1044 Pancreatitis, Acute ALG

EPIDEMIOLOGY & • Nausea and vomiting (up to 90% of cases)

BASIC INFORMATION DEMOGRAPHICS • Hypoactive bowel sounds (from ileus)
• The incidence of pancreatitis is increasing • Tachycardia, shock (from decreased intra-
DEFINITION in the U.S. Admissions for acute pancreati- vascular volume)
• Acute pancreatitis is an inflammatory process tis have increased dramatically, and acute • Confusion (from metabolic disturbances)
of the pancreas with intrapancreatic activation pancreatitis was the number-one GI-related • Fever (SIRS response or infection when pan-
of enzymes that may also involve peripancre- cause for admission across U.S. hospitals in creatic necrosis is present)
atic tissue and/or remote organ systems. The 2012. There are >270,000 cases of acute • Decreased breath sounds (pleural effusions)
diagnosis of acute pancreatitis requires at pancreatitis reported annually in the U.S., or rales (atelectasis, acute respiratory dis-
least two of the following criteria: serum amy- with 40%+ due to gallstone disease (most tress syndrome [ARDS])
lase or lipase ≥3 times normal, abdominal pain common cause) and 30% due to alcohol. • Jaundice (from obstruction or compression of
consistent with pancreatitis, and radiographic • Incidence in urban areas is twice that of rural biliary tract)
findings (CT or MRI) of acute pancreatitis. areas (20/100,000 persons in urban areas). • Ascites (from tear in pancreatic duct, leaking
• Commonly used scoring systems for acute • 20% of patients have necrotizing pancreati- pseudocyst)
pancreatitis are described in Table 1. tis; the remainder have interstitial, or edema- • Palpable abdominal mass (pseudocyst,
• T he Revised Atlanta Criteria1 use early tous, pancreatitis. phlegmon, abscess, carcinoma)
prognostic signs, organ failure, and local • Drugs are responsible for less than 5% of all • Evidence of hypocalcemia (Chvostek sign,
complications to define disease severity: cases of acute pancreatitis. Trousseau sign)
1. Mild pancreatitis: No organ failure, no • Evidence of retroperitoneal bleeding (hemor-
local or systemic complications, pancre- PHYSICAL FINDINGS & CLINICAL rhagic pancreatitis):
atitis typically resolves in first wk PRESENTATION 1. Ecchymosis around the umbilicus (Cullen
2. Moderate pancreatitis: Transient organ • Epigastric tenderness and guarding, often sign)
failure (≤48 hours) or local complications radiating to the back; pain usually developing 2. Ecchymosis involving the flanks (Grey
(e.g., pancreatic necrosis, peripancreatic suddenly, reaching peak intensity within 10 Turner sign)
fluid collections, peripancreatic necrosis) to 30 min, severe and lasting several hours • Tender subcutaneous nodules (caused by
or exacerbation of comorbid disease without relief. Rarely, some patients can have subcutaneous fat necrosis)
3. Severe pancreatitis: Persistent organ painless severe pancreatitis
failure (>48 hours)
• T he BALI Score2 evaluates only four variables: TABLE 1  Commonly Used Scoring Systems: Advantages and
1. BUN ≥25 mg/dl
Disadvantages
2. Age ≥65 yr
3. LDH ≥300 U/L System Scoring Advantages Disadvantages
4. Interleukin-6 level ≥300 pg/ml
• T hese measurements are taken at admission Ranson criteria on admission: One point for each Well known, rel- Requires 48 hr to complete
and at 48 hours. Mortality is >25% for a score factor listed; atively easy evaluation
of 3 and exceeds 50% with a score of 4. 1 . Age >55 yr score >3 indi- to calculate
2. WBC >16 × 109/L cates SAP
• Severe acute pancreatitis (SAP) is diag- 3. LDH >350 U/L
nosed by the presence of any of the following 4. AST >250 U/L
four criteria: 5. Glucose >200 mg/dl
1. Organ failure with one or more of the fol- During initial 48 hr:
lowing: Shock (systolic blood pressure <90 1. Hgb falls below 10 mg/dl
mm Hg), pulmonary insufficiency (Pao2 2. BUN rises by >5 mg/dl
≤60 mm Hg), renal failure (serum cre- 3. Ca <8 mg/dl
atinine >2 mg/dl after rehydration), and 4. Pao2 <60 mm Hg
gastrointestinal bleeding (>500 ml/24 hr) 5. Base deficit >4 mEq/L
6. Fluid sequestration >6 L
2. Local complications such as necrosis,
pseudocyst, or abscess APACHE II* Score >8 pre- Can be calcu- Requires large dataset for
dicts SAP lated within processing
3. At least three of Ranson criteria (see 24 hr of
tables) or admission
4. At least eight of the Acute Physiology and BISAP One point for Ease of use, Significantly lower sensitiv-
Chronic Health Evaluation II (APACHE II) 1. BUN >25 mg/dl each factor available ity than either Ranson or
criteria 2. Altered mental status listed; score within 24 hr APACHE II; results in greater
3. Presence of SIRS >3 indicates of admis- likelihood of missing
ICD-10CM CODES 4. Age >60 yr SAP sion severe AP
K85.0 Idiopathic acute pancreatitis 5. Pleural effusions
K85.1 Biliary acute pancreatitis CTSI Based on radio- Excellent pre- Requires 72 to 96 hr, making it
K85.2 Alcohol induced acute pancreatitis graphic data dictor of local a poor test for guiding deci-
K 85.3 Drug induced pancreatitis complica- sions at admission
K85.6 Other acute pancreatitis tions; can
K85.9 Acute pancreatitis, unspecified show infect-
ed pancreatic
necrosis

