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PANCREATITIS By; Col. Abrar Hussain Zaidi INTRODUCTION Pancreatitis is an inflammatory process in which pancreatic enzymes auto digest the gland. INTRODUCTION Inflammation of Pancreas Acute Chronic Recurrent acute Acute on chronic INTRODUCTION Acute pancreatitis - May heal without any loss of function or morphologic changes. Recurrent pancreatitis - recurs intermittently, contributing to the functional and morphologic loss of the gland. Chronic pancreatitis-persistent low grade inflammations. INTRODUCTION Clinical importance -? INTRODUCTION One of the commonest conditions that a physician or a surgeon comes across Associated morbidity is high The cost of treatment is high In severe cases the mortality may be 20-30% INTRODUCTION Prevention of disease is possible If we are aware of etiological factors and pathogenesis ANATOMY ANATOMY PHYSIOLOGY EXOCRINE FUNCTION ENDOCRNE FUNCTION Acute pancreatitis EPIDEMIOLOGY 3% of all cases of abdominal pain admitted to hospital. 40 cases per year per 100,000 adults.[International] Ranges between 5 and 80 per 100,000 population The highest incidence recorded in the United States and Finland In 80% of cases: mild and resolves without serious prob. Sex No predilection exists. Age- 35-64 years PATHOPHYSIOLOGY located in the retroperitoneal space No capsule, inflammation can spread easily. Local effects Acute edematous pancreatitis : When Parenchyma edema and peripancreatic fat necrosis occur first Haemorrhagic or narcotizing pancreatitis: When necrosis involves the parenchyma, accompanied by hemorrhage and dysfunction of the gland PATHOPHYSIOLOGY pancreatic abscesses and Pseudocysts due to necrotizing pancreatitis because enzymes can be walled off by granulation tissue PATHOPHYSIOLOGY systemic effects ; Due to cytokines: bradykinins and phospholipase A. Cytokines cause Vasodilatation, increase in vascular permeability, pain, and leukocyte accumulation in the vessel walls. Fat necrosis may cause hypocalcaemia. Pancreatic B-cell injury may lead to hyperglycemia. PATHOPHYSIOLOGY systemic effects ; in its most severe form. Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and hypotensive shock CAUSES Alcohol abuse - 44% of patients At cellular level - ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release. At ductal level - increases the permeability of ductules, enzymes reach the parenchyma, resulting in pancreatic damage. Formation of protein plugs due to increases the protein content of the pancreatic juice and decreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the that block the pancreatic outflow and obstruction. OTHER MAJOR CAUSES Biliary calculi cholelithiasis, choledocholithiasis calculi lodge in the pancreatic duct or ampulla of Vater and obstruct the pancreatic duct, leading to extravasation of enzymes into the parenchyma. Medications, including azathioprine, corticosteroids, sulfonamides, thiazides, furosemides, NSAID”S Viral infections Trauma OTHER CAUSES ERCP Hypertriglyceridemia (When the triglyceride level exceeds 1000 mg/U Peptic ulcer disease Abdominal or cardiopulmonary bypass surgery, -by ischemia Trauma –blunt+penetrating Carcinoma of the pancreas, - outflow obstruction Viral infections, including mumps, coxsackievirus, cytomegalovirus (CMV), hepatitis virus, Epstein-Barr virus (EBV), and rubella Bacterial infections, such as mycoplasma ,Tuberculosis Intestinal parasites, such as Ascaris, which can block the pancreatic outflow Pancreas divisum Scorpion and snake bites ischemia or vasculitis Autoimmune pancreatitis CLINICAL PRESENTATION History The main presentation - Epigastric pain or right upper quadrant pain radiating through, rather than around, to the back. Nausea and/or vomiting Fever History of previous biliary colic Physical Palpitations Muscular spasm –in extremities may be noted secondary to hypocalcemia. CLINICAL PRESENTATION Ask the patient about ; Recent surgery or invasive procedure e.g. ERCP Family history of hypertriglyceridemia. Alcohol consumption CLINICAL PRESENTATION EXAMINATION Patients are acutely ill Tachypnea Hypotension Fever Abdominal tenderness, distension, guarding, and rigidity Mild jaundice Diminished or absent bowel sounds CLINICAL PRESENTATION EXAMINATION Basilar rales, especially in the left lung. Pleural effusion Because of contiguous spread of inflammation from the pancreas Severe cases may have; Grey Turner sign (ie, bluish discoloration of the flanks) Cullen sign (ie, bluish discoloration of the periumbilical area) caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic pancreatitis. Differential Diagnoses Abdominal Aneurysm Hepatitis Cholangitis Mesenteric Ischemia Cholecystitis and Biliary Colic Intestinal Obstruction Cholelithiasis Choledocholithiasis Gastroenteritis Perforated viscus/du-perforation Pancreatic cancer Malabsorption syndromes Ectopic pregnancy DIAGNOSTIC WORK-UP HISTORY AND CLINICAL EXAMINATION LABORATORY TESTS IMMAGING STUDIES DIAGNOSTIC WORK-UP Laboratory Studies leukocytosis (WBC >12,000) -> polymorphs. Hyperglycemia. Disturbed in the electrolyte balance:Urea/creatinin Na, K, Cl, CO2, P, Mg---secondary to third spacing of fluids. Acid base disturbances Amylase levels, preferably the amylase P.