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Transcript
THE 34th Annual
Gastroenterology
Educational Seminar
SOUTH CENTRAL TEXAS SOCIETY OF GASTROENTEROLOGY
NURSES AND ASSOCIATES
Redefining Acute Pancreatitis
Juan Echavarria MD, MS
Gastroenterology fellow
University of Texas Health Science Center at San
Antonio
Objectives
Diagnosis Acute pancreatitis
Etiology
 Key concepts
• Phases
• Organ dysfunction
• Severity
 Morphologic classification
• Edematous vs necrotic pancreatitis
• Acute pancreatic/peripancreatic fluid collections
Treatment approach
Atlanta classification
 The Atlanta Symposium in 1992 attempted to offer a
global ‘consensus’ and a universally applicable
classification system
 Confusing and not universal
 Better understanding of physiopathology, natural
history, complications, improved diagnostic imaging
 Revised classification 2012
• Clinical assessment of severity
• Provides more objective terms to describe the local
complications of acute pancreatitis
Acute Pancreatitis Classification Working Group. Revision of the Atlanta
classification of acute pancreatitis. 2008. http://www.pancreasclub.com/resources/
AtlantaClassification.pdf
Diagnosis
 Acute pancreatitis
1. Abdominal pain consistent with acute
pancreatitis
2. Serum lipase activity (or amylase activity) at
least three times greater than the upper limit of
normal
3. Characteristic findings of acute pancreatitis on
imaging
 Onset
Acute Pancreatitis Classification Working Group. Classification of acute
pancreatitis—2012: Revision of the Atlanta classification and definitions by
international consensus. Gut 2013;62:102–111
Causes
• Readily established in most patients
• Gallstones (40-70%)
– Key role US
– Prevent recurrence, biliary sepsis
• Alcohol (25-35%)
– ≥ 5 years heavy alcohol consumption
– Discrete episodes AP to silent chronic pancreatitis
American College of Gastroenterology Guideline: Management of Acute
Pancreatitis. Am J Gastroenterol. July 2013
Medications
6MP, AZA
DDI
Infections
Metabolic causes
Hypertriglyceridemia
Hypercalcemia
Hyperparathyroidism
Malignancy
PDAC
Hereditary
PRSS
SPINK
CFTR
Idiopathic
Anatomic
Pancreas divisum
Physiologic
Sphincter of
Oddi dysdunction
Phases of acute
 Early
• 1st week
• Host response to local pancreatic injury lead to
systemic disturbances
– SIRS
• Determinant of severity: presence and duration of
organ failure
– Transient organ failure <48h
– Persistent organ failure > 48h
– MOF
Acute Pancreatitis Classification Working Group. Classification of acute
pancreatitis—2012: Revision of the Atlanta classification and definitions by
international consensus. Gut 2013;62:102–111
In this early phase, severity is entirely based on
clinical parameters
The need for treatment is determined primarily
by the presence or absence of organ failure
caused by systemic inflammatory response
syndrome
 Late
• > 1-2 weeks to months
• Characterized by persistence of systemic signs of
inflammation or by the presence of local
complications
Important to distinguish different morphologic
characteristics
• Compensatory, anti-inflammatory response
syndrome (CARS)
– Risk infection
In the second stage of the disease, the need for
treatment is determined by the presence of
symptoms and/or local complications
The type of treatment is determined mainly by
the morphologic abnormalities of the
pancreatic/peripancreatic region
Definition of Organ failure
 Why important?
