0
EPIDEMIOLOGY
17 per 100,000
 2-3% overall mortality from acute pancreatitis
 Male: female ratio is 1:3- in those with ga...
CAUSES
Obstructive(75%)







Operative trauma



Blunt/penetrating trauma





•
•



Parasitic
•
Ascariasis, cl...
Idiopathic Acute Pancreatitis
The etiology of acute pancreatitis should be
determined in at least 80% of cases and no more...
Clinical Presentation


Pain (95%)
◦ Acute onset
◦ Mid-abdominal or mid-epigastric

◦ Radiates to the back (50%)
◦ Peak i...
Cullen's sign
Grey-Turner's sign
Laboratory Diagnosis
BASELINE INVESTIGATION
 LFT’S
 Increased amylase and/or lipase >3 times
◦ Amylase levels rise w/in ...
Others
U/S ABDOMEN
 CT SCAN
 EUS
 MRCP

PREDICTION OF SEVERITY
Available prognostic features which
predict complications in acute
pancreatitis are







cl...
APACHE II score
(Acute Physiology And Chronic Health Evaluation)
Glasgow coma scale
Signs of Organ Failure


Cardiovascular



◦ Hypotension
◦ Septic physiology




HR, CO and

◦ DIC
◦ Thrombocytosis
SV...
Determining severity


Clinical assessment,





fluid status
vitals
UOP
pulse oximetry



Clinical criteria



Rad...
Ranson Score
At admission
 age in years > 55 years
 white blood cell count > 16000 cells/mm3
 blood glucose > 11 mmol/L...
Atlanta criteria
Pancreatitis Outcome Prediction
Score
When Do I Order A CT?


If the patient has…..
◦
◦
◦
◦
◦

Persisting organ failure
Signs of sepsis
Deterioration in clinic...
CT scan with pancreatic protocol


500 ml of oral contrast by mouth or
nasogastric tube. An initial scan
without iv contr...
CT Findings


Pancreas
◦
◦
◦
◦



Pancreatic enlargement
Decreased density due to edema
Intrapancreatic fluid collection...
CT Findings
Tail Indistinct

Intraperitoneal fluid
CT Findings
Severe Pancreatitis
Nonenhanci
ng
Necrosis

Peripancreatic
edema
and inflammation
Balthazar Scoring
CT grading of severity
POINTS
Grade of Acute Pancreatitis
A =Normal pancreas
B =Pancreatic enlargement
C...
When can he eat ?
TPN vs. enteral feeding




In patients with severe disease, oral intake is
inhibited by nausea; the a...
Contd…
 Tube

feed if anticipate NPO > 1 week.
 Nasogastric feeding may be feasible in up to
80% of cases. Caution shoul...
Possible pathways for pancreatic infection
There are few mechanisms by which
bacteria may enter pancreatic and
peripancrea...
Bacteriology in severe acute pancreatic












Escherichia coli
Staphylococcus aureus
Pseudomonas spp
Kleb...
Management


All patients with acute pancreatitis should receive adequate
oxygen



Start IV fluids with crystalloid
 C...
When Do I Start Antibiotics?


Acute pancreatitis is c/b infection ~ 10%
 30-50% of those with necrosis get infection

...
Antibiotic

Aminoglycosides
•Netilmicin
•Tobramycin
Acylureidopenicillins
•Mezlocillin
•Piperacillin
Cephalosporins
•Cefot...
A final word on antibiotics


Do not use empirically early in mild
pancreatitis



Fever early in the disease process is...
When Do I Consult GI ?


Evidence of biliary pancreatitis
◦ Elevated LFTs + pancreatitis
 No matter what the US shows

S...
GALL STONE PANCREATITIS AND
TREATMENT
OF GALL STONES


Q: When should I suspect it ?
◦ A: Always



Q: How do I evaluate...
Contd….


