Acute pancreatitis

Acute pancreatitis
Dr Bhupendra shah
Senior resident
BP koirala institute of health sciences
Dharan

Outline
• Introduction
• Epidemiology
• Pathophysiology
• Etiology
• Clinical Presentation
• Workup
• Severity Scoring System
• Treatment
• Prognosis
• Complications

PANCREATITIS
Inflammation in pancreas associated with injury to
exocrine parenchyma
PANCREAS
Stroma
Parenchyma
Exocrine
Primary injury causing
PANCREATITIS
Endocrine
Involved secondarily or
as a complication
PANCREAS Greek word with literal meaning ‘pan’ (all/whole) , ‘creas’ (flesh): sweatbread

DEFINITION
Atlanta Symposium definition of acute pancreatitis :
An acute inflammatory process of the pancreas with
variable involvement of other regional tissues or
remote organ systems.

CLASSIFICATION OF ACUTE PANCREATITIS
Atlanta* criteria (1992)
• Mild acute pancreatitis (80% cases)
(Acute Interstitial/edematous pancreatitis)
• Acute Absence of organ failure
• Absence of local complications
• Severe acute pancreatitis(20 % cases)
(Acute Hemorrhagic Necrotizing (fulminant)
pancreatitis)
• Local complications +/-
• Organ failure defined as
• SBP < 90 mm Hg
• PaO2 ≤ 60 mm Hg
• GI bleed ≥ 500 ml/24 hrs
• Cret ≥ 2 mg/dL after rehydration
• Ranson score ≥ 3 or APACHE ≥ 8
Revised Atlanta criteria (2012)
• Mild acute pancreatitis
• Absence of organ failure
• Absence of local complications
• Moderately severe acute
pancreatitis
• Local complications +/-
• Transient organ failure(<48 h)
• Severe acute pancreatitis
• Persistent organ failure**(>48
h) and/or death
*defined as a score of 2 or more for one of these(CVS, Renal, Resp) organ systems using
the modified Marshall scoring system

Epidemiology
World wide incidence
ranges between 5 and 80 per 100,000 population
GEOGRAPHICAL
Highest incidence(worldwide) recorded in the United States and
Finland(73.4 cases per 100,000)

Epidemiology
Gender Predilection
Generally M>F
In males more often related to alcohol
In females more often related to biliary tract
disease
Idiopathic pancreatitis no clear gender
predilection
AGE
Young males and Old Females

Mechanisms against Auto-digestion of
Pancreas
• Packing of enzyme in precursor form
• Synthesis of trypsin inhibitor
• Low calcium level inside acinar cell promote trypsin
destruction

Gallstone pancreatitis
Two factors have been suggested:
• reflux of bile into the pancreatic duct due to transient
obstruction of the ampulla during passage of gallstones
• obstruction at the ampulla secondary to stone(s) or edema
resulting from the passage of a stone .

How Alcohol  Acute Pancreatitis??
1) Effects of diet
2) Malnutrition
3) Direct toxicity of alcohol
4) Concomitant tobacco smoking
5) Hypersecretion of gastric and
pancreatic juices(rich in
protein, low in bicarbonate/
trypsin inhibitor)protein
plugsduct obstruction/reflux
6).Hyperlipidemia
7).Increased ductal
permeability enzymes
extrusion damage
8).Release of free radicals-
superoxide, hydroxyl
9).Spasm of sphincter of Oddi

Pathogenesis of Acute Pancreatitis

CLINICAL FEATURES
• Abdominal pain
• Other symptoms
• Physical examination

Other Manifestations
• Subcutaneous fat necrosis
• Small(<1 cm), red, tender nodules on extensor skin of legs
• Purtscher retinopathy(on fundoscopy)

17
Grey Turner sign
Cullen’s sign

DIFFERENTIAL DIAGNOSIS
ABDOMINAL CONDITONS
• Perforated peptic ulcer/gastroentritis
• Biliary colic/acute cholecystitis/ Cholangitis
• Mesentric Ischemia
• Ruptured Aortic Anuerysm
• Intestinal Obstruction
• Gastric/colon/pancreatic CA
• Viral Hepatitis
• IBS
SYSTEMIC CONDITIONS
• DKA
THORAX CONDITIONS
• Pneumonia/ARDS
• Pleuritic pain
• MI
GYNECOLOGICAL CONDITONS
• Ectopic pregnancy
• Salpingtis

