often not initially suspected because the clinical and radiographic findings (homogenous opacification of the lung) are delayed. In addition, pulmonary contusion can occur in the absence of any visible chest wall injury or radiographic evidence of rib fractures, particularly in children [27]. The treatment is supportive. As with any soft tissue contusion, the extent of injury can be progressive in the initial days following injury, and the patient must be monitored for respiratory failure during this time. (See "Pulmonary contusion in adults".)

Arterial injury — Blunt injury to an artery may not be immediately apparent depending upon the location and grade of the injury. High-grade injuries (pseudoaneurysm, transection) are usually symptomatic, causing hard signs of arterial injury (pain, pulsatile mass, hypotension, extremity ischemia); however, intimal tears are often asymptomatic. These lesions may remain static or progress as a subintimal dissection that can cause luminal narrowing or acute vessel occlusion over a variable period of time, reducing distal perfusion. These low-grade (minimal) injuries need to be identified so that appropriate therapy, which can be nonsurgical, can be initiated. The diagnosis and management of injuries to the vasculature is discussed in separate topic reviews.

Extremity vascular injury – (See "Severe lower extremity injury in the adult patient".)

Blunt cerebrovascular injury – (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation" and "Blunt cerebrovascular injury: Treatment and outcomes".)

Aortic injury – (See "Clinical features and diagnosis of blunt thoracic aortic injury" and "Surgical and endovascular repair of blunt thoracic aortic injury" and "Management of blunt thoracic aortic injury".)

Head and brain injury — Scalp lacerations are frequently missed on initial evaluation as they may be obscured by thick hair, so careful inspection during the tertiary survey is warranted.

Although uncommon, serious intracranial injuries may also remain undetected due to a failure to obtain an indicated head CT (penetrating injury, depressed skull fractures, altered mental status), error in interpretation of brain imaging studies, or because the injury was not apparent on the initial scan. Repeat and ongoing neurologic assessment (eg, alteration in mental status, new focal neurologic deficit) determines the need to obtain additional imaging studies.

Patients with traumatic brain injury may have indications for intracranial pressure monitoring, and repeat imaging should be used liberally for unexplained rises in intracranial pressure. (See "Management of acute moderate and severe traumatic brain injury", section on 'Intracranial pressure management'.)

Patients who remain obtunded without a discernible cause on CT scan should undergo further evaluation for possible seizures. Magnetic resonance imaging (MRI) may also be considered to evaluate for diffuse axonal injury. (See "Management of acute moderate and severe traumatic brain injury".)

MONITORING — The need for monitoring in patients who require admission for traumatic injury is determined by the nature and severity of their injuries. The presence of burned skin should not preclude attempts at intravenous access, control of hemorrhaging sites, coverage of open fractures and wounds, and fixation of closed fractures. (See 'Introduction' above.)

In general, patients with severe injuries such as intracranial hemorrhage or multiple intermediate- or high-grade organ injuries are admitted to an intensive care unit.

Patients with moderate injuries, including isolated, low-grade, conservatively managed solid organ injuries, or very minor intracerebral hemorrhage, may be admitted to a step-down unit for serial examination and close monitoring.

Patients with mild injuries such as isolated or even multiple low-grade organ injuries, including uncomplicated fractures or concussion, can be admitted to a floor unit for supportive care and close observation.

Laboratory studies — Upon admission from the emergency department or operating room, lab studies that were abnormal upon admission should be repeated. Other laboratories are obtained based upon diagnosis.

A complete blood count is obtained and compared to values obtained upon arrival in the emergency department or in the operating room. Serial hemoglobin measurement may be useful to trend slow, internal bleeding but is of limited use in guiding transfusion therapy in patients with brisk bleeding. Most importantly, an active search must be initiated to find and arrest the source of hemorrhage. Serial counts are typically obtained every six hours (and as needed based upon clinical condition) in patients with conservatively managed solid organ injuries (liver, spleen, kidney) and in patients with pelvic fracture. In patients without evidence of bleeding, the frequency of repeat blood counts depends upon the clinical situation.

Renal function – Renal function tests (blood urea nitrogen, creatinine) should be obtained daily in patients who received intravenous contrast agents, particularly if the patient is at high risk for contrast-induced nephropathy, such as patients with chronically impaired renal function and those who received contrast agents while hypovolemic. A serum creatinine concentration that begins to increase within 24 to 48 hours of contrast administration, with or without oliguria, may indicate contrast-induced nephropathy. The serum creatinine concentration generally reaches a peak after three to five days and then returns to baseline over a period of one to three weeks. Therapy of contrast-induced nephropathy is primarily supportive; dialysis is rarely required. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)

Coagulation parameters – Coagulopathy in the injured patient may be the result of physiologic derangements such as acidosis, hypothermia, hemodilution, and tissue disruption. An acute coagulopathy can occur in severely injured patients independent of these factors. Coagulopathy can be especially profound following severe traumatic brain injury due to release of brain thromboplastin into the blood stream. Early recognition and management using appropriate transfusion strategies is important to reduce morbidity and mortality. (See "Etiology and diagnosis of coagulopathy in trauma patients".)

Injured patients with normal coagulation parameters on arrival to the emergency department and who do not have signs of bleeding do not require repeat coagulation tests. Those patients who have received massive transfusions or who have ongoing transfusion requirements should have coagulation studies performed every four to six hours or following administration of procoagulant agents until the coagulation parameters are corrected. The American College of Surgeons recommends that level I and level II verified trauma centers have elastography (thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) capability. These tests may be useful in detecting the specific cause of coagulopathy, including inappropriate clot dissolution, thereby allowing more targeted component repletion or pharmacologic therapy [28-30]. TEG/ROTEM should also be repeated as appropriate throughout the resuscitation [31]. (See "Etiology and diagnosis of coagulopathy in trauma patients", section on 'Viscoelastic hemostatic assays'.)

Creatine kinase and myoglobin – Rhabdomyolysis and myoglobinuria can develop in patients with significant muscle injury, including crush injuries, prolonged immobilization, compartment syndrome, and ischemia-reperfusion following repair of vascular injuries in those who have undergone extensive arterial embolization to arrest hemorrhage (eg, hypogastric artery). Secondary compartment syndrome can also occur in the absence of a direct extremity injury following a massive resuscitation. A high index of suspicion and perhaps empiric laboratory testing in this cohort should be considered [32].

Rhabdomyolysis presents with elevated serum muscle enzymes (including creatine kinase), red-to-brown urine due to myoglobinuria if there is persistent renal function, and electrolyte abnormalities. Peak serum creatine kinase levels depend upon the volume of muscle breakdown and the muscle mass of the patient. Creatine kinase values should be measured if there is a suspicion for rhabdomyolysis until decreasing levels are observed. Urine myoglobin levels may also be assessed. A brisk urine output should be maintained with intravenous fluid therapy until the creatine kinase value starts to decrease. Additionally, the potassium level should be monitored. Potassium levels may decrease due to the brisk urine output or increase if renal function deteriorates or there is ongoing myocyte necrosis. Alkalinization of the urine is no longer routinely recommended in trauma patients. (See "Rhabdomyolysis: Clinical manifestations and diagnosis" and "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

Arterial blood gas – A baseline arterial blood gas (ABG) should be obtained in all mechanically ventilated patients to ensure appropriate ventilation and carbon dioxide tension (PaCO2). Further, an assessment of the patient's acid/base can be made based on the pH. Worsened base deficit may also be used as a marker of poor tissue perfusion. Point-of-care testing and STAT labs can be obtained for ABGs in a rapid fashion in most institutions. This allows for serial assessment as changes to pulmonary mechanics occur. (See "Arterial blood gases".)

Lactate – A serum lactate level should be drawn on all severely injured patients. Lactate clearance is a marker of end-organ perfusion and normal metabolism and can serve as a guide for ongoing resuscitation. Failure of lactate to normalize within 24 hours of injury is associated with increased mortality [33,34]. Patients who appear euvolemic and are not anemic or bleeding but have a lactate level that does not normalize should be assessed for:

Missed injury, particularly hollow visceral injury (see "Traumatic gastrointestinal injury in the adult patient")

Liver disease (see "Approach to the patient with abnormal liver biochemical and function tests")

Cardiac dysfunction (see "Initial evaluation and management of blunt cardiac injury")

Base deficit – Similar to lactate, base deficit (BD) is a biomarker that reflects tissue perfusion. Although BD has been associated with poorer clinical outcomes, lactate appears to outperform BD when used to predict mortality [35].