1 Banks PA, et  al: Acute Pancreatitis Classification
Working Group: classification of acute pancreatitis-2012:
revision of the Atlanta classification and definitions by
international consensus, Gut 62(1):102-111, 2013.
2 Spitzer AL, et  al: Applying Ockham’s razor to pan-
creatitis prognostication: a four-variable predictive
model, Ann Surg 243(3):380-388, 2006.
AP, Acute pancreatitis; APACHE, Acute Physiology and Chronic Health Evaluation; AST, aspartate aminotransferase; BISAP, Bedside
Index for Severity in Acute Pancreatitis; BUN, blood urea nitrogen; Ca, serum calcium; CTSI, Computed Tomography Severity
Index; Hgb, hemoglobin; LDH, lactate dehydrogenase; SAP, severe acute pancreatitis; SIRS, systemic inflammatory response
syndrome; WBC, white blood cell count.
*Based on diverse variables, including age, physiology, and long-term health; equation available at www.sfar.org/scores2/apache
22.html#calcul. Adding body mass index (BMI) to APACHE II (the APACHE 0 score) increases discrimination (1 point added for
BMI 26-30; 2 points for BMI >30).
From Cameron JL, Cameron AM: Current surgical therapy, ed 10, Philadelphia, 2011, Saunders.

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ETIOLOGY
• In >90% of cases: Biliary tract disease (cal-
culi or sludge) or alcohol, most common after
5 to 10 yr of heavy drinking
• Hypertriglyceridemia (usually >1000 mg/dl)
from any cause
• Drugs (e.g., thiazides, furosemide, corticoste-
roids, tetracycline, estrogens, valproic acid,
metronidazole, azathioprine, methyldopa,
pentamidine, ethacrynic acid, procainamide,
amiodarone, sulindac, nitrofurantoin, angio-
tensin-converting enzyme inhibitors, danazol,
cimetidine, piroxicam, gold, ranitidine, sul-
fasalazine, isoniazid, acetaminophen, cisplatin,
didanosine, opiates, erythromycin, metformin,
GLP-1 receptor agonists, incretin mimetics)
• Abdominal trauma
• Surgery
• Endoscopic retrograde cholangiopancreatog-
raphy (ERCP), especially with manipulation of
the pancreatic duct
• Infections (predominantly viral)
• Peptic ulcer (penetrating duodenal ulcer)
• Pancreas divisum (congenital failure to fuse
of dorsal or ventral pancreas)
• Idiopathic
• Pregnancy
• Vascular (vasculitis, ischemic)
• Hypercalcemia
• Pancreatic carcinoma (primary or metastatic)
• Renal failure
• Hereditary pancreatitis, such as in patients
with cystic fibrosis
• IgG4 disease
• Occupational exposure to chemicals: Methanol,
cobalt, zinc, mercuric chloride, creosol, lead,
organophosphates, chlorinated naphthalenes
• Others: Scorpion venom, obstruction at
ampulla region (neoplasm, duodenal diver-
ticula, Crohn disease, rarely celiac disease),
hypotensive shock, autoimmune pancreatitis
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
• PUD
• Acute cholangitis, biliary colic
• High intestinal obstruction
• Early acute appendicitis
• DKA
• Pneumonia (basilar)
• Myocardial infarction (inferior wall)
• Renal colic
• Ruptured or dissecting aortic aneurysm
• Mesenteric ischemia
LABORATORY TESTS
Pancreatic enzymes:
Amylase is increased, usually elevated in
the initial 3 to 5 days of acute pancreatitis.
Isoamylase determinations (separation of pan-
creatic cell isoenzyme components of amylase)
are useful in excluding occasional cases of sali-
vary hyperamylasemia. The use of isoamylase
rather than total serum amylase reduces the risk
of erroneously diagnosing pancreatitis and is
preferred by some as initial biochemical test in
patients suspected of having acute pancreatitis.
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ALG Pancreatitis, Acute 1045
Dilated
Inflammatory Pancreas with Normal pancreas Normal peri-
gallbladder
fat stranding inflammatory
stranding
pancreatic fat
P
Gallstone
and Disorders
Diseases
A Inferior vena cava Aorta B Normal subcutaneous fat
FIG. 1  Gallstone pancreatitis and normal pancreas for comparison, axial computed tomography
without contrast. A, Gallstone pancreatitis CT. A dilated gallbladder is visible with a hyperdense dependent
lesion consistent with a gallstone. The region of the pancreas shows significant inflammatory stranding. In this
