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334 Cards in this Set
- Front
- Back
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Steatorrhea
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excess fat in stool
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Hematochezia
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Blood in stool: bright red blood
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Melena
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black tarry stools
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Upper GI Bleed
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coffee-grounds vomitus and pink or red if esophageal varicies exist
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Lower GI Bleed
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black tarry stools (and could even be bright red if the bleed is low/ hemorrhoid)
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Anticholinergics
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scopolamine transdermal
(Tramsderm-Scop) |
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Antihistamines
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dimenhydrinate
(Dramamine) – promethazine (Phenergan) – meclizine (Antivert) – hydroxyzine (Vistaril |
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Phenothiazines
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prochlorperazine
(Compazine) – chlorpromazine (Thorazine) |
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Butyrophenones
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– droperidol (Inapsine)
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Drug therapy – Common side effects include
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• Dry mouth
• Hypotension • Sedative effects • Rashes • GI disturbances |
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Nondrug therapy
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Acupuncture
– Acupressure – Botanicals • Ginger • Peppermint oil – Breathing exercises |
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Drug therapy – Other drugs with antiemetic properties
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Benzamides
– metoclopramide (Reglan) » Prokinetic drug—increases gastric emptying • Serotonin antagonists – ondansetron (Zofran) • Dexamethasone (Decadron) – Management for chemotherapy-induced emesis |
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Nutritional Therapy
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–IV fluids to replace fluid and
electrolytes, glucose –NG tube suction to decompress stomach –Clear liquids started first • 5 to 15 ml fluid every 15 to 20 minutes • No extremely hot/cold liquids Room-temp carbonated beverages without carbonation okay •Warm tea •May advance to dry toast, crackers |
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Gerontologic Considerations- N/V
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More likely to have cardiac or renal insufficiency
– Increased risk for life-threatening fluid/electrolyte imbalances • Increased susceptibility to CNS side effects of antiemetic drugs • Caution with fluid replacement in patients with HF • Alteration in LOC—greater risk for aspiration |
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Ulcerative Colitis:
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*S/S include bloody diarrhea, abdominal cramping and distention, weight loss, anorexia, nausea, vomiting. Different because continuous inflammation, bloody stools, hemorrhage, surgery curative.
*Treatment includes a curative surgery that bypasses the bowels and leads to a permanent ostomy |
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Chohn’s Disease:
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*S/S include nonbloody diarrhea, abdominal pain, distention, weight loss, anorexia, nausea, vomiting, no surgical cure. Different because only segments of bowels are inflamed, fatty stools, fistulas, fissures, may recur after surgery.
*Treatment includes management with medications, controlling symptoms, as well as surgery but surgery is not always effective. |
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Oral Feeding
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High-calorie supplements
• Used when nutritional intake is deficient • Examples include – Milkshakes – Puddings – Ensure, Sustacal • Used as snacks |
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Tube Feeding
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Also known as enteral nutrition
• Administration of nutritionally balanced liquefied food or formula through tube inserted into – Stomach, Duodenum, Jejunum • Provide nutrients to GI tract alone or supplemental to oral or parenteral nutrition • Easily administered • Safer than parenteral • More physiologically efficient than parenteral • Less expensive than parenteral |
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Tube Feeding
• Indications include those with |
Anorexia
– Orofacial fractures – Head/neck cancer – Burns – Nutritional deficiencies – Neurologic conditions – Psychiatric conditions – Chemotherapy – Radiation therapy |
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Tube feeding
Delivery options include |
Continuous infusion by pump
– Intermittent by gravity – Intermittent bolus by syringe – Cyclic feedings by infusion pump |
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Tube feeding
Nasogastric and nasointestinal tubes |
Inserted through the nasal cavity
– Radiopaque: Allowing visualization from X-ray – ↓ Likelihood of regurgitation and aspiration when placed in intestine |
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Nasogastric, Gastrostomy, Jejunostomy tubes...