Monitoring for compartment syndromes — (See "Abdominal compartment syndrome in adults".)

Intra-abdominal pressure — Abdominal compartment syndrome (ACS) is recognized as a potentially fatal complication of aggressive fluid resuscitation in seriously injured patients. Assessment of bladder pressure (which correlates closely with intra-abdominal pressure) should be performed in patients at high risk for ACS or when there is suspicion for ACS (figure 1) but is not required in all patients. A diagnosis of ACS constitutes a surgical emergency and should prompt immediate surgical consultation. (See "Abdominal compartment syndrome in adults".)

Combined burn/trauma patients may be particularly prone to this problem, given the extent of fluid resuscitation that is required, even in the absence of intra-abdominal trauma. In a retrospective review of 1825 burn patients admitted to the United States Army Institute of Surgical Research Burn Center, acute abdominal catastrophe without intra-abdominal trauma occurred in 2.8 percent (51 patients), the majority occurring in the first few days of injury and associated with abdominal compartment syndrome [36]. The mortality rate was 78 percent.

Extremity compartment pressures — Patients with extremity injury can develop increased extremity compartment pressures as a result of crush injury, long bone fracture, ischemia-reperfusion following revascularization for arterial injury, or from burns either from constricting eschar or as a consequence of fluid resuscitation. (See "Pathophysiology, classification, and causes of acute extremity compartment syndrome".)

Patients with severe extremity injury who have combined arterial and venous injury are particularly prone to developing an extremity compartment syndrome and may require prophylactic fasciotomy or repeated evaluation for 24 hours or more following repair of injury. Although a diagnosis of extremity compartment syndrome may be suggested by an elevation in creatine kinase, the diagnosis is clinical, and the absolute level of creatine kinase is not predictive. Conversely, a low creatine kinase does not rule out the presence of an extremity compartment syndrome. The risk factors for, clinical diagnosis, measurement of compartment pressures, and treatment of acute compartment syndrome are discussed in detail elsewhere. (See "Acute compartment syndrome of the extremities" and "Lower extremity fasciotomy techniques".)

Screening for venous thromboembolism — Screening for venous thromboembolism (VTE) in injured patients using duplex ultrasound remains controversial. There are no data or guidance to support routine screening. Although the prevalence of occult deep vein thrombosis (DVT) may be significantly higher in centers that screen trauma patients [37], the incidence of pulmonary embolism (PE) is overall unchanged. The Centers for Medicare & Medicaid Services included DVT in trauma patients as a never event; however, using this endpoint as a quality measure is being questioned [38]. In spite of adequate pharmacologic anticoagulation in trauma populations, VTE persists. Many clinicians feel that a better assessment of quality of care includes evaluating adherence to an evidence-based regimen for VTE prophylaxis and, rather than using duplex testing to screen for VTE, appropriately evaluating high-risk and symptomatic patients as needed [39]. A more complete discussion of this issue can be found in a podcast [40] and in topics discussing DVT prophylaxis. (See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)

PROPHYLAXIS AND PREVENTIVE CARE — Particular attention should be paid toward preventing common complications that are associated with significant traumatic injuries.

Antibiotics — Routine antibiotic administration is not warranted in most injured patients. In particular, the presence of a penetrating injury (eg, gunshot wound, stab wound) does not indicate the need for antibiotic coverage in the absence of local signs of infection. For patients who require abdominal exploration, a single dose of prophylactic antibiotics given within one hour of incision is appropriate [41,42].

In the face of hollow viscus injury, antibiotics can be continued, and provided there has been no delay in identification and surgical management, no more than 24 hours should be needed. (See "Traumatic gastrointestinal injury in the adult patient".)

Antibiotic prophylaxis is justified in patients who require surgical intervention or have open fractures, and in those with penetrating thoracic injury who require chest tube placement. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children" and "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Antimicrobial prophylaxis' and "Thoracostomy tubes and catheters: Placement techniques and complications", section on 'Antibiotic prophylaxis'.)

Patients with moderate-to-severe burns and associated traumatic injuries are likely to develop a hypermetabolic response, which should not be confused with infection [43-48]. In general, metabolic derangements that occur to some extent in all injuries will be dominated by the burn component, and combined burn/trauma patients should be treated in accordance with practices common to those with moderate-to-severe burns. (See "Hypermetabolic response to moderate-to-severe burn injury and management".)

Thromboprophylaxis — Hospitalized trauma patients are, at minimum, at moderate risk for venous thromboembolism (VTE; deep vein thrombosis [DVT], pulmonary embolism [PE]), which remains a leading cause of preventable mortality [49]. Severely injured patients should receive early, aggressive VTE prophylaxis, which is continued until hospital discharge for all high-risk patients and beyond hospital discharge with patients with significant orthopedic injuries that limit mobility. It is generally agreed that the probability of VTE increases with each day of delay in initiation of pharmacologic prophylaxis. However, the benefit of pharmacologic prophylaxis has to be factored against the risk of hemorrhage. Furthermore, it is important to remember that inferior vena cava filter insertion does not prevent DVT and may increase the incidence of DVT; however, the filter can prevent a pulmonary embolism. Recommendations for thromboprophylaxis are discussed in more detail separately. (See "Venous thromboembolism risk and prevention in the severely injured trauma patient" and "Placement of vena cava filters and their complications".)

An area of ongoing research is the use of serum anti-Xa levels as a guide to pharmacologic prophylaxis in patients with obesity. This practice is not yet a standard of care currently but may become so as more studies evaluating this practice are published and the assays become more readily available [50]. (See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)

Stress ulcer prophylaxis — Severely injured patients (intubated, coagulopathic) and patients with a history of prior ulcer disease are at increased risk for stress ulcerations. Stress ulcerations are mucosal erosions involving the fundus and body of the stomach but sometimes occurring in the antrum, duodenum, or distal esophagus. They tend to be shallow and cause oozing of blood from superficial capillary beds, but deeper lesions can erode into the submucosa, can cause massive hemorrhage, and can occasionally perforate. Prophylaxis against stress ulcers is recommended for high-risk patients who require admission to the intensive care unit. (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention", section on 'Potential harms' and "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention", section on 'High-risk patients'.)

Some centers discontinue proton pump inhibitors or histamine-2 (H2) receptor blockers in patients who are tolerating goal enteral feeding. There is a strong association between use of proton pump inhibitors and Clostridioides difficile colitis, a risk that is further augmented by combined use of proton pump inhibitors and antibiotics. Use of Histamine-2 (H2) receptor blockers may be a better alternative to provide prophylaxis against gastritis/stress ulcers without increasing the risk of C. difficile colitis [51].

Glucocorticoids — Patients with chronic exposure to glucocorticoids may need stress dosing, but routine use of glucocorticoids in trauma patients is not indicated. (See "The management of the surgical patient taking glucocorticoids".)

Pressure ulcer prevention — Injured patients, including those requiring prolonged ventilatory support; those with brain, spine, pelvic, or extremity injury; and those being maintained on bed rest for blunt solid organ injury, are at risk for developing pressure ulcers [52]. Appropriate preventive measures should be undertaken, the choice of which depends upon the nature and severity of injuries. Preventive strategies for reducing the incidence of pressure ulcers in high-risk populations are discussed in detail elsewhere. (See "Prevention of pressure-induced skin and soft tissue injury".)

Hypothermia — Hypothermia following injury is due to cold exposure at the time of injury, during initial evaluation, compounded by the administration of cold intravenous fluids in the emergency department or prehospital setting. Hypothermia can also represent advanced shock, which is most commonly due to hemorrhage in the trauma population. Patients who require surgery are at a greater risk for hypothermia due to further physical exposure in the operating room, the effects of general anesthesia, and use of cold intravenous or intracorporeal fluids. Hypothermia may impair clot formation and platelet dysfunction, which is of particular concern in trauma patients. Injured patients with hypothermia generally have worse outcomes compared with noninjured patients with hypothermia; however, hypothermia alone is a weak independent predictor of mortality [53,54].

