acute pancreatitis

1. ACUTE PANCREATITIS
DR THANA RAM PATEL
ACADEMIC JUNIOR RESIDENT
DEPARTMENT OF SURGERY
SMS MEDICAL COLLEGE JAIPUR

2. INTRODUCTION
• The incidence of acute pancreatitis (AP) has increased during the
past 20 years. AP is responsible for more than 300,000 hospital
admissions annually in the United States.
• Most patients develop a mild and self-limited course; however, 10%
to 20% of patients hav a rapidly progressive inflammatory response
associated with prolonged length of hospital stay and significant
morbidity and mortality. Patients with mild pancreatitis have a
mortality rate of less than 1%, but in severe pancreatitis, this
increases up to 10% to 30%. The most common cause of death in
this group of patients is multiorgan dysfunction syndrome.
Mortality in pancreatitis has a bimodal distribution; in the first 2
weeks, also known as the early phase, the multiorgan dysfunction
syndrome is the final result of an intense inflammatory cascade
triggered initially by pancreatic inflammation. Mortality after 2
weeks, also known as the late period, is often caused by septic
complications.

3. Common causes
• Gallstones (including microlithiasis)
• Alcohol (acute and chronic alcoholism)
• Hypertriglyceridemia
• Endoscopic retrograde cholangiopancreatography
(ERCP), especially after biliary manometry
• Drugs (azathioprine, 6-mercaptopurine, sulfonamides,
estrogens, tetracycline,valproic acid, anti-HIV
medications, 5-aminosalicylic acid [5-ASA])
• Trauma (especially blunt abdominal trauma)
• Postoperative (abdominal and nonabdominal
operations)

4. Uncommon causes
• Vascular causes and vasculitis (ischemic-hypoperfusion states after
cardiac surgery)
• Connective tissue disorders and thrombotic thrombocytopenic
purpura (TTP)
• Cancer of the pancreas
• Hypercalcemia
• Periampullary diverticulum
• Pancreas divisum
• Hereditary pancreatitis
• Cystic fibrosis
• Renal failure
• Infections (mumps, coxsackievirus, cytomegalovirus, echovirus,
parasites)
• Autoimmune (e.g., type 1 and type 2)

5. Causes to Consider in Patients with Recurrent Bouts of Acute
Pancreatitis Without an Obvious Etiology
• Occult disease of the biliary tree or pancreatic ducts, especially
microlithiasis,
• biliary sludge
• Drugs
• Alcohol abuse
• Metabolic: Hypertriglyceridemia, hypercalcemia
• Anatomic: Pancreas divisum
• Pancreatic cancer
• Intraductal papillary mucinous neoplasm (IPMN)
• Hereditary pancreatitis
• Cystic fibrosis
• Autoimmune
• Idiopathic

6. Genetic susceptibility
• All of the major genetic susceptibility factors center on the
control of trypsin activity within the pancreatic acinar cell,
in part because they were identified as candidate genes
linked to intrapancreatic trypsin control. Five genetic
variants have been identified as being associated with
susceptibility to pancreatitis. The genes that have been
identified include
1. cationic trypsinogen gene (PRSS1),
2. pancreatic secretory trypsin inhibitor (SPINK1),
3. the cystic fibrosis transmembrane conductance regulator
gene (CFTR),
4. the chymotrypsin C gene (CTRC), and
5. the calcium-sensing receptor (CASR).

7. Pathogenesis – 3 phase
The initial phase is characterized by
• intrapancreatic digestive enzyme activation
and acinar cell injury. Trypsin activation
appears to be mediated by lysosomal
hydrolases such as cathepsin B that become
colocalized with digestive enzymes in
intracellular organelles; it is currently believed
that acinar cell injury is the consequence of
trypsin activation.

8. • Autodigestion is a currently accepted pathogenic theory;
according to this theory, pancreatitis results when
proteolytic enzymes (e.g., trypsinogen, chymotrypsinogen,
proelastase, and lipolytic enzymes such as phospholipase
A2) are activated in the pancreas acinar cell rather than in
the intestinal lumen. A number of factors (e.g., endotoxins,
exotoxins, viral infections, ischemia, oxidative stress,
lysosomal calcium, and direct trauma) are believed to
facilitate premature activation of trypsin. Activated
proteolytic enzymes, especially trypsin, not only digest
pancreatic and peripancreatic tissues but also can activate
other enzymes, such as elastase and phospholipase A2.
Spontaneous activation of trypsin also can occur.

