Diese Präsentation wurde erfolgreich gemeldet.
Wir verwenden Ihre LinkedIn Profilangaben und Informationen zu Ihren Aktivitäten, um Anzeigen zu personalisieren und Ihnen relevantere Inhalte anzuzeigen. Sie können Ihre Anzeigeneinstellungen jederzeit ändern.

Management of acute pancreatitis

6.156 Aufrufe

Veröffentlicht am

MANAGEMENT OF ACUTE PANCREATITIS, Cholelithiasis (50%)
Alcoholism (25%)
Post-operative pancreatitis Metabolic disorder
Hyperlipidemia
Diabetes
Nutritional factors
Chemotoxic and iatrogenic causes
Idiopathic pancreatitis
Miscellaneous- scorpion bite, worm infestations

Veröffentlicht in: Gesundheit & Medizin
  • Loggen Sie sich ein, um Kommentare anzuzeigen.

Management of acute pancreatitis

  1. 1. MANAGEMENT OF ACUTE PANCREATITIS DR BASHIR BIN YUNUS GENERAL SURGERY UNIT AKTH 12/19/2018 bbinyunus2002@gmail.com 1
  2. 2. OUTLINE • INTRODUCTION • Definition • Epidemiology • Etiology • PATHOGENESIS • CLINICAL FORMS • MANAGEMENT • Algorithm • Investigations and risk assessment • Treatment • PROGNOSIS • COMPLICATIONS • CURRENT TRENDS 12/19/2018 bbinyunus2002@gmail.com 2
  3. 3. DEFINITION • It is the inflammation with autodigestion of the pancreas often associated with varying degree of pancreatic ductal dilatation. • It is an acute condition presenting with abdominal pain and is usually associated with raised pancreatic enzyme levels in the blood or urine as a result of pancreatic inflammation. 12/19/2018 bbinyunus2002@gmail.com 3
  4. 4. EPIDEMIOLOGY World wide the annual incidence is varies from 5-50 per 100,000 10 fold rise in the western world reflect alcohol use. Patients age and gender: Alcohol-induced 30-40years (younger) Men >> Women Gallstone-induced 40-60 years (older) Women >> Men 12/19/2018 bbinyunus2002@gmail.com 4
  5. 5. AETIOLOGY • Cholelithiasis (50%) • Alcoholism (25%) • Post-operative pancreatitis • Genetic • Microbial agents • Endocrine factors • Cortisone and ATCH • Hyperparathyroidism and hypercalcemia • Pregnancy • Metabolic disorder • Hyperlipidemia • Diabetes • Nutritional factors • Chemotoxic and iatrogenic causes • Idiopathic pancreatitis • Miscellaneous- scorpion bite, worm infestations 12/19/2018 bbinyunus2002@gmail.com 5
  6. 6. PATHOGENESIS Obstruction- Hypersecretion theory Common channel theory Duodenal reflux Acinar cell derangement 12/19/2018 bbinyunus2002@gmail.com 6
  7. 7. 12/19/2018 bbinyunus2002@gmail.com 7
  8. 8. Acinar cell derangement 12/19/2018 bbinyunus2002@gmail.com 8
  9. 9. CLINICAL FORMS OF ACUTE PANCREATITIS • Mild form • Moderate • Severe attack 12/19/2018 bbinyunus2002@gmail.com 9
  10. 10. MILD • Epigastric pain  may be the only complaint Radiates to the back Relieve by leaning forward (Van Zant Sign) • Vomiting may be associated with persistent retching and hiccups • Constipation is a rule in the initial stage • Upper abdominal tenderness and guarding • No organ failure, local or systemic complications 12/19/2018 bbinyunus2002@gmail.com 10
  11. 11. MODERATE • Local or systemic complications without persistent organ failure • Organ failure that resolves within 48 h (transient organ failure) 12/19/2018 bbinyunus2002@gmail.com 11
