Acute Pancreatitis - Wikipedia

1/22/22, 9:25 PM Acute pancreatitis - Wikipedia
Acute pancreatitis
Acute pancreatitis (AP) is a sudden inflammation of
Acute pancreatitis
the pancreas. Causes in order of frequency include: 1) a
gallstone impacted in the common bile duct beyond the Other Acute pancreatic necrosis[1]
point where the pancreatic duct joins it; 2) heavy names
alcohol use; 3) systemic disease; 4) trauma; 5) and, in
minors, mumps. Acute pancreatitis may be a single
event; it may be recurrent; or it may progress to chronic
pancreatitis.
Mild cases are usually successfully treated with

conservative measures: hospitalization, pain control,
nothing by mouth, intravenous nutritional support, and
intravenous fluid rehydration. Severe cases often
require admission to an intensive care unit to monitor
and manage complications of the disease.
Complications are associated with a high mortality,
even with optimal management.
Contents
Pancreas
Signs and symptoms
Specialty Gastroenterology, general
Common
surgery
Uncommon
Complications
Causes
Most common
Less common
Pathology
Pathogenesis
Pathophysiology
Histopathology
3D Medical Animation still shot of Acute
Diagnosis
Pancreatitis
Differential diagnosis
Biochemical
Computed tomography
Magnetic resonance imaging
Ultrasound
Treatment
Fluid replacement
Pain control
https://en.wikipedia.org/wiki/Acute_pancreatitis 1/21
Bowel rest
Nutritional support
Oxygen
Antibiotics
ERCP
Surgery
Other measures
Classification by severity: prognostic scoring
systems
Ranson score
Alternative Ranson score
APACHE II score
Balthazar score
Glasgow score
BISAP score
Epidemiology
See also
References
External links
Signs and symptoms
Common
severe epigastric pain (upper abdominal pain) radiating to the back in 50% of cases
nausea[2]
vomiting
loss of appetite
fever
chills (shivering)
hemodynamic instability, including shock
tachycardia (rapid heartbeat)
respiratory distress
peritonitis
hiccup
Although these are common symptoms, frequently they are not all present; and epigastric pain may
be the only symptom.[3]
Uncommon
The following are associated with severe disease:
Grey-Turner's sign (hemorrhagic discoloration of the flanks)

Cullen's sign (hemorrhagic discoloration of the umbilicus)
Pleural effusions (fluid in the bases of the pleural cavity)
Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to local toxic
lesion of the vessels)
Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium,
6–7 cm above the umbilicus))
Kamenchik's sign (pain with pressure under the xiphoid process)
Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the erector spinae
muscles and below the left 12th rib (left costovertebral angle (CVA))[4]
Mayo-Robson's point – a point on border of inner 2/3 with the external 1/3 of the line that
represents the bisection of the left upper abdominal quadrant, where tenderness on pressure
exists in disease of the pancreas. At this point the tail of pancreas is projected on the abdominal
wall.
Complications
Locoregional complications include pancreatic pseudocyst (most common, occurring in up to 25% of

all cases, typically after 4–6 weeks) and phlegmon/abscess formation, splenic artery
pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic
vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal
obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites,
pleural effusion, sterile/infected pancreatic necrosis.[5]
Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia
(from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic
insulin-producing beta cell damage), malabsorption due to exocrine failure
Metabolic
Hypocalcemia, hyperglycemia, hypertriglyceridemia
Respiratory
Hypoxemia, atelectasis, Effusion, pneumonitis, Acute respiratory distress syndrome (ARDS)
Renal
Renal artery or vein thrombosis
Kidney failure
Circulatory
Arrhythmias
Hypovolemia and shock
myocardial infarction
Pericardial effusion
vascular thrombosis
Gastrointestinal
Gastrointestinal hemorrhage from stress ulceration;
gastric varices (secondary to splenic vein thrombosis)

