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Description : Check out this medical presentation on Hereditary Pancreatitis, which is titled "Acute and Chronic Pancreatitis", to know about Acute pancreatitis (Interstitial pancreatitis and Necrotising pancreatitis) and Chronic Pancreatitis.

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Published on : May 18, 2021 | Views : 4138 | Downloads : 42

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Acute and Chronic Pancreatitis Dr Farhanul Huda Additional Professor Department of Surgery
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Acute pancreatitis
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Acute pancreatitis Interstitial pancreatitis Necrotising pancreatitis
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Interstitial pancreatitis
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Necrotizing pancreatitis
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Etiology Common Causes Gallstones Alcohol Hypertriglyceridemia ERCP Trauma Postoperative Drugs (azathioprine, 6-mercaptopurine, sulfonamides, estrogens, tetracycline, valproic acid, anti-HIV medications) Sphincter of Oddi dysfunction
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Etiology Uncommon Causes Vascular causes and vasculitis (ischemic-hypoperfusion states after cardiac surgery) Connective tissue disorders TTP Cancer of the pancreas Hypercalcemia Periampullary diverticulum Pancreas divisum Hereditary pancreatitis Cystic fibrosis Renal failure
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Etiology Rare Causes Infections (mumps, coxsackievirus, cytomegalovirus, echovirus, parasites) Autoimmune (e.g., Sjögren's syndrome) Causes to Consider in Patients with Recurrent Bouts of Acute Pancreatitis without an Obvious Etiology Occult disease of the biliary tree or pancreatic ducts, especially microlithiasis, sludge Drugs Hypertriglyceridemia Pancreas divisum Pancreatic cancer Sphincter of Oddi dysfunction Cystic fibrosis Idiopathic
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Pathophysiology
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Clinical features
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Abdominal pain Nausea, vomiting, and abdominal distention Low-grade fever Tachycardia Hypotension Jaundice Erythematous skin nodules Atelectasis, pleural effusion
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Abdominal tenderness and muscle rigidity Diminished bowel sounds A faint blue discoloration around the umbilicus (Cullen's sign) may occur as the result of hemoperitoneum Blue-red-purple or green-brown discoloration of the flanks (Turner's sign) reflects tissue catabolism of hemoglobin
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Grey Turner sign Cullen’s sign
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Workup
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Laboratory Data serum amylase and lipase >threefold clinch the diagnosis No correlation between the severity and the degree of elevation After three to seven days, values tend to return toward normal Pancreatic isoamylase and lipase levels may remain elevated for 7 to 14 days
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Markers of Severity within 24 Hours SIRS [temperature >38° or < 36°C, Pulse > 90, Tachypnea > 24, WBC > 12,000] Hemoconcentration (Hct >44%) BISAP (bedside index of severity in acute pancreatitis) (B) Blood urea nitrogen (BUN) >22 mg% (I) Impaired mental status (S) SIRS: 2/4 present (A) Age >60 years (P) Pleural effusion Organ Failure Cardiovascular: systolic BP <90 mmHg, heartrate >130 Pulmonary: Pao2 <60 mmHg Renal: serum creatinine >2.0 mg% Gastrointestinal: bleeding >500 mL/24 hours
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Severity Risk Factors Age > 60 years Obesity, BMI > 30 Comorbid disease Markers during Hospitalization Persistent organ failure Pancreatic necrosis Hospital-acquired infection
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Laboratory Data Leukocytosis (15,000–20,000 leukocytes per L) Hemoconcentration with hematocrit values >44% and/or blood urea nitrogen (BUN) level >22 mg/Dl Hyperglycemia decreased insulin release, increased glucagon release, increased output of adrenal glucocorticoids and catecholamines. Hypocalcemia
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Laboratory Data Hyperbilirubinemia (>4.0 mg/dL) in 10% is transient return to normal in four to seven days Serum alkaline phosphatase and aspartate aminotransferase levels are also transiently elevated Elevated serum lactic dehydrogenase levels (>500 U/dL) Hypertriglyceridemia occurs in 5–10%
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Hypoxemia (arterial Po2 60 mmHg), which may herald the onset of ARDS Electrocardiogram ST-segment and T-wave abnormalities simulating myocardial ischemia.
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RADIOLOGY CXR Sympathetic pleural effusion Atelectasis A.R.D.S. AXR Sentinal loop Colon cutoff sign Duodenal ileus Calcifications Obscured psoas lines 79% will have radiological signs !!!
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CT Scan of acute pancreatitis CT shows significant swelling and inflammation of the pancreas
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Diagnosis Requires two of the following: typical abdominal pain, threefold or greater elevation in serum amylase and/or lipase level, and/or confirmatory findings on cross-sectional abdominal imaging.
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Differential diagnosis (1) perforated viscus, especially peptic ulcer (2) acute cholecystitis and biliary colic (3) acute intestinal obstruction (4) mesenteric vascular occlusion (5) renal colic (6) myocardial infarction (7) dissecting aortic aneurysm (8) connective tissue disorders with vasculitis (9) pneumonia (10) diabetic ketoacidosis
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Complications
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Local complications Necrosis Sterile Infected Walled-off necrosis Pancreatic fluid collections Pancreatic abscess Pancreatic pseudocyst Pain Rupture Hemorrhage Infection
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Local complications Obstruction of gastrointestinal tract (stomach, duodenum, colon) Pancreatic ascites Disruption of main pancreatic duct Leaking pseudocyst Involvement of contiguous organs by necrotizing pancreatitis Massive intraperitoneal hemorrhage Thrombosis of blood vessels (splenic vein, portal vein) Bowel infarction Obstructive jaundice
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Systemic complications Pulmonary Pleural effusion Atelectasis Mediastinal abscess Pneumonitis Acute respiratory distress syndrome Cardiovascular Hypotension Hypovolemia Sudden death Nonspecific ST-T changes in electrocardiogram simulating myocardial infarction
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Systemic complications Hematologic Disseminated intravascular coagulation Gastrointestinal hemorrhage Peptic ulcer disease Erosive gastritis Hemorrhagic pancreatic necrosis with erosion into major blood vessels Portal vein thrombosis, variceal hemorrhage Renal Oliguria Azotemia Renal artery and/or renal vein thrombosis Acute tubular necrosis
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Systemic complications Metabolic Hyperglycemia Hypertriglyceridemia Hypocalcemia Encephalopathy Sudden blindness (Purtscher's retinopathy) Central nervous system Psychosis Fat emboli Fat necrosis Subcutaneous tissues (erythematous nodules) Bone Miscellaneous (mediastinum, pleura, nervous system)
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HOW DO WE DETERMINE PROGNOSIS? 80% Will recover without any complications 20% Will develop severe cardio-pulmonary complications or septic complications Prognostic assessment : Ranson Imrie APACHE 2 CRP Classify into mild or severe acute pancreatitis ( Atlanta classification 1992)
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Treatment To limit severity of pancreatic inflammation To interrupt the pathogenesis of complications To support the patient and treat complications
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TREATMENT NON-OPERATIVE To limit severity of pancreatic inflammation Inhibition of pancreatic secretion Nasogastric suction Pharmacologic Hypothermia Pancreatic irradiation Inhibition of pancreatic enzymes Corticosteroids Prostaglandins
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TREATMENT To interrupt the pathogenesis of complications Antibiotics Antacids Heparin Low molecular weight dextran Vasopressin Peritoeal lavage
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TREATMENT To support the patient and treat complications Restoration and maintenance of intravascular volume Electrolyte replacement Respiratory support Nutritional support Analgesia Heparin
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When to operate? Diagnostic laparotomy To limit the severity of the pancreatic inflammation Biliary procedures To interrupt the pathogenesis of complications Pancreatic drainage Pancreatic resection Pancreatic debridement Peritoneal lavage To support the patient and treat complications Drainage of pancreatic infection Feeding jejunostomy To prevent recurrent pancreatitis
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Summary of treatment All patients Nasogastric suction NPO Monitor and maintenance of intravascular volume Respiratory monitoring and support Antibiotics(selective) Early laparotomy only fordiagnosis Estimate prognosis by early signs Patients with severe pancreatitis Peritoneal lavage Nutritional support Suspect and treat pancreatic sepsis Heparin if hypercoagulable