> 3 times -suggest the diagnosis .[ serum/peritoneal] Lipase - elevated / remain high for 12 days. Anemia DIAGNOSTIC WORK-UP Laboratory Studies liver function tests particularly in biliary calculi. Misc. Done in some hospitals in addition to the above, especially to identify pancreatitis post ERCP . Urinary trypsinogen activation peptide Increased serum trypsinogen2 Trypsin 2-alpha 1 antitrypsin complex values DIAGNOSTIC WORK-UP Imaging Studies Plain X-rays kidneys, ureters, bladder (KUB) Exclude viscus perforation (ie, air under the diaphragm). In patients with a recurrent episode of chronic pancreatitis, peripancreatic calcifications may be noted. DIAGNOSTIC WORK-UP Ultrasonography A screening test. poorly visualised in 25-50% of cases / overlying gas shadows Can show swollen pancreas, dilated common bile duct, and free peritoneal fluid. Useful to detect presence of gallstones. CT –scan is the most reliable imaging modality in the diagnosis of acute pancreatitis. The criteria for diagnosis are divided by Balthazar and colleagues into 5 grades: Grade A - Normal pancreas Grade B - Focal or diffuse gland enlargement Grade C - Intrinsic gland abnormality recognized by haziness on the scan Grade D - Single ill-defined collection or phlegmon Grade E - Two or more ill-defined collections or the presence of gas in or nearby the pancreas DIAGNOSTIC WORK-UP Misc. Tests Urine para-aminobenzoic acid test (ie, bentiromide [Chymex] test) is used for chronic pancreatitis to assess for the reserve function of the pancreas. In patients with severe pancreatic insufficiency and malabsorption, the sensitivity is 80–90%. In those with mild-tomoderate functional impairment, the sensitivity is as low as 37–46%. Serum trypsinogen assay or the serum trypsin test can also be used to assess the function of the pancreas in chronic pancreatitis. Only a very low level of serum trypsinogen (<20 ng/mL) is reasonably specific (90%) for chronic pancreatitis, and these are seen in advanced chronic pancreatitis with steatorhea.7 Both of these tests are available to test for the pancreatic reserve in chronic pancreatitis, and their specificity is similar in the advanced versus the moderate chronic pancreatitis. Ordering them is according to availability. Value in acute on chronic pancreatitis DIAGNOSTIC WORK-UP Peritoneal aspiration - free fluid without bacterial contamination +>amylase+>TLC. ERCP with a sphincterotomy is warranted within the first 72 hours. where a dilated obstructed common bile duct is diagnosed by CT or USG with elevated plasma bilirubin (>5 mg/dL) Laparoscopy or laparotomy: where suspicion is high but tests are inconclusive. Severity and prognostic assessment Prediction is difficult and unreliable. Clinically apparent organ failure indicates a severe attack. Scoring systems: do increase accuracy. Initially assessing the severity of an attack into mild or severe has important implications for management - and may prevent deaths. Severity and prognostic assessment Scoring systems: Glasgow Ranson Apache II scores can indicate prognosis particularly Glasgow prognostic score Age >55 years WBC >15 x109/l Urea >16mmol/l Glucose >10mmol/l pO2 <8kPa (60mmhg) Albumin <32g/l Calcium <2mmol/l LDH >600 units/l AST/ALT >200 units Ranson's criteria Present on admission: Age >55 years WBC >15 x109/l Glucose >10mmol/l LDH >600 units/l SGOT >250 units/l Developing during first 48 hours: Haematocrit fall 10% Urea increase >8mg/dl Serum Ca <8mg/dl Arterial O2 saturation <60mmHg Base deficit >4meq/l Estimated fluid sequestration >600ml Any 3 factors means severe in both systems. scoring. A Ranson score of 0-2 has a minimal mortality rate, and the patient is admitted to the regular ward for medical therapy and support. A Ranson score of 3-5 has a 10-20% mortality rate, and the patient should be admitted to the intensive care unit. A Ranson score after 48 hours higher than 5 has a mortality rate of more than 50% and is associated with more systemic complications. Treatment According to severity Mild cases in wards Severe cases to be Treat in ITU or high dependency unit. Majority - treated conservatively Emergency surgery in small proportion of cases Elective surgery in biliary calculi Treatment Emergency Department Care Most of the cases are treated conservatively, and approximately 80% respond to such treatment. Fluid resuscitation Monitor accurate intake/output and electrolyte balance of the patient. Crystalloids / packed red blood cells –[ in the case of hemorrhagic pancreatitis] CVP line with monitoring-- severe fluid loss and very low blood pressure. TREATMENT In Wards/ICU The goal -to relieve pain and minimize complications. Analgesics . Meperidine is preferred over morphine because of the greater spastic effect of the latter on the sphincter of Oddi. Parenteral NSAID”S Anti ulcer drugs Prevention of gastric/duodenal stress ulcers