9. • The second phase of pancreatitis involves the
activation, chemoattraction, and sequestration of
leukocytes and macrophages in the pancreas, resulting
in an enhanced intrapancreatic inflammatory reaction.
• Neutrophil depletion induced by prior administration
of an antineutrophil serum has been shown to reduce
the severity of experimentally induced pancreatitis.
There is also evidence to support the concept that
neutrophils can activate trypsinogen. Thus,
intrapancreatic acinar cell activation of trypsinogen
could be a two-step process (i.e., an early neutrophil-
independent and a later neutrophil-dependent phase).

10. • The third phase of pancreatitis is due to the effects of activated
proteolytic enzymes and cytokines, released by the inflamed
pancreas, on distant organs. Activated proteolytic enzymes,
especially trypsin, not only digest pancreatic and peripancreatic
tissues but also activate other enzymes such as elastase and
phospholipase A2. The active enzymes and cytokines then digest
cellular membranes and cause proteolysis, edema, interstitial
hemorrhage, vascular damage, coagulation necrosis, fat necrosis,
and parenchymal cell necrosis. Cellular injury and death result in
the liberation of bradykinin peptides, vasoactive substances, and
histamine that can produce vasodilation, increased vascular
permeability, and edema with profound effects on many organs.
The systemic inflammatory response syndrome (SIRS) and acute
respiratory distress syndrome (ARDS), as well as multiorgan failure,
may occur as a result of this cascade of local and distant effects.

11. • Pathologically, acute pancreatitis varies from
interstitial pancreatitis (pancreas blood supply
maintained), which is generally self-limited to
necrotizing pancreatitis (pancreas blood
supply interrupted), in which the extent of
necrosis may correlate with the severity of the
attack and its systemic complications.

12. Local complications
1. Pancreatic fluid collections
2. Pancreatic pseudocyst
3. Necrosis (Sterile ,Infected)
4. Walled-off necrosis
• Interstitial pancreatitis –acute peripancreatic fluid
collection –after 4 weeks – pseudocyst
• Necrotising pancreatitis – acute necrotic
collection – after 4 weeks – walled of necrosis
• Hemorrhagic pancreatitis = necrotizing
pancreatitis with hemorrhage

13. Local complications
5. Disruption of main pancreatic duct or secondary
branches
6. Pancreatic ascites
7. Involvement of contiguous organs by necrotizing
pancreatitis
8. Thrombosis of blood vessels (splenic vein, portal
vein)
9. Pancreatic enteric fistula
10. Bowel infarction
11. Obstructive jaundice

14. Systemic complications
• Metabolic [Hyperglycemia ,Hypertriglyceridemia
,Hypocalcemia, Encephalopathy ,Sudden blindness
(Purtscher’s retinopathy)]
• Fat necrosis
 Subcutaneous tissues (erythematous nodules)
 Bone
 Miscellaneous (mediastinum, pleura, nervous system)
• Hematologic-Disseminated intravascular coagulation
• Central nervous system [Psychosis,Fat emboli]
• Cardiovascular (Hypotension , Hypovolemia ,Nonspecific
ST-T changes in electrocardiogram simulating myocardial
Infarction, Pericardial effusion)

15. • Gastrointestinal hemorrhage
 Peptic ulcer disease
 Erosive gastritis
 Hemorrhagic pancreatic necrosis with erosion into
major blood vessels Portal vein thrombosis, splenic
vein thrombosis, variceal hemorrhage
• Pulmonary (Pleural effusion ,Atelectasis, Mediastinal
fluid, Pneumonitis,Acute respiratory distress syndrome
,Hypoxemia (unrecognized)
• Renal (Oliguria (<300 mL/d), Azotemia ,Renal artery
and/or renal vein thrombosis, Acute tubular necrosis)

16. MANIFESTATIONS
• The cardinal symptom of AP is epigastric or
periumbilical pain that radiates to the back. Up to 90%
of patients have nausea or vomiting that typically does
not relieve the pain. The nature of the pain is constant;
therefore, if the pain disappears or decreases, another
diagnosis should be considered.
• Dehydration, poor skin turgor, tachycardia,
hypotension, and dry mucous membranes are
commonly seen in patients with AP. Severely
dehydrated and older patients may also develop
mental status changes.

