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The Management of Acute Pancreatitis PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "The management of acute pancreatitis” by Professor Ravi Kant.

This medical PowerPoint presentation is about the management of acute pancreatitis which involves hospitalization, NPO and pain management, intravenous fluids, nutritional support, identification and treatment of complications, management of underlying causes, and supportive care when necessary.

Acute pancreatitis is a medical emergency that requires prompt evaluation and management. The primary goal of management is to relieve pain, manage complications, and prevent further damage to the pancreas.

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Published on : May 02, 2023 | Views : 2450 | Downloads : 5

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Slide 1-

THE MANAGEMENT OF ACUTE PANCREATITIS Professor Ravi Kant MB, MS, FRCS (Edinburgh), FRCS (Glasgow), FACS, FICS, DNB, FAIS, FAMS, 1
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2 INTRODUCTION
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3 Introduction “In the growing world of EBM, only 30% of surgery is based on evidence while 70% of medicine is evidence based” EJS, Sep 2005
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4 Introduction Stress will be on Diagnosis, workup, prognostic predictors and management Basic sciences
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5 DEFINITION
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6 Definition “Acute pancreatitis”: Inflammation of the pancreas without, or with minimal fibrosis.
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7 EPIDEMIOLOGY
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8 Epidemiology 300,000 annually in US 10-20% are severe Total annual cost of 2 billion $$$ (Biliary + alcoholic) 90% Even in the west, biliary pancreatitis is the most prevalent type. Incidence among AIDS patients 4-22%
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9 Epidemiology Local statistics?
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10 Epidemiology “Profile of acute pancreatitis in Jizan, Saudi Arabia” Saudi Med J. 2003 Jan;24(1):72-5. (KFCH), Jizan, KSA over 12 years regional 42% (biliary), 18% Post ERCP “Pattern of acute pancreatitis” Saudi Med J. 2001 Mar;22(3):215-8. Cross sectional, 2 years, Asir central hospital 68% found to be biliary
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11 PATHOPHYSIOLOGY
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12 Pathophysiology Causes Biliary tract disease Alcohol Hyperlipedemia Hypercalcemia Trauma ERCP Ischemia Pancreatic neoplasia Pancreas divisum Ampullary lesions Duodenal lesions Infections Venom Drugs idiopathic
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13 Pathophysiology Theories behind mechanism of biliary pancreatitis Common channel theory Incompetent sphincter theory Co-localization theory
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14 PATHOPHYSIOLOGY Common channel theory “Opie 1901” Detergent effect of bile
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15 Pathophysiology Critique of common channel theory Higher hydrostatic pressure in PD Introduction of bile into PD in animal models failed to cause AP
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16 Pathophysiology Incompetent sphincter theory Incompetent sphincter of Oddi due to stone passage  reflux  AP Critique How come papillotomy doesn’t routinely cause AP??
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17 Pathophysiology Co-localization theory “Steer & Saluja” 1998 Most acceptable Stones  PD ductal hypertension  ducutle rupture Ductal pH = 9 …… parynchemal pH = 7 trypsinogen + cathepsin B  trypsin  autodigestion cascade
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18 Pathophysiology
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19 Pathophysiology
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20 Pathophysiology
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21 Pathophysiology Support of co-localization theory CA-074me (cathepsin B inhibitor) prevented AP in 2 different models of acute pancreatitis
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22 Pathophysiology Alcoholic pancreatitis No such thing as acute alcoholic pancreatitis It is actually the first attack of chronic alcoholic pancreatitis
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23 DIAGNOSIS
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24 Diagnosis Clinical picture Investigations “Acute pancreatitis is a diagnosis of exclusion” Schwartz’s
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25 Diagnosis Hx: Epigastric pain Radiating to back Nausea, vomitting Precipitating factor?
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26 Diagnosis Physical V/S  variable Epigastric tenderness Cullen’s / Grey Turner’s (1%) Findings of complication(s)
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27 Cullen’s sign
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28 Grey Turner’s sign
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29 Diagnosis Serum markers Amylase Easiest to measure and most widely used Rises immediately Peaks in few hours Remains for 3-5 days “Three fold rise is diagnostic” May be normal in severe attacks May be falsely negative in hyperlipedimic patients Inverse correlation between severity and serum amylase level No need to repeat
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30 Diagnosis Serum markers Urine amylase Remains elevated for a few more days Increase excretion of amylase with attacks of AP Of great value when dealing with severe pancreatitis
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31 Serum markers P/S – amylase P amylase increases specificity to 93% Lipase “the serum marker of highest probability of disease” Specificity of 96% Remains elevated for longer time than total amylase Diagnosis
Slide 32-

