2.3 Nutrition and Fluid Balance, Digestive Flashcards
Elderly Nutrition
Factors affecting nutritional status in Elderly
Factors affecting nutritional status in Elderly
Changes in appetite, taste, smell and GI affect nutrition.
Decreased income contributes to food intake.
Dentures, missing teeth, pain from poor oral hygiene.
Chronic illness/ depression (leads to malnutrition)
Multiple medications
Cognitive impairment/dementia
Living in LTC facility (food not as appealing as home cooked)
Elderly Nutrition Teaching
Teaching Maintain healthy weight Chose nutrient dense foods Oral care BID Avoid processed foods & high fat foods
Elderly Nutrition
Nursing Intervention
Nursing Interventions:
Weigh as directed goal to maintain weight.
Teach nutrient dense foods
Oral care BID Safe swallow strategies.
Encourage socialization during meals.
Good lighting to see food
Use spices to add flavor instead of salt.
Chew food thoroughly to release flavors.
Vary food textures and flavors
Colorful presentations.
Grocery delivery or locate nearby grocery stores.
Meals on wheels for homebound seniors.
Refer eligible to SNAP program (supplemental nutrition assistance program)
Elderly Nutrition
Nutritional needs in Elderly
Nutritional needs in Elderly
Metabolism slows with age less calories needed
Vitamin and mineral needs same.
Iron needs drop for post-menopausal women
Vitamin D (synthesis reduced need sun or supplements)
Vitamin B12 (production of intrinsic factor in gut reduced)
Fluids-about 8 cups/day
Limit alcohol, refined sugars, fat, and salt.
Zinc deficiency can alter taste.
Elderly Nutrition
Nutritional needs in Elderly
Zinc
Zinc deficiency can alter sensitivity of taste receptors. Deficiency heightens ability to taste bitter and sour flavors and reduces sweet and salty sensations leading to more intake of sweet and added salt to food.
Dehydration in Elderly
Risk factor
Risk factors: Purposely restrict their fluids Loose sense of thirst Forget to drink Cannot get fluids on their own No A/C in summer (insensible loss)
Dehydration in Elderly
S/S
S/S Dehydration in elderly
Confusion-change in mental status early s/s dehydration.
Dry Tongue & Mucous membranes (furrowed tongue)
Skin turgor-less reliable (use sternum or inner thigh not arms)
Tachycardia
Subnormal temperature
Pinched facial expression
Hot dry body
Dehydration in Elderly Nursing interventions
Nursing interventions
I & O (1 L body fluid = 1kg/2.2lbs)
Daily weight (3% weight loss sign of dehydration)
Monitor electrolyte levels
Assessment for deficient fluid volume
Encourage fluids (approx. 8 cups sufficient)
Call light in reach
Review orders for NPO status and notify physician for late and canceled tests.
Oral Cancer
Malignancy of the oral mucosa on lips, tongue, floor of the mouth, or oral tissues.
High morbidity and mortality.
40 years old most common.
Oral Cancer Risk Factors
Risk Factors: Smoking Drinking alcohol Chewing tobacco HPV –recent studies have found contributes to risk
Oral Cancer Symptoms
Symptoms
Early: painless ulcer or lesion.
Later: difficulty speaking, swallowing or chewing, swollen lymph nodes, blood-tinged sputum.
Leukoplakia: “white patch” “smoker’s patch”
Erythroplakia: red velvety patch.
Any oral lesion that doesn’t heal/respond to Tx in 1-2 wks.. should be evaluated for malignancy.
Oral Cancer Treatment/ Prevention
Treatment/ Prevention:
Eliminate causative factors (smoking, tobacco, ETOH)
Oral sex and HPV transmission
Regular dental care
Oral Cancer Stages 1-4
Stages I and II are highly curable: Surgery and radiation. Stages III and IV require combination: Surgery, radiation and chemotherapy. Radical neck dissection with tracheostomy
Oral Cancer Post Op Surgery Nursing interventions
Nursing interventions:
Maintain a patent airway
Maintain stable weight and hydration: (I&O, wt..)
