Surgical Management of Complications of Burn Injury


Introduction

Various surgical complications can occur in burn patients resulting from pathologic progression of the burn injury itself or from iatrogenic etiologies. Multiple organ system injuries can exist that require both a thorough assessment and expeditious management according to advanced trauma life support (ATLS) guidelines. Patients with large (>30% of the total body surface area [TBSA]) burns generally require a prolonged hospital stay with numerous debridement and skin grafting procedures that can be complicated by wound infection and subsequent graft failure.

Burn patients are at risk for potential surgical complications involving multiple organ systems, particularly the gastrointestinal (GI) tract. Such complications include stress gastritis and ulceration, acalculous cholecystitis, superior mesenteric artery (SMA) syndrome, and acute pancreatitis. In this patient population, the cause for occult systemic sepsis is frequently attributed to GI sources. Necrotizing enterocolitis (NEC) is a serious GI tract complication in burn patients, representing a phenomenon of transient ischemia–reperfusion injury to the gut. It can progress to full-thickness necrosis of involved segments, perforation, and rapid clinical decline.

Abdominal compartment syndrome (ACS) can occur during the acute phase of massive fluid resuscitation in severely burned patients. Based on determination of increased intra-abdominal pressures (designated as “compartment syndrome”) and additional physiologic parameters, a decompressive laparotomy may be necessary to prevent further end-organ damage. A major burn significantly affects hemodynamics, and invasive monitoring may be necessary. As a consequence, catheter-related complications, such as distal limb ischemia and catheter-associated sepsis, can be seen with both arterial and venous vascular access. Prolonged intravascular manipulation secondary to the need for access predisposes to septic thrombophlebitis, central line-associated bloodstream infections (CLABSI), and poor outcomes.

Because of delays in diagnosis and treatment, there is a high risk of nonthermal complications in burn patients. As such, these secondary and sometimes fatal complications demand immediate recognition and treatment. This chapter reviews the frequently encountered, surgical, nonthermal complications in burn patients with respect to diagnosis and management.

Burns and Trauma

Although the overall incidence of combined burn and traumatic injury is low, the mortality is nearly twice that of burns without associated trauma. A retrospective study examined upward of 24,000 patients with burn, trauma, or combined injuries and found the overall incidence of combined burn and trauma rate to be low (3.8%), consistent with the National Trauma Data Bank and National Burn Repository data. There was no difference in length of hospital stay, injury severity scores, or mortality among burn or trauma patients alone. However, inhalational injury, length of stay, and mortality in patients suffering from combined injuries were significantly increased ( Table 37.1 ). This increase in mortality was seen despite similar burn size, demonstrating the additive effects of trauma and burns in these patients. In particular, approximately 24% of military burns are associated with concurrent traumatic injuries, compared to the 2–7% of burn/trauma injuries found in civilians in the same study. In order of frequency, injured organ systems include musculoskeletal, head and neck, abdominal, thoracic, and genitourinary. Industrial accidents, attempts to escape house fires, explosions, and electrical burns with falls account for the majority of other victims. High-voltage electrical burns rarely occur at ground level and are often accompanied by falls resulting in spinal cord injuries, solid organ injury, intracerebral hemorrhage, and multiple fractures, including vertebral, rib, pelvic, and long bone fractures.

Table 37.1
Increased Morbidity and Mortality With Combined Burn and Trauma
Trauma (n = 22,284) Burn (n = 1717) B/T (n = 92)
Age 35.1 (±27.5) 31.0 (±23.2) 40.1 (±25.4) *
TBSA N/A 17.5% (±19.7) 20.8% (±24.4)
ISS 5.5 (±10.3) 12 (±14) 23 (±16) *
LOS (days) 5.3 * (±12.2) 13.7 (±16.5) 18 (±20.8)
INH N/A 11.0% 44.5% *
Mortality 4.3% 9.8% 28.3% *
B/T, burn/trauma; TBSA, total body surface area; ISS, injury severity score; LOS, length of stay; INH, inhalation injury.

