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63 Cards in this Set
- Front
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Care of the patient undergoing ERCP
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Purposes of ERCP - X-ray contrast dye is injected into the bile duct, the pancreatic duct, or both. Most ERCPs are actually done for treatment (therapeutic ERCP)
stone removal sphincterotomy Pre-procedure teaching: NPO for 6-8 hours pre-procedure IV will be started for fluids & sedation Procedure takes 30 min – 2 hours Recovery following sedation before discharge Possible complications: pancreatitis, bleeding, infection |
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Pre-operative teaching of the patient with a “Open chole”
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Large incision with dressing
NG tube/NPO/IV fluids Drain: Jackson Pratt or Hemovac If CBD explored= ‘choledocholithotomy’ T-tube to gravity drainage |
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Nursing Care of Patient with a T-Tube
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Ensure proper connection to sterile container
Keep tube lower than level of surgical wound Monitor drainage for color and consistency (may drain up to 500 mL in first 24 hours post-op then decrease to < 200 mL in 2-3 days) Drainage may be blood-tinged changing to green-brown Semi-Fowler’s position recommended Assess skin for bile leakage around tube Teach patient how to manage tube when turning or ambulating-no pulling or tension on tube Clamp tube for 1-2 hours before and after meals when drainage subsides and stool return to normal brown color Teach patient care of t-tube and clamping if patient sent home with tube |
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Postoperative Complications for the Patient Having a Cholecystectomy with T-Tube
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Atelectasis
Pneumonia Pulmonary embolus DVT Wound dehiscence and infection Paralytic ileus Peritonitis |
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Pre-operative teaching of the patient with a “Lap chole”
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No large incision – 3-4 ‘bandaid’ incisions
Not typically NPO unless nauseous Mild to moderate pain No drains or T-tube Discharge within 1 to 2 days |
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Cholecystitis
Overview |
Inflammation of the gallbladder
Commonly associated with stones in cystic or common bile duct; also acute infection Classified as acute or chronic Acute: severe pain radiating from abdominal right upper quadrant to midline and posteriorly to scapular region Nausea and vomiting with pain Spasmodic pain results from contraction of the ducts and is initiated by high fat meal Low-grade fever or jaundice is common |
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Clinical Manifestations of Cholecystitis
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All manifestations of cholelithiasis PLUS:
Fever Elevated white blood cell count Abdominal muscle guarding with rebound tenderness and rigidity (may indicate peritonitis) Pruritis (itching) related to bile salt concentration in the skin Elevated serum bilirubin Elevated alkaline phosphatase Elevated serum amylase if pancreatic ducts are involved |
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Cholecystitis
Laboratory and Diagnostic Tests |
CBC: elevated WBC
Serum amylase and lipase: r/o pancreatitis Serum bilirubin levels> ascertain obstruction in biliary system (elevated direct) or hepatic damage (elevated indirect) X-ray of abdomen: done to visualize stones Oral cholesytogram: oral dye used to assess ability of GB to concentrate and excrete bile (non-urgent situations) Ultrasound: used if not obese; adipose tissue causes poor visualization of GB and ducts Gallbladder Scan(HIDA scan): done thru nuclear medicine to assess acute cholecytitis |
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Cholecystitis
Pharmacologic Management |
Dissolvers: oral bile acids (ursodeoxycholic acid or chenodeoxycholic acid) used to dissolve cholesterol stones under 20 mm in diameter; need to monitor hepatic enzymes and watch for diarrhea
Antibiotics if infection is suspected Questran (cholestyramine): binds with bile salts and hastens their excretion of through feces; decreases itching caused by accumulation of bile salts in skin |
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Cholecystitis
Dietary Management |
Low-fat diet
Foods to avoid Encourage weight loss If bile flow is reduced because of obstruction, may need to give fat-soluble vitamins such as A, D, E, & K Patient may be NPO in acute cases with nasogastric tube inserted |
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High-Fat Foods to Avoid for the Patient with Gallstones
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Whole-milk products