32 Diagnosis
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33 Causes of hyperamylesemia Pancreatitis p Choledocolethiasis p Parotitis s Renal failure s/p Liver cirrhosis s/p perforated bowel p mesenteric infarction p intestinal obstruction p Appendicitis p Peritonitis. P Gyne disease s Malignancies Lung CA Ovarian CA pancreatic CA Colonic CA pheochromocytoma; Thymoma multiple myeloma breast cancer
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34 RADIOLOGY (diagnostic)
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35 Radiology Diagnostic role X-ray U/S CE-CT
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36 Radiology X-ray Air in the duodenal C loop Sentinel loop sign Colon cutoff sign All these signs are non specific
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37 Radiology CE-CT Enlargement of the pancreas (focal/diffuse) Irregular enhancement Shaggy Pancreatic contour Thickening of fascial planes fluid collections. Intraperitoneal / retroperitoneal Retroperitoneal air
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38 Radiology U/S Diagnosis of gallstones F/U of pseudocysts. Dx pseudoaneurysms EAUS vs. EUS
Slide 39-

39 PROGNOSIS
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40 Prognosis Course either mild or severe Mild = edematous pancreatitis Severe = necrotic pancreatitis No such thing as moderate pancreatitis
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41 Prognosis Serum markers CT Systemic complications Prognostic scores Ranson Apache II Modified Glasgow Atlanta Atlanta Consensus 1992
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42 Prognostic scores Ranson’s Published in 1974 Predictor of morbidity/mortality <2 0% mortality 3-5 10-20% >7 >50% mortality Critique of Ranson’s 11 parameters 48 hours No predictor value beyond 48hrs Too pessimistic for today’s healthcare system
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43
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44 Prognostic scores APACHE II Immediate Acute and chronic parameters Complicated >7 = severe pancreatitis
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45 Prognostic biochemical markers Biochemical markers of prognosis Ideally High sensitivity High specificity Discriminate severe from mild Immediate Widely available Amylase & lipase Highly sens./spec. Lack prognostic value
Slide 46-

46 Prognostic biochemical markers Alternatives CRP 2 macroglobulin PMN elastase 1 antitrypsin Phospholipase A2 “CRP seems to be the marker of choice in these settings” CRP >150 is diagnostic of severe pancreatitis
Slide 47-

47 Prognostic biochemical markers Other markers IL-6 Urinary TAP These showed great promise in models and clinical trials Failed in larger scale trials
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48 CT scan (prognostic aspect) “CT scanning with bolus IV contrast has become the gold standard for detecting and assessing the severity of pancreatitis” “Currently, IV bolus contrast enhanced CT scanning is routinely performed on patients who are suspected of harboring severe pancreatitis, regardless of their Ranson’s or APACHE scores” Schwartz’s
Slide 49-

49 CT scan (prognostic aspect)
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50 CT scan (prognostic aspect)
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51 CT scan (prognostic role) Balthazar CT-severity index (CTSI) CTSI considers degree of necrosis Also considers the CT grade A final score is given and correlates with mortality and complication development
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52 CT scan (prognostic role) Balthazar grading Grade A - Normal-appearing pancreas 0 Grade B - Enlargement of the pancreas 1 Grade C - Pancreatic gland abnormalities a with peripancreatic fat infiltration 2 Grade D - A single fluid collection 3 Grade E - Two or more fluid collections 4
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53 CT scan (prognostic role) Grade of necrosis and the points assigned per grade are as follows: None 0 points Grade 0.33 2 points Grade 0.5 4 points Grade > 0.5 6 points
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54 CT scan (prognostic role) Overall prognostic outlook:
Slide 55-