* P < 0.05 (Age, B/T vs. Burn; ISS, B/T vs. Burn and Trauma; LOS, B/T vs. Trauma; Mortality, B/T vs. Burn and Trauma)

Primary Assessment

The shocking appearance of the burn injury may unduly shift attention away from the other seemingly underwhelming injuries in patients with combined trauma, resulting in potential delays in diagnosis. The initial assessment of a trauma patient, including burn victims, should focus on airway, breathing, and circulation according to the ATLS guidelines. With the exception of respiratory compromise secondary to circumferential chest burns, the burn injury itself is usually not immediately life-threatening. Inhalational injury is common in burn patients. Some of the common signs of inhalational injury include singed nasal and facial hair, erythematous oropharynx, cough, stridor, and carbonaceous sputum. Asphyxia can be seen with carbon monoxide, for which pulse oximetry is an unreliable measure of oxygenation. Intubation or a surgical airway is warranted when significant respiratory distress exists. The inhalational injury can progress rapidly over hours such that an initial chest radiograph and arterial blood gas may be normal. Smoke inhalation induces a multitude of physiologic changes that result in increased vascular permeability and pulmonary edema, infiltration by leukocytes, and bronchorrhea.

Once the airway has been secured, attention should focus on the rest of the primary assessment. Third-degree circumferential chest burns can impair respiratory mechanics and require escharotomy to release the constrictive eschar. This should be performed in a sterile manner with incisions extending from the clavicle to the costal margin in the anterior axillary line bilaterally and may be joined by transverse incisions. The more common thoracic injuries, such as pneumothorax and hemothorax, should be managed as they would be in any other blunt or penetrating thoracic injury. However, because burns carry such a high risk of infection, thoracostomy tubes should be placed away from burned skin whenever possible to reduce the risk of infectious complications such as empyema. Finally, adequate circulation should be assessed. Pericardial tamponade resulting from a heavy impact to the anterior chest wall can be detected by focused assessment with sonography for trauma (FAST) examination and managed with pericardiocentesis or a pericardial window. Myocardial dysfunction may be encountered, especially with electrical injuries, and dysrhythmias should be managed accordingly. If central venous access is necessary, it should similarly be placed away from burned tissue when possible.

Associated Injuries

Burn victims frequently present with concomitant trauma injuries. Bone fractures are the most common associated injuries; in these cases, multidisciplinary management is mandatory. Fractures anatomically distant to the burned area can be treated with reduction and/or casting, as indicated. In addition, open fractures are preferably treated within the first 24 hours; surgical treatment options include irrigation, debridement of nonviable soft tissue, and internal fixation. If the injury occurs in—or the operative incision is made through—a burned area, the wound closure must be performed to the level of the fascia. Additional considerations in the treatment of fractures in burned patients include characteristics of the fracture (stability, displacement, and complexity), need of grafting of the burned area, wound care, and prompt initiation of physical therapy.

A complete physical evaluation is needed in all patients; the cervical spine should be stabilized until spinal injuries have been ruled out. When intracranial pressure (ICP) monitoring is indicated, placement of the ICP monitor is preferably done through a nonburned area of the scalp.

Severe burn injury may mask intra-abdominal injuries that may have devastating complications due to the delay in diagnosis. Furthermore, hemodynamic fluctuations secondary to intra-abdominal injuries may be overshadowed by the massive fluid shifts and inflammatory response following thermal injury. If an intra-abdominal injury is suspected, diagnosis and treatment modalities that are used in nonburned trauma patients should be utilized. Laparoscopy may be a useful approach for the delineation of intra-abdominal injuries but achieving adequate peritoneal insufflation may be difficult with the presence of significant abdominal eschar. If laparotomy is indicated, wound dehiscence is a known complication regardless of burn wound location. Retention sutures or alternative methods of abdominal wall closure should be considered when there is increased tension when closing the abdomen. Frequently, ACS may develop in the massively burned patient that may require emergent laparotomy and temporary wound closure.