Urgent therapeutic ERCP should be performed in
patients with acute pancreatitis of gall stone etiology
who sati...
Timing of cholecystectomy
 All

patients with biliary pancreatitis should
undergo definitive management of gall
stones du...
Complications of AP


Immediate
 Shock
 DIC
 ARDS



Late








Pancreatic pseudocyst
Pancreatic abscess
Pan...
Management of Pancreatic
Complications


Acute fluid collections
◦ Occur early, seen but not felt
◦ No defined wall usual...
Infected necrosis




All patients with persistent symptoms
and greater than 30% pancreatic
necrosis, and those with sma...
Contd…


Radiological
 percutaneous wide bore drainage



Surgical
 Debridement of necrotic tissue following this abdo...
Pseudocysts


Collection of pancreatic fluid enclosed
by non-epithelialized wall of granulation
tissue



Complicates 5-...
Complications of Pseudocyst


Infection - 14%



Rupture - 6.8%



Hemorrhage - 6.5%



Common bile duct obstruction -...
Pseudocyst Management


Old thought
◦ Pseudocysts > 5 cm that have been
present > 6 weeks must be drained



Current pra...
Pseudocyst Drainage
Techniques
 Endoscopic
 Surgical
 Radiologic
Communicating Non-communicating
Endoscopic Pseudocyst Management
Percutaneous Pseudocyst Drainage
Laparoscopic Cyst
Gastrostomy
Open cyst Gastrostomy
Pancreatic abscess
◦ CT or EUS guided drainage
 Walled collection of pus
 Similar to management of pseudocyst
Closing Points
Patients with severe acute pancreatitis
have an increased risk of death.
 Patients who die usually have
ev...
Acute Pancreatitis Managment
Acute Pancreatitis Managment
Acute Pancreatitis Managment
Acute Pancreatitis Managment
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Acute Pancreatitis Managment

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Transcript of "Acute Pancreatitis Managment"

