Puntos Clave: CAPÍTULO 108: Pancreatitis Aguda

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Universidad Javeriana
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Principios de cuidados intensivos, 4e
CAPÍTULO 108: Pancreatitis aguda
Ajaypal Singh; Andrés Gelrud
PUNTOS CLAVE
La pancreatitis aguda es una causa frecuente de enfermedad crítica relacionada con el aparato digestivo.
La mayoría de los casos son causados por el alcohol y los cálculos biliares; otras etiologías incluyen hipertrigliceridemia, pancreatitis postCPRE,
hipercalcemia, traumatismos, infecciones y medicamentos.
Dos de los tres criterios siguientes establecen el diagnóstico de pancreatitis aguda: aparición repentina de dolor abdominal característico;
amilasa y / o lipasa séricas por encima de tres veces lo normal; Inflamación pancreática en estudios de imagen.
There are two types of acute pancreatitis—interstitial edematous and necrotizing. The former has pancreatic enlargement with diffuse pancreatic
and peripancreatic inflammation. The latter has necrosis of pancreatic and/or peripancreatic tissue, in addition to inflammatory changes.
Early crystalloid administration in fluidresponsive patients is important in the management of acute pancreatitis.
Early enteral nutrition has been validated as an important component of the management of acute pancreatitis; avoiding enteral feeding and/or
use of parenteral nutrition is not recommended.
There is no role for prophylactic antibiotics in the management of acute pancreatitis; however, broad spectrum antibiotics (eg, carbapenems) are
indicated in the presence of documented or suspected pancreatitic infection.
Endoscopic retrograde cholangiopancreatography (ERCP) is indicated in patients with acute gallstone pancreatitis with cholangitis and those with
pancreatic duct disruption.
Endoscopic debridement is superior to open necrosectomy for the management of mature, walledoff fluid collections.
Acute pancreatitis is currently the most frequent gastrointestinal cause of hospital admissions in the United States with a total of 275,000 admissions in
20091 and approximately $2.2 billion in annual health care costs.2 The overall mortality among patients with acute pancreatitis is around 5%, but
patients who develop severe acute pancreatitis have mortality rates as high as 15%3 and even higher when multiorgan failure is present. Appropriate
intensive care management of these patients and a multidisciplinary approach play a very important role in treatment of those patients who develop
severe acute pancreatitis. In 2012, a revised version of the original Atlanta classification was published that focused on defining the severity of acute
pancreatitis and classification of pancreatic and peripancreatic fluid collections.4
PATHOPHYSIOLOGY
Acute pancreatitis is believed to be triggered by an increase in the intraductal pressure or direct injury to acinar cells from metabolic or toxic stimuli
which leads to breakdown of the junctional barrier between acinar cells and leakage of pancreatic fluid and enzymes into the interstitial space.5
Intrapancreatic activation of proteolytic enzymes leads to autophagy and autodigestion of acinar cells.6 Lysosomal enzymes such as cathepsin B
initiate the activation of trypsinogen to trypsin which then leads to activation of more trypsin as well as other pancreatic enzymes including
phospholipase, chymotrypsin, and elastase.7 The acinar tissue death leads to an intense systemic inflammatory response syndrome (SIRS) caused by
the release of activated pancreatic enzymes and mediated by cytokines, immunocytes, and the complement system. Inflammatory cytokines (such as
tumor necrosis factor) cause macrophages to migrate into tissues distant from the pancreas, including lungs and kidneys. Immunocytes attracted by
cytokines released from macrophages release more cytokines, free radicals, and nitric oxide; the result is tissue destruction, fluid and electrolyte loss,
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hypotension, renal and pulmonary complications, late septic complications, and, in severe cases, multisystem organ failure (MSOF) and death.
CHAPTER 108: Acute Pancreatitis, Ajaypal Singh; Andrés Gelrud Page 1 / 15
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ETIOLOGY
Intrapancreatic activation of proteolytic enzymes leads to autophagy and autodigestion of acinar cells.6 Lysosomal enzymes such as cathepsin B
Pontificia Universidad Javeriana
initiate the activation of trypsinogen to trypsin which then leads to activation of more trypsin as well as other pancreatic enzymes including
phospholipase, chymotrypsin, and elastase.7 The acinar tissue death leads to an intense systemic inflammatory response syndrome (SIRS) caused by
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the release of activated pancreatic enzymes and mediated by cytokines, immunocytes, and the complement system. Inflammatory cytokines (such as
tumor necrosis factor) cause macrophages to migrate into tissues distant from the pancreas, including lungs and kidneys. Immunocytes attracted by
cytokines released from macrophages release more cytokines, free radicals, and nitric oxide; the result is tissue destruction, fluid and electrolyte loss,
hypotension, renal and pulmonary complications, late septic complications, and, in severe cases, multisystem organ failure (MSOF) and death.
ETIOLOGY
The two most common causes of pancreatitis in the United States are alcohol and gallstone pancreatitis, accounting for approximately 75% to 80% of
the cases. Other common etiologies include hypertriglyceridemia, postERCP pancreatitis, hypercalcemia, trauma, infections, drug injury, anatomical
variants such as pancreas divisum, and idiopathic pancreatitis (Table 1081). Recently, multiple studies have shown smoking to be an independent
risk factor for acute pancreatitis in a dosedependent manner.810
TABLE 1081
Etiology of Acute Pancreatitis
Toxic Alcohol
Methanol
Smoking
Organophosphates
Scorpion bite
Mechanical obstruction/duct damage Biliary pancreatitis (gallstones)
Biliary sludge
Parasitic infections (ascariasis)
Malignancy (pancreatic, ampullary, cholangiocarcinoma)
Periampullary diverticulum
Abdominal trauma/duct disruption
Metabolic Hypertriglyceridemia
Hypercalcemia
Immunerelated Autoimmune pancreatitis
Vasculitis (SLE, polyarteritis nodosa)
Drugs 5ASA/salicylates, azathioprine/6MP, didanosine, pentamidine, furosemide, tetracyclines, thiazides, estrogen
Infections Viral: mumps, varicellazoster, coxsackie, HSV, HIV
Bacterial: Mycoplasma, Leptospira, Legionella
