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Pancreatitis & pancreatic pseudocyst

Pancreatitis, mainly the acute type, necessary clinical knowledge and surgical approaches.
Pseudocyst and it's management

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Pancreatitis & pancreatic pseudocyst

  1. 1. PANCREATITIS & PANCREATIC PSEUDOCYST By :- Shweta Achuthan Kutty
  2. 2. •Introduction •History •Aetiology •Pathogenesis •Clinical Features •Complications •Diagnosis •Grading of severity •Management •Differential diagnosis HEADINGS:
  3. 3. Pancreatitis Inflammation of the pancreatic parenchyma, which is a retroperitoneal, endocrine and exocrine organ.
  4. 4. Clinical Classification
  5. 5. • Acute Pancreatitis**: inflammatory condition of the pancreas of an acute presentation characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood. • Chronic Pancreatitis: is a continuing inflammatory disease of the pancreas characterised by irreversible morphological changes typically causing pain and/or permanent loss of function. Can also have an acute on chronic presentation.
  6. 6. Pathological Classification • Are of two types: • Interstitial oedematous pancreatitis: vast majority (90-95%) • most often referred to simply as "acute pancreatitis" or "uncomplicated pancreatitis“ • Necrotising pancreatitis: necrosis develops within the pancreas and/or peripancreatic tissue
  7. 7. Blast from the Past: • Alexander the Great • Reginald Huber Fitz – On Acute Pancreatitis • Eugene Lindsey Opie – Gallstone lodging • Chiari - Autodigestion
  8. 8. ACUTE PANCREATITIS • DEFINITION: A group of reversible lesions due to inflammation of the pancreas clinically charactersied by abdominal pain and elevated levels of pancreatic enzymes in the blood. It is medical emergency, and requires to be treated as soon as possible. • GENDER PREDILECTION: Generally M>F In males more often related to alcohol In females more often related to biliary tract disease Idiopathic pancreatitis no clear gender predilection • INCIDENCE: Young men and elderly women • MORTALITY RATE: Mild pancreatitis >1%, Severe cases - 10-30% • CAUSE OF DEATH: Multi-organ Dysfunction Syndrome
  9. 9. AETIOLOGY • Gall stones - 50 to 70% cases • Alcoholism - 25% • Post ERCP - *** • Abdominal trauma • Post biliary , upper gastrointestinal or cardiothoracic surgery • Ampullary tumour • Drugs like corticosteroids, azathioprine, asparaginase, valproic acid, thiazides, oestrogens
  10. 10. • Hyperparathyroidism • Hypercalcaemia • Pancreas divisum • Autoimmune pancreatitis • Hereditary pancreatitis • Viral Infections – mumps/cockackie B • Malnutrition • Scorpion bite • Idiopathic
  11. 11. PATHOGENESIS : AUTO ACTIVATION AND AUTO DIGESTION •Two -mild pancreatitis • -severe pancreatitis, •Division is based whether the predominant response to cell injury is inflammation or necrosis, respectively. •In mild pancreatitis - inflammation and edema of the pancreas •In severe pancreatitis – also features of necrosis and secondary injury to extrapancreatic organs. •Both types share a common mechanism of abnormal inhibition of secretion of zymogens and inappropriate activation of pancreatic zymogens inside the pancreas, most notably trypsinogen.
