Nursing Care of Patients with Alterations in the GI tractPresentation Transcript
Nursing Care of Patients with Alterations in the GI tract C. Cummings RN,EdD
A & P of GI system
GI tract Hollow muscular tube, lumen surrounded by 4 tissue layers: Mucosa- innermost, thin layer of smooth muscle and exocrine cells Submucosa- connective tissue Muscularis- smooth muscle Serosa- outermost, connective tissue
GI tract Function: Secretion- secretes HCL acid, digestive enzymes Digestion- mechanical and chemical, food is broken down to chyme Absorption- from GI tract to blood supply Motility Elimination
GI tract Nerve Supply Intrinsic stimulation by myenteric plexus in smooth muscle and submucosa plexus in inner layer Autonomic system- Parasympathetic stimulation by vagus nerve, connects with intrinsic system Vagus-stimulates motor and secretory activity and relaxes spinchters Sympathetic system- thoracic and lumbar splanchnic nerves slows movement, inhibits secretions and contracts spinchters
Nerves of GI tract
Mouth Function: Mastication, taste, begin movement Glands produce 1 L of saliva/day Saliva contains mucin and salivary amylase with begins to break down CHO Oral preparatory phase- food is softened, made into a “bolus” and tongue moves to the back of the mouth Oral phase- tongue presses bolus against hard palate, elevates the larynx and forces the food bolus to the pharynx, triggering swallowing Pharyngeal phase- soft palate elevates and seals nasal cavity, inhibits respirations and allows esophagus to open Esophageal phase- is when bolus enter at cricopharyngeal juncture, peristalsis now takes food to the stomach All this takes about 10 seconds !
Esophagus Canal about 10 in long, passes through the center of the diaphragm Upper end is the upper esophageal sphincter, at rest it is closed to prevent air from entering the esophagus Lower end is the lower esophageal sphincter, it sits at the gastroesophageal junction, at rest it is closed to prevent reflux of gastric contents, this is where GERD occurs Function- to propel food and fluids and prevent reflux Mucous is secreted to move the food along Cardiac sphincter of the stomach opens to allow the food to enter
Stomach Digestive and endocrine organ, in midline and LUQ Four regions: Cardia- narrow part that is distal to the gastroesophageal junction Fundus- left above the GE junction Body or corpus- largest area Antrum- pylorus, is the distal portion and is separated from the duodenum by the pyloric sphincter, prevents backflow from the duodenum Surface is covered in rugae or folds and have smooth muscle for motility Has intrinsic and extrinsic nerves
Parietal cells secrete HCL acid and intrinsic factor, which absorbs B 12, without it, what anemia can occur?
Chief cells secrete Pepsinogenpepsin
Cephalic phase- sight, smell and taste of food, regulated by vagus, begin secretory and contractile activity
Gastric phase- G cells in the antrum secrete gastrin, which causes HCL and pepsinogen to be released. HCL changes pepsinogen to pepsin, which digest proteins. Mucous and Bicarb are secreted to protect the stomach wall
Intestinal phase- chyme produced empties into the duodenum and causes distention, this produces secretin, which stops the acid production and gastric motility !
Small Intestine Longest portion of the GI tract, 16-19 ft. Made up of 3 sections: Duodenum- first 12” and is attached to the pylorus. The CVD and pancreatic duct join to form the ampulla of Vater and empty into the duodenum at the duodenal papilla. This surrounded by a muscle, called the Sphincter of Oddi Jejunum- middle 8 ft portion Ileum- last 8-12 ft. The ileocecal valve separates the ileum form the cecum of the large intestine Inner lining is made up of intestinal villi and folds of mucosa and submucosa for digestion.
Small Intestine 3 main functions: Movement- mixing and peristalsis Moves chyme by segmental contractions and mixes with enzymes Digestion- enzymes produced by the intestinal cells make: Enterokinase, peptidases, lactase, maltase and sucrase Help to digest, CHO, proteins and lipids Absorption- absorbs most of the nutrients from food, takes 3-10 hours for the contents to pass through Major organ for absorption
Large Intestine Ileocecal valve to the anus, 5-6’, lined with columnar epithelium tha thas absorptive and mucous cells. Cecum- is the beginning, dilated pouch like structure, appendix is attached to the base Colon has 4 divisions: Ascending, transverse, descending and sigmoid Rectum- last 6-8” to the sphincter muscles and anus
Large Intestine Function: Movement- segmental contractions, to allow time for the water and electrolytes to be absorbed Absorption- absorbs most of water and electrolytes, reduces fluid volume of chyme and creates a more solid mass for elimination Elimination- 3-4 strong peristaltic contraction /day triggered by colonic distention in proximal large intestine to propel contents to rectum, until urge to defecate.