17. HISTORY
• Abdominal pain is the major symptom of acute
pancreatitis. Pain may vary from a mild
discomfort to severe, constant, and incapacitating
distress. Characteristically, the pain, which is
steady and boring in character, is located in the
epigastrium and periumbilical region, and may
radiate to the back, chest, flanks, and lower
abdomen.
• Nausea, vomiting, and abdominal distention due
to gastric and intestinal hypomotility and
chemical peritonitis are also frequent complaints.

18. Clinical exams
• Physical examination frequently reveals a distressed and anxious
patient. Low-grade fever, tachycardia, and hypotension are fairly
common.
• Shock is not unusual and may result from (1) hypovolemia
secondary to exudation of blood and plasma proteins into the
retroperitoneal space; (2) increased formation and release of kinin
peptides, which cause vasodilation and increased vascular
permeability; and (3) systemic effects of proteolytic and lipolytic
enzymes released into the circulation.
• Jaundice occurs infrequently; when present, it usually is due to
edema of the head of the pancreas with compression of the
intrapancreatic portion of the common bile duct or passage of a
biliary stone or sludge.
• Erythematous skin nodules due to subcutaneous fat necrosis may
rarely occur.

19. • In 10–20% of patients, there are pulmonary findings, including basilar
rales, atelectasis, and pleural effusion, the latter most frequently left
sided.
• Abdominal tenderness and muscle rigidity are present to a variable
degree, but compared with the intense pain, these signs may be less
impressive. Bowel sounds are usually diminished or absent. An enlarged
pancreas from acute fluid collection, walled off necrosis, or a pseudocyst
may be palpable in the upper abdomen later in the course of the disease
(i.e., 4–6 weeks).
• A faint blue discoloration around the umbilicus (Cullen’s sign) may occur as
the result of hemoperitoneum, and a blue-red-purple or green-brown
discoloration of the flanks (Turner’s sign) reflects tissue catabolism of
hemoglobin from severe necrotizing pancreatitis with hemorrhage,
resulting from retroperitoneal blood dissecting along tissue planes); more
commonly, patients may have a ruddy erythema in the flanks secondary to
extravasated pancreatic exudate

20. IMAGING STUDIES
• AXR shows
sentinel loop (isolated , dilated loop of bowel
seen in inflammatory conditions) caused by
inflammation irritating adjacent bowel
air-fluid levels suggestive of ileus, and widening
of the duodenal C loop caused by severe
pancreatic head edema
Colon cutoff -cutoff colon sign as a result of
colonic spasm at the splenic flexure.
• CXR – may shows left sided exudative pleural
effusion

21. USG
• The usefulness of ultrasound for diagnosis of
pancreatitis is limited by intra-abdominal fat and
increased intestinal gas as a result of the ileus.
Nevertheless, this test should always be ordered
in patients with AP because of its high sensitivity
(95%) in diagnosing gallstones. Combined
elevations of liver transaminase and pancreatic
enzyme levels and the presence of gallstones on
ultrasound have an even higher sensitivity (97%)
and specificity (100%) for diagnosing acute biliary
pancreatitis.

22. CECT
• Contrast-enhanced computed tomography (CT) is
currently the best modality for evaluation of the
pancreas, especially if the study is performed with a
multidetector CT scanner. The most valuable contrast
phase in which to evaluate the pancreatic parenchyma
is the portal venous phase (65 to 70 seconds after
injection of contrast material), which allows evaluation
of the viability of the pancreatic parenchyma, amount
of peripancreatic inflammation, and presence of intra-
abdominal free air or fluid collections. Noncontrast CT
scanning may also be of value in the setting of renal
failure by identifying fluid collections or extraluminal
air.