PEG tube or gastrostomy if chewing/swallowing difficulties.
Effectively communicate.
Communication boards, patient to write, yes/no questions.
Communicate an increased ability to accept changes in body image.
Oral radiation Effects of oral radiation
Effects of oral radiation
Males may experience permanent loss of hair in the area of their beard.
Skin irritation & lack of salivary function- worse as treatment continues.
Salivary function may not return to normal.
Keep mouth moist.
HOB elevated
Additional fluids.
Esophageal Cancer
Uncommon & High mortality rate
<5% survive 5 years after diagnosis.
Most tumors in lower 1/3 of esophagus
Esophageal Cancer Risk factors
Risk factors Cigarette & Chronic ETOH abuse primary. Opiate smoking Ingested carcinogens Chronic Reflux Physical mucosal damage (hot tea, radiation damage)
Esophageal Cancer Symptoms
Symptoms: Most common: Progressive dysphagia and recent weight loss. CA advanced by time this s/s presents (60% of esophagus occluded from tumor). Anemia GERD-like symptoms Anorexia Chest pain Persistent cough
Esophageal Cancer Goal & Diagnosis
Goal:
Control dysphagia and maintain nutrition regardless of treatment.
Diagnosis
Bronchoscopy
Barium swallow
Chest X-ray, CT scan, MRI look for metastasis.
Esophageal Cancer Treatment
Treatment:
Radiation therapy, and/or chemotherapy
Esophagectomy and possible anastomosis of the stomach to remaining esophagus.
NG tube often post op placed in OR.
Esophageal Cancer Complications
Complications:
Anastomosis leak
Respiratory complications (pneumonia, acute respiratory distress syndrome).
Gastric necrosis or bleeding
Infection and sepsis.
If NG tube removed, DO NOT REPLACE. CALL DR.
Do not move or manipulate NG- disrupts sutures
**After surgery high risk for aspiration and airway management r/t disruption of esophagus and incision into the thoracic cavity.
Stomach Cancer
Usually advanced when diagnosed & metastases present. Poor prognosis
Stomach Cancer Risk factor
Risk factors:
H. pylori infection is major risk factor. 60-90%
Genetic
Chronic gastritis
Gastric polyps
Carcinogens in the diet (smoked foods and nitrates)
History of partial gastric resection.
Helicobacter pylori(H. pylori)
type of bacteria. These germs can enter your body and live in your digestive tract. After many years, they can cause sores, called ulcers, in the lining of yourstomachor the upper part of your small intestine. For some people, an infection can lead tostomach cancer. Infection withH. pyloriis common
Stomach Cancer Symptoms
Symptoms: Early symptoms: very few. Vague: feeling of early satiety, anorexia, indigestion and vomiting. Ulcer-like pain unrelieved by antacids after meals. Advanced disease – metastases present Weight loss Cachectic (malnourished and poor health) Palpable abdominal mass Occult blood in stool
Stomach Cancer Diagnosis
Diagnosis Anemia may be first symptom (CBC) Upper GI with barium swallow x-ray Ultrasound Upper endoscopy with visualization and biopsy of lesion= provides definitive diagnosis
Stomach Cancer Treatment
Treatment
Removal of part or all of stomach (partial or total Gastrectomy primary Tx)
Stomach Cancer Post op Nursing care
Post op Nursing care:
Assess NG tube & suction as ordered.
Do not replace or move tube. Call Dr.
Assess color, amount and odor of gastric drainage. Initial NG output is bright red then to green-yellow over 2-3 days. If excessive amount of bright red, call Dr.
Monitor bowel sounds and distention.
Encourage ambulation
Monitor weight (significant wt.. loss common)
Stomach Cancer Post op Nursing care
Nutritional problems following surgery
Nutritional problems following surgery:
Folic acid, calcium, vitamin D absorption decreased.