Antibiotics Empiric- enteric anaerobic and aerobic gramAdjust as per c/s reports.Ceftriaxone Aminoglycosides/ Metronidazole TREATMENT Rationale for antibiotics Other conditions, such as biliary pancreatitis associated with cholangitis, also need antibiotic coverage. The preferred antibiotics are the ones secreted by the biliary system, such as ampicillin and third-generation cephalosporins. Continuous oxygen saturation should be monitored by pulse oximetry, and acidosis should be corrected. When tachypnea and pending respiratory failure develops, intubation should be performed. TREATMENT NG intubation if the patient is vomiting [for symptomatic relief and to avoid aspiration] Guided aspiration of necrotic areas, if necessary. An ERCP may be indicated for common duct stone removal Surgery in Acute pancreatitis Diagnostic/Therapeutic for complications Bleeding Pseudocysts Abscess drain, repair, or remove the affected tissues where there is fulminent infection and necrosis. open surgical debridement. Postoperative lavage or abdominal packing closure of abdomen - partial or non Establish a feeding jejunostomy. Surgery in Acute pancreatitis For phlegmon of the pancreas, surgery can achieve drainage of any abscess or scooping of necrotic pancreatic tissue. It should be followed by postoperative lavage of the pancreatic bed. In patients with hemorrhagic pancreatitis, surgery is indicated to achieve hemostasis, particularly because major vessels may be eroded in acute pancreatitis. Patients who fail to improve despite optimal medical treatment or patients who push the Ranson score even further are taken to the operating room. Surgery in these cases may lead to a better outcome or confirm a different diagnosis. Surgery in Acute pancreatitis Sphincterotomy - In biliary pancreatitis, a (ie, surgical emptying of the common bile duct) can relieve the obstruction. A cholecystectomy may be performed to clear the system from any source of biliary stones. Hyperbaric oxygen therapy - administration of 100% oxygen at a pressure of 2.5 atmospheres for 90 min twice daily for 5 days has been shown to improve Complications in Acute pancreatitis Local complications Pancreatic necrosis -Infected necrosis is almost always fatal without intervention. Acute Fluid Collections are common in patients with severe pancreatitis (occurring in 30%-50%). Pancreatic abscess is a collection of pus adjacent to pancreas presenting several months after attack. Acute pseudocyst rupture or haemorrhage in pseudocyst. Pancreatic ascites occurs when a pseudo-cyst collapses into peritoneal cavity or major pancreatic duct breaks down and releases pancreatic juices into peritoneal cavity. Complications in Acute pancreatitis Systemic complications Respiratory:Pulmonary oedema/Pleural effusions Consolidation/ARDS Cardiovascular:Hypovolaemia/Shock/arrhythmias Disseminated intravascular coagulopathy (DIC) Renal dysfunction due to hypovolaemia, intra-vascular coagulation. Usually avoided by adequate fluid replacement plus/minus low-dose dopamine but acute tubular or cortical necrosis can follow. GIT: Haemorrhage/Ileus Complications in Acute pancreatitis Metabolic: Hypocalcaemia Hypomagnesaemia Hyperglycaemia Complications in Acute pancreatitis Weber Christian disease: Subcutaneous fat necrosis - relapsing febrile nodular nonsuppurative panniculitis. Recurring crops of tender nodules in skin and subcutaneous fat of trunk, thighs and buttocks, which is more common in middle-aged women. Often ulcerate and scar on healing. Difficult to treat - prednisolone or immunosuppressives. Splenic vein thrombosis Prognosis-acute Pancreatitis Mild edematous pancreatitis occurs in about 80% cases, and the mortality rate is below 1%. Severe acute pancreatitis occurs in about 20% of presentations, with a mortality rate reaching 30%. . Follow-up acute Pancreatitis further Outpatient Care The patient should be monitored routinely with physical examination and amylase and lipase assays. Transfer Transfer patients with Ranson scores of 0-2 to a hospital floor. Transfer patients with Ranson scores 3-5 to an intensive care unit. Transfer patients with Ranson scores higher than 3 to an intensive care unit with emergency surgery as a possibility, depending on the patient's progress and findings on abdominal CT scanning. Patient Education Educate patients about the disease and advise them to avoid alcohol in binge amounts and to discontinue any risk factor, such as fatty meals and abdominal trauma. Summary –acute pancreatitis Begins with: the digestive enzymes becoming active inside the pancreas and autodigestion Could be : acute/acute recurrent /acuteon chronic Common causes: are gallstones and alcohol abuse. Sometimes no cause for pancreatitis can be found. Symptoms of acute pancreatitis include pain in the abdomen, nausea, vomiting, fever, and a rapid pulse. Treatment include: intravenous fluids, analgesics oxygen, antibiotics, anti ulcer and surgery. May becomes chronic- when pancreatic tissue is destroyed and scarring develops Questions-acute Pancreatitis ?