23. MRI
• Abdominal magnetic resonance imaging (MRI)
is also useful to evaluate the extent of
necrosis, inflammation, and presence of free
fluid. However, its cost and availability and the
fact that patients requiring imaging are
critically ill and need to be in intensive care
units limit its applicability in the acute phase.

24. MRCP
• Although magnetic resonanc
cholangiopancreatography (MRCP) is not indicated in
the acute setting of AP, it has an important role in the
evaluation of patients with unexplained or recurrent
pancreatitis because it allows complete visualization of
the biliary and pancreatic duct anatomy. In addition,
intravenous (IV) administration of secretin increases
pancreatic duct secretion, which causes a transient
distention of the pancreatic duct. For example, secretin
MRCP is useful in patients with AP and no evidence of
a predisposing condition to rule out pancreas divisum,
intraductal papillary mucinous neoplasm (IPMN), or a
small tumor in the pancreatic duct.

25. EUS
• In the setting of gallstone pancreatitis, endoscopic
ultrasound (EUS) may play an important role in the
evaluation of persistent choledocholithiasis. Several
studies have shown that routine ERCP for suspected
gallstone pancreatitis reveals no evidence of persistent
obstruction in most cases and may actually worsen
symptoms because of manipulation of the gland. EUS
has been proven to be sensitive for identifying
choledocholithiasis; it allows examination of the biliary
tree and pancreas with no risk of worsening of the
pancreatitis. In patients in whom persistent
choledocholithiasis is confirmed by EUS, ERCP can be
used selectively as a therapeutic measure.

26. Lab investigations
• Serum amylase and lipase values threefold or more above normal virtually
clinch the diagnosis if gut perforation, ischemia, and infarction are
excluded. However, it should be noted that there is no correlation
between the severity of pancreatitis and the degree of serum lipase and
amylase elevations.
• After 3–7 days, even with continuing evidence of pancreatitis, total serum
amylase values tend to return toward normal.
• It should be recognized that amylase elevations in serum and urine occur
in many conditions other than pancreatitis . Importantly, patients with
acidemia (arterial pH ≤7.32) may have spurious elevations in serum
amylase. This finding explains why patients with diabetic ketoacidosis may
have marked elevations in serum amylase without any other evidence of
acute pancreatitis.
• However, pancreatic isoamylase and lipase levels may remain elevated for
7–14 days. Serum lipase activity increases in parallel with amylase activity
and is more specific than amylase.
• Serum lipase is the preferred test.

27. Lab investigations
• Liver-associated enzymes
• Blood urea nitrogen (BUN), creatinine, and electrolytes
• Blood glucose
• Serum cholesterol and triglyceride
• Complete blood count (CBC) and hematocrit; NLR
• C-reactive protein (CRP)
• Arterial blood gas values
• Serum lactic dehydrogenase (LDH) and bicarbonate
• Immunoglobulin G4 (IgG4)

28. Definition of acute pancreatitis
• The diagnosis is established by two of the
following three criteria:
1. typical abdominal pain in the epigastrium
that may radiate to the back,
2. threefold or greater elevation in serum lipase
and/or amylase, and
3. confirmatory findings of acute pancreatitis
on cross-sectional abdominal imaging.

29. The Bedside Index of Severity in Acute Pancreatitis
(BISAP)
incorporates five clinical and laboratory parameters
obtained within the first 24 h of hospitalization —
that can be useful in assessing severity.
1. BUN >25 mg/dL,
2. impaired mental status (Glasgow coma score
<15),
3. SIRS ≥2 of 4 present
4. age >60 years,
5. pleural effusion on radiography

30. Ranson prognostic criteria
Gallstone pancreatitis Nongallstone pancreatitis
At presentation
Age (yrs) 70 55
AST (IU/L) >250 >250
Blood glucose level(mg/dL) 220 >200
LDH(4)(IU/L) >400 >350
Leukocyte count(cells /
mm3)
>18000 >16000
After 48 hrs of admission
Base deficit(mEq/L) >5 >4
PaO2(mmHg) <60 <60
Blood urea nitrogen
(increase in 2 mg/dL)
>2 >5
Serum Ca level (mg/dL) <8 <8
Fluid requirement (L) 4 L 6L