Stomach Cancer Complications of gastrectomy
Complications of gastrectomy:
Dumping syndrome is common
Food eaten enters small intestine too quickly
Gastric surgery makes it more difficult to regulate movement.
Stomach Cancer S/S
S/S: occurs 5-30 min after eating.
Full feeling, Abd cramping/pain
Nausea or vomiting
Severe diarrhea
Sweating, flushing, or light-headedness, rapid heartbeat.
Loud hyperactive bowel sounds
Hyperosmolar chyme in the jejunum causes rapid rise in glucose and release of excessive insulin. Hypoglycemia common 2-3h after meals.
Stomach Cancer Dumping syndrome management:
Dumping syndrome management:
Small frequent meals
Liquids and solids taken at separate times not together
Increase protein and fats (they exit stomach more slowly)
Reduce CHO’s, especially simple sugars.
Recumbent/ semi-recumbent 30-60 min after meals
Monitor nutritional status
Anemia common r/t decreased iron absorption
B12 deficiency r/t stomach cells decreased prod intrinsic factor.
Folic acid deficiency
Decreased absorption of Vitamin D and calcium.
What’s does the liver do?
Metabolism of proteins, carbs, fats
Metabolism of drugs & steroid hormones
Detoxifies ETOH & Toxic Substances
Converts Ammonia to urea
Synthesizes blood proteins -(Albumin & Clotting factors)
Ammonia, a toxic by-product of protein metabolism is converted to urea in the liver then is eliminated by the kidneys. The liver produces bile-an essential substance for absorbing fats and eliminating bilirubin from the body. Minerals and fat soluble vitamins are store in the liver as is glycogen (stored carbohydrate for energy reserves).
Liver regeneration
Your liver is the only organ in your body capable of regenerating. After a 75% ablation of its total mass, your body needs 4 months to regain its initial weight. A liver in good health at 80 works as efficiently as it did at the age of 20.
Liver Functions Essential functions
Essential functions:
Metabolism of proteins, fats, CHO.
Liver Functions Other functions
Other functions:
Produces bile for fat absorption & eliminates bilirubin from body.
Detoxifies ETOH & other toxic substances.
Inactivates drugs/limits duration of effects
Metabolism of steroid hormones (testosterone, estrogen etc.) & most drugs.
Makes blood proteins (albumin & clotting factors).
Ammonia (product of protein metabolism) is converted to urea for kidneys to excrete.
Minerals and fat soluble vitamin storage (stored as glycogen for energy use).
Stores iron as ferritin which is released as needed for RBC production.
LIVER METABOLIC AND DIGESTIVE FUNCTIONS
LIVER METABOLIC AND DIGESTIVE FUNCTIONS:
Secretes bile
Stores fat soluble vitamins ADEK
Metabolizes bilirubin
Stores blood and releases blood into the general circulation during hemorrhage
Synthesizes PT, fibrinogen, and factors for clotting.
Synthesizes fats from CHO and proteins for energy use or storage into adipose tissues.
Glucose release during hypoglycemia
Alters chemicals to make them less toxic —-filters
Stores iron as ferritin which is released as needed for RBC production.
Common Manifestations of Liver Disorders
3 primary effects of liver disorders regardless of cause. Manifestations: Hepatocellular failure Jaundice Portal Hypertension
Hepatocellular Failure Liver is vital to
Liver is vital to: Digestion & metabolism of nutrients. Production of plasma proteins Clotting proteins Albumin Metabolism & excretion of bilirubin, steroid hormones, toxins & ammonia.
Note: Albumin keeps fluid in the vessels. Low albumin=fluid leaks out of vessels causing edema/ascites.
Hepatocellular Failure Impaired function of liver cell causes
Impaired function of liver cell causes:
Decreased production of albumin r/t impaired protein metabolism.