Deep-fried pastries and doughnuts Avocados Sausage, bacon Gravies with fat or cream Corn and potato chips Fried foods Peanut butter Chicken pot pie Hot dogs Whole-cheese products Chocolate Most nuts |
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Nursing Care for the Patient with Cholelithiasis and Cholecystitis
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Pain Control: fat intake initiates GB contraction and causes pain
Narcotic Analgesia: Demerol is drug of choice for pain-no Morphine usually because it causes spasms of Sphincter of Oddi Monitor for fever TCDB every 2 hrs. Assess for s/s of localized infection during post-operative period Assess wound & perform abd0minal assessment every 4 hours |
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One More Type of Cholecystitis
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Acalculous (‘without stones’) cholecystitis: a gallbladder disease that is not associated with gallstones
Inflammatory in nature and often found in patients suffering or recovering from major illnesses, trauma, burns, vascular disease, or deficiencies of the immune system A rare condition |
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Pancreatitis
Overview |
Inflammation of pancreas
Release of pancreatic digestive enzymes into tissue of pancreas itself, which leads to hemorrhage and necrosis Acute and chronic types > 5,000 new cases per year in U.S. ETOH overuse and gallstones are primary risk factors |
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Normal Physiology
Pncreas |
Exocrine pancreas consists of lobules of acinar cells
Cells secrete digestive enzymes into ducts that empty into main pancreatic duct Pancreatic duct joins common bile duct and empties into duodenum thru Ampulla of Vater Pacreatic enzymes are secreted in inactive form and are activated in the intestine-this prevents digestion of pancreatic tissue by its own enzymes |
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Pancreatic Enzymes
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Trypsin, chymotrypsin, carboxypolypeptidase, ribonuclease, and deoxyribonuclease which break down proteins
Pancreatic amylase which breaks down carbohydrates (dextrin, maltose, glucose) Lipase, which breaks down fats into glycerol and fatty acids |
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Etiology of Pancreatitis
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The inflammatory process may occur following an condition or injury that causes obstruction or damage of the pancreatic duct:
Gallstones Blunt abdominal trauma Drug or alcohol (ETOH) abuse Infection Surgical manipulation or trauma This obstruction causes - direct toxic injury to the pancreatic cells - injury by release of pancreatic enzymes into the tissue due to rupture of the pancreatic duct |
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Acute Pancreatitis
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Self-destruction of pancreas by its own enzymes through autodigestion
May be mild or severe Common in middle adults Incidence higher in men than women Usually associated with gallstones in women and ETOH use in men Pancreatic enzymes activated and cause autodigestion, inflammation, edema, and/or necrosis Release of pancreatic enzymes into tissue -trypsin digests pancreatic tissue and activates other enzymes which digest cell membranes and elastic tissue of blood vessel walls Leads to edema, vascular damage, and hemorrhage Activated enzymes and vasoactive subtances produce vasodilation, which increases vascular permeability Large volume fluid shift from circulation blood into retroperitoneal, peripancreatic space, and abdominal cavity |
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Risk Factors for Pancreatitis
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Excessive alcohol intake
Biliary tract disease/gallstones Trauma 3rd trimester pregnancy Infections, particularly viral High calcium and hyperlipidemia, NSAID use High-dose estrogen therapy Heredity |
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S/S of Acute Pancreatitis
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Abrupt onset of severe epigastric and abdominal pain
Radiates to the back and is relieved by sitting forward Pain initiated by fatty meal or excessive ETOH intake Nausea/Vomiting; weight loss Abdominal distention and rigidity Tachycardia & hypotension Transient hyperglycemia (50% of pts.) Elevated temp with cold, clammy skin Mild jaundice within 24 hours Severe jaundice if the CBD is compressed or pancreatic pseudocysts exist (pocket of infected fluid becomes walled off by fibrous tissue) Pleural effusion often develop, so risk for ARDS (a severe form of pulmonary edema which can be fatal) Ascites Hypocalcemia occurs in about 30% of patients |
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DANGER!
