What Are Acute Pancreatitis Symptoms, Causes, Diagnosis, Treatment


What Are Acute Pancreatitis Symptoms, Causes, Diagnosis, Treatment

[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_single_image image=”16923″ img_size=”full” style=”vc_box_rounded”][/vc_column][/vc_row][vc_row][vc_column][vc_empty_space][/vc_column][/vc_row][vc_row equal_height=”yes” content_placement=”top”][vc_column width=”1/2″][vc_column_text]The pancreas is a gland located behind the stomach which secretes potent digestive juices or enzymes into the small intestine to aid the digestion of carbohydrates, proteins, and fat. It also releases the hormones insulin and glucagon into the bloodstream; which are involved in blood glucose metabolism, regulating how the body stores and uses food for energy.[/vc_column_text][/vc_column][vc_column width=”1/2″][vc_single_image image=”16931″ img_size=”large” alignment=”right” style=”vc_box_rounded”][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Normally, digestive enzymes secreted by the pancreas do not become active until they reach the small intestine. When the pancreas is inflamed (pancreatitis), the enzymes inside it attack and damage the tissues that produce them. Pancreatitis can be acute or chronic. Either form is serious and can lead to complications. In severe cases, bleeding, infection, and permanent tissue damage may occur. Both forms of pancreatitis occur more often in men than women.[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Acute Pancreatitis Causes

Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days with treatment. Acute pancreatitis is a leading gastrointestinal cause of hospitalization in the United States and it can be a life-threatening illness with severe complications.

The most common cause are:

Gallstones, which are small, pebble-like substances made of hardened bile – that cause inflammation in the pancreas as they pass through the common bile duct obstructing the pancreatic duct. Gallstones are the most common cause of acute pancreatitis accounting for 40 to 70% of cases.

Alcohol use is responsible for approximately 25 to 35% of cases of acute pancreatitis in the United States. Acute pancreatitis can occur within hours or as long as 2 days after consuming alcohol.

Hypertriglyceridemia — May account for 1 to 14% of cases. Serum triglyceride concentrations above 1000 mg/dL (11 mmol/L) can precipitate attacks of acute pancreatitis, although lower levels may also contribute to severity.

Post-endoscopic retrograde cholangiopancreatography (ERCP) — Acute pancreatitis occurs in about 3% of patients undergoing diagnostic ERCP.

Genetic risk — Patients with genetic risk for pancreatitis may present as recurrent acute pancreatitis, or childhood pancreatitis without a known cause and eventually progress to chronic pancreatitis.

Medications — Pancreatitis due to medications is rare (<5%). The prognosis of drug-induced pancreatitis is generally excellent and mortality is low.

– Mechanisms of drug-induced pancreatitis include immunologic reactions (eg, 6-mercaptopurine, aminosalicylates, sulfonamides), direct toxic effect (eg, diuretics, sulfonamides), accumulation of a toxic metabolite (eg, valproic acid, pentamidine, tetracycline), ischemia (diuretics, azathioprine), intravascular thrombosis (eg, estrogen), and an increased viscosity of pancreatic juice (eg, diuretics and steroids).

Abdominal trauma — Blunt or penetrating trauma can damage the pancreas, however, these injuries are uncommon due to the retroperitoneal location of the pancreas.

Other rare causes includes:

Biliary sludge and microlithiasis,
Biliary obstruction,
Infections and toxins,
Vascular disease,
Anatomic or physiologic pancreatic anomalies,
Idiopathic causes.

[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Acute Pancreatitis Symptoms:

Signs and symptoms of pancreatitis may vary, depending on which type pancreatitis the patient is experiencing, which includes:

– Epigastric abdominal pain,
– Abdominal pain that radiates to the back,
– Abdominal pain that feels worse after eating,
– Nausea,
– Vomiting,
– Tenderness when touching the abdomen, especially the epigastric area.

[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Laboratory Findings:

Pancreatic enzymes and products — Early in the course of acute pancreatitis, there is a breakdown in the synthesis-secretion coupling of pancreatic digestive enzymes; synthesis continues while there is a blockade of secretion. As a result, digestive enzymes leak out of acinar cells through the basolateral membrane to the interstitial space and then enter the systemic circulation.

Serum amylase — Serum amylase rises within 6 to 12 hours of the onset of pancreatitis. Amylase has a short half-life of approximately 10 hours and in uncomplicated attacks returns to normal within three to five days.

– Serum amylase elevation of greater than 3x the upper limit of normal elevation of serum amylase has a specificity 67 to 83% and a sensitivity of 85 to 98% for the diagnosis of acute pancreatitis.