patient, the pancreas lies just anterior to the left renal vein, which can be seen crossing anterior to the aorta
and entering the inferior vena cava. B, A normal pancreas is visible. This pancreas is surrounded by uninflamed I
fat, which is dark (nearly black). Compare this normal fat with normal subcutaneous fat. (From Broder JS:
Diagnostic imaging for the emergency physician, Philadelphia, 2011, Saunders.)
Urinary amylase determinations are use- increased as a result of tissue necrosis;
ful to diagnose acute pancreatitis in patients bilirubin and alkaline phosphatase may be
with lipemic serum, to rule out elevated serum increased from common bile duct obstruc-
amylase caused by macroamylasemia, and to tion. A threefold or greater rise in serum
diagnose acute pancreatitis in patients whose alanine aminotransferase concentrations is
serum amylase is normal. an excellent indicator (95% probability) of
Serum lipase levels are elevated in acute biliary pancreatitis.
pancreatitis; the elevation is less transient than • Serum calcium is decreased as a result of
serum amylase and more sensitive in patients saponification, precipitation, and decreased
with alcoholic pancreatitis. Concomitant evalu- parathyroid hormone response.
ation of serum amylase and lipase increas- • Arterial blood gases: Pao2 may be decreased
es diagnostic accuracy of acute pancreatitis. as a result of ARDS, pleural effusion(s);
Elevated serum trypsin levels are diagnostic of pH may be decreased as a result of lac-
pancreatitis (in absence of renal failure). tic acidosis, respiratory acidosis, and renal
Serum C-reactive protein is an excellent insufficiency.
laboratory marker of severity; a level >150 • Serum electrolytes: Potassium may be
mg/dl at 48 hours is associated with severe increased from acidosis or renal insuf-
pancreatitis. ficiency; sodium may be increased from
Rapid measurement of urinary trypsinogen-2 dehydration.
(if available) is useful in the emergency depart-
ment as a screening test for acute pancreatitis IMAGING STUDIES
in patients with abdominal pain; a negative • Abdominal plain films are useful initially to
dipstick test for urinary trypsinogen-2 rules out distinguish other conditions that may mimic
acute pancreatitis with a high degree of prob- pancreatitis (perforated viscus). They may
ability, whereas a positive test indicates need reveal localized ileus (sentinel loop), pan-
for further evaluation. creatic calcifications (chronic pancreatitis),
Interleukin-6 level: Worse prognosis with blurring of left psoas shadow, dilation of
level ≥300 pg/ml. transverse colon, calcified gallstones.
• Chest x-ray may reveal elevation of one or
ADDITIONAL TESTS both diaphragms, pleural effusions, basilar
• Complete blood count: Reveals leukocytosis; infiltrates, or platelike atelectasis.
hematocrit (Hct) may be initially increased as • Abdominal ultrasonography is useful in
a result of hemoconcentration; decreased Hct detecting gallstones (sensitivity of 60% to
may indicate hemorrhage or hemolysis. 70% for detecting stones associated with
• Blood urea nitrogen (BUN) is increased pancreatitis). Its availability and noninvasive
because of dehydration. Serial BUN mea- nature make it the initial imaging study
surements are the most valuable lab test for of choice; its major limitation is the pres-
predicting mortality during the initial 48 hr. ence of distended bowel loops overlying the
• Elevation of serum glucose in a previously pancreas.
normal patient correlates with the degree • CT scan (Fig. 1) is less sensitive than ultra-
of pancreatic malfunction and may be relat- sound in identifying gallstones and expos-
ed to increased release of glycogen, cat- es the patient to risk of contrast-induced
echolamines, and glucocorticoid release and nephropathy. It is, however, superior to ultra-
decreased insulin release. sonography in identifying pancreatitis and
• Liver profile: Aspartate aminotransferase defining its extent, and it also plays a role
(AST) and lactate dehydrogenase (LDH) are in diagnosing pseudocysts (they appear as
1046 Pancreatitis, Acute ALG

