Emergency General Surgery

The Awakening of the Sleeping Lion – Part 2

Love is like pancreatitis; it starts off slow, then builds in intensity until you become consumed and develop violent cramps.

Dana Gould

Welcome back, guys!!!

Last time we have finished our post without talking about the treatment of acute pancreatitis (AP). We can divide it into initial management, risk reduction strategies, and treatments for local complications.

The management of systemic complications and organ failure is beyond the purpose of this post.

Initial Management

Initial management of acute pancreatitis should be individualized on the patient’s conditions and severity of the inflammatory process. Grossly, there is no specific therapy for AP, and the primary treatment is represented basically just by support measures…

The initial support involves mainly fluid resuscitation, nutrition, and pain management.

1. Fluid Resuscitation

As reported last time, AP causes a shift of intravascular fluids into the so-called third space. This process reduces the circulatory volume, thus decreasing tissue perfusion and, in the long run, leading to multiorgan failure. This is confirmed by the fact that an increase in blood urea nitrogen (BUN) level within the first 24 h is associated with a higher risk of death.

To avoid this event, the fluid infusion should be initiated as soon as the diagnosis of AP has been established.

First question: which fluid should we use?… In AP, the principle is not so different from that already explained in the Damage Control Resuscitation posts. Remember that things do not get different, physiology is always the same… So then… Balanced isotonic crystalloid solutions it is… In form of lactated Ringer’s… However, in patients with AP secondary to hypercalcemia, Ringer lactate is contraindicated because of its content of calcium.

Second problem: how much and/or at what rate do we have to infuse fluids?… According to recent guidelines, the fluid infusion rate should be titrated on specific targets of perfusion such as:

  • Mean arterial pressure 65-85 mmHg;
  • Heart rate <120 bpm;
  • Urine output >0.5-1 mL/kg/h;
  • BUN level back to normal;
  • Hematocrit 35-44%.

These parameters should be reassessed every 6 h for the first 24-48 h. Along with these, other parameters should be monitored strictly:

  • Oxygen saturation (goal >90%) and arterial blood gas;
  • Electrolytes (beware of calcium and magnesium);
  • Serum glucose;
  • Urinary bladder pressure (patients in ICU should be monitored for abdominal compartment syndrome (i.e. intra-abdominal pressure >20 mmHg with new organ dysfunction)).

The infusion may be started at 3-10 mL/kg/h, and then titrated according to the parameters previously listed. If a patient is hypovolemic, the infusion may be started with a fluid bolus of 20 mL/kg given over 30 minutes.

Beware not to resuscitate too aggressively patients whose preexisting comorbidities (i.e. chronic kidney disease or heart failure) do not allow fluid overload.

Fluid resuscitation should be limited to the first 24-48 h to avoid fluid overload.

2. Nutrition

Nutrition in patients affected by acute pancreatitis should be started as soon as possible (possibly within 24-72 h) for multiple reasons:

  • To compensate the catabolic state that uprises in moderately severe and severe AP;
  • To increase bowel blood flow and to preserve the integrity of the bowel mucosa, thus reducing bacterial translocation and subsequent sepsis.

Many papers demonstrated how enteral nutrition is superior to parenteral nutrition in preserving gut motility and its barrier function and, consequently, in reducing morbidity and mortality rates.

Historically, oral nutrition has been avoided in patients admitted for AP… And we know that in many hospitals this practice is still perpetuated… So, we are going to tell you this just one time: let the poor patients eat as soon as they can (no ileus, nausea, or vomiting)!!! Most times, this means providing them a low-fat soft, or solid diet from the beginning.

If patients cannot tolerate oral nutrition within the first 72 h, enteral nutrition via a nasojejunal (or nasogastric) tube should be started. However, some patients do not stand enteral nutrition either (i.e. abdominal pain, vomiting, bloating, or diarrhea). On these occasions, the decision to start parenteral nutrition should be made as soon as possible to avoid malnourishment.

