Re: Pseudocysts to Donna

[Guest guest]

> Heidi,

> Thank you for the welcome to the group. I

> have had finals all week in school, finally have a

> little free time for pancreas reasearch. When I

> checked my email I had 157 messages from the

> pancreatitis support group. Took my all day to

> go through them but It's worth it to me to learn from

> other people.

> Heidi- you mentioned that you have articles you can

> send me about pseudocysts, I would very much be

> greatful if you could!

> Heres a little of my history: I am 29

> Nov 1992 removal of gallbladder

> Aug. 1996 and May 1998 gave birth to sons

> Sept 1999 First attack- acute pancreatitis,

> pseudocyst size 1cm x 2cm in tail of pancreas, get

> acused of being an alcoholic because I have no

> gallbladder so what else would cause it.

> frequent attacks and trips to ER, given IV fluids

> and pain meds

>

&n

bsp;

> 1st specialist- No treatment

> Jan. 2001 Another attack, pseudocyst grown, now 2.8

> x 3cm in tail of pancreas

>

> 2nd specialist- wants surgury to remove tail of

> pancreas, I declined to get 2nd opinion

>

> 3rd specialist- told me to get off birth control

> pills, I did and my labs emmediatly became normal, for

> the first time in two years my amalase, and lypase

> were normal.

> No trouble for over a year feel fairly good, I go

> back to school

> April 2001- worst attack I ever had psudocyst grown

> but only by one cm, amalase 1700, lypase 650, not

> extremely high but pain is pain, (I would rather give

> birth)

> labs normal now, have appointment with specialist

> for same old song and dance

> Have tried enzymes, felt no difference

> Just really frustrated because I dont know why I

> get this or what causes this, I wish I drank, then I

> would know what to quit!

> I do however notice a corolation of having an

> attack and having a stressful day. My last

> attack (the worst one yet) was a very high stress day,

> I had a presentaion at school (i hate getting up in

> front of people) and my babysitter did not show

> up. I started having pain in class and it only

> got worse from there, dont even know how I

> drove myself home.

> Well thanks for letting me tell my little story,

> Donna

Donna,

Your message was very difficult to read, could you please

change your settings from html to normal? We would all be able

to read the message easier.

I am pasting an article I found on psuedocysts to the bottom of

this post. It's pretty long, so sit down with a tall cool glass of

water and peruse through it. Another site to learn more about

them is this link:

http://hopkins-gi.org/

Just type in pancreas or pseudocyst into the search box.

There is also a very good articleon this message board sent in

by on May 1st on pseudocyst drainage. Go up to the box

on the message board screen and type in message # 30580.

I hope this information is of some help.

With hope and prayers,

Heidi

Heidi H. Griffeth - SC

hhessgriffeth@...

Southeastern Representative

Pancreatitis Association Intl.

Acute Pancreatitis

Etiology and Pathogenesis

Biliary tract disease and alcoholism account for >= 80% of

hospital

admissions for acute pancreatitis. The remaining 20% are

attributed to drugs

(eg, azathioprine, sulfasalazine, furosemide, valproic acid),

estrogen use

associated with hyperlipidemia, infection (eg, mumps),

hypertriglyceridemia,

endoscopic retrograde pancreatography, structural

abnormalities of the

pancreatic duct (eg, stricture, cancer, pancreas divisum),

structural

abnormalities of the common bile duct and ampullary region (eg,

choledochal

cyst, sphincter of Oddi stenosis), surgery (particularly of stomach

and

biliary tract and after coronary artery bypass grafting), vascular

disease

(especially severe hypotension), blunt and penetrating trauma,

hyperparathyroidism and hypercalcemia, renal transplantation,

hereditary

pancreatitis, or uncertain causes.

In biliary tract disease, attacks of pancreatitis are caused by

temporary

impaction of a gallstone in the sphincter of Oddi before it passes

into the

duodenum. The precise pathogenetic mechanism is unclear;

recent data

indicate that obstruction of the pancreatic duct in the absence of

biliary

reflux can produce pancreatitis, suggesting that increased ductal

pressure

triggers pancreatitis.

Alcohol intake > 100 g/day for several years may cause the

protein of

pancreatic enzymes to precipitate within small pancreatic

ductules. In time,

protein plugs accumulate, inducing additional histologic

abnormalities.

After 3 to 5 yr, the first clinical episode of pancreatitis occurs,

presumably because of premature activation of pancreatic

enzymes.

Edema or necrosis and hemorrhage are prominent gross

pathologic changes.

Tissue necrosis is caused by activation of several pancreatic

enzymes,

including trypsin and phospholipase A2. Hemorrhage is caused

by extensive

activation of pancreatic enzymes, including pancreatic elastase,

which

dissolves elastic fibers of blood vessels. In edematous

pancreatitis,

inflammation is usually confined to the pancreas, and the

mortality rate is

< 5%. In pancreatitis with severe necrosis and hemorrhage,

inflammation is

not confined to the pancreas, and the mortality rate is >= 10 to

50%.

