Jump to content
RemedySpot.com

Re: acute vs. chronic

Rate this topic


Guest guest

Recommended Posts

Chronic pancreatitis is an inflammatory disease in which progressive and

irreversible structural changes to the pancreas result in a permanent

impairment of both the exocrine and endocrine functions.

As the pancreas become progressively more scarred, some persons develop

diabetes and/or the inability to digest foods, especially fats. Because of

the lack of normal pancreatic enzymes, digestion of food and the production

of wastes are adversely affected. Abdominal pain is common, especially after

eating. Stools become bulky, greasy, foul smelling and tend to float in the

water because of their high fat content - a condition known as steatorrhea.

The formation of stones in the pancreas is also common.

The treatment of chronic pancreatitis depends on 4 factors: the cause of the

pancreatitis, the portion of the pancreas involved, the presence or absence

os symptoms, and the size of the pancreatic duct.

When symptoms are mild or absent ( " silent pancreatitis " ) no treatment is

indicated. For persons with disabling symptoms, however, treatment is

indicated. Treatment may consist of medications and possibly surgery.

The pancreas is a long, slender organ in the upper abdomen. The exocrine

area of the pancreas produces digestive juices and the endocrine area makes

hormones, such as insulin, that regulate how the body stores and uses food.

Both functions are impaired by chronic pancreatitis, an inflammatory disease

that causes progressive, irreversible structural changes. Some persons

develop diabetes and/or become unable to digest foods, especially fats. The

lack of normal pancreatic enzymes adversely affects digestion and waste

production. Abdominal pain is common, especially after eating. This illness

can make stool bulky, fatty and odiferous (that's " steatorrhea " ), and can

cause stones to form in the pancreas.

In some 70% to 80% of cases, alcoholism is a factor, but other causes can

include duct obstruction, nutritional factors and genetic abnormalities.

About 30% of cases have no known cause. Symptoms include severe abdominal

pain, weight loss and steatorrhea. When symptoms are mild, no treatment is

indicated. When needed, treatment focuses on pain control, relieving duct

obstruction, correcting digestive problems, and detecting and managing

complications.

The choice of treatment for you or for the patient you care about, depends

on the cause, the portion of the organ involved, symptoms and duct size.

This illness requires individual diagnosis and treatment. Not all patients

respond to the same therapy. Treatment may consist of medications and,

possibly, surgery. The Journal of Gastrointestinal Surgery reports that

surgery for chronic pancreatitis " can be performed safely with minimal

morbidity and excellent long-term survival. "

acute vs. chronic

> Are most of the members of this site chronic sufferers? I was just

> diagnosed with pancreatitis, but they are not sure if it is acute or

> chronic. I cant get to a specialist until early Jan.

>

> It is my understanding that acute is bad, but that many acute cases

> get better and do not come back. I am more concerned about chronic.

> Even then, there are treatments, right? Enzymes, possible

> surgeries? I am very depressed right now because I want to live for

> a good thirty more years and am concerned. I do not drink, and an

> ultrasound did not reveal any stones, just a slightly " inhomogeneous "

> pancreas and my lipase and amylase were elevated (lipase 4x normal).

>

> I am 31.

>

> Thanks

>

>

>

>

> PANCREATITIS Association, Intl.

> Online e-mail group

>

> To reply to this message hit & quot;reply & quot; or send an e-mail

to: Pancreatitis (AT) Yahoo

>

>

Link to comment
Share on other sites

Chronic pancreatitis is an inflammatory disease in which progressive and

irreversible structural changes to the pancreas result in a permanent

impairment of both the exocrine and endocrine functions.

As the pancreas become progressively more scarred, some persons develop

diabetes and/or the inability to digest foods, especially fats. Because of

the lack of normal pancreatic enzymes, digestion of food and the production

of wastes are adversely affected. Abdominal pain is common, especially after

eating. Stools become bulky, greasy, foul smelling and tend to float in the

water because of their high fat content - a condition known as steatorrhea.

The formation of stones in the pancreas is also common.

The treatment of chronic pancreatitis depends on 4 factors: the cause of the

pancreatitis, the portion of the pancreas involved, the presence or absence

os symptoms, and the size of the pancreatic duct.

When symptoms are mild or absent ( " silent pancreatitis " ) no treatment is

indicated. For persons with disabling symptoms, however, treatment is

indicated. Treatment may consist of medications and possibly surgery.

The pancreas is a long, slender organ in the upper abdomen. The exocrine

area of the pancreas produces digestive juices and the endocrine area makes

hormones, such as insulin, that regulate how the body stores and uses food.

Both functions are impaired by chronic pancreatitis, an inflammatory disease

that causes progressive, irreversible structural changes. Some persons

develop diabetes and/or become unable to digest foods, especially fats. The

lack of normal pancreatic enzymes adversely affects digestion and waste

production. Abdominal pain is common, especially after eating. This illness

can make stool bulky, fatty and odiferous (that's " steatorrhea " ), and can

cause stones to form in the pancreas.

In some 70% to 80% of cases, alcoholism is a factor, but other causes can

include duct obstruction, nutritional factors and genetic abnormalities.

About 30% of cases have no known cause. Symptoms include severe abdominal

pain, weight loss and steatorrhea. When symptoms are mild, no treatment is

indicated. When needed, treatment focuses on pain control, relieving duct

obstruction, correcting digestive problems, and detecting and managing

complications.

The choice of treatment for you or for the patient you care about, depends

on the cause, the portion of the organ involved, symptoms and duct size.

This illness requires individual diagnosis and treatment. Not all patients

respond to the same therapy. Treatment may consist of medications and,

possibly, surgery. The Journal of Gastrointestinal Surgery reports that

surgery for chronic pancreatitis " can be performed safely with minimal

morbidity and excellent long-term survival. "

acute vs. chronic

> Are most of the members of this site chronic sufferers? I was just

> diagnosed with pancreatitis, but they are not sure if it is acute or

> chronic. I cant get to a specialist until early Jan.

>

> It is my understanding that acute is bad, but that many acute cases

> get better and do not come back. I am more concerned about chronic.

> Even then, there are treatments, right? Enzymes, possible

> surgeries? I am very depressed right now because I want to live for

> a good thirty more years and am concerned. I do not drink, and an

> ultrasound did not reveal any stones, just a slightly " inhomogeneous "

> pancreas and my lipase and amylase were elevated (lipase 4x normal).

>

> I am 31.

>

> Thanks

>

>

>

>

> PANCREATITIS Association, Intl.

