eMedicine Specialties > Gastroenterology > Pancreas
Pancreatitis, Acute: Treatment & Medication
Updated: Dec 29, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
The medical management of mild acute pancreatitis is relatively straightforward. The patient is kept NPO (non per os, ie, nothing by mouth), and intravenous fluid hydration is provided. Analgesics are administered for pain relief. Antibiotics are generally not indicated. If ultrasonograms show evidence of gallstones and if the cause of pancreatitis is believed to be biliary, a cholecystectomy should be performed during the same hospital admission. Feeding should be introduced enterally as the patient's anorexia and pain resolves. Patients can be initiated on a low fat diet initially and do not need to always start their dietary advancement using a clear liquid diet.
In contrast, patients with severe acute pancreatitis require intensive care. Within hours to days, a number of complications (eg, shock, pulmonary failure, renal failure, gastrointestinal bleeding, multiorgan system failure) may develop. The goals of medical management are to provide aggressive supportive care, to decrease inflammation, to limit infection or superinfection, and to identify and treat complications as appropriate.
- Fluids: Patients are kept NPO and require intravenous hydration. Especially in the early phase of the illness, aggressive fluid resuscitation is critically important. This cannot be overemphasized. There is no universal consensus showing a definitive advantage of one type of fluid over another type. Resuscitation should be enough to maintain hemodynamic stability, which is usually an initial several liter fluid bolus followed by 250-500 cc/h continuous infusion. Careful attention should be paid to signs of overhydration, such as pulmonary edema causing hypoxia.
- Antibiotics
- Antibiotics, usually drugs of the imipenem class, should be used in any case of pancreatitis complicated by infected pancreatic necrosis. They should not be given routinely for fevers, especially early in the disease course, as this symptom is almost universally secondary to the inflammatory response and not an infectious process.
- Several controlled trials have evaluated the role of empiric antibiotics in patients with severe acute necrotizing pancreatitis for infectious prophylaxis.
- One such trial evaluated the role of imipenem/cilastatin initiated at admission to prevent infected pancreatic necrosis. This drug combination penetrates the pancreatic parenchyma and reduces the risk of intra-abdominal infection. This showed some benefit in preventing infectious complications. Unfortunately, fungal superinfection tends to develop later in the clinical course, although this risk is probably overinflated.
- A randomized trial failed to show any benefit of ciprofloxacin and metronidazole in preventing infectious complications, and thus this drug combination is not routinely used for prophylaxis in this disease.
- The bottom line is that antibiotic prophylaxis in severe pancreatitis is controversial. However, at this time, the routine use of antibiotics as prophylaxis against infection in severe acute pancreatitis is not recommended.
- ERCP: If the imaging and laboratory study findings are consistent with severe acute gallstone pancreatitis that is not responding to supportive therapy or with ascending cholangitis with worsening signs and symptoms of obstruction, early ERCP with sphincterotomy and stone extraction is indicated. (See the image below.)
This patient with acute gallstone pancreatitis underwent endoscopic retrograde cholangiopancreatography. The cholangiogram shows no stones in the common bile duct and multiple small stones in the gallbladder. The pancreatogram shows narrowing of the pancreatic duct in the area of the genu, the result of extrinsic compression of the ductal system by inflammatory changes in the pancreas.
- Nutrition
- Early initiation of enteral nutritional supplementation and maintenance of a positive nitrogen balance is important in patients with severe pancreatitis.
- Theoretical considerations regarding the ability of the enterocyte to maintain a barrier against bacterial translocation favor nasojejunal feedings. Thus, in all patients admitted to the ICU, nasojejunal feedings should be attempted beginning at admission. For patients with mild acute pancreatitis, nasojejunal feedings can be avoided unless patients are unable to tolerate oral intake for over 1 week.
- Depending on the situation, TPN, which has been shown to reduce mortality rates, may be necessary. However, TPN should generally be reserved as a second-line therapy behind enteral feeding.
- Trials are ongoing evaluating whether or not there is an advantage of nasojejunal tubes over nasogastric tubes for enteral feeding.
- Emerging treatments
- Although the role that cytokines play in systemic inflammatory response syndrome appears to be important, a large clinical trial of lexipafant, a platelet-activating factor antagonist, has shown no benefit in patients with severe acute pancreatitis.