Upon admission, the patient's temperature should be noted and measures instituted to warm the patient if the body temperature is low. Continuous temperature monitoring is essential to ensure that mild hypothermia does not worsen. Specific measures to prevent and correct mild hypothermia include controlling physical exposure, administration of warmed fluids, and passive rewarming with blankets and forced-air devices. In the case of moderate or severe hypothermia and coagulopathy, central rewarming may be needed.

Alcohol/drug screening — Injured patients have a higher-than-normal incidence of alcohol and drug use disorder. All trauma patients should be screened and appropriate interventions offered [55]. Those who have been identified as being at risk for alcohol or drug withdrawal should receive appropriate prophylactic treatment. Patients who exhibit delirium or confusion attributable to alcohol or drug withdrawal are treated accordingly. (See "Management of moderate and severe alcohol withdrawal syndromes" and "Benzodiazepine poisoning" and "Benzodiazepine withdrawal".)

Psychological support — Patients who have been assaulted, or who have suffered severe physical injury, particularly those who required intensive care unit monitoring, are susceptible to acute stress disorder and post-traumatic stress disorder (PTSD). These disorders are characterized by intrusive thoughts, nightmares and flashbacks of past traumatic events, avoidance of reminders of trauma, hypervigilance, and sleep disturbance. Patients exhibiting persistent symptoms (>2 weeks) should be referred for psychological evaluation and potentially treatment. Anxiolytics may be necessary in the interim. In more severe cases, early referral to a psychologist or psychiatrist may be beneficial. (See "Acute stress disorder in adults: Epidemiology, clinical features, assessment, and diagnosis" and "Posttraumatic stress disorder in adults: Epidemiology, pathophysiology, clinical features, assessment, and diagnosis".)

Severely injured patients who require operative intervention have an increased risk for anesthetic underdosing related to the often emergency nature of the procedure and hypotension prior to induction of anesthesia. When possible, patients should be asked if they have any recollection of intraoperative events. Patients who have experienced an awareness event and exhibit signs of psychological disturbance (eg, intrusive thoughts, flashbacks, sleep disturbance) should be referred for psychological evaluation. (See "Accidental awareness during general anesthesia".)

FLUID THERAPY AND NUTRITION SUPPORT — For patients with severe injury, the period of acute resuscitation combines several key principles: optimizing tissue perfusion, ensuring normothermia, and restoring coagulation. Specific goals include a core temperature >37ºC, base deficit <6, and normal coagulation parameters. (See 'Laboratory studies' above.)

There are a multitude of management algorithms aimed at accomplishing these goals; the majority involve goal-directed resuscitation with initial volume loading to attain adequate preload, followed by judicious use of inotropic agents or vasopressors, as needed. For patients with active hemorrhage, the focus should be on hemorrhage control and damage control resuscitation, which minimizes crystalloid exposure in favor of a balanced resuscitation of blood products and allows permissive hypotension prior to hemorrhage control for patients without significant traumatic brain injury. (See "Overview of damage control surgery and resuscitation in patients sustaining severe injury" and "Ongoing assessment, monitoring, and resuscitation of the severely injured patient".)

Excessive crystalloid resuscitation can lead to adverse sequelae, including increased intracranial pressure, pulmonary edema, and intra-abdominal visceral and retroperitoneal edema resulting in secondary abdominal compartment syndrome. (See 'Monitoring for compartment syndromes' above.)

Although the optimal hemoglobin (Hb) level remains debated, during shock resuscitation hemoglobin levels should be titrated to optimize oxygen delivery. For patients who are not bleeding, a more judicious transfusion trigger of Hb <7 g/dL in the euvolemic patient limits the adverse inflammatory effects of stored red blood cells (RBCs). (See "Massive blood transfusion" and "Approach to shock in the adult trauma patient".)

Norepinephrine is the agent of choice for patients with low systemic vascular resistance (SVR) unable to maintain a mean arterial pressure (MAP) >60 mmHg (eg, high spinal cord injuries). Some patients may have an element of myocardial dysfunction requiring inotropic support. Epinephrine may be of benefit to those with impaired cardiac output due to blunt cardiac injury because it provides better inotropic support of the heart than norepinephrine. (See "Use of vasopressors and inotropes" and "Initial evaluation and management of blunt cardiac injury" and "Management of cardiac injury in severely injured patients".)

Fluid management — Upon admission, the patient's intake and output record during the course of resuscitation and anesthesia should be obtained and the net fluid balance determined.

Hemodynamically stable euvolemic patients should receive maintenance and replacement fluids and electrolytes, as indicated, depending upon dietary status. Drainage from chest tubes, and wound sites such as an open abdomen and fasciotomy wounds, should be quantified, if possible. A preset fluid replacement regimen is rarely necessary, but these sources of fluid efflux should be considered when adjusting the volume of fluid therapy. (See "Overview of postoperative fluid therapy in adults" and "Overview of postoperative electrolyte abnormalities".)

Crystalloid boluses in addition to maintenance fluid are administered to patients who remain hypotensive or oliguric and are not actively bleeding and may be needed in hemodynamically stable patients who have a negative fluid balance. Therapy should be guided by urine output in patients with normal renal function. Ongoing bleeding requires transfusion therapy (packed red blood cells, fresh frozen plasma [FFP] or similar products [eg, PF24], platelets) to maintain an adequate oxygen carrying capacity and to reverse coagulopathy. (See "Overview of postoperative fluid therapy in adults" and "Treatment of severe hypovolemia or hypovolemic shock in adults" and "Approach to shock in the adult trauma patient".)

A positive fluid balance is likely in severely injured patients, particularly those who have received massive transfusion. Crystalloid administration is minimized in this population. Transfusion may be guided by thromboelastography parameters, where available. As discussed above, patients requiring significant fluid resuscitation should be observed for abdominal compartment syndrome. (See "Etiology and diagnosis of coagulopathy in trauma patients" and 'Monitoring for compartment syndromes' above and "Initial management of moderate to severe hemorrhage in the adult trauma patient" and "Ongoing assessment, monitoring, and resuscitation of the severely injured patient", section on 'Transfusion' and "Ongoing assessment, monitoring, and resuscitation of the severely injured patient", section on 'VHA-based dosing'.)

Similarly, patients with large body surface area burns in addition to traumatic injury may require large volume resuscitation. This will be especially true in patients who present with both hemorrhage from injury as well as insensible losses due to a large surface area burn. Whereas bleeding patients should be resuscitated with blood products as previously discussed, burn care guidelines directing the volume of fluid are used to manage large surface area burns. (See "Overview of the management of the severely burned patient".)

For patients who require repeat radiographic studies with intravenous contrast, prehydration with crystalloid for several hours prior to administering the contrast agent appears to decrease the incidence of nephrotoxicity; the addition of sodium bicarbonate or acetylcysteine may be beneficial [56-58]. However, critical imaging should not be delayed, and the risks of nephrotoxicity must be balanced against the risk of delayed diagnosis of a potentially life-threatening injury. (See "Prevention of contrast-associated acute kidney injury related to angiography".)

Enteral and parenteral nutrition — The goal of nutrition support is to maintain lean body mass to prevent the negative consequences of protein malnutrition that can lead to multisystem organ dysfunction. Early institution of high-protein nutrition support is essential in the care of the injured patient. Injured patients are susceptible to hypermetabolism, which leads to breakdown of skeletal protein and inhibition of protein synthesis [59]. In addition, fluid effluent from an open abdomen results in significant protein loss, which can be estimated as 2 g of nitrogen per liter of abdominal fluid lost. This loss needs to be taken into account when calculating daily enteral or parenteral nutrition requirements [60]. (See "Clinical assessment and monitoring of nutrition support in adult surgical patients", section on 'Trauma/surgical critical care'.)