Pancreatitis |
Retroperitoneal bleeding may occur 3-6 days after onset of acute pancreatitis
Turner’s Sign: bruising in flanks Cullen’s Sign: bruising around the umbilicus |
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Complications from Pancreatitis
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Intravascular volume depletion with acute tubular necrosis and renal failure within 24 hours
Acute respiratory distress syndrome (ARDS) within 3-7 days if extreme volume depletion Pancreatic necrosis, pseudocysts, and pancreatic ascites Infected pancreatic mass that leads to shock and multi-system organ failure Persistent increasing abdominal girth with elevated serum amylase and abdominal pai |
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Diagnostic Tests
Pancreatitits |
Ultrasound
CT scan Endoscopic Retrograde Cholangiopancreatography (ERCP) Percutaneous fine needle aspiration Serum amylase, trypsin, and lipase levels (elevated) |
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Management of Acute Pancreatitis: Nonsurgical
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Bedrest & NPO
NG tube IV fluids IV antibiotics (if needed) Narcotic analgesics H2 antagonists/antacids to decrease gastric acidity TPN/PPN Blood glucose monitoring Diet modification after acute episode: low fat, low residue diet |
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Chronic Pancreatitis
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Gradual destruction of functional pancreatic tissue
Irreversible process that leads to pancreatic insufficiency and diminished function ETOH use is primary cause Also known as CCP: chronic calcifying pancreatitis: Secretions have increased concentration of insoluble proteins that calcify and form plugs that block pancreatic juice flow and lead to ductal destruction Blockage leads to inflammation, fibrosis, & scarring of pancreatic tissue DM may develop |
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Symptoms of Chronic Pancreatitis
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Recurrent epigastric pain radiating to the back
Jaundice Anorexia, nausea, vomiting, and weight loss Flatulence, constipation Steatorrhea (fatty, frothy, pale, greasy-looking, foul-smelling stools causes by decrease in pancreatic enzyme secretion) – a hallmark sign |
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Management of the Patient with Chronic Pancreatitis
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Treatment with pancreatin (Viocase), a digestive enzyme to help replace those not being produced
Treatment with cholestyramine (Questran) & antihistamines to control the itching related to bile salt deposits in skin Treatment with diuretics to prevent pleural effusion and potential ARDS Diet modification due to decreased levels of digestive enzymes Analgesia for pain management Insulin therapy for blood glucose management H2 antagonists and/or antacids to reduce gastric acidity Eliminate ETOH use |
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Care of the Client with Pancreatic Cancer
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Pancreatic tumors are typically adenocarcinomas which affect the exocrine function of the organ
Highly malignant; spread rapidly; poor prognosis 4th leading cause of cancer deaths in U.S. Usually fatal 1-3 years after diagnosis These tumors often cause ductal obstruction; jaundice may be the first sign |
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Pancreatic CA
Etiology |
Primary cause is unknown
More common in men than women, and in African-Americans than other ethnic groups More common in smokers Linked to ETOH use and DM Linked to exposure to industrial chemicals Also linked to a high-fat diet About 25,ooo new cases per year – only 10% still confined to the pancreas |
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S/S of Pancreatic Cancer
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Jaundice – usually a late sign
Vague, dull abdominal pain Weight loss Nausea/vomiting Palpable tumor in the left upper quadrant of abdomen Live and gallbladder enlargement Thrombophlebitis: often in the form of DVT of the lower leg – a common complication |
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Diagnostic Testing
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Serum amylase (usually elevated)
Serum bilirubin (usually elevated) CT scan of the abdomen MRI of the abdomen ERCP |
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Care of the Client with Pancreatic Cancer
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Pancreatic tumors are typically adenocarcinomas which affect the exocrine function of the organ
Highly malignant; spread rapidly; poor prognosis 4th leading cause of cancer deaths in U.S. Usually fatal 1-3 years after diagnosis These tumors often cause ductal obstruction; jaundice may be the first sign |
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Management of Pancreatic Cancer
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Nonsurgical:
Chemotherapy Radiation therapy Narcotic analgesics Surgical: Whipple procedure – radical pancreaticoduodenectomy – a radical surgery which removes the head of the pancreas, the duodenum, part of the jejunum, with a partial or total gastrectomy, cholecystectomy, and anastomosis of the ducts |
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Functions of Liver
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Bile Formation
Bili excretion Ammonia Conv to Urea* Drug metabolism glucose storage and reg protein synthesis chol synthesis storage of vitamins |
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Liver Dysfunction
Common s/s |
RUQ pain
Anorexia Dark Urine Diarrhea NV Fatigu Jaundice Joint Pain |
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Liver Dysfunction
