Acute pancreatitis

109,046 views 79 slides Feb 07, 2019
Slide 1
Slide 1 of 79
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58
Slide 59
59
Slide 60
60
Slide 61
61
Slide 62
62
Slide 63
63
Slide 64
64
Slide 65
65
Slide 66
66
Slide 67
67
Slide 68
68
Slide 69
69
Slide 70
70
Slide 71
71
Slide 72
72
Slide 73
73
Slide 74
74
Slide 75
75
Slide 76
76
Slide 77
77
Slide 78
78
Slide 79
79

About This Presentation

Acute Pancreatitis general surgery undergraduate MBBS Medical School Complication of Acute Pancreatitis Ranson Criteria Alcohol Pancreatitis Gallstone Cullen sign Grey turner sign Increased serum amylase ERCP


Slide Content

Acute Pancreatitis

Outline of Presentation Anatomy of Pancreas Aetiology Pathophysiology Clinical Approach – History and Physical Examination Differential Diagnosis Investigation Assessment of Severity Management of Acute Pancreatitis Complications

ANATOMY OF PANCREAS

Anatomy Retroperitoneal organ In adults- 15cm long & 70-100 weighs 3 portions- head, body and tail Relations: Head Neck Uncinate Body Tail

Main pancreatic duct- Wirsung duct Acessory duct – Santorini duct

Incidence 3 % of all cases of abdominal pain Hospital admission rate for is 9.8 per 100 000 population anually Worldwide, 50 per 100 000 cases anually . The disease may occur at any age , with a peak in young men and older women.

Etiology Two major causes are : biliary calculi (50–70%) alcohol abuse (25%) The remaining cases may be due to rare causes or be idiopathic

Gallstone Pancreatitis Transient blockage of common bile duct  reflux of bile into pancreatic duct and impair flow of normal pancreatic juice  premature activation of pancreatic enzymes within duct system.

Alcohol Pancreatitis High risk in : 1. Long standing alcohol intake for at least 2 years or single session of heavy drinking Consumption >80g/day What Happened ? Direct toxic effect of alcohol in genetically predisposed individuals Viscid secretion of pancreatic juice  formation of protein plugs and impairment of flow

Pathophysiology Premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion . Anything that injures the acinar cell and impairs the secretion of zymogen granules , or damages the duct epithelium and thus delays enzymatic secretion, can trigger acute pancreatitis. Once cellular injury has been initiated, the inflammatory process can lead to pancreatic oedema, haemorrhage and, eventually, necrosis . As inflammatory mediators are released into the circulation, systemic complications can arise.

ACUTE PANCREATITIS History and Physical Examination

Purpose of History Taking Pain Causes Complications

History Taking 1) Abdominal Pain - Remember SOCRATES! Site: Diffuse, upper abdominal pain Onset : Sudden Character : Boring Pain Radiation : Radiates to the back Associated factor : Nausea, vomiting, dyspnea Timing : Pain escalates in intensity and peaks within 10-20 minutes of onset.

Aggravating and relieving factor : Aggravated by breathing with increased chest expansion and relieved by leaning forward. Severity : Depending on severity, patient may present in shock

2) History of underlying causes ‘I GET SMASHED’ Idiopathic (10%) Gallstone (45%) Ethanol ( 35%) Trauma (10%) Steroids Mumps Autoimmune Scorpion / Snake Hyperlipidemia ERCP Drugs (10%)

3) History of Complications Systemic : ARDS Renal Failure Shock, arrythmias Metabolic: hypocalcemia , hyperglycemia Encephalopathy

Local : Mostly develop silently Pancreatic abscess – high grade fever Pseudocyst Pancreatic effusion

Physical Examination: Acute Pancreatitis Elevation of body temperature is often is acute pancreatitis

Abdominal Examination Inspection: abdominal distension Palpation : Hepatomegaly Tenderness Cullen sign Gray turner sign Peritoneal signs Rigidity Guarding

Percussion : Dullness suggesting ascites Auscultation: auscultate the abdomen for hypoactive or an absent bowel sounds or an abdominal bruit. Ileus is common in pancreatitis. Ausculation of lungs: 10-20% of patients have pulmonary findings, commonly left sided findings. Basilar rales Atelectasis Pleural effusion

Presented by Siti Nur Rifhan Kamaruddin DIFFERENTIAL DIAGNOSIS INVESTIGATIONS SEVERITY SCORING

Differential Diagnosis For Mild Acute Pain For Severe Acute Pain Acute Cholecystitis Fecal Peritonitis due to Perforated Colon Peptic Ulcer Disease Ruptured Abdominal Aortic Aneurysm Inferior Myocardial Infarction Ruptured Ectopic Pregnancy Acute Appendicitis Massive Bowel Infarction