  12. 12. CLINICAL FEATURES  The most common symptoms and signs include: Severe epigastric pain (50% cases) radiating to the back, chest, flanks, and lower abdomen, relieved by leaning forward, that feels worse after eating Nausea, vomiting, diarrhea and loss of appetite Fever/chills Hemodynamic instability, including shock- cold clammy extremities, rapid low volume pulse, tachycardia In severe case may present with tenderness, guarding, rebound tenderness.  Respiratory symptoms: Tachypnoea, respiratory distress Hiccups
  13. 13. COMPLICATIONS/SEQUELAE 1)LOCAL: usually develop after first week • Acute fluid collection • Sterile pancreatic necrosis • Infected pancreatic necrosis • Pancreatic abcess • Pseudocyst • Pancreatic ascites • Pancreatic effusion • Haemorrhage • Portal/Splenic vein thrombosis • Pseudoaneurysm **In the long run, repeated attacks- chronic pancreatitis with irreversible damage
  14. 14. 2) SYSTEMIC: more common in the first one week • Cardiovascular: Shock, arrythmias • Pulmonary : ARDS • Renal failure • Gastrointestinal: Ileus, peritonitis • Neurological : visual disturbances, confusion, irritability, encephalopathy, coma • Miscellaneous: Subcutaneous fat necrosis, arthralgia Others include : Haematological: DIC Metabolic: hyperglycaemia, hypocalcaemia, hyperlipidaemia
  15. 15. DIAGNOSIS Proper history, clinical examination, confirmation by investigations According to the American College of Gastroenterology's guidelines, there are three criteria that must be present to diagnose acute pancreatitis, including: •Severe abdominal pain •Amylase or lipase levels that are three times higher than the upper limit of normal •"Characteristic" abdominal imaging results
  16. 16. 1. Blood • CBC - neutrophil leucocytosis, thrombocytopenia (DIC) • BUN • Clotting profile- prolonged in DIC • Glucose - hyperglycaemia in severe cases • Electrolytes: Calcium levels -decreased, Potassium levels • ABG – (hypoxemia) , pH (lactic acidosis – shock) • FDP like D-dimer– raised in DIC • Triglycerides • C-reactive protein • IgG4 – autoimmune pancreatitis INVESTIGATIONS
  17. 17. 2. Urine -24h urine ouput -Microscopy: Casts - Urinary amylase -Glycosuria (10% cases) *Trypsin and its precursor trypsinogen-2 in both the urine and the peritoneal fluid have been evaluated as possible markers for acute pancreatitis (especially post-ERCP pancreatitis) but are not widely used. *Although not currently in use clinically, polymorphisms in the chemokine monocyte chemotactic protein 1 (MCP-1) gene may also predict severity. This is the first gene identified that plays a role strictly in predicting the severity of disease. 3. Biochemical investigations - Liver function tests: Increased liver enzymes, ALT,ALP, GGT ( gallstones) - Direct bilirubin : Increase in CBD block - Renal function tests: Creatinine, BUN, Urea - Serum amylase: (amylase P): Increased (3-4 times normal diagnostic but not specific) - Serum lipase: Increased- more specific
  18. 18. 4. Radiological •X rays :- -Non specific signs – generalised or local ileus (sentinel loop), a colon cut off sign, renal halo sign, calcified gallstones/pancreatic calcifications USG abdomen:- With in 24 hours- for gallstones, rule out a/c cholecystitis, CBD dilatation diagnosis of vascular complications, i.e. thrombosis, hypoechoic lesions may indicate necrotic change •CT Abdomen with contrast:- phlegmon(inflammatory mass), pseudocyst or abscess(complications of acute pancreatitis)
  19. 19. CT: typical findings: -focal or diffuse parenchymal enlargement -calcifications may be seen within the parenchyma -changes in density because of oedema -indistinct pancreatic margins owing to inflammation -surrounding retroperitoneal fat stranding liquefactive necrosis of pancreatic parenchyma: lack of parenchymal enhancement infected necrosis abscess formation : circumscribed fluid collection, little or no necrotic tissues haemorrhage: high-attenuation fluid in the retroperitoneum or peripancreatic tissues
  20. 20. •MRI :- Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis. •ERCP :- Identification and removal of gallstones. •EUS:- not frequent, used to ultrasonographically visualize pancreas, bile tree, useful for stones, does not have complications of ERCP. More sensitive to pick up microlithiasis and periampullary lesions. •MRCP:- not frequently used, used for detection of gallstones.
