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Acute Pancreatitis

Etiology

• Although it varies geographically, the most common causes are gallstones and alcohol.

• During the passage of gallstones from the common bile duct, it blocks the pancreatic duct and creates an obstacle to pancreatic secretion and causes acute pancreatitis.

• Alcohol, on the other hand, stimulates pancreatic secretion, increases the sphincter pressure of Oddi, and also has a direct toxic effect on the pancreas.


Causes of acute pancreatitis

Common causes

Gallstones (including Microlithiasis)

Alcohol (Acute and chronic alcoholism)

hypertriglyceridemia

Endoscopic retrograde cholangiography (ERCP)

Drugs (Azathioprine, 6-mercaptopurine, sulfonamides, estrogen, tetracycline, valproic acid, HIV drugs, 5-aminosalicylic acid, GLP1 analogs, DPP4 inhibitors)

Trauma

Postoperative


Rare causes

Vascular causes and vasculitides

Connective tissue diseases and thrombotic thrombocytopenic purpura

pancreatic cancer

hypercalcemia

Periampullary diverticulum

pancreas divisium

Hereditary pancreatitis

cystic fibrosis

Kidney failure

Infections

autoimmunity


Pathogenesis

There is zymogen (inactively secreted pancreatic enzymes) activation and an increase in pancreatic duct permeability. As a result, autodigestion, fat necrosis and inflammation begin in the pancreas.


Clinic

• Abdominal pain is the most prominent symptom. It is in a girdle style and decreases when leaning forward and hunger. Lying on your back, eating, vomiting and alcohol increase the pain.

• Depending on the severity of pancreatitis, generalized abdominal tenderness, defense, distension, fever, tachycardia and hypotension may be seen on physical examination.

• If pancreatitis is due to gallstones, symptoms of jaundice and accompanying cholangitis may be seen.

• In hemorrhagic pancreatitis; Blue-violet spots may be seen secondary to the hematoma described as Gray Turner's (lumbar areas) and Cullen's sign (around the navel).

• The most important parameter in the clinical course is organ failure. organ failure; While it is usually due to SIRS (systemic inflammatory response syndrome) within the first 10 days, it is due to infections after 10 days.


Classification

• Classification of acute pancreatitis according to severity

Mild: No organ failure, local or systemic complications.

Moderate: Local or systemic complications develop without temporary organ failure (less than 48 hours) and/or permanent organ failure.

Severe: There is single or multiorgan failure for more than 48 hours.

• Classification of acute pancreatitis according to morphology

Interstitial (edematous) pancreatitis

There is acute inflammation of the pancreas and surrounding tissues, but no necrosis.

There is usually mild or mild to moderate clinical pancreatitis.

There may be a collection of peripancreatic fluid in the first 4 weeks. Later, the pseudocyst can be seen.

Necrotizing pancreatitis

There is pancreatic or peri-pancreatic necrosis.

It generally has a moderate or severe clinical course, and complications are common.

Necrosis is indicated by contrast-enhanced CT taken 72 hours after admission at the earliest.

Necrotic fluid collection in the pancreas or peripancreatic tissue can be seen in the early period. In the late period (after 4 weeks), an area of ​​well-circumscribed walled-off necrosis occurs.

Acute Pancreatitis
Lab
• Leukocytosis, hemoconcentration, hypocalcemia (due to fat necrosis and hypoalbuminemia), hyperglycemia may be seen. Sedimentation and CRP may increase.
• If pancreatitis is due to gallstones; Elevated ALP, GGT, ALT and bilirubin; If alcohol-related, AST elevation is other laboratory findings.
• Amylase and lipase are the most valuable laboratory tests in diagnosis.
• The following findings can be detected in the direct graphy:
Sentinel loop (localized small bowel obstruction)
Cut-off sign (localized descending colon obstruction)
Soap bubble appearance (in the presence of gas-producing bacteria)
Pleural fluid (usually on the left)
pulmonary edema
Calcifications due to underlying chronic pancreatitis

Diagnosis
• Serum amylase level is the most commonly used test.
• It starts to rise in the 2nd hour of the attack, peaks at the 24th hour and can remain high in the serum for 5-6 days.
• An elevation in serum amylase that exceeds 3 times the upper limit when kidney functions are normal is important for diagnosis.
• Amylase can be found to be normal in acute pancreatitis due to hypertriglyceridemia, acute attack on chronic pancreatitis, and in the late phase of acute pancreatitis.
• Pancreatic amylase can be used as a more sensitive and specific test for pancreas than total amylase level.
• Serum amylase elevation has no prognostic significance in acute pancreatitis.
• Long-term elevation of amylase suggests pseudocyst development.

Conditions that can increase serum amylase other than acute pancreatitis
Salivary gland inflammations
Tumors: genitals, breast, esophagus, lung, tonsil
Gastrointestinal perforation or obstruction
Diabetic ketoacidosis
Burns
Cholecystitis
Kidney failure
Alcohol intake

• The sensitivity of serum lipase is similar to amylase but remains higher in serum for a longer period of time. Therefore, it may be more helpful in diagnosis in late and subacute cases.
It is more useful to combine the two tests.
• Elastase, trypsin, phospholipase measurements do not provide additional information.
• Ultrasound and CT are helpful in diagnosis and follow-up (Ultrasound is more valuable in the diagnosis of gallstones and CT in the diagnosis of pancreatic necrosis).
Endoscopic ultrasonography is helpful in the diagnosis and treatment of cysts and abscesses in the late period. It does not provide additional benefit in the early period and is not used.