Serum lipase — Serum lipase has a sensitivity for acute pancreatitis ranging from 82 to 100%. Serum lipase rises within four to eight hours of the onset of symptoms, peaks at 24 hours, and returns to normal within 8 to 14 days.

Other enzymes and productsTrypsinogen activation peptide (TAP), a five amino-acid peptide that is cleaved from trypsinogen to produce active trypsin, is elevated in acute pancreatitis. Since activation of trypsin is likely an early event in the pathogenesis of acute pancreatitis, TAP may be useful in early detection and as a predictor of the severity of acute pancreatitis.

Markers of immune activation — Activation of granulocytes and macrophages in acute pancreatitis results in release of a number of cytokines and inflammatory mediators. Other associated markers includes elevations in C-reactive protein (CRP), interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF), and PMN elastase. A CRP level above 150 mg/L at 48 hours is associated with severe pancreatitis.

Other laboratory findings — Patients with pancreatitis may have:

– Leukocytosis,
– Elevated hematocrit from hemoconcentration due to extravasation of intravascular fluid into third spaces.
– Elevated blood urea nitrogen (BUN),
– Hypocalcemia,
– Hyperglycemia,
– Hypoglycemia.

[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Imaging

Several features may be seen on imaging in patients with acute pancreatitis.

Abdominal and chest radiographs — The radiographic findings in acute pancreatitis range from unremarkable in mild disease to localized ileus of a segment of small intestine (sentinel loop) or the colon cutoff sign in more severe disease. The colon cut off sign reflects a paucity of air in the colon distal to the splenic flexure due to functional spasm of the descending colon secondary to pancreatic inflammation. A ground glass appearance may indicate the presence of an acute peripancreatic fluid collection.

Abdominal ultrasound — In patients with acute pancreatitis, the pancreas appears diffusely enlarged and hypoechoic on abdominal ultrasound. Gallstones may be visualized in the gallbladder or the bile duct.

Abdominal computed tomography — Contrast-enhanced abdominal computed tomography (CT) scan findings of acute interstitial edematous pancreatitis include focal or diffuse enlargement of the pancreas with heterogeneous enhancement with intravenous contrast. Necrosis of pancreatic tissue is recognized as lack of enhancement after intravenous contrast administration.

Magnetic resonance imaging — MRI has a higher sensitivity for the diagnosis of early acute pancreatitis as compared with contrast-enhanced abdominal CT scan and can better characterize the pancreatic and bile ducts and complications of pancreatitis. Magnetic resonance cholangiopancreatogram (MRCP) is comparable to endoscopic retrograde cholangiopancreatogram (ERCP) for the detection of choledocholithiasis.[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Diagnosis
The diagnosis of acute pancreatitis should be suspected in a patient with acute onset of a persistent, severe, epigastric pain with tenderness on palpation on physical examination.

The diagnosis of acute pancreatitis requires the presence of two of the following three criteria:

1) Acute onset of persistent, severe, epigastric pain often radiating to the back,
2) Elevation in serum lipase or amylase to three times or greater than the upper limit of normal, and
3) Characteristic findings of acute pancreatitis on imaging (contrast-enhanced computed tomography [CT], magnetic resonance imaging [MRI], or transabdominal ultrasonography).

In patients with characteristic abdominal pain and elevation in serum lipase or amylase to three times or greater than the upper limit of normal, no imaging is required to establish the diagnosis of acute pancreatitis.

In patients with abdominal pain that is not characteristic for acute pancreatitis or serum amylase or lipase levels that are less than three times the upper limit of normal, or in whom the diagnosis is uncertain, imaging with a contrast-enhanced abdominal CT scan may be performed to establish the diagnosis of pancreatitis and to exclude other causes of acute abdominal pain.[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Differential Diagnosis

— Peptic ulcer disease (PUD) – Upper abdominal pain or discomfort is the most prominent symptom in patients with peptic ulcers.

 Acute cholangitis – Acute cholangitis occurs when a stone becomes impacted in the biliary or hepatic ducts, causing dilation of the obstructed duct and bacterial superinfection. It is characterized by Charcot’s triad, which includes fever, jaundice, and right upper quadrant abdominal pain.

 Hepatitis – Patients with acute hepatitis (eg, from hepatitis A, alcohol, or medications) may have fatigue, malaise, nausea, vomiting, and anorexia in addition to right upper quadrant pain. Other symptoms include jaundice, light color stool and dark urine.