  1. 1. EPIDEMIOLOGY 17 per 100,000  2-3% overall mortality from acute pancreatitis  Male: female ratio is 1:3- in those with gallstones and 6:1 in those with alcoholism The median age at onset depends on the etiology  AIDS-related - 31 years  Vasculitis-related - 36 years  Alcohol-related - 39 years  Drug-induced etiology - 42 years  ERCP-related - 58 years  Trauma-related - 66 years  Biliary tract–related - 69 years 
  2. 2. CAUSES Obstructive(75%)    Operative trauma  Blunt/penetrating trauma    • •  Parasitic • Ascariasis, clonorchiasis • Bacterial • Mycoplasma, C. jejuni, TB • MAI, Leptospirosis, Legionella • Vascular • Ischemia • Embolic • Vasculitis • MISC • • • • • • • • • Lab test(ERCP / angiography) Drugs     • Tumor Traumatic (5%)  Infection • Viral • HIV/EBV/Coxsackie/Mumps • CMV/Varicella/Hep A&C Gall Bladder stone  • 6-mercaptopurine Azathioprine DDI (2 ′ 3 ′ dideoxyinosine) Estrogens Thiazides Sulfa drugs etc Metabolic  TG ~ 4% > 1000 mg/dl  PTH < 0.5% Toxins  Alcohol  Scorpion bites  Tityus trinitatis &  T. serrulatus Hereditary Cystic Fibrosis Idiopathic: 10 to 30% microlithiasis P. divisum Annular pancreas SOD Crohn’s Dz Post Perf DU
  3. 3. Idiopathic Acute Pancreatitis The etiology of acute pancreatitis should be determined in at least 80% of cases and no more than 20% should be classified as idiopathic  Gall stone disease represents approximately half the cases of acute pancreatitis, and 20–25% are related to alcohol abuse  The correct diagnosis of acute pancreatitis should be made in all patients within 48 hours of admission.  The diagnosis of idiopathic pancreatitis should not be accepted in the absence of a vigorous search for gall stones as a minimum, it is necessary to obtain at least two good quality ultrasound examinations. 
  4. 4. Clinical Presentation  Pain (95%) ◦ Acute onset ◦ Mid-abdominal or mid-epigastric ◦ Radiates to the back (50%) ◦ Peak intensity in 30 minutes ◦ Lasts for several hours         Nausea and vomiting (80%) Fever Shock Abdominal distension (75%) Abdominal guarding and tenderness (50%) Restlessness and agitation Grey-Turner's sign (hemorrhagic discoloration of the flanks) Cullen's sign (hemorrhagic discoloration of the umbilicus)
  5. 5. Cullen's sign
  6. 6. Grey-Turner's sign
  7. 7. Laboratory Diagnosis BASELINE INVESTIGATION  LFT’S  Increased amylase and/or lipase >3 times ◦ Amylase levels rise w/in 2-12h  Peak w/in first 48hr  Remain elevated 3-5days before return to baseline ◦ Lipase much more specific Height of elevation does not correlate with severity No utility in following daily levels after the diagnosis     Serum Ca+ LDH VIRAL ANTIBODY TITERS
  8. 8. Others U/S ABDOMEN  CT SCAN  EUS  MRCP 
  9. 9. PREDICTION OF SEVERITY Available prognostic features which predict complications in acute pancreatitis are       clinical impression of severity Obesity APACHE II >8 in the first 24 hours C reactive protein levels >150 mg/l Glasgow score 3 or more Persisting organ failure after 48 hours in hospital
  10. 10. APACHE II score (Acute Physiology And Chronic Health Evaluation)
  11. 11. Glasgow coma scale
  12. 12. Signs of Organ Failure  Cardiovascular  ◦ Hypotension ◦ Septic physiology   HR, CO and ◦ DIC ◦ Thrombocytosis SVR  Respiratory Renal ◦ ATN ◦ Oliguria Hepatic ◦ Encephalopathy ◦ T bili (3 mg/dl) ◦ AST/ALT 2X nl ◦ Hypoxemia ◦ Pleural effusions  Hematologic  GI ◦ Stress ulcer ◦ Acalculous cholecystitis
  13. 13. Determining severity  Clinical assessment,     fluid status vitals UOP pulse oximetry  Clinical criteria  Radiographic criteria ◦ Ranson criteria ◦ Atlanta criteria ◦ POP score ◦ CT severity index  necrosis may not be evident until 48-72h
  14. 14. Ranson Score At admission  age in years > 55 years  white blood cell count > 16000 cells/mm3  blood glucose > 11 mmol/L (> 200 mg/dL)  serum AST > 250 IU/L  serum LDH > 350 IU/L At 48 hours  Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)  Hematocrit fall > 10%  Oxygen (hypoxemia PO2 < 60 mmHg)  BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration  Base deficit (negative base excess) > 4 mEq/L  Sequestration of fluids > 6 L
  15. 15. Atlanta criteria
  16. 16. Pancreatitis Outcome Prediction Score
  17. 17. When Do I Order A CT?  If the patient has….. ◦ ◦ ◦ ◦ ◦ Persisting organ failure Signs of sepsis Deterioration in clinical status after 6-10days Diagnostic dilemma Infection suspected  T > 101o F  Positive blood cultures  What kind of CT?  What are you looking for?  Follow up scan are recommended only if the patient’s clinical status deteriorates or fails to show continued improvement. ◦ CT scan with pancreatic protocol ◦ Necrosis: Lack of enhancement with contrast ◦ Fluid Collections ◦ Alternate diagnosis