> Online e-mail group

>

> To reply to this message hit & quot;reply & quot; or send an e-mail

to: Pancreatitis (AT) Yahoo

>

>

Link to comment
Share on other sites

Chronic pancreatitis is an inflammatory disease in which progressive and

irreversible structural changes to the pancreas result in a permanent

impairment of both the exocrine and endocrine functions.

As the pancreas become progressively more scarred, some persons develop

diabetes and/or the inability to digest foods, especially fats. Because of

the lack of normal pancreatic enzymes, digestion of food and the production

of wastes are adversely affected. Abdominal pain is common, especially after

eating. Stools become bulky, greasy, foul smelling and tend to float in the

water because of their high fat content - a condition known as steatorrhea.

The formation of stones in the pancreas is also common.

The treatment of chronic pancreatitis depends on 4 factors: the cause of the

pancreatitis, the portion of the pancreas involved, the presence or absence

os symptoms, and the size of the pancreatic duct.

When symptoms are mild or absent ( " silent pancreatitis " ) no treatment is

indicated. For persons with disabling symptoms, however, treatment is

indicated. Treatment may consist of medications and possibly surgery.

The pancreas is a long, slender organ in the upper abdomen. The exocrine

area of the pancreas produces digestive juices and the endocrine area makes

hormones, such as insulin, that regulate how the body stores and uses food.

Both functions are impaired by chronic pancreatitis, an inflammatory disease

that causes progressive, irreversible structural changes. Some persons

develop diabetes and/or become unable to digest foods, especially fats. The

lack of normal pancreatic enzymes adversely affects digestion and waste

production. Abdominal pain is common, especially after eating. This illness

can make stool bulky, fatty and odiferous (that's " steatorrhea " ), and can

cause stones to form in the pancreas.

In some 70% to 80% of cases, alcoholism is a factor, but other causes can

include duct obstruction, nutritional factors and genetic abnormalities.

About 30% of cases have no known cause. Symptoms include severe abdominal

pain, weight loss and steatorrhea. When symptoms are mild, no treatment is

indicated. When needed, treatment focuses on pain control, relieving duct

obstruction, correcting digestive problems, and detecting and managing

complications.

The choice of treatment for you or for the patient you care about, depends

on the cause, the portion of the organ involved, symptoms and duct size.

This illness requires individual diagnosis and treatment. Not all patients

respond to the same therapy. Treatment may consist of medications and,

possibly, surgery. The Journal of Gastrointestinal Surgery reports that

surgery for chronic pancreatitis " can be performed safely with minimal

morbidity and excellent long-term survival. "

acute vs. chronic

> Are most of the members of this site chronic sufferers? I was just

> diagnosed with pancreatitis, but they are not sure if it is acute or

> chronic. I cant get to a specialist until early Jan.

>

> It is my understanding that acute is bad, but that many acute cases

> get better and do not come back. I am more concerned about chronic.

> Even then, there are treatments, right? Enzymes, possible

> surgeries? I am very depressed right now because I want to live for

> a good thirty more years and am concerned. I do not drink, and an

> ultrasound did not reveal any stones, just a slightly " inhomogeneous "

> pancreas and my lipase and amylase were elevated (lipase 4x normal).

>

> I am 31.

>

> Thanks

>

>

>

>

> PANCREATITIS Association, Intl.

> Online e-mail group

>

> To reply to this message hit & quot;reply & quot; or send an e-mail

to: Pancreatitis (AT) Yahoo

>

>

Link to comment
Share on other sites

This is a medical emergency marked by acute abdominal stress. Symptoms are

caused by spillage of pancreatic fluids into the abdominal cavity. These

fluids contain enzymes which begin to digest and destroy the lining of the

intestine and the intestinal wall itself as well as any internal organs it

encounters.

Pain typically radiates from the pit of the abdomen through to the back with

nausea, vomiting, low-grade fever, and shock. Some patients exhibit none of

these save shock. There may be evidence of intra-abdominal bleeding.

Causes include direct trauma, overindulgence in alcoholic beverages, viral

and bacterial infections, duodenal ulcer perforation into the pancreas,

certain metabolic insults, and toxicity from some pharmacological drugs.

The diagnosis is made by ultrasound with supporting evidence from elevated

pancreatic enzyme levels (amylase and lipase). These people usually have

elevated white cell counts.

Acute pancreatitis is a medical emergency and must be treated in a hospital

setting. In addition to the usual management doctors in nutritional medicine

have noted that intramuscular selenium followed by repeat doses 24 hours

later, then daily doses are useful in the management of this disorder. Only

doctors who practice nutritional medicine have a clue about the use of

selenium for this indication.

In the acute stage of acute pancreatitis the patient should have nothing by

mouth, intravenous feeding should be instituted, calcium and magnesium

levels maintained, pain managed, and the cause of the disorder treated. This

may involve surgery.

Chronic pancreatitis may result from one or more bouts of acute pancreatitis

and this condition is marked by radiologic evidence of calcification of the

pancreas, passage of undigested fat in the stool, diabetes, vitamin B12

deficiency, and poor digestion due to loss of pancreatic enzymes. Also a

cyst-like condition may develop requiring surgery.

The most important aspect in the treatment of acute pancreatitis is

supportive care. This includes replacement of fluid and electrolytes,

correction of metabolic abnormalities such as symptomatic hypercalcemiaand

nutritional support. Other measures such as the use of nasogastric suction

and antibiotics should be decided on a case-by-case basis.

Agents that have been used to inhibit pancreatic secretion have not been

found to be useful in altering the course in acute pancreatitis. These

include somatostatin and glucagon. Protease inhibitors, which are effective

in laboratory studies, have not been shown to be useful in clinical

pancreatitis.

Emergency surgery is not indicated in mild acute pancreatitis. Some surgical

procedures such as resection of necrotictissue and peritoneal lavagemay have

a role in select patients with severe, progressive necrotizing pancreatitis

or pancreatic abscess. Cholecystectomy has been demonstrated to be effective

in patients with recurrent acute pancreatitis and microlithiasis (Figure

17).

Surgical sphincteroplasty of the pancreatic sphincter is an alternative

approach to endoscopic pancreatic sphincterotomy in patients with pancreatic

sphincter dysfunction. Although the patient outcome is the same as for the

endoscopic approach, it is more invasive, requiring laparotomy and .

duodenotomy

Sphincteroplasty of the minor papilla is indicated for unsuccessful or

failed endoscopic minor papilla sphincterotomy in patients with . pancreas

divisum

Endoscopic therapy has a therapeutic role in three specific areas in the

management of acute pancreatitis: 1) acute gallstone pancreatitis, 2)

recurrent pancreatitis due to pancreatic sphincter dysfunction, and 3)

recurrent pancreatitis due to . pancreas divisum The rationale for

endoscopic therapy in each area is the relief of obstruction to flow of

pancreatic juice.

