Table of Contents
Epidemiology of Pancreatitis
The per-year frequency of acute pancreatitis is about 40 for every 100,000 adults in the US. Globally, the frequency of the condition ranges between 5 and 80 cases for every 100,000 people.
The occurrence of acute pancreatitis is generally higher in males compared to females. Alcohol is a major cause of the condition in males. Biliary tract disease is the main cause of the condition in females.
Etiology of Pancreatitis
Gall stones obstructing the ampulla of Vatar is the most common cause of acute pancreatitis. It is believed that the obstruction by stone or edema from stone passage leads to backflow of the bile into the pancreatic duct leading to activation of the pancreatic enzymes and subsequently acute pancreatitis.
Ascariasis and pancreatic or ampullary tumors can also cause an ampullary obstruction and precipitate pancreatitis. Cholecystectomy in patients with gall stones prevents acute pancreatitis and guard against its recurrence.
Gall stones are more common in middle-aged overweight multiparous females. Small stones are more likely to pass through the cystic duct than the large ones causing an obstruction and acute pancreatitis.
Alcohol is responsible for up to 30 % of cases of acute pancreatitis and a major cause of chronic pancreatitis. It is believed that alcohol stimulates pancreatic cells to secrete lytic enzymes which initiate the inflammatory process and induce autolysis of the pancreas.
Elevation of the serum triglycerides levels can precipitate pancreatitis especially with TGL above 1,000 mg/dl. It is common in children with genetic disorders of lipoprotein metabolism, nephrotic syndrome, obesity, steroid therapy, hypothyroidism and diabetes mellitus.
Smoking is a risk factor for many pancreatic diseases including pancreatitis and pancreatic cancer.
Multiple drugs are involved in developing pancreatic inflammation but with good prognosis and low mortality. Common medications associated with pancreatitis include metronidazole, sulphonamides, valproic acid, Octeriotide, furosemide, didanosine, azathioprine, pentamidine, 6-mercaptopurine, and tetracycline. The mechanism of inflammation is different but they have a similar clinical presentation.
Genetic mutations including the CFTR gene in cystic fibrosis patients and PRSS1 gene are associated with pancreatitis.
- Post ERCP pancreatitis
- Viral infection, e.g. mumps and cytomegalovirus
Pathophysiology of Pancreatitis
The Pancreas gland produces insulin and manufactures and secretes digestive enzymes. About 80 % of the pancreases (by weight) is involved in the exocrine function.
The exact pathophysiology for acute pancreatitis is unclear. The current understanding is that both extracellular and intracellular factors contribute to the development of the condition.
Acute pancreatitis may result from any event that causes injury to the acinar cell and impairs the ability of the pancreas to the secrete zymogen granules.
There is also a possibility of systemic inflammatory response syndrome (SIRS), which leads to systemic shock. In the case of acute pancreatitis, the patient first develops parenchymal edema and peripancreatic fat necrosis; the phenomenon is referred to as acute edematous pancreatitis.
Clinical Presentation of Pancreatitis
The most characteristic clinical presentation of acute pancreatitis is the acute onset of severe epigastric abdominal pain that can be referred to the back and improves with leaning forward. The pain is severe and associated with nausea and vomiting. Severe pancreatitis can present with complications of pleural effusion, adult respiratory distress syndrome, and multi-organ failure.
General examination of the patients is remarkable for signs of circulatory collapse with hypotension, tachycardia, tachypnea, and hypoxemia. Signs of the causative etiology may be evident in some patients with scleral icterus in gall stones, hepatomegaly in cases of alcoholism or parotid enlargement in case of mumps.
Local examination of the abdomen reveals distension and tenderness which may be localized to the epigastrium or generalized with ileus and rigidity. Cullen’s sign is periumbilical ecchymosis while Turner’s sign is flank ecchymosis and both indicate retroperitoneal hemorrhage in case of hemorrhagic pancreatitis.
Diagnosis of Pancreatitis
This is considered a good initial screening test as a result of elevated pancreatic enzymes in the serum with acute inflammation. Serum amylase can be elevated more than 3 times normal range early in the course of inflammation and returns back to normal in a few days due to short half-life.
However, elevated serum amylase is not specific for acute pancreatitis as it can also present with acute cholecystitis, malignancy, renal failure, and ectopic pregnancy. Serum amylase can give false-negative results in case of alcoholic pancreatitis or hypertriglyceridemia as remarkable serum elevations maybe not evident.
This is more sensitive and specific than serum amylase and can last longer in the serum of patients after the resolution of symptoms. Nonspecific elevation of lipase is reported in cases of intestinal obstruction, peptic ulcer, celiac disease, and pancreatic tumors.
Elevated liver enzymes
ALT and AST are more accurate in diagnosing gall stone pancreatitis than alkaline phosphatase level.
Local complications include
- Pancreatic pseudocyst
- Acute necrosis
- Acute peripancreatic fluid collection
- Portosplenomesenteric venous thrombosis
Imaging in Pancreatitis
Abdominal ultrasound helps with detection of pancreatic enlargement or edema, fluid collection, and gall stone disease.