  12. 12. SEVERE • Patient is much iller • Pain is severer, Vomiting and retching is more persistent • The abdominal tenderness, marked guarding, rebound tenderness and diminished bowel activity • Full picture of shock may supervene • Persistent organ failure; single or multiple • Other features; left pleural effusion, jaundice 20-30%, carpopedal spasm • Could assume fulminating pancreatitis(acute haemorrhagic necrotizing) Shock is profound and coma or diabetic ketosis Retroperitoneal Haemorrhage (revealed as Cullen’s sign and grey Turner’s) 12/19/2018 bbinyunus2002@gmail.com 12
  13. 13. CULLEN’S SIGN 12/19/2018 bbinyunus2002@gmail.com 13
  14. 14. 12/19/2018 bbinyunus2002@gmail.com 14
  15. 15. MANAGEMENT 12/19/2018 bbinyunus2002@gmail.com 15
  16. 16. Management cont…. 12/19/2018 bbinyunus2002@gmail.com 16
  17. 17. Management cont….. Diagnose Resuscitate Assess severity 12/19/2018 bbinyunus2002@gmail.com 17
  18. 18. INVESTIGATIONS • HEMATOLOGICAL investigations • RADIOLOGICAL investigations • Miscellaneous investigations 12/19/2018 bbinyunus2002@gmail.com 18
  19. 19. HEMATOLOGICAL • BASELINES • CBC: • Low Hb: prolonged hemetemesis/melena, internal hemorrhage • Leucocytosis (10,000-30,000/mcL)-infection, non infectious inflammation • Low platelets-DIC • Hct –raised in hemoconcentration • LFT’s: • raised bilirubin, AST/ALT/LDH, ALP, GGTP- gall stone pancreatitis • RFT’s: • raised BUN/cretainine- ATN ARF • Coagulation profile: • increased INR-DIC • BSR: • > 180 mg/dl-diabetes as a sequelae or cause • Serum electrolytes: • Low sodium/potassium: persistent vomiting • Hypocalcemia- saponification/fat necrosis • Serum Protein: • low protein/ albumin Diabetes Mellitus AP
  20. 20. HEMATOLOGICAL • ABG’s • Etiology specific investigations • Serum fasting lipid profile • Viral titers • Serum Calcium (HypercalcemiaAPHypocalcemia) • Autoimmune markers • increased serum levels of IgG4 • serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF), Acid-Base Disturbance Etiology Metabolic (Lactic)acidosis with high anion gap Hypovolemic shock Cholride-responsive Hypokalemic Hypochloremic metabolic alkalosis (Urine chloride < 20 mEq/L) persistent vomiting Respiratory acidosis ARDS/resp failure
  21. 21. HEMATOLOGICAL • Pancreatic Enzymes’ Assays • Serum Amylase: • ONSET: almost immediately • PEAK: within several hours • 3-4 times upper limit of normal within 24 hrs (90%) • RETURN to normal depends on severity(3-5 days) • normal at time of admission in 20% cases • Compared with lipase, returns more quickly to values below the upper limit of normal. • Serum Lipase: • more sensitive/specific than amylase • Remains elevated longer than amylase(12 days) • Useful if late presentation Raised Amylase  may not AP Normal Amylase  may be AP SERUM INDICATOR OF HIGHEST PROBABILITY OF DISEASE
  22. 22. • Pancreatic Enzymes’ Assays • Urine Amylase • More sensitive than serum levels • Remain elevated for several days after serum levels returned to normal • Pancreatic-specific amylase(p-amylase) • Measuring p-amylase instead to total amylase(also includes salivary amylase) makes diagnosis more specific(88-93%)
  23. 23. CONDITIONS ASSOCIATED WITH RAISED SERUM AMYLASE ABDOMEN • Small bowel obstruction • strangulation ileus • mesenteric ischemia • Acute appendicitis • Cholecystitis • Perforated Duodenal Ulcer • Gastroenteritis • Biliary peritonitis • Spasm of sphincter of Oddi GYNE • Ruptured Ectopic pregnancy • Torsion of an ovarian cyst OTHERS • Parotitis (Mumps) • Macroamylasaemia • Opioids administration • Low GFR • Brain injury(CVA)- hyperstimulation of pancreas