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Nasogastric and nasointestinal tubes
– Can be dislodged by vomiting or coughing – Can be knotted/kinked in GI tract • Gastrostomy and jejunostomy tubes – May be used in those needing tube feedings for extended period • Patient must have intact, unobstructed GI tract – Can be placed surgically, radiologically, or endoscopically |
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TPN Administration
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Via central line and infusion pump
• Refrigerated until 30 min. before use • Solution good for 24 hours • Check label with order for each new bag • Filtered – Use correct filter – Change filter and tubing every 24h – Monitor blood sugar • Monitor for complications |
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Common Indications for PN
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Chronic diarrhea and vomiting
• Complicated surgery or trauma • Gastrointestinal obstruction • Gastrointestinal tract anomalies and fistulae • Intractable diarrhea • Malnutrition |
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Parenteral Nutrition
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Composition
– Base solutions contain dextrose and amino acids – Pharmacy adds prescribed electrolytes, vitamins, and trace elements – Three-in-one contains fat emulsion, dextrose, and amino acids • Nausea, vomiting, and elevated temperature may occur if lipids infused too rapidly |
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TPN Composition
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Amino acids
• CHO 20-50-70% glucose – (1000-2000 calories) • Vitamins, minerals, and trace elements • Electrolytes • Water • May also contain lipids • Can be customized for the patient – Insulin – Tagamet |
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Parenteral Nutrition
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Exact amount of electrolytes needed is
determined by blood testing • Vitamin K may be ordered separately as it is not included in the preparation |
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Parenteral Nutrition
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Methods of administration
– Central or peripheral use – Central parenteral nutrition through catheter whose tip lies in superior vena cava • Subclavian or jugular vein • Peripherally inserted central catheters (PICCs) • Long-term parenteral support |
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Parenteral Nutrition
• Central and peripheral nutrition differ in tonicity |
Central solutions are hypertonic
• Large central vein can handle high glucose content ranging from 20% to 50% – Peripheral solutions are hypertonic • Peripheral vein can handle glucose up to 20% |
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Parenteral Nutrition
• PN solutions prepared by pharmacist or trained technician under strict aseptic techniques |
Nothing is added to solution after it is prepared
– Solutions good for 24 hours – Must be refrigerated until 30 minutes before use – Must be labeled with nutrient content, all additives, time mixed, date and time of expiration |
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Parenteral Nutrition
• Catheter placement under sterile conditions by physician or advanced practice nurse |
Isotonic IV solution infused until x-ray confirms
correct placement – Site covered with sterile dressing – Date marked on dressing |
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Complications of
Catheter Placement |
Hemorrhage
• Hydrothorax • Pneumothorax • Hemothorax • Air embolus • Venous thrombosis |
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Parenteral Nutrition
• Complications of PN |
Infection
• Must have filter • With lipids: Tubing, filter change every 24 hours • With amino acids, dextrose: Filter, tubing change every 72 hours • Fungus, gram +/- bacteria Mechanical problems • Insertion problems • Dislodgement, thrombosis of great vein, phlebitis – Metabolic problems • Hyperglycemia, hypoglycemia, prerenal azotemia, fatty acid deficiency, electrolyte disturbances, hyperlipidemia, mineral deficiencies |
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Parenteral Nutrition
Nursing Management |
VS q 4–8 h
• Daily weights • Blood glucose – Check initially every 4 to 6 hours – May vary based on institution • Electrolytes • BUN • CBC Hepatic enzymes • Dressing changes – Site observation key • Infusion pump must be used – Need to periodically check volume infused |
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Parenteral Nutrition
Nursing Management |
Before administering, check label and
ingredients against order • Examine bag for signs of contamination • Blood and catheter cultures if infection suspected • X-ray: To check changes to pulmonary status • Daily dressing changes when discontinued until heals |
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Parenteral Nutrition
Nursing Management |
Watch for infection and septicemia
– Local manifestations • Erythema • Tenderness • Exudate at catheter insertion site – Systemic • Fever, chills • Nausea/vomiting • Malaise |
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Acute Appendicitis
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Inflammation of the appendix
• Occurs in 7-12% of the population • Peak incidence 11-19 years • > in males • Rupture-serious complication • Most common indication for emergent abdominal surgery |
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Acute Appendicitis Manifestations
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Abdominal pain (Typical)
– Periumbilical, epigastric – Later shifts to RLQ, McBurney’s point (midway between right iliac crest and umbilicus) – Constipation, unable to pass flatus – May vomit • Low grade fever • Can become gangrenous or perforate |
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Acute Appendicitis
Lab and Diagnostic Tests |
Elevated WBC with elevated immature WBCs
– (shift to the left) • Abdominal ultrasound • R/O other causes – UA, Rapid Strep • Rebound tenderness at McBurney’s point – Relief of pain with direct palpation followed by tenderness on release of pressure • Extension or internal rotation of right hip increases pain – Iliopsoas muscle test – Obturator test • Rovsing’s sign (palpate LLQ – pain felt in RLQ) |
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Acute Appendicitis
Pre-op Preparation |
Teaching
– NPO – No laxatives or enemas – Ice bag – Pain management • Used to be held until diagnosis • Studies have found increased compliance if medicate patient so no impediment with diagnosis – Ambulation, C & DB, IS, Splinting incision • Consent |
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Acute Appendicitis
Post-op Management |
Wound care
– Monitor any drainage – Assess healing of incision • Gradually increase activity – Encourage deep breathing, use of incentive spirometer – Ambulate as soon as possible |
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Hernia
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Hernia - protrusion of
tissue and/or part of an organ through a "weak spot" in the muscle of the abdominal wall. • Most occur in groin |
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Hernia: protrusion