Parasitic: Toxoplasma, cryptosporidium
Fungal: Aspergillus
Miscellaneous Idiopathic
PostERCP pancreatitis
Pancreas divisum in some patients
Ischemia
Genetic mutations in PRSS1, SPINK, CTRC, or CFTR genes
Common etiologies highlighted. CFTR, cystic fibrosis transmembrane conductance regulator; CTRC, chymotrypsin C; ERCP, endoscopic retrograde
cholangiopancreatography; HIV, human immunodeficiency virus; HSV, herpes simplex virus; PRSS1, serine protease 1; SLE, systemic lupus erythematosus; SPINK,
serine protease inhibitor Kazal type 1.
Patients who are critically ill are also at increased risk of developing pancreatitis due to ischemic injury.11 Hypoperfusion can play an important role in
The two most common causes of pancreatitis in the United States are alcohol and gallstone pancreatitis, accounting for approximately 75% to 80% of
the cases. Other common etiologies include hypertriglyceridemia, postERCP pancreatitis, hypercalcemia, trauma, infections, drug injury, anatomical
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variants such as pancreas divisum, and idiopathic pancreatitis (Table 1081). Recently, multiple studies have shown smoking to be an independent
risk factor for acute pancreatitis in a dosedependent manner.810
TABLE 1081
Etiology of Acute Pancreatitis
Toxic Alcohol
Methanol
Smoking
Organophosphates
Scorpion bite
Mechanical obstruction/duct damage Biliary pancreatitis (gallstones)
Biliary sludge
Parasitic infections (ascariasis)
Malignancy (pancreatic, ampullary, cholangiocarcinoma)
Periampullary diverticulum
Abdominal trauma/duct disruption
Metabolic Hypertriglyceridemia
Hypercalcemia
Immunerelated Autoimmune pancreatitis
Vasculitis (SLE, polyarteritis nodosa)
Drugs 5ASA/salicylates, azathioprine/6MP, didanosine, pentamidine, furosemide, tetracyclines, thiazides, estrogen
Infections Viral: mumps, varicellazoster, coxsackie, HSV, HIV
Bacterial: Mycoplasma, Leptospira, Legionella
Parasitic: Toxoplasma, cryptosporidium
Fungal: Aspergillus
Miscellaneous Idiopathic
PostERCP pancreatitis
Pancreas divisum in some patients
Ischemia
Genetic mutations in PRSS1, SPINK, CTRC, or CFTR genes
Common etiologies highlighted. CFTR, cystic fibrosis transmembrane conductance regulator; CTRC, chymotrypsin C; ERCP, endoscopic retrograde
cholangiopancreatography; HIV, human immunodeficiency virus; HSV, herpes simplex virus; PRSS1, serine protease 1; SLE, systemic lupus erythematosus; SPINK,
serine protease inhibitor Kazal type 1.
Patients who are critically ill are also at increased risk of developing pancreatitis due to ischemic injury.11 Hypoperfusion can play an important role in
the progression of mild acute pancreatitis to severe, necrotizing pancreatitis in those cases where the initial insult was due to the more common
etiologies in noncritical care setting.12
DIAGNOSIS AND ASSESSMENT OF SEVERITY
Most patients with acute pancreatitis present with sudden onset, severe, persistent epigastric, or right upper quadrant pain, with or without radiation
to the back associated with nausea and vomiting. 13,14 Physical examination findings vary according to the severity of the disease and range from mild
epigastric tenderness to a diffusely tender abdomen. Presence of ecchymotic discoloration in the periumbilical region (Cullen sign) or along the flanks
(Grey Turner sign) suggests retroperitoneal bleed.
the progression of mild acute pancreatitis to severe, necrotizing pancreatitis in those cases where the initial insult was due to the more common
etiologies in noncritical care setting.12 Access Provided by:
DIAGNOSIS AND ASSESSMENT OF SEVERITY
Most patients with acute pancreatitis present with sudden onset, severe, persistent epigastric, or right upper quadrant pain, with or without radiation
to the back associated with nausea and vomiting.13,14 Physical examination findings vary according to the severity of the disease and range from mild
epigastric tenderness to a diffusely tender abdomen. Presence of ecchymotic discoloration in the periumbilical region (Cullen sign) or along the flanks
(Grey Turner sign) suggests retroperitoneal bleed.
Serum amylase and lipase are both elevated early in the course of acute pancreatitis (within 412 hours). Amylase has a shorter halflife of 10 hours and
returns to normal within 3 to 5 days, while lipase elevations last longer, returning to baseline within 8 to 14 days. Serum lipase is more sensitive and
specific than amylase for diagnosis of acute pancreatitis.
The diagnosis of acute pancreatitis requires two of the following three criteria:
Sudden onset of characteristic abdominal pain
Elevation of serum amylase and/or lipase above three times normal
Findings of pancreatic inflammation noted on imaging (CT, MRI, or ultrasound)
Imaging is not required for diagnosis of acute pancreatitis in patients who present with characteristic abdominal pain and elevated serum amylase or
lipase.
Since the original Atlanta classification of acute pancreatitis in 1992, multiple predictive models for acute pancreatitis were proposed and there was
much confusion regarding the terminology used for local complications and fluid collections from acute pancreatitis. In an attempt to address these
issues, a revised Atlanta classification was published in 2012 which offers a detailed classification of acute pancreatitis, its severity and terminology for
early and late pancreatic and peripancreatic collections.4
Types of Acute Pancreatitis: The revised Atlanta classification (Table 1082) divides acute pancreatitis into two types, interstitial edematous
pancreatitis (Fig. 1081) and necrotizing pancreatitis (Fig. 1082). Patients with interstitial edematous pancreatitis have diffuse inflammation of the
pancreatic and peripancreatic tissue with enlargement of the pancreas. Necrotizing pancreatitis is seen in less than 10% of all patients with acute
pancreatitis. These patients have necrosis of either pancreatic or peripancreatic tissue or both, in addition to the inflammatory changes. On contrast
enhanced CT scans, interstitial edematous pancreatitis appears as homogenous enhancement, while pancreatic/peripancreatic necrosis is seen as
nonenhancing areas. Of note, the necrosis of pancreatic tissue can develop over days after onset of abdominal pain and can be missed on imaging
done early during the course of disease.15,16
TABLE 1082
Revised Atlanta Classification (2012) for Pancreatic and Peripancreatic Fluid Collections
Definition Duration CECT (ContrastEnhanced CT) Features
Acute fluid collection (AFC) <4 weeks Homogenous with fluid density