  18. 18. CT scan with pancreatic protocol  500 ml of oral contrast by mouth or nasogastric tube. An initial scan without iv contrast show extent of peripancreatic change. A post contrast series is obtained aftr iv inj of 100 ml of nonionic contrast delivered at 3 ml/s Images through the pancreatic bed should be obtained with in 40 sec and before 80 sec.
  19. 19. CT Findings  Pancreas ◦ ◦ ◦ ◦  Pancreatic enlargement Decreased density due to edema Intrapancreatic fluid collections Blurring of gland margins due to inflammation Peripancreatic ◦ Fluid collections and stranding densities ◦ Thickening of retroperitoneal fat * It may take up to 72h for inflammatory changes to become apparent on CT *
  20. 20. CT Findings Tail Indistinct Intraperitoneal fluid
  21. 21. CT Findings Severe Pancreatitis Nonenhanci ng Necrosis Peripancreatic edema and inflammation
  22. 22. Balthazar Scoring CT grading of severity POINTS Grade of Acute Pancreatitis A =Normal pancreas B =Pancreatic enlargement C =Pancreatic/peripancreatic inflammation D =Single peripancreatic fluid collection E =Multiple fluid collections 0 1 2 3 4 Grade E = 50% chance of developing an infection and 15% chance of death Degree of Necrosis No necrosis Necrosis of one third of pancreas Necrosis of one half of pancreas Necrosis of more than one half 0 2 4 6 CT Severity Index = Grade + Degree of necrosis
  23. 23. When can he eat ? TPN vs. enteral feeding   In patients with severe disease, oral intake is inhibited by nausea; the acute inflammatory response is associated with impaired gut mucosal barrier function. It has been suggested that nutritional support may help to      limit the stimulus to the inflammatory response. Reduce microbial translocation Enhance gut mucosal blood flow Promote gut mucosal surface immunity In these circumstances enteral feeding seems to be safer than parenteral feeding, with fewer septic complications.It is also cheaper
  24. 24. Contd…  Tube feed if anticipate NPO > 1 week.  Nasogastric feeding may be feasible in up to 80% of cases. Caution should be used when administering nasogastric feed to patients with impaired consciousness because of the risk of aspiration of refluxed feed.  In that case nasojeujunal tube can be used.  The use of enteral feeding may be limited by ileus. If this persists for more than five days, and if can’t maintain adequate jejunal access parenteral nutrition will be required.
  25. 25. Possible pathways for pancreatic infection There are few mechanisms by which bacteria may enter pancreatic and peripancreatic necrosis  The haematogenous route via the circulation.  Transmural migration through the colonic bowel wall either to the pancreas (translocation),or via ascites to the pancreas, or via the lymphatics to the circulation  The biliary duct system from the duodenum via the main pancreatic duct.  Intra abdominal fungal infection can also
  26. 26. Bacteriology in severe acute pancreatic            Escherichia coli Staphylococcus aureus Pseudomonas spp Klebsiella spp Proteus spp Candida Streptococcus faecalis Enterobacter spp Anaerobes Monomicrobial Polymicrobial 25% 17% 15% 9% 9% 4% 3% 3% 16% 76% 24%
  27. 27. Management  All patients with acute pancreatitis should receive adequate oxygen  Start IV fluids with crystalloid  Colloid (blood if Hct <25, albumin if serum alb <2)  Rate of fluid replacement should be monitored by frequent measurement of central venous pressure  Closely follow input output charting  0.5ml/kg /hr in absence of renal failure  Analgseics  Opioids  Antiemetics  NGT decompression  if frequent emesis or evidence of ileus on plain films  Monitor & correct electrolytes.
  28. 28. When Do I Start Antibiotics?  Acute pancreatitis is c/b infection ~ 10%  30-50% of those with necrosis get infection  Prophylactic antibiotics ◦ Controversial  No benefit in mild EtOH pancreatitis  Selective gut decontamination may be beneficial  General recommendations for use: ◦ Biliary pancreatitis with signs of cholangitis ◦ > 30% necrosis on CT scan
  29. 29. Antibiotic Aminoglycosides •Netilmicin •Tobramycin Acylureidopenicillins •Mezlocillin •Piperacillin Cephalosporins •Cefotiam •Ceftizoxime •Cefotaxime •Ceftriaxone Quinolones •Ciprofloxacin •Ofloxacin Carbapenems •Imipenem Efficacy factor 0.14 0.12 0.71 0.72 0.75 0.76 0.78 0.79 0.86 0.87 0.98
