Don't mess with the Pancreas

A 47-year-old female with epigastric abdominal pain and nausea presents to the ER for evaluation. She is an otherwise healthy female, with no prior surgical history. On further questioning, her pain started 3 days ago and radiates toward her back. It has persisted and wasn't relieved with over-the-counter Tums, Gas-X, and Pepcid. She has had nausea but no vomiting. She has had minimal appetite over the past few days. Her history is otherwise unremarkable with no prior similar symptoms.

On exam, she is uncomfortable but not in acute distress. HR 112, BP 112/63, T 99.1, O2 sat 99% on room air. Her abdominal exam is notable for focal tenderness in the epigastrium.

What is on your differential and what is your initial workup?

Peptic ulcer disease, esophagitis, hepatobiliary pathology (cholecystitis, hepatitis), pancreatitis, bowel obstruction, GERD, and bowel perforation. Labs- CBC, amylase, lipase, lactate. Imaging- acute abdominal series, possibly CT scan.

Her labs are notable for a WBC of 11K, markedly elevated lipase, normal bilirubin and normal renal function. Her acute abdominal series shows non-specific bowel gas pattern with minimally dilated loops of small bowel. Right upper quadrant ultrasound revealed gallstones without evidence of acute cholecystitis. Based on the patients clinical presentation and lab findings, she is diagnosed with acute gallstone pancreatitis and was admitted to the surgical service.

What are your initial goals of management?

Pain control, IV fluid resuscitation. NPO until pain is improving. NGT if nauseated/ vomiting. Monitor vitals and organ function (urine output, labs).

On her second hospital day, she developed worsening nausea/ vomiting, so an NGT was placed to decompress her stomach. Over the next few days, she has ongoing low grade sinus tachycardia, and then she developed intermittent low grade fever and mild leukocytosis. At that point, a CT scan is obtained.

CT abdomen and pelvis

The scan reveals peripancreatic inflammation with peripancreatic stranding, gland edema and hypoperfusion. There is also simple appearing peripancreatic fluid.

Over the next few days, the patient developed worsening pain and an uptrend in her leukocytosis. She is mildly hypotensive and she is urinating less frequently. When a Foley catheter is placed, she has a small volume of concentrated urine in the collection bag. She is transferred to the ICU and a Dobhoff tube was placed for post-pyloric enteral feeding. Over the next two days, she develops fevers, an increasingly oxygen requirement and persistent pain. A repeat CT scan was obtained.

Follow-up CT abdomen and pelvis

There is evidence of progression of her pancreatitis. There are bilateral pleural effusions as well as worsening intra-abdominal free fluid. There is evidence of non-perfusion of the midportion of her pancreas, consistent with pancreatic necrosis.

She remained in the ICU over the next several days. She did not clinically deteriorate and her pain slowly resolved. She had persistent high-volume output from her NGT.

Why would she have high volume output in her NGT?

Gastric outlet obstruction from peripancreatic fluid collection or necrosis. Ileus from ongoing intra-abdominal inflammation.

Her distension improved with NGT decompression, and she continued to have bowel function. She was started on post-pyloric enteral feeds via a nasojejunal tube, and this was continued for the next month, awaiting for the acute necrosis to wall-off and develop a rind.

Management of Acute Pancreatitis

Etiology

Gallstones and alcohol account for the vast majority of cases of pancreatitis. Other causes include hypertriglyceridemia, medication, ERCP, and hypercalcemia.

Diagnosis

Clinical presentation- epigastric pain, sometimes radiating to the back or shoulder. Nausea/ vomiting.
Labs- elevated amylase/ lipase at least 3x normal
Radiology- peripancreatic inflammation on contrast CT of abdomen. CT scan is not always mandatory on admission, but its commonly obtained for patients who have significant enough disease that they warrant a surgical consult. CT is also useful to rule out other pathology if the diagnosis is unclear.

Clinical Course

Most patients (about 80%) with acute pancreatitis suffer only mild disease and have resolution of symptoms without sequalae. The remaining 20% progress to moderate or severe pancreatitis, which is defined by the development of peri-pancreatic fluid collections or necrosis (sterile= moderate, infected= severe), or organ failure (transient= moderate, persistent= severe). Patients with organ dysfunction require ICU admission.

Initial management

Fluid resuscitation and ensuring adequate pain control.
Nutritional support is also important, and patients are allowed to eat. Enteral nutrition should be initiated if the patient doesn't have adequate intake over the first few days.
Close monitoring for development of sequalae. Patients are at risk for ARDS, abdominal compartment syndrome and infection.