• Nasogastric suction is useful only in severe

TABLE 2  Computed Tomography (CT) Severity Index Score for Pancreatitis*
Grade† CT Findings
A Normal pancreas
B Focal or diffuse enlargement of the pancreas, contour irregularities, het-
erogeneous attenuation, no peripancreatic inflammation
C Grade B plus peripancreatic inflammation
D Grade C plus a single fluid collection
E Grade C plus multiple fluid collections or gas
Percent Necrosis Present on CT
0 • Prophylactic antibiotics are not recommend-
<33
33-50
>50
*Severity Index Score = Grade score + Percent necrosis score. Maximum score = 10; severe disease = 6 or higher.
†Severity of the acute inflammatory process.
From Adams JG et al: Emergency medicine, clinical essentials, ed 2, Philadelphia, 2013, Elsevier.
a well-defined area surrounded by a high-
density capsule); gastrointestinal fistulization
or infection of a pseudocyst can also be
identified by the presence of gas within the
pseudocyst. Sequential contrast-enhanced
CT is useful for detection of pancreatic
necrosis. The severity of pancreatitis can also
be graded by CT scan (Table 2). (A = normal
pancreas, B = enlarged pancreas [1 point], C
= pancreatic and/or peripancreatic inflam-
mation [2 points], D = single peripancreatic
collection [3 points], E = at least two peripan-
creatic collections and/or retroperitoneal air
[4 points]. Percentage of pancreatic necrosis
<30% [2 points], 30% to 50% [4 points],
>50% [6 points]. The CT severity index is
calculated by adding grade points to points
assigned for percentage of necrosis.)
• Magnetic resonance cholangiopancreatogra-
phy (MRCP) has >90% sensitivity for choled-
ocholithiasis and can identify other anatomic
abnormalities.
• Endoscopic ultrasonography (EUS) is a mini-
mally invasive test that provides high-reso-
lution imaging of the pancreas. It is useful to
identify anatomic abnormalities of the pan-
creas and has good sensitivity and specificity
for small gallstones (≤5 mm).
• ERCP indications: Useful to perform biliary
sphincterotomy and stone removal in the
presence of a retained bile duct stone seen
on imaging. The role and timing of ERCP
in patients with acute biliary pancreatitis
has been controversial. Guidelines from the
American College of Gastroenterology sug-
gest that urgent ERCP (within 24 hr of
admission) is indicated in patients with biliary
pancreatitis who have concurrent acute chol-
angitis, but it is not needed in most patients
who do not have evidence of ongoing biliary
obstruction.3,4,5
3 Fogel EL, Sherman S: ERCP for gallstone pancreatitis,
N Engl J Med 370:150-157, 2014..
4 Tenner S, et al: American College of Gastroenterology
guidelines: management of acute pancreatitis, Am J
Gastroenterol 108:1400-1415, 2013.
5 Bakker OJ, et al: Early versus on-demand nasogas-
tric tube feeding in acute pancreatitis, N Engl J Med
371:1983-1993, 2014.
Score
0 Meperidine and morphine are also commonly
1 used narcotics for pain control, although mor-
2 Oddi pressure and has delayed metabolite clear-
3 ance in patients with concomitant renal failure.
4 • Correct metabolic abnormalities (e.g., replace
SPECIFIC MEASURES:
TREATMENT
NONPHARMACOLOGIC THERAPY
• Bowel rest with avoidance of liquids or
solids during the acute illness. Limited data
suggest that early feeding in patients with
acute pancreatitis does not seem to increase
adverse events and, for patients with mild to
moderate pancreatitis, may reduce length of
hospital stay.6
• Avoidance of alcohol and any drugs associ-
ated with pancreatitis.
ACUTE GENERAL Rx
GENERAL MEASURES:
• Assess severity of pancreatitis (see Table 1).
• An algorithm for the management of acute
pancreatitis is described in Fig. 2.
