MISSED DIAPHRAGMATIC INJURY

Injuries to the diaphragm are common. Approximately 5% of patients injured in motor vehicle crashes have injuries to the diaphragm. A more frequently encountered scenario involves penetrating thoracoabdominal wounds. Approximately 15% of patients with this history will have injury to the diaphragm. Unfortunately, the diagnostic modalities used routinely for evaluation of injured patients have low sensitivity and a high rate of false negatives for diaphragmatic injury. Delayed diagnosis is the usual situation with diaphragmatic injury and may occur in up to 62% of patients. Cases of delayed recognition and treatment of up to 50 years have been reported in the literature. Diaphragmatic injuries should be recognized and treated as soon as possible to prevent complications. The most serious complications of diaphragmatic injury include herniation, incarceration, and strangulation of hollow viscera. The true incidence of this devastating complication is unknown but has historically resulted in mortality rates of 20%–36%.

Optimal diagnosis of diaphragmatic injury requires a high index of suspicion. It is virtually impossible to evaluate the diaphragm with 100% certainty without operative evaluation. Direct visualization, either through laparotomy, thoracotomy, laparoscopy, or thoracoscopy, is required to make this diagnosis with certainty. Conversely, not every patient with a history of injury should be explored, as this would lead to an unacceptable rate of negative and nontherapeutic operations.

A number of physical findings should increase the surgeon’s suspicion for diaphragmatic injury. These include penetrating thoracoabdominal injury or blunt trauma involving injuries to the abdomen or chest. Unfortunately, physical examination is unreliable in patients with diaphragmatic injury. In fact, 20%–40% of patients with isolated diaphragmatic injury have an initially normal physical examination. A number of noninvasive diagnostic adjuncts are routinely used in the evaluation of trauma patients. These include chest x-ray, focused assessment with sonography for trauma (FAST), and computed tomography (CT). Unfortunately, all of these diagnostic modalities used either alone or in combination are unreliable for the diagnosis of diaphragmatic injury. Additionally, diagnostic peritoneal lavage is nonspecific and fails to diagnose isolated diaphragmatic injury in a large percentage of cases. The only methods that evaluate the diaphragm with certainty are invasive operative procedures that directly visualize the diaphragm.

Isolated diaphragmatic lacerations are rarely life-threatening immediately following the injury. Direct evaluation of the diaphragm frequently holds a lower priority than treatment of other potentially life-threatening injuries. However, it must be emphasized that eventual evaluation of the diaphragm is indicated in at-risk patients. Once identified, diaphragmatic injury should be expeditiously repaired.

FAILURE TO RECOGNIZE EXTREMITY COMPARTMENT SYNDROME

Development of a compartment syndrome occurs commonly in patients with injuries to the upper and lower extremities. Compartment syndrome may also occur in any muscular compartment encased by fascia. This includes the hand, shoulder, arm, buttocks, thigh, and foot. A commonly held misconception is that patients with open fractures are protected from the development of compartment syndrome. Approximately 10% of patients with open fractures develop a limb-threatening compartment syndrome. Compartment syndrome is diagnosed on history and physical findings as well as a few adjunctive evaluations. Physical findings suggestive of compartment syndrome include a tense extremity with increased pain. Paresthesia indicates advanced ischemia involving nerves. It is an error to assume that a compartment syndrome is not present if a distal pulse is palpable. In fact, pulselessness is a late sign of compartment syndrome and may only occur after irreversible nerve and muscular injury have taken place.

Compartment syndrome develops in injured extremities secondary to a number of factors. Hemorrhage and muscle edema within a compartment may occur secondary to fracture. As pressure within the compartment increases and compartment pressure exceeds perfusion pressures, muscle and nerve ischemia will occur. Additionally, venous outflow obstruction results when compartment pressures rise. Compartment syndrome is a well-recognized complication of electrical burns. Ischemia with reperfusion is also a well-known cause of compartment syndrome. Iatrogenic causes of compartment syndrome include misplaced intravenous catheters into a muscle compartment followed by infusion of fluids into the compartment. Prolonged utilization of military antishock trousers (MAST) has also been associated with the development of compartment syndrome.