- Because multiple pathways are involved in the inflammatory response, further research is needed in order to define which cytokine or combination of cytokines should be targeted to ameliorate the complications of acute pancreatitis.
- Anti-tumor necrosis factor-alpha therapy has been targeted as a potential therapeutic in acute pancreatitis; however, clinical trials have not begun.
- Clinical vigilance
- In the following weeks (to months) after presentation, the physician's attention shifts to developing signs of intra-abdominal infection, pancreatic pseudocyst, intra-abdominal hemorrhage, colon perforation, obstruction or fistulization, and multiorgan system failure.
- The clinician cannot rely on clinical grounds alone to differentiate infected and sterile pancreatic necrosis. When clinical signs of infection or a systemic inflammatory response is present in the setting of necrotizing pancreatitis, CT-guided needle aspiration is indicated.
Surgical Care
Surgical intervention, whether by minimally invasive or conventional open techniques, is indicated when an anatomical complication amenable to a mechanical solution is present. Depending on the situation and local expertise, this may require the talents of an interventional radiologist, interventional endoscopist, and/or surgeon (alone or in combination). The images below illustrate the treatment of severe acute pancreatitis.
CT scan of a young man referred 2 weeks into his second bout of severe acute pancreatitis. Gravely ill, he has fever and leukocytosis, as well as hypotension requiring pressors and respiratory distress requiring mechanical ventilation. His abdominal CT scan shows severe acute pancreatitis. A percutaneous drain is placed in the dominant fluid collection to establish drainage while he is given imipenem/cilastatin and his condition is stabilized.
Endoscopic retrograde cholangiopancreatography excluded suppurative cholangitis and established the presence of anular pancreas divisum. The dorsal pancreatogram showed extravasation into the retroperitoneum, and a sphincterotomy was performed on the minor papilla. As shown in this radiographic film, a pigtailed nasopancreatic tube was then inserted into the dorsal duct and out into the retroperitoneal fluid collection. The other end of the tube was attached to the bulb suction and monitored every shift.
While percutaneous drains remove loculated fluid collections elsewhere in the abdomen, the nasopancreatic tube is containing the retroperitoneal fluid collection. One week later, the retroperitoneal fluid collection is much smaller as shown in this radiographic film (the image is reversed in the horizontal direction). By this time, the patient is off pressors and is ready to be extubated.
Four months later, after the pseudocyst has been converted into a pseudocystogastrostomy using minimally invasive techniques, the pancreatogram reveals the more proximal pancreatic duct.
A guidewire is placed into the dorsal duct, crosses the stenotic area, and advances into the proximal duct. A dilating catheter is then advanced over the wire to enlarge the stenosis. The duct is subsequently stented.
Six months after severe acute pancreatitis, the patient remained symptom free and was living independently. As shown in this follow-up abdominal CT scan, minimally invasive techniques were successful in removing the pockets of infection, restoring the integrity of the pancreatic ductal system. They also preserved the endocrine function of the pancreas, and at the time of this follow-up, this patient had no evidence of diabetes mellitus.
- Pancreatic duct disruption: Damage to the pancreatic ductal system may allow pancreatic juice to leak from the gland. The sudden development of hypocalcemia or a rapid increase in retroperitoneal fluid on CT scan is suggestive of this condition.
- When imaging studies contain corroborating data, the condition is initially managed by percutaneous placement of a drainage tube into the fluid collection under the guidance of ultrasonography or CT scanning.8 Fluid amylase or lipase levels in the ten thousands strongly suggest the presence of a ductal disruption.
- In the appropriate clinical setting, endoscopic retrograde pancreatography confirms the diagnosis and provides a treatment option. Transpapillary stent placement or, preferably, placement of a 6F nasopancreatic tube attached to an external bulb suction device can successfully treat leaks by removing the sphincter tone and changing the dynamics of fluid flow in favor of ductal healing. Occasionally, leaks are associated with downstream stenoses that are also amenable to endoscopic treatment techniques.
- Refractory cases may require surgery. If the persistent leak is present in the tail of the gland, a distal pancreatectomy is preferred. If the leak is in the head of the gland, a Whipple procedure is the operation of choice.