Vascular injuries also present with a delay in diagnosis in the presence of large burned areas, anasarca, hypotension, and compartment syndromes. The assessment of vascular injuries includes the routine use of Doppler ultrasound and ankle-brachial index (ABI). Both of these modalities have their limitations in areas of significant burned or edematous skin. Computed tomography (CT) angiography is a highly sensitive and specific method useful to diagnose vascular injuries in burn patients.

Gastrointestinal Tract Complications

Although the superficial effects of burn injuries are often striking, the systemic physiological response to these injuries may result in significant end-organ dysfunction and cannot be overemphasized. Burn injuries of greater than 30% TBSA produce a physiological response leading to systemic shock, hypermetabolism, and widespread immunosuppression. The combination of intravascular fluid loss, vasoactive hormone release, catabolism, and immune dysfunction results in the development of nonthermal complications associated with burn injuries.

Physiological changes in blood flow have a dramatic effect on organ response to injury. This has been particularly well demonstrated in the GI tract, where a combination of diffuse capillary leak, hypovolemia, and the release of vasoconstrictive agents can cause a decrease in splanchnic blood flow. Splanchnic hypoperfusion occurs early in the post-burn period despite adequate cardiac output and fluid resuscitation, as demonstrated in 40% TBSA pig models that had an early reduction in superior mesenteric blood flow associated with intestinal mucosal hypoxia, acidosis, and increased bacterial translocation.

A combination of hypoperfusion and hypermetabolic response can lead to breakdown of the gut mucosal barrier resulting in bacterial translocation from the gut, systemic inflammation, and ultimately, sepsis ( Fig. 37.1 ). Several studies have demonstrated the association between massive cutaneous burn injury and bacterial translocation. Following massive burn injury, the GI tract mucosa sustains immediate atrophy, resulting in significant gut barrier dysfunction. The increase in intestinal apoptosis does not appear to be from mesenteric hypoperfusion alone, but is speculated to be related to proinflammatory mediators. An in vivo study using a 30% TBSA rat burn model confirmed that there was increased bacterial translocation and permeability to macromolecules that peaked at 18 hours post injury, lending credence to the idea that disruption of intestinal barrier integrity in severe burns can lead to sepsis from bacterial translocation. Thus, interventions aimed at preventing splanchnic hypoperfusion and hypermetabolism may circumvent complications associated with severe burns.

Fig. 37.1, Schematic representation of the role of the gastrointestinal tract in multiorgan sepsis after cutaneous burn injury.

Paralytic Ileus

Intestinal ileus is a commonly encountered condition following large burns. Multiple factors contribute to the development of ileus in burn patients, including electrolyte imbalances, narcotic use, prolonged immobilization, abdominal trauma, sepsis, and surgery. In addition, proinflammatory cytokines and proteins that are elevated as part of the postburn systemic response, such as interleukin (IL)-1α, IL-6, tumor necrosis factor (TNF)-α, p38 mitogen-activated protein kinase, and endothelins have been found to be linked to altered intestinal permeability. Electrolyte disturbances, opioids use, prolonged immobilization, abdominal trauma, sepsis, and surgery are factors that can result in decreased GI motility in burn patients

Cramping abdominal pain, abdominal distension, and intolerance to enteral feedings are the most common symptoms. The cause of ileus should be thoroughly evaluated because it may represent an early indicator of systemic sepsis and can ultimately help direct care. Physical examination must be performed to rule out fecal impaction and to identify signs of peritonitis associated with more serious complications such as acute colonic pseudo-obstruction, also known as Ogilvie's syndrome. The treatment of ileus involves correction of electrolyte derangements and adequate hydration; implementing these basic measures in burn patients can be difficult due to the pathophysiologic changes that occur after severe.