No encapsulation
Interstitial edematous pancreatitis
Acute necrotic collection (ANC) <4 weeks Heterogenous (both fluid and solid components)

No encapsulation
Acute necrotizing pancreatitis
Pseudocyst (PP) >4 weeks Homogenous with fluid density

Well defined wall
After interstitial edematous pancreatitis
Walledoff necrosis (WON) >4 weeks Heterogenous (both fluid and solid components
Well defined wall
After acute necrotizing pancreatitis
pancreatitis. These patients have necrosis of either pancreatic or peripancreatic tissue or both, in addition to the inflammatory changes. On contrast
enhanced CT scans, interstitial edematous pancreatitis appears as homogenous enhancement, while pancreatic/peripancreatic necrosis is seen as
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nonenhancing areas. Of note, the necrosis of pancreatic tissue can develop over days after onset of abdominal pain and can be missed on imaging
done early during the course of disease.15,16
TABLE 1082
Revised Atlanta Classification (2012) for Pancreatic and Peripancreatic Fluid Collections
Definition Duration CECT (ContrastEnhanced CT) Features
Acute fluid collection (AFC) <4 weeks Homogenous with fluid density

No encapsulation
Interstitial edematous pancreatitis
Acute necrotic collection (ANC) <4 weeks Heterogenous (both fluid and solid components)

No encapsulation
Acute necrotizing pancreatitis
Pseudocyst (PP) >4 weeks Homogenous with fluid density

Well defined wall
After interstitial edematous pancreatitis
Walledoff necrosis (WON) >4 weeks Heterogenous (both fluid and solid components