  30. 30. A final word on antibiotics  Do not use empirically early in mild pancreatitis  Fever early in the disease process is almost universally secondary to the inflammatory response and NOT an infectious process
  31. 31. When Do I Consult GI ?  Evidence of biliary pancreatitis ◦ Elevated LFTs + pancreatitis  No matter what the US shows Severe pancreatitis  Recurrent unexplained pancreatitis   Rule out infected necrosis  EUS FNA sampling of fluid collections  Endoscopic treatment of necrosis/abscess
  32. 32. GALL STONE PANCREATITIS AND TREATMENT OF GALL STONES  Q: When should I suspect it ? ◦ A: Always  Q: How do I evaluate for it ? ◦ A: (E)US and LFTs  Q: When is ERCP indicated ?
  33. 33. Contd….  Urgent therapeutic ERCP should be performed in patients with acute pancreatitis of gall stone etiology who satisfy the criteria for severe pancreatitis, or when there is cholangitis, jaundice, or a dilated common bile duct.  The procedure is best carried out within the first 72 hrs after the onset of pain.  All patients undergoing early ERCP for severe gall stone pancreatitis require endoscopic sphincterotomy whether or not stones are found in the bile duct. Patients with signs of cholangitis require endoscopic sphincterotomy or duct drainage by stenting to ensure relief of biliary obstruction
  34. 34. Timing of cholecystectomy  All patients with biliary pancreatitis should undergo definitive management of gall stones during the same hospital admission.  For unfit patients, endoscopic sphincterotomy alone is adequate treatment
  35. 35. Complications of AP  Immediate  Shock  DIC  ARDS  Late        Pancreatic pseudocyst Pancreatic abscess Pancreatic necrosis Progressive jaundice Persistent duodenal ileus GI bleeding Pancreatic ascites
  36. 36. Management of Pancreatic Complications  Acute fluid collections ◦ Occur early, seen but not felt ◦ No defined wall usually resolve spontaneously ◦ No routine percutaneous or operative drainage require  Infected pancreatic necrosis  Pancreatic abscess  Pseudocysts
  37. 37. Infected necrosis   All patients with persistent symptoms and greater than 30% pancreatic necrosis, and those with smaller areas of necrosis and clinical suspicion of sepsis, should undergo image guided FNA to obtain material for culture 7–14 days after the onset of the pancreatitis. Patients with infected necrosis will require intervention to completely debride all cavities containing necrotic material.
  38. 38. Contd…  Radiological  percutaneous wide bore drainage  Surgical  Debridement of necrotic tissue following this abdomen can be closed in three ways  Closed ovr drain  Packed and left open  Closed over drain and irrigated  A new approach for surgical debridement of infected necrosis offers the potential to debride necrotic tissue with minimal systemic disturbance, by approaching the cavity along the track of a percutaneously placed drain.The cavity is then debrided piecemeal with an operating nephroscope. Several sessions may be required in order to achieve complete debridement. Postoperatively the cavity is continuously irrigated
  39. 39. Pseudocysts  Collection of pancreatic fluid enclosed by non-epithelialized wall of granulation tissue  Complicates 5-10% cases of AP  ~ 4 weeks after insult  25-50% resolve spontaneously
  40. 40. Complications of Pseudocyst  Infection - 14%  Rupture - 6.8%  Hemorrhage - 6.5%  Common bile duct obstruction - 6.3%  GI obstruction - 2.6%
  41. 41. Pseudocyst Management  Old thought ◦ Pseudocysts > 5 cm that have been present > 6 weeks must be drained  Current practice ◦ Asymptomatic pseudocysts, regardless of size, do not require treatment
  42. 42. Pseudocyst Drainage Techniques  Endoscopic  Surgical  Radiologic
  43. 43. Communicating Non-communicating
  44. 44. Endoscopic Pseudocyst Management
  45. 45. Percutaneous Pseudocyst Drainage
  46. 46. Laparoscopic Cyst Gastrostomy
  47. 47. Open cyst Gastrostomy
  48. 48. Pancreatic abscess ◦ CT or EUS guided drainage  Walled collection of pus  Similar to management of pseudocyst
  49. 49. Closing Points Patients with severe acute pancreatitis have an increased risk of death.  Patients who die usually have evidence of organ failure.  All patients with severe acute pancreatitis should be managed in a high dependency unit or intensive therapy unit with full monitoring and systems support  The pancreas is mean 
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