Sunday, December 8, 2013
Tuesday, December 3, 2013
Clinical Management of Patients With Acute Pancreatitis
The diagnosis of acute pancreatitis requires
at least 2 of the following: typical upper abdominal
pain, serum levels of amylase or lipase 3 times the upper
limit of normal, and confirmatory findings from crosssectional
imaging analysis.
differential: acute cholecystitis, choledocholithiasis, DU, perforated viscus, ischaemia bowel, MI
The Revised Atlanta Classification
-consensus conference in 1992
Interstitial pancreatitis involves acute collection of
peripancreatic fluid-usually sterile and resolved or formation of pancreatic pseudocysts.
Necrotizing pancreatitis involves acute collection of
necrosis and walled-off necrosis.
can be in pancreas or peripancreatic. can be sterile or infected.
After 4 or more weeks, become smaller but rarely
disappears completely and usually evolves into walled-off
necrosis.
systemic complications
are defined as exacerbations of preexisting comorbidities
such as chronic lung disease, chronic liver
disease, or congestive heart failure, recognizing the failure
of respiratory, cardiovascular, and renal organ systems
The modified Marshall system classifies disease severity on
a scale from 0 to 4,
Mild disease is defined as acute pancreatitis
not associated with organ failure, local complications,
or systemic complications. Most patients with mild
acute pancreatitis do not require pancreatic imaging analysis
and are usually discharged within 3 to 5 days of onset
of illness.
Moderately severe acute pancreatitis is defined by the presence of transient organ failure (48h), local complications, or systemic complications. require extended hospitalization but have lower
mortality rates
Severe acute pancreatitis is defined by the presence of
persistent organ failure (>48h). Most
patients have pancreatic necrosis.meta-analysis 30% mortality rate; the risk of
in-hospital death doubles when they have persistent organ failure and infected necrosis.
The best use of an early-stage CT scan is to confirm a diagnosis, can't differentiate interstitial or necrosis
The best use of a CT scan after the 5 to 7 days is to evaluate the presence of local
complications in patients with moderately severe or severe pancreatitis to guide ongoing care.
MRCP has used for identifying retained common
bile duct stones. It also helpful in distinguishing walled-off
necrosis from a pseudocyst.
EUS is a highly sensitive test
for detecting cholelithiasis and choledocholithiasis.
MRCP, which has limited accuracy for detecting smaller gallstones or sludge
Risk factors for severe pancreatitis include
age (mortality increases among patients 60 years of age or older),
comorbid illnesses(cancer, heart failure, and chronic kidney and liver disease), a history of chronic alcohol consumption, and obesity (body mass index 30 kg/m2 increases the risk of
severe pancreatitis 3-fold and mortality 2-fold).
The initial 12 to 24 hours of hospitalization is critical, because the highest incidence
of organ dysfunction.
Ranson score, Glasgow score
bedside index of severity of acute pancreatitis
blood urea nitrogen (BUN) level 25 mg/dL,
impaired mental status, systemic inflammatory response
syndrome (SIRS), age 60 years or older, and pleural effusion
if >2 in 24 hours, 7-fold increase in risk
of organ failure and 10-fold increase in risk of mortality.
Harmless acute pancreatitis score-normal HCT, normal creat, no rebound tendrness, unlikely severe pancreatitis
Acute Physiology and Chronic Health Examination (APACHE) II score
presence of SIRS?,
2 or more :
temperature 38.3¡ãC or 36¡ãC, pulse 90 beats/
min, respirations 20 beats/min, and white blood cell
count 12,000 or 4000 cells/mm3 or 10% immature
(bands) forms.
25% to 60% of patients have SIRS when they are
admitted,but resolves in more than half
of these patients within 24 hours when they are given
appropriate fluid resuscitation.
An increasing number of SIRS criteria during the initial 24 hours increases the risk of persistent organ failure and necrosis
Patients with persistent SIRS (beyond 48 hours) have 11% to 25% mortality.
Prospective studies have shown that the level of BUN at
admission and 24 hours is a strong prognostic factor.
admission 20 mg/dL increased-have 9% to 20% mortality.
high level of BUN at admission that decreased at least 5 mg/dL - 0% to 3% mortality.
normal level of BUN followed modest increase (2 mg/dL)- 6% to 15% mortality
normal level of BUN without a subsequent increase <1% mortality.
creatinine 1.8 mg/dL within the first 24 hours of hospitalization is associated with a 35-fold
increased risk of development of pancreatic necrosis.
persistent increase in hematocrit 44% has also been shown to increase the risk of necrosis and organ failure
A prospective, randomized, controlled trial assessed
the effects of bolus infusion of 20 mL/kg, followed by continuous infusion of 3
mL · kg 1 · h 1, with interval assessment every 6 to 8
hours (comprising vital sign monitoring, pulse oximetry,
and physical examination).
Repeat volume challenge was administered if the level of BUN did not decrease.
if the BUN level decreased, the rate of the infusion was reduced to 1.5 mL · kg 1 · h 1.
head of the bed elevated, undergo continuous pulse oximetry, and receive supplemental oxygen.
Lactated Ringer¡¯s solution reduces the incidence of SIRS by 80% compared with saline resuscitation, but not for hypercalcaemia
Admit to ICU:
-respiratory failure or hypotension that fail to respond to initial resuscitation
- multiorgan dysfunction
- patients with persistent SIRS, increased levels of BUN or creatinine, increased hematocrit,
or underlying cardiac or pulmonary illness
Several practice guidelines recommend consideration of patient-controlled analgesia
and administration of intermittent doses of intravenous narcotic analgesics
Monitor saturation
Nutritional Support
2 randomized controlled trials support early-stage introduction of low-fat solid food as the initial
meal for patients who have developed mild pancreatitis; choledocholithiasis, duration of fasting, and
quickly placing patients on a full diet have been associated with recurrence of pain.
A Cochrane meta-analysis of 8 randomized controlled trials
found a reduction in mortality, systemic infection, and
multiorgan dysfunction among patients who received enteral
as opposed to parenteral nutrition.Several trials
have proposed enteral nutrition via the nasogastric route
as an alternative to nasoduodenal or nasojejunal
routes.
practice guidelines and updated meta-analyses did not find sufficient evidence to recommend routine use of prophylactic antibiotics in patients with acute necrotic collections
In a multicenter, randomized, controlled trial from The Netherlands, a step-up approach to management of infected necrosis was compared with open necrosectomy.
-percutaneous drainage catheters in addition to treatment
with antibiotics.
-72 hours, minimally invasive debridement
was performed via a retroperitoneal approach.
-4- 6 weeks after the onset of pancreatitis, an acute necrotic collection develops into walled-off necrosis. Physicians should intervene only if patients have
symptoms that can be attributed to the collection (persistent abdominal pain, anorexia, nausea, or vomiting due to mechanical obstruction or secondary infection).-direct endoscopic
necrosectomy using a transgastric approach for walled-off sterile necrosis
The median time from onset of illness to intervention was 6 to 8 weeks.
Endoscopic treatment reduced levels of inflammatory factors (such as interleukin-6), and the risk of newonset multiorgan failure, intra-abdominal hemorrhage, enterocutaneous or pancreatic fistula, or death decreased by 60%.
Pseudocyst
A longitudinal study of patients with interstitial pancreatitis reported that most collections of
acute fluid resolved within 7 to 10 days; only 6.8% of patients developed discrete pseudocysts.
Recent studies have indicated that symptomatic pseudocysts can be successfully decompressed by endoscopic cyst gastrostomy with endoscopic ultrasound guidance.
Ductal Disruption
A ductal disruption can result in unilateral pleural effusion, pancreatic ascites, or enlarging fluid collection. Symptoms include shortness of breath, abdominal pain, and even early satiety, with vomiting if the collection compresses the stomach.
MRCP might be used to identify a large disruption in ducts but detect small disruptions with low levels of sensitivity. ERCP is a valuable tool for treating symptomatic duct disruptions. Placement of a bridging stent across the disruption usually promotes duct healing when there is a focal disruption.
When a ductal disruption occurs in an area of extensive necrosis, a multidisciplinary
team of therapeutic endoscopists, interventional radiologists,
and surgeons should be consulted for optimal management.
Peripancreatic Vascular Complications
Splenic vein thrombosis has been reported in up to 20% of patients undergoing imaging for acute pancreatitis.Although gastric varices are often subsequently detected
in cross-sectional image analysis, the risk of bleeding is 5%. Routine splenectomy is not recommended.
Pseudoaneurysms are rare 4%-10%.The diagnosis can be made through CT angiography.
Rupture of a pseudoaneurysm can lead to life-threatening hemorrhage, with mortalities 50%- 90%. Mesenteric angiography with transcatheter arterial embolization is considered to be the first-line treatment for pseudoaneurysms.
Co infection -bloodstream infections, pneumonia, and UTI occur in up to 20% of patients with acute pancreatitis and increase mortality 2-fold. If sepsis is suspected during the
course of pancreatitis, it is reasonable to start antibiotic therapy while waiting for culture results. If culture results are negative, then antibiotics should be discontinued to reduce the risk of fungemia or Clostridium difficile infection.
Comorbid- monitored for exacerbation of underlying conditions such as CCF or COPD. In addition, treatment should be provided for concurrent illnesses such as alcohol withdrawal or diabetic ketoacidosis.
Timing of ERCP for Patients With Biliary Pancreatitis
severe acute biliary pancreatitis with signs of cholangitis should undergo ERCP within 24 hours. mild gallstone pancreatitis not routinely ERCP because it increase complications.
Elective ERCP with sphincterotomy can be considered for patients with persistent or incipient biliary obstruction, those who are poor candidates for cholecystectomy, or those suspected of
having bile duct stones after cholecystectomy
Drug induced pancreatitis-only 30 can cause pancreatitis when rechallenge
Hypertriglyceridemic - 1% to 4%
Serum triglyceride levels greater than 1000 mg/dL(=25.6 mmol/l) are considered necessary to
attribute an attack of pancreatitis to hypertriglyceridemia.
Case series studies have suggested use of insulin, combined with heparin or apheresis,
for treatment. Administration of fibrates should begin as early as possible.
niacin or omega-3 fatty acids can be used as second-line agents.
Hypercalcemia
hyperparathyroidism or, metastatic tumors. to treat the underlying cause of hypercalcemia to
prevent recurrence
Autoimmune Pancreatitis
Although lymphoplasmacytic sclerosing or type 1 autoimmune pancreatitis is more common, the idiopathic duct-centric type 2 form of the disease has been more frequently associated with acute pancreatitis (5% vs 34%, respectively).
Patients with type 2 autoimmune pancreatitis are less likely to have increased serum levels of
immunoglobulin G4 or significant increases in numbers of immunoglobulin G4–positive cells based on histologic analysis.
-treated with glucocorticoids (typically prednisone 40 mg/day for 4 weeks, followed by a taper of 5 mg/wk).
-For relapse, treatment with immunomodulators or possibly rituximab should be considered.
Prevention
Post-ERCP Pancreatitis
A meta-analysis of 8 randomized controlled trials calculated a pooled odds ratio of 0.22 for
development of post-ERCP pancreatitis with stent placement.
large-scale, multicenter, randomized, controlled trial showed a 45% reduction in
pancreatitis when rectal indomethacin was administered
Secondary Prevention
16.5% to 25% of patients have a repeated attack within the first several years
Continued alcohol consumption, smoking, and recurrent biliary complications are the major risk factors
-Alcohol abstinence with repeated counseling sessions at 6-month intervals is more effective than a
single counseling session
-Multiple societies recommend early cholecystectomy to prevent recurrent episodes
of gallstone-associated pancreatitis based on early recurrence rates as high as 30% among patients awaiting cholecystectomy.
- For poor candidates for surgery, endoscopic sphincterotomy can reduce the
likelihood of recurrent pancreatitis but is not as effective as cholecystectomy in reducing further biliary complications.
Factors to Consider for Outpatients
exocrine insufficiency 12% to 65%,
Patients with necrotizing pancreatitis, pancreatic
ductal obstruction, or steatorrhea should receive pancreatic enzyme supplementation while
they recover. Fecal elastase assays should be performed after 2 to 3 weeks
If exocrine insufficiency is confirmed, patients’ meals should each include pancreatic
enzyme extracts at doses of 40,000 to 50,000 IU lipase.
The dose should be determined based on patients’ symptoms,
anthropometry data, and results from biochemical
tests
For extensive necrosis, significantly higher doses may be required to achieve adequate
digestion.
Small cross-sectional studies -endocrine dysfunction of 30%-35%
Up to 30% of patients(pancreatogenic or type 3 diabetes) require insulin
Current practice guidelines do not comment on the role of screening for diabetes following acute pancreatitis.
Patients with extensive necrosis or symptoms that indicate hyperglycemia should be tested for levels of HBA1c or undergo glucose tolerance testing.
Studies using standardized quality of life instruments such as the Short Form-36 or
European Organisation for Research and Treatment of Cancer survey instrument have concluded that physical function improves over time despite persistence of mental disability.
Long-term quality of life, even among patients who have had severe episodes of acute pancreatitis,
appears to be comparable to that of the general population.
at least 2 of the following: typical upper abdominal
pain, serum levels of amylase or lipase 3 times the upper
limit of normal, and confirmatory findings from crosssectional
imaging analysis.
differential: acute cholecystitis, choledocholithiasis, DU, perforated viscus, ischaemia bowel, MI
The Revised Atlanta Classification
-consensus conference in 1992
Interstitial pancreatitis involves acute collection of
peripancreatic fluid-usually sterile and resolved or formation of pancreatic pseudocysts.
Necrotizing pancreatitis involves acute collection of
necrosis and walled-off necrosis.
can be in pancreas or peripancreatic. can be sterile or infected.
After 4 or more weeks, become smaller but rarely
disappears completely and usually evolves into walled-off
necrosis.
systemic complications
are defined as exacerbations of preexisting comorbidities
such as chronic lung disease, chronic liver
disease, or congestive heart failure, recognizing the failure
of respiratory, cardiovascular, and renal organ systems
The modified Marshall system classifies disease severity on
a scale from 0 to 4,
Mild disease is defined as acute pancreatitis
not associated with organ failure, local complications,
or systemic complications. Most patients with mild
acute pancreatitis do not require pancreatic imaging analysis
and are usually discharged within 3 to 5 days of onset
of illness.
Moderately severe acute pancreatitis is defined by the presence of transient organ failure (48h), local complications, or systemic complications. require extended hospitalization but have lower
mortality rates
Severe acute pancreatitis is defined by the presence of
persistent organ failure (>48h). Most
patients have pancreatic necrosis.meta-analysis 30% mortality rate; the risk of
in-hospital death doubles when they have persistent organ failure and infected necrosis.
The best use of an early-stage CT scan is to confirm a diagnosis, can't differentiate interstitial or necrosis
The best use of a CT scan after the 5 to 7 days is to evaluate the presence of local
complications in patients with moderately severe or severe pancreatitis to guide ongoing care.
MRCP has used for identifying retained common
bile duct stones. It also helpful in distinguishing walled-off
necrosis from a pseudocyst.
EUS is a highly sensitive test
for detecting cholelithiasis and choledocholithiasis.
MRCP, which has limited accuracy for detecting smaller gallstones or sludge
Risk factors for severe pancreatitis include
age (mortality increases among patients 60 years of age or older),
comorbid illnesses(cancer, heart failure, and chronic kidney and liver disease), a history of chronic alcohol consumption, and obesity (body mass index 30 kg/m2 increases the risk of
severe pancreatitis 3-fold and mortality 2-fold).
The initial 12 to 24 hours of hospitalization is critical, because the highest incidence
of organ dysfunction.
Ranson score, Glasgow score
bedside index of severity of acute pancreatitis
blood urea nitrogen (BUN) level 25 mg/dL,
impaired mental status, systemic inflammatory response
syndrome (SIRS), age 60 years or older, and pleural effusion
if >2 in 24 hours, 7-fold increase in risk
of organ failure and 10-fold increase in risk of mortality.
Harmless acute pancreatitis score-normal HCT, normal creat, no rebound tendrness, unlikely severe pancreatitis
Acute Physiology and Chronic Health Examination (APACHE) II score
presence of SIRS?,
2 or more :
temperature 38.3¡ãC or 36¡ãC, pulse 90 beats/
min, respirations 20 beats/min, and white blood cell
count 12,000 or 4000 cells/mm3 or 10% immature
(bands) forms.
25% to 60% of patients have SIRS when they are
admitted,but resolves in more than half
of these patients within 24 hours when they are given
appropriate fluid resuscitation.
An increasing number of SIRS criteria during the initial 24 hours increases the risk of persistent organ failure and necrosis
Patients with persistent SIRS (beyond 48 hours) have 11% to 25% mortality.
Prospective studies have shown that the level of BUN at
admission and 24 hours is a strong prognostic factor.
admission 20 mg/dL increased-have 9% to 20% mortality.
high level of BUN at admission that decreased at least 5 mg/dL - 0% to 3% mortality.
normal level of BUN followed modest increase (2 mg/dL)- 6% to 15% mortality
normal level of BUN without a subsequent increase <1% mortality.
creatinine 1.8 mg/dL within the first 24 hours of hospitalization is associated with a 35-fold
increased risk of development of pancreatic necrosis.
persistent increase in hematocrit 44% has also been shown to increase the risk of necrosis and organ failure
A prospective, randomized, controlled trial assessed
the effects of bolus infusion of 20 mL/kg, followed by continuous infusion of 3
mL · kg 1 · h 1, with interval assessment every 6 to 8
hours (comprising vital sign monitoring, pulse oximetry,
and physical examination).
Repeat volume challenge was administered if the level of BUN did not decrease.
if the BUN level decreased, the rate of the infusion was reduced to 1.5 mL · kg 1 · h 1.
head of the bed elevated, undergo continuous pulse oximetry, and receive supplemental oxygen.
Lactated Ringer¡¯s solution reduces the incidence of SIRS by 80% compared with saline resuscitation, but not for hypercalcaemia
Admit to ICU:
-respiratory failure or hypotension that fail to respond to initial resuscitation
- multiorgan dysfunction
- patients with persistent SIRS, increased levels of BUN or creatinine, increased hematocrit,
or underlying cardiac or pulmonary illness
Several practice guidelines recommend consideration of patient-controlled analgesia
and administration of intermittent doses of intravenous narcotic analgesics
Monitor saturation
Nutritional Support
2 randomized controlled trials support early-stage introduction of low-fat solid food as the initial
meal for patients who have developed mild pancreatitis; choledocholithiasis, duration of fasting, and
quickly placing patients on a full diet have been associated with recurrence of pain.
A Cochrane meta-analysis of 8 randomized controlled trials
found a reduction in mortality, systemic infection, and
multiorgan dysfunction among patients who received enteral
as opposed to parenteral nutrition.Several trials
have proposed enteral nutrition via the nasogastric route
as an alternative to nasoduodenal or nasojejunal
routes.
practice guidelines and updated meta-analyses did not find sufficient evidence to recommend routine use of prophylactic antibiotics in patients with acute necrotic collections
In a multicenter, randomized, controlled trial from The Netherlands, a step-up approach to management of infected necrosis was compared with open necrosectomy.
-percutaneous drainage catheters in addition to treatment
with antibiotics.
-72 hours, minimally invasive debridement
was performed via a retroperitoneal approach.
-4- 6 weeks after the onset of pancreatitis, an acute necrotic collection develops into walled-off necrosis. Physicians should intervene only if patients have
symptoms that can be attributed to the collection (persistent abdominal pain, anorexia, nausea, or vomiting due to mechanical obstruction or secondary infection).-direct endoscopic
necrosectomy using a transgastric approach for walled-off sterile necrosis
The median time from onset of illness to intervention was 6 to 8 weeks.
Endoscopic treatment reduced levels of inflammatory factors (such as interleukin-6), and the risk of newonset multiorgan failure, intra-abdominal hemorrhage, enterocutaneous or pancreatic fistula, or death decreased by 60%.
Pseudocyst
A longitudinal study of patients with interstitial pancreatitis reported that most collections of
acute fluid resolved within 7 to 10 days; only 6.8% of patients developed discrete pseudocysts.
Recent studies have indicated that symptomatic pseudocysts can be successfully decompressed by endoscopic cyst gastrostomy with endoscopic ultrasound guidance.
Ductal Disruption
A ductal disruption can result in unilateral pleural effusion, pancreatic ascites, or enlarging fluid collection. Symptoms include shortness of breath, abdominal pain, and even early satiety, with vomiting if the collection compresses the stomach.
MRCP might be used to identify a large disruption in ducts but detect small disruptions with low levels of sensitivity. ERCP is a valuable tool for treating symptomatic duct disruptions. Placement of a bridging stent across the disruption usually promotes duct healing when there is a focal disruption.
When a ductal disruption occurs in an area of extensive necrosis, a multidisciplinary
team of therapeutic endoscopists, interventional radiologists,
and surgeons should be consulted for optimal management.
Peripancreatic Vascular Complications
Splenic vein thrombosis has been reported in up to 20% of patients undergoing imaging for acute pancreatitis.Although gastric varices are often subsequently detected
in cross-sectional image analysis, the risk of bleeding is 5%. Routine splenectomy is not recommended.
Pseudoaneurysms are rare 4%-10%.The diagnosis can be made through CT angiography.
Rupture of a pseudoaneurysm can lead to life-threatening hemorrhage, with mortalities 50%- 90%. Mesenteric angiography with transcatheter arterial embolization is considered to be the first-line treatment for pseudoaneurysms.
Co infection -bloodstream infections, pneumonia, and UTI occur in up to 20% of patients with acute pancreatitis and increase mortality 2-fold. If sepsis is suspected during the
course of pancreatitis, it is reasonable to start antibiotic therapy while waiting for culture results. If culture results are negative, then antibiotics should be discontinued to reduce the risk of fungemia or Clostridium difficile infection.
Comorbid- monitored for exacerbation of underlying conditions such as CCF or COPD. In addition, treatment should be provided for concurrent illnesses such as alcohol withdrawal or diabetic ketoacidosis.
Timing of ERCP for Patients With Biliary Pancreatitis
severe acute biliary pancreatitis with signs of cholangitis should undergo ERCP within 24 hours. mild gallstone pancreatitis not routinely ERCP because it increase complications.
Elective ERCP with sphincterotomy can be considered for patients with persistent or incipient biliary obstruction, those who are poor candidates for cholecystectomy, or those suspected of
having bile duct stones after cholecystectomy
Drug induced pancreatitis-only 30 can cause pancreatitis when rechallenge
Hypertriglyceridemic - 1% to 4%
Serum triglyceride levels greater than 1000 mg/dL(=25.6 mmol/l) are considered necessary to
attribute an attack of pancreatitis to hypertriglyceridemia.
Case series studies have suggested use of insulin, combined with heparin or apheresis,
for treatment. Administration of fibrates should begin as early as possible.
niacin or omega-3 fatty acids can be used as second-line agents.
Hypercalcemia
hyperparathyroidism or, metastatic tumors. to treat the underlying cause of hypercalcemia to
prevent recurrence
Autoimmune Pancreatitis
Although lymphoplasmacytic sclerosing or type 1 autoimmune pancreatitis is more common, the idiopathic duct-centric type 2 form of the disease has been more frequently associated with acute pancreatitis (5% vs 34%, respectively).
Patients with type 2 autoimmune pancreatitis are less likely to have increased serum levels of
immunoglobulin G4 or significant increases in numbers of immunoglobulin G4–positive cells based on histologic analysis.
-treated with glucocorticoids (typically prednisone 40 mg/day for 4 weeks, followed by a taper of 5 mg/wk).
-For relapse, treatment with immunomodulators or possibly rituximab should be considered.
Prevention
Post-ERCP Pancreatitis
A meta-analysis of 8 randomized controlled trials calculated a pooled odds ratio of 0.22 for
development of post-ERCP pancreatitis with stent placement.
large-scale, multicenter, randomized, controlled trial showed a 45% reduction in
pancreatitis when rectal indomethacin was administered
Secondary Prevention
16.5% to 25% of patients have a repeated attack within the first several years
Continued alcohol consumption, smoking, and recurrent biliary complications are the major risk factors
-Alcohol abstinence with repeated counseling sessions at 6-month intervals is more effective than a
single counseling session
-Multiple societies recommend early cholecystectomy to prevent recurrent episodes
of gallstone-associated pancreatitis based on early recurrence rates as high as 30% among patients awaiting cholecystectomy.
- For poor candidates for surgery, endoscopic sphincterotomy can reduce the
likelihood of recurrent pancreatitis but is not as effective as cholecystectomy in reducing further biliary complications.
Factors to Consider for Outpatients
exocrine insufficiency 12% to 65%,
Patients with necrotizing pancreatitis, pancreatic
ductal obstruction, or steatorrhea should receive pancreatic enzyme supplementation while
they recover. Fecal elastase assays should be performed after 2 to 3 weeks
If exocrine insufficiency is confirmed, patients’ meals should each include pancreatic
enzyme extracts at doses of 40,000 to 50,000 IU lipase.
The dose should be determined based on patients’ symptoms,
anthropometry data, and results from biochemical
tests
For extensive necrosis, significantly higher doses may be required to achieve adequate
digestion.
Small cross-sectional studies -endocrine dysfunction of 30%-35%
Up to 30% of patients(pancreatogenic or type 3 diabetes) require insulin
Current practice guidelines do not comment on the role of screening for diabetes following acute pancreatitis.
Patients with extensive necrosis or symptoms that indicate hyperglycemia should be tested for levels of HBA1c or undergo glucose tolerance testing.
Studies using standardized quality of life instruments such as the Short Form-36 or
European Organisation for Research and Treatment of Cancer survey instrument have concluded that physical function improves over time despite persistence of mental disability.
Long-term quality of life, even among patients who have had severe episodes of acute pancreatitis,
appears to be comparable to that of the general population.
Monday, December 2, 2013
Acute cholangitis
clinical syndrome characterized by fever, jaundice, and abdominal pain
that develops as a result of stasis and infection in the biliary tract.
or ascending cholangitis
typically ascend from the duodenum;-sphincter of oddi, IgA and bile mucous
Biliary obstruction raises intrabiliary pressure increases permeability bile ductules
hematogenous spread from the portal vein is a rare
biliary calculi (28 to 70 percent), benign stenosis (5 to 28 percent), and malignancy (10 to 57 percent)
common complication of stent placement for malignant biliary obstruction (18 percent in one series)
Bile is sterile.
Bacteriology — Culture of bile, ductal stones, and blocked biliary stents
Confusion and hypotension can occur in patients with suppurative cholangitis, producing Reynolds's pentad, which is associated with significant morbidity and mortality
ALT if > 2000 reflects microabscess liver and hepatocyte necrosis.
Raised amylase suggests pancreatitis
Diagnostic criteria (the Tokyo guidelines) - two or more of the following:
all present:
If without Charcot's triad, we recommend transabdominal ultrasonography to look for common bile duct dilatation or stones. Then followed (within 24 hours) by ERCP to provide biliary drainage
If ultrasound is normal, we proceed with MRCP to look for bile duct stones or alternative diagnoses
If cannot undergo MRCP, we will proceed with ERCP if the liver tests are suggestive of biliary obstruction
If the liver tests are normal or if high risk ERCP, we will proceed with EUS to look for evidence of bile duct stones or obstruction.
If this subsequent testing fails to demonstrate biliary obstruction, an evaluation for alternative explanations for the patient's symptoms should be performed
the diagnosis confirmed by ERCP
The differential diagnosis of fever and abdominal pain includes:
Biliary drainage — Endoscopic sphincterotomy with stone extraction and/or stent insertion. If fails can proceed with percutaneous transhepatic cholangiography or open surgical decompression
Biliary drainage can then be performed on an elective basis (within 24 to 48 hours).
If the patient does not improve over the first 24 hours, urgent biliary decompression is required.
Risk factors include impacted stones, active smoker status, age >70 years, and additional stones within the GB
signs of acute suppurative cholangitis, such as:
Stones more than 2 cm require lithotripsy. Intrahepatic stones can sometimes be removed with choledochoscopy.
Endoscopic drainage has lower overall rates of mortality and morbidity compared with surgical decompression ( 4.7 to 10% VS 10 to 50 %)
If coagulopathies that prevent sphincterotomy, or large stones, or too ill, can insert nasobiliary catheter.
Placing a stent without first performing a sphincterotomy appears to permit adequate drainage and may be another option for patients with coagulopathies
PTC involves transhepatic insertion of a needle into a bile duct, followed by injection of contrast material to opacify the bile ducts. PTC permits a number of therapeutic interventions, including drainage of infected bile, extraction of biliary tract stones, dilation of benign biliary strictures, or placement of a stent across a malignant stricture.
Or placement of a percutaneous cholecystostomy tube in patients with an intact gallbladder.
Patients who are pregnant — same-antibiotic choices should take into account potential fetal toxicity . fetal shielding should be used.
mortality rates for patients with severe acute cholangitis remain high (20 to 30 percent)
if malignant stenoses- typically with stent placement, though the specific therapy chosen will depend on the patient's life expectancy and the likelihood of stent occlusion.
or ascending cholangitis
typically ascend from the duodenum;-sphincter of oddi, IgA and bile mucous
Biliary obstruction raises intrabiliary pressure increases permeability bile ductules
hematogenous spread from the portal vein is a rare
biliary calculi (28 to 70 percent), benign stenosis (5 to 28 percent), and malignancy (10 to 57 percent)
common complication of stent placement for malignant biliary obstruction (18 percent in one series)
Bile is sterile.
Bacteriology — Culture of bile, ductal stones, and blocked biliary stents
- Escherichia coli (25 to 50 percent), followed by Klebsiella (15 to 20 percent) and Enterobacter species (5 to 10 percent).
- +, Enterococcus species (10 to 20 percent).
- Anaerobes, such as Bacteroides and Clostridia, are usually present as part of a mixed infection.
Confusion and hypotension can occur in patients with suppurative cholangitis, producing Reynolds's pentad, which is associated with significant morbidity and mortality
ALT if > 2000 reflects microabscess liver and hepatocyte necrosis.
Raised amylase suggests pancreatitis
Diagnostic criteria (the Tokyo guidelines) - two or more of the following:
- A history of biliary disease
- Fever and/or chills
- Jaundice
- Abdominal pain
all present:
- Evidence of an inflammatory response (abnormal white blood cell count, elevated C-reactive protein)
- Abnormal liver tests
- Biliary dilation
If without Charcot's triad, we recommend transabdominal ultrasonography to look for common bile duct dilatation or stones. Then followed (within 24 hours) by ERCP to provide biliary drainage
If ultrasound is normal, we proceed with MRCP to look for bile duct stones or alternative diagnoses
If cannot undergo MRCP, we will proceed with ERCP if the liver tests are suggestive of biliary obstruction
If the liver tests are normal or if high risk ERCP, we will proceed with EUS to look for evidence of bile duct stones or obstruction.
If this subsequent testing fails to demonstrate biliary obstruction, an evaluation for alternative explanations for the patient's symptoms should be performed
the diagnosis confirmed by ERCP
The differential diagnosis of fever and abdominal pain includes:
- Biliary leaks-asso with lap cholecystectomy
- Acute diverticulitis
- Cholecystitis
- Appendicitis
- Pancreatitis
- Liver abscess
- Infected choledochal cysts
- Recurrent pyogenic cholangitis
- Mirizzi syndrome
- Intestinal perforation
- Right lower lobe pneumonia/empyema
In general, antibiotics should be continued for 7 to 10 days
Biliary drainage — Endoscopic sphincterotomy with stone extraction and/or stent insertion. If fails can proceed with percutaneous transhepatic cholangiography or open surgical decompression
Biliary drainage can then be performed on an elective basis (within 24 to 48 hours).
If the patient does not improve over the first 24 hours, urgent biliary decompression is required.
Risk factors include impacted stones, active smoker status, age >70 years, and additional stones within the GB
signs of acute suppurative cholangitis, such as:
- Persistent abdominal pain
- Hypotension despite adequate resuscitation
- Fever greater than 39ºC (102ºF)
- Mental confusion (a predictor of poor outcome
Stones more than 2 cm require lithotripsy. Intrahepatic stones can sometimes be removed with choledochoscopy.
Endoscopic drainage has lower overall rates of mortality and morbidity compared with surgical decompression ( 4.7 to 10% VS 10 to 50 %)
If coagulopathies that prevent sphincterotomy, or large stones, or too ill, can insert nasobiliary catheter.
Placing a stent without first performing a sphincterotomy appears to permit adequate drainage and may be another option for patients with coagulopathies
PTC involves transhepatic insertion of a needle into a bile duct, followed by injection of contrast material to opacify the bile ducts. PTC permits a number of therapeutic interventions, including drainage of infected bile, extraction of biliary tract stones, dilation of benign biliary strictures, or placement of a stent across a malignant stricture.
Or placement of a percutaneous cholecystostomy tube in patients with an intact gallbladder.
surgical exploration of the
common bile duct for stone removal. Elective surgery carries a very low
morbidity and mortality. If emergent
surgery -choledochotomy with placement of a large-bore T tube has a lower
mortality than cholecystectomy with common bile duct exploration.
Failure to perform a cholecystectomy, even after a sphincterotomy has been performed, is associated with high recurrence rates.Patients who are pregnant — same-antibiotic choices should take into account potential fetal toxicity . fetal shielding should be used.
mortality rates for patients with severe acute cholangitis remain high (20 to 30 percent)
PREVENTING RECURRENCE —
cholecystectomy is generally recommended.
If benign stenosis, as is seen following bile
duct injuries, endoscopic therapy or surgical repair may be required.if malignant stenoses- typically with stent placement, though the specific therapy chosen will depend on the patient's life expectancy and the likelihood of stent occlusion.
Splenic abscess
-results from endocarditis 4.7 % or seeding from some
other site of infection-
- recurrent or persistent despite antimicrobial therapy and left upper quadrant pain with or without splenomegaly
- may be accompanied by a left-sided pleural effusion
- splenic infarction if due to septic emboli
CT scan infarct VS abscess
antibiotic therapy and splenectomy.
CT-guided percutaneous aspiration is occasionally successful
- recurrent or persistent despite antimicrobial therapy and left upper quadrant pain with or without splenomegaly
- may be accompanied by a left-sided pleural effusion
- splenic infarction if due to septic emboli
CT scan infarct VS abscess
antibiotic therapy and splenectomy.
CT-guided percutaneous aspiration is occasionally successful
Sunday, December 1, 2013
Toxic megacolon
total or segmental nonobstructive colonic dilatation plus systemic toxicity
The most widely used criteria for the clinical diagnosis of toxic megacolon are:
non toxic- congenital megacolon (Hirschsprung's disease), idiopathic or acquired megacolon occurring with chronic constipation of any etiology, and intestinal pseudoobstruction
mucosal inflammation leads sequentially to the release of inflammatory mediators and bacterial products, increased inducible nitric oxide synthase, generation of excessive nitric oxide, and colonic dilatation.
extent of dilatation appears to be correlated with the depth of inflammation and ulceration. Damage to the myenteric plexus.
These include hypokalemia, antimotility agents, opiates, anticholinergics, antidepressants, barium enema, and colonoscopy. Discontinuing or rapid tapering of corticosteroids, sulfasalazine, or 5-ASA compounds also may contribute to the development of megacolon
Knowledge of prior attacks of IBD, the extent and type of disease, details of prior therapy, extraintestinal manifestations of IBD, recent travel, occupational exposure (eg, day care workers), antibiotic or chemotherapy use, use of antimotility agents, and HIV/AIDS status are very helpful
-diarrhea is unusual and air is absent in the colon below the point of obstruction.
High resolution ultrasonography can be used to accurately determine the extent and activity of severe ulcerative colitis and assess the response to therapy; it may also permit the early detection of toxic megacolon .
CT can determinie the etiology of megacolon. -diffuse colonic thickening
- useful in patients with AIDS who may have several intercurrent intraabdominal processes.
- identify complications of megacolon, such as perforation or vascular compromise
Limited endoscopy without bowel preparation is useful if IBD has not previously been diagnosed or an infective process is suspected, particularly CMV or acute bacillary dysentery.
full colonoscopy is extremely risky
medical treatment- preventing surgery in up to 50 percent of patients. However, a surgical consultation should be obtained upon admission,
- bowel rest and a nasogastric tube (or long intestinal tube) to decompress the gastrointestinal tract. Enteral feeding if patient shows signs of improvement to hasten mucosal healing and stimulate normal motility.
- ICU. Complete blood counts, electrolytes, and serial abdominal plain films are reviewed every 12 hours initially and then daily as the patient improves. Anemia, dehydration, and electrolyte deficits, particularly hypokalemia, may aggravate colonic dysmotility and should be treated aggressively.
(TPN) is of limited value
All antimotility agents, opiates, and anticholinergics should be discontinued.
prophylaxis for both gastric stress ulcerations and deep venous thrombosis (pneumatic compression stockings).
Antibiotic to reduce septic complications and in anticipation of peritonitis from perforation. We generally use ampicillin-gentamicin-metronidazole or a third-generation cephalosporin with metronidazole.
Intravenous corticosteroids (hydrocortisone 100 mg or equivalent every six to eight hours or by continuous infusion) - ulcerative colitis or Crohn's disease; this does not increase the risk of perforation . dexamethasone has been shown in experimental studies to decrease the colonic diameter by diminishing the expression of inducible NO synthase. methylprednisolone - its lower sodium retaining and potassium wasting properties, while others prefer prednisolone since the parenteral dose is equal to the oral dose. Steroids are not used in toxic megacolon due to C. difficile colitis or infective colitis.
Sulfasalazine and 5-ASA compounds have no role in patients with toxic megacolon due to IBD and should be initiated only after the attack begins to resolve.
Cyclosporine is useful in the treatment of severe colitis refractory to steroid therapy, but the experience in toxic megacolon is limited.
Some authors recommend intermittent rolling maneuvers or the knee-elbow position to help redistribute gas in the colon and thereby promote decompression- in patient not toxic
persistent fever after 48 to 72 hours of steroid therapy should raise the possibility of localized perforation or abscess.
Free perforation, massive hemorrhage, increasing transfusion requirements, worsening signs of toxicity, and progression of colonic dilatation are absolute indications for surgery.
surgical studies recommend colectomy if there is persistent colonic distention after 48 to 72 hours. However, we recommend prolongation of medical therapy up to seven days if the patient appears to be clinically improving despite persistent megacolon and there is no perforation
- severe C. difficile colitis, the first step is to stop the offending antibiotic, followed by vancomycin 500 mg four times daily orally or via a nasogastric tube NOT IV and intravenous metronidazole at a dose of 500 mg every eight hours. Fecal concentrations of metronidazole in the therapeutic range are achieved with this regimen because of biliary excretion of the drug.