The diagnosis of compartment syndrome is based on clinical assessment and invasive evaluation of compartment pressure. Measurement of compartment pressure is easily accomplished using a number of techniques. If pressures within a muscular compartment are greater than 30 mm Hg, then compartment syndrome must be considered. A more elegant approach to determining compartment syndrome is measurement of the compartment perfusion pressure. The compartment perfusion pressure is calculated by subtracting the compartment pressure from the mean arterial blood pressure. If the compartment perfusion pressure is less than 40 mm Hg, then compartment syndrome must be considered.

Definitive therapy for compartment syndrome exists in the form of fasciotomy. Techniques of fasciotomy for both the upper and lower extremities are well known and involve decompression of all compartments of the involved extremity.

ABDOMINAL COMPARTMENT SYNDROME

The abdominal compartment syndrome (ACS) is defined as the pathophysiology and organ dysfunction that occurs as a result of intra-abdominal hypertension (IAH). The renal, cardiovascular, and pulmonary systems are most affected. Treatment of the syndrome is early decompression. However, even when treated appropriately, mortality approaches 50%.

Appreciation of the adverse affects of intra-abdominal hypertension began in the nineteenth century. Marey (1863) and Burt (1870) demonstrated the affects of IAH on respiratory function. In 1890, Heinricius observed increased mortality in cats and guinea pigs when intra-abdominal pressure (IAP) increased from 27–46 cm H₂O.

Emerson showed the relationship between IAH and adverse cardiovascular affects in 1911. In 1913, Wendt demonstrated the relationship between IAH and renal dysfunction. Later in the century, pediatric surgeons became aware of the adverse physiologic affects of IAH and developed techniques to allow expansion of the abdominal contents. In 1984, Kron described a technique to measure intraabdominal pressure and first used the phrase “abdominal compartment syndrome.”

The cardiovascular effects of IAH are consistent and well defined. Cardiac output is reduced as a result of decreased venous return secondary to increased intrathoracic pressure. This phenomenon occurs at IAP greater than 20 mm Hg, although venous return has been shown to be impaired at pressures as low as 15 mm Hg. Elevated intrathoracic pressure also contributes to a reduction in ventricular compliance, which reduces cardiac contractility. The diminished cardiac output seen with IAH has been shown to be exacerbated by hypovolemia and inhalational anesthetics.

The respiratory effects of IAH are mechanical. As the diaphragm is displaced cephalad, increased airway pressures are required to maintain adequate ventilation. Ultimately, this leads to ventilation/perfusion mismatch with resultant hypoxia and hypercarbia.

The mechanism of renal failure with ACS is multifactorial. Inadequate renal perfusion secondary to poor cardiac output, decreased perfusion, obstruction of renal venous outflow, and compression of the kidney all contribute to the renal failure associated with increasing IAP. Numerous studies have demonstrated that the oliguria and anuria seen with ACS are reversible with abdominal decompression.

Very little evidence exists on the effects of ACS on other organ systems. However, decreased blood flow in all abdominal organs occurs when IAP is more than 40 mm Hg. Hepatic artery, portal vein, and microcirculatory perfusion decrease when IAP surpasses 20 mm Hg. Intracranial hypertension and decreased cerebral perfusion pressure consistently improve with abdominal decompression when IAH is present.

Many etiologies exist for the development of ACS. Massive fluid resuscitation with crystalloid solutions plays a prominent and potentially preventable role in the development of this syndrome. Any condition associated with intra-abdominal hemorrhage places the patient at risk for ACS. This includes abdominal trauma, ruptured abdominal aortic aneurysm, retroperitoneal hemorrhage, elective abdominal operations, complications of pregnancy, and hepatic transplantation. In addition to blood, other intraperitoneal fluid collections may contribute to the development of ACS. Edema of the bowel and retroperitoneum, abdominal packing, ileus, ascites, massive volume resuscitation for shock, and inadvisable closure of abdominal fascia, all increase the risk of IAH and ACS.

The diagnosis of ACS is based on clinical parameters and the measurement of IAP. Findings of oliguria (<0.5 ml/kg/hr), hypoxia (oxygen delivery <600 ml/min/m²) with increasing airway pressures (peak >45 cm H₂O), SVR greater than 1000, and a distended abdomen, are all suggestive of ACS. Two methods of IAP measurement are clinically useful: intragastric and intravesicular. The latter is the most widely employed. First described by Kron et al., the technique involves clamping the bladder catheter, followed by the injection of 50–100 ml of sterile saline into the bladder. The catheter is then connected to a pressure manometer.

