At Glance
Acute Pancreatitis

Acute Pancreatitis

Acute pancreatitis or acute pancreatic necrosis is a sudden inflammation of the pancreas. It can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures, such as fasting and aggressive intravenous fluid rehydration, severe cases may require admission to the intensive care unit or even surgery to deal with complications of the disease process.

Symptoms and signs

The most common symptoms and signs include:

  1.            severe epigastric pain (upper abdominal pain) radiating to the back in 50% cases
  2.            nausea
  3.            vomiting
  4.            loss of appetite
  5.            fever
  6.            chills (shivering)
  7.           hemodynamic instability, including shock
  8.            tachycardia (rapid heartbeat)
  9.            respiratory distress
  10.            peritonitis
  11.            hiccup

Although these are common symptoms, they are not always present. Simple abdominal pain may be the sole symptom.

Signs that are less common, and indicate severe disease, include:

  1.       Grey-Turner's sign (hemorrhagic discoloration of the flanks)
  2.       Cullen's sign (hemorrhagic discoloration of the umbilicus)
  3.       Pleural effusions (fluid in the bases of the pleural cavity)
  4.       Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus

        due to local toxic lesion of the vessels)                            

Causes

Most common causes

•             Alcohol

•             Gallstones

•             Post-ERCP

•             Abdominal trauma

•             Penetrating ulcers

•             Carcinoma of the head of pancreas, and other cancer

•             Structural abnormalities: choledochocele, pancreas divisum

•             Radiation X-ray[citation needed]

•             Autoimmune pancreatitis

Pathology

Pathogenesis

Acute pancreatitis occurs when there is abnormal activation of digestive enzymes within the pancreas. This occurs through inappropriate activation of inactive enzyme precursors called zymogens (or proenzymes) inside the pancreas, most notably trypsinogen. Normally, trypsinogen is converted to its active form (trypsin)) in the first part of the small intestine (duodenum), where the enzyme assists in the digestion of proteins. During an episode of acute pancreatitis, trypsinogen comes into contact with lysosomal enzymes (specifically cathepsin), which activate trypsinogen to trypsin. The active form trypsin then leads to further activation of other molecules of trypsinogen. The activation of these digestive enzymes lead to inflammation, edema, vascular injury, and even cellular death. The death of pancreatic cells occurs via two main mechanisms: necrosis, which is less organized and more damaging, or apoptosis, which is more controlled. The balance between these two mechanisms of cellular death is mediated by caspases which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate.

Pathophysiology

The two types of acute pancreatitis are mild and severe, which are defined based on whether the predominant response to cell injury is inflammation (mild) or necrosis (severe). In mild pancreatitis, there is inflammation and edema of the pancreas. In severe pancreatitis, there is necrosis of the pancreas, and nearby organs may become injured.

As part of the initial injury there is an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage.

Histopathology

The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessel necrosis (hemorrhage). These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces as well as vessel damage. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Due to the pancreas lacking a capsule, the inflammation and necrosis can extend to include fascial layers in the immediate vicinity of the pancreas.

Diagnosis

Acute pancreatitis is diagnosed clinically but requires CT evaluation to differentiate mild acute pancreatitis from severe necrotic pancreatitis. Experienced clinicians were able to detect severe pancreatitis in approximately 34-39% of patients who later had imaging confirmed severe necrotic pancreatitis. Blood studies are used to identify organ failure, offer prognostic information, determine if fluid resuscitation is adequate, and if antibiotics are indicated.

Blood investigations – Full blood count, renal function tests, liver function, serum calcium, serum amylase and lipase, Arterial blood gas, Trypsin-Selective Test.

Imaging – A triple phase abdominal CT and abdominal ultrasound are together considered the gold standard for the evaluation of acute pancreatitis. Other modalities including the abdominal x-ray lack sensitivity and are not recommended. An important caveat is that imaging during the first 12 hours may be falsely reassuring as the inflammatory and necrotic process usually requires 48 hours to fully manifest.