Nursing Assessment Family history- GI disorders, cancer Personal history- what kinds of things? Diet history- anorexia, dyspepsia- what is that? What should you question them on for diet history? Health history- diarrhea, constipation, # and color of stools, change in wt. or appetite Abdominal pain- P- precipitating Q-quality- how intense, severe, type R-region or radiation S- severity scale- 0-10 T-timing- when did it first occur, duration and frequency
Physical Assessment Abdomen: Inspection- skin, symmetry, rashes, lesions, scars Auscultation- all four quadrants, normally heard in 5-15 seconds, normal, hypoactive or hyperactive, listen 1 full minute. What is borborygmus? Why would bruits be heard? Why would there not be bowel sounds heard? Percussion- tympanic- air filled, dull- organ Palpation- light and deep palpation, masses, tenderness, look for guarding
Lab tests CBC- anemia Oncofetal antigens- CA19-9 and CEA, used to monitor for cancer in the GI tract Ca- decreased in malabsorption K – decreased with vomiting, diarrhea Xylose absorption- decreased indicates possible malabsorption in the small intesting Stool for Occult blood Stool for ova and parasite- infection Stool for fecal fat- increased with Crohn’s disease and malabsorption
Radiology Abdominal films- air in bowel and masses Upper GI and small bowel- pharynx to duodenojejunal junction, barium swallow and SBFT NPO 8 hours before, drink barium, then lie, stand and turn in multiple directions to view movement of barium SBFT- drink more barium and view passage After drink fluids to pass barium Barium enema Large intestine, done for obstructions, masses, not done is perforated colon or fistulas Only clear liquids for 12-24 hours prior, NPO, given bowel prep like Golytely Insert rectal catheter with a balloon and give 500-1500 ml of barium and hold Can be uncomfortable, must take a laxative after
Diagnostic Tests EGD- esophagogastroduodenoscopy Visualize esophagus to duodenum, NPO prior, given versed and fentanyl, maybe cetacaine to inhibit gag reflex, pass tube and visualize structures, can take biopsies Gag reflex may not return for 1-2 hours after, so no eating or drinking until then Colonoscopy- large bowel, take biopsies and remove polyps, have a bowel prep prior, given versed and fentanyl prior; Capsule enteroscopy is now done to visualize, apply a data recorder to the abdomen and the patient swallows the capsule Proctosigmoidoscopy- like colonoscopy, only a rigid tube, less invasive and does not require the cleansing of the colonoscopy
Case Study 72 year old male admitted with chest pain and nausea. He states that he awakens in the night with pain in his chest and nausea. What would you do first to evaluate his condition? What diseases could he have? What kind of lab work would you like to obtain? What past medical history do you need?
Case Study Your patient starts to have hematemesis. What does this mean? Is this life-threatening? What interventions should be done? What could have caused this condition?
Case Study It is determined that your patient can be treated non-surgically. What medications would be given? (should have 3) What type of teaching would be done for prevention? If he needed surgery, what could have been done?
Esophageal Problems GERD- gastroesophageal reflux disease Reflux causes esophageal mucosa to be irritated by the effects of gastric and duodenal contents, results in inflammation Causes: Inappropriate relaxation of the LES, sphincter tone is decreased Irritation from refluxed material Delayed gastric emptying, gastric volume or intra-abdominal pressure is increased Abnormal esophageal clearance
GERD Refluxed material has a pH of 1.5-2, whereas the esophagus normally has a pH of 6-8 erosive esophagitis, once inflammed, the mucosa can’t eliminate the material as quickly. This leads to increased blood flow and more erosion. Gastric acid and Pepsin cause the tissue injury. Can lead to Barrett’s epithelium- thicker, but can be cancerous, can also cause hemorrhage, aspiration pneumonia, asthma, laryngitis and dental deterioration.