• Important to identify patients with potentially
severe acute pancreatitis who require aggressive
early treatment
• Transfer to specialist care
• Advantages to stratifying these patients into
subgroups based on the presence of persistent
organ failure and local or systemic complications
 Mild acute pancreatitis
•
•
•
•
•
Absence of organ failure
No local or systemic complications
Usually do not require imaging
Usually discharged during early phase
Morbidity low, Mortality very rare
 Moderate severe acute pancreatitis
• Transient organ failure
• Local/systemic complications
• May resolve without intervention or require
prolonged care
• Mortality usually low, morbidity high
 Severe acute pancreatitis
• Persistent organ failure
• Single vs MOF
• During early phase is set in motion by SIRS, which
if persistent leads to persistent organ failure
• Increased mortality 36-50%
– Infected necrosis
Evolution of severity
 Most patients with severe disease present to the
emergency room with no organ failure or pancreatic
necrosis
 Patient should be classified and treated as
potentially having severe AP
 Reassess severity daily, document day 1-3, 7 days
 Imaging of early complications not as important
during 1 week
– Extent of necrosis poorly defined
– Extent of morphologic changes is not proportional to
severity
– Identification usually does not lead to change in treatment
 After 1 week (late phase), local complications
evolve
 Important to distinguish morphologic
characteristics
 Infected necrosis associated with highest risk
death
Morphologic classification
 Interstitial edematous pancreatitis
•
•
•
•
•
80-85%
No necrosis
Usually mild, self limited
Uncomplicated vs Complicated
Low mortality ~2%
 Necrotizing pancreatitis
• Parenchymal necrosis alone (<5%), peripancreatic
necrosis alone (20%), and mixed (75-80%)
• Sterile vs infected
Peri-pancreatic necrosis
Pancreatic necrosis
 Infected pancreatic necrosis
• Confers a different natural history, prognosis, and
treatment
• No absolute correlation between the extent of
necrosis and the risk of infection and duration of
symptoms
• Infected necrosis is rare during the first week
• Clues
– Presumed when there is extraluminal gas in the
pancreatic and/or peripancreatic tissues on CT
– Onset SIRS later in course
• Pancreatic abcess
Definition of pancreatic and peripancreatic collections
Acute peri-pancreatic fluid collection
 Usually develop in the early phase of IEP
• <4weeks
 Characteristics:
•
•
•
•
•
Adjacent to the pancreas
Do not have a well defined wall
Homogeneous
No solid/liquefied components
Confined by normal fascial planes in the retroperitoneum
 Most acute fluid collections remain sterile and usually
resolve spontaneously without intervention
Acute necrotic collection
 A collection containing variable amounts of
fluid and necrotic tissue
 Arises from necrotizing pancreatitis
 Within 4 weeks
 May be multiple, and may appear loculated
 Can be associated with disruption of the MPD
and become infected
Pancreatic pseudocyst
 Refers specifically to a fluid collection in the peripancreatic
tissues
 Surrounded by a well defined wall
 Contains essentially no solid material
 Usually after 4 weeks
 Arise from disruption of the main pancreatic duct or its intrapancreatic branches without any recognizable pancreatic
parenchymal necrosis
 Does not result from a ANC, but can arise in acute necrotizing
pancreatitis (disconnected duct syndrome)
Walled-off pancreas necrosis
 Mature, encapsulated collection of pancreatic
and/or peripancreatic necrosis
 Usually this maturation occurs ≥4 weeks after
onset of necrotizing pancreatitis
 CT may not readily distinguish solid from
liquid content
• MRI, trans-abdominal ultrasonography or
endoscopic ultrasonography may be required for
this distinction
Evaluation
 History very important
• Timing!!
 Imaging
• CT
– Contrast-enhanced CT is the primary tool for assessing the
imaging-based criteria
– Not all patients with acute pancreatitis need to undergo contrastenhanced CT
o Should be performed in patients who develop or are likely to develop
severe AP or complications
o Sudden change in clinical picture
o Monitor response to therapy
o 1st episode AP > age 40
• RUQ sono
– Should be performed in all patients with AP
• MRI/MRCP
American College of Gastroenterology Guideline: Management of Acute
Pancreatitis. Am J Gastroenterol. July 2013
Treatment approach
Severity assessment
Clinical
Imaging
American College of Gastroenterology Guideline: Management of Acute
Pancreatitis. Am J Gastroenterol. July 2013
 IVF
• Early aggressive intravenous fluid resuscitation provides microand macro circulatory support to prevent serious complications
such as pancreatic necrosis
• Most beneficial during the first 12 – 24 h
• LR over NS
• Monitor carefully Hct, BUN, SCr
 Antibiotics
• Should always be given for extra-pancreatic infections
• Not recommended as prophylaxis in severe AP or sterile
necrosis
• Used in proven or suspected infected necrosis
 Nutrition
• Start fast
• Enteral, not TPN
American College of Gastroenterology Guideline: Management of Acute
Pancreatitis. Am J Gastroenterol. July 2013
Management of APFC and pseudocyst
 Usually sterile and rarely become infected
 More than half of these collections
spontaneously resolve in the first several
weeks
 Intervention may only be indicated if
infection is suspected
 Most resolve spontaneously as they lose their
communication with the pancreatic ductal system
• As opposed to chronic pancreatitis pseudocysts ~ 10%
 Pseudocysts <4 cm in diameter are most likely to
resolve but a large majority of the pseudocysts which
are >10 cm require drainage
 Intervention is required in patients who develop
symptoms or in whom an infection is suspected
 Complications: tracking into pleura/mediastinum,
pseudoaneurism, obstruction
Management options
• Surgery: cyst-gastrostomy, cystenterostomy
– Morbidity 25%, mortality 5%
• Percutaneous catheter drainage
– Best results when PD is normal
– Pancreatico-cutaneous fistulas
– Recurrence (70%), Infection, dislodgement, upsizing,
duration
• Endoscopic drainage
– High success rate, low morbidity/mortality
– Several approaches, EUS-guided, Trans-papillary
drainage
– Pseudo-aneurysm – absolute contraindication
Pseudocyst
(rule out other Dx: WOPN,
Cystic neoplasm)
Asymptomatic or
Sterile
Symptomatic or
Infected
Monitor
PD features
(communication with cyst,
PD stricture, disconnect)
No
Radiologic drainage
Yes
Increasing in size?
