Chapter 47- Caring for clients with disorders of the liver, gallbladder, and pancreas

functions of liver

- metabolizes glucose

- regulates blood glucose concentration

- converts glucose to glycogen to glucose to maintain normal glucose level

- synthesizes amino acids from the breakdown of protein or form lactate that muscles produce during exercise to form glucose (gluconeogenesis)

- converts ammonia (by product of gluconeogenesis) into urea

- metabolizes proteins and fats

- stores vitamin: A, B12, D, and some B complex vitamins as well as iron and copper (remember ABDB)

- metabolizes drugs, chemical, bacteria

- forms and excretes bile

- excretes bilirubin

- synthesizes factors needed for blood coagulation (prothrombin, fibrinogen)

lobules

- single lobe of the liver

- liver has 4 lobules

liver is supported by

- intra-abdominal pressure

- mesenteries: various attachments which connect the liver to the adjacent intestine, abdominal wall, and diaphragm

liver blood supply

- gets blood from hepatic arteries that is branched indirectly from the aorta

- portal vein transport blood from the intestinal tract to the liver

- after it goes through the liver, the hepatic veins collect the blood and transport it to the inferior vena cava and then back to the heart

different ducts, veins, artery in liver include

- hepatic artery

- hepatic and portal veins

- lymphatics

- bile ducts

cellular of the liver

- hepatocytes: hepatic parenchymal cells (which performs most of the liver's metabolic functions

- Kupffer cells: which engage in the liver's immunologic, detoxifying, and blood-filtering actions

- canaliculi: small bile ducts, are between the lobules of the liver. They receive secretions from the hepatocytes, and eventually to the hepatic duct and then joins the cystic duct from the gallbaladder to form the common bile duct

sphincter of oddi

- controls the amount of bile that enters the duodenum from the common bile duct

aging process of liver

- decreases in organ weight, blood flow, and size

- decrease number of hepatocytes

- increase in fibrous tissue

- change in metabolism of medications

- lover functions is NOT SIGNIFICANTLY affected

jaundice

- is a greenish-yellow discoloration of tissue

- sign of disease, but it is not itself a unique disease

- results from abnormally high concentration of the pigment bilirubin in blood

- normal concentration of bilirubin is 0.2-1.3 mg/dL (if higher than 2.5, it is visible from skin, oral mucosa membrane and eyes

- three forms of jaundice:

a) hemolytic jaundice (excess destruction of RBC)

b) hepatocellular jaundice (liver disesae)

c) obstructive jaundice (block of duct between the liver and intestine)

bilirubin

- produced in the liver, spleen, and bone marrow

- also results from hemoglobin metabolism, and by product of hemolysis (rbc destruction)

- reticuloendothelial system also produces bilirubin

- liver removes bilirubin from the body, and excreting it in bile, which is the color of pee

- bilirubin serum increase when

a) excessive destruction of RBC

b) liver cannot excrete bilirubin normally

- two forms of bilirubin: indirect or uncongugated bilirubin and direct or conjugated bilirubin

indirect or unconjugated bilirubin

- bilirubin binds with protein as it circulates in the blood

- increased hemolysis causes level to be elevated

direct or conjugated bilirubin

- bilirubin circulates freely in blood until it reaches the liver

- liver then conjugates direct bilirubin with glucuronide, which is then excreted in the bile

- when it moves into the intestine, bacterial enzymes then transforms the direct bilirubin into urobilinogen

- some urobilinogen is changed into urobilin (brown pigment of stool), some are excreted in the urine, and some are carried back to the liver by bloodstream for re-excretion in the bile

testing for bilirubin

there are no test for indirect bilirubin level

- the only way to find the level is to calculate by subtracting direct bilirubin level from the TOTAL bilirubin level

- example: total bilirubin level - subtract direct bilirubin level = indirect bilirubin level

cirrhosis

chronic, degenerative liver disorder caused by generalized cellular damage

pathophysiology and etiology of cirrhosis

- liver cells are damaged, and become connective scar tissue thus anatomic distortion and partial or complete occlusion of blood channels in the liver

- since bile production is affected, client experience fat malabsorption and inability to absorb fat soluble vitamins (ADEK)

- several types of cirrhosis: alcohol, postnecrotic, and biliary

alcoholic cirrhosis

- most common, result from chronic alcohol intake and frequently associated with poor nutrition

- characterized by necrotic liver cells which gradually are replaced with scar tissue, which leads to non functional liver.

