Management Protocol for Acute Pancreatitis

St. Paul’s Hospital Millennium Medical College

Department of Surgery
Maheteme Bekele, MD, Assistant professor of surgery,Girmaye Tamirat, MD,
Assistant Professor of Surgery& Kirubel Abebe, General surgery Resident

Background

In our Hospital (SPHMMC) health professionals manage acute pancreatitis in different

ways based on different recommendations. This management protocol is intended to
have uniform, easy & possibly high quality care for patients with acute pancreatitis.

The protocol is developed under the auspices of SPHMMC department of surgery. It

includes fluid resuscitation, Nutritional support, use of antibiotics, pain management,
treatment of infected pancreatic necrosis, treatment of sterile pancreatic necrosis,
treatment of associated conditions& Follow up.

This protocol will be revised whenever appropriate evidence based considerations

become available.

Introduction

Acute pancreatitis is an inflammatory condition of the pancreas characterized clinically

by abdominal pain and elevated levels of pancreatic enzymes in the blood.[1]

The reported annual incidence of acute pancreatitis has ranged from 4.9 to 35 per
100,000 populations(1). The incidence & prevalence of acute pancreatitis in Ethiopia is
not well studied.

Common causes of acute pancreatitis[1]

 Gall stone -20%-40%
 Alcohol- 30%
 Idiopathic-20%

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SPHMMC Department of surgery
 Table 1-Etiology of acute pancreatitis[1]
Mechanical Gallstones, biliary sludge, ascariasis,
periampullary diverticulum, pancreatic or
periampullary cancer, ampullary stenosis,
duodenal stricture or obstruction
Toxic Ethanol, methanol, scorpion venom,
organophosphate poisoning
Metabolic Hyperlipidemia (types I, IV, V), hypercalcemia
Drugs Didanosine, pentamidine, metronidazole,
stibogluconate, tetracycline furosemide,
thiazides, sulphasalazine, 5-ASA, L-
asparaginase, azathioprine, valproic acid,
sulindac, salicylates, calcium, estrogen
Infection Viruses-mumps, coxsackie, hepatitis B, CMV,
varicella-zoster, HSV, HIV
Bacteria-mycoplasma, Legionella, Leptospira,
salmonella
Fungi-aspergillus
Parasites-toxoplasma, cryptosporidium,
Ascaris

Trauma Blunt or penetrating abdominal injury,

iatrogenic injury during surgery or ERCP
(sphincterotomy)
Congenital Cholodochocele type V, pancreas divisum
Vascular Ischemia, atheroembolism, vasculitis
(polyarteritis nodosa, SLE)
Miscellaneous Post ERCP, pregnancy, renal transplantation,
alpha-1-antitrypsin deficiency
Genetic CFTR and other genetic mutations

In general thePathophysiology of acute pancreatitis is generally considered in three

phases[2]

In the first phase, there is premature activation of trypsin within pancreatic acinar cells.
A variety of mechanisms have been proposed including disruption of calcium
signaling in acinar cells, cleavage of trypsinogen to trypsin by the lysosomal hydrolase
cathepsin-B, and decreased activity of the intracellular pancreatic trypsin inhibitor.

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Once trypsin is activated, it activates a variety of injurious pancreatic digestive enzyme
[2].

In the second phase, there is intrapancreatic inflammation through a variety of

mechanisms and pathways [2]

In the third phase, there is extrapancreatic inflammation including acute respiratory

syndrome (ARDS) .In both phases, there are four important steps mediated by
cytokines and other inflammatory mediators: [2]

1) Activation ofinflammatory cells

2) Chemoattraction of activated inflammatory cells to the microcirculation
3) Activation of adhesion molecules allowing the binding of inflammatory cells
to the endothelium
4) Migration of activated inflammatory cells into areas of inflammation

In the majority of patients, acute pancreatitis is mild. In 10–20%, the various pathways
that contribute to increased intrapancreatic and extrapancreatic inflammation result in
what is generally termed systemic inflammatory response syndrome (SIRS) [2]