GERD Physical Manifestations: Dyspepsia- heartburn, substernal or retrosternal burning that moves up and down in wavelike fashion, pain may radiate to neck or jaw or back, worsens when bends over, strains or lies on their back, occurs after meals and last 1-2 hours, helped by fluids and staying upright Regurgitation- food entering throat without nausea, watch for cough, hoarseness or wheezing Hypersalivation- water brash in response to reflux, fluid without sour or bitter taste
GERD Physical Manifestations Dysphagia and Odynophagia- difficulty swallowing, esophagus may be narrowed by inflammation or tumor, odynophagia- means what? Chronic cough, mostly at night Atypical chest pain Belching and flatulence or bloating Diagnosis: Endoscopy, 24 hour ambulatory pH monitoring- pass a small tube into esophagus and monitor pH levels
GERD Nursing Diagnoses: What diagnoses would apply to these patients? 1. 2. 3. Interventions: Diet therapy- what type of dietary modifications would be appropriate? Certain foods decrease LES pressure- chocolate, fat and mints. Also, smoking and alcohol decrease Spicy foods irritate the esophagus and Carbonated can increase gastric pressure
GERD Lifestyle changes: How should they sleep? What things increase intra-abdominal pressure? Drug therapy: Goal is to inhibit gastric acid secretion, accelerate gastric emptying and protect the gastric mucosa Antacids: Elevate the pH and deactivate pepsin, good for heartburn, take 1 hour before and 2-3 hr after a meal Name 2 antacids.
GERD Drug therapy: Histamine Receptor Antagonists Decrease acid, help promote healing of the esophagus Name 2 common ones sold OTC (generic ends in “dine”) Proton Pump Inhibitors Main treatment for GERD, long acting inhibition of gastric acid secretions by inhibiting protom pump of parietal cell, can reduce by 90%/ day Name 2 proton pump inhibitors (generic ends in “zole”)
GERD Other therapies: Consider medications that may lower LES pressure- oral contraceptives, anticholinergics, sedative, tranquilizers, B-adrenergic agonists, nitrates and Ca channel blockers Prokinetic drugs- for emptying and peristalsis- metoclopramide (reglan) Endoscopic: Enteryx procedure- spongy material in LES to tighten it Stretta procedure- radiofrequency energy through needles to inhibit the vagus nerve Surgical: Laparoscopic Nissen Fundoplication Angelchik esophageal antireflux- anchors the LES in the abdomen to increase sphincter pressure
Hiatal Hernia Protrusion of stomach through the esophagus Sliding or Rolling hernias Symptoms are similar to GERD patient Nonsurgical management is like GERD Surgical: Lap Nissen Fundoplication- reinforces the LES, wraps a portion of the stomach around the distal esophagus to anchor it Post op- risk for bleeding, infection and respiratory complications Have an NGT, begin PO once BS return Watch for gas-bloat syndrome and air swallowing
Nursing Diagnosis: GERD Impaired Nutrition: less than body requirements What things can be done to improve their intake and decrease pain? What would be the expected outcomes? How would you monitor their progress? Acute Pain r/t irritation of the esophagus What interventions can be performed? Risk for aspiration r/t reflux of gastric contents How can you determine that this does not occur?
Peptic Ulcer Disease Mucosal lesion of the stomach or duodenum Peptic can be gastric or duodenal PUD- gastric mucosal defenses become impaired and they can no longer protect the epithelium from acid and pepsin Three main types of ulcers: Gastric Duodenal Stress
Gastric Ulcers Gastric mucosa is protected by mucous and bicarbonate that maintain a normal pH on the gastric tissue and protects it from acid Gastromucosal prostaglandins increase the barrier’s resistance to ulceration by producing mucous Integrity is improved by a rich blood supply to the mucosa If there is a break in the mucosal barrier, HCL acid damages the epithelium. Gastric ulcers result from back-diffusion of acid or dysfunction of the pyloric sphincter.
