Acute pancreatitis
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  • 1. Acute pancreatitis In this disease, leakage of activated pancreatic enzymes in the intestinal and peripancreatic tissueswhich creates wide spread necrosis and reactive inflammation. This gives rise of a variety of clinicalmanifestations, which depend upon the severity of necrosis and inflammation. Pancreatic enzymes usually activated in the intestine, but when there is reflux of intestine contentwhich will lead to activation of the pancreatic enzymes in the pancreas.Embryology:The pancreas developed from 2 parts: - Dorsal: forms the neck, body, tail, and a portion of the head of pancreas (arise in the 2nd half of the 4th week) - Ventral: arises in form of diverticulum from the primitive bile duct at the point where it opens into the duodenum. Early in the 7th week the two parts of the pancreas fuse and communication is established between their ducts.Anatomy of the pancreas:  Pancreas is an elongated structure that lies in the epigastric and upper left quadrant of the abdominal cavity. It is soft and lobulated and situated on the posterior abdominal wall behind the peritoneum. It forms the bed of the stomach and separated from it by omental burs.  The pancreas is both endocrine and exocrine gland the exocrine portion produce enzymes for hydrolyzing protein fats and carbohydrates, while the exocrine portion is the islets of langerhans that produce insulin, glucagon and polypeptide.  The pancreas has 4 parts: - Head: disc shape and lies within concavity of duodenum; a part of the head is extended behind superior mesenteric vessels and called Uncinate process. - The neck: is the constricted portion of the pancreas and connect the head with the body. It lies in front of the beginning of portal vein and the origin of superior mesenteric artery from the aorta. - Body: runs upward and to the left across the midline. - Tail: passes forward in the splenicorenal ligament and comes in contact with the spleen. Relations: - Anteriorly: from right to the left, the transverse colon and attachment of the transverse mesocolon, the lesser sac and the stomach. - Posteriorly: from right to the left, bile duct, portal and splenic veins the inferior vena cava, the aorta, the origin of superior mesenteric artery, the left psoas muscle, left adrenal gland, the left kidney and hilum of the spleen.  Pancreatic ducts: 1
  • 2. - Major duodenal duct (Werrsing duct): that begins in the tail of pancreas and runs the length of the gland, receiving numerous tributaries on the way. It opens in the descending part of the duodenum and drains together with common bile duct in the major duodenal papilla. - Accessory pancreatic duct (Cenitorini): when it is present drains in the upper part of head and then opens in the minor papilla of the duodenum.  Blood and nerve supply: - Arteries: 1. Splenic artery – arises from celiac trunk 2. Superior and inferior Pancreatoduodenal arteries - arises from celiac trunk - Veins: Splenic vein, Superior and inferior Pancreatoduodenal veins drains into portal vein. - Nerves: Sympathetic and parasympathetic (vagus n.) supplies the pancreas.  Lymph drainage: Lymph nodes that lies along the arteries that supplies the gland, and drains into celiac and superior mesenteric lymph nodes.Physiology:  After meals the panaceas started to secrets enzymes in alkaline bicarbonates rich medium. The daily amount of this secretion is about one liter.  Secretin is the hormone that increases the rate of secretion of pancreas which is released by duodenal mucosa.  Pancreozymin stimulates the secretion of pancreatic enzymes.  Hormones that stimulate the secretion of pancreatic enzymes are vasoactive intestinal polypeptide and gastrin.  Hormones that inhibit the secretion are somatostatin, glucagon, and polypeptide.Pathology: Occurs when the pancreatic enzymes are activated in the pancreas and then leak out into thesurrounding tissues in which causing chemical injury to it resulting in wide spread necrosis. This givesraise it an inflammatory edema of the pancreas. The inflammatory changes also affect blood vessels inwhich eventually raptures and hemorrhage will occur. In more severe cases necrotic masses will becapsulated together with fluid and abscess will be formed. The necrotic changes reaches the duct in whichthe enzymes seeps to the peritoneum and fat necrosis of omentum will take place.Etiology: Acute pancreatitis is produced by non-bacterial injury to the pancreas and the surrounding tissuesby activated pancreatic enzymes. 2
  • 3. 1. Biliary disease: chronic cholecystitis or anomalies of biliary tract which will lead to regurgitation of Biliary content into the pancreatic duct that will give rise to pancreatitis. 2. Alcoholism: alcohol intake induces hyperlipidemia. 3. Pancreatic injury. 4. Parasites: usually caused by Ascaris which is normally resident of upper part of jejunum, Ascaris migrates to the descending part of duodenum and enters the major papilla to the pancreatic duct. 5. Metabolic disorders: like hyperparathyroidism, and hyperlipidemia. 6. Drugs: like thiazides, fursemide, and large dose of paracetamol. 7. Viral infection: mumps in children and infections with coxsackie B group viruses.Classification of acute pancreatitis: 1. Edematous. 2. Necrotic. 3. Hemorrhagic. 4. Gangrenous. 5. Fat necrosis.Fluids may accumulate in: 1. Abdominal cavity. 2. Pleural cavity. 3. Interstitial tissues. 4. Intestine.Clinical features of pancreatitis: 1. Sudden sever pain in the epigastric region which radiates to the back. The pain is improved by semi-sitting and get aggravated in lying down. The pain in acute pancreatitis is called Belt pain. 2. Vomiting. 3. Abdominal pain. 4. Paleness. 5. Peripheral circulatory failure. 6. Mild fever. 7. Jaundice may be seen. 8. Toxemia due to necrosis. 9. Paralytic ileus and peritoneal effusion developed and causing abdominal distension.Physical examination: 1. Low grade fever. 2. Abdominal tenderness. 3. Involuntary rigidity of epigastric region. 3