- Pseudocysts: By definition, peripancreatic fluid collections persisting for more than 4 weeks are termed acute pseudocysts. Pseudocysts lack an epithelial layer and, thus, are not considered true cysts. In addition, the term cyst is also a misnomer, as most of these collections are filled with necrotic debris and not fluid. A more descriptive term for these collections may be organized necrosis. Most of these can be followed clinically. When pseudocysts are symptomatic (ie, associated with pain, bleeding, or infection) or are larger than 7 cm and are rapidly expanding in an acutely ill patient, intervention is indicated. The following therapeutic approaches may be implemented, depending on anatomical relationships and the duration of the natural history of the complication. See also the diagram below for a discussion of pseudocyst treatment.
- Percutaneous aspiration: In selected patients with very large fluid collections, percutaneous aspiration of pancreatic pseudocysts is a reasonable approach. Even though treatment failures are common when the pseudocyst communicates with the pancreatic ductal system, percutaneous drainage serves as a temporizing measure that may later lead to successful endoscopic or surgical intervention. Often, an infected pseudocyst (which by definition is regarded as a pancreatic abscess) can be successfully managed by percutaneous drainage.
- Endoscopic techniques: Pseudocysts may be managed endoscopically by transpapillary or transmural techniques. Transpapillary drainage requires the main pancreatic duct to communicate with the pseudocyst cavity, ideally in the head or body of the gland. The proximal end of the stent is placed into the cyst cavity, and the stent should be smaller than the diameter of the pancreatic duct. The technical success rate is 83%, with a complication rate of 12%. Generally, however, pancreatic stents are difficult to monitor, prone to obstruction, and associated with an increased risk of infection and ductal injury.
- Some noncommunicating pseudocysts may be amenable to transmural enterocystostomy. Technical success requires a mature cyst that bulges into the foregut, and the distance from the lumen to the cyst cavity should be less than 1 cm. The success rate is 85%, with a complication rate of 17%. The transduodenal approach is associated with fewer complications and recurrences than the transgastric approach.
- Surgical cyst-enterostomy: Based on prospective data from the 1970s, surgery is recommended for persistent, large (>7 cm), pancreatic pseudocysts because complications developed in 41% of patients, 13% of whom died. Internal pseudocyst enteric anastomosis became the standard of care, with an operative mortality rate of 3-5%. This dogma has gone on to be challenged by 2 retrospective studies in which patients with smaller asymptomatic pseudocysts (ie, <5 cm) rarely developed complications (<10%).
- Infected pancreatic necrosis: Surgery is recommended when large areas of the pancreas are necrotic and percutaneous CT-guided aspiration demonstrates infection based on a positive Gram stain result. Antibiotic therapy alone is not sufficient to achieve a cure. Aggressive surgical debridement and drainage is necessary to remove dead tissue and to clear the infection.
- Pancreatic abscesses: Pancreatic abscesses generally occur late in the course of pancreatitis. Many of these respond to percutaneous catheter drainage and antibiotics. Those that do not respond require surgical debridement and drainage.
Consultations
The most effective and soundly based treatment plan for any disorder is one aimed at the mechanism responsible for the development of the disorder. With that axiom in mind, treatment of the patient must address the underlying cause of pancreatitis.
- Treatment of patients with alcohol-induced pancreatitis should go beyond the physical manifestations of this disease and address the underlying psychological addiction to alcohol. Simply telling patients they must stop drinking alcohol is not satisfactory. Successful treatment often requires the involvement and expertise of a chemical dependency counselor. The author favors in-hospital consultation with all patients admitted with alcoholic pancreatitis.
- Patients with hypertriglyceridemic- or hypercalcemic-induced pancreatitis require consultation with an endocrinologist. Rarely, such patients require surgical intervention for treatment of hyperparathyroidism or control of hyperlipidemia refractory to medical therapy.
- It is optimal for patients admitted with gallstone pancreatitis to have a cholecystectomy prior to discharge and not, for example, scheduled for a later date as an outpatient. Patients discharged with gallstone pancreatitis without a cholecystectomy are at high risk for recurrent bouts of pancreatitis.
- Patients with gallstones or microlithiasis revealed on imaging studies should have a surgical consultation for gallbladder removal. Because microlithiasis is the most common cause of idiopathic pancreatitis, a patient with recurrent idiopathic pancreatitis should undergo cholecystectomy before procedures associated with a higher risk of complications (eg, ERCP) are performed.
- Patients with medication-induced acute pancreatitis may benefit from clinical pharmacology consultation during their hospitalization to maximize their therapeutic regimen.