Decreased production of clotting factors.
Decreased bile production which impairs absorption of lipids & fat soluble vitamins. (Vit. K affects production of clotting factors).
Impaired metabolism of steroid hormones (estrogen & testosterone) causing:
Feminization of men
Irregular menses in women.
Hepatocellular Failure / Jaundice
what is it
RBC’s breakdown & form bilirubin.
When bilirubin can’t be emulsified & digested through bile it builds up causing yellow appearance.
Hepatocellular Failure / Jaundice
Accumulation of bilirubin in tissues caused by disruption in metabolism of bilirubin = yellow color reflected in skin, mucus membranes, sclera
Signs and symptoms: 1st noticeable in sclera of eyes then skin
Hepatocellular Failure Portal Hypertension
Portal Hypertension:
Impaired blood flow through liver increases pressure venous system that drains the GI tract, spleen & surface veins of the abdomen causing:
Veins in GI tract & abdominal wall to dilate causing:
Appetite suppression
Formation of collateral vessels in esophagus, rectum, & stomach
Esophageal varices, hemorrhoids, caput medusa.
Ascites: increased pressure in Abd vessels causes fluid to leak out. Worsened by low albumin levels.
Hepatic encephalopathy: build up of ammonia waste product causing mental status changes.
Cerebral edema (late disease) causing IICP.
Diagnostic Studies of Hepatic Function. Lab
Labs: enzymes released when liver cells are damaged. Will see elevation in:
ALT (Alanine Aminotransferase)
AST (Aspartate Aminotransferase)
ALP (Alkaline Phosphastase)
Diagnostic Studies of Hepatic Function Bilirubin
Bilirubin: Total, Direct (conjugated) , Indirect (unconjugated)
Bilirubin formed by breakdown of Hgb from old RBCs that is carried to liver through plasma to be excreted in the bile.
Direct: elevation usually r/t stones, tumors
Indirect: associated with increased RBC destruction
Direct (conjugated) bilirubin
Direct (conjugated) bilirubin: Increased levels usually result of
Obstructive jaundice from stones or tumor or
Damage to liver cells.
Indirect (unconjugated) bilirubin
Indirect (unconjugated) bilirubin:
Associated with increased destruction of RBC
Bilirubin- Box 25-2 p. 723- Lemone: Indirect increased with RBC hemolysis eg: transfusion reaction, sickle cell disease
Direct increase cirrhosis, Hepatitis; Total Bili increase with liver disease
Diagnostic Studies of Hepatic Function Albumin
Albumin: a protein in plasma, produced by liver, that increases osmotic pressure necessary for maintaining vascular fluid (vessels).
Albumin: decreases? increased?
Decreased levels cause fluid to shift from vessels into tissues resulting in edema and ascites. (Decreased levels seen in cirrhosis & acute liver failure).
Penicillin’s sulfonamides, asa, and ascorbic acid may decrease albumin lev
Increased levels: seen in dehydration. (Heparin may increase albumin levels)
Diagnostic Studies of Hepatic Function Ammonia
Ammonia:
A by-product of protein metabolism converted by liver to urea for excretion by kidneys.
Liver disorders or altered blood flow to liver cause ammonia levels to rise.
Increased levels can cause confusion, behavioral & personality changes in patient monitor for this.
Low protein diet
Paracentesis
Aspiration of fluid from peritoneal cavity.
Diagnostic or Therapeutic
Paracentesis NI pre procedure
NI pre procedure:
Void prior to decrease risk of bladder puncture
Weight and abdominal girth(taken at umbilicus) measurements. R: provides measure of effectiveness of procedure.
Position seated (side of bed or chair) with feet supported. Allows fluid to collect lower abdomen facilitating removal.
Therapeutic effects: relive SOB
Diagnostic: test fluid for abnormalities
Paracentesis Post Procedure
Post Procedure:
Monitor puncture site & vitals for s/s of hypovolemia.