55 Is CT superior??? “Computed Tomography Severity Index, APACHE II Score, and Serum CRP Concentration for Predicting the Severity of Acute Pancreatitis”* n=55 CTSI,APACHE and CRP had p <0.01
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56 Prognosis Recommendation for assessing severity: Mild is defined as: No systemic complications Low APACHE/Ranson scores CE-CT findings (Balthazar) CRP level <150 Santorini 1999
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57 MANAGEMENT
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58 MANAGEMENT Management depends on severity We will consider management of edematous pancreatitis separately from necrotizing pancreatitis for purpose of simplification
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59 MANAGEMENT OF MILD PANCREATITIS
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60 Management (mild) Core of treatment based on Physiological monitoring Metabolic support Maintenance of fluids and electrolytes
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61 Management (mild) NG suction H2 blockers Gastric acid reaching the duodenum will activate pancreatic secretion??? Large studies failed to show any benefit
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62 Management (mild)
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63 Management (mild)
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64 Management (mild) What is the role of anti-secretory agents? Atropin Calcitonin Somatostatin Glucagon Flurouracil Unproven benefit*
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65 Management (mild) Pancreatitis is an autodigestive process Role of protease inhibitors? Aprotinin Gabexate mesylate Camostate Phospholipase A2 inhibitors FFP No benefit
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66 Management (mild) Pancreatitis is an inflamatory process Role of anti-inflamatory drugs? Indomethacin Prostaglandin inhibitors Interleukin-10 No measurable benefit
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67 Management (mild) Vascular injury is mediated by platelet aggregating factor What’s the role of PAF inhibitors? PAF acetylhydrolase Lexipafant Great results in models Great results in small clinical trials Failed in larger studies Verdict: useless
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68 Management (mild) Question to audience: When dealing with acute pancreatitis, do u start Abx therapy? (hands please) “Antibiotic therapy has not proved to be of value in the absence of signs or documented sources of infection”
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69 Management (mild) Mainstay of management is supportive NPO IVF When to resume oral intake? Absence of pain Absence of tenderness Patient feeling hungry On average takes about 3-7 days Sips of water and build up to low protein low fat diet
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70 Management (mild) Any drug therapy for acute pancreatitis? “None of the evaluated medical treatments is recommended (level A)”* Meta-analysis considering gabexate mesylate, octreiotide, aprotinin and lexipafant
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71 MANAGEMENT OF SEVERE PANCREATITIS
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72 Management (severe) Severe pancreatitis: > Ranson / APACHE CRP >150 Systemic complications Necrosis on CE-CT Hemodynamic compromise
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73 Management (severe) Complications Local Phlegmon Abcess Pseudocyst Ascitis pseudoanurysm Adjacent organ envolvment Systemic pulmonary Cardiac Hematological GI Renal Metabolic CVS Fat necrosis
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74
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75
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76
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77
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78 Pseudocyst
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79 Management (severe) Sterile necrosis Absence of retroperitoneal air on CT Prognosis 0% mortality without complications 38% with single sys. complication
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80 Management (severe) How to approach sterile necrosis?: No sys. Comp., no infec. (i.e. uncomplicated) supportive Sys. Comp. + infection? ( mild complication) CT guided aspiration  gram stain/culture  Abx Mult. Sys comp + toxicity/shock (frank complication) surgical debridment S E V E R I T Y
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81 Management (severe) Role of prophylactic Abx? Previously thought to have no role in sterile necrosis Prophylaxis indicated whenever there is necrosis Drugs with proven benefit Imipenem Flagyl 3rd gen. Cephalosporins Abx prophylaxis reduced:* Sepsis by 21.1% Mortality by 12.3%
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82 Management (severe) Role of Antifungal medication Candida is a common inhabitant of upper GI tract Risk of secondary infection Empiric fluconazole? Clansy TE “current management of necrotizing pancreatitis”*
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83 Management (severe) Nutritional support NPO with resumption of diet when fit If NPO > 7 days… TPN vs. Jujenal tube feeding? TPN: gastric mucosal atrophy  bacterial translocation Jujenal tube feeding: induces pancreatic secretion Inconclusive studies: Jujenal T. feeding is superior*
Slide 84-

