LIVER, PANCREAS AND

BILIARY TRACT PROBLEMS

CASE STUDY
Republic of the Philippines
CAMARINES SUR POLYTECHNIC COLLEGES
Nabua, Camarines Sur
By: ELAINE FRANCES M. ILLO, RM,
GRADUATE SCHOOL
RN
 A 40-year-old white female with a past medical history
of hypertension and bipolar disorder presented with a few
hours of severe sharp epigastric abdominal pain
radiating to the back associated
with nausea and vomiting. The
patient denied any history of
pancreatitis, consuming alcohol,
or illegal drug abuse. No new
medication had recently been
started, and there was no history of abdominal trauma. She
had had a cholecystectomy in 2004.
VITAL SIGNS ON ARRIVAL:

BLOOD PRESSURE 132/84 mmHg

PULSE RATE 105 bpm
RESPIRATORY RATE 24 cpm
TEMPERATURE 36.1 C
PAIN SCALE 9/10 epigastric pain
INITIAL EVALUATION
COMPLETE BLOOD COUNT
Normal Value
WHITE BLOOD CELLS 22,100/mm3 4,500 – 11,000/mm3
NEUTROPHILS 87% 50-70%
LYMPHOCYTES 11% 25-45%
MONOCYTES 6% 4-6%
EOSINOPHILS 2% 1-3%
HEMOGLOBIN 14.0 g/dL 14-16 g/dL
HEMATOCRIT 44.6 % 40-54%
PLATELET 380,000/mm3 150,000 - 350,000/mm3
INITIAL EVALUATION
BASIC METABOLIC PANEL
Normal Value
GLUCOSE 97 mg/dL 80 – 120 mg/dL
BUN 19 mg/dL 7-30 mgg/dL
CREA 1.08 mg/dL 0.7-1.4 mg/dL
Na 138 mEq/L 135-145 mEq/L
K 2.7 mEq/L 3.5-4.5 mEq/L
Cl 107 mEq/L 95-105 mEq/L
AMYLASE 31 IU/L 20-160 IU/L
LIPASE 14 IU/L 8-78 IU/L
INITIAL EVALUATION
URINALYSIS
Normal Value
COLOR Clear Yellow
GLUCOSE Negative Negative
BILIRUBIN Negative Negative
BLOOD Negative Negative
PROTEIN Negative Negative
UROBILINOGEN Negative Negative
NITRITE Negative Negative
KETONES Negative Negative
SP GRAVITY 1.010 1.010
PH 5.0 5-7
HCG Negative Negative
 Since the patient was in severe pain with no clear diagnosis, a
CT scan of her abdomen with intravenous contrast was done in
the emergency room. The CT scan showed fat stranding in the
pancreatic head consistent with pancreatitis and reactive thickening
in the duodenum. The patient was admitted to the floor and kept
nothing by mouth. She was treated with intravenous fluids,
analgesics, potassium supplement, and antiemetics. On the next
morning, repeated measurements of her amylase and lipase were
still within normal limits. We checked her triglyceride level and it
was 53 mg/dL. Her symptoms continued to improve during her
course of hospitalization, and her leukocytosis was resolved
without the use of antibiotics. She was discharged home on day 3.
WHAT IS THE FINAL DIAGNOSIS?
ACUTE PANCREATITIS
- Acute pancreatitis is sudden inflammation of the pancreas that
may be mild or life threatening but usually subsides.
- The pancreas is an organ in the upper
abdomen that produces digestive fluids and the
hormone insulin. The part of the pancreas that
produces hormones, especially insulin, tends not to
be affected by acute pancreatitis.
- In acute pancreatitis, inflammation develops
quickly and subsides within a few days but can last
for to a few weeks. In chronic pancreatitis, the
pancreas is persistently inflamed, which causes
permanent damage, (Michael Bartel, 2019)
CLASSIFICATION
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 +/- • Ranson score > 3

• Organ failure defined as • Or APACHE > 8
 SBP < 90 mmHg
 PaO2 < 60 mmHg
 GI bleed > 500 ml/24 hrs
 Cret > mg/dL after
rehydration
 Two
phases
Early Late
1st week After 1st week

Severity Mild Moderate Severe

No organ failure Organ failure less Organ failure longer
than 48 hours than 48 hours