Every effort should be made to provide enteral nutrition to injured patients who cannot eat or who are unable to achieve adequate oral caloric intake, including patients with an open abdomen [61]. Multiple studies have demonstrated the superiority of enteral nutrition compared with parenteral nutrition. Infectious complications are lower in patients given adequate enteral nutrition [62,63]. Enteral nutrition enhanced by supplementation with glutamine and antioxidants may have additional benefits, although this is controversial [64,65]. The timing to initiation of enteral nutrition must be tailored to the individual patient based on injuries sustained and interventions performed. A delay in the initiation of parenteral nutrition may be appropriate if it is anticipated that the patient will be able to tolerate enteral nutrition within 7 to 10 days of injury [66,67].

Absolute contraindications to enteral nutrition mandate parenteral nutrition therapy and are listed in the next paragraph. A recent bowel resection and anastomosis is not a contraindication to enteral nutrition, and the presence of an open abdomen should not discourage attempts at enteral nutrition [68,69]. In a small study, enteral nutrition was successfully implemented in 52 percent of patients with open abdomen within four days of the initial laparotomy [68]. Patients with injury to the proximal gastrointestinal tract (eg, duodenal or pancreatic injury) can be fed through a more distal jejunostomy tube. (See "Overview of perioperative nutrition support".)

Patients with significant abdominal injury and operative intervention may not tolerate enteral nutrition and may require parenteral nutrition support. Indications for parenteral nutrition include patients with persistent progressive ileus, bowel obstruction, massive bowel resection refractory to enteral nutrition, malabsorption, splanchnic hypoperfusion that places the patient at high risk for nonocclusive mesenteric ischemia and bowel necrosis, high-output enteral fistula, intolerance of enteral nutrition (documented), and failure of enteral nutrition to meet caloric requirements [70]. (See "Postoperative parenteral nutrition in adults" and "Nutrition support in intubated critically ill adult patients: Parenteral nutrition".)

Glucose control — Patients with blood glucose above or below the accepted target range should be treated with insulin or glucose containing intravenous fluids, respectively. (See "Glycemic control in critically ill adult and pediatric patients".)

Increasing numbers of studies have evaluated the adverse impact of the hyperglycemic stress response in injured patents. Prospective studies of injured patients without diabetes have reported that elevated serum glucose on admission, defined as glucose >200 mg/dL, was significantly associated with an increased risk of infection (eg, urinary tract, pneumonia, wound), increased length of stay (hospital, intensive care unit), and mortality [71-77]. In a study of 6852 trauma patients, patients with stress-induced hyperglycemia had a more than twofold increased risk for mortality compared with normoglycemic patients (relative risk [RR] 2.41, 95% CI 1.81-3.23), whereas, although there was a trend toward increased mortality among patients with diabetes, the difference was not significant (RR 1.47, 95% CI 0.92-2.36) [78].

Both hyper- and hypoglycemia are associated with worsened outcomes in patients with severe traumatic brain injury (TBI). Glucose management in patients with TBI are reviewed separately. (See "Management of acute moderate and severe traumatic brain injury", section on 'Glucose management'.)

WOUND CARE — Injured patients present with a myriad of different wounds depending upon the injury mechanism. At admission, the location and size of each wound should be documented. Deep and more extensive wounds, particularly those in proximity to major vessels, should be explored in the operating room where lighting is optimal, debridement can be undertaken, and any disrupted vessels can be managed in a controlled fashion. For patients involved in criminal events (eg, explosion, terrorism), debrided materials (eg, penetrating objects, bomb fragments) gathered from the patients are included as evidence [79,80].

Individual wounds are managed with moist dressings, and closure or coverage, as indicated. Negative pressure wound therapy may be useful for management of large wounds but should be used cautiously in the setting of active soft tissue infection. (See "Basic principles of wound management" and "Negative pressure wound therapy".)

Open abdomen — Open abdomen is an abdominal wall defect created by intentionally leaving the fascia and skin open at the completion of surgery. Damage control surgery and suspected abdominal compartment syndrome are the most frequent reasons for open abdomen. The open abdomen is managed using temporary abdominal closure techniques that control abdominal fluid losses and assist with the progressive closure of the defect (picture 1). (See "Management of the open abdomen in adults".)

In euvolemic patients without an acute kidney injury and normal sodium levels, hypertonic saline can be used to promote abdominal wall closure. Hypertonic saline acts to decrease bowel and mesenteric edema and thus can be given prior to attempts at abdominal wall closure [81].

Fasciotomy wounds — Patients with acute extremity compartment syndrome are treated with fasciotomy. Prophylactic fasciotomy may be indicated in some patients (eg, ischemia-reperfusion following arterial repair, tibial fracture). The fasciotomy wounds are managed with moist dressings or negative pressure dressings initially with subsequent closure of the skin when muscle edema has resolved. (See "Lower extremity fasciotomy techniques", section on 'Indications' and "Patient management following extremity fasciotomy", section on 'Wound management'.)

CATHETERS, TUBES, DRAINS, AND LINES — During the initial assessment in the emergency department, most severely injured patients will have received an indwelling bladder catheter, various intravenous catheters, and possibly a nasogastric tube or an endotracheal or chest tube. Postoperative patients, particularly those who underwent damage control surgery, may also have had intraoperative drains placed.

At admission, the correct positioning of each tube and line should be confirmed, using radiographs if needed. Intravenous lines are often placed under duress during resuscitation, and frequent breaks in sterile precautions occur. These lines should be changed, whenever possible. Indications for use, placement, and appropriate care and management of these tubes and drains helps prevent complications. Issues related to surgical tubes and drains are discussed in detail elsewhere.

Bladder catheters – (See "Placement and management of urinary bladder catheters in adults" and "Complications of urinary bladder catheters and preventive strategies".)

Central lines – (See "Central venous access: acute and emergency access in adults" and "Central venous access: Device and site selection in adults" and "Routine care and maintenance of intravenous devices".)

Nasogastric and nasoenteric tubes – (See "Inpatient placement and management of nasogastric and nasoenteric tubes in adults".)

Chest tubes – (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children" and "Thoracostomy tubes and catheters: Placement techniques and complications" and "Thoracostomy tubes and catheters: Management and removal".)

PAIN MANAGEMENT — Pain management in the injured patient follows similar principles for managing postoperative pain. Critically injured patients in the intensive care unit are assessed frequently to ensure that pain control is adequate. It is imperative that a multimodality treatment strategy be used whenever possible to minimize narcotic use [82]. (See "Pain control in the critically ill adult patient" and "Approach to the management of acute pain in adults".)

Chest wall injures can cause significant pain that can compromise respiratory function. Management should include the use of non-narcotic medications, including acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs); neuraxial anesthesia; or non-narcotic parenteral medications, such as ketamine and/or lidocaine infusions. Operative fixation of multiple rib fractures, particularly flail chest, has gained renewed acceptance as a means to control chest wall pain and improve respiratory mechanics. The most common cause of death from rib fractures is pneumonia related to inability to breathe deeply, cough, and move. Thus, controlling pain in this population is critically important. (See "Inpatient management of traumatic rib fractures and flail chest in adults".)

Approaches to pain control in combined burn patients are discussed separately. (See "Management of burn wound pain and itching" and "Paradigm-based treatment approaches for management of burn pain".)

NONOPERATIVE MANAGEMENT — Nonoperative management of hemodynamically stable patients with solid organ injury (eg, liver, spleen, kidney) is appropriate for selected patients. (See "Management of splenic injury in the adult trauma patient", section on 'Nonoperative management' and "Management of hepatic trauma in adults", section on 'Nonoperative management'.)

Similarly, nonoperative management of pancreatic injury may be indicated in stable patients who do not require laparotomy for another indication [83]. (See "Management of duodenal trauma in adults", section on 'Role of conservative management' and "Management of pancreatic trauma in adults", section on 'Role of conservative management'.)

A nonoperative management approach may include the use of interventional techniques (eg, arteriography with embolization, endoscopic retrograde cholangiopancreatography). When applied correctly, nonoperative management is associated with shorter hospital stays and improved outcomes. However, it also requires the availability of appropriate institutional resources and a commitment to ongoing patient assessment and monitoring [84-86]. (See 'Monitoring' above.)