- eventually becomes 'hobnail' appearance (looks like a bag of marbles)

- can follow poisoning with chemicals such as carbon tetrachloride, a cleaning agent, or ingestion of hepatotoxic drugs like acetaminophene

- disease develops over years (30)

postnecrotic cirrhosis

- destruction of liver cells secondary to infection

- usually related to chronic biliary obstruction and infection, liver disease, or exposure to hepatotoxins or industrial chemicals

biliary cirrhosis

- scarring occurs around the bile ducts in the liver

- related to chronic biliary obstruction and infection

- primary biliary cirrhosis refers to progressive autoimmune disease of the liver

- chronic inflammation causes destruction to the small intrahepatic biliary ducts, preventing flow of bile into small intestine

- eventually cirrhosis and liver failure

assessment findings of Cirrhosis:

S&S

- categorized as compensated (where it is less severe and S&S are vague) or decompensated (where the disease has progressed and S&S are very pronounced and indicate liver failure)

- clients experience: fatigue, anorexia, dyspepsia, nausea vomiting diarrhea or constipation, with weight loss

- pass gray color stool due to no bile in the GI tract

- dark or tea colored urine due to concentration of urobilin

- many mention bleeding from gums, nose, easy bruising, and itch from accumulated bile salts

- client has enlarged liver due to cirrhosis and causes the abdomen to appear distended and causes shortness of breath and discomfort due to compression of chest

- edema in legs and feet and veins over abdomen may be dilated (caput medusae)

- since estrogen cant be fully metabolize, men may have enlarged breasts (gynecOmastia) and testicular atrophy (wasting away)

- palmar erythema (bright pink palms)

- cutaneous spider angiomata (tiny spider like blood vessels)

compensated S&S of cirrhosis

- intermittent mild fever

- vascular spiders

- palmar erythema (reddened palms)

- unexplained epistaxis

- ankle edema

- vague morning indigestion

- flatulent dyspepsia

- abdominal pain

- firm enlarged liver

- splenomegaly

decompensated S&S of cirrhosis

- ascites (hypertension in liver)

- hypotension

- jaundice

- weakness

- muscle wasting

- weight loss

- continuous mild fever

- clubbing of fingers

- purpura (non blanching purple on skin due to decreased platelet count)

- spontaneous bruising

- epistaxis (nose bleed)

- sparse body hair

- white nails

-gonadal atrophy

assessment findings of cirrhosis:

Diagnostic findings

- most conclusive diagnostic procedure: liver biopsy

- done in radiology dept with ultrasound or CT to identify appropriate placement of trochar or biopsy needle

- vitamin K is given before biopsy to prevent bleeding

- ultrasound for density of scar tissue and parenchymal (bulk) cells

- ct, mri, and radioisotope liver scan demonstrate the liver's enlarge size, nodular config, and distorted blood flow

common blood test findings in cirrhosis

- high unconjugated and conjugated bilirubin levels

- high enzymes levels of AST, ALT, GGT

- high globulin level

- low RBC count, cells appear large

- low platelet count

- low leukocytes and thrombocytes

- low fibrinogen level

- slow Prothrombin time (PT)

- low serum albumin level

- hypokalemia

med and surge management of cirrhosis

- no cure for cirrhosis

- preserving what liver function remains

- if hypoproteinemia is severe, IV albumin is given

- vitamin K is given for prolonged PT and partial thromboplastin time (clot time)

- hepatic encephalopathy (ammonia affecting the brain) requires lactulose to detoxify ammonium by drawing water into the bowel, which sometimes causes diarrhea

- Histamine2 (h2) receptors antagonists to reduce gastric disturbance

- pironolactone for potassium-sparing antidiuretics to treat ascites (liver hypertemsion and low level protein or albumin)

- transfusion of platelets to correct thrombocytopenia

- RBC for anemia or blood loss

- cholestyramine for binding bile salt and relieve pruritus (itch), or cleanse skin with non drying agent