Based on the adverse physiologic changes at different IAP levels, most experienced surgeons suggest that the abdomen be decompressed with IAP above 25 mm Hg and that all patients be decompressed above 35 mm Hg. Early decompression, which may be performed in the intensive care unit (ICU), can reverse the pathophysiology of ACS. To avoid hypotension upon decompression, it is important to ensure that adequate intravascular volume resuscitation has been accomplished. Complications of abdominal decompression include hyperkalemia, respiratory alkalosis, hemorrhage, and reperfusion injury. The final step in decompressive laparotomy is to provide temporary abdominal closure that prevents recurrent IAH. Additional concerns include infection, fluid loss, evisceration, enterocutaneous fistula formation, and exposure of the abdominal viscera. Many methods of closure are available, including absorbable mesh, plastic intravenous (IV) (Bogota) bags, and vacuum-assisted closure. The large ventral hernia which results from temporary closure frequently requires delayed repair with nonabsorbable mesh. The mortality rate of ACS, despite decompression, still approaches 50%. Left untreated, it is routinely fatal. Early clinical suspicion in patients at risk, combined with aggressive measurement of IAP, can lead to life-saving decompression.

THE MYTH OF MANDATORY COLOSTOMY

Interpersonal violence remains prevalent in North America. The colon is the second most commonly injured abdominal organ in penetrating trauma (Table 1). Multiple associated injuries and infectious complications are common. When these patients present, the trauma surgeon must decide to primarily repair the colon, resect and perform an anastomosis, or create a colostomy. There is continuing debate as to the optimal treatment for penetrating colon injuries. During World War I, many patients underwent primary repair. Colostomy was reserved for extensive injuries or left colon injuries. No matter what treatment was employed, there was a high mortality rate. These dismal survival statistics occurred in an era of delayed treatment, inadequate volume resuscitation, no blood transfusions or antibiotics, and the absence of critical care. The dogma of mandatory colostomy began after the U.S. Army Surgeon General W. H. Ogilvie published a letter in 1943 that required the performance of colostomy for colon injuries:

Table 1 American Association for the Surgery of Trauma (AAST) Colon Injury Scale

This mandate was based on scant evidence but was issued in response to a mortality rate of greater than 50%. From Ogilvie’s own data, 50% of patients primarily repaired died, while 59% of patients treated with colostomy died. As military surgeons returned home, they continued to treat colon injuries with colostomy. But, as early as 1951, Woodhall and Ochsner reported decreased mortality with primary repair compared to colostomy in civilian practice (8.3% vs. 35%). In recent decades, surgeons have become more comfortable with primary repair of colon injuries that previously would have been diverted. More surgeons accept repair or resection and anastomosis of right colon injury, but treatment of left colon injuries are increasingly treated without colostomy. In previous decades, surgeons had to justify primary repair of a colon injury, but now the tide has turned. In 1991, Chappuis et al. reported the first prospective, randomized study of primary repair versus diversion in penetrating colon injuries. Patients were randomized irrespective of injury, contamination, transfusions, or shock. There was no difference in morbidity between the groups (17.9% vs. 21.4%). Length of hospitalization was 6 days longer in the colostomy group.

A 1996 prospective, randomized study by Gonzalez evaluated patients with penetrating colon injuries. These patients were randomized to either primary repair with or without resection versus mandatory colostomy. Randomization occurred irrespective of concomitant injuries or other risk factors. Septic complications were lower in the primary repair group (20% vs. 25%,) although this was not statistically significant. In severely injured patients with a PATI (penetrating abdominal trauma index) score higher than 25, there was a lower complication rate in the primary repair group as compared with the diversion group. Although these differences were not statistically significant, this experience demonstrated that primary repair was at least equal to, if not superior to, mandatory colostomy.

Subsequently, Gonzalez et al. reported their 6-year experience with 181 patients with penetrating colon injury. These patients were again randomized to primary repair or colostomy, regardless of other injuries, heavy fecal contamination, or hypotension. Septic complications were lower in the primary repair group (18% vs. 21%, p = 0.05). In hemodynamically unstable patients, the complication rate was also lower in the primary repair group (26% vs. 50%). Complications declined over time in both groups, which can be explained by improvement in the overall care of trauma victims.

