Acute Pancreatitis

[Acute inflammation of abdominal

tiger]

By Dr. Ibrahim Odeh

Resident, Surgical Unit
Al-Salt Hospital \ Jordan
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

Blood Ductal
Exocrine Endocrine
vessels system

Primary injury causing Involved secondarily

PANCREATITIS or as a complication
Physiology
ACUTE PANCREATITIS
 CLINICAL DEFINITION
◦ An acute condition presenting with abdominal pain-usually
associated with raised pancreatic enzymes as a result of
pancreatic inflammation

 PATHOLOGICAL DEFINITION
◦ Reversible* pancreatic parenchymal injury associated with
inflammation

_____________________________________________________

*if underlying cause of pancreatitis is removed, heal without any

impairment of function or morphologic loss of gland

*Recurrent attacks with irreversible parenchymal injury leading to

impairment of function and morphologic loss is chronic pancreatitis
 CLINICAL CLASSIFICATION

*Considered a phase of chronic pancreatitis

** resulting from fibrosis within pancreas
CLASSIFICATION OF ACUTE
PANCREATITIS
 Mild acute pancreatitis (80%
cases)
(Acute Interstitial/edematous pancreatitis)
◦ 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
Epidemiology
World wide incidence

ranges between 1 and 80 per 100,000 of population

The incidence in USA 73,3 per 100,000 per year
In Jordan 1,6 per 100,00 of population per year
In Saudia Arabia 7,5 per 100,00 of population per year
In Egypt 19,1 per 100,00 of population per year
In Turkey 22.4 per 100,00 of population per year

[Link]
Epidemiology
Median ages of onset for various
Etiology etiologiesMedian Ages of onset
Alcohol-related 39 years

Biliary tract–related 69 years

Trauma-related 66 years

Drug-induced etiology 42 years

ERCP-related 58 years

AIDS-related 31 years

Vasculitis-related 36 years
Epidemiology
Gender Predilection
Generally M>F
In males more often related to alcohol
In females more often related to biliary tract
disease

Race
3 times higher for blacks than whites
PATHOPHYSIOLOGY

Autodigestion of pancreatic substance

by inappropriately activated pancreatic
enzymes (especially trypsinogen)
Pathophysiology
 PATHOPHYSIOLOGY

Activation of Hageman Activation of clotting and

factor-XII complement systems
thrombosis
 Splenic vein thrombosis

Lipase activation Fatty acids+ calcium 

Triglycerides Glycerol + Saponification
TRYPSINOGE Fatty acids  Hypocalcemia
N  TRYPSIN
Elastase activation 3rd space Sequestration of
Digestion of elastic fibers blood/fluid
Capillary leak/rupture  Hemorrhage+
Psudoanurysm Hypovolemic shock
Activation of Membrane damage Necrosis
Lysolecithinase (derived
from bile)

Release of inflammatory systemic complications

mediators into circulation
Etiology
1. Mechanical causes
2. Metabolic causes
3. Infective causes
4. Genetic causes
5. Vascular causes
6. Idiopathic AP
 Etiology of Pancreatitis

Mechanical Metabolic Infective Genetic Vascular Idiopathic

Pancreatic
Gall Stone Alcoholism Mumps Shock 70 %
devisim
due to
microlithiasis
Ampullary tumor Hypercalcemia Cocsaki – B Annular pancreas Hypothermia

Pancreatic Ca Hyperlipidimia Ascares Cystic fibrosis Atheroembolism

Iatrogenic (ERCP) Malnutrition Scorpion bite Autoimmune Vasculitis

(Polyarteritis
nodosa, SLE)
Trauma Azotemia Snake bite

Porphyries

Drugs
Tetracycline
Azathioprine
Steriods
Furosemide
Valproic acid
Ethanol can induce pancreatitis by several
methods:
1- Ethanol is a metabolic toxin to pancreatic acinar cells, where it can
interfere with enzyme synthesis and secretion also by Release of free
radicals- superoxide, hydroxyl produced by ethanol metabolism .

2- The "secretion with blockage" mechanism is possible because ethanol

causes spasm of the sphincter of Oddi,

3- Elevation of enzyme proteins that can precipitate within the pancreatic

duct.
Calcium then can precipitate within this protein matrix, causing multiple
ductal obstructions by protein bulges .

