Introduction

Various surgical complications can occur in burn patients, resulting from pathologic progression of the burn injury itself to 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 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 pancreatitis. In this patient population, the cause for occult systemic sepsis is frequently attributed to GI sources, as evidenced by the development of acute cholecystitis, ischemic bowel, hollow viscus perforation, and intra-abdominal abscess. Necrotizing enterocolotitis 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 can occur during the acute phase of massive fluid resuscitation in large TBSA burned patients. Based on determination of increased intra-abdominal pressures, a decompressive laparotomy may be necessary to prevent further end-organ damage (cardiovascular collapse, oliguria, elevated peak pressures, and intestinal ischemia). A major burn significantly affects hemodynamics, and invasive monitoring may be necessary. As a consequence, catheter-related vascular 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 and is associated with poor outcomes.

Because of delays in diagnosis and treatment, there is a substantial increase in morbidity and mortality associated with non-thermal complications in burn patients. As such, these secondary and sometimes fatal complications demand immediate recognition and treatment. Patients who suffer major burn injury need diligent care and attention throughout their hospital course to avoid complications arising from various organ systems. This chapter reviews the frequently encountered general surgical, non-thermal 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.¹ A retrospective study examined upwards 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%),² consistent with the National Trauma Data Bank and National Burn Repository data. Although there was no difference in length of stay, injury severity scores, or mortality among burn or trauma patients alone, there were significant increases in inhalational injury, length of stay, and mortality in patients suffering from combined injuries (Table 37.1). This increase in mortality was seen despite similar TBSA burns, demonstrating the additive effects of trauma and burns in these patients.² In particular, approximately 24% of military burn injuries are associated with concurrent traumatic injuries, compared to the 2–7% of burn/trauma injuries found in civilians in the same study.³ The most common civilian cause of burn/trauma injury remains motor vehicle collisions (MVC). Of the 500 000 individuals in the United States treated for burn injuries, an estimated 7.2% are secondary to street or highway accidents (American Burn Association, National Burn Repository 2009). MVA victims that require extrication and those that are ejected typically have the most severe multitraumatic injuries. 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 bones.

Table 37.1 Increased morbidity and mortality with combined burn and trauma ¹

Primary assessment

In trauma patients with multiple organ system injuries, the shocking appearance of the burn injury may unduly shift attention away from the other seemingly underwhelming injuries, resulting in delays in diagnosis. The initial assessment of patients with combined thermal and other traumatic injuries should center 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 injuries are common in burn patients. Some of the common signs of inhalational injury include cough, stridor, singed nasal hair, carbonaceous sputum, and a hyperemic oropharynx. Asphyxia can be seen with carbon monoxide and cyanide poisoning, for which pulse oximetry is an unreliable measure of oxygenation. If the respiratory distress is significant, intubation or a surgical airway may be required, and although hypoxemia is usually evident, the inhalational injury can evolve over hours such that an initial chest radiograph and arterial blood gas may be normal. Smoke inhalation induces a multitude of physiologic changes which result in increased vascular permeability and pulmonary edema, infiltration by leukocytes, and bronchorrhea. Therefore, it is not unusual for patients to escalate to unconventional modes of ventilation, such as volumetric diffusive ventilation.

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 rib fractures, 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.

Associated injuries

Burns may also be associated with other traumatic injuries. The cervical spine should be considered unstable until a complete evaluation has been performed. Unstable cervical spine fractures may be managed appropriately with traction via halo or tongs. When necessary, intracranial pressure monitoring via a bolt placed through unburned scalp is preferred over a ventriculostomy. If a neurosurgical procedure is required, debridement of the scalp and non-viable tissue is completed at the same time as the craniotomy.

Orthopedic injuries – primarily fractures – comprise the most commonly associated traumatic injury in thermally injured patients. The burn surgeon and the orthopedist must coordinate the optimal management of these patients. Therapeutic decisions are based upon the following considerations: stability of the fracture, the need for excision and grafting of the burn, access required for adequate burn wound care, and early aggressive physical therapy after the injury. Although fractures away from the burns may be managed with reduction and casting, in cases where fractures are associated with severe soft tissue damage, internal fixation should be performed within 24–48 hours, prior to bacterial colonization of the wound. All open fractures must have incision and drainage performed in the operating room within 24 hours of the injury, and when open reduction occurs through a burn, the wound should only be closed to the level of fascia without drain placement. Using this approach, early aggressive fracture treatment has been shown to reduce orthopedic complications without further risks of infection, poor healing, or amputation. Antibiotic coverage should be provided as deemed appropriate for the orthopedic injury.