Sasaki et al. published a prospective randomized study of 71 patients with penetrating colon injuries. There were no exclusionary criteria used in the randomization. Sixty percent of patients were treated with primary repair or resection and anastomosis. There was no significant difference in the grade of injury. There was a 19% complication rate (colon and non-colon related) in the primary repair group as compared with a 36% complication rate in the diversion group. In patients with a PATI greater than 25, the complication rate was 33% in primarily repaired patients and 93% in diverted patients. The PATI score has been used as an argument for mandatory colostomy in the past, but in this and other studies, the complication rate is higher in patients with higher PATI scores regardless of the choice of treatment. The authors also report a 7% complication rate at the time of colostomy reversal. Berne et al. performed a retrospective review of 40 patients who underwent colostomy reversal after trauma. They found a morbidity rate of 55% in patients initially treated with colostomy for colon injury.

The decision to perform a diverting colostomy may seem inherently sound. But contemporary trauma care must be based on evidence and not intuition. Diverting colostomy condemns patients to a subsequent operation for reanatomosis and exposes them to stoma-specific complications, including peristomal hernia, stenosis of the ostomy, ostomy retraction, necrosis and skin damage at the ostomy site. Based on current evidence, mandatory colostomy for penetrating colon injury should be abandoned. Consideration of colostomy for any colon injury, regardless of the coexisting injuries or comorbidities, must be justified based on current evidence and the status of the individual patient.

DELAYED DAMAGE-CONTROL LAPAROTOMY

“Damage control,” a term originating from the U.S. Navy definition of a ship’s ability to absorb damage and maintain mission integrity, is now a phrase that describes a surgical strategy utilized in many body regions. It describes a modified operative sequence in which the immediate repair of injuries is abandoned in favor of a staged approach. This is done in recognition of the physiologic insult suffered by the critically injured patient, and the continued deterioration during the operation which may render that insult irreversible. The concept of abbreviated laparotomy dates to 1908, when Pringle described the principles of compression and hepatic packing for control of portal venous hemorrhage. This practice fell out of favor after World War II, but reports emerged in the 1960s and 1970s that suggested improved outcomes with this technique. In 1983, Stone et al. introduced the modern concept of the abbreviated laparotomy with subsequent resuscitation and interval completion laparotomy after physiologic restoration. In 1993, Rotondo and associates popularized the term “damage control,” and it has rapidly become a standard in the treatment of critically injured patients with deteriorating physiologic parameters.

Three stages of damage-control laparotomy were originally described. The first stage is the truncated laparotomy in the face of life-threatening physiologic circumstances. It involves the control of hemorrhage with intra-abdominal packing and control of contamination from bowel, pancreatic, or biliary tract injuries. Lengthy vascular repairs are not pursued, but temporary shunting is used liberally. Enteric contamination is controlled by rapid suture, stapling, or resection. No attempt at definitive reconstruction of bowel continuity is required. Most authors describe the use of laparotomy pads for packing; however, the use of Kerlex gauze has also been described. Overpacking can lead to increased intra-abdominal pressure and abdominal compartment syndrome. Underpacking may fail to stop hemorrhage. Packing should provide pressure in vectors that recreate the disrupted tissue planes. It is difficult to obtain hemostasis of arterial injuries with packing. If rapid repair, ligation, or stenting cannot be accomplished, then other methods, such as angiographic embolization, should be employed. Biliary tract and pancreatic injuries can be managed with external tube drainage. Rarely, a pancreatoduodenectomy without reconstruction may be required. Once the abbreviated laparotomy is completed, the abdomen is closed by temporary methods. Many techniques for temporary closure have been described, including penetrating towel clamp closure, running skin sutures, use of an IV bag (Bogota bag) and vacuum closure device. Whichever method is used, the goals are identical: prevent evisceration, protect the bowel, and minimize the risk of intra-abdominal hypertension and abdominal compartment syndrome.