[top]

Although it would seem logical that removal of the gallstones from the

common bile duct early in acute gallstone pancreatitis would improve the

clinical course, there is a lack of a " predictable " good outcome as

suggested by propective clinical trials. It appears, however, that the

patients with suspected stones who benefit from early ERCP are those with

evidence of biliary obstruction such as jaundice or dilation of the bile

duct and severe pancreatitis. Further clinical trials are needed before more

definitive recommendations can be made. In a subgroup of patients with acute

recurrent pancreatitis and ,microlithiasis endoscopic sphincterotomy has

been shown to significantly reduce the frequency of attacks (Figure 18).

[top]

With the advent of manometric studies of the pancreatic sphincter, many

cases of so-called idiopathic recurrent pancreatitis are now known to be a

result of pancreatic sphincter dysfunction. Endoscopic pancreatic

sphincterotomy may be expected to have a good outcome in up to 90% of these

patients. There are two techniques for endoscopic pancreatic sphincterotomy;

one is with a pull-type sphincterotome followed by stenting of the

pancreatic duct and the second is with a needle-knife sphincterotome

performed over a pancreatic stent. Following pancreatic sphincterotomy there

may be tissue swelling that could result in obstruction to pancreatic

outflow. Therefore, short-term pancreatic stenting is indicated when

pancreatic sphincterotomy is performed to maintain patency of pancreatic

outflow (Figure 19).

[top]

Endoscopic minor papilla sphincterotomy is effective treatment for patients

with recurrent pancreatitis and pancreas divisum (Figure 20). Good long-term

results are found in about 70% of patients but may be significantly less if

there are changes of chronic pancreatitis.

There are two techniques for endoscopic minor papilla sphincterotomy; one is

with a pull-type sphincterotome followed by stenting of the pancreatic duct

and the second is with a needle-knife sphincterotome performed over a

pancreatic stent (Figure 21). Following pancreatic sphincterotomy there may

be tissue swelling that could result in obstruction to pancreatic outflow.

Therefore short-term pancreatic stenting is indicated when pancreatic

sphincterotomy is performed to maintain patency of pancreatic outflow.

[top]

acute vs. chronic

> Are most of the members of this site chronic sufferers? I was just

> diagnosed with pancreatitis, but they are not sure if it is acute or

> chronic. I cant get to a specialist until early Jan.

>

> It is my understanding that acute is bad, but that many acute cases

> get better and do not come back. I am more concerned about chronic.

> Even then, there are treatments, right? Enzymes, possible

> surgeries? I am very depressed right now because I want to live for

> a good thirty more years and am concerned. I do not drink, and an

> ultrasound did not reveal any stones, just a slightly " inhomogeneous "

> pancreas and my lipase and amylase were elevated (lipase 4x normal).

>

> I am 31.

>

> Thanks

>

>

>

>

> PANCREATITIS Association, Intl.

> Online e-mail group

>

> To reply to this message hit & quot;reply & quot; or send an e-mail

to: Pancreatitis (AT) Yahoo

>

>

Link to comment
Share on other sites

INTRODUCTION

Background: Pancreatitis is an inflammatory process in which pancreatic

enzymes autodigest the gland.

The gland can sometimes heal without any impairment of function or any

morphologic changes. This process is known as acute pancreatitis. It can

recur intermittently, contributing to the functional and morphologic loss of

the gland. Recurrent attacks are referred to as chronic pancreatitis. Both

forms of pancreatitis are present in the ED with acute clinical findings.

Pathophysiology: Because the pancreas is located in the retroperitoneal

space with no capsule, inflammation can spread easily. In acute

pancreatitis, parenchymal edema and peripancreatic fat necrosis occur first.

This process is known as acute edematous pancreatitis.

When necrosis involves the parenchyma, accompanied by hemorrhage and

dysfunction of the gland, the inflammation evolves into hemorrhagic or

necrotizing pancreatitis.

Pseudocysts and pancreatic abscesses can result from necrotizing

pancreatitis because of enzymes being walled off by granulation tissue (ie,

pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic

tissue (ie, pancreatic abscess formation). An ultrasound or, preferably, a

CT scan can be used detect both.

The inflammatory process can cause systemic effects because of the presence

of cytokines, such as bradykinins and phospholipase A. These cytokines may

cause vasodilation, increase in vascular permeability, pain, and leukocyte

accumulation in the vessel walls. Fat necrosis may cause hypocalcemia.

Pancreatic B cell injury may lead to hyperglycemia.

Frequency:

In the US: Annual incidence of acute pancreatitis is 19.5 per 100,000

population and chronic pancreatitis is 8.3 per 100,000 population per year.

Mortality/Morbidity:

Although acute pancreatitis should be noted, chronic pancreatitis has a more

severe presentation as episodes recur.

Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac

depression, hemorrhage, and hypotensive shock all may be systemic

manifestations of acute pancreatitis in its most severe form.

Race: Annual incidence of acute pancreatitis in Native American persons is 4

per 100,000 population, in white persons is 5.7 per 100,000 population, and

in black persons is 20.7 per 100,000 population.

Sex: No predilection exists.

Age: The risk for African American persons aged 35-64 years is 10 times

higher than for any other group. African American persons are at higher risk

than white persons in that same age group.

Clinical

History:

The main presentation of acute pancreatitis is epigastric pain or right

upper quadrant pain radiating to the back

Nausea and/or vomiting

Fever

Query the patient about recent surgeries and invasive procedures (ie,

endoscopic retrograde cholangiopancreatography) or family history of

hypertriglyceridemia.

Patients frequently have a history of previous biliary colic and binge

alcohol consumption, the major causes of acute pancreatitis.

Physical:

Tachycardia

Tachypnea

Hypotension

Fever

Abdominal tenderness, distension, guarding, and rigidity

Mild jaundice

Diminished or absent bowel sounds

Because of contiguous spread of inflammation (effusion) from the pancreas,

lung auscultation may reveal basilar rales, especially in the left lung.

Occasionally, in the extremities, muscular spasm may be noted secondary to

hypocalcemia.

Severe cases may have a Grey sign (ie, bluish discoloration of the

flanks) and Cullen sign (ie, bluish discoloration of the periumbilical area)

caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic

pancreatitis.