COMPLICATIONS — Complications in injured patients are often related to the nature of the patient's specific injuries (eg, pancreatic fistula, intra-abdominal abscess). These complications are discussed in separate reviews that discuss specific injuries. Complications may also arise as a result of resuscitative efforts, prolonged ventilation, or immobilization. Complications may also be iatrogenic in nature. Significant complications are briefly reviewed below.

Deep vein thrombosis and pulmonary embolism — Patients sustaining major trauma have a high risk of developing venous thromboembolism, in part due to the number of patients whose injuries contraindicate antithrombotic prophylaxis. The incidence of lower extremity deep vein thrombosis in injured patients who have received thromboprophylaxis ranges from 12 to 65 percent [87-90].

The incidence of pulmonary embolism (PE) is estimated between 0.7 and 20 percent, depending upon the population studied [90-93]. In a review of the United States National Trauma Data Bank (NTDB), the overall incidence of pulmonary embolism was 0.35 percent [94]. The prevalences for those with isolated traumatic brain injury, lower extremity, pelvic fracture, liver and/or spleen, thorax, spine, multiple injuries, and none of the studied injuries were 0.25, 0.36, 0.35, 0.37, 0.52, 0.37, 1.1, and 0.12 percent, respectively.

Acute respiratory distress syndrome — Severe trauma predisposes to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) and may be related to the mechanism of injury (eg, lung contusion, long bone fracture leading to fat embolism) or resuscitation (eg, transfusion). The definition, clinical features, diagnosis, and management of ALI/ARDS are discussed in detail elsewhere. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults".)

In a study that included 1762 patients with major traumatic injury, acute respiratory distress syndrome occurred in 24 percent [95]. Predictors of acute respiratory distress syndrome after trauma included increasing subject age; increasing Acute Physiology and Chronic Health Evaluation II (APACHE II) score; increasing injury severity score (ISS); and the presence of blunt injury, pulmonary contusion, massive transfusion, or flail chest.

Transfusion-associated complications — Acute lung injury and noncardiogenic pulmonary edema can develop in response to transfusion of packed red blood cells or, more commonly, plasma transfusion. The diagnosis, distinction of this disorder from transfusion-related circulatory overload, and management are discussed in detail elsewhere. (See "Transfusion-related acute lung injury (TRALI)".)

Ventilator-associated pneumonia — Injured patients appear to have a higher risk for ventilator-associated pneumonia (VAP) compared with noninjured patients. In a study of 2591 patients at a single institution that included 511 trauma patients, the incidence of VAP was significantly greater in the trauma population (18 versus 3.4 percent); however, mortality was significantly less (11 versus 31 percent), compared with nontrauma patients [96]. VAP occurred earlier in the hospital course in the trauma group. A multivariate regression for VAP in the trauma cohort identified the total ventilator days as the major independent risk factor for VAP. Injury severity score (ISS) was not a significant factor. No differences in mortality were seen between those with and without VAP. Several other studies have likewise found no significant differences in mortality rates in trauma patients with and without VAP [97,98]. The diagnosis and general management of VAP is discussed elsewhere. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

Acute kidney injury

In a review that used the Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE) classification to define acute kidney injury (AKI), the incidence was 26 percent among 982 patients with severe blunt trauma (82 percent with ISS >25) who survived past 24 hours [99]. The adjusted risk for hospital death was three times higher for patients with AKI compared with those without AKI (odds ratio [OR] 3.05, 95% CI 1.73-5.40). Risk factors for AKI included any increase in serum creatinine on admission greater than that expected (based upon patient age, sex, and race), an increase in lactic acid, low body temperature, and any transfusion of packed red blood cells or cryoprecipitate within the first 24 hours of trauma.

In another review, risk factors for AKI among trauma patients who required intensive care management included older age, medical comorbidities (particularly diabetes), higher ISS, massive transfusion, and volume loading with hydroxyethyl starch [100]. A subsequent meta-analysis also found that colloid administration compared with crystalloids significantly increased the risk of AKI (OR 1.21, 95% CI 1.07-1.37), with a subgroup analysis identifying increased risks for pentastarch (OR 1.8, 95% CI 1.24-2.62) and tetrastarch (OR 1.16, 95% CI 1.01-1.32) but not hypertonic saline-dextran or gelatin [101]. However, mortality and renal injury attributable to colloids were observed only in critically ill patients with sepsis.

Among patients with penetrating torso injury, a review of the NTDB reported an incidence of severe AKI of 2.3 percent [102]. The incidence of dialysis was 0.9 percent. The definition of AKI in NTDB corresponded to stage 3 AKI according to the Acute Kidney Injury Network classification. Independent risk factors for severe AKI included older age, male sex, diabetes, hypertension, Glasgow Coma Scale score, sepsis, hollow viscus injury, and injury severity score. Patients requiring dialysis had a higher mortality rate compared with patients with severe AKI who didn't require dialysis, and those without AKI (28.4 versus 20 and 8.8 percent, respectively).

An absolute correlation between extensive intravenous contrast loading (>150 mL) and kidney dysfunction has not been found in this population [99,100]. The true incidence of nephrotoxicity is unknown but is probably less than 1 percent. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)

There is evolving evidence on the utility of serum and urine biomarkers to predict onset of AKI and probability of renal recovery. However, these studies are mostly in the overall critically ill population and not specific to the trauma cohort. Similarly, there have been reports on the use of a "furosemide stress test" as a means to predict progression of acute kidney injury and need for renal replacement therapy [103]. These studies suggest that this test is more sensitive than serum or urine biomarkers of AKI for predicting progression of AKI, but, as before, the studies were performed in the general intensive care unit (ICU) population and are not unique to injured patients. Regardless, once AKI is established, the treatment is primarily supportive. (See "Overview of the management of acute kidney injury (AKI) in adults".)

Catheter-associated blood stream infection — The incidence of catheter-associated infection is higher in trauma populations, which may be due to the placement of lines under less-than-ideal conditions. Issues related to catheter-associated blood stream infection are discussed in detail elsewhere. When possible, central venous catheters (which include peripherally inserted central catheters or PICC lines) should be exchanged to peripheral IVs or midline catheters when the indication for central access is no longer present. (See "Central venous access: Device and site selection in adults" and "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology" and "Intravascular non-hemodialysis catheter-related infection: Treatment".)

OUTCOMES — Injury severity scores have been devised to quantitate injury and predict outcome for multitrauma patients; however, each scoring system has limitations [104-108]. Examples of scoring systems include the anatomical scoring system Injury Severity Score (ISS), the physiologic scoring system Revised Trauma Score (RTS), TRISS (age plus ISS and RTS), and A Severity Characterization of Trauma (ASCOT) [104-110]. TRISS can accurately predict the probability of survival in blunt trauma patients and provides a reasonable assessment of survival in patients with penetrating injuries [104]. Trauma scores have not been typically used to quantitate burn injuries, as burns are assessed as total body surface area (TBSA) burned. Burns are a component of ISS, but the contribution of the burn injury to TRISS is often inaccurate and cannot be used for prognostication.

Morbidity and mortality — Early recognition and treatment of patients at risk for complications may help reduce morbidity and mortality. Multivariate analysis of data from over 30,000 patients identified the following independent risk factors for multiorgan failure (MOF), which has a high rate of death: increasing age, higher injury severity score, head abbreviated injury scale (AIS) ≥3, thoracic AIS ≥3, male sex, Glasgow Coma Scale (GCS) ≤8, massive transfusion, base excess <-3, systolic blood pressure <90 mmHg on admission, and presence of coagulopathy. A scoring system using parameters obtained within four hours of presentation to the emergency department may help predict those who could develop MOF within seven days of hospitalization [111]. Elements of the Denver Emergency Department Trauma Organ Failure (TOF) scoring system include age ≥54 years (1 point), emergency intubation (3 points), hematocrit <20 percent (2 points), hematocrit ≥20 percent and <35 percent (1 point), emergency department systolic blood pressure <90 mmHg (1 point), and white blood cell count ≥20,000/microL (1 point). Based on this scoring system, the risk of MOF can be considered low, moderate, or high for scores of 0 to 1, 2 to 3, or >4, respectively. Among 2072 patients in a multicenter study, 120 (6 percent) developed MOF [112]. MOF developed in 3 percent of those with low score, 26 percent of those with moderate score, and 36 percent of those with high scores.