4- Ethanol also increases ductal permeability, making it possible for

improperly activated enzymes to leak out of the activated enzymes into
the surrounding tissue.
lysosomes (L)
Zymogen granules (ZG)
Cholesteryl esters (CE)
fatty acid ethyl esters
(FAEE)
 Hyperlipidemia induced 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 >
1,000 mg /dl

•  Lipase without increasment of serum amylase

Post-ERCP Pancreatitis
 3rd Most common cause of AP(after gallstone and alcohol) i.e. 4%
 Most common complication of ERCP

 INCIDENCE
◦ 2-4 % patients undergoing ERCP develop acute pancreatitis
◦ Risk of severe AP < 1/500.

 CAUSE
◦ Duct disruption , enzyme extravasation

 PREDISPOSING FACTORS
◦ Sphincter of Oddi dysfunction(risk increases to 30 %)
◦ H/O recurrent pancreatitis
◦ Sphincterotomy
◦ Balloon dilation of sphincter
◦ Inexperienced endoscopist
ABDOMINAL PAIN-Cardinal Symptom
 SITE: usually experienced first in the epigastrium but may be localized to either
upper quadrant or felt diffusely throughout the abdomen or lower chest

 ONSET: characteristically develops quickly, generally following substantial meal.

 SEVERITY: frequently severe, reaching max. intensity within minutes rather than
hours

 NATURE: “boring through”, “knifing” (illimitable agony)

 DURATION: hours-days

 COURSE: constant (refractory to usual doses of analgesics, not relieved by

vomiting)

 RADIATION: directly to back(50%), chest or flanks

 RELEIVING FACTOR: sitting or leaning/stooping forward (Muslims PRAYER

SIGN)
◦ due to shifting forward of abdominal contents and taking pressure off from inflamed
pancreas

 AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine

 OTHER MANIFESTATIONS
 Nausea, frequent and effortless vomiting, anorexia,diarrhea
◦ Due to reflex pylorospasm
◦ More intense in necrotizing than in edematous pancreatitis

 Persistent retching
◦ despite empty stomach

 Hiccups
◦ Due to gastric distension/diaphragmatic irritation

 Fever
◦ Low grade, seen in infective pancreatitis

 Weakness, Anxiety, Sweating

◦ Indicates severe attack.
 General Physical Examination
 Appearance: well  gravely ill with profound shock, toxicity
and confusion

 Vitals:
◦ Tachypnea(and dyspnea-10%),
◦ Tachycardia(65%).
◦ Hypotension
◦ temp  high(76%)/normal/low (acute swinging pyrexia in
cholangitis)

 Icterus(28%)
◦ gallstone pancreatitis or due to edema of pancreatic head

 Pallor, cold clammy skin, diaphoresis, dehydration

ABDOMEN EXAMINATION
 Tenderness + Rebound tenderness:
◦ epigastrium/upper abdomen

 Distension:
◦ Ileus(BS decreased or absent)
◦ ascites with shifting dullness

 Mass in epigastrium(usually absent)

◦ due to inflammation

 Guarding(also called “defense musculaire” )-upper abdomen

◦ tensing of the abdominal wall muscles to guard inflamed organs
within the abdomen from the pain of pressure upon them(i.e.
during palpation)

 Rigidity(involuntary stiffness)-unusual
◦ Tensing of the abdominal wall muscles to guard inflamed organs
even if patient not touched
 Cutaneous Ecchymosis(1 %
cases)*

Acute Hemorrhagic (Necrotizing/fulminant) Pancreatitis

Periperitoneal/retroperitoneal
Hemorrhage

Methemalbumin formed from digested blood

tracks around Fascial planes  hemorrhagic spots and

ecchymosis

FALCIFORM LIGAMENT
in flanks  around umbilicus Below inguinal ligament
(GREY TURNER’S SIGN) (FOX SIGN)
(CULLEN’S SIGN)
Differential Diagnosis for
coetaneous ecchemosis
 Acute Pancreatitis
 Pancreatic Hemorrhage
 Ruptured AAA
 Blunt abdominal trauma
 Ruptured ectopic pregnancy
 Retroperitoneal hemorrhage
 Coagulopathy
 GREY TURNER1 SIGN CULLEN2 SIGN FOX3
SIGN