The second phase of damage control involves ongoing resuscitation in the ICU with the reversal of the lethal triad: hypothermia, acidosis, and coagulopathy. Each of these devastating physiologic complications has a compounding effect on the others. Hypothermia, defined as a core temperature less than 35° C, is exacerbated by prolonged exposure, inadequate perfusion, and inadequate warming in the emergency department or operating room. Hypothermia exists in as many as half of injured patients following trauma laparotomy. Hypothermia increases the requirement for fluid resuscitation, vasopressors, inotropes, and transfusions. It is associated with increased morbidity, organ dysfunction, coagulopathy, and mortality. In the ICU, the ambient temperature, airway circuit, intravenous fluids, and blood products should all be warmed. Warm blankets and a forced-air heater should be used aggressively. Acidosis results from inadequate oxygen delivery secondary to hemorrhage which results in anaerobic metabolism and the release of lactic acid. Acidosis worsens coagulopathy, depresses myocardial contractility, diminishes inotropic response to catecholamines, and predisposes to ventricular dysrhythmias. Correction of acidosis is directed at improvement of oxygen delivery and optimizing cardiac output. Failure to correct elevated lactic acid levels or base deficit within 48 hours is associated with rates of mortality approaching 100%. Coagulopathy is worsened by the combined effects of hypothermia, acidosis, and dilution of clotting factors by massive crystalloid resuscitation. Correction of coagulopathy is achieved by the reversal of hypothermia and acidosis, as well as the aggressive replacement of clotting factors with fresh frozen plasma, cryoprecipitate, and platelets. Recombinant factor VIIa may be beneficial in reversing recalcitrant coagulopathy in trauma.

The third phase of damage control refers to definitive operative repair of injuries after reversal of physiologic impairments. The timing of definitive repair is based on clinical parameters rather than the clock. It may be necessary to perform more than one subsequent laparotomy to repair all injuries. The decision to employ damage control techniques is ultimately made by the surgeon. The decision should be made early if the benefits of the technique are to be fully realized. Indications for the damage control approach include the inability to achieve hemostasis, inaccessible source of hemorrhage, multiple severe injuries, poor response to resuscitation, and as dictated by the direct measurement of physiologic parameters of temperature, pH, and the vital signs. Complications of damage control include wound infection, abscess formation, enterocutaneous fistula formation, dehiscence, bile leak, pancreatic pseudocyst formation, intestinal necrosis, abdominal compartment syndrome, multisystem organ failure, acute respiratory distress syndrome (ARDS), and death.

Damage control represents a unique surgical philosophy which can be life-saving in a select population of critically injured patients. Success is dependent on timing, patient selection, rapid operative control of hemorrhage and contamination, aggressive resuscitation, and the reversal of the lethal triad of hypothermia, acidosis, and coagulopathy.

MISSED HOLLOW VISCUS INJURY

With the increasing utilization of nonoperative management of solid organ injuries in blunt trauma, the incidence of missed hollow viscus must be considered. Hollow viscus injury affects about 1% of all trauma patients and 15% of patients with blunt abdominal trauma. Motor vehicle collisions are the most common mechanism of injury. Even as diagnostic imaging has evolved, it is still inferior to laparotomy in establishing the diagnosis of hollow viscus injury. Some of these injuries are evident on close examination of initial computed tomography (CT) scans, but others become apparent after hours or days. The FAST exam has proven useful to diagnose hemoperitoneum, but it is not capable of reliably identifying hollow viscus injury. Physical examination, diagnostic peritoneal lavage (DPL), and laboratory tests are similarly unreliable.

The use of CT has dramatically increased over recent years. The ability to identify solid organ injuries with CT scans is far superior to the ability to diagnose hollow viscus injury. Killeen et al. examined 150 CT scans of blunt trauma victims and compared these to operative findings. Helical CT scan showed a sensitivity of 94% for bowel injuries and 96% for mesenteric injuries. The number of solid organ injuries influences the diagnosis of hollow viscus injuries. With a single solid organ injury, a hollow viscus injury was found in 7.3% of patients. The incidence doubled (15.4%) with two solid organ injuries and was 34.4% with three solid organ injuries. Malhotra et al. also found that the following findings on CT were predictive of hollow viscus injury: unexplained intraperitoneal fluid, pneumoperitoneum, bowel wall thickening, mesenteric fat streaking, mesenteric hematoma, extravasation of luminal contrast, and extravasation of vascular contrast. They recommend that patients with a single positive finding undergo confirmatory DPL, and those with more than one finding should undergo urgent exploration.