Complications
• Early complications (usually < 2 weeks); Shock, ARDS, acute kidney injury, hyperglycemia, acidosis, hypocalcemia, hypomagnesemia, colon obstruction, necrosis, bleeding, DIC, metastatic fat necrosis (brain, bone, skin), sudden blindness (retinal artery occlusion) can be seen.
• Late complications: The most common late complication is pseudocyst. Abscess should be considered in fever that lasts longer than two weeks.
pseudocyst
It is a localized collection of tissue, fluid, debris, pancreatic enzymes, and blood that occurs in the pancreas within 1-4 weeks following acute pancreatitis.
Since the cyst wall consists of necrotic, fibrous and granulation tissue and does not contain a true epithelial layer, it is defined as a pseudocyst.
The diagnosis is made by ultrasonography as the most practical and reliable way.
Most recover with up to 6 weeks of follow-up.
Pseudocyst can be followed unless symptomatic, and should be drained in the presence of symptoms.
Major complications of pseudocyst; It is rupture, abscess and hemorrhage.

Local and systemic complications in the course of pancreatitis
local complications
Necrosis
walled necrosis
Pancreatic fluid collection
pancreatic pseudocyst
pancreatic acid
Disruption in the main pancreatic duct
Involvement of adjacent organs with necrotizing pancreatitis
Thrombosis of blood vessels (splenic vein, portal vein)
Pancreaticoenteric fistula
intestinal infarction
obstructive jaundice

Systemic Complications
Pulmonary (Pleural effusion, atelectasis, mediastinal fluid, pneumonia, ARDS, hypoxemia)
Cardiovascular (Hypotension, hypovolemia, ECG changes, pericardial effusion)
Hematological (DIC)
Gastrointestinal hemorrhage (Peptic ulcer disease, erosive gastritis, portal vein thrombosis, splenic vein thrombosis, varicose bleeding)
Renal (oliguria, azotemia, renal artery and/or vein thrombosis, acute tubular necrosis)
Metabolic (Hyperglycemia, hypertriglyceridemia, hypocalcemia, encephalopathy, sudden blindness)
Central nervous system (Psychosis, fat embolism)
Fat necrosis (Erythematous nodules)

Prognosis
• The criteria defined by Ranson in acute pancreatitis are widely used to determine the prognosis.
Ranson criteria
At the time of application or
. Age > 55
. Leukocytes> 16,000/mm3
. Glucose > 200 mg/dl
. LDH > 350 IU/L
. AST> 250 U/L


Within 48 hours
. BUN> 45 mg/dl (> 5 mg/dl increase)
. Calcium < 8 mg/dl
. PO2 < 60 mmHg
. Fluid deficit > 6 lt
. Base deficit > 4 mEq/L
. > 1% O decrease in hematocrit
These criteria were first defined for alcoholic pancreatitis. Minor changes were made to the modified Ranson criteria for gallstone pancreatitis.

Disease severity risk factors
- Age >60
- Obesity (BMl>30)
- Comorbid disease (Charlson comorbidity index)

Indicators of Sevirity at the time of application or within the first 24 hours
- SIRS- In the presence of 2 or more criteria:
Body temperature <36 or >38°C
Heart rate > 90 bpm
Respiratory rate > 20/min or PcO2<32 mmHg
White blood cell count > 12.000/mm3, <4000/m3 or 10% band cells
- APACHE 2
- Hemoconcentration (Hematocrit >44%)
- BUN (>22 mg/dl) at the time of application
 (B) BUN>25 mg/dl
 (1) Impaired mental state
 (S) SIRS: >= 2 findings
 (A) Age >60 years
 (P) Pleural effusion
- Organ failure (Modified Marshall score)
- Cardiovascular: Systolic blood pressure <90 mmHg, heart rate>130 bpm
- Pulmonary: Pa02 <60 mmHg
- Renal: Serum creatinine >2.0 mg

Sevirity markers during hospitalization
-Persistent organ failure
-Pancreatic necrosis

Treatment
• Treatment of acute pancreatitis is conservative (closing the patient's oral intake, IV fluid, acid suppression, treatment of electrolyte disorders, etc.).
• Appropriate hydration, especially at the beginning, is the most important approach in reducing morbidity and mortality.
• Pain relief opioid analgesics can be given.
• Antibiotics are used if cholangitis is suspected or infected pancreatic necrosis is present.
Antibiotics with good penetration into the pancreas (imipenem, etc.) should be preferred for infected pancreatic necrosis.
• If there is biliary pancreatitis, stones are removed with ERCP and papillotomy.
• Less invasive endoscopic methods are the primary choice in the treatment of pseudocyst, infected fluid, necrotic collection and walled necrosis requiring drainage. For this purpose, endoscopic ultrasound is widely used.
• Surgical treatment is performed only if there is an acute abdomen, organ perforation cannot be excluded, drainage of infected fluid that cannot be treated endoscopically or for the treatment of necrosis.
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