Causes:

The major causes are long-standing alcohol consumption and biliary stone

disease.

In developed countries, the most common cause of acute pancreatitis is

alcohol abuse.

On the cellular level, ethanol leads to intracellular accumulation of

digestive enzymes and their premature activation and release.

On the ductal level, ethanol increases the permeability of ductules, which

allow enzymes to reach the parenchyma, resulting in pancreatic damage.

Ethanol increases the protein content of the pancreatic juice and decreases

bicarbonate levels and trypsin inhibitor concentrations. This leads to the

formation of protein plugs that block the pancreatic outflow and

obstruction.

Another major cause of acute pancreatitis is biliary stone disease (eg,

cholelithiasis, choledocholithiasis). A biliary stone may lodge in the

pancreatic duct or ampulla of Vater and obstruct the pancreatic duct,

leading to extravasation of enzymes into the parenchyma.

Minor causes of acute pancreatitis

Medications, including azathioprine, corticosteroids, sulfonamides,

thiazides, furosemides, NSAIDs, mercaptopurine, methyldopa, and

tetracyclines

Endoscopic retrograde cholangiopancreatography (ERCP)

Hypertriglyceridemia (When the triglyceride (TG) level exceeds 1000 mg/U, an

episode of pancreatitis is more likely.)

Peptic ulcer disease

Abdominal or cardiopulmonary bypass surgery, which may insult the gland by

ischemia

Trauma to the abdomen or back, resulting in sudden compression of the gland

against the spine posteriorly

Carcinoma of the pancreas, which may lead to pancreatic outflow obstruction

Viral infections, including mumps, sackievirus, cytomegalovirus (CMV),

hepatitis virus, Epstein-Barr virus (EBV), and rubella

Bacterial infections, such as mycoplasma

Intestinal parasites, such as ascaris, which can block the pancreatic

outflow

Pancreas divisum

Scorpion and snake bites

Vascular factors, such as ischemia or vasculitis

DIFFERENTIALS

Other Problems to be Considered: Perforated viscus

Acute peritonitis

Choledocholithiasis

Macroamylasemia

Macrolipasemia

Intestinal obstruction

Pancreatic cancer

Malabsorption syndromes/processes

Workup

Lab Studies:

A complete blood count (CBC) demonstrates leukocytosis (WBC >12000) with the

differential being shifted towards the segmented polymorphs.

If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis,

obtain type and crossmatch.

Measure blood glucose level because it may be elevated from B cell injury in

the pancreas.

Obtain measurements for BUN, creatine (Cr), and electrolytes (Na, K, Cl,

CO2, P, Mg); a great disturbance in the electrolyte balance is usually

found, secondary to third spacing of fluids.

Measure amylase levels, preferably the Amylase P, which is more specific to

pancreatic pathology. Levels more than 3 times higher than normal strongly

suggest the diagnosis of acute pancreatitis

Lipase levels also are elevated and remain high for 12 days. In patients

with chronic pancreatitis (usually caused by alcohol abuse), lipase may be

elevated in the presence of a normal serum amylase level

Perform liver function tests (eg, alkaline phosphatase, serum

glutamic-pyruvic transaminase [sGPT], serum glutamic-oxaloacetic

transaminase [sGOT], G-GT) and bilirubin, particularly with biliary origin

pancreatitis.

Imaging Studies:

Perform a plain KUB (Kidneys, ureters, bladder) with the patient in the

upright position to exclude viscus perforation (ie, air under the

diaphragm). In cases with a recurrent episode of chronic pancreatitis,

peripancreatic calcifications may be noted

Ultrasound can be used as a screening test. If overlying gas shadows

secondary to bowel distention are present, it may not be specific

CT scan is the most reliable imaging modality in the diagnosis of acute

pancreatitis. The criteria for diagnosis are divided by Balthazar and

colleagues into 5 grades, as follows:

Grade A - Normal pancreas

Grade B - Focal or diffuse gland enlargement

Grade C - Intrinsic gland abnormality recognized by haziness on the scan

Grade D - Single ill-defined collection or phlegmon

Grade E - Two or more ill-defined collections or the presence of gas in or

nearby the pancreas

Other Tests:

Para-aminobenzoic acid test (ie, bentiromide [Chymex] test) for chronic

pancreatitis

Treatment

Emergency Department Care: Most of the cases presenting to the ED are

treated conservatively, and approximately 80% respond to such treatment.

Fluid resuscitation

Monitor accurate intake/output and electrolyte balance of the patient.

Crystalloids are used, but other infusions, such as packed red blood cells

(PRBCs), are occasionally administered, particularly in the case of

hemorrhagic pancreatitis.

Central lines and Swan-Ganz catheters are used in patients with severe fluid

loss and very low blood pressure.

Patients should have nothing by mouth, and a nasogastric tube should be

inserted to assure an empty stomach and to keep the GI system at rest.

Begin parenteral nutrition if the prognosis is poor and if the patient is

going to be kept in the hospital for more than 4 days.

Analgesics are used to relieve pain. Meperidine is preferred over morphine

because of the greater spastic effect of the latter on the sphincter of

Oddi.

Antibiotics are used in severe cases associated with septic shock or when

the CT scan indicates that a phlegmon of the pancreas has evolved.

Other conditions, such as biliary pancreatitis associated with cholangitis,

also need antibiotic coverage. The preferred antibiotics are the ones

secreted by the biliary system, such as ampicillin and third generation

cephalosporins.

Continuous oxygen saturation should be monitored by pulse oxymetry and

acidosis should be corrected. When tachypnea and pending respiratory failure

develops, intubation should be performed.

Perform CT-guided aspiration of necrotic areas, if necessary.

An ERCP may be indicated for common duct stone removal.

Consultations: Consult a general surgeon in the following cases:

For phlegmon of the pancreas, surgery can achieve drainage of any abscess or

scooping of necrotic pancreatic tissue. It should be followed by

postoperative lavage of the pancreatic bed.

In patients with hemorrhagic pancreatitis, surgery is indicated to achieve

hemostasis, particularly because major vessels may be eroded in acute

pancreatitis.

Patients who fail to improve despite optimal medical treatment or patients

who push the Ranson score even further are taken to the operating room.

Surgery in these cases may lead to a better outcome or confirm a different

diagnosis.

In biliary pancreatitis, a sphincterotomy (ie, surgical emptying of the

common bile duct) can relieve the obstruction. A cholecystectomy may be

performed to clear the system from any source of biliary stones.

