Acute Pancreatitis

Acute pancreatitis is a sudden inflammation of the pancreas. The most common symptoms and signs include severe, dull epigastric pain, nausea, vomiting, diarrhea, anorexia and fever. Alcohol consumption and biliary stone disease cause most cases of acute pancreatitis.

  • Processes: auto immune
  • Incidence: 63 / 100.000

Overview

Acute pancreatitis is a clinical emergency defined as the sudden onset inflammation of the pancreas that may resolve in a few days. Inflammation of the pancreas may lead to auto-digestion of the organ.

The pancreas is a digestive organ found behind the stomach that secretes enzymes and aids in the digestion of carbohydrates, proteins and fats. It is also an endocrine organ that helps the regulation of plasma glucose by secreting the hormones insulin and glucagon. Acute pancreatitis may be managed medically without the need of surgery.

Etiology

The most common cause of acute pancreatitis is gallstone formation that is lodged in the bile duct. Alcoholism is also a common cause of acute pancreatitis that could clinically resolve within two days. The less common causes of acute pancreatitis include infections, infestations, genetic defects and tumors of the pancreas.

Patients with celiac disease have a very high prevalence of acute pancreatitis due to pancreatic insufficiency [1]. Abdominal trauma and some elicit medications may trigger the inflammation of the pancreas in some cases.

In rare occasions, acute pancreatitis may be initiated after its inadvertent manipulation with some diagnostic procedures like endoscopic retrograde cholangio-pancreatography (ERCP) [2].

Epidemiology

In the United States, approximately 40 cases of adult pancreatitis in 100,000 population per year is observed [3]. The incidence of acute pancreatitis worldwide is 5 to 80 per 100,000 population with the highest prevalence in Finland and the US [4]. Other European countries and Hong Kong has a predominance of gallstone pancreatitis compared to the alcoholic type observed in the US.

Alcohol related acute pancreatitis has a median age of onset at 39 years old while those cases related to the biliary tract has median age of 69 years old [5]. Patients suffering from AIDS may manifest pancreatitis early at a median age of 31 years old.

Males are more predisposed to acute pancreatitis than females due to alcohol related issues. The relative risk of African American for acute pancreatitis within the age group of 35 to 64 years is 10 times higher than any other age group risk in the United States.

Pathophysiology

The pathophysiology of acute pancreatitis is grossly due to the imbalance of the gland’s homeostasis or normal functioning. Common inciting factors like alcohol use, gallstones, and certain drugs injure the exocrine acinar cells of the pancreas and impair the secretion of zymogen granules.

Once the process of acute pancreatitis is triggered, lysosomal and zymogen granule compartments fuse which advertently activate the trypsinogen to trypsin that initiates autodigestion. The intracellular trypsin activates the entire zymogen cascade of events aggravating the autodigestive process. The molecular fragments formed from the secretory vesicles of the exocrine membranes attract inflammatory cells that further damage the organ.

The increase in early mediators in bloodstream like plasma tumor necrosis factor–alpha (TNF-a), interleukin 6 (IL-6), and interleukin 8 (IL-8) suggests that an inflammatory response triggered by the macrophages and activated neutrophils is in effect in acute pancreatitis. These same mediators cause an increase in vascular permeability in the pancreas which may lead to necrosis, edema and hemorrhage.

A systemic cascade of mediators and cytokines leads to complications like acute respiratory distress syndrome (ARDS), bacteremia, pleural effusion, gastrointestinal hemorrhage, and renal failure. Systemic inflammation may lead to hypotensive shock which may lead to mortality.

Prognosis

Out of 100 cases of acute pancreatitis 10 to 15 cases die. Mortality cases are more pronounced in biliary pancreatitis compared to alcoholic ones. Acute pancreatitis patients who complicate with organ failures has a mortality rate of 30% [6].

However, in cases of pancreatitis with necrosis presenting with no organ failure mortality rate is almost zero. Majority of deaths in the first week of illness is due to multi-organ failure. Recent studies have demonstrated that an increased neutrophil-lymphocyte ratio (NLR) in the first 48 hours of the disease increases the likelihood of a severe pancreatitis attack carrying a grimmer prognosis [7].

Complications

The following disease conditions may complicate from acute pancreatitis:

  • Recurrence: The pancreas may inflame again if the inciting factors aren’t dealt with accordingly.
  • Acute renal failure: The kidneys are the most sensitive organ to hypotensive and hypovolemic shock.
  • Acute respiratory distress syndrome (ARDS): The systemic inflammatory response may incapacitate the lung function and cause acute dyspnea.
  • Heart Failure: Persistent shock may lead to cardiac pump overload and results to failure.
  • Pancreatic cysts or abscess: The unabated exocrine auto-digestion may form abscess or cyst in the pancreatic parenchyma.
  • Ascites: The irritation of the retroperitoneum from the inflammation may propagate extracellular fluid build-up in the abdominal cavity.
  • Fungal superinfection: This may develop late in the clinical course [8].
  • Hypotension: The systemic inflammatory response to acute pancreatitis dilates the vessels and cause a drop in blood pressure.