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Reducible
• Truss – Not reducible/incarcerated • Surgery (herniorraphy, hernioplasty) – Strangulated • Emergency surgery |
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Nursing Care: Herniorraphy
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If open inguinal hernia
• Pain management – Pain meds – Scrotal support with ice • Discharge instructions – No heavy lifting 2-6 weeks – No driving for 2 weeks – Monitor incision |
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Nursing Care: Herniorraphy
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If laproscopic repair
• Pain management • Discharge instructions – No heavy lifting 2 weeks – No driving 3-5 days – Monitor stab wounds |
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Colorectal Cancer
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Third most common type of cancer
• Risk factors – Over age 40 – Male – Polyps of colon and/or rectum • familial polyposis (nearly 100%risk) – IBD, esp. ulcerative colitis – high fat, high calorie, low fiber (???) diet Benign Polyps: More likely to become cancerous if >2cm in size |
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Colorectal Cancer
Etiology and Pathophysiology |
More common in men
• Risk factors – Family or personal history of colorectal cancer – Increased age – Colorectal polyps – Inflammatory bowel disease (IBD) – Lifestyle factors • Obesity, Smoking, Alcohol, Large amounts of red meat Cancer elsewhere in the body – Family history – Radiation exposure – Immunodeficiency disease – Low calcium |
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Colorectal Cancer
Etiology and Pathophysiology |
Adenocarcinoma is most common type
• Most arise from adenomatous polyps • Tumors spread through the walls of the intestine into musculature into the lymphatic and vascular system • Most common sites of metastasis – Regional lymph nodes, Liver, Lungs, Peritoneum |
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Colorectal Cancer
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Vague symptoms in early stages
– Rectal bleeding/blood in stool (hematochezia) – Change in bowel habits – Abd fullness, pain – later, wt. loss, malaise • Treatment – Surgery – Chemotherapy and radiation |
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Colorectal Cancer
Clinical Manifestations |
Symptoms (cont’d)
– Anemia – Weight loss – Rectal bleeding • Most common symptom • Most often with left-sided lesions |
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Colorectal Cancer
Clinical Manifestations |
Left-sided lesions
– Rectal bleeding – Alternating constipation and diarrhea – Narrow, ribbonlike stools – Sensation of incomplete evacuation |
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Colorectal Cancer
Clinical Manifestations |
Right-sided lesions
– Usually asymptomatic – Vague abdominal discomfort – Colicky abdominal pain – Iron-deficiency anemia – Occult bleeding |
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Colorectal Cancer
Diagnostic Studies |
Family history
• Physical examination • Digital rectal examination • Colonoscopy Colonoscopy – Gold standard – Entire colon is examined – Biopsies can be obtained – Polyps can be immediately removed and sent to laboratory for examination • Fecal occult blood tests – Cancerous tumors bleed intermittently into colon – Used to detect very small quantities of blood – Does not detect nonbleeding tumors Fecal occult blood tests (cont’d) – Guaiac-based tests (FOBT) • Avoid NSAIDs, vitamin C, citrus juices, red meat for 3 days before test • Six samples from three consecutive bowel movements – Fecal immunochemical test (FIT) • No special restrictions • Two stool specimens |
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Colorectal Cancer
Diagnostic Studies |
Stool DNA test
– DNA markers are shed from premalignant adenomas and cancer cells in stool and not degraded – Stools collected and analyzed – Not yet sensitive enough to replace other screening methods Colonoscopy and tissue biopsies confirm diagnosis • Additional laboratory studies must be done – CBC – Coagulation studies – Liver function tests • Carcinoembryonic antigen (CEA) – Complex glycoprotein – Produced by 90% of colorectal cancers – Helpful in monitoring disease recurrence CT scan or MRI – Helpful in detecting • Liver metastases • Retroperitoneal and pelvic disease • Depth of penetration of tumor in bowel wall |
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Detection & Diagnosis
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Occult blood tests, rectal exam annually after age 40
– Barium enema, double-contrast BE – CT scan – Annual guiac tests after age 50 – Primary diagnostic tests: endoscopies ie flexible sigmoidoscopy q 3-5 yrs after age 50, colonoscopy, biopsy – CEA test • Non-specific for colorectal cancer • Used to monitor tumor status after surgery |
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Colorectal Cancer
Collaborative Care |
Prognosis and treatment correlate with
pathologic staging of the disease – Duke’s classification – TNM system-Preferred classification system • Surgical therapy – Polypectomy during colonoscopy used to resect colorectal cancer in situ – If cancer is localized, can be resected with healthy tissue and cancer-free ends sewn together • Lymph nodes removed Chemotherapy and radiation therapy – If cancer has spread to lymph nodes or nearby tissue • Once cancer has spread to distant sites, surgery is palliative • Optimal procedure: Bowel resection with reanastomosis of remaining segments • ↓ Colonic bacteria to prevent infection and breakdown at site |
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Colorectal Cancer
Collaborative Care |
Surgical goals
– Complete resection of tumor • Site of cancer dictates site of resection – Thorough exploration of abdomen – Removal of all lymph nodes that drain the area – Restoration of bowel continuity – Prevention of surgical complications Chemotherapy – Positive lymph nodes at time of surgery – Metastatic disease – Used as an adjuvant following colon resection – As primary treatment for nonresectable colorectal cancer • Preoperative preparation – Bowel cleansing agent • Unless patient has bowel obstruction or perforation – Oral antibiotics |
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Pre Op Care
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Preparation of patient
– General instructions – Antibiotics • To clean the bowel and reduce risk of peritoneal contamination by bowel contents • Often given Go-Lytely – NG • To empty stomach contents and secretions. • Prepare for colostomy – Be sure location is marked – Prepare psychologically |
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Types of Colon Surgeries
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hemicolectomy (rt. or left)
– anterior rectosigmoid resection – abdominoperineal resection (AP resection) |
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Ostomy surgery
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Ileostomy-Opening
between the ileum and abdominal wall • Colostomy-Opening between the colon and abdominal wall |
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Postop Care after Bowel Surgery
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Monitor bowel sounds!