Medications

The goal of pharmacotherapy is to relieve pain and minimize complications.

Drug Category: Antibiotics - Used to cover the microorganisms that may grow

in biliary pancreatitis and acute necrotizing pancreatitis. The empiric

antibiotic regimen usually is based on the premise that enteric anaerobic

and aerobic gram-bacilli microorganisms are often the cause of pancreatic

infections. Once culture sensitivities are made, adjustments in the

antibiotic regimen can be done. Drug Name

Ceftriaxone (Rocephin)- Third-generation cephalosporin with broad-spectrum

gram-negative activity; lower efficacy against gram-positive organisms;

higher efficacy against resistant organisms. Arrests bacterial growth by

binding to one or more penicillin binding proteins.

Adult Dose 1-2 g IM/IV once or divided bid

Pediatric Dose 50-75 mg/kg/d IM/IV divided q12h

Contraindications Documented hypersensitivity

Interactions Probenecid may increase levels; coadministration with

ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Adjust dose in renal impairment; caution in breastfeeding women

and allergy to penicillin

Drug Name

Ampicillin (Marcillin, Omnipen)- Bactericidal activity against susceptible

organisms. Alternative to amoxicillin when unable to take medication orally.

Adult Dose 250-500 IM/IV mg q6h

Pediatric Dose 25-50 mg/kg/d IM/IV divided q6-8h

Contraindications Documented hypersensitivity; viral mononucleosis

Interactions Probenecid and disulfiram elevate levels; allopurinol decreases

effects and has additive effects on ampicillin rash; may decrease effects of

oral contraceptives

Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Adjust dose in renal failure; evaluate rash and differentiate

from hypersensitivity reaction

Drug Category: Analgesics - Pain control is essential to quality patient

care. It ensures patient comfort, promotes pulmonary toilet, and has

sedating properties, which are beneficial for patients who have sustained

trauma or have painful lesions.

Drug Name

Meperidine (Demerol)- Analgesic with multiple actions similar to those of

morphine. May produce less constipation, smooth muscle spasm, and depression

of cough reflex than similar analgesic doses of morphine.

Adult Dose 15-35 mg/h IV; 50-150 mg IM q3-4h

Pediatric Dose 1.1-1.8 mg/kg IM q3-4h

Contraindications Documented hypersensitivity; MAOIs; upper airway

obstruction or significant respiratory depression; during labor when

delivery of premature infant is anticipated

Interactions Monitor for increased respiratory and CNS depression with

coadministration of cimetidine; hydantoins may decrease effects; avoid with

protease inhibitors

Pregnancy C - Safety for use during pregnancy has not been established.

Precautions Caution in head injuries because may increase respiratory

depression and CSF pressure (use only if absolutely necessary); caution when

using postoperatively and with history of pulmonary disease (suppresses

cough reflex; substantially increased dose levels may aggravate or cause

seizures because of tolerance, even if no prior history of convulsive

disorders; monitor closely for morphine-induced seizure activity if seizure

history exists

Drug Category: Antibiotics - Used to cover the microorganisms that may grow

in biliary pancreatitis and acute necrotizing pancreatitis. The empiric

antibiotic regimen usually is based on the premise that enteric anaerobic

and aerobic gram-bacilli microorganisms are often the cause of pancreatic

infections. Once culture sensitivities are made, adjustments in the

antibiotic regimen can be done. Drug Category: Analgesics - Pain control is

essential to quality patient care. It ensures patient comfort, promotes

pulmonary toilet, and has sedating properties, which are beneficial for

patients who have sustained trauma or have painful lesions.

Followup

Further Inpatient Care:

Transfer patients with Ranson scores of 0-2 to a hospital floor.

Transfer patients with Ranson scores 3-5 to an intensive care unit.

Transfer patients with Ranson scores higher than 5 to an intensive care unit

with emergency surgery as a possibility.

Further Outpatient Care:

The patient should be followed routinely with physical examination and

amylase and lipase assays.

Complications:

Infected pancreatic necrosis may result from seeding of bacteria into the

inflammation.

An acute pseudocyst is an effusion of pancreatic juice that is walled off by

granulation tissue after an episode of acute pancreatitis.

Hemorrhage into the GI tract retroperitoneum or the peritoneal cavity is

possible because of erosion of large vessels.

Intestinal obstruction or necrosis may occur.

Common bile duct obstruction may be caused by a pancreatic abscess,

pseudocyst, or biliary stone that caused the pancreatitis.

An internal pancreatic fistula from pancreatic duct disruption or a leaking

pancreatic pseudocyst may occur.

Prognosis:

Ranson developed a series of different criteria for the severity of acute

pancreatitis.

Present on admission

Older than 55 years

WBC higher than 16,000 per mcL

Blood glucose higher than 200 mg/dL

Serum lactate dehydrogenase (LDH) more than 350 IU/L

SGOT (ie, aspartate aminotransferase [AST]) greater than 250 IU/L

Developing during the first 48 hours

Hematocrit fall more than 10%

BUN increase more than 8 mg/dL

Serum calcium less than 8 mg/dL

Arterial oxygen saturation less than 60 mm Hg

Base deficit higher than 4 mEq/L

Estimated fluid sequestration higher than 600 mL

A Ranson score of 0-2 has a minimal mortality rate.

A Ranson score of 3-5 has a 10%-20% mortality rate.

A Ranson score higher than 5 has a mortality rate of more than 50% and is

associated with more systemic complications.

Patient Education:

Educate patients about the disease and advise then to avoid alcohol in binge

amounts and to discontinue any risk factor, such as fatty meals and

abdominal trauma.

acute vs. chronic

> Are most of the members of this site chronic sufferers? I was just

> diagnosed with pancreatitis, but they are not sure if it is acute or

> chronic. I cant get to a specialist until early Jan.

>

> It is my understanding that acute is bad, but that many acute cases

> get better and do not come back. I am more concerned about chronic.

> Even then, there are treatments, right? Enzymes, possible

> surgeries? I am very depressed right now because I want to live for

> a good thirty more years and am concerned. I do not drink, and an

> ultrasound did not reveal any stones, just a slightly " inhomogeneous "

> pancreas and my lipase and amylase were elevated (lipase 4x normal).

>

> I am 31.

>

> Thanks

>

>

>

>

> PANCREATITIS Association, Intl.

> Online e-mail group

>

> To reply to this message hit & quot;reply & quot; or send an e-mail

to: Pancreatitis (AT) Yahoo

>

>

Link to comment
Share on other sites

INTRODUCTION

Background: Pancreatitis is an inflammatory process in which pancreatic

enzymes autodigest the gland.