  24. 24. Plain CXR-PA view • Left sided Pleural effusion: blunting of costophrenic and cardiophrenic angles + haziness in lower zones • Elevated diaphragm on left side • Linear focal atelactasis of lower lobe of lungs • ARDS: diffuse alveolar interstitial shadowing • Pulmonary edema: prominent vascular markings _________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
  25. 25. Plain X-ray abdomen erect AP view • Sentinel* loop sign • Localized isolated Distended gut loop (Ileus) seen near the site of injured viscus or inflamed organ • RATIONALE: body's effort to localize the traumatic or inflamed lesions • ETIOLOGY: Localized paralysis followed by accumulation of gas • SITE: • Acute Pancreatitis Left hypochondrium (PROXIMAL JEJUNUM) • Acute Appendicitis Right iliac fossa • Acute Cholecystitis Right Hypochondrium • Diverticulitis Left iliac fossa *SENTINEL:A soldier stationed as a guard to challenge all comers and prevent a surprise attack _______________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
  26. 26. SENTINEL LOOP SIGN
  27. 27. Plain X-ray abdomen erect AP view • Colon cut-off sign • Gas filled (Distended) segment of proximal(mainly transverse) colon associated with narrowing of the splenic flexure • abruptly ending at the area of pancreatic inflammation • with collapse of descending colon • RANTIONALE: Extension of inflammatory process from the pancreas into the phrenicocolic ligament via the transverse mesocolon • resulting in functional spasm and/or mechanical narrowing of the splenic flexure at the level where the colon returns to the retroperitoneum. • Differential DIAGNOSIS: • IBD • Carcinoma of colon • Mesenteric Ischemia ____________________________________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
  28. 28. COLON CUT-OFF SIGN
  29. 29. Plain X-ray abdomen erect AP view • Renal halo sign • RATIONALE: peripancreatic inflammatory reaction extension into pararenal space • ETIOLOGY: water-density (radiolucent-halo)of inflammation in anterior pararenal space contrasts with perirenal fat; more common on left side • OTHERS _______________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis • Air in the duodenal C-loop • increased gastrocolic separation • Gastric curvature distortion • To rule out perforated DU(gas under diaphragm) • Obliteration of psoas shadow • Localized ground glass appearance ( localized increased high soft tissue density) • Calcified gall stones • Pancreatic calcification(chronic pancreatitis)
  30. 30. Renal Halo Sign NORMAL RENAL HALO SIGN
  31. 31. Transcutaneous Abdominal Ultrasonography • Not diagnostic • Should be performed within 24 hours in all patients to • detect gall stones* as a potential cause • Rule out acute cholecystits as differential diagnosis • Detect dilated CBD • sensitivity-(70-80%) • DEMERIT: overlying gas shadows 2ndary to bowel distension • THERAPEUTIC: • USG-guided aspiration for gram staining and culture • USG-guided pig tail catheter insertion ______________________________________________________________________ ________ * Identification of gallstones as the etiology should prompt referral for cholecystectomy to prevent recurrent attacks and potential biliary sepsis. Gallstone pancreatitis is usually an acute event and resolves when the stone is
  32. 32. IV Contrast enhanced Computed Tomography Scan • Provides over 90 % sensitivity and specificity for the diagnosis of AP….. BUT • Routine use in patients with AP is unwarranted, as the diagnosis is apparent in many patients and most have a mild, uncomplicated course.