lab values |
Increase: ALT AST Serum ALk phos, Bili, PT prolonged Ammonia, GGT
Decrease: alb, glob, neutropenia |
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Cirrhosis
Overview |
Chronic, progressive
Scarring of the liver that involves the formation of the fibrous tissue ass with destruction of normal architecture of the organ Scarring causes serious flow alteration in the vascular system and lymphatic duct |
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Cirrhosis
Types |
Laennec's- ETOH, nutritional
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Cirrhosis
Early s/s |
Jaundice
Anorexia Dyspepsia weakness NV Bowel changes Flatulance Hepatomegly spleenomegly abd pain liver tenderness acites pulm congestion |
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Cirrhosis
Later manifestations |
Decreae bili excretion
spider nevi palmer erythema edma hepatomegly splenomegly dark urine bowel changes fector hepaticus endocdrine neuro peripheral neuropathy |
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Assesing for Compensated cirrhosis
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Mild fever
vascular spiders unexpalined nosebleed dyspepsia abd pain firm,enlarged lever large spleen |
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Decomp cirrhosis
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sig impairment of live
severe fatigue weight loss muscle wasting edema portal HTN ascites neruo SPB |
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Cirrhosis
Nursing Interventions |
nutritious diet
rest stop ETOH skin care eval for edema and ascites prevent inf ed client |
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Portal HTN
Overview |
Persistant > in pressure within portal vein
increase in venous pressure in portal circulation as well as spleenomegly Persistant increase on blood pressure in the portal venouse system occuring as a results of > resistance to or obstruction of blood flow through the portal venoussystem into the liver |
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Portal HTN causes
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lagre colateral veins
Varices- esopg, gastric, rectal spleenomegly ascites systemic HTN |
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Ascities
Management |
Corrrect F/E imbalance
diet promote resp promotes skin integ medications surgical interventions |
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Potenetial for portal systemic encephalopathy
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seen in severe liver inj or failure
also as an outcome of tips the liver soes not detxify ammonia ammonia ia a CNS depressent |
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Encephalopathy
Interventions |
low protein diet
lactulose,neoymycin, flagyl, vanco monitor for GI hemmorhage maintain fluid balance bowel habits asses neuro |
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hepato renal syn
overview |
functional renal failure- vaso constriction and then renal failure
Primary cause of death in end stage cirrhosis |
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hepato renal syn
s/s |
sudden < in urine
elevates blood urea decrease nitrogen and cr decrease in urine NA ASA tylen, indocin can precipitate s/s |
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Hepato renal syn
lab tests |
Increased- AST,ALT,LDH, alk phos, Bili,PT Ammonia
Lowered- serum portein and alb |
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Hepatitis
Overview |
develop from exp to chemicals, ETOH, toxins, med, blood trans
Secondary inf |
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Phases of Hepatitis
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Prodromal
Icteric postcteric |
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prodromal phase
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begins with inf and the start of s/s
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iIcetric
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starts with onset of jaundice and last 4-6 weeks
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posticteric
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Recovery. damaged cells are removed and liver regenerates NL funtion in 4months
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HAV overview
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Most common form
Usually mild Non chronic Spred by fecal oral route Incubation 1 1/2 months Inf for 7-10 days after symptoms appear Course 4-8 weeks |
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HAV increased risk
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Yound children
Institutional settings travelers shellfish |
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HAv symptoms
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anicteric or Jaundice
no symptoms mild, flu like anorexia GI distress dark urine aversion to odors |
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No symptoms
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Mild flu like
anorexia dark usrine Gi distress aversion to odors |
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HAV dx
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Serum HAV antibodies
Jaundice Hep a antigen in stool |
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Hep focus of care
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Res to progressive ambulation
cleanliness no ffod prep nut diet no OTC meds noETOH f/u blood work |
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Hep B
Overview |
Transmitted via blood, seman, vag secretions, mucous membranes and skin tears
Incubation 1-6 monhts can progress to carries stateor develop chronic HBV Mahor cause of cirrhosis and hepatomegly |