Two
types Oedematous Necrotizing
< 4 wk: acute peripancreatic collection < 4 wk: acute necrotic collection
Complications
> 4 wk: pseudocyst > 4 wk: walled-off necrosis
ETIOLOGY
According to Ahmed, 2019 the etiologic factors of acute pancreatitis includes:
METABOLIC VASCULAR
 Alcoholism
 Shock
 Cigarette smoking  Atheroembolism
 Azotemia
 Vasculitis (Polyarteritis nodosa, SLE)
 Porphyries
 Malnutrition
GENETIC
 Hyperlipoproteinemia
 Hypercalcemia  Mutations in the cationic trypsinogen
 Drugs (e.g. azathioprine, angiotensin- (PRSSI) and trypsin inhibitor (SPINK
I) genes
converting enzyme (ACE)
inhibitors, azathioprine, furosemide, 6-
mercaptopurine, pentamidine, sulfa drugs,
and valproate)
MECHANICAL SOME CAUSES OF ACUTE PANCREATITIS
according to Odeh, 2016
 Gallstones
 Trauma  Estrogen use in women with high levels of
 Iatrogenic injury (ERCP) lipids in the blood
 Hereditary pancreatitis, including a small
 Pancreatic CA
percentage of people with cystic fibrosis or
 Perioperative injury
cystic fibrosis genes
 Endoscopic Procedures with dye  Kidney transplantation
injection  Pregnancy (rare)
 Tropical pancreatitis
INFECTIOUS
 Estrogen use in women with high levels of
 Mumps lipids in the blood
 Coxsackievirus
 Cytomegalovirus
 Scorpion Bite
 Snake Bite
 Ascares
EPIDEMIOLOGY
• United States statistics
Acute pancreatitis has an approximate incidence of 40-50 cases per year per
100,000 adults, Dhiraj Yadav, et. al, 2013.

• International statistics
Worldwide, the incidence of acute pancreatitis ranges between 5 and 80 per
100,000 population, with the highest incidence recorded in the United States and
Finland.  In Luneburg, Germany, the incidence is 17.5 cases per 100,000 people.
In Finland, the incidence is 73.4 cases per 100,000 people. Similar incidence
rates have been reported in Australia. The incidence of disease outside North
America, Europe, and Australia is less well known. In Europe and other
developed nations, such as Hong Kong, more patients tend to have gallstone
pancreatitis, whereas in the United States, alcoholic pancreatitis is most
common, and in the Philippines, 25,365 of the estimated population of
84,241,697, (Odeh, 2016).
MEDIAN AGES OF ONSET FOR VARIOUS ETIOLOGIES

Etiology Median 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
• Sex-related demographics
Generally - M>F
In males - more often related to alcohol
In females - more often related to biliary tract disease

• Race-related demographics
times higher for blacks than whites
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS
ABDOMINAL PAIN – Cardinal Symptoms
• SITE: usually experienced first in the epigastrium but maybe localized to ether 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 chest or flanks
• RELIEVING FACTOR: sitting or leaning/stooping forward (Muslims PRAYER SIGN)
due to shifting forward of abdominal contents taking pressure off from 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 -Y 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

ABDOMINAL 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
DIAGNOSTICS
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 hours after
hospital admission (e.g., persistent pain, fever, nausea, unable to begin
oral feeding)
– to evaluate complications
HEMATOLOGICAL WORKUPS
• BASELINES
– CBC.
• Low Hb: prolonged
hemetemesis/melena, internal
hemorrhage
• Leucocytosis non infectious
inflammation
• Low platelets – Disseminated
Intravascular Coagulation
• 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:
• Low protein/ albumin
HEMATOLOGICAL WORKUPS
• ABG’s
Acid – Base Disturbance Etiology
Metabolic (Lactic) acidosis with high anion gap Hypovolemic shock
Hypokalemic Hypochloremic
metabolic alkalosis persistent vomiting

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 Il antibody, and rheumatoid factor (RF),
HEMATOLOGICAL WORKUPS
• Pancreatic Enzymes' Assays
Raised Amylase - may not AP
– Serum Amylase: Normal Amylase - may be AP
• ONSET: almost immediately
• PEAK: within several hours
– 3-4 times upper limitof 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 Lipase: SERUM INDICATOR OF HIGHEST

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
HEMATOLOGICAL WORKUPS

• 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
 Small bowel Obstruction
• strangulation ileus
OTHERS
• mesenteric ischemia
 Acute appendicitis  Parotitis (Mumps)
 Cholecystitis  Macroamylasaemia
 Perforated Duodenal Ulcer  Opioids administration
 Gastroenteritis  Low GFR
 Biliary peritonitis  Brain injury (CVA)- hyperstimulation
 Spasm of sphincter of Oddi of pancreas
GYNE