SIRS predisposes to multiple organ dysfunction and/or pancreatic necrosis. The

factors that determine severity are not clearly understood, but appear to involve a
balance between proinflammatory and anti-inflammatory factors. Recent evidence
suggests that the balance may be tipped in favor of proinflammatory factors by
genetic polymorphisms of inflammatory mediators that increase severity of acute
pancreatitis. [2]

Table 2-Systemic inflammatory response syndrome (SIRS)-two or more of the

following[3]
Temperature >38.3ºC or <36ºC
Heart rate >90 beats/min
Respiratory rate >20 breaths/min or PaCO2 <32 mmHg
WBC >12,000 cells/mm3, <4000 cells/mm3, or >10 percent immature (band) forms

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Hypovolemia is another important feature in the course of acute pancreatitis which is
caused by [2]
 Third space losses
 Vomiting
 Diaphoresis
 Greater vascular permeability caused by inflammatory mediators
Intravascular volume depletion
 Compromises the microcirculation of the pancreas and is a major contributor
to the development of necrotizing pancreatitis. [2]
 Leads to hemoconcentration (hematocrit ≥44), tachycardia, hypotension,
scanty urine output, and prerenal azotemia. [2]
 Leads to intestinal ischemia which increases intestinal permeability to bacteria,
products of bacteria, and endotoxins which results in secondary pancreatic
infection & stimulation of cytokine release and increases in nitric oxide that
contribute both to ongoing pancreatic injury and also to organ failure
(particularly respiratory failure) [2]
Two factors have been suggested as the possible initiating event in gallstone
pancreatitis: [4]
 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 which leads to premature activation of trypsin
Alcohol-induced pancreatitis — several mechanisms have been proposed: [4]
 Sensitization of acinar cells to CCK-induced premature activation of zymogens
 Potentiation of the effect of CCK on the activation of transcription factors,
nuclear factor kB, and activating protein-1
 Generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters
 Activation of pancreatic stellate cells by acetaldehyde and oxidative stress and
subsequent increased production of collagen and other matrix proteins

Differential Diagnosis
To Diagnose Clinical, biochemical, and radiologic features need to be considered
together [1, 2, 7,8 ]
The diagnosis of acute pancreatitis requires two of the following three features: [2]
1) Characteristic abdominal pain
2) Serum amylase and/or lipase≥3 times the upper limit of normal
3) Characteristic findings of acute pancreatitis on CT scan

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History
Abdominal pain [1, 7, 8]
 The pain israpid onset but not as abrupt as that with a perforated viscus,
reaching maximum intensity in many cases within 10 to 20 minutes.
 Site- upper abdominal pain (mid-epigastrium, right upper quadrant), diffuse,
or, infrequently, confined to the left side
 Band-like radiation to the back(suggests a pancreatic origin)
 If related to alcohol frequently occurs one to three days after a binge or
cessation of drinking
 Associated with- Nausea and vomiting, Restlessness & agitation (90%)
 Relief on bending forward
History of drug intake
Family History

Physical findings
Depends upon the severity [1, 7, 8]
 Systemic features include fever, tachycardia, shock and coma
 Obstruction of the common bile duct- jaundice
 Respirations may be shallow
o Diaphragmatic irritation
o Pleural effusion
 Abdominal distention( epigastrium) ,tenderness and guarding,Epigastric mass,
Ecchymosis discoloration in the flank (Grey-Turner's sign) or the periumbilical
region (Cullen's sign)
 Less common - subcutaneous nodular fat necrosis (panniculitis),
thrombophlebitis in the legs, and polyarthritis
 Underlying disorders- hepatomegaly in alcoholic pancreatitis, xanthomas in
hyperlipidemic pancreatitis, and parotid swelling associated with mumps

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Possible Deferential Diagnoses are shown below (Figure 1)

Figure 1- Common differential diagnoses for AP [1, 7, 8]

Investigations

The following investigations should be ordered for patients with acute pancreatitis [1,
2, 7, 8, 9}