  21. 21. Assessment of Severity • AIM: to define patients with severe pancreatitis • Based on history, clinical assessment , investigations - scoring systems – Ranson score, Glasgow scale, APACHE II, BISAP, Balthazar scoring •Grade severity , provide adequate appropriate treatment/interventions, ward off/better control of another attack
  22. 22. This calculator evaluates the following Clinical Criteria: BUN >25 mg/dL (8.9 mmol/L) Impairment of mental status with a Glasgow coma score <15 SIRS (systemic inflammatory response syndrome) Age >60 years old Pleural effusion Each determinant is given one point SIRS is defined as 2 or more of the following variables; Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F) Heart rate of more than 90 beats per minute Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO2) of less than 32mm Hg Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10% immature [band] forms) Bedside index of severity in acute pancreatitis (BISAP) score
  23. 23. BISAP Score BISAP Score Observed Mortality 0 0.1% 1 0.4% 2 1.6% 3 3.6% 4 7.4% 5 9.5% Wu et al, Gut 2008
  24. 24. MANAGEMENT Early management Management of risk factors Management of complications Early Management: aims to provide immediate care and resuscitation •Admission to HDU/ICU •Analgesia •Aggressive fluid rehydration, electrolyte imbalance correction •Oxygenation •Monitoring vitals, CVP, urine output, blood gases
  25. 25. • Frequent monitoring : haematological + biochemical parameters- RFT, LFT, clotting profile, serum Calcium, blood sugar levels • NG drainage •Antibiotic prophylaxis • CT scan : essential for organ failure, clinical deterioration or signs or sepsis develops • ERCP within 72 hours for severe gallstone pancreatitis or signs of cholangitis • Supportive therapy for organ failure if it develops – inotropes, ventilatory support, haemofiltration, etc • If nutritional support is required consider enteral feeding using NG tube
  26. 26. SPECIFIC MANAGEMENT OF COMPLICATIONS 1) Acute fluid collection: •Small sterile collections resolve •large collections- CT/USG guided percutaneous aspiration 2) Sterile/infectious pancreatic necrosis and pancreatic abscesses: A) CT/USG guided wide bore needle aspiration •Microbiological assessment of pus, •AB sensitivity- start Abs,
  27. 27. If conservative measures fail especially in very severe cases– B) NECROSECTOMY- thorough removal of necrotic tissues and collections •Based on clinical symptoms and imaging studies via endoscopy/ midline laparotomy •Asso high morbidity and mortality •If tail and body involved – left flank approach •If gallstones are cause – Cholecystectomy- endoscopic/laparotomy •After Necrosectomy- more necrotic tissue may form, re-exploration may be needed
  28. 28. C) Management of Post Necrosectomy necrotic tissue: Closed continuous lavage of Berger: Tube drains are left in and the raw areas flushed Closed drainage: Incision is closed but cavity is packed with gauze filled Penrose drains and closed suction drains. The Penrose drains are brought out through the flank and slowly pulled out and removed after 7 days. Open packing: Incision is left open and cavity packed with intention of returning to the OT at regular intervals and repacking until there is a clean granulation cavity.
  29. 29. Closure and relaparotomy: incision is closed with drains with intention of performing a series of planned relaparotomies every 48-72 hours until raw area granulates 3) Pancreatic ascites: Wide bore needle drainage, NG tubing, Octreotide 4) Pancreatic effusion: Imaging guided percutaneous drainage 5) Haemorrhage : Fatal, embolisation and surgery 6) Portal/Splenic vein thrombosis: If Portal HTN – esophageal banding/sclerosing agents, In case of thrombocytosis – antiplatelets like aspirin, clopidogrel, systemic anticoagulation – double edged sword?
  30. 30. DIFFERENTIAL DIAGNOSIS •Perforated peptic ulcer •Biliary colic------------- •Acute cholecystitis---- •Pneumonia---------------- •Pleuritic pain-------------- •Myocardial infarction--- •Oesophageal spasm----- •Perforated viscus •Acute mesentric ischaemia •Acute respiratory distress syndrome *rule out any cause of acute abdomen Right upper quadrant pain Radiation to chest
