Evidence Based Treatment of Acute Pancreatitis 2013

Dr. Waleed Khalid Mahrous
Consultant Internal Medicine
)

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

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

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

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

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

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

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.

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

STRATIFICATION

STRATIFICATION
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
STRATIFICATION

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
STRATIFICATION

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

ICU
Transfer 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/h
 Tachycardia 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):205-208
Fluid 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

 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

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

 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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