 Ruptured Ectopic pregnancy

 Torsion of an ovarian cyst
Transcutaneous Abdominal Ultrasonography
• Not diagnostic
• Should be performed within 24 hours in al/ 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.
ABDOMINAL RADIOGRAPHY
Abdominal radiographs have a
limited role in acute pancreatitis.
Kidneys-ureters-bladder (KUB)
radiography with the patient in the
upright position is primarily performed to
detect free air in the abdomen, indicating
a perforated viscus, as would be the case
in a penetrating, perforated duodenal
ulcer. In some cases, the inflammatory
process may damage peripancreatic
structures, resulting in a colon cut-off
sign, a sentinel loop, or an ileus. The
presence of calcifications within or
around the pancreas may indicate chronic
pancreatitis, (Jeffrey C F Tang, 2019).
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
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.
• INDICATIONS
– 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
– Initial assessment of prognosis (CT severity index).
• Perfusion CT at 3rd day area of ischemia predict pancreatic necrosis
BALTHAZAR CT SEVERITY INDEX
Mild (0-3)
Moderate (4 – 6)
Severe (7 – 10)
Prognostic Indicator Points
Pancreatic Inflammation
Normal Pancreas 0
Focal or diffuse enlargement of the pancreas 1
Intrinsic pancreatic abnormalities with inflammatory changes in peripancreatic fat 2
Single, ill-defined fluid collections or presence of gas in or adjacent to the pancreas 3
Two or more poorly defined collections or presence of gas in or adjacent to the 4
pancreas
Pancreatic necrosis
None 0
< 30% 2
> 30 – 50 % 4
> 50% 6
MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY (MRCP)
• INDICATION:
– diagnosis of suspected biliary and pancreatic duct obstruction in the setting of pancreatitis.
– Repeated attacks of idiopathic acute pancreatitis (Microlithiasis)

ENDOSCOPIC RETROGRADE CHOLANGIOEANCREATOGRAPHY

• INDICATION:
- cholangltis/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/moflality
• NOT INDICATED
- Not needed early in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of
ongoing biliary obstruction

o As most Of gallstones causing AP readily pass to duodenum and are lost in stool
o MRCP or EUS recommended if CBD stone still suspected
- as risk of post-ERCP pancreatitis is greater with normal calibre bile duct normal bilirubin
- MRCP /EIJS as accurate as diagnostic ERCP
SEVERITY SCORING SYSTEMS
ACUTE PANCREATITIS SPECIFIC SCORING SYSTEMS
• Ranson score
• Glagsow score
• Bedside Index for Severity in Acute Pancreatitis(BlSAP) 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) Il score
• Sequential Organ Failure Assessment(SOFA) score
RANSON SCORE
(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
LDH > 350 IU/L Fluid Sequestration >6000 mL
Hct fall >100%

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

REVISED RANSON SCORE
(FOR GALLSTONE PANCREATITIS)

ON ADMISSION AFTER 48 HOURS

Age > 70 yrs 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
LDH > 400 IU/L Fluid Sequestration > 4000 mL
Hct fall >10%

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

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 sons or sources of infection
• Pain results in ongoing cholinergic discharge, stimulating gastric and
pancreatic secretions
• Avoid Morphine-cause sphincter of Odd spasm
– Metabolic support
• Correction of electrolyte imbalance
• Nasogastric suction
• H2 blockers
• Secretion-inhibiting drugs
• Atropine, calcitonin, somatostatin and its
analogue(Octreotide)
• glucagon and fluorouracil
• Protease inhibiting drugs
• Aprotinin, aabexate mesylate,camostate, phospholipase A2
inhibitors, FFP
• Indomethacin or PG inhibitors
SEVERE ACUTE PANCREATITIS
P: A:
 Pain relief  Admit in HDU/ICU
 Proton pump inhibitors – omeprazole  Antibiotics
 Peritoneal lavage C:
N:  Calcium Gluconate
 Nasogastric intubation (if vomiting) E:
 Nasal oxygen  Endotracheal intubation
 Nutrition Support  Electrolytes management
R:  ERCP
 Rehydration by IV fluids, plasma, S:
blood  Swan-Ganz Catheter for CVP and TPN
 Ranitidine (for stress ulcer)  Suction-in case of aspiration
 Radiology: CT Scan, USG)  Steroids in case of ARDS
 Resuscitation when required)
A:  Supportive therapy for organ failure
 Inotropes
 Antacids  Hemofiltration
 Ventilator (PEEP)
EARLY AGRESSIVE IV HYDRATION
Lactated Ringer 's solution may be the preferred isotonic
crystalloid replacement fluid
– 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— 24 hours, and may have little benefit beyond this time period
EARLY AGRESSIVE IV HYDRATION
Aggressive hydration, defined as 250 — 500 ml per
hour of isotonic 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
within 6 hours of admission and for the next 24 - 48 hrs
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
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
ANTIBIOTICS
•Routine use* NOT recommended 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, UTI's,
pneumonia

Routine use of antifungal agents along with prophylactic or therapeutic antibiotics

NOT recommended
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

– Rather than preventing infection, the role of antibiotics in

patients with necrotizing AP is NOW to treat established
infected necrosis
NUTRITION
MILD AP
• OraI 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
SEVERE
AP – Enteral route is recommended to prevent infectious complications

• Parenteral nutrition should be avoided, unless enteral route is not

available not tolerated or not meeting calorie
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)