- ursodeoxycholic acid for promotion of bile flow from liver

nursing management for cirrhosis

- if alcoholism, monitor for rise in BP, pulse and temp from alcohol withdrawal

- weight daily and record I&O

- measure abdomen

- small frequent meals

nutrition for cirrhosis clients

- dietary restrictions are used ONLY when expected to improve symptoms

- medium-chain triglyceride oil for fat restricted or intake is limited

- sodium restricted to 2 g/day when ascites

- fluid restriction for hyponatremia

- high calorie for malnutrition, weight loss or infection

- high protein to prevent muscle wasting

- carbohydrate controlled for diabetes or insulin resistance

- multiple small frequent meals to boost intake who have nausea, vomiting or fatigue

complications of cirrhosis:

portal hypertension

- portal system consist of: gastric veins from stomach mesenteric vein from the intestines, splenic vein from the spleen and pancreas, and portal vein

- all these drain into and through the liver and out to vena cava

- if scarred cirrhotic liver, veins may be compressed and blood backs up into the portal system which is the venous pathway through the liver (also called portal hypertension)

- collateral veins become engorged with blood: esophagus (esophageal varices), rectum (hemorrhoids), and abdominal surface (caput medusae)

-S&S of portal hypertension:

a) GI bleeding as evidence by vomiting of blood, black tarry stools or bloody stools

b) acites

c) decrease platelets

- surgical shunt can be created

- transjugular intrahepatic portosystemic shunt (TIPS)

surgical shunt

- procedure uses graft to decompress the portal system by diverting blood flow into the system circulation

- not frequently performed

transjugular intrahepatic portosystemic shunt (TIPS)

- invasive radiologic procedure involves the creation of a tract from the hepatic to the portal vein

- cannula with an expandable stent is inserted into the portovenous system through the jugular vein

- serves as a intrahepatic shunt between the hepatic vein and portal circulation

- can be carried out using conscious sedation or anesthesia

treatment of cirrhosis:

portal hypertension

- aim to reduce fluid accumulation and venous pressure

- propranolol: beta-adrenergic blocker to reduce BP

- sodium restrictions

- spironolactone: for diuretic

- furosemide: for diuretic

- caution with diuretic for long term use because of sodium depletion

complications of cirrhosis:

esophageal varices

- bulging esophageal veins

- Varix: single dilated bulging esophageal vein

- result of portal hypertension (overfill)

- easy to bleed due to superficially in the mucosa, contain little protective elastic tissue (can cause bleeding from rough foods or chemicals)

- can be slight but chronic or massive and rapid

treatment of cirrhosis:

esophageal varices

- barium swallow or esophagocopy confirm esophageal varices

- CT and/or MRI can help further identify

- antitussives and stool softeners are prescribed when the client is sympomatic to reduce coughing or straining which increases vascular pressure

- injection of sclerotherapy

- variceal banding

- Distal splenorenal shunt

- IV octreotide: reduce pressure in the portal venous system. preferred over the agents: vassopressin or terlipressin

- injection sclerotherapy

- also called endoscopic sclerotherapy

- doctor passes an endoscope orally to locate the varix

- passes a thin needle through the endoscope into the varix and then directly injects a sclerosing agent (sodium tetradecyl, sodium morrhuate)

- the agent solidifies and stops circulation to the varix

.

- if skilled endoscopist is not available, or bleeding is too rapid to permit endoscopy: ballooning tamponade with a sengstaken-blakemore tube is used to compress the varices and stemming the flow of blood

complications of cirrhosis:

ascites

- collection of fluid in the peritoneal cavity

- causes by portal hypertension

- is a hepatorenal syndrome: leading to a cascade of events, that ultimately alter fluid distribution and interfere with fluid excretion

- increase pressure forces serum proteins into peritoneal cavity

- proteins draw plasma from the circulating blood by osmosis, therefore the kidneys respond to decrease in blood volume and renal BP by initiating the renin-angiotensin-aldosterone system

- the body then conserves sodium ions, which futher contributes to fluid retention

- since low renal blood volume, it also contributes to re absorption of water rather than eliminating as urine