Surgery — Subtotal colectomy with end-ileostomy - lower morbidity and mortality than single stage proctocolectomy and allows subsequent re-anastomosis. Early surgery without perforation results has much lower mortality than after perforation (8 VS 40 %)
The most widely used criteria for the clinical diagnosis of toxic megacolon are:
- Radiographic evidence of colonic distension
- PLUS at least three of the following:
- Fever >38ºC
- Heart rate >120 beats/min
- Neutrophilic leukocytosis >10,500/microL
- Anemia
- PLUS at least one of the following:
- Dehydration
- Altered sensorium
- Electrolyte disturbances- Metabolic alkalosis secondary to volume depletion and potassium loss is associated with a poor prognosis. Metabolic acidosis suggests the presence of ischemic colitis.
- Hypotension
non toxic- congenital megacolon (Hirschsprung's disease), idiopathic or acquired megacolon occurring with chronic constipation of any etiology, and intestinal pseudoobstruction
mucosal inflammation leads sequentially to the release of inflammatory mediators and bacterial products, increased inducible nitric oxide synthase, generation of excessive nitric oxide, and colonic dilatation.
extent of dilatation appears to be correlated with the depth of inflammation and ulceration. Damage to the myenteric plexus.
These include hypokalemia, antimotility agents, opiates, anticholinergics, antidepressants, barium enema, and colonoscopy. Discontinuing or rapid tapering of corticosteroids, sulfasalazine, or 5-ASA compounds also may contribute to the development of megacolon
Knowledge of prior attacks of IBD, the extent and type of disease, details of prior therapy, extraintestinal manifestations of IBD, recent travel, occupational exposure (eg, day care workers), antibiotic or chemotherapy use, use of antimotility agents, and HIV/AIDS status are very helpful
Radiography — Plain
abdominal radiographs
- The transverse or right colon is usually the most dilated, frequently greater than 6 cm and occasionally up to 15 cm on supine films . Repositioning results in redistribution of air in the colon,
- Multiple air-fluid levels, colonic haustral pattern is either absent or severely disturbed.
- Deep mucosal ulcerations may appear as air-filled crevices
-diarrhea is unusual and air is absent in the colon below the point of obstruction.
High resolution ultrasonography can be used to accurately determine the extent and activity of severe ulcerative colitis and assess the response to therapy; it may also permit the early detection of toxic megacolon .
CT can determinie the etiology of megacolon. -diffuse colonic thickening
- useful in patients with AIDS who may have several intercurrent intraabdominal processes.
- identify complications of megacolon, such as perforation or vascular compromise
Limited endoscopy without bowel preparation is useful if IBD has not previously been diagnosed or an infective process is suspected, particularly CMV or acute bacillary dysentery.
full colonoscopy is extremely risky
medical treatment- preventing surgery in up to 50 percent of patients. However, a surgical consultation should be obtained upon admission,
- bowel rest and a nasogastric tube (or long intestinal tube) to decompress the gastrointestinal tract. Enteral feeding if patient shows signs of improvement to hasten mucosal healing and stimulate normal motility.
- ICU. Complete blood counts, electrolytes, and serial abdominal plain films are reviewed every 12 hours initially and then daily as the patient improves. Anemia, dehydration, and electrolyte deficits, particularly hypokalemia, may aggravate colonic dysmotility and should be treated aggressively.
(TPN) is of limited value
All antimotility agents, opiates, and anticholinergics should be discontinued.
prophylaxis for both gastric stress ulcerations and deep venous thrombosis (pneumatic compression stockings).
Antibiotic to reduce septic complications and in anticipation of peritonitis from perforation. We generally use ampicillin-gentamicin-metronidazole or a third-generation cephalosporin with metronidazole.
Intravenous corticosteroids (hydrocortisone 100 mg or equivalent every six to eight hours or by continuous infusion) - ulcerative colitis or Crohn's disease; this does not increase the risk of perforation . dexamethasone has been shown in experimental studies to decrease the colonic diameter by diminishing the expression of inducible NO synthase. methylprednisolone - its lower sodium retaining and potassium wasting properties, while others prefer prednisolone since the parenteral dose is equal to the oral dose. Steroids are not used in toxic megacolon due to C. difficile colitis or infective colitis.
Sulfasalazine and 5-ASA compounds have no role in patients with toxic megacolon due to IBD and should be initiated only after the attack begins to resolve.
Cyclosporine is useful in the treatment of severe colitis refractory to steroid therapy, but the experience in toxic megacolon is limited.
Some authors recommend intermittent rolling maneuvers or the knee-elbow position to help redistribute gas in the colon and thereby promote decompression- in patient not toxic
persistent fever after 48 to 72 hours of steroid therapy should raise the possibility of localized perforation or abscess.
Free perforation, massive hemorrhage, increasing transfusion requirements, worsening signs of toxicity, and progression of colonic dilatation are absolute indications for surgery.
surgical studies recommend colectomy if there is persistent colonic distention after 48 to 72 hours. However, we recommend prolongation of medical therapy up to seven days if the patient appears to be clinically improving despite persistent megacolon and there is no perforation
- severe C. difficile colitis, the first step is to stop the offending antibiotic, followed by vancomycin 500 mg four times daily orally or via a nasogastric tube NOT IV and intravenous metronidazole at a dose of 500 mg every eight hours. Fecal concentrations of metronidazole in the therapeutic range are achieved with this regimen because of biliary excretion of the drug.
Surgery — Subtotal colectomy with end-ileostomy - lower morbidity and mortality than single stage proctocolectomy and allows subsequent re-anastomosis. Early surgery without perforation results has much lower mortality than after perforation (8 VS 40 %)
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