Acute pancreatitis and necrotizing colitis following extensive burn injury

Abstract

Case

We describe a patient with severe pancreatitis and ischemic colitis after extensive burn injury. An 81‐year‐old man presented with a 55% total body surface area burn with inhalation injury. A low‐density area was detected in the pancreas on the abdominal computed tomography scan on admission. The clinical course of the patient was good until 28 days after injury when he complained of abdominal pain and distension. Abdominal computed tomography revealed acute pancreatitis and ischemic colitis.

Outcome

The patient died 59 days after burn injury.

Conclusions

Extensive burn injury can cause acute pancreatitis. Further work‐up is necessary to identify pancreatic complications after severe burn injury.

Introduction

Extensive burn injury is accompanied by many complications, such as burn‐induced compartment syndrome, acute kidney injury, and burn sepsis. Pancreatitis, however, is an unusual complication with burn injury. To the best of our knowledge, only two reports of postburn pancreatitis have been documented in Japanese published works.1, 2 Here, we report a patient with severe pancreatitis after extensive burn injury who then developed ischemic colitis.

Case

A previously well 81‐year‐old man suffered 55% total body surface area burns (30% 2nd degree burns and 25% 3rd degree burns) to the face, neck, trunk, and lower limbs with associated inhalation injury in a fire while at work. There were no witnesses, but some kind of explosion was suspected. Initial fluid resuscitation and intubation were carried out at the receiving hospital, and the patient was transferred to our center for further management. Because the patient was intubated and sedated, we could not take the detailed history of injury or physical findings. So we decided to carry out computed tomography (CT) as screening for trauma. The patient, who did not drink alcohol and had no obvious history of trauma, had a low‐density area in the pancreas detected by abdominal CT on admission (Fig. 1) and no amylase elevation. The clinical course of this patient, which included four sessions of debridement and grafting, was good until 28 days after the injury, when he began to complain of abdominal distention. Peritoneal fluid was detected by ultrasonography, and abdominal CT revealed a pancreatic pseudocyst without either biliary duct dilatation or gallstones. Until 28 days after injury, the patient was not given any medication that could induce pancreatitis on drug information sheets. He had no history of hyperlipidemia and a value of serum triglyceride on the day of 76 mg/dL. On day 43, his serum amylase level, white blood cell count, and C‐reactive protein level were increased (Fig. 2), and repeat abdominal CT revealed portal air and partial ischemia of the ascending colon (Fig. 3). On day 44, the patient had voluminous rectal bleeding and went into shock. Diagnostic colonoscopy revealed mucosal necrosis, and a laparotomy was carried out. We observed no findings suggestive of serosa necrosis. The amylase level in the peritoneal fluid collected during the operation was high (5,840 IU/L). On day 56, the patient had massive rectal bleeding again, and on day 59, the patient died.

Figure 1.

Abdominal computed tomography image of an 81‐year‐old man on the first day after extensive burn injury. The white circle indicates an area of low density in the pancreas.

Figure 2.

Changes in serum amylase levels, white blood cell counts, and C‐reactive protein levels throughout the clinical course of an 81‐year‐old man treated for extensive burn injury. After 40 days, levels of serum amylase and C‐reactive protein were increased. These increases may have represented the development of acute pancreatitis and ischemic colitis.

Figure 3.

Peritoneal fluid, portal air, and partial ischemic change in the ascending colon on abdominal computed tomography in an 81‐year‐old man 43 days after extensive burn injury. White arrows indicate air in the portal vein (A), superior mesenteric vein (C), and right colic vein (D). The white circle (B) indicates a ruptured pancreatic pseudocyst. These findings are suggestive of acute pancreatitis and ischemic colitis.

Discussion

There are two clinically important issues relating to this case. Pancreatitis can develop after extensive burn injury, and a low‐density area detected in the pancreas on CT early after injury may predict the development of pancreatitis.

First, postburn pancreatitis is relatively uncommon in Japan.2 A retrospective review of 121 adult burn patients identified elevation of amylase and lipase levels in 40% (49/121) of the patients with large burns (≥20% total body surface area). Of these patients, most (40/49) had symptoms of pancreatitis, and three had pancreatic pseudocysts or abscesses.3 A recent study examining pediatric burn patients found an incidence of acute pancreatitis of 0.05%.4 Despite its rarity, acute pancreatitis is associated with a significant increase in mortality.3, 4 Severe pancreatitis can cause non‐occlusive mesenteric ischemia5 leading to ischemic colitis, which results in high mortality in burn patients.

Second, pancreatic pseudocysts usually appear several weeks after the onset of pancreatitis and usually resolve spontaneously.6 In our patient, the low‐density area seen at the first presentation was not accompanied by amylase elevation. This area could have represented a pancreatic pseudocyst, pancreatic cyst, or other tumorous lesion. Unfortunately, we did not investigate this low‐density area further because of the patient's severe burn injury. The low‐density area and the pancreatic pseudocyst that developed later were located the same area in the pancreas. To the best of our knowledge, there are no reports on the timing of pancreatic pseudocyst development after burn injury, so the present case might shed some light on the importance of early diagnosis, which may lead to adequate treatment.

In general, acute pancreatitis after extensive burn injury is an under‐recognized complication and is easily missed. Pancreatitis seems more likely to occur in patients with inhalation injury, deep burns, and associated trauma. Importantly, the pancreatitis develops 3–4 weeks after burn injury with onset of infection.3 The etiology of postburn pancreatitis is not fully understood. One reason why postburn acute pancreatitis develops is thought to be that pancreatic ischemia occurs as a result of hypovolemia due to extensive burn injury.1, 2, 3, 4 According to this theory, acute pancreatitis should develop soon after burn injury. We speculate that pancreatic ischemia occurring after burn injury can trigger pancreatic injury, and bacteremia induced by burn sepsis can cause infection in the injured pancreas that leads to the development of postburn acute pancreatitis. Management of acute pancreatitis in the burn patient is the same as that in non‐burn patients. However, in the burn patient, invasive management such as necrosectomy or drainage can increase the risk of infection due to burn wounds. Continuous regional arterial infusion therapy7 and/or early venovenous hemofiltration might be considered.8 Due to the difficulty of medical treatment, prevention and early recognition of pancreatitis after severe burn injury are extremely important.

The course of our patient provides four clinical suggestions: (i) acute pancreatitis can developed after severe burn injury, (ii) abnormal presence of peritoneal fluid can indicate the development of acute pancreatitis, (iii) postburn acute pancreatitis can lead to ischemic colitis, (iv) a low‐density area detected on CT in the early phase after burn injury might predict postburn pancreatitis.

In conclusion, this case reminds clinicians of the necessity of detailed examination to identify potential pancreatic complications in extensive burn patients.

Conflict of Interest

None.