Gastric Ulcers If the pyloric sphincter doesn’t function, bile backs up into the stomach, produces H+ ion back diffusion and mucosal inflammation Toxic agents and bile destroy the lipid plasma membrane of the mucosa. Delayed gastric emptying also affects. What drug can be given to improve emptying? Gastric Ulcers are deep and penetrating and usually are in the lesser curvature of the stomach, near the pylorus
Duodenal Ulcers Occur in the first portion of the duodenum. Deep lesions that penetrate through the mucosa and submucosa into the muscle layer. The floor of the ulcer consists of a necrotic area on granulation tissue and surrounded by fibrosis High gastric acid secretion, pH levels are low for long periods Protein rich meals, calcium and vagal excitation stimulate acid secretion Hypersecretion, rapid emptying of food from stomach reduces the buffering effect of food and delivers a large acid bolus to the duodenum Inhibitory secretory mechanisms and pancreatic secretion may be insufficient to control the acid Many patients have H. pylori infection. H. pylori produces urease changes urea to ammonia, H+ ions released contribute to damage
Stress Ulcers Acute gastric mucosal lesions occurring after and acute medical crisis or trauma Associated with head injury, major surgery, burns, respiratory failure, shock and sepsis Bleeding is the principle manifestation Multifocal areas often in the proximal portion of the stomach and duodenum Usually elevated HCL acid levels and hospital stay longer than 11 days
Complications of Ulcers Hemorrhage: 15-25% of patients with PUD, most serious complication Most often with gastric ulcers and elderly After initial bleed, 40% have a recurrence if untreated, especially if H. pylori untreated and no H2 antagonist Have Hematemesis- bleeding at or above the duodenojejunal junction Smaller amounts of bleeding are seen as melena, more often seen in duodenal ulcers, stool may appear black.
Complications of Ulcers Perforation Gastric or duodenal may perforate or bleed Stomach or duodenal contents can leak into the abdomen, acid peptic juice, bile and pancreatic juice empty through the anterior wall of the stomach into the peritoneal cavity Sudden, sharp pain in midepigastric region and spread over the abdomen Amount of pain correlates with the amount and type of GI contents spilled Abdomen is tender, rigid and boardlike, go into a fetal position to decrease tension of abdomen Chemical peritonitis, bacterial septicemia and hypovolemic shock follow paralytic ileus and possible death
Complications of Ulcers Pyloric obstruction Small number of patients, vomiting caused by stasis and gastric dilation Obstruction occurs at the pylorus and is caused by scarring, edema, and/or inflammation Gastric outlet obstruction abdominal bloating, nausea and vomiting May go into metabolic alkalosis from loss of large quantities of acid gastric juice (H+ and Cl-) Hypokalemia may result from the vomiting
Complications of Ulcers Intractable disease Disease may recur throughout life, stressors, inability to adhere to therapy, no longer responds to management Cause: Use of NSAID’s- break down the mucosal barrier and disrupt the protection by COX inhibition. Cause the depletion of prostaglandins, have a high rate of recurrence Drugs such as Theophylline, corticosteroids and caffeine stimulate HCL acid production H pylori infection is transmitted person to person 50% of people with PUD have a first or second line relative with PUD, usually the same type of ulcer
Physical Manifestations Epigastric tenderness, midline between the umbilicus and xiphoid process May begin as hyperactive BS, then diminish if perforation Dyspepsia- discomfort around the epigastrium, sharp, burning or gnawing Gastric- occurs in upper epigastrium with localization to the left of the midline and may be relieved by food Duodenal- located to the right of the epigastrium, occurs 90 min to 3 hours after eating and awaken at night, may be aggravated by spicy foods, onions, alcohol, caffeine and ASA, NSAIDS
Physical Manifestations Vomiting may occur Appetite is maintained, unless pyloric obstruction occurs Fluid volume deficit, if bleeding, take orthostatic BPs Watch for Hematemesis and melena Monitor H & H Dx- barium swallow and EGD Test for H. pylori is IgG serologic testing and urea breath testing
Nursing Diagnoses Name 5 diagnoses r/t PUD 1. 2. 3. 4. 5. What would be an expected outcome for this disorder?