  31. 31. PANCREATIC PSEUDOCYST Definition: Is a collection of amylase rich fluid enclosed in a wall of fibrous or granulation tissue. Aetiology: after an attack of acute pancreatitis**, in chronic pancreatitis, and post pancreatic trauma Pathogenesis: Formation >/= 4 weeks from the onset of acute pancreatitis. Thick fibrous capsule – no true epithelial lining. Due to ductal distruption, strictures, calculi, tumours. Composition: Similar electrolyte concentrations to plasma High concentration of amylase, lipase, and trypsin. Occurrence: Most common cystic lesions of pancreas, accounting for 75-80% of such masses Single *, maybe multiple, or loculated Location: Lesser peritoneal sac in proximity to the pancreas Large pseudocysts can extend into the paracolic gutters, pelvis, mediastinum, neck or scrotum
  32. 32. CLINICAL FEATURES •Asymptomatic when small •Symptoms Abdominal pain > 3 weeks (80 – 90%) Nausea / vomiting Early satiety Bloating, indigestion •Signs: Abdominal fullness Tenderness Palpable mass in the abdomen Peritoneal signs suggesting rupture of the cyst or infection Fever Scleral icterus Pleural effusion
  33. 33. COMPLICATIONS/SEQUELAE: Infection: Abscess, systemic sepsis Rupture: Into gutGI bleeding, internal fistula Into peritoneum Peritonitis Enlargement: Bowel obstruction, biliary compression, pain Erosion into vessel: Haemorrhage into the cyst, haemoperitoneum
  34. 34. DIAGNOSIS Clinically suspicion in case : •Episode of pancreatitis fails to resolve •Amylase levels persistantly high •Persistent abdominal pain •Epigastric mass palpated after pancreatitis
  35. 35. INVESTIGATIONS Labs: Persistently elevated serum amylase Cyst fluid analysis(EUS+A): Carcinoembryonic antigen (CEA) and CEA-125 (low in pseudocysts and elevated in tumors); fluid viscosity (low in pseudocysts and elevated in tumors); amylase (usually high in pseudocysts and low in tumors)CEA (cystic neoplasm) Radiological Investigations •Plain X-ray: Not very useful •Ultrasound TransAbd: 75 -90% sensitive •EUS: helps plan therapy, not useful for Dx •CT : Most accurate (sensitivity 90-100%) •MRI –detection of solid component of cyst and in differentiating between organized necrosis and a pseudocyst
  36. 36. NATURAL HISTORY OF PSEUDOCYST: •~50% resolve spontaneously •Nearly all <4cm resolve spontaneously •Those >6cm, >12weeks duration asso c/c pancreatitis persist, necessitate intervention • Multiple cysts – few spontaneously resolve
  37. 37. MANAGEMENT  If asymptomatic/small – wait for spontaneous resolution DEFINITIVE TREATMENT DRAINAGE INDICATIONS : Complications Symptoms Concern about possible malignancy • 3 approaches to drain a pseudocyst:  Percutaneous Endoscopic Surgical**
  38. 38. A) PERCUTANEOUS DRAINAGE: 1) Percutaneous catheter drainage: Done under USG/CT guidance, but has several disadvantages. High recurrence rate, contraindicated In cysts that are communicating with duct lumen- Pancreticocutaneous fistula- and in neoplastic cysts Hence not common 2)Percutaneous transgastric cystgastrostomy: radiological guidance Recurrence <15% B) ENDOSCOPIC DRAINAGE: 1) Under EUS guidance 2) ERCP and Stenting of Ampulla – communicating cyst
  39. 39. C) SURGICAL DRAINAGE: cystogastrostomy •most preferred, least recurrence rate ( <5%), best for complicated pseudocysts •Open incision laparotomy or laproscopy (also shows similar rates)
  40. 40. DIFFERENTIAL DIAGNOSIS: •Acute fluid collections •Organized necrosis •Pancreatic abscesses •Cystic neoplasm
  41. 41. “Never in medical history have so many owed so much to a single stone”. – Reginald Huber Fitz 
  42. 42. The following are the latest terms according to the updated Atlanta classification to describe fluid collections associated with acute pancreatitis: fluid collections in interstitial oedematous pancreatitis acute peripancreatic fluid collections (APFC): in the first 4 weeks: non-encapsulated peripancreatic fluid collections pseudocysts: develop after 4 weeks; encapsulated peripancreatic or remote fluid collections fluid collections in necrotising pancreatitis acute necrotic collections (ANCs): in the first 4 weeks; non- encapsulated heterogeneous non-liquefied material walled-off necrosis (WON or WOPN): develop after 4 weeks; encapsulated heterogeneous non-liquefied material
  43. 43.  Peritonitis Signs that are less common, and indicate severe disease, include: Pleural effusions: Grey-Turner's sign (hemorrhagic discoloration of the flanks) Cullen's sign (hemorrhagic discoloration of the umbilicus) Grünwald sign Körte's sign ) Kamenchik's sign Mayo-Robson's sign ) Mayo-Robson's point - a point on border of inner 2/3 with the external 1/3 of the line that represents the bisection of the left upper abdominal quadrant, where tenderness on pressure exists in disease of the pancreas. At this point the tail of pancreas is projected on the abdominal wall.