– What will promote return of peristalsis? • Monitor stoma and/or incision – If AP resection, both abdominal and perineal incision, stoma. • Close monitoring of NG tube for patency – Facilitates healing of anastomosis. – Low suction (intermittent or continuous) • Sitz baths • Medicate for pain – Incisional and possibly phantom rectal pain Assess color, odor, and amt. of drainage from drains and colostomy; note changes – Would indicate a complication ie hemorrhage, obstruction, or infection • Initial drainage: may be bright red then become dark and finally clear or greenish yellow over first 2-3 days. • Avoid rectal temps, suppositories, enemas, etc. if rectum involved in surgery – To avoid disruption of anal suture line |
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Ostomy care
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Stoma –beefy red
• Keep stoma site clean & dry • Skin barrier to protect skin • Empty pouch frequently • Well balanced diet with adequate fluid intake • Avoid gas producing foods |
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Colorectal Cancer
Collaborative Care |
Biologic and targeted therapy
– Two monoclonal antibodies • Targets epidermal growth factor receptor – cetuximab (Erbitux) • Targets vascular endothelial growth factor – bevacizumab (Avastin) • Radiation therapy – May be used postop as an adjuvant to surgery and chemotherapy or as palliative for metastasis |
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Nursing Management
Nursing Implementation |
Health promotion
– American Cancer Society recommends starting at age 50 • Yearly fecal occult blood test or fecal immunochemical test • Double contrast enema every 5 years • Sigmoidoscopy every 5 years • Colonoscopy every 10 years Health promotion – Screening for high-risk patients should begin before age 50 and at more frequent intervals • Health promotion – Colonoscopy only detects polyps when bowel has been adequately prepared – Ingesting clear liquids for 24 hours before colonoscopy and using an oral preparation required before colonoscopy |
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Nursing Management
Nursing Implementation |
Acute intervention
– Postoperative care • Management differs depending on the type of wound • Type of management is individualized • If drains present, remain in place until drainage is less than 50 ml per 24 hours Drainage must be assessed for amount, color, consistency • Wound should be examined regularly – Record bleeding, excessive drainage, and odor • Monitor suture line for infection • Pain control • Sexual dysfunction education |
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Peptic Ulcer Disease (PUD)
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Erosion of GI mucosa resulting from digestive
action of HCl acid and pepsin Ulcer development can occur in – Lower esophagus – Stomach – Duodenum – Margin of gastrojejunal anastomosis after surgical procedures |
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Types of PUD
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Acute
– Superficial erosion –Minimal inflammation – Short duration, resolves quickly when cause is identified and removed Chronic – Muscular wall erosion with formation of fibrous tissue – Long duration—present continuously for many months or intermittently – Four times as common as acute erosion |
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Peptic Ulcer Disease
Etiology and Pathophysiology |
Develops only in presence of acid environment
• Excess of gastric acid not necessary for ulcer development • Stomach normally protected from autodigestion by gastric mucosal barrier • Surface mucosa of stomach is renewed about every 3 daysMucosa can continually repair itself except in extreme instances • Water, electrolytes, and water-soluble substances can pass through barrier • Mucosal barrier prevents back-diffusion of acid and pepsin from gastric lumen through mucosal layers to underlying tissue |
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Peptic Ulcer Disease
Etiology and Pathophysiology |
Destroyers of mucosal barrier
– Helicobacter pylori • Produces enzyme urease – Mediates inflammation making mucosa more vulnerable – Aspirin and NSAIDs • Inhibit syntheses of prostaglandins – Cause abnormal permeability – Corticosteroids • ↓Rate of mucosal cell renewal ↓Protective effects Lipid-soluble cytotoxic drugs • Pass through and destroy it • Destroyers of mucosal barrier (cont’d) – ↑Vagal nerve stimulation • Emotions • ↑in HCl acid |
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Gastric Ulcers
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Prevalent in women, older adults
• Peak incidence >50 years of age • Characterized by – Normal to low secretion of gastric acid • Some intraluminal acid essential Causes – Drugs • Aspirin, NSAIDs, corticosteroids – Chronic alcohol abuse – Chronic gastritis – Bile reflux – Nicotine • 60% to 80% present with H. pylori • H. pylori—more destructive when drugs or smoking involved |
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Duodenal Ulcers
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Occur at any age and in anyone
– ↑Between ages of 35 to 45 years • Account for ~80% of all peptic ulcers • Familial tendency – Person with blood group O ↑risk • Associated with increased HCl acid secretion • H. pylori is found in 90% to 95% of patients – Not all individuals with H. pylori develop ulcers Increased risk of duodenal ulcers in those with – COPD – Cirrhosis of liver – Chronic pancreatitis – Hyperparathyroidism Chronic renal failure – Zollinger-Ellison syndrome – Treatment for these conditions may promote ulcer development – Smoking and alcohol use |
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Peptic Ulcer Disease
Clinical Manifestations |
Common—no pain or
other symptoms – Due to lack of sensory pain fibers • If pain exists – Gastric ulcer pain • High in epigastrium • 1 to 2 hours after meals • Burning or gaseous Duodenal ulcer pain • Midepigastric region beneath xiphoid process • Back pain—if located posterior aspect • 2 to 4 hours after meals • Tendency to occur, then disappear, then occur again |
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Peptic Ulcer Disease
Hemorrhage (Complication) |
Most common complication of peptic ulcer
disease • Develops from erosion of – Granulation tissue found at base of ulcer during healing – Ulcer through a major blood vessel |
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Peptic Ulcer Disease
Perforation (Complication) |
Most lethal complication of peptic ulcer
• Common in large penetrating duodenal ulcers that have not healed and are located on posterior mucosal wall • Bacterial peritonitis may occur within 6 to 12 hours • Difficult to determine from symptoms alone if gastric or duodenal ulcer has perforated When ulcer penetrates serosal surface with spillage of contents into peritoneal cavity • Size proportional to length of time ulcer existed • Large perforations: Immediate surgical closure Clinical manifestations – Sudden, dramatic onset – Severe upper abdominal pain spreads throughout abdomen – Possible shoulder pain – Rigid, boardlike abdominal muscles Shallow, rapid respirations – Bowel sounds absent – Nausea/vomiting – History reporting symptoms of indigestion or previous ulcer |
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Peptic Ulcer Disease
Nursing Implementation • Perforation |
Sudden, severe abdominal pain unrelated in
intensity and location to pain that brought patient to hospital • Possibility of perforation – Indicated by a rigid, boardlike abdomen – Surgical or laparoscopic closure may be necessary if perforation does not heal spontaneously Severe generalized abdominal/ shoulder pain – Shallow, grunting respirations – Bowel sounds diminished or absent – Vital signs every 15 to 30 minutes – Stop all oral, NG feeds/drugs until health care provider notified – IV fluids may be increased to replace volume lost – Ensure any known allergies are reported on chart • Antibiotic therapy is usually started |
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Peptic Ulcer Disease
Nursing Implementation |
Gastric outlet obstruction
– Can occur at any time • Likely in patients whose ulcer is located close to pylorus – Gradual onset |
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Peptic Ulcer Disease
Therapy Related to Complications |
Perforation
– Immediate focus: • Stop spillage of gastric or duodenal contents into peritoneal cavity • Restore blood volume – NG tube is placed into stomach • Continuous aspiration • Placement of tube near to perforation site facilitates decompression Circulating blood volume: Replaced with lactated Ringer’s and albumin solutions – Blood replacement in form of packed RBCs may be necessary – Central venous pressure line inserted and monitored hourly – Indwelling urinary catheter inserted and monitored hourly – ECG—if history of cardiac disease Broad-spectrum antibiotics – Pain medication – Open or laparoscopic repair |
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Peptic Ulcer Disease
Gastric Outlet Obstruction |
Clinical manifestations
– Usually long history of ulcer pain – Pain progresses to generalized upper abdominal discomfort – Pain worsens toward end of day as stomach fills and dilates – Relief obtained by belching or vomiting – Vomiting is common Constipation is a common complaint • Dehydration, lack of roughage in diet – Swelling in stomach and upper abdomen – Loud peristalsis – Visible peristaltic waves – If stomach grossly dilated, may be palpable |
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Peptic Ulcer Disease
Therapy Related to Complications • Gastric outlet obstruction |
Decompress stomach
– Correct any existing fluid and electrolyte imbalances – Improve patient’s general state of health – NG tube inserted in stomach, attached to continuous suction Continuous decompression allows • Stomach to regain its normal muscle tone • Ulcer to begin to heal • Inflammation and edema to subside – After several days, NG clamped and residual volumes checked – Common to clamp tube overnight for 8 to 12 hours and measure residual in morning |
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Peptic Ulcer Disease
Therapy Related to Complications • Gastric outlet obstruction (cont’d) |
When aspirate below 200 ml
• Within normal range • Oral intake of clear liquids can begin – Watch patient carefully for signs of distress or vomiting – As residual ↓solid foods added and tube removed IV fluids and electrolytes • Administered according to degree of dehydration, vomiting, electrolyte imbalance – Pyloric obstruction: Endoscopically treated with balloon dilations – Surgery may be necessary to remove scar tissue |
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Peptic Ulcer Disease
Diagnostic Studies |
To determine presence and location of ulcer
• Endoscopy with biopsy – Most often used • Allows for direct viewing of mucosa – Determines degree of ulcer healing after treatment – During procedure, tissue specimens can be obtained to identify H. pylori and rule out gastric cancer |
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Tests for H. pylori
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Noninvasive tests
• Serum or whole blood antibody tests • Urea breath test – Urea is by product of metabolism of H. pylori – Can determine active infection • Stool antigen test – Not as accurate as breath test Invasive tests • Endoscopic procedure • Biopsy of stomach – Rapid urease test |
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Peptic Ulcer Disease
Diagnostic Studies |
Barium contrast studies
– Widely used – Not accurate for shallow, superficial ulcers – Used in diagnosis of gastric outlet obstruction X-ray studies – Ineffective in distinguishing a peptic ulcer from a malignant tumor – Do not show degree of healing like that of endoscope |
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Peptic Ulcer Disease
Diagnostic Studies |
Gastric analysis
– Analyze gastric contents for acidity and volume – NG tube is inserted, and gastric contents are aspirated – Contents analyzed for HCl acid Laboratory analysis – CBC • Anemia – Urinalysis – Liver enzyme studies – Serum amylase determination • Pancreatic function – Stool examination • Blood presence |
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Peptic Ulcer Disease
Collaborative Care |
Medical regimen consists of