Nursing Interventions Drug Therapy Goals: Provide pain relief, eradicate H. pylori, heal ulcerations, prevent recurrence Eliminate H. pylori- triple treatment: Bismuth product (pepto-bismol) or a a proton pump inhibitor and two antibiotics (metronidazole (Flagyl) and tetracycline or amoxicillin) May have to take medications 4 x’s/day for 14 days and often they don’t complete the series
Nursing Interventions Drug therapy: Hyposecretory drugs- reduce gastric acid secretions Antisecretory agents- proton pump inhibitors, “zole” ending, suppress H, K-ATP ase enzyme system of gastric acid production, can be given IV or PO H2 receptor antagonists- block histamine-stimulated gastric secretions, “dine” ending Prostaglandin analogues- reduce gastric acid secretion and enhance gastric mucosal resistance to tissue injury, Misoprostol (Cytotec) helps prevent NSAID induced ulcers, does cause uterine contraction and can not be given to pregnant women
Nursing Interventions Antacids Buffer gastric acid and prevent formation of pepsin, heal duodenal ulcers Aluminum hydroxides and magnesium hydroxide, may affect those with renal impairment Take 2 hours after meals to reduce the H+ion load Calcium carbonate (TUMS) is an antacid, but it triggers gastrin release and causes a rebound acid secretion Antacids can interact with other drugs- tetracycline, dilantin, also may have a high sodium content Mucosal Barrier fortifiers- sucralfate (Carafate) supplies a protect coating by forming a complex with proteins, binds with bile acids and pepsin, should be given on an empty stomach and not within 1 hour of eating or taking antacids
Nursing Interventions Diet therapy Bland diet may help to relieve symptoms Food may help to neutralize acids, rebound may follow when more acid is released Avoid foods that stimulate gastric acid release They are?? Yoga for stress relief, herbals, such as licorice and vitamins may help
Gastrointestinal Bleeding What would be a nursing diagnosis for GI Bleeding? 1. 2. What would be the expected outcome and how would you know that this was met?
Gastrointestinal Bleeding Hypovolemia Management Monitor vital signs and I&O, assess for bleeding and vomiting, monitor CBC Fluid and electrolyte replacement is necessary, usually NSS or LR, may give PRBC’s or FFP Watch for signs of shock, what are they?? Bleeding reduction Monitor labs, insert and NGT to decompress the stomach, give an H2 blocker, may need gastric lavage, what is that??
Nursing Interventions for GI bleeding Endoscopic therapy EGD, can do: cautery on the bleeding sites inject a sclerosing agent with diluted epipherine Laser therapy Clip the bleeding vessel Somastatin Analogue- Sandostatin may be used to suppress gastric acid secretion on parietal and chief cells, vasoconstricts the splanchnic arteries which reduce hemorrhage
Surgical management of GI bleeding MIG- minimally invasive gastrectomy- laproscopic to remove chronic gastric ulcer or treat hemorrhage, make several small incisions, may partially remove the stomach and/or vagotomy to control acid secretion Gastroenterostomy- creates a passage between the body of the stomach and jejunum, reduces motor activity in the pyloroduodenal area, diverts acid, a vagotomy may be done with it to decrease secretion. Can do truncal, selective or proximal. Billroth I- connect to duodenum, Billroth II connects to jejunum Pyloroplasty- widens the exit of the pylorus and empties the stomach
Postop care for GI surgery NGT management Monitor for complications of: Dumping syndrome- vasomotor symptoms, rapid emptying of gastric contents into the small intestine, shifts fluid into the gut and cause abdominal distention, 30 min after eating have vertigo, tachycardia, syncope, sweating, pallor, palpitations. 90 min later have excessive amount of insulin released, this dizziness, palpitations, diaphoresis and confusion Should eat smaller amounts, take less liquid with food, high protein and fat, low CHO diet, sandostatin may be given and pectin with food
Postop Care of GI surgery Reflux gastropathy- bile reflux, when pylorus is bypassed, bile in stomach and have abdominal discomfort and vomiting Delayed gastric emptying- usually resolves in 1 week, edema at the anastomosis or adhesions may occur, hypokalemia, hypoproteinemia and hyponatremia may also cause Afferent loop syndrome- duodenal loop is partially obstructed, pancreatic and biliary secretions fill the intestinal loop, it becomes distended painful contractions, bloating and pain 20-60 min after eating
Post op GI surgery Recurrent ulceration- occurs in 5% of patients, may have ulcers at the anastomosis Nutritional management: Deficiencies of B12, folic acid and iron Impaired Ca metabolism and reduced absorption of Ca and vitamin D Shortage of intrinsic factor, r/t the resection and rapid emptying of the food pernicious anemia- weak, anemic, atrophic glossitis- beefy shiny tongue Give back B12 and folic acid
Irritable Bowel Syndrome Chronic GI disorder, with chronic or recurrent diarrhea, constipation, abdominal pain and bloating Spastic colon, impairment of the motor/sensory function diarrhea alternating with constipation Usually begin as a young adult Stress, anxiety and familial factors may predispose patient
IBS Assessment: History of bowel pattern Manning criteria- abdominal pain relieved by defection, abdominal distention, sensation of incomplete evacuation of stool, presence of mucus with the stool Pain in LLQ and cramps, may be tenderness and air in bowels Dx- flexible sigmoidoscopy or colonoscopy if >40 Barium enema
IBS Interventions Diet therapy- limit caffeine, alcohol, beverages with sorbitol, take in fiber and bulk, 30-40 gm/day Drug therapy: Bulk forming laxatives (Metamucil) antidiarrheals (loperamide) anticholinergics (bentyl) antidepressants (elavil) 5-HT4 agonists(Zelnorm) for prokinetic activity, imitates serotonin to stimulate peristalsis Stress management- relaxation techniques
Nursing Diagnoses Constipation r/t low residue diet and stress What can be done to manage this? Diarrhea r/t increased motility of intestines How can this be corrected or treated? What can be done to correct constipation and impaction? What role may analgesics play in constipation?
