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Acute and Chronic Pancreatitis

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Dr. Gregory HouseAcute pancreatitis is an acute inflammation of the pancreas associated with varying degrees of severity and pain, whilst chronic pancreatitis is a painful progressive destruction of the pancreas in which the predominant symptom is pain
Acute pancreatitis is an acute inflammation of the pancreas associated with varying degrees of severity and pain, whilst chronic pancreatitis is a painful progressive destruction of the pancreas in which the predominant symptom is pain

Basics

Description: acute pancreatitis is an acute inflammation of the pancreas associated with varying degrees of severity and pain, whilst chronic pancreatitis is a painful progressive destruction of the pancreas in which the predominant symptom is pain; therapy should be directed toward alleviating pain. It eventually results in loss of exocrine function and later of endocrine function

Prevalence: 10-46/100,000

Risk Factors: obesity is a risk factor mainly for acute pancreatitis (more severe pancreatitis) and alcoholism is a risk factor  mainly for chronic pancreatitis:  

Genetics: Hereditary pancreatitis is rare and is autosomal dominant. A mutation in gene cationic trypsinogen can induce chronic pancreatitis.

Pathophysiology: ✓ Activation of pancreatic proteases results in tissue necrosis. Inflammatory mediators directly affect sensory fibers of the celiac plexus (T5-T9) to cause visceral pain.

✓ Postulated causes of pain:

    • Inflammation of the pancreatic parenchyma
    • Increased pressure in the pancreatic duct system
    • Neuritis
    • Recurrent ischemia of the parenchyma.

✓ Early in disease, pain is severe and function is preserved.

✓ Late in disease, pain is less severe and function is impaired.

Etiology:

  • Gallstones (45%)
  • Alcohol abuse (45%)
  • Hypercalcemia
  • Hypertriglyceridemia
  • Trauma/surgery
  • Infectious agents

General Prevention:

✙ Avoid excessive alcohol consumption

✙ Avoid pancreatic toxins

✙ Prevention of progressive chronic pancreatitis:

    • Avoid smoking
    • Avoid alcohol consumption
    • Multivitamins may help reduce progression

Associated Conditions: chief associated condition at pancreatitis is HIV: in patients with a CD4 count of <500, pancreatitis is more common. It may be associated with medication used to treat AIDS (didanosine or pentamidine), or it may be the result of infections associated with AIDS (cytomegalovirus [CMV], toxoplasmosis).

Diagnosis

In acute pancreatitis, it is important to distinguish between mild and severe disease because the prognosis is quite different for each condition.

History: pain is localized to the upper abdomen, but may spread over a large portion of the abdomen; it often radiates to the back and is frequently nocturnal. Pain is intermittent in severity and is often worse after meals. Weight loss is typically secondary to fasting and malabsorption. Also nausea and vomiting often are present.

Physical Exam:

★ varies according to severity of disease

★ possible fever, tachycardia, shock

★  mild abdominal pain upon palpation to guarding with palpation

★ discoloration of the flank (Grey-Turner sign) or periumbilical region (Cullen sign)

Lab Test of Acute Pancreatitis:

  • Amylase, lipase levels plus Ransom criteria. For amylase, expect greater than threefold increase and for lipase expect greater than threefold increase in levels.
  • Triglycerides.
  • Serum calcium.

Lab Test of Chronic Pancreatitis:

  • Pancreatic function testing (secretin, para-aminobenzoic acid [PABA]), fecal elastase, serum trypsinogen, fecal chymotrypsin.
  • C-reactive protein.
  • Polymorphonuclear leukocyte (PMN)-elastase.
  • Trypsinogen activation peptide.
  • Procalcitonin.

Imaging: dynamic, contrast-enhanced CT (preferred) or MRI are the imaging modalities of choice for staging and detection of complications (especially necrosis), fluid collection, and abscesses.

Diagnostic Procedures/Surgery:

  • Laparotomy
  • Endoscopic retrograde cholangiopancreatography (ERCP) (removal of stones from pancreatic duct or bile duct)
  • Fine needle aspiration of fluid collections and abscesses

Pathological Findings: interstitial edema, hemorrhage, cell and fat necrosis for   acute pancreatitis and calcification&fibrosis for chronic one.

Differential Diagnosis:

➲ Pancreatic cancer

➲ Gallstones

➲ Peptic ulcer disease

➲ Irritable bowel syndrome

➲ Mesenteric ischemia

➲ Dyspepsia

Medication (Drugs)

Acute pancreatitis:

  • Parenteral opioids; consider IV patient-controlled analgesia in inpatients.
  • Some practitioners prefer meperidine because of a presumed lack of constrictor response on the Sphincter of Oddi; however these effects are usually of no clinical importance.
  • Morphine, hydromorphone, and fentanyl are reasonable choices for IV opioid therapy.

Chronic pancreatitis:

Three stages of treatment: Careful consideration is warranted before transitioning to next phase because of greater side-effect profile associated with progressive phases:

  • Phase 1: paracetamol (acetaminophen)
  • Phase 2: dextropropoxyphene
  • Phase 3: opioids

Adjuncts can be added at any phase:

  • NSAIDs
  • Tricyclic antidepressants; nortriptyline, desipramine are preferred over amitriptyline due to more favorable side effect profile with similar efficacy.
  • Oral enzyme preparations (Viokase)
  • Antiepileptics (Neurontin)
  • H2-blockers or proton pump inhibitors (PPIs) are useful adjuncts to decrease risk of ulcer formation associated with acute pancreatitis.

