Acute Pancreatitis

Presentation/etiology:

▪ mild to severe epigastric pain, with radiation to the flank, the back, or both.
▪ pain is characterized as constant, dull and boring, and is worse when the patient is
supine.
▪ discomfort may lessen when patient is sitting or in a fetal position.
▪ nausea and nonfeculent vomiting are present in 75-90% of patients.
▪ many causes, but the mechanisms by which these trigger acute pancreatitis have not
been identified.
▪ a heavy meal or a drinking binge often triggers the pain.
- patients as young as 30 can present with acute pancreatitis secondary to alcohol
consumption. Estimated amounts are 150 g of alcohol per day, but can be as
minimal as 50 g (4 beers). It usually develops after 4 to 7 years of drinking.
- Biliary pancreatitis usually occurs in older adults. These patients usually have a
history of cholelithiasis or intermittent, postprandial right upper-quadrant pain.
▪ 2-5% of cases are drug related—hypersensitivity reaction or production of a toxic
metabolite.
▪ autodigestion is one pathogenetic theory, where pancreatitis results when proteolytic
enzymes are activated in the pancreas rather than in the intestinal lumen.

Signs:

▪ between 50 and 90% of patients have signs of abdominal distension or muscle spasms
with epigastric pain and left upper-quadrant tenderness.
▪ other signs are fever, tachycardia, and jaundice.
▪ patient is often restless and dehydrated on presentation.
Lab:

▪ Amylase serum amylase levels start increasing from 2 to 12 hours after the onset of
symptoms and peaks at 12 to 72 hours. It usually returns to normal within one week.
This method is quick, easily obtained, and inexpensive. 75-92% sensitive, 20 to 60%
specific.
▪ Lipase lipase levels increase within 4 to 8 hours of the onset of clinical symptoms
and peak at about 24 hours. Levels decrease within eight to 14 days. 86-100% sensitive,
50-99% specific.
▪ Trypsin/Elastase elevated trypsin level has a better likelihood ratio for detecting
pancreatitis than the amylase level and is probably the most accurate serum indicator for
acute pancreatitis. Serum trypsin assay is not widely available and therefore is not
routinely used.
▪ Hepatic Function Studies hepatic transaminase levels may be elevated in patients
with pancreatitis caused by alcohol abuse or cholelithiasis with obstruction. However,
these tests are not sufficiently reliable for diagnosing acute biliary pancreatitis or
determining its etiology.
Radiology:

▪ Plain Radiographs may support diagnosis when certain findings are present—a gas-
filled duodenum (sentinal loop) secondary to obstruction is the most specific for
pancreatitis.
▪ Ultrasonography an acceptable study for initial evaluation when biliary causes are
suspected. It is non-invasive, relatively inexpensive and may be performed at he bedside.
In 35% of cases, the pancreas is obscured secondary to bowel gas.
▪ Computed Tomography contrast-enhanced CT provides the best imaging of the
pancreas and surrounding structures. Useful when other diagnostic studies are
inconclusive, when the patient has severe symptoms, when fever is present or in the face
of persistent leukocytosis that suggests secondary infection.
▪ Endoscopic Retrograde Cholangiopancreatography (ERCP) ERCP has a limited role
in management of acute pancreatitis. It is indicated in patients with severe disease who
are suspected of having biliary obstruction. The risks include precipitating an acute
episode of pancreatitis, introducing infection and causing hemorrhage and perforation.

Complications:

▪ most complications and subsequent deaths occur within two weeks of onset of pain.
▪ 2º pancreatic infection is the most common cause of death, 70-80% of deaths.
▪ complications frequently manifest as necrosis and organ failure, which often includes
cardiovascular (bleeding into the retroperitoneal space and decreased vascular resistance),
pulmonary (mild atelectasis to life threatening adult respiratory distress syndrome) and
renal systems (rise in creatinine 2º to cardiovascular collapse and hypotension, resulting
in acute tubular necrosis).
▪ Purtscher’s retinopathy unusual complication, it is a sudden loss of vision in a patient
with acute pancreatitis. It is characterized by a peculiar funduscopic appearance with
cotton-wool spots and hemorrhages confined to an area limited by the optic disk and
macula.

Treatment:

▪ if no complications occur, it usually improves on its own. Analgesics are given for
pain, intravenous fluids and colloids to maintain normal intravascular volume, no oral
alimentation, and nasogastric suction to decrease gastrin release from the stomach and
prevent gastric contents from entering the duodenum.
▪ treatment is designed to support vital functions and prevent complications.
▪ antibiotics may be prescribed if an infection develops.
▪ surgery may be necessary.