Colorectal Cancer 95% are adenocarcinomas, most come from adenomatous polyps 2/3 occur in rectosigmoid region Can metastasize through blood and lymph, liver most common site with 15-30% spread there, can also go to the lungs, brain, bones and adrenals May form fistulas into bladder and vagina Genetics- autosomal dominant disorder- familial adenomatous polyposis only 1%, 100% malignant, usually starting at age 20. Also, hereditary nonpolyposis colorectal cancer- autosomal dominant, 10% of cancers, develop by age 45
Colorectal cancer 75% have no known cause Age is a risk factor Dietary- decreased bowel emptying time, foods with carcinogens- red meat, fatty food, fried meats and fish, concentrated sweets High fat diet increases bile acid secretion and anaerobic bacteria Irritable bowel diseases Third most common malignancy
Colorectal cancer Manifestations: Rectal bleeding, anemia and change in stool Gas pains, cramping or incomplete evacuation Hematochezia- bright red blood when in rectum Tumors can grow large when in upper abdomen, mostly liquid stool, more pain when in lower Tests- stool for occult blood, CEA, barium enema, CT of abdomen Colonoscopy or sigmoidoscopy
Colorectal cancer Nursing Diagnoses- Name 4 diagnoses, associated with colorectal cancer 1. 2. 3. 4. What would be the expected outcomes?
Colorectal cancer Nonsurgical management: Duke’s staging classification A- tumor has penetrated into, but not through the bowel wall B- tumor has penetrated through the bowel wall C-tumor has penetrated through the bowel wall and there is lymph node involvement D- tumor has metastasized to distant sites Radiation therapy Drug therapy-chemotherapy IV 5-FU and leucovorin, side effects are diarrhea, mucositis, leucopenia and mouth ulcers Eloxatin, Camptosar, Avastin are also being used, along with monoclonal antibodies- cetuximab
Colorectal cancer Surgical management: Colon resection- removal of tumor and lymph nodes Colectomy- colon removal Abdominal perineal resection- removes sigmoid colon, rectum and anus, colostomy is performed Colostomies may be ascending, descending, sigmoid, transverse or double barreled Stool returned depends on the site of the colostomy
Colorectal cancer Postoperative Care: Colostomy management What types of nursing diagnoses may accompany this procedure? How should the stoma appear? Report any bleeding, breakdown of the sutures from the wall and signs of ischemia or necrosis Wound care management- JP drains, monitor for infection Fluid volume deficit and electrolyte imbalance
Colorectal cancer Teaching: Colostomy care- what kinds of things should be covered? Dietary measures to control stool and gas, what would they be? Psychological adjustment to the colostomy, what diagnosis relates to this? Grief and family coping- what resources may be needed? Genetic testing if familial type
Intestinal Obstruction Partial or complete Mechanical- bowel is physically obstructed by adhesions, tumors Nonmechanical- paralytic ileus or adynamic ileus, neuromuscular distrubance- slow movement or backup Contents accumulate at or above the obstruction distention, peristalsis increases to aid movement, stimulates more secretions more distention edema of the bowel, increased capillary permeability
Intestinal Obstruction Plasma leaks into the peritoneal cavity and trapped fluid decreases the absorption of fluid and electrolytes into the vascular space reduced blood volume and electrolyte imbalances, can hypovolemic shock Can also lead to metabolic alkalosis if high and there is a loss of gastric acid, if low, metabolic acidosis occurs with the loss of alkaline fluids Bacterial peritonitis and septic shock can also occur from the release of endotoxins
Intestinal Obstruction Adhesions account for 45-60%, r/t scar tissue Intussusception- telescoping bowel and volvulus- twisting of the bowel Paralytic ileus- decreased peristalsis from trauma, toxin or autonomic, can result from surgery, MI’s, rib fracture, pneumonia, peritonitis and vascular insufficiency from heart failure or shock