Alert: the belief that meperidine causes less constriction of the sphincter of Oddi than do other opioids is based on outdated research and is incorrect when the doses are equipotent. Meperidine's principal metabolite, normeperidine, is neurotoxic and causes seizures, especially in patients with renal impairment. Propoxyphene is a weak opioid and has a low dose ceiling due to cardiotoxicity. Acetaminophen may not be appropriate in patients with liver disease, and it is potentially hepatotoxic in healthy persons in doses of >4 g/day.

Interventional:

Acute pancreatitis:

  • Maintain intravascular volume and start enteral/oral feeding as soon as the patient is able to tolerate nutrition. Consider either duodenal or jejunal feedings.
  • Drain fluid collections/pseudocysts.

Chronic pancreatitis:

  • In select cases, endoscopic decompression of the pancreatic duct with or without a stent may be warranted.
  • Drain fluid collections/pseudocysts.
  • Thoracic epidural analgesia leads to rapid pain relief and a decreased need for parenteral/oral opioids so that side effects can be minimized.
  • Blockade/neurolysis of celiac plexus or splanchnic nerves may provide effective analgesia for 3 to 6 months, although pain will recur if the underlying condition is still active. It is a good alternative in some patients for whom indwelling regional analgesia (epidural) is inappropriate.
  • Intrathecal opioids/local anesthetics/clonidine may be appropriate for long-term neuraxial analgesia, especially if systemic opioids lead to adverse effects.
  • Celiac ganglia resection may be appropriate.
  • Dorsal column stimulation may be warranted; nine case reports demonstrate a reduction of abdominal visceral pain and opioid use with single- or dual-lead placement between T5-6.

Rehabilitation: in alcoholic pancreatitis, cessation of alcohol may slow course of disease.

Mental Health/Behavioral: cognitive behavioral therapy may be useful to enhance healing behavior, increase relaxation, and improve self-control.

Surgery:

  • Surgical decompression of the main pancreatic duct can reduce pain secondary to distension.
  • Pancreatic resection relieves pain secondary to inflammation.
  • Thoracoscopic splanchnicectomy
  • Puestow procedure
  • Distal pancreatectomy

Follow-Up

Prognosis:

Acute pancreatitis:

  • Mild edematous disease (75% to 85% of cases) has a mortality rate of <1%.
  • Severe hemorrhagic-necrotizing pancreatitis (15% to 25% of cases) has a mortality rate of 10% to 24%.

Chronic pancreatitis: prognosis varies widely from disease resolution to death.

Issues for Referral: consider pain medicine consultation for patients suffering from abdominal pain due to chronic pancreatitis for pharmacotherapy, multidisciplinary treatment, and/or interventional therapy. Gastroenterology consultation is warranted for diagnosis, endoscopic evaluation, and treatment. Nutrition consultation is warranted for assistance with parenteral and enteral nutrition. General surgery consultation may be considered for surgical management of patients, where indicated.

Complications:

  • Pancreatic duct strictures
  • Pancreatic duct stenosis
  • Pseudocyst
  • Pancreatic abscess
  • Ascites
  • Bile duct stenosis with cholestasis
  • Duodenal stenosis
  • Maldigestion
  • Chronic abdominal pain

Patient Monitoring: varies, depending on activity of disease. In acute pancreatitis, serum markers (e.g., lipase) provide an index of disease (but not necessarily pain). For patients with indwelling percutaneous neuraxial (epidural or intrathecal) catheters, weekly or biweekly follow-up is recommended, along with home nursing. For patients having had splanchnic or celiac plexus denervation, 3 month follow-up is recommended.For patients with chronic indwelling intrathecal drug administration systems, pump refill and maintenance will be necessary on a 3- to 4-month interval, in general.

Miscellaneous:

✎ No correlation occurs between lab results, imaging, and severity of pain.

✎ The treatment of pain secondary to pancreatitis must be individualized and directed toward improving quality of life.

References

  1. Andren-Sandberg, et al. Pain management in chronic pancreatitis. Eur J Gastroenterol Hepatol. 2002;14(9):957-970.
  2. Bernhardt A, et al. Using epidural analgia in patients with acute pancreatitis: Prospective study of 121 patients. Anesthesiol Reanim. 2002;27(1):16-22.
  3. Bradley E, et al. Nerve blocks and neuroablative surgery for chronic pancreatitis. World J. Surg. 2003;27(11):1241-1248.
  4. Dassopoulos, et al. Acute pancreatitis in human immunodeficiency virus-infected patients: A review. Am J Med. 1999;107:78-84.
  5. Griffith H, et al. The Five-Minute Clinical Consult. Philadelphia: Lippincott. 794-795
  6. Kahn YN, Raza SS, Kahn EA. Application of spinal cord stimulation for the treatment of abdominal visceral pain syndromes: Case reports. Neuromodulation. 2005;8(1):14-27.
  7. Leksowski K. Thorascopic splanchnicectomy for the relief of pain due to pancreatitis. Surg Endosc. 2001;15(6):592-596.
  8. Mayerle J, et al. Medical treatment of acute pancreatitis. Gastroenterol Clin. 2004;33(4).
  9. Wilmer A. ICU management of severe acute pancreatitis. Eur J Intern Med. 2004;15(5):274-280.
  10. McCloy R. Chronic pancreatitis at Manchester, UK. Digestion. 1998;59:(Supply 4).
11th October, 2011