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: