Downloaded 68 times
More Related Content
![Acute pancreatitis [Autosaved].pptx surgery](https://cdn.slidesharecdn.com/ss_thumbnails/acutepancreatitisautosaved-240829144740-b197e85a-thumbnail.jpg?width=640&height=640&fit=bounds)
More from mauryaramgopal
Pancreatitis
- 1. Pancreatitis By: Dr. RamGopal Maurya
- 2. Outline • Introduction • Epidemiology •Pathophysiology • Etiology • Clinical Presentation • Workup • Severity Scoring System • Treatment • Prognosis • Complications
- 3. Introduction • Inflammation inpancreas associated with injury to exocrine parenchyma. • Types: 1. Acute: Emergency condition. 2. Chronic: Prolonged & frequently lifelong disorder resulting from the development of fibrosis within the pancreas
- 4. Acute Pancreatitis • Definition: Acutecondition of diffuse pancreatic inflammation & autodigestion, presents with abdominal pain, and is usually associated with raised pancreatic enzyme levels in the blood & urine. • Reversible inflammation of the pancreas
- 5. Epidemiology • The annualincidence ranges from 13– 45/100,000 persons. • Acute pancreatitis results in >250,000 hospitalizations per year. • higher among males than females. • It may occur at any age, peak incidence is between 50 and 60 years.
- 6. Pathophysiology • Pathologically, acutepancreatitis varies from interstitial pancreatitis (pancreas blood supply maintained), which is generally self-limited to necrotizing pancreatitis (pancreas blood supply interrupted). • Autodigestion is a currently accepted pathogenic theory; according to this theory, pancreatitis results when proteolytic enzymes (e.g., trypsinogen, chymotrypsinogen, proelastase, and lipolytic enzymes such as phospholipase A2) are activated in the pancreas acinar cell rather than in the intestinal lumen.
- 8. • A numberof factors (e.g., endotoxins, exotoxins, viral infections, ischemia, oxidative stress, lysosomal calcium, and direct trauma) are believed to facilitate premature activation of trypsin. Activated proteolytic enzymes, especially trypsin, not only digest pancreatic and peripancreatic tissues but also can activate other enzymes, such as elastase and phospholipase A2.
- 9.
- 10. Clinical Presentation • Symptoms:Upper Abdominal pain, sudden onset, sharp, severe, continuous, radiates to the back, reduced by leaning forward. • Patient lies very still. • Nausea, non-projactile vomiting, retching • Anorexia • Fever, weakness
- 11. ABDOMEN PAIN-Cardinal Symptom •SITE: usually experienced first in the epigastrium – but may be localized to either upper quadrant or felt diffusely throughout the abdomen or lower chest • ONSET: characteristically develops quickly, generally following substantial meal and precedes N&V • SEVERITY: frequently severe, reaching max. intensity within minutes rather than hours • NATURE: “boring through”, “knifing” (illimitable agony) • DURATION: hours-days • COURSE: constant (refractory to usual doses of analgesics, not relieved by vomiting) • RADIATION: directly to back(50%), chest or flanks • RELEIVING FACTOR: sitting or leaning/stooping forward (MUHAMMEDAN PRAYER SIGN) – due to shifting forward of abdominal contents and taking pressure off from inflamed pancreas • AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine
- 12. General Physical Examination •Appearance: well to critically ill with profound shock, toxicity and confusion • Vitals: Tachypnea(and dyspnea-10%), Tachycardia(65%), Hypotension, temp : high(76%)/normal/low • Icterus(28%) – gallstone pancreatitis or due to edema of pancreatic head • Cyanosis – Improper lung perfusion • Pallor, cold clammy skin,diaphoretic
- 13. ABDOMEN EXAMINATION • Tenderness+ Rebound tenderness: – epigastrium/upper abdomen. • Distension: – Ileus(BS decreased or absent) – ascites with shifting dullness. • Guarding(also called “defense musculaire” )-upper abdomen – tensing of the abdominal wall muscles to guard inflamed organs within the abdomen from the pain of pressure upon them(i.e. during palpation). • Rigidity(involuntary stiffness)-unusual – Tensing of the abdominal wall muscles to guard inflamed organs even if patient not touched.