1. Named after British surgeon George Grey Turner(1877-1951)

2. Named for Thomas Stephen Cullen (1869-1953), Canadian gynecologist who

first described the sign in ruptured ectopic pregnancy in 1916

[Link] after George Henry Fox(1846-1937), American dermatologist

 RESPIRATORY
EXAMINATION
Left sided* Pleural effusion(10-20%) -
exudative

* Due to close approximation of body and tail of pancreas to the left sided
Other Manifestations
 Subcutaneous fat necrosis
◦ Small(<1 cm), red, tender nodules on
extensor skin of legs

 Purtscher retinopathy(on
fundoscopy)
◦ Activation of complement and agglutination
of blood cells within retinal vessels causing
Ischemic injury of retina
◦ It may cause temporary or permanent
blindness
MANIFESTAIONS OF
COMPLICATIONS
 Hypocalcaemia
◦ circumoral numbness or paresthesia (1st symtpom to
develop).
◦ carpopedal spasm .
◦ Laryngospasm.
◦ generalized seizures
◦ Chvostek sign :
 Depending on calcium level, graded response occur: twitching
first at angle of mouth, then by nose, the eye and the facial
muscles
 Positive in 10 % population in absence of hypocalcaemia
◦ Trousseau sign :
 BP cuff around arm and inflating to 20 mmHg above SBP for 3-5
minutes
 Carpal spasm observed
 More specific and sensitive than chvostek sign(postive even
before tetany/hyperreflxia)
MANIFESTAIONS OF COMPLICATIONS

Peripancreatic (duodenal)
necrosis

Gastric
DIC
erosions

Hematemesis/
melena
(5%)
ABDOMINAL CONDITONS THORAX CONDITIONS

 Perforated peptic ulcer/gastroentritis  Pneumonia/ARDS

 Pleuritic pain
 Biliary colic/acute cholecystitis/  MI
Cholangitis

 Mesentric Ischemia
GYNECOLOGICAL CONDITONS
 Ruptured Aortic Anuerysm
• Ectopic pregnancy
• Salpingtis
 Intestinal Obstruction

 Gastric/colon/pancreatic CA
SYSTEMIC CONDITIONS
 Viral Hepatitis
 DKA
 IBS

DIFFERENTIAL DIAGNOSIS
Diagnostic criteria
 Most often established by the presence of two of
the three following criteria:
◦ (i) abdominal pain consistent with the disease,
◦ (ii) serum amylase and/or lipase greater than three
times the upper limit of normal, and/or
◦ (iii) characteristic findings from abdominal imaging.
 CT and/or MRI of the pancreas should be
reserved for patients
◦ in whom the diagnosis is unclear(typical pain with
normal enzymes)
◦ who fail to improve clinically within the first 48–72 h
after hospital admission (e.g., persistent pain, fever,
nausea, unable to begin oral feeding)
◦ to evaluate complications
WORKUP
 HEMATOLOGICAL investigations
 RADIOLOGICAL investigations
 HEMATOLOGICAL
 BASELINES
◦ CBC:
 Low Hb: prolonged hemetemesis/melena, internal hemorrhage
 Leucocytosis (10,000-30,000/mcL)-infection, non infectious
inflammation
 Low platelets-DIC
 Hct –raised in hemoconcentration
◦ LFT’s:
 raised bilirubin, AST/ALT/LDH, ALP, GGTP- gall stone
pancreatitis
◦ RFT’s:
 raised BUN/cretainine- ATN ARF
◦ Coagulation profile:
 increased INR-DIC
◦ BSR:
 > 180 mg/dl-diabetes as a sequelae or cause
◦ Serum electrolytes:
 Low sodium/potassium: persistent vomiting
 Hypocalcemia- saponification/fat necrosis
◦ Serum Protein:
HEMATOLOGICAL
 ABG’s
Acid-Base Disturbance Etiology
Metabolic (Lactic)acidosis Hypovolemic shock
with high anion gap
Hypokalemic Hypochloremic persistent vomiting
metabolic alkalosis
Respiratory acidosis ARDS

 Etiology specific investigations

◦ Serum fasting lipid profile
◦ Serum Calcium (Hypercalcemia  AP
Hypocalcemia)
◦ Autoimmune markers:
 serum autoantibodies such as anti-nuclear antibody
(ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II
antibody, and rheumatoid factor (RF),
 HEMATOLOGICAL
 Pancreatic Enzymes’ Assays
◦ Serum Amylase: Raised Amylase  may not AP
 ONSET: almost immediately Normal Amylase  may be AP
 PEAK: within several hours
 3-4 times upper limit of normal within 24 hrs (90%)
 RETURN to normal in (3-5 days)
 normal at time of admission in 20% cases
 Compared with lipase, returns more quickly to normal values.