Patients with signs of malabsorption (e.g. steatorrhea) should be considered for high protein, low fat, semi-elemental formulations and, in case of exocrine pancreas insufficiency (high risk in necrotic pancreatitis and alcohol-related pancreatitis), pancreatic enzyme supplementation.

3. Pain Management

In the setting of pain management, the usual rules should be applied…

Opioids can be used safely but try not to use more than one at a time. In case of persistent abdominal pain, a patient-controlled analgesia pump may be a good alternative to boluses.

Even if some studies showed that morphine causes an increase in the sphincter of Oddi pressure, there is no evidence of AP or worsening of AP caused by its use.

4. Others

Do you think something is missing in the Initial Management section, aren’t you?… Maybe antibiotics?… Well, about one patient out of five indeed develops an extrapancreatic infection, but this is not a good reason to use antibiotics randomly… Antibiotic prophylaxis is not recommended in AP. If you suspect the patient has an infection, you must start antibiotics as soon as possible, but if no source of infection is identified, they should be discontinued immediately.

Beware that a high white cell count at admission is not a specific sign of infection… Remember that these patients may have hemoconcentration.

Similarly, the use of prophylactic antifungals and protease inhibitors is not recommended in patients with AP.

Risk Reduction Strategies

After the first episode of AP is mandatory to set up all the possible strategies to reduce the risk of recurrence. Obviously, these strategies are strictly related to the etiological process beyond the disease.

  • Gallstones – The risk of recurrence is about 8% within 40 days after the first episode. Cholecystectomy (via laparoscopy, if possible) should be performed as soon as possible. In the case of predicted mild AP, no contraindications exist for early (i.e. within 24-48 h) cholecystectomy. If same-admission cholecystectomy cannot be made, it should be planned within 2-4 weeks after discharge, and an ERCP with sphincterotomy should be considered to lower the risk of recurrence. In patients with pancreatic collections, cholecystectomy should be delayed for at least 6 weeks, and imaging (e.g. CT scan, MRCP) should be repeated before surgery to confirm their resolution.
  • Alcohol – Alcohol consumption must be stopped to avoid recurrent episodes of AP and, with time, the onset of chronic pancreatitis.
  • Hypertriglyceridemia – Weight reduction is the first goal in obese patients. The use of fibrates, statins, niacin and omega 3 fatty acids may be useful to decrease triglyceride levels (fibrates are the best).
  • Hypercalcemia – The cause beyond this condition should be explored and treated accordingly (e.g. primary hyperparathyroidism, malignancy, thyrotoxicosis).

Treatments for Local Complications

Books can be written on this matter. In this post, we are going to overview the principal treatments, but we are not discussing them in detail…

The basic strategy in managing local complications is the so-called step-up approach… This means starting with the less invasive treatment and, along with its failure, moving up with more and more aggressive procedures.

Most of the time local complications are asymptomatic and resolve spontaneously so that the only thing to do is having patience.

However, when these local complications cause symptoms and/or become infected, appropriate treatment must be undertaken.

1. Infected Necrosis

About 30% of patients with pancreatic necrosis develop infected necrosis. Usually, the infection is caused by bowel organisms (e.g. E. Coli, Enterococcus, Pseudomonas, and Klebsiella) and it happens about 10 days after the onset of AP.

No correlation exists between the extension of necrosis and risk of infection, and, as already stated, antimicrobial prophylaxis has no role in patients with sterile necrosis.

Infected necrosis may be suspected in case of new onset of fever, leukocytosis, increased CRP and/or procalcitonin levels, or in patients who fail to improve after 7-10 days. If pancreatic necrosis infection is suspected, a CEACT should be performed to look for signs of infection (i.e. gas bubbles inside necrotic collections). Remember that there is no need to start antibiotics on admission just because the patient has a fever, elevated CRP, and/or leukocytosis; they may only reflect the inflammation of the pancreatic gland.