- 14. Cutaneous Ecchymosis(1 %cases) • Acute Hemorrhagic Necrotizing/fulminant Pancreatitis--Periperitoneal/retroperitoneal Hemorrhage. • Methemalbumin formed from digested blood tracks around. • GREY TURNER’S SIGN • CULLEN’S SIGN • FOX SIGN
- 15. GREY TURNER’S SIGN hemorrhagicspots and ecchymosis in flanks, ruddy erythema in flanks due to extravasated pancreatic exudate.
- 16. CULLEN’S SIGN FALCIFORM LIGAMENTBluish Discoloration around umbilicus.
- 17. FOX SIGN Below inguinalligament.
- 18. Panniculitis • Subcutaneous nodularfat necrosis • Tender red nodules • Usually measures 0.5 – 2 cm • Usually over the extremities
- 19. WORKUP • HEMATOLOGICAL investigations •RADIOLOGICAL investigations • Miscellaneous investigations
- 20. HEMATOLOGICAL investigations Blood tests: CompleteBlood Count Serum amylase & lipase C-reactive Protein Serum electrolytes Blood glucose Renal Function Tests Liver Function Tests LDH Coagulation profile Arterial Blood Gas Analysis
- 21. Serum Amylase • Sensitivity:72% Specificity: 99% • Released within 6-12 hours of the onset, & Remains elevated for 3-5 days. • Elevation ˃ 3X normal is significant. • Undergoes renal clearance. After its serum levels decline, its urinary level remains elevated. • Its level doesn't correlate with the disease activity
- 22. Serum Lipase • Morepancreatic-specific than s. Amylase. • Sensitivity: about 100% Specificity: 96% • Remains elevated longer than amylase (up to week). • Useful in patients presenting late to the physician. • S. Amylase tends to be higher in gallstone pancreatitis. • S. Lipase tend to be higher in alcoholic pancreatitis.
- 24. • Patients withmore severe disease may show hemoconcentration with hematocrit values >44% and/or prerenal azotemia with a blood urea nitrogen (BUN) level >22 mg/dL resulting from loss of plasma into the retroperitoneal space and peritoneal cavity. • Hyperglycemia is common d/t including decreased insulin release, increased glucagon release, and an increased output of adrenal glucocorticoids and catecholamines. • Hypocalcemia occurs in ~25% of patients.
- 25. • Hyperbilirubinemia (serumbilirubin >68 mmoL or >4.0 mg/dL) occurs in ~10% of patients. • Hypertriglyceridemia occurs in 5–10% of patients. • Approximately 5–10% of patients have hypoxemia (arterial PO2≤60 mmHg), which may herald the onset of ARDS.
- 26. Imaging Investigations • Plainerect chest X-ray: not diagnostic on pancreatitis, but to rule out other D/D • Pleural effusion, diffuse alveolar infiltrate (ARDS) • Pleural effusion, common on left side.
- 28.
- 29.
- 31. CT Scan Not indicatedin every patient, only in: 1. Diagnostic uncertainty. 2. Severe acute pancreatitis. 3. Clinical deterioration, with multi-organ failure, sepsis, progressive deterioration. 4. Local complications occurs (fluid collection, pseuodocyst, pseudo-aneurysm).
- 32. • Axial CTScan: Peripancreatic stranding (arrow). Multiple gallstones in the gallbladder
- 33. Contrast-enhanced CT: acutenecrotising pancreatitis. Pancreatic area of reduced enhancement, peripancreatic edema and stranding of the fatty tissue
- 35. Magnetic Resonant Cholangiopancreatography • INDICATION: –diagnosis of suspected biliary and pancreatic duct obstruction in the setting of pancreatitis. – Repeated attacks of idiopathic acute pancreatitis • Merit – used if choledocholithiasis is suspected but there is concern that pancreatitis might worsen is ERCP is performed – Provide non-invasive/fast/safe high-quality (Heavily T2– weighted) imaging for diagnostic and/or severity purposes
- 36.
- 37. Endoscopic Retrograde Cholangiopancreatography INDICATION Severe gallstoneAP or AP with concurrent acute cholangitis/biliary obstruction/ biliary sepsis/jaundice (due to persistent stone) NOT INDICATED • Not needed early in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction • As most of gallstones causing AP readily pass to duodenum and are lost in stool • MRCP /EUS as accurate as diagnostic ERCP
- 38.
