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2024 | Volume 25 | Issue 2

General Surgery

 

Case summary

Case summary

A 74-year-old woman with comorbidities including chronic obstructive pulmonary disease, obesity, and associated metabolic syndrome was admitted to the emergency department after several hours of severe acute upper abdominal pain with nausea and vomiting.

She had contacted emergency services 9.5 hours earlier. On arrival, the patient was pale, tachycardic and hypertensive. She was triaged as Category 2 but not reviewed medically until two hours later. At that time, she was noted to be dehydrated. She remained tachycardic and tachypnoeic, likely from acute pancreatitis with a mild acute renal injury (lipase 1,500 units/L, creatinine 90 mmol/L, white cell count 17 x109/L, C-reactive protein 80 mg/L).

The patient was assessed by the acute surgical unit. The initial diagnosis of severe acute pancreatitis was confirmed, and a care plan implemented including fluid resuscitation, monitoring of urine output, abdominal computed tomography (CT) scan (with contrast) and an upper abdominal ultrasound (to detect cholelithiasis or choledocholithiasis). Her initial CT revealed severe extensive (75 per cent) acute necrotising pancreatitis from an unknown origin, with suspicion of non-occlusive superior mesenteric vein (SMV) and splenic vein thrombosis. Bilateral lower lobe atelectasis was noted based on abdominal CT findings. There was no cholelithiasis or choledocholithiasis observed on ultrasound; liver function was normal.

The patient was referred to a hepatobiliary specialist team. Supportive care in the intensive care unit was recommended, with fluid resuscitation without anticoagulation due to the concern of haemorrhagic pancreatitis. She developed systemic inflammatory response syndrome (SIRS) with multiple organ dysfunction that progressed to multiorgan failure. She became disoriented and had abdominal pain, distension, high bile aspirate via a nasogastric tube, and increased intra-abdominal pressure (IAP) (12.6 mm Hg). She became anuric and hypotensive and developed acute respiratory distress syndrome. She required ketamine, intubation for ventilation, renal dialysis and vasopressors. She commenced on meropenem (later changed to piperacillin/tazobactam after Enterococcus was cultured) and fluconazole due to concerns of complicating infected necrotic pancreatitis, despite no gas in the retroperitoneal cavity or pancreas on repeated abdominal CT scan on day 3 of hospitalisation, and normal procalcitonin.

The patient was weaned from sedatives between days 8 and 10 and was extubated on day 11. Her multiorgan function slightly improved and vasopressors were ceased.

On day 13 of admission, the patient suddenly became hypotensive and anaemic. She had a tense and distended abdomen with evolving severe extensive necrotic pancreatitis with early encapsulation, peripancreatic fluids but no drainable collection, non-occlusive proximal SMV thrombosis, newly iatrogenic nearly occlusive right external iliac and common iliac veins, and bi-basal pneumoniae. Following a multidisciplinary meeting and counselling of the family, the patient was provided with palliative care and died on day 15.

Discussion
This case highlights the significant mortality of severe acute necrotic pancreatitis with persistent (>48 hours) single or multiorgan failure as defined by the revised Atlanta classification or by determinant-based classification.1, 2 This is also consistent with the abdominal CT severity index of Balthazar et al, where extensive pancreatic oedema, swelling, peripancreatic stranding and fluids with >50 per cent necrotic pancreas would yield a score of 9/10, predicting 92 per cent morbidity and 17 per cent mortality.3 It does not account for the advanced age and significant comorbidities of the patient, which compounded the fatality in this case.

It is unclear when fluid resuscitation commenced. It is well known that early optimal fluid resuscitation is crucial to prevent microcirculatory collapse (thereby preventing the development of mild pancreatitis to severe pancreatitis with initial SIRS), then to sterile pancreatic necrosis, and further to infected pancreatic necrosis and ultimately death.

There were significant delays in intervention at multiple stages of this case, even though they may not have affected the eventual outcome:
•    initial delay in calling the ambulance, followed by further significant delays in ambulance attendance
•    patient triaged as Category 2 (to be seen within 15 minutes) on admission, but not medically assessed until after 120 minutes (Category 4).

Clinical lessons
For scenarios of persistent increased IAP (and associated multiorgan failure), the development of acute compartment syndrome (IAP >20 mm Hg) should be questioned. Decompressive laparotomy and simultaneous open necrosectomy and drainage of ongoing pancreatic leak from unstable ductal anatomy of necrotic pancreatic neck would be options worth considering, despite a trend away from invasive, early open necrosectomy toward a step-up approach (endoscopic, percutaneous, videoscopic, laparoscopic late necrosectomy). However, this would be a final attempt to save a patient in a critical condition, particularly if the patient was young with no pre-existing conditions. It was not applicable for the patient in this case.

References
1.    Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62(1):102–11.
2.    Dellinger EP, Forsmark CE, Layer P, Levy P, Maravi-Poma E, Petrov MS, et al. Determinant-based classification of acute pancreatitis severity: an international multidisciplinary consultation. Ann Surg. 2012;256(6):875–80.
3.    Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174(2):331–6.