31. Acute physiology and chronic health
evaluation APACHE-II SCORE
(12 parameters)1. Glasgow coma scale
2. Temperature
3. Heart rate
4. Mean arterial blood pressure
5. Respiratory rate
6. Arterial pH
7. Oxygenation
8. Serum Sodium
9. Serum Potassium
10. Creatinine
11. Hematocrit
12. WBC counts

32. Modified Marshall scoring system for
organ failure-parameters
1. Shock (systolic blood pressure <90 mm Hg)
2. Pulmonary insufficiency (Pao2 <60 mm Hg)
3. Renal failure (creatinine level >2 mg/dL after
fluid resuscitation)
4. Gastrointestinal bleeding (>500 mL/24 hr)

33. Computed tomography severity index
(CTSI) highest attainable score=10
• Pancreatic inflammation (Balthazar grade)
• Pancreatic necrosis
Normal pancreas 0 A
Pancreatic enlargement (focal or diffuse) 1 B
Instrinsic pancreatic alterations with
peripancreatic fat inflammatory changes
2 C
Single fluid collection / or phlegmon 3 D
Two or more fluid collection or gas , in adjacent
to the pancreas
4 E
None 0
<30 2
30-50 4

34. The Revised Atlanta Classification
1. defines phases of acute pancreatitis,
2. defines severity of acute pancreatitis, and
3. clarifies imaging definitions

35. Phases of Acute Pancreatitis
• Two phases of acute pancreatitis have been defined, Which primarily describes the
hospital course of the disease.
• early (<2 weeks) phase of acute pancreatitis, which lasts 1–2 weeks, severity is
defined by clinical parameters rather than morphologic findings. Most patients
exhibit SIRS, and if this persists, patients are predisposed to organ failure. Three
organ systems should be assessed to define organ failure: respiratory,
cardiovascular, and renal. Organ failure is defined as a score of 2 or more for one
of these three organ systems using the modified Marshall scoring system.
Persistent organ failure (>48 h) is the mostimportant clinical finding in regard to
severity of the acute pancreatitis
• late (>2 weeks), phase is characterized by a protracted course of illness and may
require imaging to evaluate for local complications. The important clinical
parameter of severity, as in the early phase, is persistent organ failure. These
patients may require supportive measures such as renal dialysis, ventilator
support, or need for supplemental nutrition via the nasojejunal or parenteral
route. The radiographic feature of greatest importance to recognize in this phase is
the development of necrotizing pancreatitis on CT imaging. Necrosis generally
prolongs hospitalization and, if infected, may require operative, endoscopic, or
percutaneous intervention.

36. The revised Atlanta criteria
• clearly outlined the morphologic features of
acute pancreatitis on computed tomography (CT)
scan as follows:
• (1) interstitial pancreatitis,
• (2) necrotizing pancreatitis,
• (3)acute pancreatic fluid collection,
• (4) pancreatic pseudocyst,
• (5) acute necrotic collection (ANC),
• (6) walled-off pancreatic necrosis (WON)

37. EVALUATION & DD
• The differential diagnosis should include the following
disorders:
• (1) perforated viscus, especially peptic ulcer; (2) acute
cholecystitis and
• biliary colic; (3) acute intestinal obstruction; (4)
mesenteric vascular
• occlusion; (5) renal colic; (6) inferior myocardial
infarction; (7) dissecting
• aortic aneurysm; (8) connective tissue disorders with
vasculitis;
• (9) pneumonia; and (10) diabetic ketoacidosis.

38. TREATMENT
• The most important treatment intervention
for acute pancreatitis is safe, aggressive
intravenous fluid resuscitation. The patient is
made NPO to rest the pancreas and is given
intravenous narcotic analgesics to control
abdominal pain and supplemental oxygen (2 L)
via nasal cannula.