In 1999, Fang et al. examined patients with a delayed diagnosis of small bowel injury. Their retrospective review of 111 blunt trauma victims with small bowel injury showed no difference in mortality if the injury was treated within 24 hours. But patients with a delay in diagnosis of greater than 4 hours had an increased incidence of wound infection, abscess formation, enterocutaneous fistula, wound dehiscence, and sepsis. Those whose injury was repaired after 24 hours averaged a 20-day increase in hospital stay and a 6-day delay in initiation of oral intake when compared with those whose injury was repaired between 12 and 24 hours. Fakhry et al. found an increase in mortality and morbidity with diagnostic delays in small bowel injuries. Mortality was 2% when the injury was treated within 8 hours, 9.1% when treated between 8 and 16 hours, 16.7% when treated between 16 and 24 hours, and 30.8% when delayed more than 24 hours.

Missed injuries are not isolated to blunt mechanism of injury. Sung et al. found, in a retrospective review of 607 patients with penetrating trauma, a missed injury rate of 2%. These injuries were missed at the initial operation. These injuries included two gastric perforations, two retroperitoneal rectal injuries, one pancreatic transection, and one duodenal injury. Forty-two percent of patients with missed injuries developed sepsis, and 17% developed renal failure. Mortality was significantly higher in patients with missed injuries (17% vs. 6.4%, p = 0.007). This study highlights the need for a standard, systematic approach to trauma laparotomy. In our institution, after a physical exam, all patients undergo a surgeon-performed FAST exam. In the stable patient with free fluid, we then obtain a contrast-enhanced CT. If the patient’s physical findings change or a hollow viscus injury is still suspected, but unproven, a repeat CT scan and/or diagnostic laparoscopy is then considered. The increased mortality and morbidity associated with diagnostic delays mandates an aggressive search for suspected hollow viscus injuries.

FAILURE TO PERFORM TERTIARY SURVEY

Missed injuries plague all trauma centers. The Advanced Trauma Life Support Course (ATLS) has become the gold standard for initial recognition and treatment of life-threatening injuries in the initial evaluation period through the use of a primary and secondary survey. However, it is clear from published reports that this approach allows injuries to go undetected. While there is no consensus on the specific criteria to define a missed injury, it refers to any injury not appreciated in the initial evaluation. The reported rates of missed injuries vary from 2%–50%. The majority of these may not be clinically significant, but some are potentially fatal. Even less severe injuries can cause prolonged disability, expense, pain, and deterioration in the relationship between the trauma team and the patient. Factors that contribute to the prevalence of missed injuries include the attention focused on more urgent treatment priorities, altered patient sensorium, poorly appreciated physical findings, and radiologic studies that are not appropriately performed, are misinterpreted, or are omitted. Missed injuries are more common in patients involved in motor vehicle crashes, those with higher injury severity scores (ISS), and those with a greater number of injuries. One other factor reported to increase the frequency of missed injuries is the level of experience of the treating physician.

There are a number of reports that recommend the use of a tertiary survey as a mechanism to address this issue. The tertiary survey is a thorough re-examination of the trauma patient within the first 24 hours of admission and after all contributing sources of examination difficulty have resolved. This exam includes symptom review, physical examination, and review or ordering of appropriate radiologic or laboratory studies. Since factors of hemodynamic instability and altered sensorium may still exist after 24 hours of treatment, it is important to complete the tertiary survey again when a patient is stabilized and neurologically competent. Many surgeons have suggested formal radiology rounds as a standard part of the tertiary survey, since over 25% of missed injuries can be correctly identified on the original x-ray studies. Enderson et al. reported identifying additional injuries in 9% of blunt trauma patients with the routine use of a tertiary survey. Janjua et al. detected 56% of early missed injuries and 90% of clinically significant missed injuries with the performance of a tertiary survey within 24 hours of admission. Biffl et al. were able to reduce the incidence of missed injuries from 2.4%–1.5% after implementation of a tertiary survey policy. Soundappan et al. reported similar results in a pediatric population.

