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Dr. Waleed Khalid Mahrous
Consultant Internal Medicine
)
Evidence-Based Treatment of
Acute Pancreatitis
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218
Guideline: Management of Acute Pancreatitis
DIAGNOSIS
AP established by the presence of 2 of the 3 following criteria:
(i) Abdominal pain consistent with the disease
(ii) Serum amylase and / or lipase greater than three times the upper limit of normal
(iii) Characteristic findings from abdominal imaging
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
DIAGNOSIS
The onset of acute pancreatitis is
defined as the time of onset of abdominal pain
(not the time of admission to the hospital)
Gut 2013;62:102–111. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
DIAGNOSIS
Contrast-enhanced computed tomography (CECT) and / or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom
The diagnosis is unclear Who fail to improve clinically within the first
48– 72 h after hospital admission Evaluate complications
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
DIAGNOSIS
Serum amylase alone cannot be used reliably for the diagnosis of AP and serum lipase is preferred.
Serum lipase appears to be more specific and remains elevated longer than amylase after disease presentation.
Upper limit of normal greater than 3– 5 times
may be needed in diabetics who appear to have higher median lipase compared with nondiabetic patients for unclear reasons
DIAGNOSIS
MRI is helpful in patients with : A contrast allergy Renal insufficiency where T2-weighted
images without gadolinium contrast can diagnose pancreatic necrosis
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
ETIOLOGY
Abdominal ultrasound US should be
performed in all patients with AP In the absence of gallstones and / or history
of significant history of alcohol use, a
serum triglyceride should be obtained and considered the etiology if
>1000 mg/dl In a patient > 40 years old, a
pancreatic tumor should be considered as a possible cause of AP The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218
Guideline: Management of Acute Pancreatitis
ETIOLOGY
Endoscopic investigation of an elusive etiology in patients with AP should be limited
Patients with idiopathic AP (IAP) should be referred to centers of expertise
Genetic testing may be considered in young patients ( < 30 years old) if :
No cause is evident & a family history of pancreatic disease is present The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218
Guideline: Management of Acute Pancreatitis
ETIOLOGY
Identification of gallstones as the etiology should prompt referral for cholecystectomy to prevent recurrent attacks
Alcohol-induced pancreatitis the diagnosis should not be entertained unless a person has a history of over 5 years of heavy alcohol consumption ( > 50 g per day, but is often much higher )
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
ETIOLOGY
A fasting triglyceride level should be re-evaluated 1 month after discharge when hypertriglyceridemia is suspected
Patient at age of 40 or higher with prolonged or recurrent pancreatitis contrast-enhanced CT scan or MRI is needed
A more extensive evaluation including endoscopic ultrasound (EUS) and /o r MRCP may be needed initially or after a recurrent episode of IAP
ETIOLOGY
IDIOPATHIC AP
IAP is defined as pancreatitis with no etiology established after initial laboratory
(including lipid and calcium level)
and imaging tests (transabdominal ultrasound and CT in the appropriate patient)
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
INITIAL ASSESSMENT AND RISK STRATIFICATION
Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as
Risk assessment should be performed to stratify patients into higher- and lower-risk categories to assist triage, such as admission to an intensive care
Patients with organ failure should be
admitted to an intensive care unit ICU or intermediary care setting whenever possible
INITIAL ASSESSMENT AND RISK STRATIFICATION
Definition of severity of acute pancreatitis
Mild acute pancreatitis Is characterised by the absence of organ
failure and the absence of local or systemic complications.
- Usually be discharged during the early phase - Usually do not require pancreatic imaging - Mortality is very rare Gut 2013;62:102–111. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
INITIAL ASSESSMENT AND RISK STRATIFICATION
Moderately severe acute pancreatitis
Is characterised by the presence of :
- Transient organ failure (present for <48 h)
- Local or systemic complications in the absence of persistent organ failure
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
INITIAL ASSESSMENT AND RISK STRATIFICATION
Severe acute pancreatitis Is characterised by persistent organ failure
(persists for >48 hr)
When SIRS is present and there is an increased risk that the pancreatitis will be complicated by persistent organ failure, and the patient should be treated as if they have severe acute pancreatitis.
Gut 2013;62:102–111. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
INITIAL ASSESSMENT AND RISK STRATIFICATION
Develop persistent organ failure within the first few days of the disease are at increased risk of death, with a mortality
reported to be as great as 36–50%
The development of infected necrosis among patients with persistent organ failure is associated with an extremely high mortality
Gut 2013;62:102–111. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
INITIAL ASSESSMENT AND RISK STRATIFICATION
INITIAL ASSESSMENT AND RISK STRATIFICATION
Revised Atlanta Criteria Define Organ Failure
Gut 2013;62:102–111. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
Pancreatic necrosis
Defined as diffuse or focal areas of non- viable pancreatic parenchyma > 3 cm in size or > 30% of the pancreas .