Diet
General guidelines for nutritional support of patients with acute pancreatitis include the following:
- In patients with mild uncomplicated pancreatitis, no benefit is observed from nutritional support, and the energy (caloric) intake received with intravenous dextrose 5% in water (D5W) suffices. Oral feedings should be initiated once the patient's pain and anorexia resolve.
- In patients with moderate-to-severe pancreatitis, begin nutritional support early in the course of management, as soon as stabilization of fluid and hemodynamic parameters permits. Optimally, nasojejunal feedings with a low-fat formulation should be initiated at admission. The success of nasogastric tube feedings has also been compared to nasojejunal feedings in one randomized study. The study showed equivalent outcomes for patients with severe pancreatitis fed with nasogastric feedings compared with nasojejunal feedings.
- However, TPN may be required in patients who are unable to maintain their caloric needs with enteral nutrition or because adequate jejunal access cannot be maintained. TPN should include fat emulsions in amounts sufficient to prevent essential fatty acid deficiency.
- If surgery is required for diagnosis or complications of the disease, place a feeding jejunostomy at the time of the operation. Use a low-fat formula.
- Begin oral feedings once abdominal pain has resolved and the patient regains appetite. The diet should be low in fat and protein. A prospective, randomized study showed that initiating feeding with a low-fat solid diet was as well tolerated as initiating feeding with a clear liquid diet, but it did not result in a shorter length of stay.
Medication
Currently, no medications are used to treat acute pancreatitis specifically. Therapy is primarily supportive and involves intravenous fluid hydration, analgesics, antibiotics (in severe pancreatitis), and treatment of metabolic complications (eg, hyperglycemia, hypocalcemia).
Analgesics
Used to reduce pain and inflammation, which is essential to quality patient care.
Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)
Peripherally acting DOC for mild pain and elevation of body temperature.
Adult
325-1000 mg PO q4h prn; not to exceed 4 g/d
Pediatric
10-15 mg/kg PO q4-6h; not to exceed 5 doses/d
Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity; decreases zidovudine levels; concurrent use with warfarin may result in increased risk of bleeding; sulfinpyrazone may result in increased hepatotoxicity in acetaminophen overdose; concurrent use with diflunisal may result in an increased risk of acetaminophen toxicity
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hepatotoxicity is possible in patients who chronically abuse alcohol following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative doses exceeding recommended maximum dose
Acetaminophen and propoxyphene (Darvocet N 100)
DOC for moderately severe pain.
Adult
Acetaminophen 650 mg and propoxyphene 100 mg PO q4h; not to exceed 600 mg propoxyphene qd
Pediatric
Not established
May increase serum concentrations of MAOIs, TCAs, carbamazepine, phenobarbital, and warfarin; concurrent use with diflunisal may result in an increased risk of acetaminophen toxicity; sulfinpyrazone may result in increased hepatotoxicity in acetaminophen overdose; decreases zidovudine levels
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Pregnancy category D in prolonged use; caution in patients dependent on opiates as substitution may result in acute opiate withdrawal symptoms; caution in patients with severe renal or hepatic dysfunction, hepatotoxicity may occur even at normal therapeutic doses
Tramadol (Ultram)
Centrally acting analgesic for moderately severe pain. Inhibits ascending pain pathways, altering perception of and response to pain. Also inhibits reuptake of norepinephrine and serotonin.
Adult
50-100 mg PO q4-6h; not to exceed 400 mg/d
Pediatric
<1 year: Not established
>1 year: 1-2 mg/kg/dose PO
Significantly decreases effects of carbamazepine; cimetidine increases toxicity; risk of serotonin syndrome with coadministration of antidepressants; increases effects of MAOIs; chlorpromazine, cyclobenzaprine, desipramine, fluoxetine, paroxetine, haloperidol, imipramine, sertraline, thioridazine, and venlafaxine increase risk of seizures; concurrent use with digoxin may increase risk of digoxin toxicity (nausea, vomiting, cardiac arrhythmia); concurrent use with diphenhydramine, hydrocodone, meperidine, morphine, oxycodone, and trazodone may cause CNS depression (sedation, lethargy, speech difficulties); concurrent use with warfarin may increase risk of bleeding
Documented hypersensitivity; patients dependent on opioids; concurrent use of MAOIs or within 14 days; use of SSRIs, TCAs, or opioids; acute alcohol intoxication
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Can cause dizziness, nausea, constipation, sweating, and pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, and hypoadrenalism; pregnancy and breastfeeding; seizure; development of tolerance or dependency with extended use
Meperidine (Demerol)
Analgesic with multiple actions similar to those of morphine. May produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine. Synthetic opioid narcotic analgesic for the relief of severe pain.