The gland can sometimes heal without any impairment of function or any

morphologic changes. This process is known as acute pancreatitis. It can

recur intermittently, contributing to the functional and morphologic loss of

the gland. Recurrent attacks are referred to as chronic pancreatitis. Both

forms of pancreatitis are present in the ED with acute clinical findings.

Pathophysiology: Because the pancreas is located in the retroperitoneal

space with no capsule, inflammation can spread easily. In acute

pancreatitis, parenchymal edema and peripancreatic fat necrosis occur first.

This process is known as acute edematous pancreatitis.

When necrosis involves the parenchyma, accompanied by hemorrhage and

dysfunction of the gland, the inflammation evolves into hemorrhagic or

necrotizing pancreatitis.

Pseudocysts and pancreatic abscesses can result from necrotizing

pancreatitis because of enzymes being walled off by granulation tissue (ie,

pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic

tissue (ie, pancreatic abscess formation). An ultrasound or, preferably, a

CT scan can be used detect both.

The inflammatory process can cause systemic effects because of the presence

of cytokines, such as bradykinins and phospholipase A. These cytokines may

cause vasodilation, increase in vascular permeability, pain, and leukocyte

accumulation in the vessel walls. Fat necrosis may cause hypocalcemia.

Pancreatic B cell injury may lead to hyperglycemia.

Frequency:

In the US: Annual incidence of acute pancreatitis is 19.5 per 100,000

population and chronic pancreatitis is 8.3 per 100,000 population per year.

Mortality/Morbidity:

Although acute pancreatitis should be noted, chronic pancreatitis has a more

severe presentation as episodes recur.

Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac

depression, hemorrhage, and hypotensive shock all may be systemic

manifestations of acute pancreatitis in its most severe form.

Race: Annual incidence of acute pancreatitis in Native American persons is 4

per 100,000 population, in white persons is 5.7 per 100,000 population, and

in black persons is 20.7 per 100,000 population.

Sex: No predilection exists.

Age: The risk for African American persons aged 35-64 years is 10 times

higher than for any other group. African American persons are at higher risk

than white persons in that same age group.

Clinical

History:

The main presentation of acute pancreatitis is epigastric pain or right

upper quadrant pain radiating to the back

Nausea and/or vomiting

Fever

Query the patient about recent surgeries and invasive procedures (ie,

endoscopic retrograde cholangiopancreatography) or family history of

hypertriglyceridemia.

Patients frequently have a history of previous biliary colic and binge

alcohol consumption, the major causes of acute pancreatitis.

Physical:

Tachycardia

Tachypnea

Hypotension

Fever

Abdominal tenderness, distension, guarding, and rigidity

Mild jaundice

Diminished or absent bowel sounds

Because of contiguous spread of inflammation (effusion) from the pancreas,

lung auscultation may reveal basilar rales, especially in the left lung.

Occasionally, in the extremities, muscular spasm may be noted secondary to

hypocalcemia.

Severe cases may have a Grey sign (ie, bluish discoloration of the

flanks) and Cullen sign (ie, bluish discoloration of the periumbilical area)

caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic

pancreatitis.

Causes:

The major causes are long-standing alcohol consumption and biliary stone

disease.

In developed countries, the most common cause of acute pancreatitis is

alcohol abuse.

On the cellular level, ethanol leads to intracellular accumulation of

digestive enzymes and their premature activation and release.

On the ductal level, ethanol increases the permeability of ductules, which

allow enzymes to reach the parenchyma, resulting in pancreatic damage.

Ethanol increases the protein content of the pancreatic juice and decreases

bicarbonate levels and trypsin inhibitor concentrations. This leads to the

formation of protein plugs that block the pancreatic outflow and

obstruction.

Another major cause of acute pancreatitis is biliary stone disease (eg,

cholelithiasis, choledocholithiasis). A biliary stone may lodge in the

pancreatic duct or ampulla of Vater and obstruct the pancreatic duct,

leading to extravasation of enzymes into the parenchyma.

Minor causes of acute pancreatitis

Medications, including azathioprine, corticosteroids, sulfonamides,

thiazides, furosemides, NSAIDs, mercaptopurine, methyldopa, and

tetracyclines

Endoscopic retrograde cholangiopancreatography (ERCP)

Hypertriglyceridemia (When the triglyceride (TG) level exceeds 1000 mg/U, an

episode of pancreatitis is more likely.)

Peptic ulcer disease

Abdominal or cardiopulmonary bypass surgery, which may insult the gland by

ischemia

Trauma to the abdomen or back, resulting in sudden compression of the gland

against the spine posteriorly

Carcinoma of the pancreas, which may lead to pancreatic outflow obstruction

Viral infections, including mumps, sackievirus, cytomegalovirus (CMV),

hepatitis virus, Epstein-Barr virus (EBV), and rubella

Bacterial infections, such as mycoplasma

Intestinal parasites, such as ascaris, which can block the pancreatic

outflow

Pancreas divisum

Scorpion and snake bites

Vascular factors, such as ischemia or vasculitis

DIFFERENTIALS

Other Problems to be Considered: Perforated viscus

Acute peritonitis

Choledocholithiasis

Macroamylasemia

Macrolipasemia

Intestinal obstruction

Pancreatic cancer

Malabsorption syndromes/processes

Workup

Lab Studies:

A complete blood count (CBC) demonstrates leukocytosis (WBC >12000) with the

differential being shifted towards the segmented polymorphs.

If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis,

obtain type and crossmatch.

Measure blood glucose level because it may be elevated from B cell injury in

the pancreas.

Obtain measurements for BUN, creatine (Cr), and electrolytes (Na, K, Cl,

CO2, P, Mg); a great disturbance in the electrolyte balance is usually

found, secondary to third spacing of fluids.

Measure amylase levels, preferably the Amylase P, which is more specific to

pancreatic pathology. Levels more than 3 times higher than normal strongly

suggest the diagnosis of acute pancreatitis

Lipase levels also are elevated and remain high for 12 days. In patients

with chronic pancreatitis (usually caused by alcohol abuse), lipase may be

elevated in the presence of a normal serum amylase level

Perform liver function tests (eg, alkaline phosphatase, serum

glutamic-pyruvic transaminase [sGPT], serum glutamic-oxaloacetic

transaminase [sGOT], G-GT) and bilirubin, particularly with biliary origin

pancreatitis.