Intestinal Obstruction Assessment: History of symptoms and occurrence Abdominal pain and cramping Obstipation, vomiting with brown and foul smelling Borborygni above the obstruction, then absent Abdominal distention and tympanic abdomen Abdominal films and CT of abdomen WBC elevated in some cases
Intestinal Obstruction Nonsurgical management: NGT to decompress to LCS Nasointestinal tubes- Miller-Abbott, mercury balloons and migrate down the intestine by peristalsis, don’t irrigate with fluid- it will increase edema at the obstruction Fluid and electrolyte replacement- NPO, give NSS or LR, replace K Pain control- not normally given opioids, mask pain and peritonitis Antibiotics if suspect perforation Surgical management: Exploratory laparotomy
Case Study 24 year old female admitted with frequent bloody diarrhea stools, weight loss and anemia. What do you suspect? What labwork should you do? What treatment may be needed?
Case Study Your patient tells you that the diarrhea has been occurring for months. How do you differentiate between U.C. and Crohn’s disease? What may be her treatment options?
Case Study How do you help your patient decide about a colostomy? If she does want a colostomy, what type of teaching needs to be done?
Chronic Inflammatory Bowel Disease Ulcerative Colitis and Crohn’s Ulcerative Colitis: Remissions and exacerbations Loose stools with blood and mucous 10-20/day Poor absorption of nutrients and thickening of the colon wall Abdominal distention and cramping Complications are: hemorrhage, perforation, fistulas and nutritional deficiencies May be familial tendency, inflammation r/t response to normal flora
Chronic Inflammatory Bowel Disease Crohn’s disease Terminal ileum, patching involvement through all layers of the bowel Deep fissures and ulcers occur 5-8 loose stools/day, rarely bloody Complications are: Fistulas, nutritional deficiencies Cause is thought to be mycobacterium paratuberculosis, genetic predisposition
Crohn’s Disease Garrard Crohn's story
Ulcerative Colitis Manifestations: Abdominal pain, bloody diarrhea, tenesmus- uncontrolled straining Dx- barium enema Nursing Diagnoses: Diarrhea r/t inflammation of the bowel Acute and chronic pain Imbalance nutrition: less than body requirements Disturbed body image
Ulcerative Colitis Diarrhea management- Drugs- salicylate compounds- Sulfasalazine (Azulfidine) inhibits prostaglandins to reduce inflammation, also use Asacol, Pentasa Corticosteroids- Prednisone to decrease edema Immunosuppressive- cyclosporine Antidiarrheals Monoclonal antibody- Remicade neutralizes the activity of tumor necrosis factor and prevents toxic megacolon
Ulcerative Colitis Diet therapy: NPO at first, then TPN, may have low fiber or low residue, what foods would be included? Surgical management: Total Proctocolectomy with permanent Ileostomy Total colectomy with a continent ileostomy Total colectomy with ileoanal anastomosis and ileoanal reservoir or pouch Postop- teaching for ostomy, pain control and monitoring for GI bleeding and fluid volume deficit
Crohn’s Disease Aggravated by bacterial infection, inflammation and smoking History of fever, abdominal pain and loose stools, weight loss Steatorrhea is common- fatty stools Fistulas may occur between bladder and vagina Drug therapy- same as UC, except may take metronidazole if fistulas and imuran as an immunosuppressant Diet therapy- may be on TPN, supplements like ensure, vivonex
Crohn’s Disease Monitor for fistulas- infections, skin problems, malnutrition, fluid and electrolyte imbalances Fluid and electrolyte therapy- what would this entail? Name one antidiarrheal. Surgical management: Bowel resections Fistula repairs Ileostomies may also be required to rest the bowel or repair damaged areas.