The diagnosis of intra-abdominal injury may prove difficult, as the abdominal examination is rather unreliable in the face of a severe burn. In addition, hemodynamic changes that occur with an intra-abdominal injury can be masked by the physiologic response seen with intravascular volume shifts and the exaggerated inflammatory response. Nonetheless, imaging modalities that are currently used to evaluate trauma patients with blunt or penetrating mechanisms should also be considered when evaluating a burned patient with a suspected intra-abdominal injury. Diagnostic laparoscopy can be a helpful adjunct in the evaluation of various intra-abdominal injuries, such as bowel perforation and ischemia, that are difficult to diagnose with computed tomography (CT) alone. However, adequate abdominal CO₂ insufflation is often difficult to achieve in patients with significant eschar of the trunk. If laparotomy is warranted, dehiscence of abdominal wounds is a frequent complication, independent of whether or not the burn wound was traversed. If abdominal wall closure demonstrates significant tension, the use of retention sutures should be considered. Occasionally, a temporary abdominal closure may be required to prevent abdominal compartment syndrome. In cases where the bowel becomes massively edematous, a vacuum-pack for the open abdomen will act as a temporizing measure for a delayed abdominal wall closure.

Vascular injuries may be difficult to diagnose in the presence of burned skin, significant soft tissue edema, compartment syndrome, or hypotension. The principles in their diagnosis remain the same, with an assessment of capillary refill, neurologic deficits, and palpable pulses. A Doppler ultrasound is a non-invasive bedside study that can easily be performed to assess adequacy of arterial blood flow and can be supplemented with an ankle–brachial index (ABI). However, the data, especially the ABI, can be difficult to interpret when extremities are burned full thickness or circumferentially. Although conventional angiography continues to be the gold standard in the diagnosis of major vascular injuries, its benefits do not seem to outweigh its invasive risks in the era of CT angiography. One study found that CT angiography had a >95% sensitivity and specificity in the diagnosis of traumatic arterial injuries of the extremity, with poor arterial opacification being a disadvantage.⁴ Thus, CT angiography is a reasonable tool in the diagnosis of major vascular injuries. Should a vascular insult require repair, substantial consideration should be given to the choice of graft (autologous versus synthetic), as contamination is not infrequent and only complicates the care of these critical patients. The liberal use of prophylactic muscle flaps for graft coverage has proved helpful.

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 >30% TBSA produce a physiological response leading to systemic shock, hypermetabolism, and widespread immunosuppression.⁵ The combination of intravascular fluid loss, vasoactive hormone release, catabolism, and immune dysfunction results in the non-thermal complications of burn injuries and has consequently become the focus of preventative treatment and molecular models in the design of future therapies.

Physiological changes in blood flow have a dramatic effect on organ response to injury, healing, and permanent dysfunction. 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 selective decrease in splanchnic blood flow.⁶ 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.^7,⁸ The GI tract ischemia has multiple effects, including ulcer formation (Curling’s ulcer), enterocolitis, and acalculous cholecystitis secondary to gallbladder ischemia and bile stasis. Other abdominal organs, such as the kidneys and liver, may endure end-organ damage when exposed to the ‘low-flow’ state associated with hypoperfusion following burns, leading to surgical complications and worsened outcomes.

The hypermetabolic response to burn injury plays a key role in non-thermal complications and is characterized by catabolic metabolism, hyperdynamic circulation, insulin resistance, delayed wound healing, while increased risk of infection.⁹ Poor fibroblast function contributes to impaired wound healing, while leukocyte dysfunction and reduced cellular immunity cause immunological compromise. Alterations in stress hormone responses, cardiac output, lean body mass, and sex hormones may persist for several years post burn. Previous studies have demonstrated typical stress responses to a variety of traumatic injuries, with a so-called ‘ebb’ phase resulting in a decrease in metabolism and tissue perfusion, followed by a ‘flow’ phase 3–5 days following injury.¹⁰ Early enteral feeding has been shown to blunt the hypermetabolic response.¹¹

Of all the potential mechanisms of injury, severe burns result in the most dramatic metabolic response. The hypermetabolic phase results in the activation of the hypothalamopituitary axis, sympathetic outflow, the acute-phase response that promotes fat and protein breakdown, and gluconeogenesis.¹² Excessive catabolism following a burn injury encourages hyperglycemia and insulin resistance within the first week after injury, both of which are associated with an increase in morbidity and mortality in severely burned patients. Recent trials have demonstrated that intensive insulin therapy aimed at maintaining a daily average glucose of 140 mg/dL improves immune function and reduces sepsis, along with an attenuation of the inflammatory and acute-phase response.^13,¹⁴ As such, tight glucose control is thought to be critical in improving the overall recovery of burn patients.

As mentioned, 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). Numerous studies have demonstrated the association between massive cutaneous burn injury and bacterial translocation.^8,¹⁵ 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 produced by the burn wound.¹⁵ An in vivo study using a 30% TBSA burn model in rats 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.¹⁶ Thus, interventions aimed at preventing splanchnic hypoperfusion and hypermetabolism may circumvent complications associated with severe burns.