The distribution of missed injuries involves almost every anatomic region. The most commonly missed injuries are fractures. These include fractures of the extremities, spine, and pelvis. Missed skull and facial fractures are reported routinely. Strategies to avoid delayed diagnosis include a thorough physical examination of all extremities and the back to search for deformity, swelling, ecchymosis, and decreased range of motion. In neurologically intact patients, a meticulous interrogation of symptoms is warranted. Radiologic evaluation of any questionable area should be performed and reviewed in a timely fashion. Delays in the diagnosis of abdominal injuries, including both solid organ, intestinal, and diaphragm injuries, can cause preventable trauma deaths. Inability to perform a meaningful abdominal exam, hemodynamic instability precluding the ability to perform a CT scan, and the immediacy of an operative procedure for other serious injuries, can all contribute to a delay in diagnosis. Useful measures to reduce these delays include repeat physical examination, the use of serial sonography, and repeat CT scan to improve the diagnosis of a hollow viscus injury. Frequently missed injuries in the thorax include aortic rupture, rib fractures, pneumothorax, and hemothorax. Careful physical examination and radiologic evaluation can reduce the rate of diagnostic delays.

Missed injuries occur with significant frequency and with the potential for significant morbidity and mortality. The tertiary survey is a comprehensive patient evaluation that occurs after the initial resuscitation period. Tertiary survey should become a standard and necessary feature of the care of every trauma patient.

FUTILE RESUSCITATIVE THORACOTOMY

One of the most dramatic procedures performed is the emergency department (ED) thoracotomy. It is performed in a hectic environment, but when carried out in the proper patient, can be life saving. Unfortunately, it is frequently performed in poorly selected patients without valid indications, with predictably dismal results. There is little doubt that a patient with cardiac tamponade secondary to a small stab wound to the right ventricle who loses vital signs in the trauma bay may be salvaged. But in many instances, indications for resuscitative thoracotomy are less clear. Futile thoracotomy performed for patients with lethal injuries is distressingly common.

Rhee et al. recently retrospectively reviewed a 25-year multicenter experience with resuscitative thoracotomy. Blunt trauma victims undergoing ED thoracotomy had a survival rate of 1.4%. Survival of blunt trauma victims ranged from 0%–12.5% for the various trauma centers. If the 12.5% rate of survival from one center is excluded, most survival rates are less than 2%. Many blunt trauma “survivors” of ED thoracotomy were not neurologically intact. In 2004, Powell et al. evaluated their experience with ED thoracotomy for victims of penetrating and blunt trauma who required prehospital cardiopulmonary resuscitation (CPR). They documented four blunt trauma survivors, all of whom had a severe neurologic deficit. Even in blunt trauma patients with cardiac tamponade, the outcome after ED thoracotomy is routinely fatal. In a retrospective review of ED thoracotomy patients, Grove et al. reported four blunt trauma victims with cardiac tamponade who survived ED thoracotomy and were admitted to the ICU; all died within 9 days. Clearly, blunt trauma victims without signs of life in the field or upon arrival in the trauma bay should be declared dead. The blunt trauma patient who loses vital signs shortly after arrival in the ED will have a dismal outcome with any therapy, and we believe that thoracotomy should not be performed.

Some victims of penetrating trauma clearly may benefit from ED thoracotomy. Proper selection of potentially salvageable patients is key. Powell found that the duration of CPR was critical. All survivors of ED thoracotomy had CPR for 15 minutes or less. Any penetrating trauma patient with prolonged CPR (>15 minutes) should be pronounced dead upon arrival.

Few patients will survive if the duration of prehospital CPR is greater than 5 minutes. ED thoracotomy is a potentially life-saving procedure, but there are few survivors. Utilization of this intervention should be limited to patients with penetrating mechanisms of injury. Those with noncardiac injuries have a poor prognosis. The FAST exam may help to delineate treatable intrathoracic injury and decrease the number of futile ED thoracotomies in the future.

SUMMARY

The circumstances involved in the evaluation and treatment of injured patients makes errors likely. It is inevitable that delays in diagnosis and intervention will occur in multiply injured patients. However, it is incumbent upon all those who care for trauma patients to have a high index of suspicion for common errors so that the frequency of these may be minimized. A low threshold of suspicion for difficult to diagnose injuries must be maintained if optimal care is to be delivered to injured patients. Futile attempts to salvage lethally injured patients are costly and time consuming and should be minimized.