Duration
Transpapillary
drainage alone
Cyst features
Small/remote/
solitary
Large/close to
stomach or duodenum
Transmural
drainage +- TP
Treatment of sterile pancreas necrosis
 Serial CT (7–10 days)
• Evolution of the pancreatic necrosis
• Assess evidence of complications
– Infection (air bubbles)
– Increased peripancreatic necrotic collections
– Hemorrhage
• FNA if worsening clinically but no radiologic evidence of infection
– Retroperitoneal approach preferred
 If sterile necrosis but persistent symptoms
• Main PD disruption, increasing/additional collections, pain,
obstruction (GD, biliary, colonic)
• Consider percutaneous drainage, PD drainage, DEN  delayed 4-6
weeks
• Avoid surgery
“Asymptomatic WON does not mandate
intervention regardless of the size and extension
of the collection, and may resolve spontaneously
over time”
“Symptomatic WON generally requires
intervention late in the course (ie, >4 weeks) if
there is intractable pain, obstruction of a viscus
such as the stomach or bile duct, or in the
presence of infection”
Treatment of infected pancreas necrosis
Traditionally treated with surgical debridement and antibiotics
• 34-95% complication rate
• 11-39% Death
Avoid early surgical intervention as much as possible
• 242 pts: 0 –14 days, 56%; 14 –29 days, 26%; and 29 days, 15% (P <.001)
If a patient is too unstable for surgery, percutaneous catheter
drainage may help stabilize the patient
“Step-up approach”
• Reduced the rate of the composite end point of major complications
among patients with necrotizing pancreatitis and infected necrotic
tissue
• In 37% cases, percutaneous drainage was enough
“Intervention by any method is optimal when
infected necrosis is walled-off and demarcated
with at least partial liquefaction, and discrete
encapsulation. This typically requires a delay of
4 to 6 weeks”
Interventions to drain/debride necrosis can be
categorized into open surgical, minimally invasive
surgical approaches, image-guided percutaneous,
endoscopic, and hybrid approaches
• Transperitoneal (through the abdominal wall),
retroperitoneal usually through a flank approach, and/or
orally via a transmural approach
• Percutaneous catheter drainage (PCD) is most useful for
– Collections that do not resolve, to control sepsis, and the first step in
the step-up approach, in combination with endoscopic transmural
debridement, as a bridge to surgery, or to treat residual collections
after surgery
– Considerations
• Minimally invasive retroperitoneal necrosectomy
– Sinus tract endoscopy, laparoscopic transabd necrosectomy, VARD
– Morbidity 24-54%, mortality up to 8%
• Endoscopic necrosectomy
– Primary success was achieved in 80% and 91% of patients
– Median of 3 to 6 necrosectomies
– Adverse events occur in 15% to 26% of patients (perforation,
peritonitis, bleeding, and air embolism)
Treatment of necrotizing pancreatitis
Dutch Pancreatitis Study Group. CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
2012;10:1190–1201
Take home points
 Be aware of terminology
 Monitor closely for organ damage
 Timing of imaging important
 Tailor treatment based on clinical picture and imaging findings
 Multidisciplinary approach
 Be aware of complications
Take home points
 Step-up approach utilizing percutaneous or endoscopic
drainage followed by minimally invasive or endoscopic
necrosectomy
 Traditional open necrosectomy reserved as a second-line
intervention
 No single approach can be applied universally to all patients
with necrotizing pancreatitis
 The ideal approach for a particular patient should be
determined based on the individual clinical scenario
QUESTIONS??