Acute pancreatitis

Acute pancreatitis

Dr Bhupendra shahSenior residentBP koirala institute of health sciencesDharan

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

PANCREATITIS

Inflammation in pancreas associated with injury to exocrine parenchyma

PAN

CREA

S

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

DEFINITIONAtlanta 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 incidenceranges between 5 and 80 per 100,000 population

GEOGRAPHICALHighest incidence(worldwide) recorded in the United States and

Finland(73.4 cases per 100,000)

Epidemiology

Gender Predilection

Generally M>FIn males more often related to alcohol

In females more often related to biliary tract disease

Idiopathic pancreatitis no clear gender predilection

AGEYoung males and Old Females

Pathogenesis

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 plugsduct 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 signCullen’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


ETIOLOGICAL INVESTIGATIONS• 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)


SENTINEL LOOP SIGN

COLON CUT-OFF SIGN

SEVERITY SCORING SYSTEMSACUTE 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 signs15-20% mortality risk with 3-4 signs40% mortality risk with 5-6 signs99% 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) Blood urea nitrogen (BUN) >22 mg%(I) Impaired mental status(S) SIRS: 2/4 present(A) Age >60 years(P) Pleural effusion

BISAP Score Observed Mortality0 0.1%1 0.4%2 1.6%3 3.6%4 7.4%

5 9.5%

Wu et al, Gut 2008

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. 3 rd edition Pg 3-12

33

0-3 = 3% mortality4-6 = 6% mortality7-10 = 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

Acute Physiology And Chronic Health Evaluation II score-1985

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

Modified Marshall Scoring System for organ failure

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

ICUTransfer 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 hospitalizationThe American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218

Guideline: Management of Acute Pancreatitis

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 subsided2) Parenteral narcotics are no longer required 3) Abdominal tenderness has markedly decreased4) Nausea and vomiting have ceased5) 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 APNasogastric 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

http://www.ncbi.nlm.nih.gov/pubmed/21775915

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

http://www.ncbi.nlm.nih.gov/pubmed/21775915

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

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%

• 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 analgesia2) 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 examinationand amylase and lipase assays) is needed to monitor for potential

complications of the pancreatitis, especially pseudocysts.Within 7-10 days

PrognosisTYPE 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

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Acute pancreatitis

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