- all of the above causes fluid accumulation in the abdomen

treatment of cirrhosis:

ascites

- abdominal paracentesis

- maintenance of diuretic therapy

- sodium restrictions

- last resort, physician surgically insert an internal catheter to redirect the ascitic fluid back into the vascular space

abdominal paracentesis

- performed to remove acitic fluid

- needle through the abdominal wall allowing the fluid to drain

- up to 5 or 6 L of fluid may be removed over 60 to 90 min

- IV albumin is simultaneously infused to pull back into the vascular space

- monitor BP and output

complications of cirrhosis:

hepatic encephalopathy

- portosystemic encephalopathy (CNS) manifestation of liver failure that leads to coma or death

- excessive amounts of ammonia forms from the break down of protein in intestine, but liver fails to convert it to urea to excrete in urine

- ammonia can cross blood brain barrier and enter brain cells, where it interferes with brain metabolism, cell membrane pump mechanisms, and neurotransmission

- indications of CNS effects include: deep coma, lethargy disorientation, drowsiness, confusion, personality change, memory loss, agitation, flapping tremor called asterixis (a positive Babinski reflex), sulfurous fecal breath called fetor hepaticus

- CNS effects worsen after eating high protein meal or active GI bleeding (digesting blood)

-

treatment of cirrhosis:

hepatic encephalopathy

- depleting intestinal microorganisms with drugs: neomycin or kanamycin (poorly absorbed antibiotics) destroy intestinal microorganisms thereby decrease ammonia production)

- laxatives

- enema therapy

- lactulose: reduces serum ammonia concentration by splits into lactic acid and acetic acid, attracts ammonia from the blood and forms a compound that can be eliminated in the feces

- levodopa: precursor of dopamine that restores normal neurotransmission

- TPN, IV electrolyte

- only a few survive without transplant

hepatitis

- inflammation of the liver

- acute or chronic

pathophysiology and etiology of hepatitis

- most common cause is viral infection (ABCDEG)

- modes of transmission and icubation periods differentiate each virus

- virus invades liver cells and alter their structure thus cells that are infected become inflamed and dysfunctional

- active disease process affects the: uptake, conjugation and excretion of bilirubin

- chronic persistent hepatitis (common with BCD), liver damage does not worsen but it does not improve and the liver remains enlarged

- Hepatitis A virus (HAV) and hepatitis E virus are transmitted via the oral-fecal route, and sometimes blood transfusion. rarely leads to chronic illness but may need to be hospitalized

- Hepatitis E is not common. Self- limited and no chronic form of the disease.

- Hepatitis B and C are transmitted through blood or sex. commonly are associated with hepatocellular carcinoma

- Hepatitis D occurs with some that are infected with B (therefore similar to B and how infection occurs and is treated). Antidelta antibodies are present when blood tests are done (this confirms the diagnosis)

- Hepatitis G considered to be non A, non B, and non C disease. occurs 14-145 days after a blood transfusion. cant be identified like other types. G is similar to C.

- other hepatitis include: autoimmune hepatitis, toxic hepatitis, drug induced hepatitis

autoimmune hepatitis

results from abnormal immune system response

- treatment by administration of corticosteroids and immuneomodulating agents (azathioprine or 6-mercaptopurine)

- many will die or require liver transplant if not treated

toxic hepatitis

- develops when certain chemicals toxic to the liver causes liver necrosis

- treatment includes removing toxins and treating symptoms

- if liver damage is severe and prolonged, prognosis is not good without a liver transplant

drug-induced hepatitis

- drug reaction damages liver

- sever reactions include anesthetic agents, antidepressants, or anticonvulsants

- high dose corticosteroids are administered to treat reaction

- liver transplant may be necessary

Assessment findings of hepatitis

S&S

- phase of all forms of hepatitis are as follows:

1) incubation phase

2) preicteric or prodromal phase

3) icteric phase

4) posticteric phase

- not all clients experience the listed and severity may vary

- not all clients develop jaundice

incubation phase

- virus replicates within the liver, with client asymptomatic (no showing of symptoms)