- 41. MISCELLANEOUS • Peritoneal(sensitivity 54%,specificity 93%)/Pleuralfluid tap – High amylase/lipase/protein • Urine Complete Examination – Proteinuria, granular cast, glycosuria • Electrocardiography – ST-T wave changes • Bile Aspiration – Crystal analysis, if suspicion of microlithiasis
- 45. SEVERITY SCORING SYSTEMS •Ranson score • Glagsow score • Bedside Index for Severity in Acute Pancreatitis(BISAP) score • CT severity index • Acute Physiology And Chronic Health Evaluation(APACHE) II score
- 46. Each system hasmerits and demerits, and none is currently recognized as a criterion standard. Although amylase/lipase are used in diagnosing pancreatitis, they are NOT use for predicting severity of disease
- 47. RANSON SCORE-1974 (foralcohol pancreatitis) ON ADMISSION • Age > 55 yrs • TLC > 16,000/mm3 • BSR> 200 mg/dL • AST > 250 IU/L • LDH > 350 IU/L WITHIN 48 HOURS • BUN rise >5 mg/dL • Pa02 < 60 mmHg ( 8 KPa) • Serum Calcium < 8 mg/dL • Base deficit > 4 meq/L • Fluid Sequestration > 6000 mL • Hct fall > 10 % NOTE: Disease classified as SEVERE when 3 or more factors are present
- 48. Revised RANSON SCORE-1979(for Gallstone pancreatitis) ON ADMISSION • Age > 70 years • TLC > 18000/mm3 • BSR > 220 mg/dL • AST> 250 IU/L • LDH >400 IU/L WITHIN 48 HOURS • BUN rise >5 mg/dL • Pa02 < 60 mmHg ( 8 KPa) • Serum Calcium < 8 mg/dL • Base deficit > 5 meq/L • Fluid Sequestration > 4 litres • Hct fall > 10 % NOTE: Disease classified as SEVERE when 3 or more factors are present
- 49. RANSON SCORE Ranson score Mortality rateSEVERITY Interpretation 0-2 ≈ 0-2 %i.e. minimal mortality Mild AP Admit in regularward 3-5 10-20 % SevereAP Admit in ICU/HDU 6-7 40 % Associated with moresystemic complications >7 >50% Sameas above
- 50. Glasgow-Imrie score ON ADMISSION •Age > 55 yrs • TLC > 15 x 109 l-1 • BSR>180 mg/dL (10 mmol l- 1) (no H/O diabetes) • BUN > 16 mmol l-1 (no response to IV fluids) • Pa02 < 60 mmHg ( 8 KPa) WITHIN 48 HOURS • Serum Calcium < 2.0 mmol l-1 • Serum albumin <32 g l-1 • LDH > 600 units l-1 • AST/ALT > 200 units l-1 NOTE: Disease classified as SEVERE when 3 or more factors are present
- 51. Modified Glasgow/PANCREAS score •PaO2 < 8kPa (60mmhg) • Age > 55 years • Neutrophils: WBC >15 x109/l • Calcium < 2mmol/l • Renal function: (Urea > 16mmol/l) • Enzymes: (AST/ALT > 200 iu/L or LDH > 600 iu/L) • Albumin < 32g/l • Sugar: (Glucose >10mmol/L) • *Applicable for both gallstone and alcohol induced pancreatitis within 48 hours of admission • *Omission of age/serum transaminase increases the predictive valve of scoring system as serum transaminase did not differ significantly between mild and severe pancreatitis.
- 52. Bedside Index forSeverity in Acute Pancreatitis(BISAP) score
- 53.