• Maintain adequate intravascular volume
with vigorous IV hydration. Aggressive fluid
resuscitation (250 to 500 ml/hr) with iso-
tonic crystalloids is critical in managing acute
pancreatitis, unless cardiac or renal disease
precludes it.
• Patient should remain NPO until clinically
improved, stable, and hungry. Enteral feed-
ings are preferred over total parenteral nutri-
tion if supplemental nutrition is necessary.
Enteral nutrition reduces mortality, multiple
organ failure, systemic infections, and opera-
tive interventions more than total parenteral
nutrition does in patients with acute pancre-
atitis. Parenteral nutrition may be necessary
in patients who do not tolerate enteral feed-
ing or in whom an adequate infusion rate
cannot be reached within 2 to 4 days. Early
(within 24 to 48 hr of admission) enteral
feeding through a nasogastric (NG) feeding
tube has limited evidence to support this
strategy. A recent trial did not show superiori-
ty of early NG tube feeding, as compared with
oral diet after 72 hours, in reducing the rate
of infection or death in patients with acute
pancreatitis at high risk for complications.
6 Vaughn VM, et  al: Early versus delayed feeding in
patients with acute pancreatitis, a systematic review,
Ann Intern Med 66:883-892, 2017.
pancreatitis to decompress the abdomen in
patients with ileus.
• Control pain: IV hydromorphone or fentanyl.
phine has been shown to increase sphincter of
calcium and magnesium as necessary).
ed, regardless of the severity or presence of
pancreatic necrosis.
• An algorithm for the management of acute
pancreatitis at various stages is described in
Fig. 2.
• Pancreatic or peripancreatic infection devel-
ops in 30% of patients with pancreatic
necrosis. The use of antibiotics is justified
if the patient has evidence of septicemia,
pancreatic abscess, or pancreatitis caused
by biliary calculi with concomitant cholan-
gitis. Their use should generally be limited
to 5 to 7 days to prevent development of
fungal superinfection. Appropriate empiric
antibiotic therapy should penetrate pancre-
atic necrosis. Options include a carbapenem
alone (due to anaerobic coverage) or a qui-
nolone, ceftazidime, or cefepime, combined
with an enteric anaerobic agent such as
metronidazole. CT-guided fine-needle aspi-
ration (FNA) can be performed to culture the
infected necrosis and tailor antibiotic therapy.
If sampling of infected necrosis occurs and is
sterile, antibiotics should be discontinued
• Surgical therapy has a limited role in acute
pancreatitis; it is indicated in the following:
1. G allstone-induced pancreatitis:
Cholecystectomy when acute pancreati-
tis subsides. However, randomized trials
have shown that patients with mild gall-
stone pancreatitis can undergo cholecys-
tectomy safely during the first 48 hr of
hospitalization
2. Perforated peptic ulcer
3. Necrotizing pancreatitis with infected
necrotic tissue is associated with an elevat-
ed rate of complications and increased risk
of death. Traditional treatment has been
open necrosectomy; surgical necrosec-
tomy induces a proinflammatory response
and is associated with a high complication
rate. Recent trials have shown that a step-
up approach consisting of percutaneous
drainage followed, if necessary, by mini-
mally invasive retroperitoneal necrosec-
tomy may have a lower rate of complica-
tions and death. Endoscopic transgastric
necrosectomy, a form of natural orifice
transluminal endoscopic surgery, has been
shown in recent trials to be effective in
reducing the proinflammatory response as
well as reducing complications
• Identification and treatment of complications:
1. Pseudocyst: Round or spheroid collec-
tion of fluid, tissue, pancreatic enzymes,
and blood