SERUM INDICATOR OF HIGHEST

◦ Serum Lipase: PROBABILITY OF DISEASE
 more sensitive/specific than amylase
 Remains elevated longer than amylase(12 days)
 Useful in late presentation and if the cause is High TG
 Pancreatic Enzymes’ Assays
◦ Urine Amylase
 More sensitive than serum levels
 Remain elevated for several days after serum levels
returned to normal

◦ Pancreatic-specific amylase (p-amylase)

 Measuring p-amylase instead to total amylase(also
includes salivary amylase) makes diagnosis more
specific(88-93%)
CONDITIONS ASSOCIATED WITH RAISED SERUM
AMYLASE

ABDOMEN GYNE

 Small bowel obstruction  Ruptured Ectopic pregnancy

◦ strangulation ileus
◦ mesenteric ischemia  Torsion of an ovarian cyst

 Acute appendicitis OTHERS

 Cholecystitis  Parotitis (Mumps)

 Perforated Duodenal Ulcer  Macroamylasaemia

 Gastroenteritis  Opioids administration

 Biliary peritonitis  Low GFR

 Spasm of sphincter of Oddi  Brain injury(CVA)- hyperstimulation of

pancreas
Plain CXR-PA view
 Left sided Pleural effusion: blunting of costophrenic and
cardiophrenic angles + haziness in lower zones

 Elevated diaphragm on left side

 Linear focal atelactasis of lower lobe of lungs

 ARDS : diffuse alveolar interstitial shadowing

Plain X-ray abdomen erect AP
view
 Sentinel* loop sign
◦ Localized isolated Distended gut loop (Ileus) seen near the site of injured
viscus or inflamed organ

◦ RATIONALE: body's effort to localize the traumatic or inflamed lesions

◦ ETIOLOGY: Localized paralysis followed by accumulation of gas

◦ SITE:
 Acute Pancreatitis Left hypochondrium (PROXIMAL JEJUNUM)
 Acute Appendicitis Right iliac fossa
 Acute Cholecystitis Right Hypochondrium
 Diverticulitis Left iliac fossa
SENTINEL LOOP SIGN
Plain X-ray abdomen erect AP
view
 Colon cut-off sign
◦ Gas filled (Distended) segment of proximal(mainly transverse)
colon associated with narrowing of the splenic flexure
◦ with collapse of descending colon

◦ RANTIONALE: Extension of inflammatory process from the

pancreas into the phrenicocolic ligament via the transverse
mesocolon
 resulting in functional spasm and/or mechanical narrowing of the
splenic flexure at the level where the colon returns to the
retroperitoneum.

◦ Differential DIAGNOSIS:
 IBD
 Carcinoma of colon
 Mesenteric Ischemia
COLON CUT-OFF SIGN
Transcutaneous Abdominal
Ultrasonography
 Not diagnostic
 Should be performed within 24 hours in all patients to
◦ detect gall stones* as a potential cause
◦ Rule out acute cholecystits as differential diagnosis
◦ Detect dilated CBD.

* Identification of gallstones as the etiology should prompt referral for

cholecystectomy to prevent recurrent attacks and potential biliary sepsis.