May be some leaking at puncture site- normal depending on how much fluid remains.
Weight and abdominal girth- @ umbilicus.
Record amount, color, clarity of fluid removed. No more than 2L removed generally.
Albumin often given(when lg vol fluid removal) to retain fluid in vascular system & decrease complications.
Liver Biopsy
Uses ultrasound guided biopsy where needle inserted into liver specimen obtained.
Liver Biopsy Performed to
Performed to:
r/o cancer, detect cysts
Detect cirrhosis.
Liver Biopsy Nursing Implications
Nursing Implications:
Need driver home
NPO 4-6h prior , signed consent
Place on right side 1-2 h after procedure r/t increased bleeding risk
Bedrest 8-10 h after procedure at home as prescribed.
Light activity 1-2 wks.. after procedure.
Ask about anticoagulants taken or NSAID use.
Teach: pain in right shoulder common as local anesthetic wears off
Diagnostic Studies of Hepatic Function Coagulation Studies
Coagulation Studies: Prothrombin is made by the liver & is an inactive precursor in the clotting process.
Liver synthesizes Vitamin K for clotting factors. If liver function impaired Vitamin K not functioning properly
Diagnostic Studies of Hepatic Function Prothrombin Time (PT/ Pro time
Prothrombin Time (PT/ Pro time):
Measures the clotting ability of fibrinogen and prothrombin.
Increased levels can indicate liver diseases
Normal range 10-13 seconds
COMMON HEPATOTOXINS
Drugs: Isoniazid, Acetaminophen, Thiazides, Tetracycline, statins, steroids.
Alcohol
Some herbal supplements
Hepatotoxins are toxic to the liver and cause damage to liver function.
What is Cirrhosis?
Fibrosis (scar tissue) of the liver tissue leading to:
Decreased mass
Impaired liver function
Altered blood flow.
Thought to be irreversible but fibrosis may be reversed when underlying cause eliminated.
Liver Cirrhosis Types
Types of Cirrhosis:
Alcoholic: (Lannec’s)
Posthepatic: (hepatotoxic; viral hepatitis, non-alcoholic fatty liver r/t obesity, autoimmune hepatitis)
Biliary (obstructions)
Functional liver tissue gradually destroyed & replaced with scar tissue.
Scar tissue disrupts blood & bile flow causing liver size and function to decrease.
Alcoholism major cause! NI assess for ETOH use and frequency.
Liver Cirrhosis Post-hepatic
Post-hepatic: The immune response is responsible for producing liver damage and fibrosis in chronic and autoimmune hepatitis. The liver is shrunken and nodular with extensive liver cell loss and fibrosis.
Multisystem Effects of Cirrhosis Ascites
Ascites- accumulation of plasma fluid in abdominal cavity. (low albumin causes fluid to shift) Pt in Semi-Fowler’s position to facilitate breathing.
Multisystem Effects of Cirrhosis Bleeding
Bleeding- decreased clotting factor, platelet destruction, & impaired Vit K absorption.
Multisystem Effects of Cirrhosis Esophageal Varices & hemorrhoids
Esophageal Varices & hemorrhoids: Increased pressure in portal system & thin walled vessels cause this.
Multisystem Effects of Cirrhosis Encephalopathy
Encephalopathy: r/t build up of ammonia as liver cannot convert to urea for excretion.
Multisystem Effects of Cirrhosis Integumentary
Integumentary: Pruritis r/t build up of toxins
Multisystem Effects of Cirrhosis Malnutrition
Malnutrition- r/t impaired fat & nutrient absorption. Supplements needed.