Gastrointestinal obstruction
Hepatobiliary
Jaundice
Portal vein thrombosis
Neurologic
Psychosis or encephalopathy (confusion, delusion and coma)
Cerebral Embolism
Blindness (angiopathic retinopathy with hemorrhage)
Hematologic
Anemia
DIC
Leucocytosis
Dermatologic
Painful subcutaneous fat necrosis
Miscellaneous
Subcutaneous fat necrosis
Arthalgia
Causes
Most common
Biliary pancreatitis due to gallstones or constriction of ampulla of Vater in 40% of cases
Alcohol in 30% of cases
Idiopathic in 15-25% of cases
Metabolic disorders: hereditary pancreatitis, hypercalcemia, elevated triglycerides, malnutrition
Post-ERCP
Abdominal trauma
Penetrating ulcers
Carcinoma of the head of pancreas, and other cancer
Drugs: diuretics (e.g., thiazides, furosemide), gliptins (e.g., vildagliptin, sitagliptin, saxagliptin,
linagliptin), tetracycline, sulfonamides, estrogens, azathioprine and mercaptopurine, pentamidine,
salicylates, steroids, Depakote
Infections: mumps, viral hepatitis, coxsackie B virus, cytomegalovirus, Mycoplasma pneumoniae,
Ascaris
Structural abnormalities: choledochocele, pancreas divisum
Radiotherapy
Autoimmune pancreatitis
Severe hypertriglyceridemia[6]
Less common
Scorpion venom
Chinese liver fluke[7]
Ischemia from bypass surgery
Heart valve surgery[8]
Fat necrosis
Pregnancy
Infections other than mumps, including varicella zoster[7]
Hyperparathyroidism
Valproic acid
Cystic fibrosis
Anorexia or bulimia
Codeine phosphate reaction[9][10]
Pathology
Pathogenesis
Acute pancreatitis occurs when there is abnormal activation of digestive enzymes within the pancreas.
This occurs through inappropriate activation of inactive enzyme precursors called zymogens (or
proenzymes) inside the pancreas, most notably trypsinogen. Normally, trypsinogen is converted to its
active form (trypsin) in the first part of the small intestine (duodenum), where the enzyme assists in
the digestion of proteins. During an episode of acute pancreatitis, trypsinogen comes into contact with
lysosomal enzymes (specifically cathepsin), which activate trypsinogen to trypsin. The active form
trypsin then leads to further activation of other molecules of trypsinogen. The activation of these
digestive enzymes lead to inflammation, edema, vascular injury, and even cellular death. The death of
pancreatic cells occurs via two main mechanisms: necrosis, which is less organized and more
damaging, or apoptosis, which is more controlled. The balance between these two mechanisms of
cellular death is mediated by caspases which regulate apoptosis and have important anti-necrosis
functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through
inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If,
however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult
then necrosis can predominate.
Pathophysiology
The two types of acute pancreatitis are mild and severe, which are defined based on whether the
predominant response to cell injury is inflammation (mild) or necrosis (severe). In mild pancreatitis,
there is inflammation and edema of the pancreas. In severe pancreatitis, there is necrosis of the
pancreas, and nearby organs may become injured.
As part of the initial injury there is an extensive inflammatory response due to pancreatic cells
synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of
acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of
neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of
pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome,

disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal
hemorrhage.
Histopathology
The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute

inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and
vessel necrosis (hemorrhage). These are produced by intrapancreatic activation of pancreatic
enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and
peripancreatic spaces as well as vessel damage. Necrotic fat cells appear as shadows, contours of cells,
lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates
(hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage.
Inflammatory infiltrate is rich in neutrophils. Due to the pancreas lacking a capsule, the inflammation
and necrosis can extend to include fascial layers in the immediate vicinity of the pancreas.
Diagnosis
Acute pancreatitis is diagnosed using clinical history and physical examination, based on the presence
of at least 2 of 3 criteria: abdominal pain, elevated serum lipase or amylase, and abdominal imaging
findings consistent with acute pancreatitis.[11] Additional blood studies are used to identify organ
failure, offer prognostic information, and determine if fluid resuscitation is adequate and whether
ERCP is necessary.
Blood investigations – complete blood count, kidney function tests, liver function, serum calcium,
serum amylase and lipase
Imaging – A triple phase abdominal CT and abdominal ultrasound are together considered the
gold standard for the evaluation of acute pancreatitis. Other modalities including the abdominal x-
ray lack sensitivity and are not recommended. An important caveat is that imaging during the first
12 hours may be falsely reassuring as the inflammatory and necrotic process usually requires 48
hours to fully manifest.
Differential diagnosis
The differential diagnosis includes:[12]
Perforated peptic ulcer