Gallstone pancreatitis is usually an acute event and resolves when the

stone is removed or passes spontaneously.
IV Contrast enhanced Computed Tomography Scan

 Provides over 90 % sensitivity and specificity for the

diagnosis of AP….. BUT

 Routine use in patients with AP is unwarranted, as the

diagnosis is apparent in many patients and most have a mild,
uncomplicated course.
IV Contrast enhanced Computed Tomography Scan*

 INDICATIONS-DIAGNOSTIC

◦ Diagnostic uncertainty (differentiating pancreatitis from other

possible intra-abdominal catastrophes)

◦ Severe acute pancreatitis- distinguish interstitial from necrotizing

pancreatitis
 Necrosis( non enhancement area > 30 % or 3 cm) done at 72
hrs

◦ Systemic complications:
 Progressive deterioration, MOF, sepsis

◦ Localized complications:
 Altered fat and fascial planes, Fluid collection, pseudocyst,
psduoaneurysm,
 Bowel distension, mesenteric edema, hemorrhage
IV Contrast enhanced Computed Tomography Scan

 INDICATIONS-DIAGNOSTIC
◦ Initial assessment of prognosis (CT severity index).
◦ Perfusion CT at 3rd day  area of ischemia predict
pancreatic necrosis
BALTHAZAR CT severity index(CTSI)-1994

Mild (0-3)
moderate (4-
6)
severe (7-10)

CT Severity Inflammation score + Necrosis score

Index
Magnetic Resonant
Cholangiopancreatography

 INDICATION:
◦ diagnosis of suspected biliary and pancreatic duct
obstruction in the setting of pancreatitis.
◦ Repeated attacks of idiopathic acute pancreatitis
(Microlithiasis)
Endoscopic Ultrasonography
 INDICATIONS

◦ Repeated idiopathic acute pancreatitis*

 occult biliary disease- small stones/sludge
 secretin-stimulated EUS study may reveal
resistance to ductal outflow at the level of the
papilla,
 as evidenced by dilatation of the pancreatic duct to a
greater extent and longer duration than in a healthy
population

◦ Age >40 to exclude malignancy

 especially those with prolong or recurrent course
 RATIONALE: 5 % CA pancreas present as AP
Endoscopic Retrograde
Cholangiopancreatography
INDICATION
 Severe gallstone AP or AP with concurrent acute
cholangitis/biliary obstruction/ biliary sepsis/jaundice (due to
persistent stone)
 ERCP within 24(-72) h of admission
 Sphincterotomy /stent and bile duct clearance
 It reduces infective complications/mortality

NOT INDICATED
 Not needed early in most patients with gallstone pancreatitis
who lack laboratory or clinical evidence of ongoing biliary
obstruction

◦ As most of gallstones causing AP readily pass to duodenum and are

lost in stool

◦ MRCP or EUS recommended if CBD stone still suspected

 as risk of post-ERCP pancreatitis is greater with normal calibre bile duct and
normal bilirubin
 MRCP /EUS as accurate as diagnostic ERCP
 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

Although amylase/lipase are used in
diagnosing pancreatitis, they are NOT
use for predicting severity of disease
____________________________
◦ i.e. patient with normal amylase(raised in
90 % cases) levels may still have severe
acute pancreatitis
 RANSON SCORE-1974
(for alcohol pancreatitis)
ON ADMISSION AFTER 48 HOURS

 Age > 55 yrs  BUN rise >5 mg/dL

 WBC > 16,000/mm3  Pa02 < 60 mmHg ( 8 KPa)

 BSR > 200 mg/dL  Serum Calcium < 8 mg/dL

 AST > 250 IU/L  Base deficit > 4 meq/L

 Fluid Sequestration > 6000 mL

 LDH > 350 IU/L

 Hct fall > 10 %

NOTE: Disease classified as SEVERE when 3 or more factors are

 Revised RANSON SCORE-1979
(for Gallstone pancreatitis)
ON ADMISSION AFTER 48 HOURS

 Age > 70 years  BUN rise >5 mg/dL

 WBC > 18,000/mm3  Pa02 < 60 mmHg ( 8 KPa)

 BSR > 220 mg/dL  Serum Calcium < 8 mg/dL

 AST> 250 IU/L  Base deficit > 5 meq/L

 Fluid Sequestration > 4000 ml

 LDH >400 IU/L

 Hct fall > 10 %

NOTE: Disease classified as SEVERE when 3 or more factors are present
RANSON SCORE

Ranson Mortality rate SEVERITY Interpretation

score
0-2 0-2 % Mild Admit in regular ward
3-5 10-20 % Moderate Admit in ICU/HDU
6-7 40 % Associated with more
Severe systemic complications
>7 >50 % Same as above
APACHE Scoring System
 Immediate assessment of the severity
of pancreatitis possible