INVESTIGATIONS

Investigations The diagnosis if made on basis of clinical presentation, an elevated serum Amylase level and characteristic Imaging features. Biological : - Serum Amylase increase 3x than normal or more than 1000IU/mL (Peak within the first 24hours after onset of Symptom) - Serum Lipase has longer half life thus more useful in delayed cases. - Serum Lipase: more sensitive & specific for Pancreatitis than Amylase

Other Causes of Increased Serum Amylase : Renal Failure Liver Cirrhosis Peritonitis GIT Inflammation Ruptured Ectopic Pregnancy/ Salphingitis Salivary Gland Inflammation ( Parotitis )

Other Blood Tests.. Full Blood Count Elevated Leucocytes count for Ranson’s Criteria and to predict prognosis LFT To asses cause of Pancreatitis/obstructive jaundice BUSE To determine level of dehydration Random Blood Glucose Damage to beta cells interferes with insulin production causing Hyperglycemia (in severe cases) Serum Calcium Hypocalcaemia suggests saponification

Role of Imaging in Acute Pancreatitis To clarify diagnosis when the clinical picture is confusing To determine possible causes To assess severity (Balthazar Score) and thus to determine prognosis To detect complications

Imaging : Ultrasound Trans abdominal USG : Does not establish a diagnosis. USG should be performed within 24 hours in ALL patients To detect gallstones To rule out Acute Cholecystitis To determine whether the common bile duct is dilated T o evaluate change on pancreas i.e. edema, mass in Pancreas

Transverse Transbadominal Ultrasound shows a swollen pancreatic body with ill-defined heterogeneous hypoechoic pattern.

ERCP Diagnostic and therapeutic To look for Gallstones, CBD stones or CBD dilatation In patient with severe acute gallstone pancreatitis & signs of on going biliary obstruction and cholangitis – an urgent ERCP should be sought.

ERCP : Gallstone Pancreatitis

Plain Abdominal X-Ray Plain erect chest & abdominal X-ray are not diagnostic of Acute Pancreatitis but are useful in differential diagnosis. Non specific findings in Pancreatitis : Generalized or local ileus (Sentinel Loop), a colon cut off sign, and calcified gallstones. Erect CXR. Look for pleural effusion. In severe cases, a diffuse alveolar shadowing (Acute Respiratory Distress Syndrome)

A focal dilated proximal jejunal loop in the left upper quadrant. A focal area of adynamic ileus close to an intraabdominal inflammatory process . The sentinel loop sign may aid in localizing the source of inflammation. Sentinel Loop in upper abdomen may indicate Pancreatitis

Colon Cut-off Sign describes gaseous distension seen in proximal colon Associated with narrowing of splenic flexure in cases of Acute Pancreatitis This Appearance results from inflammatory process extending from Pancreas into the phrenicolic ligament via transverse mesocolon

CT Scan Not necessary for all patients. May reveal pseudo cyst or abscess (complication of acute pancreatitis ) A contrast-enhanced CT is indicated in following : If there is diagnostic uncertainty In Pt. with severe acute Pancreatitis to distinguish interstitial from necrotizing pancreatitis. In Pt. with organ failure, signs of sepsis or progressive clinical deterioration When a localized complication is suspected I.e. fluid collection, pseudo cyst.

CT Anatomy Pancreatic Level

CT shows significant swelling & Inflammation of the Pancreas

Morphologic Types of Acute Pancreatitis THE REVISED ATLANTA CLASSIFICATION Interstitial Edematous Pancreatitis Necrotizing Pancreatitis Parenchymal necrosis Peripancreatic necrosis Combined Type

Interstitial Edematous Pancreatitis Pancreatic Enlargement due to edema Pancreatic Parenchyma shows relatively homogenous enhancement & peripancreatic fat stranding Outcome : Symptoms usually resolve within first week

- Inflammation associated pancreatic parenchymal necrosis orperipancreatic necrosis - Cause impairment of pancreatic perfusion - Impairment evolve over several days - Early CECT may underestimate extent of disease Necrotizing Pancreatitis (5-10%)

Pancreatic Fluid Collection : Revised Atlanta 2012 85% 15%

Local Complications should be suspected if : Persistence or recurrence of abd . pain Secondary increases in Serum Pancreas activity Increasing organ dysfunction Development of clinical signs of Sepsis i.e. fever, leucocytosis Prompt CECT to be done in these cases. Pancreatic Fluid Collection : REVISED ATLANTA 2012 Acute Peripancreatic Fluid Collection (APFC) Pancreatic Pseudocyst (PP) Acute Necrotic Collection (ANC) Walled-off Necrosis (WOPN)