Table 3–Investigations for acute pancreatitis

Laboratory Tests* Mandatory  Serum Amylase & Lipase
 CBC
 Blood glucose level
 Cr. & BUN
 AST,ALT,ALP & bilirubin (Total & Indirect)
 Serum calcium, potassium, sodium, chlorine
& magnesium
 Serum Triglyceride
 LDH
 Arterial blood gas test (PH & HCO3)
Optional  Coagulation profile
 Autoimmune markers
 Viral antibody titers
 Serum IgG4 levels
 C-reactive protein
 Trypsinogen-activating peptide(TAP)

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 Radiologic Mandatory  Chest X-ray(PA &Erect)
Investigations  Plain abdominal X-ray(PA & erect)
 Abdominal ultrasound
Optional  CT scan**(contrast enhanced)
 MRCP
 ERCP
 ECG
*the lab tests are in order of importance
**CT scan- indicated in patients who are deteriorating or have severe pancreatitis
determined clinically and by APACHE II score & not required on the first day unless
there are other diagnoses are being considered

Treatment

Assessment of severity

About 15-25% of patients with acute pancreatitis develop severe acute pancreatitis
Severe necrotizing pancreatitis is associated with a high rate of complications (local
and systemic) and mortality (approximately 17 percent). SIRS accounts for nearly one-
half of the mortality from severe AP. Local complications from pancreatic necrosis,
such as pseudocysts and abscesses, can occur from 24 hours to up to six weeks
following the onset of AP and account for many of the deaths that occur more than
two weeks after the onset of AP.[2,5,6,7,9]

The International Symposium, held in Atlanta, GA, in 1992, established a clinically

based classification system for acute pancreatitis. [2,10]Two major classifications

 Mild (edematous and interstitial) acute pancreatitis

 Severe (necrotizing) acute pancreatitis

Table 4-Severe Acute Pancreatitis & organ failure as Defined by Atlanta Symposium
[2,10]
Sever acute pancreatitis Organ failure
 A Ranson's score of 3 or more  Shock–systolic pressure <90 mmHg
 An APACHE II score of 8 or more  PaO2 ≤60 mmHg
within the first 48 hours  Creatinine >2.0 mg/L after
 Organ failure rehydration
 Local complications (pancreatic  Gastrointestinal bleeding >500 cc/24
necrosis, abscess, or pseudocyst). h

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NB: There are subgroups with intermediate features and classified as moderately
severe acute pancreatitis. These patients have local complications without organ
failure. The mortality is low as compared to severe acute pancreatitis but have similar
morbidity [6, 10]

Clinical predictors [2, 6, 9,10]

o Older age( 55 to 75 years)

o Alcoholic pancreatitis-increased risk of pancreatic necrosis & intubation
o Short time interval to symptom onset
o Obesity- BMI >30
o Organ failure
o Intra-abdominal pressure (> 15 mm Hg)

Laboratory & Radiologic Predictors [2, 6,9, 10]

o Hemoconcentration-Associated with a milder clinical course

 Normal or low hematocrit at admission and during the first 24 hours
o C-reactive protein
 At 48 hours ( level > 150mg/dl)
o Blood urea nitrogen–Associated with high mortality& local complications
 33 mg/dL or more
 Any increase at 24 hours
o Serum Creatinine –associated with pancreatic necrosis
 Elevated serum Creatinine (greater than 1.8 mg/dL) within the first 48
hours
o Plasma glucose (RBS)
 >190 mg/dL
o CXR-associated with necrosis and organ failure
 Pleural effusion and/or pulmonary infiltrates during the first 24 hours
o CT scan
 Used to look for pancreatic necrosis and extrapancreatic inflammation.
 Intravenous contrast-enhanced CT distinguishes between edematous
and necrotizing pancreatitis
 CT is more accurate than ultrasonography for the diagnosis of severe
pancreatic necrosis
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Table 5- Computed tomography (CT) grading of severity[9]
CT-grade Score
(A) Normal pancreas 0
(B) Oedematous pancreatitis 1
(C) B plus mild extrapancreatic changes 2
(D) Severe extrapancreatic changes 3
including one fluid collection
(E) Multiple or extensive extrapancreatic 4
collections
Necrosis Score
None 0
<One third 2
>One third,<one half 4
>Half 6
CT severity index = CT grade+necrosis Complications
score
0–3 8%
4–6 35%
7–10 92%
Deaths
0–3 3%
4–6 6%
7–10 17%
Modified from the World Association guidelines and based on Balthazar and
colleagues.