- 54. • NOTE: Diseaseclassified as SEVERE if clinical impression of very ill patient with APACHE II score above 8
- 55. APACHE II SCORE MERIT •Immediate assessment of the severity of pancreatitis possible. • Can be used even after 48 hours. • Unlike ALL pancreatic specific scoring systems, APACHE (and SOFA) also includes clinical features of patient besides laboratory values. (Clinical findings are more important than lab findings in predicting SIRS,sepsis and other complications)
- 56. MANAGEMENT • Mild acutepancreatitis – Conservative Approach – Admit in general ward – Non invasive monitoring • (Moderate)Severe acute pancreatitis – Aggressive Approach – Admit in HDU/ICU – Invasive monitoring __________________________________________________ Recognizing patients with severe acute pancreatitis ASAP is critical for achieving optimal outcomes
- 57. Mild Acute Pancreatitis •mild and self-limiting, needing only brief hospitalization. • Rehydration by IV fluids • Frequent non-invasive observation/monitoring(atleast 8 hrly) • Brief period of fasting till pain/vomiting settles – Little physiological justification for prolonged NPO • No medication required other than analgesics(important) and anti-emetics – Antibiotics not indicated in absence of signs or documented sources of infection – Pain results in ongoing cholinergic discharge, stimulating gastric and pancreatic secretions – Analgesics: Avoid Morphine-cause sphincter of Oddi spasm • Metabolic support – Correction of electrolyte imbalance
- 58. Severe Acute Pancreatitis •P:– Pain relief – Proton pump inhibitors- omeprazole – Peritoneal lavage • A:– Admit in HDU/ICU – Antibiotics • N:– Nasogastric intubation – Nasal oxygen – Nutrition support • C:– Calcium gluconate – CVP line – Catherisation- Foley • R:– Rehydration by IV fluids,plasma,blood – Ranitidine(for stress ulcer) – Radiology: CT scan, USG – Resuscitation when required • E:-Endotracheal intubation – Electrolytes managemen – ERCP • A – Antacids • S:– Suction-in case of aspiration – Steroids in case of ARDS – Supportive therapy for organ failure • Inotropes • Hemofiltration • Ventilator(PEEP)
- 59. ACG 2013 Recommendations •Despite dozens of randomized trials, no medication has been shown to be effective in treating AP. • However, an effective intervention has been well described: EARLY AGRESSIVE IV hydration.
- 60. • Rationale forEARLY AGRESSIVE IV hydration • Frequent hypovolemia due to – vomiting, – reduced oral intake, – third spacing of fluids(increased vascular permeability) – increased respiratory losses, and – diaphoresis.
- 61. Kon sa? Lactated Ringer ’ssolution may be the preferred isotonic crystalloid replacement fluid •Ringer lactate is better electrolyte balance and more pH-balanced •Normal saline given in large volumes may lead to the development of a non-anion gap, hyperchloremic metabolic acidosis and increased chances of SIRS •Low pH activates the trypsinogen, makes the acinar cells more susceptible to injury and increases the severity of established AP Kab? Early aggressive IV hydration is most beneficial during the first 12 – 24 h, and may have little benefit beyond this time period Kitna? Aggressive hydration, defined as 250 – 500 ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular, renal, or other related comorbid factors exist. • In a patient with severe volume depletion, manifest as hypotension and tachycardia, more rapid repletion (bolus) may be needed • Fluid requirements should be reassessed at frequent intervals within 6 h of admission and for the next 24 – 48 h. EARLY AGRESSIVE IV hydration
- 62. Antibiotics • Routine use*NOT recommended(ACG 2013) as – Prophylaxis in severe AP – Preventive measure in sterile necrosis to prevent development of infected necrosis • Indicated in – Established infected pancreatic necrosis or – Extraperitoneal infections -- Cholangitis, -- catheter-acquired infections, bacteremia, UTIs, pneumonia
- 63. • As SIRSmay be indistinguishable from sepsis syndrome, so if infection is suspected, antibiotics should be given while source of infection is being investigated – Once blood and other cultures are found negative, antibiotics should be discontinued. • Few antibiotics penetrate due to consistency of pancreatic necrosis – cefuroxime, or imipenem, or ciprofloxacin plus metronidazole.