Well defined wall
After acute necrotizing pancreatitis
FIGURE 1081
A 52yearold man admitted with sudden onset of postprandial severe abdominal pain. On abdominal CT scan, the pancreas enhances uniformly with
intravenous contrast. There is fat stranding particularly in the head and neck of the pancreas (arrows).
FIGURE 1082
A 68yearold man with severe abdominal pain 30 minutes after eating fried chicken. Abdominal CT scan with IV contrast reveals a nonenhancing area
on the pancreatic body consistent with necrotizing pancreatitis (arrows)
FIGURE 1082 Pontificia Universidad Javeriana
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A 68yearold man with severe abdominal pain 30 minutes after eating fried chicken. Abdominal CT scan with IV contrast reveals a nonenhancing area
on the pancreatic body consistent with necrotizing pancreatitis (arrows)
The clinical course after an episode of acute pancreatitis is quite variable and it is of utmost importance to detect highrisk patients who will progress
to severe, necrotizing pancreatitis in an effort to improve outcomes. Multiple clinical scoring systems have been used to predict the severity of acute
pancreatitis. These scoring systems are very important because they can help recognize patients with severe acute pancreatitis who would require
aggressive care in the intensive care unit. Ranson criteria have been shown to be moderately accurate in predicting the severity of acute pancreatitis,17
19 but it takes 48 hours after initial hospitalization to be calculated and involves laboratory values that are not routinely checked. As such, it is not
frequently used. The Acute Physiology and Chronic Health Examination II (APACHE II) score was initially developed for critically ill patients and is
currently the most widely used scoring system for severity of acute pancreatitis. It is as accurate as the Ranson criteria and is faster to calculate.20
Recently, a new scoring method known as bedside index for severity in acute pancreatitis (BISAP) was developed in an attempt to recognize early
disease severity.21 It is based on blood urea nitrogen (BUN) >25 mg/dL, impaired mental status, presence of systemic inflammatory response syndrome
(SIRS), age >60 years, and presence of pleural effusions. Even though it is simpler and quick to calculate, it has been found to have lower sensitivity
than both Ranson and APACHE II scores in predicting severity, pancreatic necrosis, and mortality in patients with acute pancreatitis.22
The revised Atlanta classification has attempted to simplify this classification of severity of acute pancreatitis and it divides acute pancreatitis into mild
acute pancreatitis, moderately severe acute pancreatitis, and severe acute pancreatitis.4 This classification is based on the presence or absence of
organ failure and local or systemic complications. In the classification, transient organ failure refers to organ failure that is present for <48 hours, while
persistent organ failure is present for >48 hours after onset. Local complications refer to acute peripancreatic fluid collections or pancreatic necrosis.
Exacerbation of previously present comorbidities is considered systemic complication. The modified Marshall scoring system is used for assessing
organ failure. It involves assessment of cardiovascular, respiratory, and renal systems.
Mild acute pancreatitis is associated with very low mortality and is characterized by the absence of organ failure, local and systemic complications.
Most of these patients do not require crosssectional imaging and have a short hospital stay. Moderately severe pancreatitis is characterized by
presence of transient organ failure or local or systemic complications but persistent organ failure is absent; mortality rate is also low. Severe acute
pancreatitis is indicated by the presence of persistent organ failure and carries a higher mortality rate.
INITIAL RESUSCITATION AND MANAGEMENT
EARLY FLUID RESUSCITATION
Aggressive management of patients with acute pancreatitis should begin early after diagnosis (eg, in the emergency department). Published data
suggest that initial resuscitation can affect the outcomes of acute pancreatitis significantly. The first 24 hours have been referred to as the “golden
hours” of management of acute pancreatitis23 and both underresuscitation as well as overresuscitation can lead to worse outcomes; accordingly,
very close monitoring of these patients is needed.2426 There is no benefit of using colloids for fluid resuscitation over crystalloids in acute
pancreatitis.27 Lactated Ringer’s solution has been found to be associated with a markedly decreased incidence of SIRS compared to 0.9% sodium
chloride. Though the exact mechanism for this is not known, it is hypothesized that hyperchloremic metabolic acidosis caused by normal saline can
promote activation of trypsinogen in a pH dependent manner.28 Hence, lactated Ringer’s should be the initial choice for volume resuscitation in all
patients with acute pancreatitis except those with hypercalcemia since it contains 3 mEq/L of calcium. Serial measurements of blood urea nitrogen and
hematocrit should accompany fluid resuscitation along with close assessment of clinical condition, vital signs, and urine output. An evidencebased
approach to fluid resuscitation should be utilized (see Chap. 34 on “Judging the Adequacy of Fluid Resuscitation”) and fluid resuscitation should begin