Severity scoring system

There are different severity scoring systems such as:[2,6,7,8,9,10]
o Ranson’s score
o APACHE (acute physiology and chronic health examination) II score
o Systemic inflammatory response syndrome score
o BISAP(bedside index of severity in acute pancreatitis) score
o Harmless acute pancreatitis score(HAPS)
o Organ failure-based scores
o CT severity index
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SPHMMC Department of surgery
There is no perfect scoring system. Different institutions prefer different scoring
system depending on the availability of laboratory and radiologic tests. All the above
scoring systems can be used in our hospital. The American college of
gastroenterology & many other colleges’ recommend using the APACHE II score
because it has good negative predictive value and modest positive predictive value
for predicting severe AP and can be performed daily.[2,10]

Ranson’s score [2,6,7,8,9,10]

Consist of 11 parameters
o Five of the factors are assessed at admission
o Sixare assessed during the next 48 hours
Mortality
o Score <3-0 to 3 percent (mild pancreatitis)
o Score ≥3-11 to 15 percent
o Score≥6-40 percent

Table 6- Ranson criteria to predict severity of acute pancreatitis[10]

0 hours
Age >55
White blood cell count >16,000/mm3
Blood glucose >200 mg/dL (11.1 mmol/L)
Lactate dehydrogenase >350 U/L
Aspartate aminotransferase (AST) >250 U/L
48 hours
Hematocrit Fall by ≥10 percent
Blood urea nitrogen Increase by ≥5 mg/dL (1.8 mmol/L)
despite fluids
Serum calcium <8 mg/dL (2 mmol/L)
pO2 <60 mmHg
Base deficit >4 MEq/L
Fluid sequestration >6000 mL

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SPHMMC Department of surgery
APACHE II Score[7,8,10]

o Most widely studied severity scoring system

o Has 12 physiologic measures and extra points based upon age and presence of
chronic disease
o Has good negative predictive value and modest positive predictive value for
predicting severe AP and can be performed daily.
o Decreasing values during the first 48 hours suggest a mild attack, while increasing
values suggest a severe attack
o Mortality
 Score <8 – less than 4 percent
 Score >8-11 to 18 percent

Summary (Recommendation for our hospital)

 For all patient with acute pancreatitis determine severity & prognosis by using
combination of Ranson's score & APACHE II score ( if CT scan is done include
CT severity score)
 At admission the following investigation should be ordered

Table 8-Lab & Radiologic Evaluations at admission

Laboratory tests Radiologic tests
 Serum Amylase & Lipase  Chest X-ray(PA &Erect)
 CBC  Plain abdominal X-ray(PA &
erect)
 Blood glucose level  Abdominal ultrasound
 Cr. & BUN  CT scan (contrast
enhanced)**
 AST,ALT,ALP & bilirubin
(Total & Indirect)
 Serum calcium, potassium,
sodium, chlorine &
magnesium
 Serum Triglyceride
 LDH
 Arterial blood gas test (PH &
HCO3)

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& **indicated in patients who are deteriorating or have severe pancreatitis
determined clinically and by APACHE II score & not required on the first
day unless there are other diagnoses are being considered[2,10]
 Following admission [2,9,10]
o Do CBC(HCT) , RFT (Cr & BUN), LFT (AST,ALP &Bilirubin),serum
electrolyte every 24 hr until adequate resuscitation is obtained
o Repeat Serum amylase & lipase after 48hrs
o Serum glucose level measured per sliding scale protocol
o Other investigations including imaging’s can be done according to
patient’s condition& need