84 Management (severe) Benefit of enteral feeding Prospective randomized trial n=34 Severe acute pancreatitis “enteral feeding modulates the inflamatory and sepsis response in acute pancreatitis”*
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85 Management (severe) NG vs. NJ feeding Prospective randomized trial N=50 Mortality as endpoint No statistically significant benefit of NJ*
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86 Management (severe) Something very important has been missing in the presentation… Where is pain management? Also missing from the research scene
Slide 87-

87 Specific considerations of biliary pancreatitis
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88 Management (severe) Specific consideration of biliary pancreatitis: Majority of stones will pass within hours Some might impact Patient at risk of subsequent stone obst. NECROSECTOMY
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89 Management (severe) If hyperbili is dropping: Lap chole with surgical duct clearance <72 hours vs. >72 (within admission) If patient critical  ERCP stone clearance Routine ERCP NOT ADVOCATED
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90 Management (severe) If hyper bili persists: confirm presence of stone before ERCP (MRCP, EUS)
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91 Suggested algorithm
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92
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93 Conclusion Acute pancreatitis is a hot area for research Advances at the cellular level show promise to “halt”pancreatitis Most patients need just supportive care No indication for Antibiotics in mild type Severe pancreatitis needs antibiotics Surgical management ►gallstones / complications
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94 Your comments….
Slide 95-

95 Pancreatic Psudocyst
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96 Definition: Pseudocysts are encapsulated localized collection of pancreatic enzyme, inflammatory fluid and necrotic debris on pancreas or in part or the whole of the lesser sac. They are distinguished from other types of pancreatic cysts by their lack of an epithelial lining.
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97 Causes Acute or chronic pancreatitis abdominal trauma. Duct obstruction.
Slide 98-

98 Presenting symptoms Epigastric pain Nausea Vomiting Weight loss Mild Fever Jaundice
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99 Physical Examination The sensitivity of physical examination findings is limited. Tender abdomen. Palpable mass in the abdomen with an indistinct lower edge. The upper limit is not palpable .
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100 Physical Examination The sensitivity of physical examination findings is limited. tender abdomen. palpable mass in the abdomen with an indistinct lower edge. The upper limit is not palpable .
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101 Physical Examination Its usually resonant to percussion because it is covered by the stomach. It moves very slightly with respiration. it is not possible to elicit fluctuation or a fluid thrill. Peritoneal signs suggest rupture of the cyst or infection
Slide 102-

102 Differential diagnosis: Acute pancreatic fluid collections. Serous cystadenoma of the pancreas Mucinous cystadenoma of the pancreas Mucinous cystadenocarcinoma Pancreatic retention cyst
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103 Investigations: Lab studies Imaging studies E.R.C.P
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104 Serum tests: Amylase and lipase levels are often elevated but may be normal Bilirubin and LFT findings may be elevated if the biliary tree is involved.
Slide 105-

105 Lab Studies Analysis of the cyst fluid may help differentiate pseudocysts from tumors. Attempt to exclude tumors in any patient who does not have a clear history of pancreatitis.
Slide 106-

106 Analysis of cyst fluid Carcinoembryonic antigen (CEA) and carcinoembryonic antigen-125 (CEA-125) tumor marker levels are low in pseudocysts and elevated in tumors. Fluid viscosity is low in pseudocysts and elevated in tumors. Amylase levels are usually high in pseudocysts and low in tumors. Cytology is occasionally helpful in diagnosing tumors, but a negative result does not exclude tumors.
Slide 107-

107 Abdominal CT scan CT scan is the investigation of choice in pancreatic pseudocysts. It has a sensitivity of 90-100% and is not operator dependent. The usual finding on CT scan is a large cyst cavity in and around the pancreas. Multiple cysts may be present.
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108 Abdominal CT scan The pancreas may appear irregular or have calcifications. Pseudoaneurysms of the splenic artery, bleeding into a pseudocyst, biliary and enteric obstruction, and other complications may be noted on CT scan. The CT scan provides a very good appreciation of the wall thickness of the pseudocyst, which is useful in planning therapy.
Slide 109-