Imaging Studies:

Perform a plain KUB (Kidneys, ureters, bladder) with the patient in the

upright position to exclude viscus perforation (ie, air under the

diaphragm). In cases with a recurrent episode of chronic pancreatitis,

peripancreatic calcifications may be noted

Ultrasound can be used as a screening test. If overlying gas shadows

secondary to bowel distention are present, it may not be specific

CT scan is the most reliable imaging modality in the diagnosis of acute

pancreatitis. The criteria for diagnosis are divided by Balthazar and

colleagues into 5 grades, as follows:

Grade A - Normal pancreas

Grade B - Focal or diffuse gland enlargement

Grade C - Intrinsic gland abnormality recognized by haziness on the scan

Grade D - Single ill-defined collection or phlegmon

Grade E - Two or more ill-defined collections or the presence of gas in or

nearby the pancreas

Other Tests:

Para-aminobenzoic acid test (ie, bentiromide [Chymex] test) for chronic

pancreatitis

Treatment

Emergency Department Care: Most of the cases presenting to the ED are

treated conservatively, and approximately 80% respond to such treatment.

Fluid resuscitation

Monitor accurate intake/output and electrolyte balance of the patient.

Crystalloids are used, but other infusions, such as packed red blood cells

(PRBCs), are occasionally administered, particularly in the case of

hemorrhagic pancreatitis.

Central lines and Swan-Ganz catheters are used in patients with severe fluid

loss and very low blood pressure.

Patients should have nothing by mouth, and a nasogastric tube should be

inserted to assure an empty stomach and to keep the GI system at rest.

Begin parenteral nutrition if the prognosis is poor and if the patient is

going to be kept in the hospital for more than 4 days.

Analgesics are used to relieve pain. Meperidine is preferred over morphine

because of the greater spastic effect of the latter on the sphincter of

Oddi.

Antibiotics are used in severe cases associated with septic shock or when

the CT scan indicates that a phlegmon of the pancreas has evolved.

Other conditions, such as biliary pancreatitis associated with cholangitis,

also need antibiotic coverage. The preferred antibiotics are the ones

secreted by the biliary system, such as ampicillin and third generation

cephalosporins.

Continuous oxygen saturation should be monitored by pulse oxymetry and

acidosis should be corrected. When tachypnea and pending respiratory failure

develops, intubation should be performed.

Perform CT-guided aspiration of necrotic areas, if necessary.

An ERCP may be indicated for common duct stone removal.

Consultations: Consult a general surgeon in the following cases:

For phlegmon of the pancreas, surgery can achieve drainage of any abscess or

scooping of necrotic pancreatic tissue. It should be followed by

postoperative lavage of the pancreatic bed.

In patients with hemorrhagic pancreatitis, surgery is indicated to achieve

hemostasis, particularly because major vessels may be eroded in acute

pancreatitis.

Patients who fail to improve despite optimal medical treatment or patients

who push the Ranson score even further are taken to the operating room.

Surgery in these cases may lead to a better outcome or confirm a different

diagnosis.

In biliary pancreatitis, a sphincterotomy (ie, surgical emptying of the

common bile duct) can relieve the obstruction. A cholecystectomy may be

performed to clear the system from any source of biliary stones.

Medications

The goal of pharmacotherapy is to relieve pain and minimize complications.

Drug Category: Antibiotics - Used to cover the microorganisms that may grow

in biliary pancreatitis and acute necrotizing pancreatitis. The empiric

antibiotic regimen usually is based on the premise that enteric anaerobic

and aerobic gram-bacilli microorganisms are often the cause of pancreatic

infections. Once culture sensitivities are made, adjustments in the

antibiotic regimen can be done. Drug Name

Ceftriaxone (Rocephin)- Third-generation cephalosporin with broad-spectrum

gram-negative activity; lower efficacy against gram-positive organisms;

higher efficacy against resistant organisms. Arrests bacterial growth by

binding to one or more penicillin binding proteins.

Adult Dose 1-2 g IM/IV once or divided bid

Pediatric Dose 50-75 mg/kg/d IM/IV divided q12h

Contraindications Documented hypersensitivity

Interactions Probenecid may increase levels; coadministration with

ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Adjust dose in renal impairment; caution in breastfeeding women

and allergy to penicillin

Drug Name

Ampicillin (Marcillin, Omnipen)- Bactericidal activity against susceptible

organisms. Alternative to amoxicillin when unable to take medication orally.

Adult Dose 250-500 IM/IV mg q6h

Pediatric Dose 25-50 mg/kg/d IM/IV divided q6-8h

Contraindications Documented hypersensitivity; viral mononucleosis

Interactions Probenecid and disulfiram elevate levels; allopurinol decreases

effects and has additive effects on ampicillin rash; may decrease effects of

oral contraceptives

Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Adjust dose in renal failure; evaluate rash and differentiate

from hypersensitivity reaction

Drug Category: Analgesics - Pain control is essential to quality patient

care. It ensures patient comfort, promotes pulmonary toilet, and has

sedating properties, which are beneficial for patients who have sustained

trauma or have painful lesions.

Drug Name

Meperidine (Demerol)- Analgesic with multiple actions similar to those of

morphine. May produce less constipation, smooth muscle spasm, and depression

of cough reflex than similar analgesic doses of morphine.

Adult Dose 15-35 mg/h IV; 50-150 mg IM q3-4h

Pediatric Dose 1.1-1.8 mg/kg IM q3-4h

Contraindications Documented hypersensitivity; MAOIs; upper airway

obstruction or significant respiratory depression; during labor when

delivery of premature infant is anticipated

Interactions Monitor for increased respiratory and CNS depression with

coadministration of cimetidine; hydantoins may decrease effects; avoid with

protease inhibitors

Pregnancy C - Safety for use during pregnancy has not been established.

Precautions Caution in head injuries because may increase respiratory

depression and CSF pressure (use only if absolutely necessary); caution when

using postoperatively and with history of pulmonary disease (suppresses

cough reflex; substantially increased dose levels may aggravate or cause

seizures because of tolerance, even if no prior history of convulsive

disorders; monitor closely for morphine-induced seizure activity if seizure

history exists

Drug Category: Antibiotics - Used to cover the microorganisms that may grow

in biliary pancreatitis and acute necrotizing pancreatitis. The empiric

antibiotic regimen usually is based on the premise that enteric anaerobic

and aerobic gram-bacilli microorganisms are often the cause of pancreatic

infections. Once culture sensitivities are made, adjustments in the

antibiotic regimen can be done. Drug Category: Analgesics - Pain control is

essential to quality patient care. It ensures patient comfort, promotes

pulmonary toilet, and has sedating properties, which are beneficial for

patients who have sustained trauma or have painful lesions.