Ogilvie's Syndrome

Ogilvie's syndrome, first described in 1948, is characterized by massive colonic dilation without a mechanical cause for obstruction. This entity has been well described in burns, with a reported incidence of 0.3%. Clinical presentation includes insidious and progressive abdominal distension. Some patients may report a history of diarrhea prior to the onset of distension. Nausea, vomiting, and bowel sounds are not reliable indicators of this condition. Mild abdominal pain can develop as distension increases. Diagnosis and management of pseudo-obstruction require that mechanical bowel obstruction be absolutely excluded. Radiologic studies showing colonic air in all colonic segments, including the rectum, are warranted before considering pharmacologic therapy.

The goal of the management is to decompress the colon in order to minimize the risk of colonic perforation and ischemia, which are associated with high mortality. Close monitoring including serial physical examinations and plain abdominal radiographs every 12–24 hours to evaluate colonic diameter are recommended. Initial management is conservative in patients without significant abdominal pain, severe colonic distension (>12 cm), or signs of peritonitis. In patients with cecal diameter of greater than 12 cm or who have failed 24–48 hours of supportive management, intravenous neostigmine can be used. In patients who fail or who have contraindications to neostigmine, colonic decompression is indicated. Acute colonic pseudo-obstruction secondary to opiates can benefit from methylnaltrexone prior to decompression. Endoscopic decompression is the preferred method to decompress the colon; surgical decompression (e.g., surgical cecostomy) is performed if endoscopic decompression and pharmacologic therapy fail or if there is evidence of perforation or signs of peritonitis. Percutaneous cecostomy should be reserved for patients who are not surgical candidates.

Abdominal Compartment Syndrome

ACS refers to the onset of new organ dysfunction caused by increased intra-abdominal pressure. Intra-abdominal pressure measurements have allowed grading of ACS; however, for clinical purposes, ACS is defined as new organ dysfunction secondary to increased intra-abdominal pressure without a strict threshold. Aggressive fluid resuscitation, severe burns (>30% TBSA), and sepsis increase the risk for ACS. Secondary ACS is commonly related to the extent of volume resuscitation. For this reason, the amount of fluid being administered and the development of early signs of ACS should be closely monitored. Mortality for patients who have progressed to ACS ranges from 40% to 100%.

Nearly all patients have a tense and distended abdomen; however this clinical finding is a poor predictor of ACS. Oliguria and increased ventilator requirements are common in patients with ACS. Tachycardia, hypotension, jugular venous distension, and peripheral edema can also be found. Imaging studies are not helpful to diagnose ACS; however expected findings include decreased lung volumes, atelectasis, or elevated hemidiaphragms in chest radiographs. Compression of the inferior vena cava, massive abdominal distension, renal compression or displacement, bowel wall thickening, and bilateral inguinal herniation can be demonstrated in CT of the abdomen.

Management of ACS consists of supportive care and surgical abdominal decompression. However, in patients with abdominal burns, mechanical limitations due to burn eschars can be a significant contributing factor for increased intra-abdominal pressure; thus early escharotomy is advocated. Supportive care includes measures that can decrease intra-abdominal pressure, such as evacuation of intraluminal contents (e.g., nasogastric and rectal drainage) and improvement of abdominal wall compliance (supine positioning without head elevation, adequate pain control and sedation, chemical paralysis).

Surgical decompression is the definitive management of ACS; however a specific threshold for decompression has not been defined. Several factors can be considered to decide the need for this intervention, including progression of organ dysfunction after supportive measures, intra-abdominal pressure of greater than 25 mm Hg, or abdominal perfusion pressure (difference between the mean arterial pressure and the intra-abdominal pressure) of less than 50 mm Hg. Decompression is achieved by making a midline incision through the linea alba to open the abdominal cavity. A temporary abdominal wall closure is often used to maintain an open abdomen.

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