NECROSIS

TREATMENT OF INFECTED NECROSIS Antibiotics, drainage, necrosectomy

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

MERITS OF NASOGASTRIC DEMERITS OF NASOGASTRIC

ROUTE ROUTE
NG tube placement is far easier Slight increased risk Of
than nasojejunal tube aspiration (Can be overcome by
placement( requiring interventional placing patient in upright position and
radiology or endoscopy, thus be placed on aspiration precautions)
expensive) especially in HDU/ICU
setting
ENDOSCOPIC RETROGRADE
CHOLANGIOPANCREATOGRAPHY
• Soon after a person is admitted to the hospital with suspected narrowing of
the pancreatic duct or bile ducts, a physician with specialized training
performs ERCP.
• After lightly sedating the patient and giving medication to numb the throat,
the doctor inserts an endoscope-a long, flexible, lighted tube with a camera-
through the mouth, throat, and stomach into the small intestine. The
endoscope is connected to a computer and screen. The doctor guides the
endoscope and injects a special dye into the pancreatic or bile ducts that
helps the pancreas, gallbladder, and bile ducts appear on the screen while x
rays are taken.
The following procedures can be performed
using ERCP:
Sphincterotomy
  Using a small wire on the endoscope, the doctor finds the muscle that
surrounds the pancreatic duct or bile ducts and makes a tiny cut to enlarge the
duct opening. When a pseudocyst is present, the duct is drained.
Gallstone removal
The endoscope is used to remove pancreatic or bile duct stones with a
tiny basket. Gallstone removal is sometimes performed along with a
sphincterotomy.
Stent placement
Using the endoscope, the doctor places a tiny piece of plastic or metal
that looks like a straw in a narrowed pancreatic or bile duct to keep it open.
The following procedures can be performed
using ERCP:

Balloon dilatation
  Some endoscopes have a small balloon that the doctor uses to dilate, or
stretch, a narrowed pancreatic or bile duct. A temporary stent may be placed for
a few months to keep the duct open.

People who undergo therapeutic ERCP are at slight risk for complications, including severe
pancreatitis, infection, bowel perforation, or bleeding. Complications of ERCP are more common
in people with acute or recurrent pancreatitis. A patient who experiences fever, trouble
swallowing, or increased throat, chest, or abdominal pain after the procedure should notify a
doctor immediately.
SURGICAL MANAGEMENT
In case of mild gallstone AP, cholecystectomy should be performed before
discharge to prevent a recurrence of AP
• Within 48-72 hour admission or briefly delay hrs. but during same admission
• Along with intraoperative cholangiography and any remaining CBD stones can be dealt with
Intra/postoperative ERCP or
• Along with preoperative ELIS 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

Cholecystectomy 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 Does not mandate
Surgical, radiologic and/or Stable
intervention regardless of
endoscopic drainage should be
size, location and
delayed preferably for more than
extension 4 weeks
• To allow liquefaction of the
contents and the development
of a fibrous wall around the
necrosis
• Initially treated with antibiotics
Symptomatics Minimally invasive • Urgent debridement unstable
(associated with methods of necrosectomy
GOO or bile are 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
CT • If neoplasia or chronic pancreatitis is found addressed and treated accordingly
Scan
• Shows developmental abnormalities, strictures, or evidence of chronic pancreatitis
MRCP endoscopic or surgical treatment may be of benefit in a subset of patients

• Microlithiasis/biliary sludge – Cholecystectomy

EUS • Periampullary mass missed on CT or MRCP

• Cationic trysinogen mutations, SPINK 1 mutations, or CFTR mutations

Genetic

• Sphincter of Oddi manometry

ERC • Placed last because very high rate of post-ERCP pancreatitis (benefits <risk)
P
PROGNOSIS
TYPE OF AP MORTALITY
Overall 10 – 15 % (Biliary > Alcoholic

Mild Acute 1%
Pancreatitis (80%
cases)
Severe Acute Severe  20 – 50 %
Pancreatitis (20% < 1 week 1/3 Cases Multiple Organ
Failure
cases)
> 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 HEMOTOLOGICAL

 Oliguria  Hemoconcentration
 Azotemia  Disseminated intravascular Coagulopathy (DIC)
 Renal Artery/ vein thrombosis
SYSTEMIC COMPLICATIONS
METABOLIC NEUROLOGICAL
 Hypocalcemia  Visual disturbances-Sudden blindness
 Hyperglycemia (purtscher's retinopathy)
 Hyperlipidemia  Confusion, irritability psychosis
 Fat emboli
GASTROINTESTINAL  Alcohol withdrawal syndrome

 Peptic Ulcer/Erosive gastritis  Encephalopathy

 Ileus MISCELLANEOUS
 Portal vein or splenic vein thrombosis  Subcutaneous fat necrosis
with varices
 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.