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Chronic Pancreatitis 46
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Definition and Prevalence Defined as chronic inflammatory condition that causes irreversible damage to pancreatic structure and function. Incurable 5 To 27 Persons Per 100,000 47
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Etiology Alcohol, 70% Idiopathic (including tropical), 20% Other, 10% Hereditary Hyperparathyroidism Hypertriglyceridemia Autoimmune pancreatitis Obstruction Trauma Pancreas divisum 48
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Classification: 1.Calcific pancreatitis 2. Obstruction pancreatitis 3. Inflammatory pancreatitis 4. Auto immune pancreatitis 5. Asymptomatic fibrosis 6. Tropical pancreatitis 7. Hereditary pancreatitis 8. Idiopathic pancreatitis 49
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Signs and Symptoms Steady and Boring Pain Not Colicky Nausea /Vomiting Anorexia- Most Common Malabsorption And Weight Loss Diabetes Mellitus 50
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Classic triad “ pancreatic calcification , steatorrhea , and diabetes mellitus” Found in <1/3 secretin stimulation test (abnormal when 60% or more of pancreatic exocrine function has been lost) decreased serum trypsinogen (<20ng/ml) or a fecal elastase level of <100ug/mg of stool strongly suggests severe pancreatic insufficiency
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Laboratory Studies 52
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Imaging techniques A. Plain film radiography of abdomen B. Ultrasonography C. Computed tomography D. ERCP E. MRCP F. EUS
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Plain films : Pancreatic calcifications : 30% most common with alcoholic pancreatitis
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55 Pancreatic calcifications. CT scan showing multiple, calcified, intraductal stones in a patient with hereditary chronic pancreatitis Endoscopic retrograde cholangiopancreatography in chronic pancreatitis. The pancreatic duct and its side branches are irregularly dilated
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CT features Pancreatic atrophy, calcifications, and main pancreatic duct dilation 56
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ERCP 57 ERCP is a highly sensitive radiographic test for CP
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MRCP 58 MRCP allows a noninvasive alternative to ERCP for imaging the pancreatic duct.
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EUS EUS is a minimally invasive test that allows simultaneous assessment of ductal and parenchymal structure 59
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Treatment Analgesia Enzyme Therapy Antisecretory Therapy Neurolytic Therapy Endoscopic Management Surgical Therapy 60
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Complications Pseudocyst Pancreatic Ascites Pancreatic-Enteric Fistula Head-of-Pancreas Mass Splenic and Portal Vein Thrombosis 61
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Management 63
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A 45-year-old man presents to the emergency room complaining of severe epigastric pain that radiates to his back and left scapula. He has had severe nausea and vomiting associated with the pain for 3 days. Nothing seems to relieve his pain. He drinks about a fifth of bourbon a day. He has not had a bowel movement in several days. He also complains of a very dry mouth. He is afebrile and normotensive with a heart rate of 110 beats/min. He is mildly tender on abdominal examination. His serum amylase level is 650 IU/L. Which of the following is the most appropriate initial step in the management of this patient? (A) Exploratory laparotomy and pancreatic débridement (B) Discharge and close follow up as outpatient (C) Obtain an abdominopelvic computed tomography (CT) scan (D) Perform esophagogastroduodenoscopy (EGD) (E) Admit for intravenous (IV) hydration and withhold oral feeding
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A 48-year-old, alcoholic male has been hospitalized over the last 20 years more than 30 times for episodes of acute pancreatitis. He now presents to the emergency department complaining of mid-back pain and horribly malodorous and frequent soft stools. He describes that the stools float in the toilet. He also explains that he has lost 30 lb over the last 6 months. Which of the following therapeutic measures is the best option to improve this patient's health maintenance? (A) Total pancreatectomy (B) Oral pancreatic enzyme replacement (C) Total parenteral nutrition (D) Octreotide therapy (E) High-fat diet