Mortality among victims of civilian trauma is substantially increased in the presence of one or more underlying chronic conditions. As an example, one study of approximately 7800 patients admitted with traumatic injures found that patients with at least one underlying medical condition had a significantly higher mortality compared with patients without such conditions (9 versus 3 percent), despite similar Glasgow Coma and Injury Severity Scores [113]. Underlying renal disease, malignancy, or cardiac disease were particularly ominous indicators. Similar associations have been observed in the APACHE and other models of illness severity. (See "Predictive scoring systems in the intensive care unit".)

Obesity also appears to worsen outcomes in trauma patients [114,115]. A systematic review of 18 studies compared outcomes in 7751 patients with a body mass index [BMI] ≥30 with patients with BMI <30 [115]. The ISS was similar between the groups. Using a random effects model, the pooled estimate of effect showed that patients with obesity had a significantly increased risk of death, complications (acute renal failure, multiorgan failure, adult respiratory distress), and length of stay in the intensive care unit.

Organ donation — Impending trauma deaths should be called in to the local organ procurement organization (OPO) regardless of age, injury, or comorbidity. Management of the potential organ donor can be very challenging and is discussed in detail elsewhere. (See "Diagnosis of brain death" and "Evaluation of the potential deceased organ donor (adult)".)

A cooperative relationship between trauma centers and the local OPO is essential. Importantly, members of the treating team should not engage in discussions related to organ donation with the patient's family or health care proxy. Procurement rate improves when trained personnel initiate these discussions, and as such, all discussion should be deferred to the OPO.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Abdominal compartment syndrome" and "Society guideline links: General issues of trauma management in adults" and "Disaster management: Links to UpToDate resources and society guidelines".)

SUMMARY AND RECOMMENDATIONS

Initial assessment – The injured patient admitted from the emergency department or operating room warrants full reassessment of the medical history. Patients with alcohol or drug use disorder are more likely to have complications during their hospital stay, while patients with medical comorbidities have an increased risk of mortality. (See 'Patient assessment' above.)

Repeat assessment – Repeat head-to-toe trauma examination (tertiary survey) on all patients decreases the frequency of missed injuries. Missed injuries are more common in multiply injured patients who require emergent surgical intervention shortly after hospital arrival. Extremity injuries are commonly missed. Significant injuries that can be missed during the initial evaluation include intra-abdominal injury, diaphragm injury, pulmonary contusion, arterial injury, and intracranial injury. (See 'Consider other potential injuries' above.)

Preventive strategies – Preventive strategies are important to reduce the incidence of common complications and include monitoring to identify and treat extremity and abdominal compartment syndromes, as indicated by the patient's injuries, and prophylactic therapies such as antibiotics prior to surgical intervention, thromboprophylaxis, stress ulcer prophylaxis, steroid prophylaxis for those on chronic therapy, and prophylaxis for drug/alcohol withdrawal. (See 'Monitoring for compartment syndromes' above and 'Prophylaxis and preventive care' above.)

Complications – Complications that may arise in injured patients are often related to specific injuries (eg, biliary fistula) but may also be due to incomplete or absent prophylaxis (eg, deep vein thrombosis), lack of monitoring (eg, abdominal compartment syndrome), or complications arising from diagnostic and resuscitative efforts (eg, contrast-media-associated nephropathy, transfusion-associated acute lung injury), prolonged ventilation (eg, ventilator-associated pneumonia), or immobilization (eg, pressure ulcers). (See 'Complications' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges C Crawford Mechem, MD, FACEP, who contributed to earlier versions of this topic review.