Abdominal CT scan with contrast can detect the severity and extent of pancreatic inflammation and necrosis if present. It also can help with identifying the etiology of pancreatitis.
MRI with and without gadolinium enhancement can detect pancreatic enlargement and necrosis.
Endoscopic retrograde cholangiogram can be diagnostic and therapeutic in gall stone pancreatitis. Papillotomy can be performed endoscopically in cases where surgery is contraindicated.
Prognosis of Pancreatitis
Acute pancreatitis can be mild or severe. Most patients with mild disease recover in few days while severe disease develops necrosis, organ failure, and the mortality is high. Some patients develop recurrent or chronic pancreatitis.
Management of Pancreatitis
Acute physiology and chronic health evaluation (APACHE) II score and systemic inflammatory response syndrome (SIRS) score are both used to evaluate the severity of pancreatitis.
APACHE score depends on patient’s age and different physiologic variants including Pa o2, temperature, pulse, mean arterial blood pressure, respiratory rate, conscious level, urine output, serum sodium, serum potassium, PH, serum glucose and calcium.
Treatment of acute pancreatitis is mainly supportive and depends on the severity of the disease. ICU admission is mandatory in cases with high APACHE score and severe disease.
Fluid resuscitation of patients to compensate for the fluid loss in the retroperitoneal and intraperitoneal spaces is the initial step in management.
Patients should be followed up with the measurement of urine output and central venous pressure to ensure optimal hydration. NPO and parenteral feeding are initiated as long as the patient complains of abdominal pain and nausea then enteral feeding starting with a liquid diet low in fat can be introduced within the first 48 hours.
Pain control with fentanyl or meperidine is indicated for severe abdominal pain. Morphine should be avoided in cases with gall stone pancreatitis as it increases the pressure of the sphincter of Oddi.
Antibiotic therapy is mainly reserved for patients with infection but not for routine administration. Imipenem and cilastatin are proven effective in penetrating pancreatic tissue and preventing abdominal infection.
Surgical intervention in acute pancreatitis is reserved for patients with necrotic pancreatitis to avoid infection and for hemorrhagic pancreatitis that leads to circulatory compromise. In case of infection or pancreatic abscess, CT guided needle aspiration is indicated or percutaneous drainage otherwise opens surgery with debridement of the necrotic and infected tissues.
Cholecystectomy or endoscopic retrograde intervention is indicated in gall stone pancreatitis in the same hospital setting to avoid recurrence.
One of the complications that can follow acute pancreatitis is persistent peripancreatic fluid collection known as pseudocysts. They lack epithelialized wall but are surrounded by adjacent structures such as pancreas, colon, omentum, and stomach.
Pseudocysts are usually asymptomatic but sometimes they present with dull pain and dyspepsia. Intestinal obstruction with nausea and vomiting due to the expansion of large cysts may develop. Digestion of the wall of blood vessels can lead to pseudoaneurysms and GI bleeding.
Pancreatic ascites and pleural effusion from leakage of the pancreatic enzymes in the abdomen or chest through a pancreatic fistula can lead to infection and sepsis. Treatment is usually surgical following control of pancreatic secretions with octreotide. Endoscopic drainage of the fluid via transpapillary approach or transmural approach is used to drain the fluid and prevent recurrence through a stent in the pancreatic duct or communicating the cyst with the small bowel (transmural enterocystostomy). Open surgical drainage is used for large pseudocysts by utilizing enteric anastomosis.
Progression of acute pancreatitis or recurrent attacks can lead to chronic pancreatitis with major structural and functional impairment of the exocrine and endocrine gland of the pancreas. Complications of chronic pancreatitis include pseudocyst formation, obstruction of the bile duct which may lead to jaundice and liver cirrhosis, duodenal obstruction with dyspepsia, portal hypertension, splenic vein thrombosis, and endocrine pancreatic insufficiency.
Patients with chronic pancreatitis can develop diabetes mellitus with fluctuations in blood glucose level. Follow up with serum glucose and HbA1c is indicated to determine diabetic potential and appropriate management. Symptoms of weight loss, anorexia, and abdominal pain should raise the suspicion of pancreatic adenocarcinoma in patients with chronic pancreatitis. Serial tumor markers and imaging for early diagnosis of pancreatic cancer are indicated.
Treatment of the patient with chronic pancreatitis starts with abstinence from alcohol and smoking. Frequent small meals with medium-chain fatty acids and pancreatic enzyme supplements are dietary modifications to decrease pancreatic stimulation and limit the pain. Opiates and amitriptyline can be used also to limit the pain and sometimes patients can benefit from hospitalization and a short period of NPO.
Surgical treatment of chronic pancreatitis is directed for pain control and correction of structural complications. Surgical intervention in the form of total pancreatectomy or partial resection of the pancreas is utilized to relieve intestinal obstruction or treatment of pancreatic cancer. Some patients with consistent pain are a good candidate to denervation of the afferent pathways through the celiac ganglion or radiation therapy.