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 ALG Pancreatitis, Acute 1047

Early course: 0-72 hours intervention, whereas those >5 cm

Is there organ failure?
require surgical intervention after the
wall has matured. P
No Yes 2. Phlegmon: Represents pancreatic
edema. It can be diagnosed by CT scan
Admission to medical/surgical floor Admission to an ICU
or sonography. Treatment is supportive as
NPO, IV hydration (250-400 cc/hr) Same orders as for floor admission it usually resolves spontaneously
Nasal oxygen Central line placement 3. Pancreatic abscess: Diagnosed by CT
Frequent evaluation of oxygen saturation Evaluate need for assisted ventilation scan (presence of air in the retroperito-
Hematocrit daily/BUN twice daily for 48 hours Assess for bile duct obstruction neum); Gram staining and cultures of fluid
Serum electrolytes daily If bilirubin rising, consider urgent ERCP obtained from guided percutaneous aspi-
Pain control ration usually identify bacterial organism.
Therapy is surgical (or catheter) drainage

and Disorders
Diseases
and IV antibiotics (carbapenem is the
Later course: >72 hours
drug of choice)
Evidence of severe 4. Pancreatic ascites: Usually caused by
disease or organ failure?
leaking of pseudocyst or tear in pancre-
No Yes
atic duct. Paracentesis reveals very high

Early refeeding To ICU if patient not already there

amylase and lipase levels in the pancre-
atic fluid; ERCP may demonstrate the I
Evaluate for etiology Observe for biliary sepsis; if present, lesion. Treatment is surgical correction if
If gallstones, early cholecystectomy consider emergency ERCP exudative ascites from severe pancreati-
If alcohol, address psychosocial issues Enteral feedings (NJ or NG) tis does not resolve spontaneously
If high serum TG, medical therapy CT to evaluate for necrosis 5. Abdominal compartment syndrome:
Caused by intraabdominal leakage of flu-
ids from volume resuscitation or ascites.
Diagnosed with sustained intraabdominal
pressure >20 mm Hg with new-onset
Interstitial pancreatitis on CT without Pancreatic/peripancreatic necrosis on CT: organ failure
peripancreatic necrosis: Continue supportive care 6. Gastrointestinal bleeding: Caused
Continue supportive care Enteral feedings by alcoholic gastritis, bleeding varices,
Observation If infection suspected, consider
antibiotics
stress ulceration, or disseminated intra-
vascular coagulation (DIC)
7. Renal failure: Caused by hypovolemia,
Late course: 7-28 days resulting in oliguria or anuria, cortical or
Patient improving? tubular necrosis (shock, DIC), or thrombo-
sis of renal artery or vein
Yes No 8. Hypoxia: Caused by ARDS, pleural effu-
sion, or atelectasis
Consider oral refeeding If on antibiotics, consider FNA 9. Vascular: Splenic, portal, or superior
of pancreas for culture and mesenteric vein thrombosis; pseudoan-
change of antibiotics eurysm
If not on antibiotics and FNA
negative, keep off antibiotics THERAPY OF UNCOMMON
FORMS OF PANCREATITIS
• A utoimmune pancreatitis (AIP):
Beyond 28 days
Fibroinflammatory disease characterized by
Patient improving? an IgG4 lymphoplasmacytic infiltrate. It is a
Yes No variant of chronic pancreatitis and has been
associated with other autoimmune disorders
(e.g., primary sclerosing cholangitis, Sjögren
Consider refeeding Consider necrosectomy by syndrome). The inflammatory process is gen-
If patient cannot tolerate feedings, endoscopic, radiologic, or
consider necrosectomy surgical means
erally responsive to corticosteroid therapy.
Older men aged 60 to 70 yr are primarily
affected. Patients present with abdominal
FIG. 2  Algorithm for the management of acute pancreatitis at various stages in its course. NJ,
pain, weight loss, anorexia, and obstruc-
Nasojejunal. (From Feldman M, Friedman LS, Brandt LJ: Sleisenger and Fordtran’s gastrointestinal and liver
tive jaundice. Immunoglobulin G4 levels are
disease, ed 10, Philadelphia, 2016, Elsevier.)
elevated. Radiographically on CT, the pan-
creas is diffusely enlarged, with a charac-
teristic smooth, capsulelike rim (“sausage
a. D iagnosed by CT scan or sonography. in place for continuous drainage) can pancreas”). Features of type 1 and type 2
b. Treatment: Pancreatic pseudocysts be used, but the recurrence rate is autoimmune pancreatitis are summarized in
can be drained surgically or endo- high; the conservative approach is to Table 3. Type II autoimmune hepatitis (idio-
scopically. The endoscopic approach reevaluate the pseudocyst (with CT pathic duct-centric chronic pancreatitis) is
is preferable when the patient’s anat- scan or sonography) after 6 to 7 wk associated with inflammatory bowel disease
omy is suitable and an experienced and surgically drain it if the pseudo- and not related to IgG4 cell deposition.
endoscopist is available. CT scan cyst has not decreased in size. • Hypertriglyceridemic pancreatitis (HTGP):
or ultrasound-guided percutaneous c. Generally, pseudocysts <5 cm in IV insulin therapy is the cornerstone of
drainage (with a pigtail catheter left diameter are reabsorbed without immediate treatment, with supplemental IV