Biliary colic
Acute cholecystitis
Pneumonia
Pleuritic pain
Myocardial infarction
Biochemical
Elevated serum amylase and lipase levels, in combination with severe abdominal pain, often
trigger the initial diagnosis of acute pancreatitis. However, they have no role in assessing disease
severity.
Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days
after treatment.
Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis
(depleted acinar cell mass) and hypertriglyceridemia.
Reasons for false positive elevated serum amylase include salivary gland disease (elevated
salivary amylase), bowel obstruction, infarction, cholecystitis, and a perforated ulcer.
If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to
alcohol.[13]
Decreased serum calcium
Glycosuria
Regarding selection on these tests, two practice guidelines state:
"It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be
preferable because it remains normal in some nonpancreatic conditions that increase serum
amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase
is thought to be more sensitive and specific than serum amylase in the diagnosis of acute
pancreatitis"[14]
"Although amylase is widely available and provides acceptable accuracy of diagnosis, where
lipase is available it is preferred for the diagnosis of acute pancreatitis (recommendation grade
A)"[15]
Most, but not all individual studies support the superiority of the lipase.[16] In one large study, there
were no patients with pancreatitis who had an elevated amylase with a normal lipase.[17] Another
study found that the amylase could add diagnostic value to the lipase, but only if the results of the two
tests were combined with a discriminant function equation.[18]
While often quoted lipase levels of 3 or more times the upper-limit of normal is diagnostic of
pancreatitis, there are also other differential diagnosis to be considered relating to this rise.[19]
Computed tomography
Regarding the need for computed tomography, practice guidelines

state:
CT is an important common initial assessment tool for acute

pancreatitis. Imaging is indicated during the initial presentation
if:
the diagnosis of acute pancreatitis is uncertain

there is abdominal distension and tenderness, fever >102 F
(38,9 C), or leukocytosis
Axial CT in a patient with acute
there is a Ranson score > 3 or APACHE score > 8
exudative pancreatitis showing
there is no improvement after 72 hours of conservative extensive fluid collections
medical therapy surrounding the pancreas.
there has been an acute change in status: fever, pain, or
shock
CT is recommended as a delayed assessment tool in the following situations:
acute change in status

to determine therapeutic response after surgery or interventional radiologic procedure
before discharge in patients with severe acute pancreatitis
Abdominal CT should not be performed before the first 12 hours of onset of symptoms as early CT
(<12 hours) may result in equivocal or normal findings.
CT findings can be classified into the following categories for easy recall:
Intrapancreatic – diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts

and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
Peripancreatic / extrapancreatic – irregular pancreatic outline, obliterated peripancreatic fat,
retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
Locoregional – Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes
visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic
ileus, etc.
The principal value of CT imaging to the treating clinician is the capacity to identify devitalised areas
of the pancreas which have become necrotic due to ischaemia. Pancreatic necrosis can be reliably
identified by intravenous contrast-enhanced CT imaging,[20] and is of value if infection occurs and
surgical or percutaneous debridement is indicated.
Magnetic resonance imaging
While computed tomography is considered the gold standard in diagnostic imaging for acute
pancreatitis,[21] magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the
visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris.[22]
Additional utility of MRI includes its indication for imaging of patients with an allergy to CT's contrast
material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms,
and venous thrombosis.[23]
Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP)

sequences. MRCP provides useful information regarding the etiology of acute pancreatitis, i.e., the
presence of tiny biliary stones (choledocholithiasis or cholelithiasis) and duct anomalies.[22] Clinical
trials indicate that MRCP can be as effective a diagnostic tool for acute pancreatitis with biliary
etiology as endoscopic retrograde cholangiopancreatography, but with the benefits of being less
invasive and causing fewer complications.[24][25]
Ultrasound
On abdominal ultrasonography, the finding of a hypoechoic and bulky pancreas is regarded as

diagnostic of acute pancreatitis.
Treatment
Initial management of a patient with acute pancreatitis consists of

supportive care with fluid resuscitation, pain control, nothing by
mouth, and nutritional support.
Fluid replacement
Aggressive hydration at a rate of 5 to 10 mL/kg per hour of

