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Acute Pancreatitis - Coggle Diagram
Acute Pancreatitis
Key assessment findings
The most common symptom of acute pancreatitis is a sudden onset of sharp, twisting, deep, upper abdominal pain.
It frequently radiates to the back and is associated with nausea and vomiting.
Localized pain commonly reflects mild acute pancreatitis, while more diffuse pain may be associated with severe or necrotizing pancreatitis.
The degree of pain may or may not reflect the severity of the disease process.
Other common signs and symptoms of acute pancreatitis are anorexia, hypoactive bowel sounds, upper abdominal tenderness without rigidity, abdominal distension, and diarrhea.
In more severe cases, the patient may have fever, tachycardia, hypotension, weakness, diaphoresis, shock, jaundice, and peritoneal signs, such as guarding and rebound tenderness.
Managing the acute episode
Treating an episode of acute pancreatitis includes supportive care and curative interventions when possible.
The first goal is to stabilize the patient hemodynamically.Administer I.V. crystalloids such as lactated Ringer’s solution or colloids and plasma expanders for more critically ill patients, as prescribed.
Early aggressive I.V. hydration has been associated with less complications and improved outcomes.
Monitor vital signs, oxygen saturation, pain intensity level, intake and output, hematocrit, and BUN levels to help assess hemodynamic stability.
A patient with severe acute pancreatitis may need support with an inotropic drug such as I.V. dobutamine, hemodynamic monitoring, mechanical ventilation, and monitoring of intra-abdominal pressure via the bladder for development of abdominal compartment syndrome.
As prescribed, manage pain with an opioid such as fentanyl or hydromorphone.Besides making the patient more comfortable, these drugs decrease pancreatic enzyme secretion.
Consistently assess the patient’s pain using the same pain intensity rating scale each time to determine changing patterns of pain and evaluate the patient’s response to treatment.
Eating stimulates pancreatic secretions, so keep the patient N.P.O. until nausea and vomiting have resolved, serum amylase levels start returning to normal, and pain subsides.
The patient may need a nasogastric tube to manage vomiting or paralytic ileus.
Enteral feeding stabilizes gut bacteria, which prevents bacterial translocation and subsequent infection, and is more physiologic than parenteral nutrition (PN).
What diagnostic tests reveal？
An abdominal ultrasound can help determine the presence of gallstones quickly, noninvasively, and without radiation.
An abdominal CT scan is usually performed with contrast to confirm an unclear diagnosis and to evaluate the extent of damage to the pancreas and surrounding region.
Endoscopic retrograde cholangiopancreatography (ERCP), an invasive diagnostic procedure, uses an endoscope to view the ampulla of Vater, pancreas, and bile ducts.ERCP requires contrast medium and fluoroscopy.
An advantage of ERCP is that it can also be used to remove obstructions such as gallstones, perform biopsies, and/or insert a stent to promote drainage.
Magnetic resonance cholangiopancreatography (MRCP) is a noninvasive procedure that allows visualization of the biliary tree and pancreatic ducts.This doesn’t involve contrast media and is less risky for the patient than ERCP.
Inflammation triggers autodigestion
Acute pancreatitis is characterized by pancreatic inflammation resulting in autodigestion, or the breakdown of pancreatic tissue by its own activated enzymes.
During pancreatitis, however, inflammation delays release of activated enzymes, giving them time to attack pancreatic cells and leak into surrounding tissues.
This process causes more inflammation.
The damage in acute pancreatitis occurs in stages：
Premature activation of trypsin, amylase, lipase, and other enzymes occurs inside the pancreas.
Intrapancreatic inflammation through the release of cytokines and other proinflammatory mediators leads to micro and macrovascular failure as the activated digestive enzymes autodigest the pancreas and peripancreatic tissues.
In the last stage, extrapancreatic or systemic inflammation and injury may occur.
Severity of pancreatitis
Moderately severe acute pancreatitis
Organ failure that resolves in 48 hours
Local or systemic complications without persistent organ failure
Severe acute pancreatitis
Persistent single or multiple organ failure (> 48 hours)
Mild acute pancreatitis
No organ failure
Lack of local or systemic complications
A diagnosis of acute pancreatitis requires at least two of the following：
characteristic abdominal pain
serum amylase and/or lipase level at least three times the upper limit of normal.These enzymes leak into the blood as pancreatic cells are damaged.
characteristic findings from abdominal imaging (CT scan, magnetic resonance imaging, or ultrasound).
Assessment
BISAP
uses vital signs, mental status, age, blood urea nitrogen (BUN), white blood cell count, and pleural effusion detected on imaging
HAPS
uses absence of rebound tenderness, creatinine< 2 mg/dL, and normal hematocrit to predict mild cases of acute pancreatitis
Looking at factors such as age, body mass index, comorbidities, lab values, and systemic inflammatory response syndrome (SIRS) to deter- mine those most at risk for developing organ failure is recommended.
SIRS criteria
SIRS is defined as two or more of the following：
temperature, < 36 ̊ C (96.8 ̊ F) or > 38 ̊ C (100.4 ̊ F)
respiratory rate > 20 breaths/minute or PaCO2 < 32 mm Hg
pulse > 90 beats/minute
WBC count < 4.0 or > 12.0 cells/mm3 or > 10% immature neutrophils (bands)
Possible systemic complications
For example, most patients with severe acute pancreatitis experience hypoxemia or other respiratory issues in the first 2 days.
Risk factors such as obesity, age (>55), medical comorbidities, presence of hypovolemia, SIRS, mental status changes on presentation, pleural effusion or infiltrates, and multiple or extensive fluid collections outside of the pancreas are associated with development of severe disease.
Routine nursing care should include the following：
Monitor patients for early signs and symptoms of complications, such as increased abdominal pain and tenderness, fever, and WBC count.Changes in mental status are early signs of impending respiratory failure or shock.
Assess for a bluish discoloration around the umbilicus (Cullen sign) or a reddish-brown discoloration along the flanks (Grey-Turner sign); these may indicate hemorrhagic pancreatitis or expelled exudates from necrotic areas.
Assess for dizziness or lightheadedness and hypotension.
Document intake and output and assess for signs and symptoms of fluid overload, including dyspnea, peripheral edema, crackles in the lung fields especially the bases, and electrolyte imbalances.
Document urine/stool characteristics
Monitor intra-abdominal pressure for development of abdominal compartment syndrome.
Watch for Chvostek or Trousseau signs as indicators of hypocalcemia.