1) Acute Peripancreatic Fluid Collection (APFC) Peripancreatic Fluid associated with IEP with no necrosis Usually seen within first 4 weeks Homogenous collection of fluid Usually resolve spontaneously When a localised APFC persists > 4 weeks – develop into a Pseudocyst

2) Pancreatic Pseudo cyst Encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas With minimal or no necrosis Usually round or oval Appears after 4 weeks of onset IEP Note the two round, homogenous fluid collection with a well defined borders White stars denote normal enhancing pancreas

3) Acute Necrotic Collection (ANC) A collection containing of both fluid & necrosis < 4 weeks Occurs only in setting of NP Single or multiple heterogeneous collection No defined wall Note enhancement of entire pancreatic Parenchyma (Whitestars ) Note the heterogeneous, non-liquid component in retroperitoneum (White arrows pointing at the borders of ANC)

4) Walled-off Necrosis (WON) A mature, encapsulated collection of pancreatic / peripancreatic necrosis that has developed a well-defined inflammatory wall Appears >4 weeks after onset of NP Heterogeneous with liquid & non-liquid density Note the Area of non-liquid components of high attenuation (black arrows) in the collection It has a well defined, enhancing wall (White arrows)

- Homogenous, low attenuation fluid density - NO solid component Pseudocyst (PC) vs. Walled-off Necrosis (WON) Heterogeneous with liquid and solid densities

SUMMARY: Local Complications of AP

CT Severity Index: Balthazar + Necrosis Score A B C D E

Assessment of Severity Ranson Score Glasgow Scale APACHE II Score

Severity: RANSON’S SCORE To predict severity of acute pancreatitis . On Admission (LEGAL) L – Leucocytes >16000 E – Enzyme AST > 250 G – Glucose > 200 A – Age > 55 L – LDH > 350 During Next 48 Hours (C.HOBBS) C – Calcium 8mg/dl H – Hematocrit fall of >10% O2 – Pa02 < 60mmHG B – Base deficit > 4mmol/L B – BUN rise > 5 S – Sequestration (Fluid) > 6 litres 3 or more factors present – SEVERE

Glasgow Scale 3 OR MORE FACTORS PRESENT - SEVERE

APACHE II SCORE Score > 8 : Severe Acute Pancreatitis

Management of Acute Pancreatitis Presented By Fariza Asilah Ahmad Rahim

Mild Acute Pancreatitis Nil by mouth Fluid resuscitation : 4 pints Analgesia : IM Tramal 50mg TDS Treat underlying cause No role for antibiotics

Severe Acute Pancreatitis Admission to intensive care or high-dependency unit Oxygen supplementation Analgesia Aggressive fluid rehydration 4. Monitor vital signs 5. Monitor haematological & biochemical parameters

6. Nasogastric drainage 7. Antibiotic prophylaxis –imipenem, cefuroxime 8. CT scan 9. ERCP within 72 hours 10. Supportive therapy for organ failure 11. Nutritional support

Complications of Acute Pancreatitis

SYSTEMIC Cardiovascular - shock - arrhythmia Pulmonary - ARDS Renal failure Haematological - DIC Gastrointestinal - Ileus

SYSTEMIC Metabolic - Hypocalcaemia - Hyperglycaemia - Hyperlipidaemia Neurological - Visual disturbance - Confusion - Encephalopathy Miscellaneous - Arthralgia

Acute fluid collection Sterile pancreatic necrosis Infected pancreatic necrosis Pacreatic abscess Pseudocyst LOCAL

Pancreatic ascites Pleural effusion Portal or systemic vein thrombosis Pseudocyst LOCAL

Complications & their Management Acute fluid collection No intervention unless pressure effect Aspirate under US or CT guidance OR Transgastric drainage under EUS guidance Pancreatic necrosis No intervention

Infected pancreatic necrosis Aspirate under CT guidance Percutaneous drainage Prophylactic antibiotic

If patient deteriorates Necrosectomy Closed continuous lavage C losed drainage Open packing Closure and relaparotomy

Pancreatic abscess Percutaneous drainage Antibiotic cover Pancreatic ascites Drainage Parenteral or jejunal feeding

Pancreatic effusion Percutaneous drainage under CT guidance Portal or systemic vein thrombosis Aspirin in the early process

Pseudocyst Percutaneous transgastric cystogastrotomy and place double-pigtail drain Endoscopic under EUS guidance and place tube drain Surgical drainage – internal drainage into gastric or jejunum lumen

Cystogastrotomy

Reference BAILEY, H., LOVE, R. J. M., MANN, C. V., & RUSSELL, R. C. G. (1992). Bailey and Love's short practice of surgery. London, Chapman & Hall Medical. COLLEDGE, N. R., WALKER, B. R., RALSTON, S., & DAVIDSON, S. (2010). Davidson's principles and practice of medicine. Edinburgh, Churchill Livingstone/Elsevier.