- late in phase: virus can be found in blood, bile, and stools (client is considered infectious)

preicteric or prodromal phase

- nausea, vomiting

- anorexia, malaise, weight loss

- fever

- arthralgia

- headache

- RUQ discomfort

- enlarge of the spleen, liver and lymph nodes

- rash, urticaria (hives)

icteric phase

- jaundice

- pruritus,

- clay colored ir light stools

- dark urine

- fatigue

- symptoms of preicteric phase may continue

posticteric phase

- liver enlargement

- malaise

- fatigue

- other symptoms subside

- liver function test begin to return to normal

Assessment findings of hepatitis:

diagnostic findings

- RNA can identify the virus itself

- can take up to 1 week

- WBC count may be elevated

- cholestasis (ineffective bile drainage) is seen with elevated bilirubin levels

- hepatic aminotransferase levels rise during the incubation period and begin to fall once symptoms appear

- chronic disease result in persistent elevation of transaminases

- poor synthetic functions includes prolonged OT or low blood glucose and serum albumin level

med and surg management of hepatitis

- bed rest

- balanced diet of small feedings at intervals

- IV fluid administration

- intron A may be given to clients with chronic hepatitis BCD to force the virus into remission

- ribavirin, synthetic antiviral used to treat respiratory syncytial virus infection (birth defects for pregnant clients, so birth control methods are used)

- both used increase likelihood of sustained virus-free response

tumors of the liver

- an abnormal mass of cells in the liver

- can be benign or malignant

- malignant can be metastasis or primary lesion (hepatoma)

pathophysiology and etiology of tumors of the liver

- Hepatomas are rare but appear with people with previous hepatitis B or D virus infections or cirrhosis of the postnecrotic form

- most common liver malignancy is a metastatic lesion from the breast, lung, or GI tract

- cause of benign liver tumors are tuberculosis and fungal and parasitic infections

- oral contraceptives and anabolic steroids can also develop benign hepatic lesions

assessment findings of tumors of the liver

- can be vague and confused with those of cirrhosis

- jaundice is common

- Pain in RUQ when tumor is large

- weight loss

- bleeding tendencies

- alpha-fetoprotein: serum protein produced during fetal development, if elevated, can indicate a primary malignant liver tumor

- total bilirubin and serum enzyme levels are high

- Liver scan, ultrasonography, MRI or CT scan identifies the tumor and location

- biopsy can disclose damage to adjacent liver tissues

medi and surg management of tumors of liver

- Hepatic lobectomy may be attempted to remove primary malignant or benign tumors if it is a single lobe

- Metastatic tumors are inoperable and liver transplant is eliminated for therapeutic option

- percutaneous biliary or transhepatic drainage

- cryosurgery or cryoablation

- for malignant tumors, short-term improvement can be achieved by IV chemotherapy or infusions into hepatic artery or in the peritoneum

- results from chemotherapy tend to be short term

- radiation therapy may be administered to reduce pain and discomfort

percutaneous biliary or transhepatic drainage

- biliary ducts obstructed by disease are bypassed with a catheter that is inserted under fluroscopy through the abdominal wall past the obstruction into the duodenum

- procedure relieves the pressure and pain caused by bile buildup and decreases jaundice and pruritus

-

- cryosurgery or cryoablation

- technique uses liquid nitrogen at -196°C to destroy tumors

- two or three freeze and thaw cycles

disorders of the gallbladder

- several disorder affect the biliary system which refers to the gallbladder and bile ducts, which carry bile

- disorders impair the drainage of bile into the duodenum

cholelithiasis and cholecystitis

- cholelithiasis: denotes stones that form in the gallbladder

- choledocholithiasis: if the stones are located in the common bile duct

- cholecystitis: an inflammation or infection of the gallbladder. can be chronic or acute

terms related to biliary system

- cholecystitis: inflammation of gallbladder

- cholelithiasis: presence of calculi in the gallbladder

- cholecystectomy: removal of the gallbladder

- cholecystostomy: opening and drainage of the gallbladder

- choledochotomy: opening into the common duct

- choledocholithiasis: stones in the common bile duct

- choledocholithotomy: incision of the common bile duct for removal of stones

- choledochoduodenostomy: anastomosis of common duct to duodenum

- choledochojejunostomy: anastomosis of common duct to jejunum

- lithotripsy: disintegration of gallstones by shock waves

- laparoscopic cholecystectomy: removal of gallbladder through endoscopic procedure