– Adequate rest – Dietary modification – Drug therapy – Elimination of smoking and alcohol – Long-term follow-up care – Stress management Aim of treatment program – Reduce degree of gastric acidity – Enhance mucosal defense mechanisms – Minimize harmful effects on mucosa Complete healing may 3 to 9 weeks – Should be assessed by means of x-rays or endoscopic examination • Aspirin and nonselective NSAIDs may be stopped |
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Peptic Ulcer Disease
Drug Therapy |
Use of
– H2R blockers – PPIs – Antibiotics – Antacids – Anticholinergics – Cytoproctective therapy |
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Peptic Ulcer Disease
Nutritional Therapy |
Dietary modifications: Food and beverages
irritating to patient are avoided/eliminated: Hot, spicy foods and pepper, alcohol, carbonated beverages, tea, coffee, broth • Foods high in roughage may irritate mucosa • Bland diet • Six small meals a day during symptomatic phase |
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Peptic Ulcer Disease
Surgical Therapy |
Vagotomy
• Severing of vagus nerve • Done in conjunction with gastrectomy – Pyloroplasty • Surgical enlargement of pyloric sphincter • Commonly done after vagotomy • ↓Gastric motility and gastric emptying • If accompanying vagotomy, ↑gastric emptying |
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Peptic Ulcer Disease
Gerontologic Considerations |
↑Patients >60 years of age
– ↑Use of NSAIDs • First manifestation may be frank gastric bleeding or ↓ hematocrit • Treatment similar to younger adults • Emphasis placed on prevention of both gastritis and peptic ulcers |
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Diverticular Disease
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Diverticula-small out pouchings of
the colon • Incidence increases with age • Most patients are asymptomatic • Low fiber diet may be the cause • 2 types – Diverticulosis – Diverticulitis |
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Diverticulosis
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The presence of
diverticula • Usually asymptomatic • About 15% of patient progress to diverticulitis |
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Diverticulitis
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Inflammation of diverticular
sac • Symptoms – Abdominal pain over involved area of colon – Tender left lower quadrant • Diagnosis – CT scan with oral contrast – Barium enema – Colonoscopy-r/o polyps |
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Diverticular Disease Tx
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Uncomplicated diverticular disease
– High fiber diet – Bulk laxatives – Increase po fluids • Acute diverticulitis – Bowel rest (NPO with IV fluids or TPN) – Oral antibiotics (Flagyl, Cipro, Bactrim) – Pain management |
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Irritable Bowel Syndrome (IBS)
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Motility disorder of lower GI tract-Characterized by intermittent
and recurrent abdominal pain and stool pattern irregularities • Abdominal pain – Relieved by defecation – Intermittent and colicky, dull and continuous – Abdominal bloating and flatulence • Altered bowel elimination – Constipation – Diarrhea – Mucous stools |
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IBS
Psychosocial Factors in IBS |
Common in patients with IBS
– Anxiety, panic disorder – Depression – Post-traumatic stress disorder – Abuse history • Stress can exacerbate stress symptoms • May influence health care seeking behavior |
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IBS
Diagnostic Studies |
No specific findings
• Diagnosis made based on symptoms and ruling out other conditions • Physical examination • Past health history – Psychosocial factors – Family history – Drug/diet history Standardized symptom-based criteria (Rome II criteria) – Abdominal discomfort/pain for at least 12 weeks (not necessarily consecutive) within 12 months with at least two of following characteristics • Relieved with defecation • Onset associated with change in stool frequency • Onset associated with change in stool appearance |
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IBS
Collaborative Care |
Diet modification
• Fiber therapy (20 g/day) • Antispasmodics • Antidiarrheals • Laxatives • Serotonergic agents • Antidepressants |
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IBS
Nutritional Therapy |
Eliminate gas-producing foods
– Brown beans – Brussels sprouts, cabbage, cauliflower, raw onions – Grapes, plums, raisins – Eliminate fructose, sorbitol • Determine if lactose intolerant |
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IBS
Drug Therapy: Antispasmodics |
Anticholinergics
– Dicyclomine (Bentyl) – Reduce colonic motility after meals – Take before meals – Side effects • Dry mouth, urinary retention, tachycardia |
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IBS
Drug Therapy: Antidiarrheals Drug Therapy: Antidepressants |
Loperamide (Imodium)
– Decrease intestinal transit – Enhances intestinal water absorption and sphincter tone Antidepressant:Symptomatic treatment: Pain – Reserved for patients with severe or refractory pain |
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IBS
Drug Therapy: Serotonin Agonist |
5-HT3 receptor blockers
– ↓ Urgency, pain, and diarrhea in diarrheaprominent women – Alosetron (Lotronex) • FDA approved for women only • Must be monitored due to potential side effects Tegaserod (Zelnorm) – Used in women with constipation- predominant IBS – Current widespread use suspended by FDA • March, 2007 – May be released for use again with close monitoring |
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Similarities in Crohn’s and UC
|
Cause unknown
• Exacerbation's and remissions • Effects young adults • Stress symptoms – Decreased intake or absorption of nutrients – Abdominal cramps – Diarrhea |
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Ulcerative Colitis
|
Diffuse inflammation
– Begins in rectum and distal colon and spreads upward • Affects mucosal layer • Symptoms – Bloody diarrhea – Abdominal cramping and distention – Weight loss – Anorexia, nausea, vomiting • Surgery is curative |