In patients with high suspicion of infected pancreatic necrosis is important to start empiric antibiotic therapy even without cultures. The recommended antibiotic regimens for infected necrosis are:

  • Carbapenem (i.e. imipenem, meropenem);
  • Quinolone, ceftazidime or cefepime along with metronidazole.

In patients who fail to respond to antimicrobials, the second step is necrosectomy (endoscopic, percutaneous radiologic, or surgical). However, this procedure should be made in patients with mature collections (i.e. walled-off necrosis). So, bridge therapy with percutaneous drainage may be a good choice. Moreover, this procedure allows taking samples to perform cultures and, consequently, to set up a targeted antimicrobial therapy. If cultures came back negative, antibiotics should be discontinued.

We will skip the necrosectomy techniques because they are beyond the purpose of this post. However, before going on, we want to say a couple of words about acute cholecystitis diagnosed during an episode of acute pancreatitis… Even if these two entities may appear simultaneously, we must be very cautious in diagnosing acute cholecystitis during acute pancreatitis, because it will change completely our approach to the patient… Most of the time, acute cholecystitis is diagnosed by the radiologist because of gallbladder walls thickening and free fluid around it… However, you have to consider that the gallbladder lies over the pancreas, and during an episode of acute pancreatitis reactive changes to the gallbladder’s structure may happen. Though, this does not mean that there is acute cholecystitis… Sometimes imaging may be misleading… You must look for other clues…

2. Symptomatic Sterile Collections

Pancreatic pseudocystis

In sterile collections, indications for treatment are:

  • Gastrointestinal or biliary obstruction due to mass effect 4-8 weeks after the onset of AP;
  • Persistent symptoms (abdominal pain, nausea, vomiting, inability to assume oral nutrition, etc…) more than 8 weeks after the onset of AP;
  • Complete transection of the main pancreatic duct with persistent symptoms more than 8 weeks after the onset of AP.

Remember that it takes about 8 weeks for pancreatic collections to resolve and that it is better (and safer) to intervene on well-defined collections than on immature ones.

The same as for infected necrosis, the interventional approach may be endoscopic, percutaneous radiologic, or surgical… And the treatment attempts should follow this precise order…

3. Others

Porto-spleno-mesenteric venous thrombosis usually resolves spontaneously after the resolution of AP. However, if the clot involves the portal vein or the superior mesenteric vein, anticoagulation should be started. On the other hand, in case of retroperitoneal bleeding, a quite rare but life-threatening complication, angioembolization must be done if the patient’s condition allows it.

Well, we think it is enough… We know that we have left aside a lot of topics (maybe too much)… However, the main goal of this two-episode series was to give you an overview of how to manage patients with acute pancreatitis… And we think we succeeded with that…

We have so much to talk about… And we are sure we will come back on this in the future… But for now, that’s all folks!!!

References

  1. Mederos MA, et al. Acute pancreatitis – a review. JAMA 2021;325:382-90.
  2. Greenberg JA, et al. Clinical practice guideline: management of acute pancreatitis. J Can Chir 2016;59:128-40.
  3. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 2013;13:e1-e15.
  4. Crockett SD, et al. American Gastroenterological Association Institute guideline on initial management of acute pancreatitis. Gastroenterology 2018;154:1096-101.
  5. Vivian E, et al. Acute pancreatitis task force on quality. Am J Gastroenterol 2019;114:1322-42.
  6. Ketwaroo G, et al. Quality of care indicators in patients with acute pancreatitis. Dig Dis Sci 2019;64:2514-26.
  7. Pereira J, et al. Accuracy of ultrasound in the diagnosis of acute cholecystitis with coexistent acute pancreatitis. Eur J Trauma Emerg Surg 2017;43:79-83

How to Cite This Post

Bellio G, Marrano E. The Awakening of the Sleeping Lion – Part 2. Surgical Pizza. Published on July 24, 2021. Accessed on September 18, 2021. Available at [https://surgicalpizza.org/emergency-surgery/the-awakening-of-the-sleeping-lion-part-2/].

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