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1048 Pancreatitis, Acute ALG

TABLE 3  Features of Type 1 and Type 2 Autoimmune Pancreatitis
Feature
Histology
Average age at pre-
sentation
Gender predomi-
nance
Usual clinical pre-
sentations
Pancreatic imaging
IgG4
Other organ involve-
ment
Associated diseases
Long-term outcome
HPF, High power field; IBD, inflammatory bowel disease; IgG4, Immunoglobulin G, subclass 4.
From Feldman M, Friedman LS, Brandt LJ: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 10, Philadelphia, 2016,
Elsevier.
TABLE 4  Prognostic Criteria for Acute Pancreatitis
Ranson Criteria*
On admission: Age >55 yr
WBC >16,000/μL
AST >250 U/L LDH >350 U/L
Glucose >200 mg/dl
48 hr after admission:
Hematocrit decrease by >10
BUN increase by >5 mg/dl
Ca2+ <8 mg/dl
Arterial Po2 <60 mm Hg
Base deficit >4 mEq/L
Fluid sequestration >6 L
REFERRAL
• Hospitalization is indicated in moderate to
Type 1 Type 2 severe cases of pancreatitis.
• Surgical consultation is needed in suspect-
Lymphoplasmacytic infiltration Periductal lymphoplasmacytic and ed gallstone pancreatitis, perforated peptic
Dense periductal infiltrate without damage neutrophilic infiltration
to ductal epithelium Destruction of the duct epithelium by
ulcer, or presence of necrotic or infected
Storiform fibrosis neutrophils (granulocytic epithelial foci. Acute pancreatitis can generally be
Obliterative phlebitis lesion, or GEL) attributed to gallstones when patients have
Abundant (>10 cells/HPF) IgG4-positive Obliterative phlebitis is rare both abnormal liver enzymes and gallstones
cells No IgG4-positive cells (or sludge) on imaging. Such patients should
Fibroinflammatory process may extend to consider cholecystectomy prior to discharge
peripancreatic region to prevent recurrent pancreatitis.
60-70 yr 40-50, but may present in young • Gastroenterology consultation in severe or
adults and even children recurrent pancreatitis, when ERCP is needed
Male Equal for gallstone pancreatitis, or when the cause
of pancreatitis is unclear.
Obstructive jaundice (75%) Obstructive jaundice (50%) • Consider intensive care unit transfer for
Acute pancreatitis (15%) Acute pancreatitis (33%) patients who require aggressive fluid resus-
Diffuse pancreatic enlargement (40%) Diffuse pancreatic enlargement citation and are at risk of volume overload
Focal pancreatic enlargement (60%) (15%) from cardiac or renal causes. Similarly, con-
Focal pancreatic enlargement (85%) sider transfer for patients with developing
Level elevated in serum (~2/3 of patients) Not associated ARDS, patients with abdominal compartment
Positive in staining of involved tissues syndrome (with surgical consultation), and
Biliary strictures Not associated those who require apheresis.
Pseudotumors
Kidney
Lung PEARLS &
Others
Retroperitoneal fibrosis
CONSIDERATIONS
Sialoadenitis • Acute pancreatitis is the most common major
See above (other organ involvement) IBD complication of ERCP. NSAIDs are potent
Frequent relapses Rare or no relapse inhibitors of phospholipase A2, cyclooxygen-
ase, and neutrophil-endothelial interactions,
which play an important role in the pathogen-
esis of acute pancreatitis. Preliminary trials
show that among patients at high risk for
post-ERCP pancreatitis, rectal indomethacin
(given as two 50-mg indomethacin supposi-
Simplified Glasgow Computed Tomography tories administered immediately after ERCP)
Criteria† Criteria‡ significantly reduced the incidence of post-
ERCP pancreatitis.
Within 48 hr of admission: Age Normal
>55 yr Enlargement • Pancreatic stent placement decreases the
WBC >15,000/μL Pancreatic inflammation risk of post-ERCP pancreatitis.
LDH >600 U/L Single fluid collection • Statins reduce risk for pancreatitis in adults.
Glucose >180 mg/dl Multiple fluid collection Fibrates do not affect risk for pancreatitis
Albumin <3.2 g/dl other than in patients with hypertriglyceride-
Ca2+ <8 mg/dl mia-induced pancreatitis.
Arterial Po2 <60 mm Hg • Diabetes mellitus may develop from exten-
BUN >45 mg/dl sive pancreatic necrosis.