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Crohn’s Disease
|
Inflammation of segments of the
bowel, mainly in the terminal ileum – “Skip lesions” • Affects ALL layers of bowel wall • Symptoms – Diarrhea (nonbloody) – Abdominal pain, distention – Weight loss – Anorexia, nausea, vomiting • No surgical cure |
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Differences Crohn's VS UC
|
Crohn’s
– Segments of bowel are inflamed – Fatty stools – Fistulas, fissures – May recur after surgery Ulcerative colitis – Continuous inflammation – Bloody stools – Hemorrhage – Surgery curative |
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Management goals
|
Decrease inflammation
• Rest the inflammed bowel • Correct nutritional deficiencies • Correct fluid and electrolyte imbalances • Control diarrhea • Manage abdominal pain and cramping |
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Management
|
Medications
– Azulfidine (Sulfasalazine) – Corticosteroids (Prednisone) – Immunomodulators (Remicade) • Surgery – Proctocolectomy – Total colectomy |
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Exacerbations and remissions
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Crohn's and Ulcerative Colitis
|
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Segments of bowel are inflamed (skip
lesions), affecting all layers of the bowel |
Crohns
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Continuous colitis affecting mucosal
layer |
Ulcerative Colitis
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Surgery is curative
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Ulcerative colitis
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Can have 10-20 liquid, bloody stools
per day |
Ulcerative colitis
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Diarrhea and abdominal
cramps/pain |
Crohns and Ulcerative Colitis
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Peritonitis
|
Inflammation of peritoneum
• Caused by – Appendicitis with rupture – Trauma to abdominal organs – Ruptured diverticuli – Pancreatitis – Perforated peptic ulcer – Peritoneal dialysis – Postop abdominal surgery |
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Peritonitis
|
Inflammation of peritoneum results in:
– Fluid shift ie 3rd spacing – Increased circulation to inflamed area causing a decreased circulating blood volume – Respiratory problems – Abd pressure and pain, slowed peristalsis • abdomen tender with guarding • boardlike, rebound tenderness • Possible bacteremia and septicemia shock |
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Manifestations of Peritonitis
|
Severe abdominal pain
– Generalized or localized – Worse with movement – Tenderness with guarding • Abdominal distension • N/V, anorexia • Low-grade fever • Absent or diminished bowel sounds |
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Management of Peritonitis
|
Broad spectrum antibiotics
• Pain meds • NPO, NG, IV fluids • May require surgery • Fluid and GI assessment • Watch renal function! WHY? |
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Intestinal Obstructions
|
Mechanical
– Small bowel obstruction – Large bowel obstruction • Nonmechanical – Paralytic ileus most common |
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Diagnostic Studies - Intestinal obstruction
|
CBC
• Electrolytes • Abdominal x-ray • Endoscopy • CT |
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Tube Feeding
|
Feedings can be started when bowel
sounds are present, usually 24 hours after placement • Immediately after insertion, tube length from insertion site to distal end should be measured and recorded • Tube should be marked at skin insertion site • Insertion length should be checked regularlyTube feeding administration – Patient position • Patient should be sitting or lying with HOB at 30 to 45 degrees • HOB remains elevated for 30 to 60 minutes for intermittent delivery – Tube patency • Irrigated with water before/after each feeding, drug administration, residual checks • Continuous feedings administered on feeding pump with occlusion alarm |
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Tube Feeding
|
Tube position
• Placement checked before each feeding/drug administration or every 8 hours with continuous feeds • Methods used to check placement – Aspiration of stomach contents – pH check » pH less than 5: Indicative of stomach – Most accurate assessment: X-ray visualization • Check gastric residual volumes – ↑Volume leads to aspiration Formula • Before feeding – Aspirate gastric contents and measure amount » Volume greater than 150 ml and clinical signs of intolerance—feeding held for 1 hour and residual rechecked » Residual should be given back to patient • Room/body temperature |
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Tube feeding
General Nursing Considerations |
Daily weights
• Assess for bowel sounds before feedings • Accurate I&O • Initial glucose checks • Label with date and time started • Feedings infusing >8 hours discarded • Pump tubing changed q24h |
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Tube Feeding
• Complications |
Vomiting
– Diarrhea – Constipation – Dehydration • More calorically dense, less water • Check for high protein content |
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Gastrostromy or jejunostomy feedings
• Two potential problems |
Skin irritation
– Skin assessment – Skin care • Pulling out of tube – Education to patient/family regarding feeding administration, tube care, and complications |
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Tube Feeding
• Gerontologic considerations |
More vulnerable to complications
• Fluid and electrolyte balances • Glucose intolerance • Decreased ability to handle large volumes • Increased risk of aspiration |
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Esophageal Varices
|
Dilated veins in
esophageal wall • Occur 2o to hepatic cirrhosis, common in EtOH abusers • Obstruction of hepatic portal blood flow results in dilation, thinning of esophageal veins |
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Esophageal Varices
• Portal hypertension |
Hepatic scarring slows
blood flow – Blood backs up in portal circulation – Pressure rises – Vessels in portal circulation become distended |