Treatment Components of acute pancreatitis [2,6,7,8,9,10]

Figure 2-Treatment guidelines for acute pancreatitis

SPHMMC Department of surgery

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 1. The initial measure in the treatment of acute pancreatitis is to determine the
severity (See above). If one of the following criteria is met it is considered as
severe pancreatitis[2,6,9,10]
 A Ranson's score of 3 or more
 An APACHE II score of 8 or more within the first 48 hours
 Organ failure
 Local complications (pancreatic necrosis, abscess, or pseudocyst).
o Criteria for ICU care[1,5,9]
 Severe pancreatitis
 Mild pancreatitis which progressed to severe form
 Sustained hypoxemia, hypotension refractory to a bolus of IV fluids, and
possibly renal insufficiency that does not respond to a fluid bolus
Three most important issues initially are pain relief, fluid replacement and nutrition [6].
2. Fluid Replacement- Aggressive IV fluid replacement is of critical importance
tocounteract hypovolemia &in the prevention of systemic
complications[2,6,8,9,10}
There is abundant experimental evidence that early aggressive fluid resuscitation
and improved delivery of oxygen prevent or minimize pancreatic necrosis and
improve survival [2]
o Type of fluid
 Ringer lactate is the preferred fluid[5]
 Use normal saline in the face of hypercalcemia[5]
o Amount to give
 2oml/Kg over 1-2 hrs then 250-300 ml/hr over 48 hrs. (fluid can
be adjusted according to patient condition & responses)[5]
o Response is Assessed by(5)
 Improvement in vital signs
 Urine output (>0.5 ml|Kg|hr)
 Reduction in hematocrit and blood urea nitrogen (BUN)
3. Oxygen supplementation
o Maintain arterial oxygen saturation above 95%[2,5,9]
o If below 95% start supplementation
 Nasal Catheter (2L/min-5L/min) either continuous or intermittently
depending on response
 Facemask from 5L/min-15L/min continuous( if no response with nasal
catheter)
 Mechanical ventilation if there is

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  Persistent or progressive hypoxia
 Respiratory failure
4. Correct electrolyte & Metabolic abnormalities
o Hypocalcium- correct if ionized calcium is low (<4.65mg/dl) or symptomatic
 Calcium gluconate 10% 1 to 2 g in 50 mL of 5 percent dextrose
infused over 10 to 20 minutes then 11g in 1000ml of normal saline or 5
percent dextrose water over 24 hr [11]
o Hypercalcemia
o Serum glucose level should be controlled with sliding scale insulin(follow the
hospital recommendation)[2,5,9]
5. Pain Management
o Adequate fluid resuscitation should be the first priority in addressing severe
abdominal pain[2,5,6]
o There is no evidence to suggest an advantage of any particular type of
medication[2]
o Start with NSAIDs Diclofenac 75mg IM daily or BID depending on patients
response [6]
o If no response add Tramadol 50-100mg IV TID or QID[5]
o Still if no response to the above combination switch to pethidine 50mg-
100mg IM or IV TID Or QID
o Doses should be adjusted if there is renal function impairment
o Studies showed that morphine causes an increase in sphincter of Oddi
pressure[5]
6. Nutritional Support
o Since acute pancreatitis is a hypercatabolic condition, prompt and adequate
provision of nutrition is essential. [2,5,6]
o In Mild pancreatitis Intravenous hydration alone is enough (Maintenance fluid &
Estimated loss)[2,5,9]
 Normal saline, Ringer lactate & D5NS each 1L every 8 hr alternatively &
add 2o MEq potassium in each liter
o Early Nutritional support (24 to 48 hours)- Enteral feeding[2,5,6,9]
 Sever pancreatitis
 In those who are unlikely to resume oral intake for more than five to
seven days