Pancreatic necrosis can be sterile or infected
INITIAL ASSESSMENT AND RISK STRATIFICATION
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
Predicting severe AP In general, AP-specific scoring systems
have a limited value, as they provide little additional information to the clinician in the evaluation of patients and may delay appropriate management
When the score demonstrates severe disease, the patient’ s condition is obvious regardless of the score
INITIAL ASSESSMENT AND RISK STRATIFICATION
INITIAL ASSESSMENT AND RISK STRATIFICATION
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
INITIAL ASSESSMENT AND RISK STRATIFICATION
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
INITIAL ASSESSMENT AND RISK STRATIFICATION
Obtain vital signs at frequent intervals (such as every 4-6 h)
Supplemental oxygen be administered during the first 24–48 h, especially if narcotic agents are used to control pain
ABG should be performed when oxygen saturation is ≤95% , hypoxemia or hypotension refractory to a bolus of IV fluids
INITIAL MANAGEMENT
ICUTransfer to ICU) (or possibly a step-down care unit should be
considered If there are :
Signs that suggest that the pancreatitis is severe or is likely to be severe
Need for very aggressive fluid resuscitation to overcome hemoconcentration, especially in an older person who may have underlying cardiovascular disease
If a patient does not have hypoxemia but is showing signs of
labored respiration, transfer should be considered to monitor pulmonary status carefully in anticipation
INITIAL MANAGEMENT
Close supervision by physicians and nursing staff in a step down unit but not necessarily urgent transfer to an intensive care unit include :
Obesity (BMI >30)Oliguria with urine output <50 mL/hTachycardia with pulse >120 beats/min, Evidence of encephalopathy Increasing need of narcotic agents to
counteract pain
INITIAL MANAGEMENT
Fluid therapy in acute pancreatitis: anybody's guess
Adequate prompt fluid resuscitation
- Fluids are given intravenously- Aim to maintain urine output >0.5 ml/kg body
weight
- Clinically relevant questions remain regarding the - - Type of fluid (crystalloid or colloid - Ringer’s
lactate or normal saline ) !!- - Rate of administration (Fast or slow) - - Goal of FT ??
INITIAL MANAGEMENT
An early elevated :
- Hematocrit- Blood urea nitrogen- Creatinine
Should prompt clinicians to institute more intensive early resuscitation measures.
INITIAL MANAGEMENT
INITIAL MANAGEMENT
Aggressive hydration, defined as 250-500ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular, renal, or other related comorbid factors exist
Early aggressive intravenous hydration is
most beneficial during the first 12 – 24 hr, and may have little benefit beyond this time period
In a patient with severe volume depletion, manifest as hypotension and tachycardia, more
rapid repletion (bolus) may be needed
Lactated Ringer ’ s solution may be the preferred isotonic crystalloid replacement fluid
Fewer patients developing SIRS as compared with patients receiving normal (0.9% ) saline
Normal saline given in large volumes may lead
to the development of a non-anion gap, hyperchloremic metabolic acidosis
INITIAL MANAGEMENT
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
Crystalloids - Ringer’s lactate or normal saline
While crystalloids appear to be the ideal choice based on expert opinion and the guidelines/recommendations from America, Italy and Japan
These recommendations are not based on high-level evidence in patients with acute pancreatitis
JOP. J Pancreas 2011 Mar 9; 12(2):205-208Fluid Therapy in Acute Pancreatitis. A Systematic Review of Literature
INITIAL MANAGEMENT
Fluid requirements should be reassessed at frequent intervals within 6 hr of admission and for the next 24 – 48 hr
The goal to decrease hematocrit (demonstrating hemodilution) and BUN (increasing renal perfusion) and maintain a normal creatinine during the first day of hospitalization
INITIAL MANAGEMENT
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
Patients not responding to intravenous hydration early (within 6 –1 2 h ) may not benefit from continued aggressive hydration.