Computed tomography

Regarding the need for computed tomography, practice guidelines state:

CT is an important common initial assessment tool for acute pancreatitis. Imaging is indicated during the initial presentation if:

  1. the diagnosis of acute pancreatitis is uncertain
  2. there is abdominal distension and tenderness, fever >102, or leukocytosis
  3. there is a Ranson score > 3 or APACHE score > 8
  4. there is no improvement after 72 hours of conservative medical therapy
  5. there has been an acute change in status: fever, pain, or shock

CT is recommended as a delayed assessment tool in the following situations:

  1. acute change in status
  2. to determine therapeutic response after surgery or interventional radiologic procedure
  3. before discharge in patients with severe acute pancreatitis

CT abdomen should not be performed before the first 12 hours of onset of symptoms as early CT (<12 hours) may result in equivocal or normal findings.

CT Findings can be classified into the following categories for easy recall:

  1. Intrapancreatic – diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
  2. Peripancreatic / extrapancreatic – irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
  3. Locoregional – Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus, etc.

Magnetic resonance imaging

While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis, magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris. Additional utility of MRI includes its indication for imaging of patients with an allergy to CT's contrast material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms, and venous thrombosis.

Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP) sequences. MRCP provides useful information regarding the etiology of acute pancreatitis, i.e., the presence of tiny biliary stones (choledocholithiasis or cholelithiasis) and duct anomalies. Clinical trials indicate that MRCP can be as effective a diagnostic tool for acute pancreatitis with biliary etiology as endoscopic retrograde cholangiopancreatography, but with the benefits of being less invasive and causing fewer complications.

Treatment

Initial management of a patient with acute pancreatitis consists of supportive care with fluid resuscitation, pain control, and nutritional support.

Fluid replacement

Aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (e.g., normal saline or lactated Ringer’s solution) to all patients with acute pancreatitis, unless cardiovascular, renal, or other related comorbid factors preclude aggressive fluid replacement. In patients with severe volume depletion that manifests as hypotension and tachycardia, more rapid repletion with 20 mL/kg of intravenous fluid given over 30 minutes followed by 3 mL/kg/hour for 8 to 12 hours.

Fluid requirements should be reassessed at frequent intervals in the first six hours of admission and for the next 24 to 48 hours. The rate of fluid resuscitation should be adjusted based on clinical assessment, hematocrit and blood urea nitrogen (BUN) values.

In the initial stages (within the first 12 to 24 hours) of acute pancreatitis, fluid replacement has been associated with a reduction in morbidity and mortality.

There is some evidence that fluid resuscitation with lactated Ringer’s solution may reduce the incidence of Systemic Inflammatory Response Syndrome (SIRS) as compared with normal saline.

Pain control

Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics.

Opioids are safe and effective at providing pain control in patients with acute pancreatitis.[39] Adequate pain control requires the use of intravenous opiates, usually in the form of a patient-controlled analgesia pump. Hydromorphone or fentanyl (intravenous) may be used for pain relief in acute pancreatitis. Fentanyl is being increasingly used due to its better safety profile, especially in renal impairment. As with other opiates, fentanyl can depress respiratory function. It can be given both as a bolus as well as constant infusion. Meperidine has been historically favored over morphine because of the belief that morphine caused an increase in sphincter of Oddi pressure. However, no clinical studies suggest that morphine can aggravate or cause pancreatitis or cholecystitis.[40] In addition, meperidine has a short half-life and repeated doses can lead to accumulation of the metabolite normeperidine, which causes neuromuscular side effects and, rarely, seizures.

Bowel rest

In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving them nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest.[citation needed] Approximately 20% of patients have a relapse of pain during acute pancreatitis.[41] Approximately 75% of relapses occur within 48 hours of oral refeeding.[citation needed]

The incidence of relapse after oral refeeding may be reduced by post-pyloric enteral rather than parenteral feeding prior to oral refeeding.[41] IMRIE scoring is also useful.

Nutritional support

Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as fungemia). The additional advantages of post-pyloric feeding are the inverse relationship of pancreatic exocrine secretions and distance of nutrient delivery from the pylorus, as well as reduced risk of aspiration.

Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the trachea even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea). Oxygen may be provided in some patients (about 30%) if Pao2 levels fall below 70mm of Hg.

 

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