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 o Endoscopic placement of a jejunal feeding (Nasojejunal) tube beyond the
ligament of Treitz (if not possible NG tube feeding is alternative)[5]
o Start with 25ml|hr & advance as tolerated to at least 30% of the calculated daily
requirement (25 kcal/kg ideal body weight) (5)
o Type of diet
 High protein & low fat(5)
 BMD( butter milk Diet)-1ml=1cal(preparation see at end)
o Initiation of oral feeding[2,5,9]
 In Mild acute pancreatitis in the absence of ileus, nausea, vomiting, or as
soon as pain starts improving ( 24 to 48 hours)
 In Sever acute pancreatitis when the local complications start improving
 Advance from a clear liquid diet to solid food as tolerated
 Enteral feeding rather than total parenteral nutrition (TPN) is suggested for
patients who require nutritional support[2,5,9]
o Its ability to maintain the intestinal barrier and prevent bacterial
translocation& endotoxins (which stimulate nitric oxide and cytokine
production that contribute to organ failure) from the gut
o Avoidance of the complications associated with parenteral nutrition
(catheter sepsis, arterial laceration, pneumothorax, vein thrombosis,
thrombophlebitis, and catheter embolism)

7. Infection control

Pancreatic infection is a leading cause of morbidity and mortality in acute necrotizing

pancreatitis. Approximately one-third of patients with pancreatic necrosis develop
infected necrosis. Infection can occur early but more often late after 10 days [5]

Aerobic and anaerobic gastrointestinal floras are the primary organisms involved, and
infections may be monomicrobial or polymicrobial. The predominant microbes seen
were Escherichia coli (35%), Klebsiella pneumoniae (24%), Streptococcus (24%),
Staphylococcus (14%), and Pseudomonas (11%).[7]

The majority of infections (about 75 percent) are monomicrobial. Fungal infections

occur in approximately 9 percent of necrotizing pancreatitis (more frequently in the
setting of prophylactic antibiotic use for severe acute pancreatitis, especially when
used for more than 10 to 14 days) [5]
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SPHMMC Department of surgery
Approaches taken to decrease bacterial infections in acute necrotizing pancreatitis
include [5]
 Enteral feeding
 Systemic antibiotics
 Necrosectomy

Prophylactic antibiotics
There are conflicting recommendations from recent studies addressing the use of
systemic antibiotic prophylaxis in severe pancreatitis
 Indication
 Necrotizing pancreatitis involving >30% of the pancreases[6,7,9]
 Drugs
 Meropenem 1g IV QID (Drug of choice)[5]
 Ceftriaxone 1g-2g IV BID & Metronidazole 500mg-1g IV TID-QID (Alternative)
[5]
 Duration
 Discontinue after 7 to 10 days unless infection is confirmed (CT-guided
percutaneous aspiration-Gram's stain or culture positive) or clinical
evidences[5]

8. Treatment of pancreatic Necrosis

One-third of patients with pancreatic necrosis develop infected necrosis usually after
10 days of illness.[5]
Definitions according to International Symposium on Acute Pancreatitis (the Atlanta
Symposium) shown below [7]

Table 8-Definitions Proposed by the International Symposium on Acute Pancreatitis

(the Atlanta Symposium), 1992
Acute Acute inflammatory process of the pancreas with variable involvement of
pancreatitis other regional tissues or remote organ systems.
Severe AP Association with organ failure and/or local complications, such as
necrosis, abscess, or pseudocyst.
Acute fluid Occurs early in the course of AP, located in or near the pancreas, always
collection lacking a wall of granulation or fibrous tissue; bacteria variably present;

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 occurs in 30–50% of severe AP; most acute fluid collections regress, but
some progress to pseudocyst or abscess.
Pancreatic Diffuse or focal area(s) of nonviable pancreatic parenchyma, typically
necrosis associated with peripancreatic fat necrosis, diagnosed by CT scan with
intravenous contrast enhancement.
Acute Collection of pancreatic juice enclosed by a wall of fibrous or granulation
pseudocyst tissue, which arises as a consequence of AP, pancreatic trauma, or chronic
pancreatitis; formation requires 4 or more weeks form onset of AP.
Pancreatic Circumscribed intra-abdominal collection of pus usually in or near the
abscess pancreas, containing little or no pancreatic necrosis, arises as a
consequence of AP or pancreatic trauma.