isotonic crystalloid solution (e.g., normal saline or lactated
Ringer's solution) to all patients with acute pancreatitis, unless Abdominal ultrasonography of acute
cardiovascular, renal, or other related comorbid factors preclude pancreatitis.
aggressive fluid replacement. In patients with severe volume
depletion that manifests as hypotension and tachycardia, more
rapid repletion with 20 mL/kg of intravenous fluid given over 30 minutes followed by 3 mL/kg/hour
for 8 to 12 hours.[26][27]
Fluid requirements should be reassessed at frequent intervals in the first six hours of admission and
for the next 24 to 48 hours. The rate of fluid resuscitation should be adjusted based on clinical
assessment, hematocrit and blood urea nitrogen (BUN) values.
In the initial stages (within the first 12 to 24 hours) of acute pancreatitis, fluid replacement has been
associated with a reduction in morbidity and mortality.[28][29][30][31]
Pain control
Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be
treated with analgesics.
Opioids are safe and effective at providing pain control in patients with acute pancreatitis.[32]
Adequate pain control requires the use of intravenous opiates, usually in the form of a patient-
controlled analgesia pump. Hydromorphone or fentanyl (intravenous) may be used for pain relief in
acute pancreatitis. Fentanyl is being increasingly used due to its better safety profile, especially in
renal impairment. As with other opiates, fentanyl can depress respiratory function. It can be given
both as a bolus as well as constant infusion.
Meperidine has been historically favored over morphine
because of the belief that morphine caused an increase in sphincter of Oddi pressure. However, no
clinical studies suggest that morphine can aggravate or cause pancreatitis or cholecystitis.[33] In
addition, meperidine has a short half-life and repeated doses can lead to accumulation of the
metabolite normeperidine, which causes neuromuscular side effects and, rarely, seizures.
Bowel rest
In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving them
nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As
the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food
pass through the system allows the pancreas to rest. Approximately 20% of patients have a relapse of
pain during acute pancreatitis.[34] Approximately 75% of relapses occur within 48 hours of oral
refeeding.
The incidence of relapse after oral refeeding may be reduced by post-pyloric enteral rather than
parenteral feeding prior to oral refeeding.[34] IMRIE scoring is also useful.
Nutritional support
Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to
early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically
introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more
physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as
fungemia). The additional advantages of post-pyloric feeding are the inverse relationship of
pancreatic exocrine secretions and distance of nutrient delivery from the pylorus, as well as reduced
risk of aspiration.
Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube
remains in place greater than two weeks) and a still-present risk of accidentally intubating the trachea
even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always
sufficient to prevent NG tube entry into the trachea).
Oxygen
Oxygen may be provided in some patients (about 30%) if Pao2 levels fall below 70mm of Hg.
Antibiotics
Up to 20 percent of people with acute pancreatitis develop an infection outside the pancreas such as
bloodstream infections, pneumonia, or urinary tract infections.[35] These infections are associated
with an increase in mortality.[36] When an infection is suspected, antibiotics should be started while
the source of the infection is being determined. However, if cultures are negative and no source of
infection is identified, antibiotics should be discontinued.
Preventative antibiotics are not recommended in people with acute pancreatitis, regardless of the type
(interstitial or necrotizing) or disease severity (mild, moderately severe, or severe)[11][37]
ERCP
In 30% of those with acute pancreatitis, no cause is identified. ERCP with empirical biliary
sphincterotomy has an equal chance of causing complications and treating the underlying cause,
therefore, is not recommended for treating acute pancreatitis.[38]
If a gallstone is detected,
Endoscopic retrograde cholangiopancreatography (ERCP), performed within 24 to 72 hours of
presentation with successful removal of the stone, is known to reduce morbidity and mortality.[39]
The indications for early ERCP are:
Clinical deterioration or lack of improvement after 24 hours

Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on abdominal
CT
The risks of ERCP are that it may worsen pancreatitis, it may introduce an infection to otherwise
sterile pancreatitis, and bleeding.
Surgery
Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii)
complications. The most common cause of death in acute pancreatitis is secondary infection.
Infection is diagnosed based on 2 criteria
Gas bubbles on CT scan (present in 20 to 50% of infected necrosis)

Positive bacterial culture on FNA (fine needle aspiration, usually CT or US guided) of the
pancreas.
Surgical options for infected necrosis include:
Minimally invasive management – necrosectomy through small incision in skin (left flank) or
abdomen
Conventional management – necrosectomy with simple drainage
Closed management – necrosectomy with closed continuous postoperative lavage
Open management – necrosectomy with planned staged reoperations at definite intervals (up to
20+ reoperations in some cases)
Other measures
Pancreatic enzyme inhibitors are proven not to work.[40]
The use of octreotide has been shown not to improve outcomes.[41]
Classification by severity: prognostic scoring systems