Perforated viscus – Patients with a perforated viscus present with sudden onset abdominal pain and have peritoneal signs with guarding, rigidity and rebound tenderness that are not associated with pancreatitis. Patients may have an elevated amylase but elevations are unlikely to be three times the upper limit of normal.

— Intestinal obstruction – Patients with intestinal obstruction have abdominal pain with anorexia, emesis, obstipation, or constipation and elevation in serum amylase and lipase. These patients may have a history of prior abdominal surgeries or Crohn’s disease.

Mesenteric ischemia – Acute mesenteric ischemia presents with the acute and severe onset of diffuse and persistent abdominal pain, often described as pain out of proportion to examination.

 Hepatitis – Patients with acute hepatitis (eg, from hepatitis A, alcohol, or medications) may have fatigue, malaise, nausea, vomiting, and anorexia in addition to right upper quadrant pain. Other symptoms include jaundice, light color stool and dark urine.[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Treatment

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

Fluid replacement — The only effective treatment in the first 24 to 48 hours after the diagnosis of acute pancreatitis is intravenous hydration.

Pain control — Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics. Uncontrolled pain can contribute to the hemodynamic instability.

Monitoring — Patients should be monitored closely in the first 24 to 48 hours. Patients with organ failure will need ongoing monitoring for other complications that might arise.

Vital signs including oxygen saturation should be monitored and supplemental oxygen administered to maintain arterial oxygen saturation of greater than 95%,

Urine output,

Electrolytes should be monitored frequently in the first 48 to 72 hours and especially with aggressive fluid resuscitation.

Hypocalcemia should be corrected if ionized calcium is low or if there are signs of neuromuscular irritability (Chvostek’s or Trousseau’s sign).

Low magnesium levels can also cause hypocalcemia and should be corrected.

Serum glucose levels should be monitored hourly in patients with severe pancreatitis and hyperglycemia should be treated as it can increase the risk of secondary pancreatic infections,

Intensive care unit (ICU) patients should be monitored for potential abdominal compartment syndrome with serial measures of urinary bladder pressures.

Nutrition — Patients with mild pancreatitis can often be managed with intravenous hydration alone since recovery occurs rapidly, allowing patients to resume an oral diet within a week. Nutritional support is often required in patients with moderately severe pancreatitis if they are unlikely to resume oral intake within five to seven days Nasojejunal tube feeding (using an elemental or semi-elemental formula) is preferred to total parenteral nutrition (TPN).

Oral feeding — depends on the severity of the pancreatitis,

Enteral — Enteral feeding rather than parenteral nutrition is recommended in patients with moderately severe and severe acute pancreatitis who cannot tolerate oral feeding,

Parenteral — Parenteral nutrition should be initiated only in patients who do not tolerate enteral feeding.

Antibiotics — Up to 20% of patients with acute pancreatitis develop an extrapancreatic infection (eg, bloodstream infections, pneumonia, and urinary tract infections). Extrapancreatic infections are associated with an increase in mortality[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_separator color=”sky” border_width=”2″][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Treating the underlying cause of pancreatitis:

Once pancreatitis is brought under control, it is very important to start treating the underlying cause(s) of pancreatitis, for example:

Procedures to remove bile duct obstructions. Pancreatitis caused by a narrowed or blocked bile duct may require procedures to open or widen the bile duct. A procedure called endoscopic retrograde cholangiopancreatography (ERCP) uses a long tube with a camera on the end to examine your pancreas and bile ducts. The tube is passed down your throat, and the camera sends pictures of your digestive system to a monitor. ERCP can aid in diagnosing problems in the bile duct and in making repairs.

Gallbladder surgery. If gallstones caused your pancreatitis, your doctor may recommend surgery to remove your gallbladder (cholecystectomy).

Lipid management — Patients recovering from Hypertriglyceridemia-induced acute pancreatitis require long-term therapy to prevent recurrent pancreatitis and to prevent other complications of hypertriglyceridemia. This consists of both pharmacologic therapy (eg, oral gemfibrozil 600 mg twice daily) and dietary modification with restriction of fat content to 10 to 15% of the diet and avoidance of concentrated sugars.

Pancreas surgery. Surgery may be necessary to drain fluid from your pancreas or to remove diseased tissue.

Treatment for alcohol dependence. Drinking several drinks a day over many years can cause pancreatitis. If this is the cause of your pancreatitis, your doctor may recommend you enter a treatment program for alcohol addiction. Continuing to drink may worsen your pancreatitis and lead to serious complications.[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_empty_space][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]Sources: [1][2][3][4][5][6][/vc_column_text][/vc_column][/vc_row]

Leave a Reply