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

HEMATOLOGICAL
• Pancreatic Enzymes’ Assays
• Serum Amylase:
• ONSET: almost immediately
• PEAK: within several hours
• 3-4 times upper limit of normal within 24 hrs (90%)
• RETURN to normal depends on severity(3-5 days)
• normal at time of admission in 20% cases
• Compared with lipase, returns more quickly to values below the upper
limit of normal.
• Serum Lipase:
• more sensitive/specific than amylase
• Remains elevated longer than amylase(12 days)
• Useful if late presentation
Raised Amylase  may not AP
Normal Amylase  may be AP
SERUM INDICATOR OF HIGHEST
PROBABILITY OF DISEASE

DIAGNOSIS
Contrast-enhanced computed tomography (CECT) and / or
magnetic resonance imaging (MRI) of the pancreas should be reserved for
patients in whom (3- 5 days later )
• The diagnosis is unclear
• Who fail to improve clinically within the first 48– 72 h after hospital
admission
• Evaluate complications

DIAGNOSIS
MRI is helpful in patients with :
• A contrast allergy
• Renal insufficiency where T2-weighted images without
gadolinium contrast can diagnose pancreatic necrosis

ETIOLOGICALINVESTIGATIONS
• 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, serum triglyceride should be obtained and considered the
etiology if >1000 mg/dl
• 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 )
• In a patient > 40 years old, a pancreatic tumor should be
considered as a possible cause of AP

• Genetic testing may be considered in young patients (
< 30 years old) if :
No cause is evident & a family history of pancreatic disease is
present

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)

SEVERITY SCORING SYSTEMS
ACUTE PANCREATITIS SPECIFIC SCORING SYSTEMS
• Ranson score
• Glagsow score
• Bedside Index for Severity in Acute Pancreatitis(BISAP) score
• Harmless Acute Pancreatitis Score(HAPS)
• Hong Kong Criteria
ACUTE PANCREATITIS NON-SPECIFIC SCORING SYSTEMS
(ICU SCORING SYSTEMS)
• Acute Physiology And Chronic Health Evaluation(APACHE) II score
• Sequential Organ Failure Assessment(SOFA) score

Ranson Criteria
• Admission
• Age > 55(70 years)
• WBC > 16,000(18000)
• Glucose > 200(220)
• LDH > 350(400)
• AST > 250
wagla
• During first 48 hours
• Hematocrit drop > 10%
• Serum calcium < 8
• Base deficit > 4.0(6.0)
• Increase in BUN > 5(2)
• Fluid sequestration > 6L
(4L)
• Arterial PO2 < 60
hbo fuc 30
5% mortality risk with <2 signs
15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signs

Glasgow-Imrie score
ON ADMISSION
• Age > 55 yrs
• TLC > 15 x 109 l-1
• BSR>180 mg/dL (10 mmol l-1)
(no H/O diabetes)
• BUN > 16 mmol l-1
(no response to IV fluids)
• Pa02 < 60 mmHg ( 8 KPa)
WITHIN 48 HOURS
• Serum Calcium < 2.0 mmol l-1
• Serum albumin <32 g l-1
• LDH > 600 units l-1
• AST/ALT > 200 units l-1
NOTE: Disease classified as SEVERE when 3 or more factors are present

BISAP Score:
(B)Bloodureanitrogen(BUN)>22mg%
(I)Impairedmentalstatus
(S)SIRS:2/4present
(A)Age>60years
(P)Pleuraleffusion
BISAPScore ObservedMortality
0 0.1%
1 0.4%
2 1.6%
3 3.6%
4 7.4%
5 9.5%
Wuetal,Gut2008

CT SEVERITY INDEX
• CT Grade (Balthazar grade)
• A : normal pancreas- 0
• B : enlarged pancreas but
without inflammation- 1
• C : pancreatic or
peripancreatic inflammation-2
• D : single peripancreatic fluid
collection-3
• E :>= 2 peripancreatic fluid
collections or gas in pancreas
or retroperitoneum-4
• Necrosis score
• None -0
• <33% - 2
• 33-50% - 4
• > 50% - 6
• TOTAL SCORE =
CT grade + Necrosis
Sabistine S. Marc The massachusetts General hospital handbook of Internal Medicine. 3rd edition Pg 3-12
33
0-3 = 3% mortality
4-6 = 6% mortality
7-10 = 17% mortality

Harmless Acute Pancreatitis Score
• Absence of rebound tenderness
• Absence of Guarding
• Normal Hct level
• Normal serum creatine level
• Accuracy of nonseverity is 98%
Stephen et al.Current medical diagnosis and treatment:2012;692-
693

AcutePhysiologyAndChronicHealthEvaluationIIscore-1985
NOTE: Disease classified as SEVERE if clinical impression of very ill patient with
APACHE II score above 8

Modified MarshallScoringSystemfor organfailure

Predicting Severe AP(ACG 2013)
So rather than depending on a scoring system to predict severity
of AP,
one need to be aware of intrinsic patient-related risk factors,
including laboratory and imaging risk factors, for the development of
severe disease.