early in the course of management. A large single center retrospective study showed that those patients with acute pancreatitis who received early
resuscitation (receiving more than onethird of total 72hour fluid volume within first 24 hours of presentation) had significantly lower incidence of
hours” of management of acute pancreatitis and both underresuscitation as well as overresuscitation can lead to worse outcomes; accordingly,
very close monitoring of these patients is needed.2426 There is no benefit of using colloids for fluid resuscitation over crystalloids in acute
pancreatitis.27 Lactated Ringer’s solution has been found to be associated with a markedly decreased incidence of SIRS compared to 0.9% sodium
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chloride. Though the exact mechanism for this is not known, it is hypothesized that hyperchloremic metabolic acidosis caused by normal saline can
promote activation of trypsinogen in a pH dependent manner.28 Hence, lactated Ringer’s should be the initial choice for volume resuscitation in all
patients with acute pancreatitis except those with hypercalcemia since it contains 3 mEq/L of calcium. Serial measurements of blood urea nitrogen and
hematocrit should accompany fluid resuscitation along with close assessment of clinical condition, vital signs, and urine output. An evidencebased
approach to fluid resuscitation should be utilized (see Chap. 34 on “Judging the Adequacy of Fluid Resuscitation”) and fluid resuscitation should begin
early in the course of management. A large single center retrospective study showed that those patients with acute pancreatitis who received early
resuscitation (receiving more than onethird of total 72hour fluid volume within first 24 hours of presentation) had significantly lower incidence of
SIRS, organ failure, admission to intensive care unit, and a reduced length of stay compared to those with late resuscitation (receiving less than one
third of total 72 hours fluid volume within first 24 hours).29
A general approach is to start with a 1000 to 2000mL crystalloid fluid bolus followed by fluid resuscitation at a rate of 250 to 300 mL/h for 1000 to 3000
mL, to target a urine output of at least 0.5 mL/kg per hour. However, one should utilize the tools outlined in Chap. 34 to judge the adequacy of fluid
resuscitation rather than following an exact recipe. Some patients with cardiopulmonary disease, particularly those with ARDS, may progress to
respiratory failure and require endotracheal intubation.
NUTRITION IN ACUTE PANCREATITIS
The nutritional therapy in acute pancreatitis has significantly evolved from the concept of “pancreas rest” to efforts directed at early resumption of
enteral nutrition with an aim to maintain the gut integrity and prevent bacterial translocation and associated complications. Enteral nutrition should
be initiated as soon as possible. It is safe in patients with acute pancreatitis and it has been shown to be associated with lower rates of systemic
infections, multiorgan failure, and mortality in comparison to parenteral nutrition.30,31 Until recently, the general practice was to avoid oral intake until
resolution of abdominal pain; however, patients with mild acute pancreatitis can be fed as soon as they are hungry, without any restriction on the
consistency of food. A low fat solid diet seems to be as safe as clear liquid diet.32 Nutritional support is often needed in patients with moderately severe
and severe acute pancreatitis and should be started within 24 to 48 hours of initial presentation, especially when it is likely that the patient will be
unable to start oral intake within the next 5 to 7 days. As noted above, enteral nutrition is preferred over parenteral nutrition. Multiple studies and
metaanalyses have shown that parental nutrition is associated with vascular catheterrelated complications and infections, while enteral nutrition
appears to help maintain gut mucosal integrity and hence decrease bacterial translocation;30,31,33 it is associated with decreases in infections, organ
failure, and length of stay.34 There has been significant debate regarding nasogastric versus nasojejunal feeding in these patients but no data are
currently available to strongly favor any one approach over the other. Though traditionally nasojejunal feedings have been preferred in patients with
acute pancreatitis, nasogastric tube feeding has been shown to as safe as the jejunal feeding.31,35,36 Aspiration precautions, including elevation of
head end of bed, should be applied in all patients. Checking gastric residuals to guide gastric feeding has not been shown to be beneficial. In patients
who cannot tolerate gastric feeding due to large fluid collections causing gastric compression or duodenal obstruction, nasojejunal tube placement is
usually needed.
ROLE OF PROPHYLACTIC ANTIBIOTICS
Approximately onefourth of patients with acute pancreatitis develop infectious complications and those with severe acute pancreatitis are at
particularly high risk. Patients with infected pancreatic necrosis have a mortality of around 30%14 (Fig. 1083). The use of prophylactic antibiotics was
common in the early 2000s in patients with severe acute pancreatitis. Multiple studies and a recently published Cochrane metaanalysis have shown
