Page 465 - Concise Pathology for Exam Preparation ( PDFDrive )

450 SECTION II Diseases of Organ Systems

Pathology

• Damage to microvasculature leads to oedema.
• Fat necrosis by lipases causes fat cells to become indistinct and ghost like (loss of inter-
nal structure). The entire field appears bluish due to the deposition of calcium salts.
These areas appear chalky white on gross examination.
• Acute inflammatory reaction
• Destruction of pancreatic parenchyma (pancreatic acini and ducts)
• Destruction of blood vessels with resulting haemorrhage.
• Ascites is found in severe cases. The fluid is turbid, brownish yellow, or blood tinged.

Occurs in Two Forms

• Milder form: Mostly, there is interstitial oedema with mild inflammation. Focal mild
necrosis of acinar cells may sometimes be seen. This form occurs in terminally ill
patients, various forms of shock and after prolonged operations. It is recognized by
mild elevation of pancreatic enzymes in the blood, is self-limiting and usually resolves
spontaneously.
• Acute necrotizing/haemorrhagic pancreatitis: May be life-threatening. Caused by
enzyme-mediated destruction of pancreatic and peripancreatic tissue. Neutrophils in-
vade the necrotic tissue. In later stages, neutrophils are replaced by macrophages and
the entire area undergoes fibrosis.

Clinical Features
• Sudden onset of severe abdominal pain usually in the left upper quadrant of the abdomen;
may radiate to the back
• Nausea and vomiting, fever, sweating, tachypnea and tachycardia followed by periph-
eral vascular collapse

Laboratory Findings

• Neutrophilic leukocytosis: Increase in neutrophil count
• Serum amylase: It is a sensitive marker for acute pancreatitis in the first 24 h; especially,
if the elevation is four times above normal values.
• Urinary amylase: Amylase is excreted in urine. Amylase levels in urine become elevated
from the second day onwards and may remain elevated for 7–10 days. This test has
little specificity and sensitivity.
• Serum lipase: It appears little later than amylase in blood, but it is more specific.
• Trypsin: This enzyme has the highest specificity and sensitivity for pancreatic injury,
but its measurement requires the use of a radioimmunoassay, which is not available in
all hospitals.
• Hypocalcaemia: Due to precipitation of calcium in the areas of fat necrosis. If persistent
indicates a poor prognosis.
• X-rays: Plain X-rays are important to exclude perforation of an ulcer (visible air under
the diaphragm), and CT scan aids in demonstrating the enlarged pancreas and ascites
(fluid if analysed biochemically shows increased amount of pancreatic enzymes).

Complications
• Shock: It is multifactorial, but mostly due to increased vascular permeability caused by
the action of pancreatic enzymes.
• DIC: Endothelial injury caused by pancreatic enzymes in circulation leads to the forma-
tion of platelet and fibrin thrombi in small vessels.
• ARDS: It is a manifestation of shock.
• Renal failure: It is mostly a consequence of shock.
• Pseudocyst formation: Massive necrosis leads to liquefactive necrosis of the tissue. The
necrotic area becomes walled off by granulation tissue, which transforms later into a
fibrous scar. The cyst contains fluid full of pancreatic enzymes.

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