 Unlike ALL pancreatic specific scoring systems,

APACHE includes clinical features of patient
besides laboratory values

 (Clinical findings are more important than lab

findings in predicting SIRS,sepsis and other
complications)
DEMERITS OF AP-specific scoring
systems(ACG 2013)

 No single laboratory test is accurate to predict

severity in patients with AP.
◦ Even the acute-phase reactant CRP, the most
widely studied inflammatory marker in AP, is not
practical as it takes 72h to become accurate.
 CT and/or MRI imaging also cannot
determine severity early in the course of AP,
as necrosis usually is not present on
admission and may develop after 24 – 48 h.
_________________________________________
Thus, in the absence of any available test to
determine severity, close examination to
assess early fluid losses, hypovolemic shock,
and symptoms suggestive of organ dysfunction
is crucial.
Mild Acute Pancreatitis
 mild and self-limiting, needing only brief hospitalization.

 Rehydration by IV fluids

 Frequent non-invasive observation/monitoring

 Brief period of fasting till pain/vomiting settles

◦ Little physiological justification for prolonged NPO

 No medication required other than analgesics(important) and

anti-emetics
◦ Antibiotics not indicated in absence of signs or documented sources of
infection
◦ Pain results in ongoing cholinergic discharge, stimulating gastric and
pancreatic secretions
◦ Avoid Morphine-cause sphincter of Oddi spasm

 Metabolic support
◦ Correction of electrolyte imbalance
Modified WHO analgesic
Ladder
No or little role of………………..
 Nasogastric suction

 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
Severe Acute Pancreatitis
 P:  R
◦ Pain relief ◦ Rehydration by IV fluids,plasma,blood
◦ Ranitidine(for stress ulcer)
◦ Proton pump inhibitors-
omeprazole ◦ Radiology: CT scan, USG
◦ Resuscitation when required
◦ Peritoneal lavage
 E
◦ Endotracheal intubation
 A ◦ Electrolytes management
◦ Admit in HDU/ICU ◦ ERCP
 A
◦ Antibiotics
◦ Antacids
 S
 N ◦ Swan-Ganz catheter for CVP and
TPN
◦ Nasogastric intubation(if
◦ Suction-in case of aspiration
vomiting)
◦ Steroids in case of ARDS
◦ Nasal oxygen ◦ Supportive therapy for organ failure
◦ Nutrition support  Inotropes
 Hemofiltration
 C  Ventilator(PEEP)

◦ Calcium gluconate
 CLINICAL INVESTIGATIONS

 Vitals  Baselines

 UOP  Serial ABGs

 CV pressure  Serial BSR

 Serum
calcium/magnesium

Monitoring
ACG 2013 Recommendations

 Despite dozens of randomized trials,

no medication has been shown to be
effective in treating AP.

 However,an effective intervention

has been well described: EARLY
AGRESSIVE IV hydration.
Rationale for EARLY AGRESSIVE IV hydration

 Frequent hypovolemia due to

◦ vomiting,
◦ reduced oral intake,
◦ third spacing of fluids(increased vascular permeability)
◦ increased respiratory losses, and
◦ diaphoresis.

 Combination of microangiopathic effects and edema of the

inflamed pancreas decreases blood flow, leading to increased
cellular death, necrosis, and ongoing release of pancreatic
enzymes activating numerous cascades.

_____________________________________________________
____
*provides micro- and macrocirculatory support to prevent serious
complications such as pancreatic necrosis
 EARLY AGRESSIVE IV hydration
Lactated Ringer ’s solution may be the preferred isotonic
Kon crystalloid replacement fluid
sa? • Ringer lactate is better electrolyte balance and more pH-
balanced
• Normal saline given in large volumes may lead to the
development of a non-anion gap, hyperchloremic
metabolic acidosis and increased chances of SIRS
• Low pH activates the trypsinogen, makes the acinar cells
more susceptible to injury and increases the severity of
established AP
Early aggressive IV hydration is most beneficial during the first 12 –
Kab? 24 h, and may have little benefit beyond this time period
Aggressive hydration, defined as 250 – 500 ml per hour of isotonic
Kitna? crystalloid solution should be provided to all patients, unless
cardiovascular, renal, or other related comorbid factors exist.
• In a patient with severe volume depletion, manifest as
hypotension and tachycardia, more rapid repletion (bolus) may
be needed