39. Fluid resuscitation & monitoring
response to therapy
• Intravenous fluids of lactated Ringer’s or normal saline are initially
bolused at 15–20 cc/kg (1050–1400 mL), followed by 3 mg/kg per
hour (200–250 mL/h), to maintain urine output >0.5 cc/kg per hour.
• Serial bedside evaluations are required every 6–8 h to assess vital
signs, oxygen saturation, and change in physical examination.
Lactated Ringer’s solution has been shown to decrease systemic
inflammation and may be a better crystalloid than normal saline. A
targeted resuscitation strategy with measurement of hematocrit
and BUN every 8–12 h is recommended to ensure adequacy of fluid
resuscitation and monitor response to therapy, noting less
aggressive resuscitation strategy may be needed in milder forms of
pancreatitis. A rising BUN during hospitalization is not only
associated with inadequate hydration but also higher in-hospital
mortality.

40. • A decrease in hematocrit and BUN during the first 12–24 h is strong
evidence that sufficient fluids are being administered. Serial
measurements and bedside assessment for fluid overload are
continued, and fluid rates are maintained at the current rate.
• Adjustments in fluid resuscitation may be required in patients with
cardiac, pulmonary, or renal disease.
• A rise in hematocrit or BUN during serial measurement should be
treated with a repeat volume challenge with a 2-L crystalloid bolus
followed by increasing the fluid rate by 1.5 mg/kg per hour. If the
BUN or hematocrit fails to respond (i.e., remains elevated or does
not decrease) to this bolus challenge and increase in fluid rate,
consideration of transfer to an intensive care unit is strongly
recommended for hemodynamic monitoring.

41. Nutritional therapy
A low-fat solid diet can be administered to
subjects with mild acute pancreatitis after the
abdominal pain has resolved. Enteral nutrition
should be considered 2–3 days after admission in
subjects with more severe pancreatitis instead of
total parenteral nutrition (TPN). Enteral feeding
maintains gut barrier integrity, limits bacterial
translocation, is less expensive, and has fewer
complications than TPN. The choice of gastric
versus nasojejunal enteral feeding is currently
under investigation.

42. Management of Local Complications
• Patients exhibiting signs of clinical deterioration
despite aggressive fluid resuscitation and
hemodynamic monitoring should be assessed for
local complications, which may include necrosis,
pseudocyst formation, pancreas duct disruption,
peripancreatic vascular complications, and
extrapancreatic infections. A multidisciplinary
team approach is recommended including
gastroenterology, surgery, interventional
radiology, and intensive care specialists, and
consideration should also be made for transfer to
a pancreas center.

43. The management of necrosis requires a multidisciplinary
team approach.
• The benefits of percutaneous aspiration of necrosis with Gram stain
and culture should be considered or discussed if there are ongoing
signs of possible pancreatic infection such as sustained leukocytosis,
fever, or organ failure. There is currently no role for prophylactic
antibiotics in necrotizing pancreatitis.
• It is reasonable to start broad-spectrum antibiotics in a patient who
appears septic while awaiting the results of Gram stain and
cultures. If cultures are negative, the antibiotics should be
discontinued to minimize the risk of developing opportunistic or
fungal superinfection.
• Repeated fine-needle aspiration and Gram stain with culture of
pancreatic necrosis may be done every 5–7 days in the presence of
persistent fever. Repeated CT or MRI imaging should also be
considered with any change in clinical course to monitor for
complications (e.g., thromboses, hemorrhage, abdominal
compartment syndrome).

44. • In general, sterile necrosis is most often managed conservatively unless
complications arise. Once a diagnosis of infected necrosis is established and an
organism identified, targeted antibiotics should be instituted. Pancreatic
debridement (necrosectomy) should be considered for definitive management of
infected necrosis, but clinical decisions are generally influenced by response to
antibiotic treatment and overall clinical condition.
• Symptomatic local complications as outlined in the Revised Atlanta criteria may
require definitive therapy. A step-up approach (percutaneous or endoscopic
transgastric drainage followed, if necessary, by open necrosectomy) has been
successfully reported by some pancreatic centers. One-third of the patients
successfully treated with the step-up approach did not require major abdominal
surgery. A randomized trial reported advantages to an initial endoscopic approach
compared to an initial surgical necrosectomy approach in select patients requiring
intervention for symptomatic WON. Taken together, a more conservative approach
to the management of infected pancreatic necrosis has evolved under the close
supervision of a multidisciplinary team. If conservative therapy can be safely
implemented for 4–6 weeks, to allow the pancreatic collections to resolve or “wall-
off,” surgical or endoscopic intervention is generally much safer and better
tolerated by the patient.