Caution for certain groups of patients, such as the elderly, or cardiac and / or renal disease in order to avoid complications such as volume overload, pulmonary edema, and abdominal compartment syndrome
Other studies have suggested that aggressive hydration may be associated with an increased morbidity and mortality
INITIAL MANAGEMENT
Nine studies looked at aggressive versus nonaggressive resuscitation protocols,
- 4 concluded that an aggressive approach
yielded better outcomes
- 5 concluded that a nonaggressive approach was better
Ann Surg. 2013 Feb;257(2):182-8. doi: 10.1097/SLA
INITIAL MANAGEMENT
Rapid hemodilution increases incidence of sepsis within 28 days and in-hospital mortality
HCT should be maintained between 30% and 40% in acute response stage
Controlled fluid resuscitation offers better prognosis in patients with severe volume deficit within 72 h of severe acute pancreatitis onset
Patients with severe acute pancreatitis should receive 1/3 or more of initial 72 h cumulative i.v. fluid volume during first 24 h
INITIAL MANAGEMENT
Ringer’s lactate: 60-160 mL/kg body weight/day About 1/3-1/2 of amount required for first 24 h,
within the first 6 h Hourly: pulse, blood pressure, urine output, Central venous
pressure monitoring
Severe volume depletion: 500-1,000 mL/h for several hours with amount of fluid reduced once signs of severe volume depletion have subsided
- Non pancreatic fluid loss: 300-500 mL/h- No clinical volume depletion: 250-300 mL/h
Fluid rates reassessed 1-2 hourly for severely depleted patients or at least 4 hourly for other patients
INITIAL MANAGEMENT
1 to 2 L of crystalloids bolus, preferably
Lactated Ringer’s (approximately 20 mL/kg), followed by a
Continuous infusion of 150 to 300
cc/hour (approximately 3 mL/kg/h) for the first 24 hours
INITIAL MANAGEMENT
NUTRITIONAL SUPPORT
NBO
INITIAL MANAGEMENT
NUTRITION IN AP
In mild AP, oral feedings can be started immediately if there is no nausea and vomiting, and the abdominal pain has resolved
In mild AP, initiation of feeding with a
low-fat solid diet appears as safe as a clear liquid diet
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
Oral intake of limited amounts of calories is usually
initiated when : Abdominal pain has subsided Parenteral narcotics are no longer required Abdominal tenderness has markedly
decreased Nausea and vomiting have ceased Bowel sounds are present, Overall assessment of the physician is that the
patient has improved
INITIAL MANAGEMENT
NUTRITION IN AP
In severe AP, enteral nutrition is recommended to prevent infectious complications.
Parenteral nutrition should be avoided, unless the enteral route is
- - Not available- - Not tolerated- - Not meeting caloric requirements
Nasogastric delivery and Nasojejunal delivery of enteral feeding appear comparable in efficacy and safety
NUTRITION IN AP
In mild AP, oral feedings can be started immediately if there is no nausea and vomiting, and the abdominal pain has resolved
In mild AP, initiation of feeding with a
low-fat solid diet appears as safe as a clear liquid diet
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
NUTRITION IN AP
In severe AP, enteral nutrition is recommended to prevent infectious complications.
Parenteral nutrition should be avoided, unless the enteral route is
- - Not available- - Not tolerated- - Not meeting caloric requirements
Nasogastric delivery and Nasojejunal delivery of enteral feeding appear comparable in efficacy and safety
Enteral Feeding Stabilizes gut barrier function, prevent systemic complications
and improve morbidity and mortality
Enteral feeding is safer and less expensive than TPN, but there is not major improvements in morbidity and mortality of acute pancreatitis
NUTRITION IN AP
Nasogastric Feeding Was found to be comparable to
nasojejunal feeding in terms of safety, morbidity ,and mortality
Whether pancreatic rest has a role to play in patients with severe AP is still uncertain !!
Animal studies have shown that pancreatic exocrine secretion in experimental AP in response to CCK stimulation is suppressed
Pancreas. 2012 Jan;41(1):153-9. doi: 10.1097/MPA.Evaluation of early enteral feeding through nasogastric and nasojejunal tube in severe acute pancreatitis: a noninferiority randomized controlled trial
NUTRITION IN AP
Role of immediate oral feeding versus fasting in 60 patients with AP
The orally fed group had a significant 2-day shorter length of hospital stay without differences in recurrent attacks of pancreatitis in a follow-up of 3 months.
Pancreas. 2012 Jan;41(1):153-9. doi: 10.1097/MPA.Evaluation of early enteral feeding through nasogastric and nasojejunal tube in severe acute pancreatitis: a noninferiority randomized controlled trial
NUTRITION IN AP
These concepts should now be replaced by the principle that :
- Pancreatic stimulation should be reduced to basal rates, but that gut integrity should be maintained and that the stress response should be contained to reduce the likelihood of multi-organ failure, nosocomial infections, and mortality
Gastroenterology Research and Practice Volume 2011
NUTRITION IN AP
ERCP IN AP
Patients with AP and concurrent acute cholangitis should undergo ERCP within 24 hr of admission
ERCP is not needed early in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218
Guideline: Management of Acute Pancreatitis
During the course of biliary pancreatitis :
- Progressive increases in serum bilirubin - Increase in LFT- Persistent dilatation of the common bile
duct
All are strongly suggestive of common bile duct obstruction by gallstones & in this circumstance, it is reasonable to proceed directly to ERCP
ERCP IN AP
Benefit of early ERCP is seen in patients with AP complicated by acute cholangitis and biliary tree obstruction, but not severe AP in the absence of acute cholangitis.