- laser cholecystectomy: removal of gallbladder using laser rather than scalpel and surgical instruments

pathophysiology and etiology of cholelithiasis and cholecystitis

risk factors for cholelithiasis:

- obesity

- native americans or US sw hispanic

- rapid weight loss

- treatment with high-dose estrogen

- low-dose estrogen therapy- small increase in the risk of gallstones

- ileal resection or disease

- cystic fibrosis

- diabetes

assessment findings of cholelithiasis and cholecystitis:

S&S

initally:

- belching, nausea, and RUQ discomfort with pain or cramps after high fat meals

- with acute cholecystitis, clients are sick with fever, vomiting, tenderness over the liver and severe pain called biliary colic

- slight jaundice

- urine appears dark brown

- stool may be light colored

assessment findings of cholelithiasis and cholecystitis:

diagnostic findings

- cholecystography: gallbladder imaging

- ultrasonography, ct scan, or radionuclide imaging (last resort)

- percutaneous transhepatic cholangiography distinguishes jaundice caused by liver disease from gallbladder disease

- MRI detects gallstones and gallbladder disorders

medi and surgi management of cholelithiasis and cholecystitis

- when gallbladder is inflamed, client is NPO

- nasgastric tube is inserted and antibiotic and parenteral fluids are prescribed

- low fat diet

- fat soluble vitamins

- cholestyramine for a bile-binding resin to relieve pruritus

- chenodeoxycholic acid or ursodenoxycholic acid: oral bile acid to dissolve the gallstones. takes up to 6 to 12 months to be effective. therapy can last for 2 years

- methyl tert-butyl ether can be instilled into gallbladder or commonbile duct through a percutaneously placed catheter. stones clear in hours or few days

- lithotripsy: non surgical procedures using shock waves generated by a machine called lithotriptor to break up stones while client lays in a water tank

- sphincterotomy: opening of the sphincter of oddi using an endoscope and then stone is snared using a basketlike attachment on the endoscope

-laparoscopic cholecystectomy: surgical procedure to remove gallbladder by one of the three or four small puncture sites in the abdomen.

- open cholecystectomy: when a laparoscopic cant not be performed and removal through a small opening is impossible

- after a cholecystectomy, a penrose or a vacuum drain is inserted to drain serosanguineous fluid

- choledochotomy: during cholecystectomy a T-tube is inserted while the surgical wound is healing. bile salt is prescribed to promote drainage.

nurse management of cholelithiasis and cholecystitis:

cholecystectomy and t-tube

- measure bile drainage every 8 hours or according to policy

- if more than 500 mL of bile drains within 24 hours or if drainage is significantly reduced, nurse must notify the doctor

-

acute pancreatitis

- inflammation of the pancreas

pathophysiology and etiology of acute pancreatitis

- autodigestion happens when there is reflux of bile and duodenal contents into the pancreatic duct

- swelling obstructs the release of bicarbonate which neutralizes chyme

- obstructs the release of enzymes trypsin which digest protein

- obstructs amalase which digest carbs

- obstructs lipase which digest fat

- cause can vary widely: structural abnormalities, trauma, infections, metabolic disorders, vascular abnormalities, inflammatory bowel disease, hereditary factors, alcohol, drugs re feeding after prolonged fasting or anorexia

assessment findings of acute pancreatitis:

S&S

- most common complaint is severe mid-abdominal to upper abdominal pain

- radiating both sides and straight to the back

- worse after eating

- nausea, vomit, and gas

- steatorrhea: stool is FROTHY and FOUL SMELLING (increased fat in stool)

- relieve when sit up and leans forward or curls into fetal position

- may reveal jaundice

- bowel sounds are diminished to absent and distention

- abdomen is tender to palpation

- can be hypotensive indicating hypovolemia and shock caused by the release of large amounts of protein- rich fluid into the tissues and peritoneal cavity

- can feel feverish and tachycardic

- breathing is shallow from severe pain

- bruising around the umbilicus or on the flanks

-

assessment findings of acute pancreatitis:

diagnostic findings

- elevated serum and urine amylase, lipase, and liver enzyme levels

- if bile duct is obstructed: bilirubin is up

- blood glucose level and WBC up

- serum electrolyte levels are low

medi and surge management of acute pancreatitis

- medical treatment concentrates on

a) relieving pain

b) reducing pancreatic secretions

c) restoring fluid and electrolyte losses

d) respiratory distress syndrome

e) acute (renal) tubular necrosis

f) bleeding abnormalities

- client is NPO with nasogastric with suction if nausea and vomiting

- IV albumin to pull fluid trapped in the peritoneum back into the circulations

- clear liquid diet with a slow progression to a low fat diet

- if pancreatic exocrine function is impaired, pancreatic enzyme replacement therapy is administered with meals to promote digestion

.