  33. 33. IV Contrast enhanced Computed Tomography Scan*• INDICATIONS-DIAGNOSTIC • Diagnostic uncertainty (differentiating pancreatitis from other possible intra- abdominal catastrophes) • Severe acute pancreatitis- distinguish interstitial from necrotizing pancreatitis • Necrosis( non enhancement area > 30 % or 3 cm) done at 72 hrs* • Systemic complications: • Progressive deterioration, MOF, sepsis • Localized complications: • Altered fat and fascial planes, Fluid collection, pseudocyst, psduoaneurysm, • Bowel distension, mesenteric edema, hemorrhage _____________________________________________________________ *INVESTIGATION OF CHOICE **Seldom needed within first 72 hrs after symptom onset unless the diagnosis is uncertain, because inflammatory changes are often not radiological present until this time
  34. 34. IV Contrast* enhanced Computed Tomography Scan • INDICATIONS-DIAGNOSTIC • Initial assessment of prognosis(CT severity index) • Perfusion CT at 3rd day  area of ischemia predict pancreatic necrosis • INDICATIONS-THERAPEUTIC: • CT-guided aspiration of fluid collection/necrotic tissue for gram staining and culture(sterile vs infected necrosis) • specimen should be delivered to the laboratory within an hour and interpreted promptly • CT-guided pig tail catheter insertion ______________________________________________________________ *Use of IV contrast may increase risk of complications of pancreatitis and AKI *Avoided if serum creatinine >1.5 mg/dL *MRI suitable alternative
  35. 35. BALTHAZAR CT severity index(CTSI)-1994 ___________________________________________________________________ Mild (0-3) moderate (4-6) severe (7-10) CT Severity Index Inflammation score + Necrosis score
  36. 36. Magnetic Resonant Imaging Suitable alternative to CT in patients with a contrast allergy and renal insufficiency where T2-weighted images without gadolinium contrast can diagnose pancreatic necrosis
  37. 37. 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
  38. 38. Endoscopic UltraSonography • INDICATIONS • Repeated idiopathic acute pancreatitis* • occult biliary disease- small stones/sludge • secretin-stimulated EUS study may reveal resistance to ductal outflow at the level of the papilla, • as evidenced by dilatation of the pancreatic duct to a greater extent and longer duration than in a healthy population • Age >40 to exclude malignancy • especially those with prolong or recurrent course • RATIONALE: 5 % CA pancreas present as AP _________________________________________ *Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the risks and benefits of investigation in these patients are unclear and should be referred to centers of expertise.
  39. 39. Endoscopic Retrograde Cholangiopancreatography INDICATION • Severe gallstone AP or AP with concurrent acute cholangitis/biliary obstruction/ biliary sepsis/jaundice (due to persistent stone) • ERCP within 24(-72) h of admission • Sphincterotomy/stent and bile duct clearance reduces infective complications/mortality 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 or EUS recommended if CBD stone still suspected • as risk of post-ERCP pancreatitis is greater with normal calibre bile duct and normal bilirubin • MRCP /EUS as accurate as diagnostic ERCP
  40. 40. ASSESSMENT OF SEVERITY • Early identification of patient at risk of severe pancreatitis and serious complication thereby decrease mortality. • Haemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed • Ranson’s scoring system • Glasgow scoring system • Apache II scoring system • Contrast enhance CTScan • C-reactive protein 12/19/2018 bbinyunus2002@gmail.com 40
  41. 41. RANSON’S SCORING SYSTEM • 11 Parameters, 5 on admission, 6 within 48hours. ≥3 factors indicate severe acute pancreatitis • ON ADMISSION 12/19/2018 bbinyunus2002@gmail.com 41
  42. 42. RANSON SCORE-1974 (for alcohol 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
  43. 43. 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
  44. 44. RANSON SCORE Ranson score Mortality rate SEVERITY Interpretation 0-2 ≈ 0-2 % i.e. minimal mortality Mild AP Admit in regular ward 3-5 10-20 % Severe AP Admit in ICU/HDU 6-7 40 % Associated with more systemic complications >7 >50 % Same as above SCORING SYSTEM SENSITIVITY SPECIFICITY Ranson Criteria 73% 77% APACHE II 77% 84% CRP 73% 71%