CIRRHOSIS- Manifestations
Malaise, Fatigue r/t anemia GI-gastritis, anorexia, diarrhea Malnutrition- malabsorption of vitamins Fluid Retention- edema/ascites Jaundice- liver & bile duct inflammation prevents bilirubin from being excreted into small intestine causing jaundice. Bleeding-Bruising Encephalopathy Pain & Pruritis
Cirrhosis Management TIPS
TIPS procedure (trans jugular intrahepatic portosystemic shunt) Relieves portal HTN & complications of esophageal varices & ascites. Needle inserted transcutaneous creating a channel. Expandable metal stent inserted to allow blood to flow directly from portal vein into the hepatic vein Bypasses the cirrhotic liver Short term treatment until liver transplant.
Liver Tumors
Primary liver cancer uncommon.
Prognosis poor r/t advanced by time diagnosed.
Liver Tumor Risk factor
Risk factors Chronic Hep B & C infections Cirrhosis Chronic Alcohol consumption Non alcoholic fatty liver
Manifestations of LIVER TUMORS Signs and Symptoms
Signs and Symptoms Jaundice Ascites, edema Extreme weakness GI bleeding, bleeding tendencies High AFP alpha-fetoprotein Encephalopathy Spreads quickly Painful palpable mass RUQ
Manifestations of LIVER TUMORS Diagnostics
Diagnostics:
CT Scan
MRI
Liver Biopsy
Manifestations of LIVER TUMOR Treatment:
Treatment:
Radiation, Chemo
Tumor excisions
Liver transplant (stage I /II)
Hepatitis
Inflammation of the liver usually caused by a virus.
Can be acute or chronic
Chronic hepatitis = increase risk of liver CA
Hepatitis Types / causes
Types / causes
Viral- Hep A,B,C,D,E virus
Chronic – Primary cause of liver damage leading to cirrhosis and liver cancer. (caused by HBV, HCV,HDV)
Fulminant- Rare rapid progression liver failure 2-3 weeks (associated with HBV & HDV infections)
Toxic- ETOH, hepatotoxic meds,
Autoimmune- body attacks itself.
Regardless of cause of hepatitis inflammatory process disrupts liver function.
Common Symptom is Fatigue!!!
3 Phases of Hepatitis
Pre-icteric (prodromal)
Icteric (jaundiced)
Recovery/posticteric phase
3 Phases of Hepatitis Pre-icteric
Pre-icteric (prodromal)
Begins abrupt or insidiously
Malaise, fatigue, anorexia, muscle aches
Often mistaken for flu
3 Phases of Hepatitis Icteric
Icteric (jaundiced)
Begins 5-10 days after onset of symptoms
Jaundice sclera, skin, mucous membranes
Pruritus r/t bile salts on skin
Stools light brown or clay r/t bile not excreted in stool
Brown urine from bile pigment excreted by kidneys instead.
3 Phases of Hepatitis Recovery/posticteric phase
Recovery/posticteric phase
Follows jaundice and last several weeks
S/S gradually improve. Serum enzymes decrease.
Hepatitis jaundice
Patients with acute hepatitis A or B are likely to develop jaundice whereas people with Hep C do not resulting in the infection going undiagnosed for an extended period of time.
What is a Carrier State?
Carrier state is when an infected individual harbors the active virus and is capable of spreading it to others even though there are no manifestations of the disease.
Hepatitis B & C associated
With carrier states.
Hepatitis A
Sometimes called infectious hepatitis.
Prevent: Hep A vaccine; Give immunoglobulin IM within 2 weeks of exposure.
Hepatitis A Transmission
Transmission:
Fecal-oral via contaminated food, water, or direct contact with infected person. Virus present in stool up to 2 wks. before s/s present. Once jaundice occurs amount of virus in stool & risk of spreading decreases significantly.
Hepatitis A Risk Factors & Onset
Risk Factors & Onset:
International travel primary reason.
Close household contact with infected person
Abrupt onset, self-limiting disease (not chronic)
Hepatitis A, B, C, D, E transmission
Hep A and E are fecal oral transmission.
Hep B,C,D are blood and body fluid transmission.
Hepatitis B
Can cause acute, chronic, rapid progressing hepatitis. It is associated with a carrier state.