///////////////////////
Clinical findings associated with a severe course for initial risk assessment
Patient characteristics Age > 55 years
Obesity (BMI > 30 kg/m2)
Altered mental status
Comorbid disease
SIRS (> 2 of the following criteria) pulse > 90 bpm
Resp rate > 20/min or PaCO2 >4.3 KPa(32 mmHg)
Temperature > 38 °C (100.4oF)or < 36 °C(96.8oF)
TLC >12,000 or <4 ,000 cells/mm3 or > 10%
immature neutrophils (bands)
Laboratory findings BUN > 20 mg/dl
Rising BUN
Hct > 44%
Rising Hct
Elevated creatinine
Radiology findings Pleural effusions
Pulmonary infiltrates
Multiple or extensive extrapancreatic collections

TREATMENT GUIDELINES
• Supportive
• Transfer to intensive care
• Nutritional support
• Use of prophylactic antibiotics
• Treatment of infected necrosis
• Treatment of sterile necrosis
• Role of ERCP and biliary sphinchterotomy

INITIAL MANAGEMENT
• NPO
• 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

PAIN MANAGEMENT
• Parenteral analgesics usually needed.
• A number of parenteral narcotics are used
• In past, morphine avoided due to a concern it cause spasm of the
SOD and worsens although no evidence in humans .
• Meperidine with the accumulation of a neurotoxic metabolite
(normeperidine) ,relatively short duration of action, and many
hospitals have severely limited its use..
• Hydromorphine may thus be preferred.

INITIAL MANAGEMENT
ICU
Transfer to ICU 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
• Fluid therapy in acute pancreatitis:
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
• 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

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

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

INITIAL MANAGEMENT
Oral intake of limited amounts of calories is usually initiated
when :
1) Abdominal pain has subsided
2) Parenteral narcotics are no longer required
3) Abdominal tenderness has markedly decreased
4) Nausea and vomiting have ceased
5) Bowel sounds are present
6) Overall assessment of the physician is that the patient has
improved

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
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

ROLE OF ANTIBIOTICS IN AP
• 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
• Antibiotics should be given for an extra-pancreatic infection,
such as cholangitis, catheter-acquired infections, bacteremia,
urinary tract infections, pneumonia

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– 10 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 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 ( MCQ )
• Routine administration of antifungal agents along with
prophylactic or therapeutic antibiotics is not recommended

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

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

TREATMENTOFINFECTED 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%

• 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).

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.

No or little role of………………..
• Nasogastric suction and H2-blockers
• Secretion-inhibiting drugs
• Atropine, calcitonin, somatostatin and its analogue(Octreotide)
• glucagon and fluorouracil
• Protease inhibiting drugs
• Aprotinin, gabexate mesylate , camostate , phospholipase A2
inhibitors, FFP
• Indomethacin or PG inhibitors
• PAF antagonists
• PAF acetylhydrolase, Lexipafant

When to Discharge
1) Pain is well controlled with oral analgesia
2) Able to tolerate an oral diet that maintains their caloric needs, and
3) all complications have been addressed adequately
Follow up
• Routine clinical follow-up care (typically including physical examination
and amylase and lipase assays) is needed to monitor for potential
complications of the pancreatitis, especially pseudocysts.
Within 7-10 days

Prognosis
TYPE OF AP MORTALITY
Overall 10-15 %
(Biliary>alcholic)
Mild Acute Pancreatitis(80 % cases) 1 %
Severe Acute Pancreatitis(20 % cases) Severe  20-50 %
<1 week 1/3 cases MOF
>1 week 2/3 cases Sepsis
(+MOF)

REFERENCES:
Harrison principal of internal medicine 18th edition
• The American Journal of Gastroenterology , (30 July 2013)
• Guideline: Management of Acute Pancreatitis
• Robbins & Cotran Pathologic Basis of Disease - 8th Ed
• Bailey and Love’s short practice of surgery 25th edition
• Washington Manual® of Medical Therapeutics, The, 33rd Edition
• Meta-analysis of parenteral nutrition versus enteral nutrition in patients
with acute pancreatitis BMJ 2004; 328
•
• Acute Pancreatitis.Frossard JL, Steer ML, Pastor CM.Lancet 2008;
• 371:14
• Kun Jiang et al .world journal of Gastroenterology ‘present and future
antibiotics for severe acute pancreatitis ,2012-1-21:279-286
• Ryan Van Woerkom et al .Acute pancreatitis review and clinical update;2009-1
;9-19

Acute pancreatitis

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