that the use of prophylactic antibiotics is not associated with decreased incidence of infected pancreatic necrosis, mortality, or need for surgical
interventions,3739 even though a decreased incidence of infection in pancreatic necrosis and a trend toward lower mortality were noted in patients
receiving imipenem.40 However, all patients with severe acute pancreatitis requiring critical care should be monitored closely for development of any
signs of sepsis or infection, since delay in starting antibiotic therapy has been shown to be associated with declining survival. Hence, recent guidelines
from American College of Gastroenterology published in 2013 suggest that when an infection is suspected, it is justifiable to start empiric antibiotics
covering both gram, negative and grampositive organisms; antibiotics should be discontinued if cultures are negative and no definite source is
identified.33
FIGURE 1083
A 34yearold man with a history biliary pancreatitis with epigastric abdominal pain and new onset of fever and chills 48 hours prior to admission. CT
Scan reveals walled off necrosis (WON) in the tail of the pancreas area with air (white arrow). This finding and associated symptoms are diagnostic of
infected WON.
FIGURE 1083
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A 34yearold man with a history biliary pancreatitis with epigastric abdominal pain and new onset of fever and chills 48 hours prior to admission. CT
Scan reveals walled off necrosis (WON) in the tail of the pancreas area with air (white arrow). This finding and associated symptoms are diagnostic of
infected WON.
ROLE OF ERCP IN ACUTE PANCREATITIS
The role of endoscopic retrograde cholangiopancreatography in ERCP in management of acute pancreatitis is limited to patients with acute gallstone
pancreatitis with cholangitis and those with pancreatic duct disruption. Patients with acute pancreatitis and biliary sepsis (cholangitis) should have
ERCP performed within 24 hours of admission since it has been shown to be associated with decreased morbidity and mortality.41,42 The beneficial role
of ERCP in patients with gallstone pancreatitis without cholangitis is not clear. A large multicenter study and a recent metaanalysis involving 717
patients have both shown that there is no beneficial role for early ERCP in acute pancreatitis patients with severe acute biliary pancreatitis without
biliary sepsis.43,44
When acute pancreatitis is mild interstitial, and biliary in origin, it is favorable to proceed with cholecystectomy prior to discharging the patient home.45
With moderate or severe biliary pancreatitis, it is favored to wait and reimage a month after the episode to assure that no fluid collections are present;
if so, the gallbladder can be removed and the fluid collection treated, both during the same surgery.46 ERCP with biliary sphincterotomy should be
performed to protect the pancreas against another attack of pancreatitis while waiting for the cholecystectomy or in those patients who are poor
candidates for cholecystectomy.47
PANCREATIC AND PERIPANCREATIC COLLECTIONS
The recent Atlanta classification has led to a major change in the classification of the pancreatic and peripancreatic fluid collections based on the
presence or absence and duration of solid material in these collections.4 The four types of fluid collections as a sequel of acute pancreatitis include
acute fluid collection (AFC), pancreatic pseudocyst (PP) (Fig. 1084), acute necrotic collection (ANC), and walledoff necrosis (WON) (Fig. 1085). All
these types of fluid collections have significantly different management strategies and hence it is very important to distinguish one from the others.
AFCs develop early in acute interstitial edematous pancreatitis, are homogenous on contrastenhanced imaging (no solid debris), do not have well
developed demarcation, and usually resolve without any intervention. If these persist beyond 4 weeks, they develop a welldemarcated wall and are
known as pseudocysts, which do not contain any solid material. Acute necrotic collection (ANC), usually seen during the first 4 weeks in necrotizing
pancreatitis, contains both fluid and necrotic components and is without a welldemarcated wall. These can progress to a welldefined encapsulation
after 4 weeks, a condition known as walledoff necrosis. Both ANCs and WONs can become infected, which is associated with morbidity and mortality.
FIGURE 1084
A 42yearold woman with early satiety, nausea, abdominal pain, and weight loss 6 weeks after an episode of interstitial pancreatitis. Abdominal CT
scan reveals a large pancreatic pseudocyst compressing the stomach. She was successfully treated with endoscopic cystgastrostomy with stent
placement.
FIGURE 1084
A 42yearold woman with early satiety, nausea, abdominal pain, and weight loss 6 weeks after an episode of interstitial pancreatitis. Abdominal CT
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scan reveals a large pancreatic pseudocyst compressing the stomach. She was successfully treated with endoscopic cystgastrostomy with stent
placement.
FIGURE 1085
A 39yearold woman with history of hypertriglyceridemiainduced necrotizing pancreatitis with early satiety, nausea, abdominal pain, and weight loss.
Abdominal CT scan reveals a large pancreatic and peripancreatic collection with walledoff necrosis compressing the stomach. She was successfully