  1. Shamir MY, Rivkind A, Weissman C, et al. Conventional terrorist bomb incidents and the intensive care unit. Curr Opin Crit Care 2005; 11:580.
  2. Rotondo MF, Schwab CW, McGonigal MD, et al. 'Damage control': an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993; 35:375.
  3. Schreiber MA. Damage control surgery. Crit Care Clin 2004; 20:101.
  4. Parr MJ, Alabdi T. Damage control surgery and intensive care. Injury 2004; 35:713.
  5. MacKenzie EJ, Morris JA Jr, Edelstein SL. Effect of pre-existing disease on length of hospital stay in trauma patients. J Trauma 1989; 29:757.
  6. Soderstrom CA, Smith GS, Dischinger PC, et al. Psychoactive substance use disorders among seriously injured trauma center patients. JAMA 1997; 277:1769.
  7. Jurkovich GJ, Rivara FP, Gurney JG, et al. The effect of acute alcohol intoxication and chronic alcohol abuse on outcome from trauma. JAMA 1993; 270:51.
  8. Milzman DP, Soderstrom CA. Substance use disorders in trauma patients. Diagnosis, treatment, and outcome. Crit Care Clin 1994; 10:595.
  9. Biffl WL, Harrington DT, Cioffi WG. Implementation of a tertiary trauma survey decreases missed injuries. J Trauma 2003; 54:38.
  10. Hajibandeh S, Hajibandeh S, Idehen N. Meta-analysis of the effect of tertiary survey on missed injury rate in trauma patients. Injury 2015; 46:2474.
  11. Richards CF, Mayberry JC. Initial management of the trauma patient. Crit Care Clin 2004; 20:1.
  12. Committee on Trauma of the American College of Surgeons. Advanced Trauma Life Support: Course for Physicians, 5th ed, American College of Surgeons, Chicago 1993. p.17.
  13. Yeh DD, Imam AM, Truong SH, et al. Incidental findings in trauma patients: dedicated communication with the primary care physician ensures adequate follow-up. World J Surg 2013; 37:2081.
  14. Pfeifer R, Pape HC. Missed injuries in trauma patients: A literature review. Patient Saf Surg 2008; 2:20.
  15. Giannakopoulos GF, Saltzherr TP, Beenen LF, et al. Missed injuries during the initial assessment in a cohort of 1124 level-1 trauma patients. Injury 2012; 43:1517.
  16. Leeper WR, Leeper TJ, Vogt KN, et al. The role of trauma team leaders in missed injuries: does specialty matter? J Trauma Acute Care Surg 2013; 75:387.
  17. Kalemoglu M, Demirbas S, Akin ML, et al. Missed injuries in military patients with major trauma: original study. Mil Med 2006; 171:598.
  18. Brooks A, Holroyd B, Riley B. Missed injury in major trauma patients. Injury 2004; 35:407.
  19. Vles WJ, Veen EJ, Roukema JA, et al. Consequences of delayed diagnoses in trauma patients: a prospective study. J Am Coll Surg 2003; 197:596.
  20. Haste AK, Brewer BL, Steenburg SD. Diagnostic Yield and Clinical Utility of Abdominopelvic CT Following Emergent Laparotomy for Trauma. Radiology 2016; 280:735.
  21. Todd SR. Critical concepts in abdominal injury. Crit Care Clin 2004; 20:119.
  22. Enderson BL, Maull KI. Missed injuries. The trauma surgeon's nemesis. Surg Clin North Am 1991; 71:399.
  23. Rostas J, Cason B, Simmons J, et al. The validity of abdominal examination in blunt trauma patients with distracting injuries. J Trauma Acute Care Surg 2015; 78:1095.
  24. Sung CK, Kim KH. Missed injuries in abdominal trauma. J Trauma 1996; 41:276.
  25. Allen GS, Coates NE. Pulmonary contusion: a collective review. Am Surg 1996; 62:895.
  26. Cohn SM. Pulmonary contusion: review of the clinical entity. J Trauma 1997; 42:973.
  27. Wanek S, Mayberry JC. Blunt thoracic trauma: flail chest, pulmonary contusion, and blast injury. Crit Care Clin 2004; 20:71.
  28. Moore HB, Moore EE, Gonzalez E, et al. Hyperfibrinolysis, physiologic fibrinolysis, and fibrinolysis shutdown: the spectrum of postinjury fibrinolysis and relevance to antifibrinolytic therapy. J Trauma Acute Care Surg 2014; 77:811.
  29. CRASH-2 trial collaborators, Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376:23.
  30. Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg 2012; 147:113.
  31. Gonzalez E, Moore EE, Moore HB, et al. Goal-directed Hemostatic Resuscitation of Trauma-induced Coagulopathy: A Pragmatic Randomized Clinical Trial Comparing a Viscoelastic Assay to Conventional Coagulation Assays. Ann Surg 2016; 263:1051.
  32. Goaley TJ Jr, Wyrzykowski AD, MacLeod JB, et al. Can secondary extremity compartment syndrome be diagnosed earlier? Am J Surg 2007; 194:724.
  33. Ouellet JF, Roberts DJ, Tiruta C, et al. Admission base deficit and lactate levels in Canadian patients with blunt trauma: are they useful markers of mortality? J Trauma Acute Care Surg 2012; 72:1532.
  34. Régnier MA, Raux M, Le Manach Y, et al. Prognostic significance of blood lactate and lactate clearance in trauma patients. Anesthesiology 2012; 117:1276.
  35. Callaway DW, Shapiro NI, Donnino MW, et al. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma 2009; 66:1040.
  36. Markell KW, Renz EM, White CE, et al. Abdominal complications after severe burns. J Am Coll Surg 2009; 208:940.
  37. Dietch ZC, Edwards BL, Thames M, et al. Rate of lower-extremity ultrasonography in trauma patients is associated with rate of deep venous thrombosis but not pulmonary embolism. Surgery 2015; 158:379.
  38. Thorson CM, Ryan ML, Van Haren RM, et al. Venous thromboembolism after trauma: a never event?*. Crit Care Med 2012; 40:2967.
  39. Bandle J, Shackford SR, Kahl JE, et al. The value of lower-extremity duplex surveillance to detect deep vein thrombosis in trauma patients. J Trauma Acute Care Surg 2013; 74:575.
  40. http://www.east.org/resources/traumacast-detail/23 (Accessed on April 28, 2016).
  41. Goldberg SR, Anand RJ, Como JJ, et al. Prophylactic antibiotic use in penetrating abdominal trauma: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg 2012; 73:S321.
  42. Smith BP, Fox N, Fakhro A, et al. "SCIP"ping antibiotic prophylaxis guidelines in trauma: The consequences of noncompliance. J Trauma Acute Care Surg 2012; 73:452.
  43. Hart DW, Wolf SE, Mlcak R, et al. Persistence of muscle catabolism after severe burn. Surgery 2000; 128:312.
  44. Murray CK, Hoffmaster RM, Schmit DR, et al. Evaluation of white blood cell count, neutrophil percentage, and elevated temperature as predictors of bloodstream infection in burn patients. Arch Surg 2007; 142:639.
  45. Wolf SE, Jeschke MG, Rose JK, et al. Enteral feeding intolerance: an indicator of sepsis-associated mortality in burned children. Arch Surg 1997; 132:1310.
  46. Greenhalgh DG, Saffle JR, Holmes JH 4th, et al. American Burn Association consensus conference to define sepsis and infection in burns. J Burn Care Res 2007; 28:776.
  47. Jeschke MG, Mlcak RP, Finnerty CC, et al. Burn size determines the inflammatory and hypermetabolic response. Crit Care 2007; 11:R90.
  48. Williams FN, Jeschke MG, Chinkes DL, et al. Modulation of the hypermetabolic response to trauma: temperature, nutrition, and drugs. J Am Coll Surg 2009; 208:489.
  49. O'Donnell M, Weitz JI. Thromboprophylaxis in surgical patients. Can J Surg 2003; 46:129.
  50. Ko A, Harada MY, Barmparas G, et al. Association Between Enoxaparin Dosage Adjusted by Anti-Factor Xa Trough Level and Clinically Evident Venous Thromboembolism After Trauma. JAMA Surg 2016; 151:1006.
  51. Kwok CS, Arthur AK, Anibueze CI, et al. Risk of Clostridium difficile infection with acid suppressing drugs and antibiotics: meta-analysis. Am J Gastroenterol 2012; 107:1011.
  52. Berg GM, Spence M, Patton S, et al. Pressure ulcers in the trauma population: are reimbursement penalties appropriate? J Trauma Acute Care Surg 2012; 72:793.
  53. Tsuei BJ, Kearney PA. Hypothermia in the trauma patient. Injury 2004; 35:7.
  54. Shafi S, Elliott AC, Gentilello L. Is hypothermia simply a marker of shock and injury severity or an independent risk factor for mortality in trauma patients? Analysis of a large national trauma registry. J Trauma 2005; 59:1081.
  55. Dischinger PC, Mitchell KA, Kufera JA, et al. A longitudinal study of former trauma center patients: the association between toxicology status and subsequent injury mortality. J Trauma 2001; 51:877.
  56. Rudnick MR, Berns JS, Cohen RM, Goldfarb S. Contrast media-associated nephrotoxicity. Semin Nephrol 1997; 17:15.
  57. Deray G, Jacobs C. Radiocontrast nephrotoxicity. A review. Invest Radiol 1995; 30:221.
  58. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 2004; 291:2328.
  59. Biffl WL, Moore EE, Haenel JB. Nutrition support of the trauma patient. Nutrition 2002; 18:960.
  60. Cheatham ML, Safcsak K, Brzezinski SJ, Lube MW. Nitrogen balance, protein loss, and the open abdomen. Crit Care Med 2007; 35:127.
  61. Burlew CC, Moore EE, Cuschieri J, et al. Who should we feed? Western Trauma Association multi-institutional study of enteral nutrition in the open abdomen after injury. J Trauma Acute Care Surg 2012; 73:1380.
  62. Moore EE, Jones TN. Benefits of immediate jejunostomy feeding after major abdominal trauma--a prospective, randomized study. J Trauma 1986; 26:874.
  63. Dissanaike S, Pham T, Shalhub S, et al. Effect of immediate enteral feeding on trauma patients with an open abdomen: protection from nosocomial infections. J Am Coll Surg 2008; 207:690.