109 Abdominal ultrasound: While cystic fluid collections in and around the pancreas may be visualized via ultrasound, the technique is limited by operator skill, the patient's habitus, and overlying bowel gas. As such, ultrasound is not the study of choice for diagnosis.
Slide 110-

110 MR MR is not necessary for the diagnosis of pseudocysts; however, it is useful in detecting a solid component to the cyst and in differentiating between organized necrosis and a pseudocyst.
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111 MRI A solid component makes catheter drainage difficult; therefore, in the setting of acute necrotizing pancreatitis with resultant pseudocyst, an MRI may be very important before a planned catheter drainage procedure.
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112 Endoscopic Retrograde Cholangiopancreatography (ERCP) is not necessary in diagnosing pseudocysts; however, it is useful in planning drainage strategy.
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113 Complications Infection of the pseudocyst patients develop fever or an elevated WBC count. Treat infection with antibiotics and urgent drainage. Gastric outlet obstruction, manifesting as nausea and vomiting, is an indication for drainage.
Slide 114-

114 Complications Rupture A controlled rupture into an enteric organ occasionally causes GI bleeding. On rare occasions, a profound rupture into the peritoneal cavity causes peritonitis
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115 Continue Bleeding is the most feared complication and is caused by the erosion of the pseudocyst into a vessel. Consider the possibility of bleeding in any patient who has a sudden increase in abdominal pain coupled with a drop in hematocrit level or a change in vital signs.
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116 Continue Bleeding is the most feared complication and is caused by the erosion of the pseudocyst into a vessel. Therapy is emergent surgery or angiography with embolization of the bleeding vessel.
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117 Management: 4X4, 5X5, 6X6 All cysts do not require treatment. In many cases the pseudocysts may improve and go away on their own. In a patient with a small (less than 5cm) cyst that is not causing any symptoms, careful observation of the cyst with periodic CT scans is indicated.
Slide 118-

118 Management: If a pseudocyst is persistent over many months or causing symptoms then treatment of the cyst is required.
Slide 119-

119 External Drainage Catheter drainage: Percutaneous catheter drainage is the procedure of choice for treating infected pseudocysts, allowing for rapid drainage of the cyst and identification of any microbial organism. A high recurrence and failure rate exist.
Slide 120-

120 Continue Percutaneous catheter drainage is contraindicated in patients who are poorly compliant and cannot manage a catheter at home. It is also contraindicated in patients with strictures of the main pancreatic duct and in patients with cysts containing bloody or solid material.
Slide 121-

121 Internal drainage: The majority of patients who require treatment for their pseudocysts are treated by surgery.
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122 Internal drainage: In the surgical procedure a connection is created between the cyst and an adjacent intestinal organ to which the cyst is adherent to such as the stomach. This connection allows the cyst to drain into the stomach.
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123 Continue Cysto-gastrostomy a connection is created between the back wall of the stomach and the cyst , the cyst drains into the stomach. Cysto-jejunostomy: a connection is created between the cyst and the small intestine. Cysto-duodenostomy: a connection is created between the duodenum and the cyst. During surgical drainage procedure biopsy of cyst wall must be done to rule out a cystic carcinoma.
Slide 124-

124 Endoscopic technique In this procedure a gastroenterologist drains the pseudocyst through the stomach by creating a small opening between the cyst and the stomach during endoscopy.
Slide 125-

125 Endoscopic technique In selected patients this treatment can successfully treat pseudocyst. The disadvantage of this technique is that if there is dead tissue in the pseudocyst cavity or if the cyst is very large then infection or recurrence of pseudocyst with this technique may occur.
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126 Insertion of a pancreatic stent: In this technique the gastroenterologist may insert a drain into the cyst during an ERCP. If the drain is placed directly into the cyst then the fluid from the cyst is drained into the intestine through this tube.
Slide 127-

127 Prognosis Most pseudocysts resolve without interference, and patients do well without intervention. Outcome is much worse for patients who develop complications or who have the cyst drained.
Slide 128-

128 Prognosis The failure rate for drainage procedures is about 10%, the recurrence rate is about 15%, and the complication rate is 15-20%.
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129 Thank You