Pancreatic exudate containing toxins and activated pancreatic

enzymes

permeates the retroperitoneum and at times the peritoneal

cavity, inducing a

chemical burn and increasing the permeability of blood vessels.

This causes

extravasation of large amounts of protein-rich fluid from the

systemic

circulation into " third spaces, " producing hypovolemia and

shock. On

entering the systemic circulation, these activated enzymes and

toxins

increase capillary permeability throughout the body and may

reduce

peripheral vascular tone, thereby intensifying hypotension.

Circulating

activated enzymes may damage tissue directly (eg,

phospholipase A2 is

thought to injure alveolar membranes of the lungs).

Symptoms and Signs

In pancreatitis, pancreatic enzymes activate complement and the

inflammatory

cascade, thus producing cytokines. Patients typically present

with fever and

an elevated WBC count. It may thus be difficult to determine if

infection is

the cause or has developed during the course of pancreatitis.

Most patients suffer severe abdominal pain, which radiates

straight through

to the back in about 50%; rarely, pain is first felt in the lower

abdomen.

Pain usually develops suddenly in gallstone pancreatitis versus

over a few

weeks in alcoholic pancreatitis. Pain is severe, often requiring

large doses

of parenteral narcotics. The pain is steady and boring and

persists without

relief for many hours and usually for several days. Sitting up and

leaning

forward may reduce pain, but coughing, vigorous movement, and

deep breathing

may accentuate it. Most patients experience nausea and

vomiting, at times to

the point of dry heaves.

The patient appears acutely ill and is sweating. Pulse rate is

usually 100

to 140 beats/min. Respirations are shallow and rapid. BP may

be transiently

high or low, with significant postural hypotension. Temperature

may be

normal or even subnormal at first but may increase to 37.7 to

38.3° C (100

to 101° F) within a few hours. Sensorium may be blunted to the

point of

semicoma. Scleral icterus is occasionally present. Examination

of the lungs

may reveal limited diaphragmatic excursion and evidence of

atelectasis.

About 20% of patients experience upper abdominal distention

caused by

gastric distention or a large pancreatic inflammatory mass

displacing the

stomach anteriorly. Pancreatic duct disruption may cause

ascites (pancreatic

ascites). Abdominal tenderness always occurs and is often

severe in the

upper abdomen and less severe in the lower abdomen.

Mild-to-moderate

muscular rigidity may exist in the upper abdomen but is rare in

the lower

abdomen. The entire abdomen rarely exhibits severe peritoneal

irritation in

the form of a rigid boardlike abdomen. Bowel sounds may be

hypoactive.

Rectal examination usually discloses no tenderness, and the

stool usually

tests negative for occult blood.

Complications

Death during the first several days of acute pancreatitis is

usually caused

by cardiovascular instability (with refractory shock and renal

failure) or

respiratory failure (with hypoxemia and at times adult respiratory

distress

syndrome) and occasionally by heart failure (secondary to

unidentified

myocardial depressant factor). Circulating enzymes and toxins

are thought to

play a large role in early death.

Death after the first week is usually caused by pancreatic

infection or

pancreatic pseudocyst.

Pancreatic infection of devitalized retroperitoneal tissue is

usually caused

by gram-negative organisms. Infection should be suspected if

the patient

maintains a generally toxic appearance with elevated

temperature and WBC

count or if deterioration follows an initial period of stabilization.

The

diagnosis is supported by positive blood cultures and

particularly by the

presence of air bubbles in the retroperitoneum on abdominal

CT. Percutaneous

aspiration of pancreatic exudate guided by abdominal CT may

reveal organisms

on Gram stain or culture, which should lead to prompt surgical

debridement.

Mortality rate is usually 100% without extensive surgical

debridement of

infected retroperitoneal tissue.

A pancreatic pseudocyst is a collection of enzyme-rich pancreatic

fluid and

tissue debris arising within areas of necrosis or an obstructed

smaller

duct. It is not surrounded by a true capsule. Death is caused by

secondary

infection, hemorrhage, or rupture.

Diagnosis

Acute pancreatitis should be considered in the differential

diagnosis of

every acute abdomen. The differential diagnosis of acute

pancreatitis

includes a perforated gastric or duodenal ulcer, mesenteric

infarction,

strangulating intestinal obstruction, ectopic pregnancy,

dissecting

aneurysm, biliary colic, appendicitis, diverticulitis, inferior wall MI,

and

hematoma of abdominal muscles or spleen.