AST, Aspartate aminotransferase; BUN, blood urea nitrogen; LDH, lactate dehydrogenase; WBC, white blood cells.
SUGGESTED READINGS
*Three or more Ranson criteria predict a complicated clinical course. Data from Ranson JH et al: Prognostic signs and nonoperative Available at ExpertConsult.com
peritoneal lavage in acute pancreatitis, Surg Gynecol Obstet, 143:209-219, 1976.
†Data from Blamey SL et al: Prognostic factors in acute pancreatitis, Gut 25:1340, 1984.
‡Grades A and B represent mild disease with no risk of infection or death. Grade C represents moderately severe disease with a RELATED CONTENT
minimal likelihood of infection and essentially no risk of mortality. Grades D and E represent severe pancreatitis with an infection
rate of 30% to 50% and mortality rate of 15%. Data from Balthazar EJ et al: Acute pancreatitis value of CT in establishing
Acute Pancreatitis (Patient Information)
prognosis, Radiology, 174:331, 1990. AUTHOR: David J. Lucier, Jr., MD, MBA, MPH
From Goldman L, Ausiello D (eds): Cecil textbook of medicine, ed 24, Philadelphia, 2012, Saunders.

glucose infusion if the serum glucose levels
are not elevated. IV heparin was previously
used as well, but its effectiveness has come
into question. Antihyperlipidemic agents
(fibrates) should be initiated as adjuvant
therapy as soon as possible for long-term
control. Beneficial results have been reported
with early (within 48 hr) initiation of apher-
esis with therapeutic plasma exchange when
there is concomitant hypocalcemia, lactic
acidosis, or other signs of organ dysfunction.
DISPOSITION
Prognosis varies with the severity of pancreati-
tis; overall mortality rate in acute pancreatitis
is 5% to 10%. Prognostic criteria for acute
pancreatitis are described in Table 4.

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Pancreatitis, Acute 1048.e1

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Forsmark CE et al: Acute pancreatitis, N Engl J Med 375:1972-1981, 2016.
Quinlan JD et al: Acute pancreatitis, Am Fam Physician 90(9):632-639, 2014.
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Med 170:178-181, 2019.
Trna J et  al: Lack of significant liver enzyme elevations and gallstones and/or
sludge on ultrasound on day 1 of acute pancreatitis is associated with recur-
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Descargado para Juan Sebastian Valencia Quintero (juans-valenciaq@unilibre.edu.co) en Free University de ClinicalKey.es por Elsevier en febrero 24, 2021.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.