  45. 45. RANSON SCORE……. DRAWBACKS • One has to measure all 11 signs to achieve the best predictability of prognosis • 2 full days are needed to complete the profile. • A delay of 48 hours after admission merely for assessment may squander a valuable opportunity to prevent a complication during this time. • Best used within the initial 48 hours of hospitalization and have not been validated for later time intervals. • Threshold for abnormal valve depends on whether cause is gallstone or alcohol • Only 73 % sensitive and 77 % specific in predicting mortality
  46. 46. TREATMENT OF MILD/MODERATE 12/19/2018 bbinyunus2002@gmail.com 46
  47. 47. Mild/moderate 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: WHO analgesic ladder-1986 • Avoid Morphine-cause sphincter of Oddi spasm • Metabolic support • Correction of electrolyte imbalance
  48. 48. Severe Acute Pancreatitis • P: • Pain relief • Proton pump inhibitors-omeprazole • Peritoneal lavage • A • Admit in HDU/ICU • Antibiotics • N • Nasogastric intubation(if vomiting) • 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 management • ERCP • A • Antacids • S • Swan-Ganz catheter for CVP and TPN • Suction-in case of aspiration • Steroids in case of ARDS • Supportive therapy for organ failure • Inotropes • Hemofiltration • Ventilator(PEEP)
  49. 49. Monitoring CLINICAL • Vitals • UOP • CV pressure INVESTIGATIONS • Baselines • Serial ABGs • Serial BSR • Serum calcium/magnesium
  50. 50. Role of Surgery in AP • In case of mild gallstone AP, cholecystectomy should be performed before discharge to prevent a recurrence of AP • Within 48-72 hour od admission or briefly delay intervention(after 72 hrs but during same admission • Along with intraoperative cholangiography and any remaining CBD stones can be dealt with intra/post operative ERCP or • Along with preoperative EUS or MRCP • 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 • Cholecysectomy done for recurrent AP (IAP) with no stones/sludge on USG and no significant elevation of LFTs is associated with >50 % recurrence of AP _________________________________________________________ If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone may be effective to reduce further attacks of AP
  51. 51. Sterile necrosis infected necrosis Asymptomatic doesnot mandate intervention regardless of size, location and extension surgical, radiologic, and/or endoscopic drainage should be delayed preferably for more than 4 weeks • to allow liquefaction of the contents and the development of a fibrous wall around the necrosis • Initially treated with antibiotics Stable Symptomatic (associated with GOO or bile obstruction) minimally invasive methods of necrosectomy are preferred to open necrosectomy Urgent debridement unstable Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach), percutaneous radiologic catheter drainage or debridement, video-assisted or small incision- based left retroperitoneal debridement, and endoscopy
  52. 52. 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 Follow up • Routine clinical follow-up care (typically including physical examination and amylase and lipase assays) is needed to monitor for potential complications of the pancreatitis, especially pseudocysts. • Within 7-10 days
  53. 53. PROGNOSIS • Mortality rate for all patient with acute pancreatitis is about 10% • Necrotizing pancreatitis associated with infection has mortality of 20% • Earlier diagnosis of infection and aggressive intervention may lower this figure. 12/19/2018 bbinyunus2002@gmail.com 53
  54. 54. COMPLICATIONS • Pancreatic abscess • Pancreatic pseudocyst • Pancreatic fistula • Acute renal failure • Diabetic ketosis • Gastric erosion • Intestinal obstruction • Splenic rupture • Hypocalcaemia and tetany • Hypomagnesaemia 12/19/2018 bbinyunus2002@gmail.com 54
  55. 55. CURRENT TREND • Treatment with platelet-activating factor (PAF) antagonists appears to ameliorate the severity of acute pancreatitis and reduction in organ failure. Lexipafant • Interleukin 1 antagonist and IL-10 administration may prove beneficial to patient with severe disease, still under trial. 12/19/2018 bbinyunus2002@gmail.com 55
  56. 56. REFERENCES 12/19/2018 bbinyunus2002@gmail.com 56

×