Laboratory tests cannot confirm a diagnosis of acute pancreatitis

but can

support the clinical impression. Serum amylase and lipase

concentrations

increase on the first day of acute pancreatitis and return to

normal in 3 to

7 days. Both may remain normal if destruction of acinar tissue

during

previous episodes precludes release of sufficient amounts of

enzymes to

raise serum levels. Serum amylase may remain normal if there

is coexisting

hypertriglyceridemia (which may contain a circulating inhibitor

that must be

diluted before an elevation in serum amylase can be detected).

Both serum

amylase and lipase may be increased in other disorders, such

as renal

failure and abdominal conditions requiring urgent surgical

therapy (eg,

perforated ulcer, mesenteric vascular occlusion, intestinal

obstruction

associated with ischemia). Other causes of increased serum

amylase include

salivary gland dysfunction, macroamylasemia, and tumors that

secrete

amylase.

The amylase:creatinine clearance ratio does not appear to have

sufficient

sensitivity or specificity to confirm a diagnosis of pancreatitis. It is

generally used to diagnose macroamylasemia when no

pancreatitis truly

exists. In macroamylasemia, amylase bound to serum

immunoglobulin falsely

elevates the serum amylase level. Fractionation of total serum

amylase into

pancreatic type (p-type) and salivary-type (s-type) isoamylase is

now

possible in most commercial laboratories. p-Type increases on

the first day

of pancreatitis and, along with serum lipase, remains elevated

longer than

total serum amylase. However, p-type also increases in renal

failure and in

other severe abdominal conditions in which amylase clearance

is altered.

The WBC count usually increases to 12,000 to 20,000/µL. Third

space fluid

losses may increase the Hct to as high as 50 to 55%, indicating

severe

inflammation. Hyperglycemia may occur. Serum Ca

concentration falls as early

as the first day because of the formation of Ca " soaps "

secondary to excess

generation of free fatty acids, especially by pancreatic lipase.

Serum

bilirubin increases in 15 to 25% of patients because pancreatic

edema

compresses the common bile duct.

Supine and upright plain x-rays of the abdomen may disclose

calculi within

pancreatic ducts (evidence of prior inflammation and hence

chronic

pancreatitis), calcified gallstones, or localized ileus in the left

upper

quadrant or central abdomen (a " sentinel loop " of small bowel,

dilation of

the transverse colon, or duodenal ileus). Chest x-ray may reveal

atelectasis

or a pleural effusion (usually left-sided or bilateral but rarely

confined

to the right pleural space). Ultrasound should be performed; it

may detect

gallstones or dilation of the common bile duct, indicating biliary

tract

obstruction. Edema of the pancreas may be visualized, but

overlying gas

frequently obscures the pancreas. CT usually offers better

visualization of

the pancreas (unless the patient is very thin). CT is

recommended for severe

pancreatitis or if a complication ensues (eg, hypotension or

progressive

leukocytosis and elevation of temperature). Although > 80% of

patients with

gallstone pancreatitis pass the stone spontaneously, ERCP with

sphincterotomy and stone removal is indicated for patients who

do not

improve over the initial 24 h of hospitalization. Patients who

spontaneously

improve generally undergo elective laparoscopic

cholecystectomy. Elective

cholangiography in these patients remains controversial.

However, the advent

of MRI cholangiography may make imaging of the biliary tree

noninvasive and

simple.

The patient's nutritional needs must be adequately met. A

seriously ill

patient should not be fed for >= 2 to 3 wk (often 4 to 6 wk). Thus,

TPN

should be initiated within the first few days (see Nutritional

Support in

Ch. 1).

Surgical intervention during the first several days is justified for

severe

blunt or penetrating trauma. Other indications for surgery include

uncontrolled biliary sepsis and inability to distinguish acute

pancreatitis

from a surgical emergency. The value of surgery during the first

several

days to counteract a progressive downhill course remains

unclear, although

there are reports of marked improvement after pancreatic

debridement.

It was once believed that a pancreatic pseudocyst that persisted

for > 4 to

6 wk, was > 5 cm in diameter, and caused abdominal symptoms

(especially

pain) required surgical decompression. However, pseudocysts

<= 12 cm have

been managed expectantly. A pseudocyst that is expanding

rapidly, is

secondarily infected, or is associated with bleeding or

impending rupture

requires drainage. Whether this is performed percutaneously,

surgically, or

endoscopically depends on location of the pseudocyst and

institutional

expertise.

[Guest guest]

Donna,

My oldest sister had the tail end of her pancreas removed back in 1986.

She is doing great, although she is a diabetic. She takes a shot every

morning.

I had a pseudocysts on the tail end of my pancreas. It was the size of a

grapefruit.

The DR, tried to drain it with a needle and that didn't work, so he placed a

drain tube in my side. That didn't work either, the fluid was too thick. So,

I was taken to surgery. I was 26 weeks pregnant at the time. All he done was

cut a hole into the cyst so that it would drain into the stomach. And I also

had the NG Tube, so it drain off the stomach.

I wish you the best of luck and hope that you get some relief soon.

Tammy - TN