• Fluid requirements should be reassessed at frequent intervals

EARLY AGRESSIVE IV hydration

◦ Hematocrit and BUN has been widely recommended

as surrogate markers for successful hydration
 No absolute numbers recommended
 Goal to decrease Hct and BUN and maintain normal cret

◦ In elderly and cardiac/renal comorbidities hydration

is monitored by
 Central venous pressure via CV line or
 Intrathoracic blood volume index
 Better/more accurate correlate with cardiac index than CVP
 Antibiotics
 Routine use* NOT recommended(ACG 2013) as
◦ Prophylaxis in severe AP
◦ Preventive measure in sterile necrosis to prevent
development of infected necrosis

 Indicated in
◦ Established infected pancreatic necrosis or
◦ Extraperitoneal infections
 Cholangitis, catheter-acquired infections, bacteremia, UTIs,
pneumonia

_________________________________________
_____
*Routine use of antifungal agents along with prophylactic or therapeutic antibiotics
NOT recommended(ACG 2013)
Antibiotics
 As SIRS may be indistinguishable from
sepsis syndrome, so if infection is
suspected, antibiotics should be given
while source of infection is being
investigated
◦ Once blood and other cultures are found
negative, antibiotics should be discontinued

 Few antibiotics penetrate due to

consistency of pancreatic necrosis
◦ cefuroxime, or imipenem, or ciprofloxacin
plus metronidazole
 Antibiotics
 Use of probiotics is associated with increased
mortality in severe AP

 Selective decontamination of bowel, targeting both

bacteria and fungi, in order to prevent infected
necrosis
◦ Controversial

 Relatively stable patients with infected necrosis

can be managed conservatively on antibiotics
without needing surgery(necrosectomy) or
intervention (percutaneous or endoscopic
drainage)
◦ Surgical debridement recommended if no response to
conservative treatment or deteriorates clinically
Rather than preventing infection, the role of antibiotics in patients
with necrotizing AP is NOW to treat established infected
necrosis …………………………………
………………….
 Nutrition
 In mild AP
◦ oral feedings can be started immediately if there is no
nausea/vomiting, and the abdominal pain/tenderness/Ileus
has resolved(amylase return to normal, patient feel hunger)

◦ Initiation of feeding with a small and slowly increasing low-fat

(low-protein) soft diet appears as safe as a clear liquid diet,
providing more calories
 Stepwise manner increase from clear liquids to soft diet NOT necessary

 In severe AP
◦ Enteral route is recommended to prevent infectious
complications

◦ Parenteral nutrition should be avoided, unless enteral route is

RATIONALE OF EARLY ENTERAL
NUTRITION
 The need to place pancreas at rest until complete
resolution of AP no longer seem imperative
◦ Bowel rest associated with intestinal mucosal atrophy
and bacterial translocation from gut and increased
infectious complications

 Early enteral feeding maintains the gut mucosal

barrier, prevents disruption, and prevents
translocation of bacteria that seed pancreatic
necrosis
◦ Decrease in infectious complications, organ failure and
mortality
 RATIONALE MANAGEMENT

PREVENTION OF STERILE NECROSIS Early aggressive IV hydration

PREVENTION OF INFECTED Early enteral feeding( NOT antibiotics)

NECCROSIS
TREATMENT OF INFECTED Antibiotics, drainage, necrosectomy
NECROSIS

………………………………
Rather than using antibiotics to prevent infected necrosis………….start early
………………..
enteral feeding to prevent translocation of bacteria
 Route of enteral Nutrition
 Traditionally nasojejunal route has been
preferred to avoid the gastric phase of
stimulation BUT
◦ Nasogastric route appears comparable in efficacy
andOFsafety
MERITS NASOGASTRIC ROUTE DEMERITS OF NASOGASTRIC ROUTE

