Case Report: Acute pancreatitis as a complication for the use of furosemide during transurethral resection of the prostate

Introduction

Acute pancreatitis caused after transurethral resection of the prostate (TURP) is an uncommon complication, with few reports found in the literature. It usually occurs in those who develop TURP syndrome¹.

The prognosis depends on suspicion of this complication in a timely manner because it lead to multi-organ failure and even death¹.

The case presented herein describes the case of a middle-aged patient who develops pancreatitis after TURP. The report describes how this was managed, the treatment used, and a review of the literature to identify similar cases.

Clinical case

A timeline of the patient’s case can be seen in Figure 1.

Figure 1. Timeline of the important points in the patient’s medical history, interventions and follow-up.

Diagnostic assessment

At 24 hours post-surgery, the patient presented elevation of azoles (Cr = 3.7mg/dl; Urea = 92 mg/dl) and oliguria, therefore furosemide 20mg was administered twice a day. After 72 hours of follow-up, the condition persisted, and it was decided to increase treatment with furosemide to 20 mg EV three times a day; despite this, it evolves in an unfavourable manner. On the fifth day after surgery, elevation azoles continued (Cr = 12.43 mg/dl; Urea = 235mg/dl), and there was also an increase in pancreatic enzymes (Amylase = 329U/L(Normal value <105); Lipase = 304U/L(Normal value: <50) ; leukocytes = 20880ml/mm3 ( Normal value = 4500 ml/mm3 to 10500 ml/mm3). The aggregate infectious process was improved. An abdominal-pelvic CT scan was performed, finding a slight increase in the density of peripancreatic mesenteric fat with the presence of low laminar free fluid (Figure 2). The patient was transferred to the Intensive Care Unit (ICU) for emergency dialysis and stabilization.

Figure 2. Abdominopelvic CT scan.

Pancreas is not increased in size, no pancreatic necrosis, no peripancreatic collections. Slight increase in the density of mesenteric fat. Presence of low laminar free liquid.

Discussion

Acute pancreatitis is an inflammatory disease of the pancreas that can also involve neighbouring tissues or organs, with a highly variable clinical presentation. In some cases, it has significant morbidity and mortality^1,2; 20% of patients adopt a severe evolutionary course, with persistent organ failure leading to mortality in 25%. The reported age range is between 50 and 75 years, as the incidence of acute pancreatitis increases with age^1,2.

Approximately 80–90% of cases are due to alcohol consumption and gallbladder lithiasis, while 10–20% have variable aetiology, including idiopathic, hyperlipaemias, viral infections, impaired pancreatic perfusion, ductal obstructions, drugs, and hypercalcemia^3,4.

Drug-associated pancreatitis is an underreported entity with an incidence of 0.1 to 2%⁵. Drugs that have been associated with causing pancreatitis that have been reported in the literature include antihypertensive agents, proton pump inhibitors, anticonvulsants, and chemotherapeutic agents⁵.

Lesions in the pancreatic tissue is caused by aggressor factors (drugs, infection, or metabolic disorder) and by the secondary activation of digestive zymogens within acinar cells, which trigger a subsequent inflammatory response³. The mechanisms by which these complications develop are not fully understood, but intestinal endotoxins and inflammatory mediators play an important role¹.

The diagnosis of drug-associated pancreatitis is by exclusion, so it is recommended to use the “Naranjo Scale of drug adverse reaction probability” in order to calculate the probability of adverse drug effect (Table 1). In 1981 Naranjo et al. validated this scale for cases of adverse drug reactions. In our case, the total score of our patient was 5 (answered affirmatively in questions 1, 2, 3 and 10), classified as probable in relation to furosemide⁶.

Drugs such as furosemide have been described that could damage pancreatic perfusion by decreasing intravascular volume, affecting blood flow, producing ischemia and the subsequent development of acute pancreatitis. It may also stimulate the exocrine pancreas producing a hypersensitivity reaction^1,6,7.

In our patient, Valsartan was suspected of having contributed to the presentation. However, due to the prolonged exposure time, it was dismissed as a possible aetiology.

In the literature, risk factors associated with drug pancreatitis have been described, of which our patient presented advanced age and vascular risk factors. As a result of these factors an increase in pancreatic toxicity may have occurred, due to atherosclerosis of mesenteric vessels, resulting in furosemide making the perfusion worse by diuresis and intravascular volume depletion⁸. However, the exact mechanism is not yet known. However, some hypotheses include that furosemide could stimulate exocrine secretion of the pancreas, or mechanisms of hypersensitivity or immune response against a drug-protein. As evidenced in multiple reports, there are many confounding factors, but they only increase pancreatic susceptibility. In our case, the precipitating event is the administration of furosemide.

The present patient did not present capsule perforation or post-surgery bleeding. Berber-Deseusaa et al. present the case of a patient who presents capsule perforation during the intraoperative period¹. In our case, pancreatitis was mild, presenting improvement on the eighth post-surgery day after dialysis. However, the case reported by Berber-Deseusaa et al. presented severe necrotizing pancreatitis, leading to the death of the patient¹.

Acute pancreatitis is an infrequent complication reported after TURP^1,9–11; it can delay diagnosis if it is not considered as a possibility¹. In our patient, the surgery was without complication, unlike previous cases presented in the literature where capsule perforation was observed¹. The present surgical time was 55 minutes.

On the other hand, the evolution of our patient was favourable in contrast to what was presented by Berber et al., where the two patients presented unfavourable evolution with acute renal failure, ventilatory-circulatory deterioration, and death¹.

Conclusions

The clinical features of pancreatitis following TURP surgery has been reported previously in the literature but infrequently. This condition should be suspected when dealing with pain in the epigastrium post TURP. If this complication is suspected, imaging tests and pancreatic enzyme levels should be immediately requested, as it can have an unfavourable evolution until death.

Data availability

All data underlying the results are available as part of the article and no additional source data are required.

Consent

Written informed consent for publication of their clinical details and clinical images was obtained from the patient.