UNUSUAL COMPLICATIONS OF ACUTE NECROTISING PANCREATITIS

UNUSUAL COMPLICATIONS OF ACUTENECROTISING PANCREATITIS: A Report of Three Cases

BHAAMA S ACHARYA*, SANJAY NAGRAL**
*Lecturer; **Ex-Associate Professor, Department of General Surgery, King Edward VII Memorial Hospital,Mumbai 400 012.

We report three patients of acute pancreatitis with unusual complications. One had multiple splenic haematomas, another developed a colonic fistula and the third had pancreatic ketoacidosis. All three patients developed their complications in their second week, after a period of initial apparent stability. They were all treated surgically for infected pancreatic necrosis and for regional complications as indicated. All three succumbed to multi-organ system failure.

In patients with pancreatic necrosis, development of loco-regional and systemic complications is associated with a high mortality rate. These three cases are a reminder of the uncommon presentations, and the need for a high degree of awareness and suspicion to enable early intervention.

INTRODUCTION

Acute necrotising pancreatitis is a deadly disease with high morbidity and mortality. Its presentation is fairly typical and management strategies are now well elucidated. Sometimes the disease presents with unusual delayed manifestations as a result of loco-regional or systemic complications. We report three such patients seen in our department over a two-year period.
CASE REPORTS

CASE 1

A 45-year old man who presented with acute abdomen was diagnosed as acute alcoholic pancreatitis in another hospital, and was discharged after eight days of treatment, since he had an apparent recovery. There was no preceding history of trauma. He was apparently alright for two days at home. Following this, he presented to us with acute left hypochondrial pain, fever and left pleural effusion. A contrast-enhanced computed tomogram (CECT) of the abdomen revealed extensive pancreatic necrosis with splenomegaly and multiple patchy hypodensities with no contrast enhancement, suggestive of intrasplenic haematomas (Fig. 1). Since the patient continued to have signs of sepsis on conservative management, he was explored and drainage of peripancreatic and interloop abscesses was done with placement of multiple drains. Splenectomy had been planned but could not be done due to extensive adhesions and bleeding. The patient subsequently deteriorated and died due to multi-organ system failure (MOSF) on post-operative day three.

CASE 2

A 40-year old chronic alcoholic male presented to us with acute epigastric pain radiating to the back. The clinical suspicion of pancreatitis was confirmed by an ultrasound (USG) of the abdomen, which showed a bulky pancreas. He made an apparent recovery in our intensive care unit and was started on full orals gradually. He remained stable for 8 days and had no obvious signs of sepsis. However on day 10 of his stay, he developed diarrhoea and bleeding per rectum, which was initially treated as infective diarrhoea. He had no significant abdominal or systemic signs at the time. Patient did not respond to the therapy and developed tachycardia, hypotension, abdominal distension and tenderness. A CECT abdomen revealed extensive pancreatic necrosis, with an area in the transverse colon strongly suspicious of a colo-pancreatic fistula (Fig. 2). On exploratory laparotomy, there was an area of transverse colonic necrosis with perforation and fistulation into the lesser sac, with infected pancreatic necrosis. Patient underwent a colonic resection, with colostomy, pancreatic necrosectomy and placement of multiple drains. In spite of appropriate antibiotics and intensive care, patient continued to show signs of sepsis and succumbed to MOSF.

CASE 3

A 20-year-old non-smoker, teetotaler man presented with acute upper abdominal pain of one-day duration. After a chest radiograph (including both domes of diaphragm) ruled out a perforated viscus, a USG abdomen was done, which showed a bulky, inflamed pancreas and no gallstones. He was diagnosed to have acute idiopathic pancreatitis. He made an apparent recovery and was started on full orals. On day eight of his hospital stay, he developed severe tachypnoea and acidotic pattern of breathing. Arterial Blood Gases (ABG) revealed severe acidosis. The urine ketones were found to be in large quantity, with a normal random blood sugar. The ketoacidosis persisted for 48 hours despite appropriate corrective measures, while the sugar level remained persistently normal. A CECT abdomen revealed extensive pancreatic necrosis with air in the peripancreatic area. The patient was explored and necrosectomy with placement of drains was performed. However the patient continued to be septic and expired five days after the surgery.

Fig. 1: Pancreatic necrosis with multiple intrasplenic hematomas.

Fig. 2: Area suspicious of colo-pancreatic fistula with central pancreatic necrosis seen.

DISCUSSION

Necrotising pancreatitis is seen in 15% of patients with acute pancreatitis.[1] It has a typical presentation and should be suspected in any patient with a fulminant clinical course and persistent MOSF, especially one that is non-responsive to intensive medical therapy. In a majority of patients with pancreatic necrosis loco-regional complications have been reported to occur after operation.[2] Most of these can be managed conservatively. However, local complications may also result from erosion by the necrotic process itself and adversely affect outcome.

Splenic involvement in acute pancreatitis is rare. The lesions described include haematomas, infarction, rupture, erosion of splenic artery or thrombosis of splenic vein;[3,4] these may occur due to discussion of pancreatic secretion into the splenic hilum. Splenectomy is usually required.[3]

Colonic complications develop in about 2% of patients, and include ileus, fistula formation, perforation and colonic necrosis.[5] Although colonic involvement is well described, spontaneous direct fistulisation as seen in the above case is rare. Mortality rates for colonic fistula may exceed 50%.[6] The accepted treatment is resection of nonviable colon and proximal colostomy, which was done in our patient.

Kabadi[7] has described ketonaemia in acute pancreatitis, in a report of three patients. When the ketoacidosis is not due to the other well-known factors such as ethanol, diabetes mellitus or prolonged starvation, it is thought that the ketogenesis is promoted and maintained by extremely high circulating pancreatic lipase concentration. In our patient, although we were not able to obtain concomitant serum lipase levels, we believe this may have been the mechanism, since other factors were ruled out. Since some patients with necrotising pancreatitis could have acidosis due to other factors, it would be important to keep in mind ‘pancreatic ketoacidosis’ as one of the rare causes.

In all the three patients, there was an apparent period of recovery lasting 1-2 weeks before these unusual complications set in. This led to diagnostic dilemma and may be delay in treatment. The increased awareness of the existence of such complications can prevent the delay in aggressive and timely management.

REFERENCES

1.Shah SR, Nagral SS. Surgical management of acute pancreatitis. Bombay Hosp J 1997; 39 : 542-7.

2.Choudhary A, Dhar P, Sachdev A, et al. Surgical management of pancreatic necrosis presenting with local complications. Br J Surg 1997; 84 : 1-4.

3.Warshaw AL, Chesney TM, Evans GW, et al. Intrasplenic dissection by pancreatic pseudocysts. N Engl J Med 1972; 287 : 72-5.

4.Shafiroff BB, Berkowitz D, Li JK, et al. Splenic erosion and hemorrhage secondary to pancreatic pseudocyst. A review of the literature and additional case report. Am J Gastroenterol 1977; 68 : 145-53.

5.Abcarian H, Eftaiha M, Kraft AR, et al. Colonic complications of acute pancreatitis. Arch Surg 1979; 114 : 996-1001.

6.Schein M, Saadia R, Decker G. Colonic necrosis in acute pancreatitis. A complication of massive retroperitoneal suppuration. Dis Colon Rectum 1985; 28 : 948-50.
7.Kabadi UM. Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis. Postgrad Med J 1995; 71 : 32-5.

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Fig. 1: Pancreatic necrosis with multiple intrasplenic hematomas.	Fig. 2: Area suspicious of colo-pancreatic fistula with central pancreatic necrosis seen.