May be asymptomatic or have prodromal symptoms (urticarial and other rashes, arthralgia’s, serum sickness or glomerulonephritis) Preventative Vaccine is available; Hep B immunoglobulin IM within 24 h of exposure.
Hepatitis B Transmission
Transmission:
Contact with infected blood & body fluids
Hepatitis B High Risk Populations
High Risk Populations:
Injection drug users
Multiple sex partners & gay sex
Exposure to frequent blood products (hemodialysis pts)
Healthcare workers thru blood & needle stick injuries
Hepatitis B Complications
Complications:
Primary liver cancer- especially if infected perinatally.
Hepatitis C
Primary cause of chronic hepatitis, cirrhosis, & liver cancer.
Acute hepatitis usually asymptomatic or mild
Hepatitis C Transmission
Transmission:
Infected blood & body fluids
Hepatitis C Risk Factors
Risk Factors:
Injection drug use primary risk factor
Hepatitis C S/S Chronic
S/S Chronic:
Fatigue, hepatomegaly
Occasional jaundiced periods No Vaccine Available!!
Liver enzymes elevated Treat with Interferon (antiviral). Many new meds available.
Hepatitis & Labs
ALT increased
AST increased
ALP increased
Serum Bilirubin increased
Viral Antigen & Specific antibodies- identifies virus and state of activity.
Liver Biopsy- detect & evaluate for chronic hepatitis.
Pancreas Function
Glandular organ that provides 2 functions (exocrine & endocrine)
Produce enzymes that affect control of digestive enzymes. (exocrine)
Produce hormones for carbohydrate, fat, and protein metabolism.(insulin, glucagon)- endocrine function
Pancreatitis
Inflammatory disorder involves self destruction of pancreas by its own enzymes. Leads to hemorrhage & necrosis.
Exact causes unknown
Alcoholism & gallstones primary risk factors for acute pancreatitis.
Can be either Acute or Chronic
Diagnostic Tests of Pancreatic Function
Serum Amylase increases in pancreatitis
Serum Lipase increases in pancreatitis
Endoscopic Retrograde Cholangiopancreatography (ERCP) diagnostic for chronic pancreatitis to differentiate fibrosis from carcinoma
Chronic Pancreatitis-Gallstones labs
Chronic Pancreatitis-Gallstones, ETOH abuse. Labs = increase Lipase, increase Blood Glucose. Have increase lipase from pancreatic cell injury. Decrease insulin production from pancreas.
Acute Pancreatitis
Often mild and self limiting
Reversible
Abrupt onset of epigastric & LUQ pain
Gallstones leading cause, ETOH 2nd cause
Acute Pancreatitis 2 forms
2 forms:
Interstitial edematous pancreatitis- milder leads to inflammation & edema of pancreatic tissue.
Necrotizing: more severe leads to inflammation, hemorrhage, and necrosis of pancreatic tissue.
Acute Pancreatitis Pathophysiology
Pathophysiology:
Activated pancreatic enzymes released into pancreas.
Enzymes, trypsin, digests pancreatic tissue & activates other enzymes
Other enzymes digest blood vessel walls causing vasodilation leading to edema, hemorrhage, necrosis.
Fluid volume shifts from circulating blood into retroperitoneal spaces of abdomen.
Hypovolemic shock & renal failure can develop 24h after onset.
*Organ failure leading cause of death- respiratory failure particularly.
Chronic Pancreatitis
Chronic inflammation, fibrosis, & gradual destruction of pancreatic tissue.
Irreversible
Alcoholism primary risk factor in U.S.
ETOH- pancreatic secretions have insoluble proteins that calcify and block pancreatic ducts & flow of pancreatic juices.
10-20% idiopathic
Recurrent inflammation causes fibrous (scar) tissue leading to malabsorption.
Can lead to diabetes if endocrine function of pancreas disrupted.