NG tube placement is far easier than Slight increased risk of aspiration

nasojejunal tube placement( requiring
interventional radiology or endoscopy, thus (Can be overcome by placing patient in
expensive) especially in HDU/ICU setting upright position and be placed on
aspiration precautions)
 Role of Surgery in AP
 In case of mild gallstone AP, cholecystectomy should be performed before
discharge to prevent a recurrence of AP
◦ Within 48-72 hour od admission or briefly delay intervention(after 72 hrs but during
same admission
◦ Along with intraoperative cholangiography and any remaining CBD stones can be dealt
with intra/post operative ERCP or
◦ Along with preoperative EUS or MRCP

 In case of necrotizing biliary AP, in order to prevent infection,

cholecystectomy is to be deferred until active inflammation subsides and
fluid collections resolve or stabilize

 Cholecysectomy done for recurrent AP (IAP) with no stones/sludge on USG

and no significant elevation of LFTs is associated with >50 % recurrence of
AP
_________________________________________________________
If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone may
be effective to reduce further attacks of AP
 Sterile necrosis infected necrosis
Asymptomatic doesnot mandate surgical, radiologic, and/or Stable
intervention regardless of endoscopic drainage should
size, location and be delayed preferably for
extension more than 4 weeks
• to allow liquefaction of
the contents and the
development of a
fibrous wall around the
necrosis
• Initially treated with
antibiotics
Symptomatic minimally invasive Urgent debridement unstable
(associated methods of
with GOO or necrosectomy are
bile preferred to open
obstruction) necrosectomy

Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach),

percutaneous radiologic catheter drainage or debridement, video-assisted or small
incision-based left retroperitoneal debridement, and endoscopy
 When to Discharge

 Pain is well controlled with oral analgesia

 Able to tolerate an oral diet that maintains their caloric needs, and
 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
 Recurrent AP
• If neoplasia or chronic pancreatitis is found
• addressed and treated accordingly.
CT scan

• shows developmental abnormalities, strictures, or evidence of chronic pancreatitis

• endoscopic or surgical treatment may be of benefit in a subset of patients
MRCP

• Microlithiasis/biliary sludge Cholecystectomy

EUS • Periammpullary mass missed on CT or MRCP

Genetic • cationic trypsinogen mutations, SPINK1 mutations, or CFTR mutations

• sphincter of Oddi manometry

ERCP • Placed last because very high rate of post-ERCP pancreatitis(benefits< risk)
Prognosis
TYPE OF AP MORTALITY
Overall 10-15 %
(Biliary>alcholic)
Mild Acute Pancreatitis(80 % 1%
cases)
Severe Acute Pancreatitis(20 % Severe  20-50 %
cases) <1 week 1/3 cases MOF
>1 week 2/3 cases Sepsis
(+MOF)
 SYSTEMIC
COMPLICATIONS
 CARDIOVASCULAR
◦ Shock- hypovolemic and septic
◦ Arrhythmias/pericardial effusion/sudden death
◦ ST-T nonspecific changes

 Pulmonary
◦ Respiratory failure/pneumonia/atelectasis/pleural effusion
◦ Acute Respiratory Distress Syndrome (ARDS)

 Renal Failure
◦ Oliguria
◦ Azotemia
◦ Renal artery/vein thrombosis

 Hematological
◦ Hemoconcentation
◦ Disseminated Intravascular Coagulopathy (DIC)
 SYSTEMIC

COMPLICATIONS
Metabolic
◦ Hypocalcemia
◦ Hyperglycemia
◦ Hyperlipidemia

 Gastrointestinal
◦ Peptic Ulcer/Erosive gastritis
◦ Ileus
◦ Portal vein or splenic vein thrombosis with varices

 Neurological
◦ Visual disturbances-Sudden blindness(Purtscher’s retinopathy)
◦ Confusion,irritability,psychosis
◦ Fat emboli
◦ Alcohol withdrawal syndrome
◦ Encephalopathy

 Miscellaneous
◦ Subcutaneous fat necrosis
◦ Intra-abdominal saponification
◦ Arthralgia
LOCAL COMPLICATIONS
 Peripancreatic fluid collections

 (Peri)Pancreatic necrosis( sterile + infected)

 Pancreatic abscess(Phlegmon)

 Pseudocyst

 Pancreatic ascites

 Pseudoaneurysm

 Involvement of adjacent organs, with hemorrhage,

thrombosis, bowel infraction, obstructive jaundice, fistula
formation, or mechanical obstruction
THANK YOU……….