  • 4. 4. Signs of shock: sweating, tachycardia, and hypertension. 5. Discoloration of skin around the umbilicus (grey turner sign, and Cullen sign). 6. Abdominal distension.Signs of acute pancreatitis: 1. Gobbier sign: accumulation of gases in the transverse colon 9due to development of paralytic illeus) 2. Horse shoe sign: in X-ray picture the duodenum will appear as a horse shoe due to swelling of the head of pancreas. 3. Turner & Grey sign: bluish discoloration of the skin around the umbilicus and lateral abdomen due to development of disseminated intravascular coagulation. 4. Vaskinsky sign: during deep palpation of the abdomen we can fell aortic pulsation, but when pancreatitis is present we can’t feel the pulsation due to edema of the pancreas. 5. Myo-Robinson sign: pain in the left costodiphragm angle.Investigations: 1. Blood: Raised serum amylase, hypocalcaemia and hyperglycemia, Increase of WBC 2. Abnormalities of liver function test: may seen in gallstone-associated pancreatitis; increase of bilirubin, alkaline phosphatase, alanine aminotransferase. 3. Cretain serum enzymes are increased. 4. Serum and urinary lipase are increased. 5. X-ray of abdomen will show dilation of small bowel segment in the upper abdomen. 6. Ultrasound and CT scan will reveal swelling of the gland. 7. Chest X-ray: may show pleural effusion and rise of the diaphragm of the left side. 8. MRI 9. Laproscopy.Complications: Local complications: 1. Pancreatic phlegmon: when the disease resolves some of necrotic tissues gets encapsulated with very little fluid inside and surrounded by inflammatory tissues. It gives rise to pancreatic mass. 2. Pseudocyst: when the pancreatic ruptures and the enzymes leak out of the gland. It may develop in pancreas or in the surrounding tissues. 3. Haemorrhage: when erosive process affects the vessels in the intestinal tissues. 4. Abscess: infection of the necrotic tissues lead to formation of an abscess, if it is not treated properly it may lead to septicemia. 5. Pseudoaneurysm: is afalse aneurysm of major pancreatic vessels confined as a clot by surrounding tissues and often associated with infection. 6. External pancreatic fistula 7. Gastrointestinal fistula. 8. Diabetes mellitus 4
  • 5. 9. Intestinal fistula. 10. Chronic pancreatitis. 11. Multiple organ dysfunctions. 12. Pancreatic necrosis. Systemic complications: 1. Cardiovascular: hypotension, tachycardia and arrhythmia. 2. Pulmonary. 3. Renal: decrease of urine output, increase of urea and creatinine level. 4. Metabolic: decrease level of calcium, magnesium, and albumin. 5. Hematological: decrease of haematocrit, disseminated intravascular coagulation. 6. Neurological: irritability and confusion. 7. GIT: paralytic ileus.Treatment:Surgery is always deferred in acute appendicitis and the treatment of choice is conservative treatment.Conservative treatment: 1. Management of shock and electrolytes imbalance: IV fluids are started immediately; plasma and dextran may be infused. 3-4 L/ day 2. NIL by mouth and gastric aspiration. 3. Analgesia: Meperidine hydrochloride 50 – 100 mg every 4 hrs. 4. Suppression of pancreatic secreation: a. NIL by mouth. b. Antacids (aluminum hydroxide and magnesium trisilicate). c. Naso-gastric aspiration. d. Inhibitors of gastric secretion (H2 antagonist) e. Glucagon – to reduce exocrine function of pancreas. f. Calcitonin – suppress exocrine function of pancreas and gastric acid secretion. g. Somatostatin – inhibitor of pancreatic exocrine secretion. 5. Anti enzyme preparations: 6. Antibiotics: a. Imipenem is the antibiotic of choice, because it has the maximum blood pancreas diffusion, widest spectrum against the enteric flora and anaerobes. b. Floxacilin. c. 3rd generation of cephalosporin. 7. Peritoneal lavage:  It is effective to decrease of early death in acute pancreatitis, it remove the toxic products.  A lower midline or lower left quadrant incision is used, a catheter is introduced. Then 2 liters of peritoneal dialysis solution introduced containing 1.5g/100 glucose, potassium and heparin. 5
  • 6. Surgical treatment: Indications for surgery: 1. Uncertain diagnosis: many conditions of acute abdomen resemble acute appendicitis. 2. Deterioration of clinical condition and presence of necrosis: if there is necrosis, necrotomy is required 3. Correction of associated Biliary disease: when diagnosis of gallstone-associated acute pancreatitis. 4. Secondary pancreatic infections: This includes pancreatic abscess, infected pancreatic necrosis, and infected pancreatic psudocyst. 5. In case of local complications: such as psudocyst and abscess. - Bursa-omento-pancreato-pixy: We take the omentum and surround the pancreas with it, then we make and opening through the skin and start to drain the infected fluids. 6