Adult
50-150 mg PO/IV/IM/SC q3-4h
Pediatric
Not established
Monitor for increased respiratory and CNS depression with coadministration of cimetidine; hydantoins may decrease effects; avoid with protease inhibitors; concurrent use with cimetidine may result in toxicity; fosphenytoin may decrease effectiveness; furazolidone may result in cardiovascular instability, hyperpyrexia, coma, or death; isoniazid may cause hypotension and CNS depression; methohexital may cause CNS depression; naltrexone may result in precipitation of opioid withdrawal symptoms; phenelzine may result in CV instability, hyperpyrexia, coma, or death; phenytoin may decrease effectiveness; concurrent use of procarbazine, selegiline, and tranylcypromine may result in cardiac instability, hyperpyrexia, or coma; concurrent use with ritonavir may result in an increased risk of CNS stimulation and excitation; sibutramine may increase risk of serotonin syndrome (hypertension, hypothermia, myoclonus, mental status changes)
Documented hypersensitivity; MAOIs; upper airway obstruction or significant respiratory depression; during labor when delivery of premature infant is anticipated
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Pregnancy category D in prolonged use; caution in patients with head injuries because may increase respiratory depression and CSF pressure (use only if absolutely necessary); caution when using postoperatively and with history of pulmonary disease (suppresses cough reflex); substantially increased dose levels (due to tolerance) may aggravate or cause seizures even if no prior history of convulsive disorders is present; monitor closely for morphine-induced seizure activity if prior seizure history is present
Antibiotics
For prophylaxis against infection in severe acute necrotizing pancreatitis.
Imipenem and cilastatin (Primaxin)
For treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of potential for toxicity. Generally administered in a 1:1 combination. Thienamycin derivative with broad-spectrum antimicrobial coverage. A thienamycin derivative with greater potency and broader antimicrobial spectrum than other beta-lactam antibiotics. Cilastatin inhibits dehydropeptidase activity and reduces cilastatin metabolism.
Adult
500 mg to 1 g IV q6-8h over 30 min
Pediatric
<12 years: Do not administer
>12 years: Not established
Coadministration with cyclosporine may increase adverse CNS effects of both agents; coadministration with ganciclovir may result in generalized seizures
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adjust dose in renal insufficiency; CNS events, including seizures, have occurred; may increase risk for superinfection
More on Pancreatitis, Acute |
| Overview: Pancreatitis, Acute |
| Differential Diagnoses & Workup: Pancreatitis, Acute |
 Treatment & Medication: Pancreatitis, Acute |
| Follow-up: Pancreatitis, Acute |
| Multimedia: Pancreatitis, Acute |
| References |
| Further Reading |
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Further Reading
Clinical guidelines
AGA Institute medical position statement on acute pancreatitis.
American Gastroenterological Association Institute - Medical Specialty Society. 2007 May. 3 pages. NGC:005792
Role of EUS.
American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2000 (revised 2007 Sep). 10 pages. NGC:006206
ACR Appropriateness Criteria® acute pancreatitis.
American College of Radiology - Medical Specialty Society. 1998 (revised 2006). 5 pages. NGC:005114
Clinical trials
Diagnostic and Interventional Therapy in Acute Pancreatitis
Early Goal-Directed Volume Resuscitation in Severe Acute Pancreatitis (EAGLE)
Goal-directed Fluid Resuscitation in Acute Pancreatitis
Related eMedicine topics
Pancreatitis
Pancreatitis, Acute (Radiology)
Pancreatic Necrosis and Pancreatic Abscess
Pancreatic Pseudocysts
Acute Renal Failure
Keywords
acute pancreatitis, pancreas, pancreatitis, chronic pancreatitis, pancreatic enzymes, endoscopic retrograde cholangiopancreatography, ERCP, magnetic resonance cholangiopancreatography, zymogen, biliary disease, biliary tract disease, elevated pancreatic enzymes, inflammation of the pancreas, pancreatitis diet, pancreatitis treatment, autoimmune pancreatitis, pancreatic disease, alcohol pancreatitis, alcoholic pancreatitis, pancreas inflammation