ERCP before cholecystectomy has been shown to be of limited value and may be harmful.
ERCP IN AP
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
In the absence of cholangitis and / or jaundice, MRCP or EUS rather than diagnostic ERCP should
be used to screen for choledocholithiasis if highly suspected
Post-ERCP pancreatitis is greater in a patient with normal caliber bile duct & normal bilirubin
Pancreatic duct stents and / or post-procedure rectal (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients
ERCP IN AP
Rectal diclofenac and / or indomethacin should be considered before ERCP, especially in high-risk patients
ERCP IN AP
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
ERCP is indicated for clearance of bile duct stones in patients with :
- Severe worsening biliary pancreatitis
- Cholangitis- Poor candidates for cholecystectomy - Post cholecystectomy- Strong evidence of persistent biliary
obstruction
ERCP IN AP
THE ROLE OF ANTIBIOTICS IN AP
Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheter-acquired infections, bacteremia, urinary tract infections, pneumonia
Routine use of prophylactic antibiotics in patients with severe AP is not recommended
The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended
THE ROLE OF ANTIBIOTICS IN AP
Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis who deteriorate or fail to improve after 7– 1 0 days of hospitalization
(i) Initial CT-guided (FNA) for Gram stain and culture to guide use of appropriate antibiotics or
(ii) Empiric use of antibiotics after obtaining necessary cultures for infectious agents, without CT FNA, should be given
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
TREATMENT OF INFECTED NECROSIS Treatment of choice in infected necrosis is
surgical debridement (NOW minimal invasive procedure preferred )
33% of patients with necrotizing pancreatitis develop infected necrosis, usually after 10 days of illness
48% of patients with infected necrosis have persistent organ failure, either documented initially at admission or sometime after admission
Organ failure may occur in a substantial percentage of patients with both sterile 45% & infected necrosis 62%
THE ROLE OF ANTIBIOTICS IN AP
Once blood and other cultures are found to be negative and no source of infection is identified, antibiotics should be discontinued.
In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole
Routine administration of antifungal agents along with prophylactic or therapeutic antibiotics is not recommended
THE ROLE OF ANTIBIOTICS IN AP
Infected necrosis Antibiotics alone can lead to resolution of infection and, in select patients, avoid surgery
64% of the patients with infected
necrosis could be managed by conservative antibiotic treatment with 12% mortality, and only 26% underwent surgery.
In stable patients with infected necrosis, surgical, radiologic, and/ or endoscopic drainage should be delayed by preferably 4 weeks to allow the development of a wall around the necrosis (walled-off pancreatic necrosis).
THE ROLE OF ANTIBIOTICS IN AP
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
MANAGEMENT OF PANCREATIC NECROSIS WHEN INFECTION IS SUSPECTED
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
TREATMENT OF STERILE NECROSIS
Sterile necrosis is best managed medically during the first 2–3 wk
After this interval, if abdominal pain persists and prevents oral intake, debridement should be considered.
This is usually accomplished surgically, but percutaneous or endoscopic debridement is a reasonable choice in selected circumstances with the appropriate expertise.
TREATMENT OF STERILE NECROSIS
There is now an increasing consensus that patients with sterile necrosis should continue to be managed medically during the first 2–3 wk for the following reasons:
Delay in surgical necrosectomy and at times a total avoidance of surgery results in less morbidity and mortality than early surgical debridement
TREATMENT OF STERILE NECROSIS
When sterile necrosis is debrided surgically, a common sequela is the development of infected necrosis and the need for additional surgery
Patients with sterile necrosis, there was a trend to greater mortality among those operated on within 4 days
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218 Guideline: Management of Acute Pancreatitis
TREATMENT OF STERILE NECROSIS
If surgery is delayed for at least 2-3 wk ,the diffuse inflammatory process in the retroperitoneum resolves considerably, and gives rise to an encapsulated structure that envelops the necrotic pancreas and peripancreatic area
This structure has frequently been called organized necrosis.
By this time, organ failure has usually subsided, and many patients are now asymptomatic and do not require additional therapy.