Evidence Based Treatment of Acute Pancreatitis 2013

Dr. Waleed Khalid Mahrous

Consultant Internal Medicine

)

Evidence-Based Treatment of

Acute Pancreatitis

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448904/




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


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


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


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


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 )


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)


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


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


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



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.



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



Revised Atlanta Criteria Define Organ Failure


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



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


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


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


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

http://www.ncbi.nlm.nih.gov/pubmed/23207241

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


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


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


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


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


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


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


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%


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


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).



MANAGEMENT OF PANCREATIC NECROSIS WHEN INFECTION IS SUSPECTED


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.


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


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



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.

Evidence Based Treatment of Acute Pancreatitis 2013

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