  64. Heyland DK, Dhaliwal R, Day AG, et al. REducing Deaths due to OXidative Stress (The REDOXS Study): Rationale and study design for a randomized trial of glutamine and antioxidant supplementation in critically-ill patients. Proc Nutr Soc 2006; 65:250.
  65. Todd SR, Gonzalez EA, Turner K, Kozar RA. Update on postinjury nutrition. Curr Opin Crit Care 2008; 14:690.
  66. Casaer MP, Hermans G, Wilmer A, Van den Berghe G. Impact of early parenteral nutrition completing enteral nutrition in adult critically ill patients (EPaNIC trial): a study protocol and statistical analysis plan for a randomized controlled trial. Trials 2011; 12:21.
  67. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Rice TW, Wheeler AP, et al. Initial trophic vs full enteral feeding in patients with acute lung injury: the EDEN randomized trial. JAMA 2012; 307:795.
  68. Byrnes MC, Reicks P, Irwin E. Early enteral nutrition can be successfully implemented in trauma patients with an "open abdomen". Am J Surg 2010; 199:359.
  69. Cothren CC, Moore EE, Ciesla DJ, et al. Postinjury abdominal compartment syndrome does not preclude early enteral feeding after definitive closure. Am J Surg 2004; 188:653.
  70. Kudsk KA, Tolley EA, DeWitt RC, et al. Preoperative albumin and surgical site identify surgical risk for major postoperative complications. JPEN J Parenter Enteral Nutr 2003; 27:1.
  71. Yendamuri S, Fulda GJ, Tinkoff GH. Admission hyperglycemia as a prognostic indicator in trauma. J Trauma 2003; 55:33.
  72. Laird AM, Miller PR, Kilgo PD, et al. Relationship of early hyperglycemia to mortality in trauma patients. J Trauma 2004; 56:1058.
  73. Sung J, Bochicchio GV, Joshi M, et al. Admission hyperglycemia is predictive of outcome in critically ill trauma patients. J Trauma 2005; 59:80.
  74. Bochicchio GV, Sung J, Joshi M, et al. Persistent hyperglycemia is predictive of outcome in critically ill trauma patients. J Trauma 2005; 58:921.
  75. Bochicchio GV, Joshi M, Bochicchio KM, et al. Early hyperglycemic control is important in critically injured trauma patients. J Trauma 2007; 63:1353.
  76. Bochicchio GV, Salzano L, Joshi M, et al. Admission preoperative glucose is predictive of morbidity and mortality in trauma patients who require immediate operative intervention. Am Surg 2005; 71:171.
  77. Bochicchio GV, Bochicchio KM, Joshi M, et al. Acute glucose elevation is highly predictive of infection and outcome in critically injured trauma patients. Ann Surg 2010; 252:597.
  78. Kerby JD, Griffin RL, MacLennan P, Rue LW 3rd. Stress-induced hyperglycemia, not diabetic hyperglycemia, is associated with higher mortality in trauma. Ann Surg 2012; 256:446.
  79. Frykberg ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma 2002; 53:201.
  80. Frykberg ER. Triage: principles and practice. Scand J Surg 2005; 94:272.
  81. Harvin JA, Mims MM, Duchesne JC, et al. Chasing 100%: the use of hypertonic saline to improve early, primary fascial closure after damage control laparotomy. J Trauma Acute Care Surg 2013; 74:426.
  82. Compton WM, Volkow ND. Major increases in opioid analgesic abuse in the United States: concerns and strategies. Drug Alcohol Depend 2006; 81:103.
  83. Mohseni S, Holzmacher J, Sjolin G, et al. Outcomes after resection versus non-resection management of penetrating grade III and IV pancreatic injury: A trauma quality improvement (TQIP) databank analysis. Injury 2018; 49:27.
  84. van Haarst EP, van Bezooijen BP, Coene PP, Luitse JS. The efficacy of serial physical examination in penetrating abdominal trauma. Injury 1999; 30:599.
  85. Brooks AJ, Rowlands BJ. Blunt abdominal injuries. Br Med Bull 1999; 55:844.
  86. Al-Mulhim AS, Mohammad HA. Non-operative management of blunt hepatic injury in multiply injured adult patients. Surgeon 2003; 1:81.
  87. Velmahos GC, Kern J, Chan LS, et al. Prevention of venous thromboembolism after injury: an evidence-based report--part I: analysis of risk factors and evaluation of the role of vena caval filters. J Trauma 2000; 49:132.
  88. Geerts WH, Jay RM, Code KI, et al. A comparison of low-dose heparin with low-molecular-weight heparin as prophylaxis against venous thromboembolism after major trauma. N Engl J Med 1996; 335:701.
  89. Chung SB, Lee SH, Kim ES, Eoh W. Incidence of deep vein thrombosis after spinal cord injury: a prospective study in 37 consecutive patients with traumatic or nontraumatic spinal cord injury treated by mechanical prophylaxis. J Trauma 2011; 71:867.
  90. Ho KM, Burrell M, Rao S, Baker R. Incidence and risk factors for fatal pulmonary embolism after major trauma: a nested cohort study. Br J Anaesth 2010; 105:596.
  91. Tuttle-Newhall JE, Rutledge R, Hultman CS, Fakhry SM. Statewide, population-based, time-series analysis of the frequency and outcome of pulmonary embolus in 318,554 trauma patients. J Trauma 1997; 42:90.
  92. O'Malley KF, Ross SE. Pulmonary embolism in major trauma patients. J Trauma 1990; 30:748.
  93. Spencer Netto F, Tien H, Ng J, et al. Pulmonary emboli after blunt trauma: timing, clinical characteristics and natural history. Injury 2012; 43:1502.
  94. Jeremitsky E, St Germain N, Kao AH, et al. Risk of pulmonary embolism in trauma patients: Not all created equal. Surgery 2013; 154:810.
  95. Watkins TR, Nathens AB, Cooke CR, et al. Acute respiratory distress syndrome after trauma: development and validation of a predictive model. Crit Care Med 2012; 40:2295.
  96. Cook A, Norwood S, Berne J. Ventilator-associated pneumonia is more common and of less consequence in trauma patients compared with other critically ill patients. J Trauma 2010; 69:1083.
  97. Rello J, Ollendorf DA, Oster G, et al. Epidemiology and outcomes of ventilator-associated pneumonia in a large US database. Chest 2002; 122:2115.
  98. Cavalcanti M, Ferrer M, Ferrer R, et al. Risk and prognostic factors of ventilator-associated pneumonia in trauma patients. Crit Care Med 2006; 34:1067.
  99. Bihorac A, Delano MJ, Schold JD, et al. Incidence, clinical predictors, genomics, and outcome of acute kidney injury among trauma patients. Ann Surg 2010; 252:158.
  100. Eriksson M, Brattström O, Mårtensson J, et al. Acute kidney injury following severe trauma: Risk factors and long-term outcome. J Trauma Acute Care Surg 2015; 79:407.
  101. Qureshi SH, Rizvi SI, Patel NN, Murphy GJ. Meta-analysis of colloids versus crystalloids in critically ill, trauma and surgical patients. Br J Surg 2016; 103:14.
  102. Athavale AM, Fu CY, Bokhari F, et al. Incidence of, Risk Factors for, and Mortality Associated With Severe Acute Kidney Injury After Gunshot Wound. JAMA Netw Open 2019; 2:e1917254.
  103. Koyner JL, Davison DL, Brasha-Mitchell E, et al. Furosemide Stress Test and Biomarkers for the Prediction of AKI Severity. J Am Soc Nephrol 2015; 26:2023.
  104. Millham FH, LaMorte WW. Factors associated with mortality in trauma: re-evaluation of the TRISS method using the National Trauma Data Bank. J Trauma 2004; 56:1090.
  105. Wolf SE, Kauvar DS, Wade CE, et al. Comparison between civilian burns and combat burns from Operation Iraqi Freedom and Operation Enduring Freedom. Ann Surg 2006; 243:786.
  106. Moreau AR, Westfall PH, Cancio LC, Mason AD Jr. Development and validation of an age-risk score for mortality predication after thermal injury. J Trauma 2005; 58:967.
  107. Chawda MN, Hildebrand F, Pape HC, Giannoudis PV. Predicting outcome after multiple trauma: which scoring system? Injury 2004; 35:347.
  108. Rutledge R, Osler T, Emery S, Kromhout-Schiro S. The end of the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS): ICISS, an International Classification of Diseases, ninth revision-based prediction tool, outperforms both ISS and TRISS as predictors of trauma patient survival, hospital charges, and hospital length of stay. J Trauma 1998; 44:41.
  109. Champion HR, Copes WS, Sacco WJ, et al. Improved predictions from a severity characterization of trauma (ASCOT) over Trauma and Injury Severity Score (TRISS): results of an independent evaluation. J Trauma 1996; 40:42.
  110. Champion HR, Sacco WJ, Copes WS, et al. A revision of the Trauma Score. J Trauma 1989; 29:623.
  111. Vogel JA, Liao MM, Hopkins E, et al. Prediction of postinjury multiple-organ failure in the emergency department: development of the Denver Emergency Department Trauma Organ Failure score. J Trauma Acute Care Surg 2014; 76:140.
  112. Vogel JA, Newgard CD, Holmes JF, et al. Validation of the Denver Emergency Department Trauma Organ Failure Score to Predict Post-Injury Multiple Organ Failure. J Am Coll Surg 2016; 222:73.
  113. Milzman DP, Boulanger BR, Rodriguez A, et al. Pre-existing disease in trauma patients: a predictor of fate independent of age and injury severity score. J Trauma 1992; 32:236.
  114. Winfield RD, Bochicchio GV. The critically injured obese patient: a review and a look ahead. J Am Coll Surg 2013; 216:1193.
  115. Liu T, Chen JJ, Bai XJ, et al. The effect of obesity on outcomes in trauma patients: a meta-analysis. Injury 2013; 44:1145.
Topic 7956 Version 46.0

References

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