- 64. • Relatively stablepatients with infected necrosis can be managed conservatively on antibiotics without needing surgery(necrosectomy) or intervention (percutaneous or endoscopic drainage) – Surgical debridement recommended if no response to conservative treatment or deteriorates clinically
- 65. Nutrition • In mildAP – oral feedings can be started immediately if there is no nausea/vomiting, and the abdominal pain/tenderness/Ileus has resolved(amylase return to normal, patient feel hunger). – Initiation of feeding with a small and slowly increasing low-fat (low-protein) soft diet appears as safe as a clear liquid diet, providing more calories. -- Stepwise manner increase from clear liquids to soft diet NOT necessary. • In severe AP – Enteral route is recommended to prevent infectious complications – Parenteral nutrition should be avoided, unless enteral route is not available, not tolerated, or not meeting caloric requirements
- 66. RATIONALE OF EARLYENTERAL NUTRITION • The need to place pancreas at rest until complete resolution of AP no longer recommended – Bowel rest associated with intestinal mucosal atrophy and bacterial translocation from gut and increased infectious complications • Early enteral feeding maintains the gut mucosal barrier, prevents disruption, and prevents translocation of bacteria that seed pancreatic necrosis – Decrease in infectious complications, organ failure and mortality
- 67. Rather than usingantibiotics to prevent infected necrosis………….start early enteral feeding to prevent translocation of bacteria
- 68. Route of enteralNutrition • Traditionally nasojejunal route has been preferred to avoid the gastric phase of stimulation BUT – Nasogastric route appears comparable in efficacy and safety MERITS OF NASOGASTRIC ROUTE DEMERITS OF NASOGASTRIC ROUTE NG tube placement is far easier than nasojejunal tube placement( requiring interventional radiology or endoscopy, thus expensive) especially in HDU/ICU setting Slight increased risk of aspiration (Can be overcome by placing patient in upright position and be placed on aspiration precautions)
- 69. FEEDING REGIMEN • Thejejunum does not have the reservoir capacity of the stomach, so jejunal feedings should be advanced more slowly than gastric feedings • The diluting effect of gastric secretions is also lost in the jejunum, so isotonic feeding formulas are preferred to hypertonic formulas • Standard (polymeric) tube feedings can be used for jejunal feedings, but in patients with diarrhea, elemental feeding formulas may be preferred. (Elemental formulas are low in fat, and the protein is available as individual amino acids, which are presumably easier to digest.)
- 70. Role of Surgeryin AP • In case of mild gallstone AP, cholecystectomy should be performed before discharge to prevent a recurrence of AP. • In case of necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize. • If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone may be effective to reduce further attacks of AP.
- 71. When to Discharge •Pain is well controlled with oral analgesia • Able to tolerate an oral diet that maintains their caloric needs, and • all complications have been addressed adequately
- 72. Prognosis TYPEOFAP MORTALITY Overall 10-15% (Biliary>alcholic) Mild Acute Pancreatitis(80 %cases) 1 % SevereAcute Pancreatitis(20 %cases) Severe 20-50 % <1week 1/3 cases >1week 2/3 cases
- 73. SYSTEMIC COMPLICATIONS • CARDIOVASCULAR –Shock- hypovolemic and septic – Arrhythmias/pericardial effusion/sudden death – ST-T nonspecific changes • Pulmonary – Respiratory failure/pneumonia/atelectasis/pleural effusion – Acute Respiratory Distress Syndrome (ARDS) • Renal Failure – Oliguria – Azotemia – Renal artery/vein thrombosis • Hematological – Hemoconcentation – Disseminated Intravascular Coagulopathy (DIC)
- 74. • Metabolic – Hypocalcemia –Hyperglycemia – Hyperlipidemia • Gastrointestinal – Peptic Ulcer/Erosive gastritis – Ileus – Portal vein or splenic vein thrombosis with varices • Neurological – Visual disturbances-Sudden blindness(Purtscher’s retinopathy) – Confusion,irritability,psychosis – Fat emboli – Alcohol withdrawal syndrome – Encephalopathy • Miscellaneous – Subcutaneous fat necrosis – Intra-abdominal saponification – Arthralgia
- 75. LOCAL COMPLICATIONS • Peripancreaticfluid collections • (Peri)Pancreatic necrosis( sterile + infected) • Pancreatic abscess(Phlegmon) • Pseudocyst • Pancreatic ascites • Pseudoaneurysm • Involvement of adjacent organs, with hemorrhage, thrombosis, bowel infraction, obstructive jaundice, fistula formation, or mechanical obstruction