 Indications for laparotomy & Necrosectomy (Surgical debridement of pancreatic

necrosis)[5,8]
 Infected pancreatic necrosis
 Sterile symptomatic pancreatic necrosis with chronic low grade fever, nausea,
lethargy, and abdominal pain preventing oral intake
 Diagnostic uncertainty
 Intra-abdominal catastrophe unrelated to necrotizing pancreatitis such as
perforated viscus
All patients with pancreatic necrosis undergoing debridement should have contrast
enhanced CT scanning of the abdomen and pelvis to define the extent and location of
necrotic areas.[5]
 Timing of debridement
 The optimal timing is at least three to four weeks following the onset of
acute pancreatitis [5]
 Approaches [5,7,8]
 Open debridement under general anesthesia with closure over drains is the
gold standard.[5,7,8]
o Midline &Bilateral subcostal incision
o Reserve as much viable tissue as possible
o Consider cholecystectomy if technically possible
o Enteral access should be established through a gastrojejunal feeding
tube placed via a Stamm-type gastrostomy
o Place 2 to 4 large size (19 French) drain

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Figure 3-Operative approaches to open pancreatic debridement & external drainage
tubes [7]
 Post-operative management [5,7,8]
o Volume replacement, blood glucose control, maintenance of normothermia,
and adequate pain control.
o After the first 48 hours of resuscitation start enteral feeding
9. Treatment of Associated conditions
 Cholecystectomy -prevent recurrence (25% to 30% risk of recurrent acute
pancreatitis, cholecystitis, or cholangitis within 6 to 18 weeks).[5,7,8,9]
o Indications
 Cholelithiasis
 Biliary sludge
o Timing
 Same admission after 7 days & 3 weeks after recovery from mild
& severe pancreatitis respectively
 Counseling on cessation of alcohol
 Treat associated Hypertriglyceridemia[5]
10.Others
 Deep vein thrombosis prophylaxis
o Heparin (LMW) 500 units subcutaneous QID to BID
 Ulcer (duodenal) prophylaxis[5,2]
o Indication
 In subtotal or total pancreatic necrosis
o Drugs
 Esomeprazole/omeprazole 20mg IV daily or BID(preferred)

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  Cimetidine 200mg-400mg IV daily or BID (alternative)
11.Follow up
o Vital signs including oxygen saturation every 2-4 hr for the first 24-48
hrs. & subsequently based on patients condition
o Strict input & output monitoring(urine output should be (>0.5 ml|Kg|hr)
o Laboratory investigations should be done per this protocol(see above)

Acknowledgements
First, we would like to express our deep gratitude to the SPHMMC department of
surgery for giving us this chance to prepare the protocol then to all of those who have
participated in the preparation.

References
1. Santhi Swaroop Vege, MD. (2012). Etiology of acute pancreatitis. UpToDate
20.3
2. Peter A. Banks, M.D., M.A.C.G., 1 Martin L. Freeman, M.D., F.A.C.G., 2. (2006).
Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379–
2400.
3. Remi Neviere, M. (2012). Sepsis and the systemic inflammatory response
syndrome: Definitions, epidemiology, and prognosis. UpToDate 20.1
4. Santhi Swaroop Vege, M. (2012). Pathogenesis of acute pancreatitis. UpToDate
20.1.
5. Santhi Swaroop Vege, M. (2012). Treatment of acute pancreatitis. UpToDate
20.1.
6. Tandon, R. K. (2009). Management of Acute Pancreatitis. Indian Guidelines and
Protocols, 267-270.
7. J.Zinner, M., & w.Ashely, Maingot's Abdominal Operations (11th ed.). McGraw
Hills.
George D.Zuidema, M., & Charles J.Yeo, M. (20002). Shackelford's Surgery of the
Alimentary Tract (5th ed.). USA: W. B. Saunders Company.

8.

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