treated with endoscopic transgastric cystnecrosectomy and two percutaneous drains.
It is usually difficult to differentiate between AFC and ANC during the first week or two of acute pancreatitis since both can appear homogenous with
fluid consistency on contrast imaging. Hence, delaying imaging for the first 2 weeks after admission is acceptable, unless indicated for clinical
management.
Management: Majority of the AFCs resolve within a few weeks of acute pancreatitis onset and do not require any intervention; however, 6% to 7% of
these can persist beyond 4 weeks as pseudocysts or walledoff pancreatic necrosis. Only symptomatic patients require treatment—asymptomatic
collections do not require treatment irrespective of their size. The symptoms from pancreatic or peripancreatic collections are usually due to
obstruction of adjacent viscera (gastric or duodenal outlet obstruction with early satiety, nausea and vomiting, biliary or pancreatic obstruction),
infection, rupture, or bleeding. Therapy can be provided in the form of drainage or drainage along with necrosectomy in patients with walledoff
necrosis. The approach depends on the local expertise and includes: endoscopic drainage (transpapillary, transgastric or transduodenal), placement
of percutaneous drains by interventional radiology, or surgical intervention (videoassisted retroperitoneal debridement, laparoscopic or open
surgery). While rupture requires urgent surgical exploration, bleeding into the pseudocyst and pseudoaneurysms can be treated with angiographic
embolization.48 Endoscopic drainage can be used in symptomatic collections. It is important to assess the ductal anatomy in these cases since
transpapillary drainage should be performed if the pseudocyst is communicating with the main pancreatic duct or there is pancreatic duct disruption.
Otherwise, transgastric or transduodenal approaches should be sufficient.
Both acute pancreatic necrosis and walledoff necrosis can become infected and have high mortality necessitating antibiotics and debridement.
Previously, early surgical approach was the only option available for these patients, but transgastric endoscopic necrosectomy has been increasingly
performed since 2000 with excellent results. It has dramatically changed the way we now treat symptomatic patients with walledoff necrosis.49
Drainage procedures (endoscopic, interventional radiology, or surgical) should be avoided in the first 4 weeks until a welldefined wall develops
necrosis. The approach depends on the local expertise and includes: endoscopic drainage (transpapillary, transgastric or transduodenal), placement
of percutaneous drains by interventional radiology, or surgical intervention (videoassisted retroperitoneal debridement, laparoscopic or open
surgery). While rupture requires urgent surgical exploration, bleeding into the pseudocyst and pseudoaneurysms can be treated with angiographic
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embolization.48 Endoscopic drainage can be used in symptomatic collections. It is important to assess the ductal anatomy in these cases since
transpapillary drainage should be performed if the pseudocyst is communicating with the main pancreatic duct or there is pancreatic duct disruption.
Otherwise, transgastric or transduodenal approaches should be sufficient.
Both acute pancreatic necrosis and walledoff necrosis can become infected and have high mortality necessitating antibiotics and debridement.
Previously, early surgical approach was the only option available for these patients, but transgastric endoscopic necrosectomy has been increasingly
performed since 2000 with excellent results. It has dramatically changed the way we now treat symptomatic patients with walledoff necrosis.49
Drainage procedures (endoscopic, interventional radiology, or surgical) should be avoided in the first 4 weeks until a welldefined wall develops
around these collections. A direct correlation exists between success of endoscopic intervention and degree of encapsulation,50 and early intervention
is associated with poor outcomes.51 Multiple studies have now shown that endoscopic debridement is superior to open necrosectomy,52,53 due to
lower morbidity and mortality rates.54 But it is very important to recognize that not all patients with necrotizing pancreatitis will need necrosectomy.
Hence, a stepup approach has been proposed in managing these patients. In one of the largest prospective cohort studies on patients with
necrotizing pancreatitis, it was shown that up to twothirds of the patients with necrotizing pancreatitis can be managed conservatively with aggressive
intensive care support. In those who develop infected necrosis, onethird can be managed by simple catheter drainage without debridement (either
transcutaneous or endoscopic), while those who fail drainage require necrosectomy.3
The therapy for patients with severe acute pancreatitis must be individualized and decisions must be made in a multidisciplinary fashion including
gastroenterologist/pancreatologist, critical care physician, surgeon, and interventional radiologist to ensure the best outcome.
KEY REFERENCES
Aboulian A, Chan T, Yaghoubian A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a
randomized prospective study. Ann Surg. 2010; 251(4):615619.
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Puntos Clave: CAPÍTULO 108: Pancreatitis Aguda