- worst case, surgical opening to debride necrotic tissue, and repeated ever 2 to 3 days to prevent infection

- multiple sump drains are inserted into the cavity to remove debris, and attached to continuous irrigation

nurse management for acute pancreatitis

- if gastric decompression is prolonged: client can receive nasojejunal feeding of a low fat formula or TPN

- if client has artery or central venous catheter: monitor pressure measurements

pathophysiology and etiology chronic pancreatitis

- alcohol can be the problem ( edema of duodenum and decrease the tone of the sphincter of oddi

- with chronicity, glands undergoes fibrotic scarring

assessment findings of chronic pancreatitis

S&S

- severe to persistent pain

- weight loss

- digestive disturbance such as flatulence, vomiting and diarrhea

- firm mass palpated upper left quad

- urine can be dark, stool light and foul smelling with fatty streaks

-

assessment findings of chronic pancreatitis

diagnostic findings

same as acute

- ct scans, mari, ultrasound, and ERCP

- islet of langerhans in pancreas cannot metabolize carbohydrates

-

medi management of chronic pancreatitis

drug therapy:

- meperidine (demerol) instead of morphine because it causes spasm of the sphincter of oddi

.

pancreatic enzyme replacement therapy:

- pancreatin (require ph of under 4 to avoid being brokein down)

.

help with fat proteins and carbs absorb:

- pancrelipase (require ph of 4 or above to work well)

surge management of chronic pancreatitis

partial or total pancreatectomy: removal of pancreas

- if scarring, with stricture and stenosis of portions of the pancreatic duct, then pancreaticojejunostomy (joining of the pancreatic duct to the jejunum) to relieve ductal obstruction

- pancreatic autotransplantation: to treat pain symptoms, endocrine function and normal insulin production are preserved, but exocrine functions is lost (enzyme replacement)

carcinoma of the pancreas

- can be head body or tail

- head tumors can cause obstructive jaundice

pathophysiology and etiology of carcinoma of the pancreas

- tumors in body or tail can press the portal vein and cause bleeding and varices

- can spread to liver or spleen

- can correlate with cancer include

a) diabetes mellitus,

b)high fat diet

c) chronic exposures to carcinogenic substances (petro chemicals)

assessment findings of carcinoma of the pancreas:

S&S

- left upper ab pain referred to the back, jaundice, anorexia, and weight loss

- palpation of mass in same area

- can also be gallbladder enlarged due to obstructive duct

- light color stool, dark urine (obstructive jaundice)

- pruritus (itch of skin)

- acites is later stage (fluid in peritoneal)

- some develop thrombophlebitis from pancreatic tumor products, which increase the bloods coagulability

assessment findings of carcinoma of the pancreas:

diagnostic findings

- ultra sound CT: can see but cant indicate cause

- ERCP:Endoscopic retrograde cholangiopancreatography or percutaneous needle aspiration to provide evidence of malignant cells

medical and surgical management of carcinoma of the pancreas

- radical pancreatoduodenectomy (whipple procedure): removal of the head of pancreas, resecting the dupdenum and stomach, and redirecting the flow of secretions from the stomach, gallbladder, and pancreas into the jejunum

- spleen is also removed if metastasis from tumor

- some do a total pancreatectomy, which creates a malabsorption syndrome and historically brittle diabetes which must be treated after surgery. some complcations associated with this surgery include bleeding tendencies cause by vitamin k deficiency and liver and kidney failure.

.

- cholecystojejunostomy: rerouting of pancreatic and bilary drainage for obstructive jaundice and is only palliative

- for inoperable tumors, mitomycin may be tried

- most clients die within 3 to 12 months