Pancreatitis Acute
Acute Reversible Onset: Abrupt/ 24h Gallstones leading cause Complications: Intravascular volume depletion. Renal failure Acute respiratory distress syndrome.
Pancreatitis Chronic
Chronic Irreversible Onset: gradual destruction Alcoholism leading cause Complications: Malabsorption & malnutrition. Increased risk pancreatic cancer. Opioid addiction r/t pain
ACUTE PANCREATITIS
ACUTE PANCREATITIS: Why hypovolemia and renal failure?
Pancreatic enzymes released into pancreatic tissue.
Activated enzymes, trypsin, digest pancreatic tissue & activate other enzymes that digest elastic tissue of blood vessel walls.
This leads to: vascular damage and hemorrhage and necrosis
Cellular damage produces vasodilation increasing vascular permeability and causes edema.
Large fluid volume may shift from circulating blood into the retroperitoneal space and abdominal cavity (causing respiratory distress from fluid accumulation) LeMone 721
ACUTE PANCREATITIS ONSET
ONSET:
Acute: abrupt usually complications develop 24 hours of onset renal and hypovolemia
Chronic: gradual destruction of pancreatic function.
Pancreatitis Manifestations Acute
Acute: Abrupt severe epigastric LUQ pain may radiate to back.
N/V fever
Decreased bowel sounds, ABD rigidity & distension
Tachycardia, hypotension, cold clammy skin
Possible jaundice
+ Turner (flank bruising) & Cullen sign (peri-umbilical bruising)
Pancreatitis Manifestations Chronic
Recurrent epigastric & LUQ pain radiating to back.
Anorexia
Nausea / vomiting
Weight loss
Flatulence, constipation
Steatorrhea (fatty, frothy, foul smelling stool from decrease in pancreatic enzyme secretion
Pancreatitis Treatment Acute
Acute: Supportive: pain meds
NPO to reduce pancreatic secretions promote rest of pancreas. NG tube to sx
IVF to maintain vascular vol
TPN for nutrition while NPO
Low fat High CHO diet when: bowel sounds +, pain relieved, & amylase normalizes (3-4 days)
Surgery if cause gallstone
Pancreatitis Treatment Chronic
Chronic
Pain meds- monitor dependence .
Enzyme supplements- manage ABD pain & reduce steatorrhea. (pancrealipase enhances digestion of fats & starches and decreases # of BM’s)
High CHO low fat diet with frequent feedings
H2 blockers & PPI to neutralize gastric secretions.
Pancreatitis Treatment
Foods
Food best tolerated during convalescence in pancreatitis. No Fried, greasy, or acid foods. Pt could have baked chicken, boiled potatoes. Day 4 NPO order changed to small frequent meals, high CHO, Low Fat
Pancreatic Cancer
Uncommon <3% of cancers but one of most lethal forms.
Pancreatic Cancer Risk Factors
Risk Factors: Cigarette smoking 2 x higher risk than non-smokers. Chronic pancreatitis DM Cirrhosis Obesity, high fat diet Genetic predisposition
Pancreatic Cancer Manifestations
Manifestations
Few s/s until advanced.
Dull epigastric pain that increases as tumor grows.
wt. loss, flatulence
Pancreatic Cancer Treatment
Treatment Early may be able to resect the head of the pancreas (Whipple) Pancreatoduodenectomy (Whipple) Radiation, chemo Post-op Whipple complications Hypovolemic shock Hemorrhage Bile leak, hepatorenal failure
Whipple Procedure
Done when cancer found early. Removes Head of pancreas Entire duodenum Distal 1/3 of stomach Portion of jejunum.
Whipple Procedure Nursing Care
Nursing Care:
Semi-fowlers- facilitate lung expansion reduce stress on suture line
Maintain NG low int. sx., keep patent, DO NOT REPOSITION!!!! Puts stress on suture lines.
No forceful NG irrigations- stress on suture lines