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Puntos Clave: CAPÍTULO 108: Pancreatitis Aguda

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Pontificia

Definition Duration CECT (ContrastEnhanced CT) Features

Acute fluid collection (AFC) <4 weeks Homogenous with fluid density

Acute necrotic collection (ANC) <4 weeks Heterogenous (both fluid and solid components)

Pseudocyst (PP) >4 weeks Homogenous with fluid density

Definition Duration CECT (ContrastEnhanced CT) Features

Acute fluid collection (AFC) <4 weeks Homogenous with fluid density

Acute necrotic collection (ANC) <4 weeks Heterogenous (both fluid and solid components)

Pseudocyst (PP) >4 weeks Homogenous with fluid density

Walledoff necrosis (WON) >4 weeks Heterogenous (both fluid and solid components

You might also like

Puntos Clave: CAPÍTULO 108: Pancreatitis Aguda

Uploaded by

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Original Title

Copyright

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Puntos Clave: CAPÍTULO 108: Pancreatitis Aguda

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Copyright:

Available Formats

Pontificia

Definition Duration CECT (Contrast­Enhanced CT) Features

Acute fluid collection (AFC) <4 weeks Homogenous with fluid density

Acute necrotic collection (ANC) <4 weeks Heterogenous (both fluid and solid components)

Pseudocyst (PP) >4 weeks Homogenous with fluid density

Definition Duration CECT (Contrast­Enhanced CT) Features

Acute fluid collection (AFC) <4 weeks Homogenous with fluid density

Acute necrotic collection (ANC) <4 weeks Heterogenous (both fluid and solid components)

Pseudocyst (PP) >4 weeks Homogenous with fluid density

Walled­off necrosis (WON) >4 weeks Heterogenous (both fluid and solid components

You might also like

Definition Duration CECT (ContrastEnhanced CT) Features

Definition Duration CECT (ContrastEnhanced CT) Features

Walledoff necrosis (WON) >4 weeks Heterogenous (both fluid and solid components