Acute pancreatitis patients recover in majority of cases. Some may develop abscess, pseudocyst or
duodenal obstruction.
In 5 percent cases, it may result in ARDS (acute respiratory distress syndrome),
DIC (disseminated intravascular coagulation)
Acute pancreatitis can be further divided into mild and
severe pancreatitis.
Mostly the Ranson Criteria are used to determine severity of acute pancreatitis. In severe pancreatitis
serious amounts of necrosis determine the further clinical outcome. About 20% of the acute
pancreatitis are severe with a mortality of about 20%. This is an important classification as severe
pancreatitis will need intensive care therapy whereas mild pancreatitis can be treated on the common
ward.
Necrosis will be followed by a systemic inflammatory response syndrome (SIRS) and will determine
the immediate clinical course. The further clinical course is then determined by bacterial infection.
SIRS is the cause of bacterial (Gram negative) translocation from the patients colon.
There are several ways to help distinguish between these two forms. One is the above-mentioned
Ranson Score.
In predicting the prognosis, there are several scoring indices that have been used as predictors of
survival. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and
Chronic Health Evaluation) indices. Most,[42][43] but not all[44] studies report that the Apache score
may be more accurate. In the negative study of the APACHE-II,[44] the APACHE-II 24-hour score was
used rather than the 48-hour score. In addition, all patients in the study received an ultrasound twice
which may have influenced allocation of co-interventions. Regardless, only the APACHE-II can be
fully calculated upon admission. As the APACHE-II is more cumbersome to calculate, presumably
patients whose only laboratory abnormality is an elevated lipase or amylase do not need assessment
with the APACHE-II; however, this approach is not studied. The APACHE-II score can be calculated
at www.sfar.org (https://web.archive.org/web/20070205031526/http://www.sfar.org/scores2/apach
e22.html).
Practice guidelines state:
2006: "The two tests that are most helpful at admission in distinguishing mild from severe acute
pancreatitis are APACHE-II score and serum hematocrit. It is recommended that APACHE-II
scores be generated during the first 3 days of hospitalization and thereafter as needed to help in
this distinction. It is also recommended that serum hematocrit be obtained at admission, 12 h
after admission, and 24 h after admission to help gauge adequacy of fluid resuscitation."[14]
2005: "Immediate assessment should include clinical evaluation, particularly of any

cardiovascular, respiratory, and renal compromise, body mass index, chest x ray, and APACHE
II score"[15]
Ranson score
The Ranson score is used to predict the severity of acute pancreatitis. They were introduced in 1974.
At admission
age in years > 55 years
white blood cell count > 16000 cells/mm3
blood glucose > 11.1 mmol/L (> 200 mg/dL)
serum AST > 250 IU/L
serum LDH > 350 IU/L
At 48 hours
Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
Hematocrit fall >10%
Oxygen (hypoxemia PO2 < 60 mmHg)
BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
Base deficit (negative base excess) > 4 mEq/L
Sequestration of fluids > 6 L
The criteria for point assignment is that a certain breakpoint be met at any time during that 48 hour
period, so that in some situations it can be calculated shortly after admission. It is applicable to both
gallstone and alcoholic pancreatitis.
Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2]
Alternative Ranson score
Ranson's score of ≥ 8
Organ failure
Substantial pancreatic necrosis (at least 30% glandular necrosis
according to contrast-enhanced CT)
Interpretation
If the score ≥ 3, severe pancreatitis likely.
If the score < 3, severe pancreatitis is
unlikely
Or
Score 0 to 2 : 2% mortality

Score 7 to 8 :
100% mortality
APACHE II score
"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 8 points predicts 11% to 18%
mortality[14]
Hemorrhagic peritoneal fluid

Obesity
Indicators of organ failure
Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO2 <60 mmHg
Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>
Balthazar score
Developed in the early 1990s by Emil J. Balthazar et al.,[45] the Computed Tomography Severity
Index (CTSI) is a grading system used to determine the severity of acute pancreatitis. The numerical
CTSI has a maximum of ten points, and is the sum of the Balthazar grade points and pancreatic
necrosis grade points:
Balthazar grade
Balthazar grade Appearance on CT CT grade points