Assessment of Disease Severity

Ranson's Criteria: Classic criteria for estimating pancreatitis severity[1]
- Admit data: WBC >16K, age >55, glucose >200, AST >250, LDH >250
- 48 hours: ↓Hct >10%, ↑BUN >5, Ca <8, PaO2 <60, Base deficit >4, >6L IVF.
CT Severity has also been used to grade pancreatitis- inflammation, fluid collections and necrosis.[2]

Management of Complicated Pancreatitis- Fluids Collections, Necrosis, Infection

Diagnosis and Classification of peri-pancreatic fluid collections and necrosis [3]

Acute interstitial edematous pancreatitis
- Less than 4 weeks, the fluid collection is an acute peripancreatic fluid collection.
- After 4 weeks, it becomes walled-off/ encapsulated and is a pancreatic pseudocyst.
Acute necrotizing pancreatitis [non-enhancing pancreatic parenchyma]
- Less than 4 weeks, the fluid collection is an acute necrotic collection.
- After 4 weeks, it becomes walled-off/ encapsulated and is walled-off necrosis.
Infected pancreatic necrosis- diagnosed by air in the necrosis, clinical symptoms consistent with infection and confirmed by aspiration and culture. A negative culture does not definitely rule out infection, so in the appropriate setting of clinical deterioration, there must be a high index of suspicion for infection.

Indication for Antibiotics

Antibiotics are NOT indicated for severe pancreatitis or pancreatic necrosis as a prophylaxis for infection.[4, 5] They are only indicated in known or highly-suspected infected necrosis. The antibiotics chosen must penetrate pancreatic tissue to be effective- quinolones and carbapenems are both broad-spectrum antibiotics (cover gram positive and gram negative) that penetrate pancreatic tissue.
Carbapenems also cover anaerobes. Metronidazole covers gram negatives. Regimen: carbapenem or quinolone + metronidazole. Also consider antifungal coverage in severely ill patients.[6]

Diagnosis of Infected Necrotizing Pancreatitis

Infected pancreatic necrosis can be a challenging clinical diagnosis because the inflammatory state associated with pancreatitis can present with similar signs and symptoms, including fever, tachycardia, leukocytosis and ileus. CT evidence of air in the pancreatic necrosis is highly suggestive of infection, although absence of air does NOT definitively rule out infection. Fine-needle aspiration (FNA) can be used to obtain a sample for culture. There is a risk of infecting a sterile necrotic collection by performing an FNA, so this requires careful clinical decision-making.

Management of Infected Necrotizing Pancreatitis

These patients need broad spectrum antibiotics. Some patients may improve with antibiotics alone, but a drainage procedure is often needed. Percutaneous IR drain placement has a low rate of complications, but frequently fails to fully resolve the infection. Upsizing the drain or proceeding to more invasive intervention (see below) is required if that patient deteriorates despite drain placement and antibiotics.

Previously, open necrosectomy was the standard. This is a highly morbid procedure, that requires maintaining an open abdomen, repeat washouts, and a prolonged ICU stay. Now, the step up approach is being increasingly utilized to manage these patients less invasively with similar or better outcomes (percutaneous retroperitoneal drainage or endoscopic transgastric drainage, endoscopic necrosectomy, followed by retroperitoneal necrosectomy).[7-10]

Management of peri-pancreatic fluid collections [11-13]

Enteral nutrition and pain control. A trial of a regular diet is appropriate, but if the patient is able to tolerate a regular diet, supplemental nutrition is required. Enteral nutrition is ideal, as it is associated with improved outcomes compared to TPN. Enteral access distal to the 3rd portion of the duodenum may theoretically avoid stimulation of the pancreas, but there is no evidence that jejunal feeds are superior to gastric feeds. However, depending on the location of the fluid collection, gastric outlet obstruction is a potential complication. Ideally, post-pyloric access would be obtained prior to obstruction, and can be used for long-term feeding while the fluid collection is allowed to resolve/ mature.
Most resolve without intervention. As long as the patient is not systemically ill, drainage of pancreatic necrosis should be delayed as long as possible, ideally 6-8 weeks. Goal is to avoid procedural intervention until the fluid/ necrosis have become walled off, and then only intervene if the patient remains symptoms (pain, early satiety). However, if the patient clinically worsens, earlier intervention is necessary.
Open pancreatic necrosectomy is associated with significant morbidity and mortality. An algorithm starting with least invasive (percutaneous or endoscopic drainage) and progressing to more invasive if the patient continues to do poorly is associated with decreased morbidity and mortality.

References