45. pseudocyst
• The incidence of pseudocyst is low, and most acute collections
resolve over time. Less than 10% of patients have persistent fluid
collections after 6 weeks that would meet the definition of
pseudocyst. Only symptomatic collections should be drained with
surgery or endoscopy or by percutaneous route.
• there is increasing evidence that transgastric and transduodenal
endoscopic drainage are safe and effective approaches for patients
with pancreatic pseudocysts in close contact (defined as <1 cm)
with the stomach and duodenum, respectively. In addition
transpapillary drainage can be attempted in pancreatic pseudocysts
communicating with the main pancreatic duct. For patients in
whom a pancreatic duct stricture is associated with a pancreatic
pseudocyst, endoscopic dilation and stent placement are indicated.

46. pseudocyst
• Surgical drainage is indicated for patients with pancreatic pseudocysts that
cannot be treated with endoscopic techniques and for patients who fail to
respond to endoscopic treatment. Definitive treatment depends on the
location of the cyst. Pancreatic pseudocysts closely attached to the
stomach should be treated with a cystogastrostomy. In this procedure, an
anterior gastrostomy is performed. Once the pseudocyst is located, it is
drained through the posterior wall of the stomach using a linear stapler.
The defect in the anterior wall of the stomach is closed in two layers.
Pancreatic pseudocysts located in the head of the pancreas that are in
close contact with the duodenum are treated with cystoduodenostomy.
Finally, some pseudocysts are not in contact with the stomach or
duodenum. The surgical treatment for these patients is a Roux-en-Y
cystojejunostomy. Surgical cyst enterostomy is successful in achieving
immediate cyst drainage in more than 90% of cases. After initial
resolution, pseudocyst formation may recur in up to 12% of cases during
long-term follow-up, depending on the location of the cyst and underlying
cause of the disease.

47. • PANCREATIC DUCT DISRUPTION Pancreatic duct disruption may present
with symptoms of increasing abdominal pain or shortness of breath in the
setting of an enlarging fluid collection. Diagnosis can be confirmed on
magnetic resonance cholangiopancreatography (MRCP) or ERCP.
Placement of a bridging pancreatic stent for at least 6 weeks is >90%
effective at resolving the leak. Nonbridging stents are less effective (25–
50%).
• PERIVASCULAR COMPLICATIONS Perivascular complications may include
splenic vein thrombosis with gastric varices and pseudoaneurysms. Gastric
varices bleed <5% of the time. Life-threatening bleeding from a ruptured
pseudoaneurysm can be diagnosed and treated with mesenteric
angiography and embolization.
• EXTRAPANCREATIC INFECTIONS Hospital-acquired infections occur in up
to 20% of patients with acute pancreatitis. Patients should be continually
monitored for the development pneumonia, urinary tract infection, and
line infection. Continued culturing of urine, monitoring of chest x-rays, and
routine changing of intravenous lines are important during hospitalization.

48. FOLLOW UP
• Hospitalizations for moderately severe and severe
acute pancreatitis can be prolonged and last weeks to
months and often involve a period of intensive care
unit admission and outpatient rehabilitation or
subacute nursing care. Follow-up evaluation should
assess for development of diabetes, exocrine
insufficiency, recurrent cholangitis, or development of
infected fluid collections.
• cholecystectomy should be performed during
hospitalization or within 4–6 weeks of discharge if
possible for patients with uncomplicated gallstone
pancreatitis.

49. Clinical vignette
• A 35-year-old man complains of rapid onset of
midepigastric pain with radiation to the back
after eating a large meal. Physical exam shows
low grade fever, epigastric tenderness, and
decreased bowel sounds. Abdominal CT scan
shows localized dilation of the upper
duodenum and a small collection of fluid in
the left pleural cavity.

50. THANK YOU