Followup

Further Inpatient Care:

Transfer patients with Ranson scores of 0-2 to a hospital floor.

Transfer patients with Ranson scores 3-5 to an intensive care unit.

Transfer patients with Ranson scores higher than 5 to an intensive care unit

with emergency surgery as a possibility.

Further Outpatient Care:

The patient should be followed routinely with physical examination and

amylase and lipase assays.

Complications:

Infected pancreatic necrosis may result from seeding of bacteria into the

inflammation.

An acute pseudocyst is an effusion of pancreatic juice that is walled off by

granulation tissue after an episode of acute pancreatitis.

Hemorrhage into the GI tract retroperitoneum or the peritoneal cavity is

possible because of erosion of large vessels.

Intestinal obstruction or necrosis may occur.

Common bile duct obstruction may be caused by a pancreatic abscess,

pseudocyst, or biliary stone that caused the pancreatitis.

An internal pancreatic fistula from pancreatic duct disruption or a leaking

pancreatic pseudocyst may occur.

Prognosis:

Ranson developed a series of different criteria for the severity of acute

pancreatitis.

Present on admission

Older than 55 years

WBC higher than 16,000 per mcL

Blood glucose higher than 200 mg/dL

Serum lactate dehydrogenase (LDH) more than 350 IU/L

SGOT (ie, aspartate aminotransferase [AST]) greater than 250 IU/L

Developing during the first 48 hours

Hematocrit fall more than 10%

BUN increase more than 8 mg/dL

Serum calcium less than 8 mg/dL

Arterial oxygen saturation less than 60 mm Hg

Base deficit higher than 4 mEq/L

Estimated fluid sequestration higher than 600 mL

A Ranson score of 0-2 has a minimal mortality rate.

A Ranson score of 3-5 has a 10%-20% mortality rate.

A Ranson score higher than 5 has a mortality rate of more than 50% and is

associated with more systemic complications.

Patient Education:

Educate patients about the disease and advise then to avoid alcohol in binge

amounts and to discontinue any risk factor, such as fatty meals and

abdominal trauma.

acute vs. chronic

> Are most of the members of this site chronic sufferers? I was just

> diagnosed with pancreatitis, but they are not sure if it is acute or

> chronic. I cant get to a specialist until early Jan.

>

> It is my understanding that acute is bad, but that many acute cases

> get better and do not come back. I am more concerned about chronic.

> Even then, there are treatments, right? Enzymes, possible

> surgeries? I am very depressed right now because I want to live for

> a good thirty more years and am concerned. I do not drink, and an

> ultrasound did not reveal any stones, just a slightly " inhomogeneous "

> pancreas and my lipase and amylase were elevated (lipase 4x normal).

>

> I am 31.

>

> Thanks

>

>

>

>

> PANCREATITIS Association, Intl.

> Online e-mail group

>

> To reply to this message hit & quot;reply & quot; or send an e-mail

to: Pancreatitis (AT) Yahoo

>

>

Link to comment
Share on other sites

,

You are correct that you can have acute panc, recover and never have another

problem. The thing I would think is important would be to try and find the

cause of the acute panc and then prevent future attacks.

I have found that diagnosing chronic panc is anything but simple and

straightforward. At this point I have not been diagnosed with chronic panc. I

have 'recurring acute panc'.

W

acute vs. chronic

Are most of the members of this site chronic sufferers? I was just

diagnosed with pancreatitis, but they are not sure if it is acute or

chronic. I cant get to a specialist until early Jan.

It is my understanding that acute is bad, but that many acute cases

get better and do not come back. I am more concerned about chronic.

Even then, there are treatments, right? Enzymes, possible

surgeries? I am very depressed right now because I want to live for

a good thirty more years and am concerned. I do not drink, and an

ultrasound did not reveal any stones, just a slightly " inhomogeneous "

pancreas and my lipase and amylase were elevated (lipase 4x normal).

I am 31.

Thanks

PANCREATITIS Association, Intl.

Online e-mail group

To reply to this message hit & quot;reply & quot; or send an e-mail to:

Pancreatitis (AT) Yahoo

Link to comment
Share on other sites

,

You are correct that you can have acute panc, recover and never have another

problem. The thing I would think is important would be to try and find the

cause of the acute panc and then prevent future attacks.

I have found that diagnosing chronic panc is anything but simple and

straightforward. At this point I have not been diagnosed with chronic panc. I

have 'recurring acute panc'.

W

acute vs. chronic

Are most of the members of this site chronic sufferers? I was just

diagnosed with pancreatitis, but they are not sure if it is acute or

chronic. I cant get to a specialist until early Jan.

It is my understanding that acute is bad, but that many acute cases

get better and do not come back. I am more concerned about chronic.

Even then, there are treatments, right? Enzymes, possible

surgeries? I am very depressed right now because I want to live for

a good thirty more years and am concerned. I do not drink, and an

ultrasound did not reveal any stones, just a slightly " inhomogeneous "

pancreas and my lipase and amylase were elevated (lipase 4x normal).

I am 31.

Thanks

PANCREATITIS Association, Intl.

Online e-mail group

To reply to this message hit & quot;reply & quot; or send an e-mail to:

Pancreatitis (AT) Yahoo

Link to comment
Share on other sites

,

You are correct that you can have acute panc, recover and never have another

problem. The thing I would think is important would be to try and find the

cause of the acute panc and then prevent future attacks.

I have found that diagnosing chronic panc is anything but simple and

straightforward. At this point I have not been diagnosed with chronic panc. I

have 'recurring acute panc'.

W

acute vs. chronic

Are most of the members of this site chronic sufferers? I was just

diagnosed with pancreatitis, but they are not sure if it is acute or

chronic. I cant get to a specialist until early Jan.

It is my understanding that acute is bad, but that many acute cases

get better and do not come back. I am more concerned about chronic.

Even then, there are treatments, right? Enzymes, possible

surgeries? I am very depressed right now because I want to live for

a good thirty more years and am concerned. I do not drink, and an

ultrasound did not reveal any stones, just a slightly " inhomogeneous "

pancreas and my lipase and amylase were elevated (lipase 4x normal).

I am 31.

Thanks

PANCREATITIS Association, Intl.

Online e-mail group

To reply to this message hit & quot;reply & quot; or send an e-mail to:

Pancreatitis (AT) Yahoo

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...