Grade A Normal CT 0 points
Grade B Focal or diffuse enlargement of the pancreas 1 point
Grade C Pancreatic gland abnormalities and peripancreatic inflammation 2 points
Grade D Fluid collection in a single location 3 points
Grade E Two or more fluid collections and / or gas bubbles in or adjacent to pancreas 4 points
Necrosis score
Necrosis percentage Points

No necrosis 0 points
0 to 30% necrosis 2 points
30 to 50% necrosis 4 points
Over 50% necrosis 6 points
CTSI's staging of acute pancreatitis severity has been shown by a number of studies to provide more
accurate assessment than APACHE II, Ranson, and C-reactive protein (CRP) level.[46][47][48]
However, a few studies indicate that CTSI is not significantly associated with the prognosis of
hospitalization in patients with pancreatic necrosis, nor is it an accurate predictor of AP
severity.[49][50]
Glasgow score
The Glasgow score is valid for both gallstone and alcohol induced pancreatitis, whereas the Ranson
score is only for alcohol induced pancreatitis. If a patient scores 3 or more it indicates severe
pancreatitis and the patient should be considered for transfer to ITU. It is scored through the
mnemonic, PANCREAS:
P - PaO2 <8kPa
A - Age >55-years-old
N - Neutrophilia: WCC >15x10(9)/L
C - Calcium <2 mmol/L
R - Renal function: Urea >16 mmol/L
E - Enzymes: LDH >600iu/L; AST >200iu/L
A - Albumin <32g/L (serum)
S - Sugar: blood glucose >10 mmol/L
BISAP score
Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be
taken from the first 24 hours of the patient's evaluation.
BUN >25 mg/dL (8.9 mmol/L)

Abnormal mental status with a Glasgow coma score <15
Evidence of SIRS (systemic inflammatory response syndrome)
Patient age >60 years old
Imaging study reveals pleural effusion
Patients with a score of zero had a mortality of less than one percent, whereas patients with a score of
five had a mortality rate of 22 percent. In the validation cohort, the BISAP score had similar test
performance characteristics for predicting mortality as the APACHE II score.[51] As is a problem with
many of the other scoring systems, the BISAP has not been validated for predicting outcomes such as
length of hospital stay, need for ICU care, or need for intervention.
Epidemiology
In the United States, the annual incidence is 18 cases of acute pancreatitis per 100,000 population,
and it accounts for 220,000 hospitalizations in the US.[52] In a European cross-sectional study,
incidence of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995;
however, mortality remained stable as a result of better outcomes.[53] Another study showed a lower
incidence of 9.8 per 100,000 but a similar worsening trend (increasing from 4.9 in 1963–74) over
time.[54]

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1/22/22, 9:25 PM Acute pancreatitis - Wikipedia

Mild cases are usually successfully treated with

Signs and symptoms

The following are associated with severe disease:

Grey-Turner's sign (hemorrhagic discoloration of the flanks)

Locoregional complications include pancreatic pseudocyst (most common, occurring in up to 25% of

Hypocalcemia, hyperglycemia, hypertriglyceridemia

Hypoxemia, atelectasis, Effusion, pneumonitis, Acute respiratory distress syndrome (ARDS)

gastric varices (secondary to splenic vein thrombosis)

pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome,

The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute

The differential diagnosis includes:[12]

Perforated peptic ulcer

Regarding selection on these tests, two practice guidelines state:

Regarding the need for computed tomography, practice guidelines

CT is an important common initial assessment tool for acute

the diagnosis of acute pancreatitis is uncertain

CT is recommended as a delayed assessment tool in the following situations:

acute change in status

Intrapancreatic – diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts

Magnetic resonance imaging

Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP)

On abdominal ultrasonography, the finding of a hypoechoic and bulky pancreas is regarded as

Initial management of a patient with acute pancreatitis consists of

Aggressive hydration at a rate of 5 to 10 mL/kg per hour of

Clinical deterioration or lack of improvement after 24 hours

Gas bubbles on CT scan (present in 20 to 50% of infected necrosis)

Surgical options for infected necrosis include:

Classification by severity: prognostic scoring systems

Practice guidelines state:

2005: "Immediate assessment should include clinical evaluation, particularly of any

Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2]

Alternative Ranson score

Score 0 to 2 : 2% mortality

Hemorrhagic peritoneal fluid

Balthazar grade Appearance on CT CT grade points

Necrosis percentage Points

BUN >25 mg/dL (8.9 mmol/L)

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