Presentation

The most common presenting sign of acute pancreatitis is pain on the epigastric area involving the upper left quadrant of the abdomen. Abdominal pain is aggravated with intake of drinks and food especially those with high fat content. Patient usually appears prostrated because pain becomes worst when lying flat on the back. Referred pain is usually felt at the back by the edge of the lower left shoulder blades.

General appearance will convey an ill-looking person with heavy sweating. Patients may also complain of fever, nausea and vomiting in the early part of the disease. Other gastrointestinal symptoms like feeling of fullness, intractable hiccups, clay-colored stools, indigestion and sometimes jaundice are also associated with acute pancreatitis.

Workup

The following diagnostic tests are used to evaluate acute pancreatitis:

  • Serum amylase: An increase in serum amylase level is always present with acute pancreatitis.
  • Urine amylase: In the same way, amylase excretion in the urine is also evident.
  • Serum lipase: An increase in serum lipase correlates well with the disease.
  • Complete blood count: Demonstrates the acuteness of the disease while the neutrophil to lymphocyte ratio is valuable a predictor of pancreatitis prognosis.
  • Serum electrolyte: Determines any instability in the electrolyte balance during the inflammatory process.
  • Imaging methods like CT-scan, ultrasound and MRI can demonstrate the inflaming pancreas in the acute phase of the disease.

Treatment

The medical approach in the treatment of acute pancreatitis revolves on pain management with intravenous analgesics and bowel rest. Parenteral feeding or fluid maintenance may ensue for weeks till full recovery. A nasogastric tube (NGT) may be inserted for a week or two to drain the contents of the stomach especially with paralytic ileus.

The introduction of intravenous antibiotics may prevent necrosis if given early in the course. Surgical intervention may be imployed in the removal of gallstones or any blockage in the bile ducts that incites the disease. A cohort study was performed demonstrating that an early cholecystectomy in the first 48 hours shortens the clinical course of pancreatitis [9]. Fluid drainage of the pancreas may be performed in some cases to relieve inflammation.

Prevention

The early diagnosis of the disease and early medical interventions may prevent serious complications in acute pancreatitis. The early demonstration of gallstone in the biliary tree through imaging must be promptly performed to prevent pancreatitis. Pancreatic tumors and cysts must also be dealt with accordingly for the same purpose. Alcohol binge drinking must be avoided to prevent occurrence of the disease.

Patient Information

Acute pancreatitis is the sudden onset of inflammation of the pancreas. Proper education about the disease and how it is prevented to high risk individuals is of paramount importance. Patients who have just recovered from acute pancreatitis may tolerate low fat diet and clear liquids initially [10]. Avoidance of fatty foods and alcohol binges may lessen the risk of recurrence. Encourage them to inform their physicians about any abdominal trauma they may have incurred recently to avoid any risk in the future.

References

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  2. Ito K, Fujita N, Kanno A, Matsubayashi H, Okaniwa S, Nakahara K, Suzuki K, Enohara R. Risk factors for post-ERCP pancreatitis in high risk patients who have undergone prophylactic pancreatic duct stenting: a multicenter retrospective study. Intern Med. 2011; 50(24):2927-32 
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  7. Suppiah A, Malde D, Arab T, Hamed M, Allgar V, Smith AM, et al. The Prognostic Value of the Neutrophil-Lymphocyte Ratio (NLR) in Acute Pancreatitis: Identification of an Optimal NLR. J Gastrointest Surg. Feb 1 2013;
  8. Maraví-Poma E, Gener J, Alvarez-Lerma F, Olaechea P, Blanco A, Domínguez-Muñoz JE. Early antibiotic treatment (prophylaxis) of septic complications in severe acute necrotizing pancreatitis: a prospective, randomized, multicenter study comparing two regimens with imipenem-cilastatin. Intensive Care Med. Nov 2003;29(11):1974-80.
  9. Aboulian A, Chan T, Yaghoubian A, Kaji AH, Putnam B, Neville A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. Apr 2010;251(4):615-9.
  10. Jacobson BC, Vander Vliet MB, Hughes MD, Maurer R, McManus K, Banks PA. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. Aug 2007;5(8):946-51; quiz 886.

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