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Esophageal Varices
• Signs and Symptoms |
Hematemesis (usually bright red)
– Nausea, vomiting – Evidence of hypovolemia – Melena (uncommon) |
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Diagnostic tests for UGI Bleed
|
Upper GI Endoscopy
Esophagogastroduodenoscopy (EGD)- direct observation – Pre • NPO • Consent • Preop med if ordered – Post • NPO until gag reflex returns • Warm saline gargles for sore throat |
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Management of UGI Bleeds
|
Nasogastric (NG) tube to evacuate contents
• Lavage the stomach – cold water or not; saline • Vasopressin (ADH), a vasoconstrictor • Clotting or sclerosing agent into bleeding vessel • Laser or electric coagulation • IV fluids • Treat underlying cause |
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Esophageal Cancer
|
Adenocarcinomas
– Arise from glands lining esophagus – Resemble cancers of stomach and small intestine – 30% to 70% of esophageal cancers – Incidence in distal esophagus currently ↑ • Squamous cell – Incidence currently ↓in United States |
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Esophageal Cancer
Etiology and Pathophysiology |
Cause is unknown
• Incidence ↑ with age • ↑Incidence in African Americans and Alaska Natives |
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Esophageal Cancer
Etiology and Pathophysiology |
Risk factors
– Smoking – Excessive alcohol intake – Barrett’s esophagus – Diets low in fruits and vegetables – Exposure to lye, asbestos, and metal Majority of tumors located in middle and lower portion of esophagus • Malignant tumor – Usually appears as ulcerated lesion – May penetrate muscular layer and outside wall of esophagus – Obstruction in later stages |
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Esophageal Cancer
Clinical Manifestations |
Symptom onset is late
• Progressive dysphagia is most common – Initially with meat, then soft foods and liquids • Pain develops late – Substernal, epigastric, or back areas • Increases with swallowing • May radiate Weight loss • Regurgitation of bloodflecked esophageal contents • If tumor is in upper third of esophagus – Sore throat – Choking – Hoarseness |
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Esophageal Cancer
Complications |
Hemorrhage
– If erodes into aorta • Esophageal perforation with fistula formation • Esophageal obstruction • Metastasis – Liver and lung common |
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Esophageal Cancer
Diagnostic Studies |
Endoscopy with biopsy
– Necessary for definitive diagnosis • Endoscopic ultrasonography (EUS) – Important tool to stage • Barium swallow with fluoroscopy Bronchoscopic examination – Detect involvement of lung • Computed tomography (CT) • Magnetic resonance imaging (MRI) |
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Esophageal Cancer
Collaborative Care |
Treatment depends on location and spread
• Poor prognosis-Usually not diagnosed until advanced • Best results with combination therapy • Photodynamic and/or laser therapy – Used to ablate mucosal adenocarcinoma • Endoscopic mucosal resection (EMR) – Removes superficial lesions – Submucosal neoplasms |
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Esophageal Cancer
Collaborative Care |
Surgical procedures
– Esophagectomy • Removal of part or all of the esophagus • Use of Dacron graft to replace resected part – Esophagogastrostomy • Resection of a portion of esophagus and anastomosis of remaining portion to stomach • Surgical procedures – Esophagoenterostomy • Resection of a portion of esophagus and anastomosis of segment of colon to remaining portion • May be open or laparoscopic |
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Esophageal Cancer
Collaborative Care |
Concurrent radiation and chemotherapy
– Slows progression – Sometimes started before surgery • Nutritional therapy – After surgery, parenteral fluids given – Jejunostomy feeding tube may be used – Swallowing study may be done before patient can have oral fluids |
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Hiatal Hernia
|
Herniation of portion of the stomach into
esophagus through an opening or hiatus in diaphragm • Also referred to as diaphragmatic hernia and esophageal hernia • Most common abnormality found of x-ray of upper GI • More common in older adults and in women |
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Hiatal Hernia
Etiology and Pathophysiology |
Cause is unknown
• Many factors involved – Structural changes • Weakening of muscles in diaphragm – Increased intraabdominal pressure • Obesity • Pregnancy • Heavy lifting Many factors involved – Increasing age – Trauma – Poor nutrition – Forced recumbent position – Congenital weakness |
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Hiatal Hernia
Clinical Manifestations |
May be asymptomatic
• Symptoms include – Heartburn • After meal or lying supine – Dysphagia |
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Hiatal Hernia
Complications |
GERD
• Esophagitis • Hemorrhage from erosion • Stenosis • Ulcerations of herniated portion • Strangulation of hernia Ulcerations of herniated portion • Strangulation of hernia • Regurgitation with tracheal aspiration • Increased risk of respiratory problems |
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Hiatal Hernia
Diagnostic Studies |
• Barium swallow
– May show protrusion of gastric mucosa through esophageal hiatus • Endoscopy – Visualize lower esophagus – Information on degree of inflammation or other problems |
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Hiatal Hernia
Conservative Therapy |
Lifestyle modifications
– Eliminate alcohol – Elevate HOB – Stop smoking – Avoiding lifting/straining – Weight reduction, if appropriate |
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Hiatal Hernia
Surgical Therapy |
Reduction of herniated stomach into abdomen
Example: Herniorrhaphy • Closure of hiatal defect • Laparoscopically performed Nissen and Toupet techniques are standard antireflux surgeries • Goals – Reduce hernia – Provide acceptable lower esophageal sphincter (LES) pressure – Prevent movement of gastroesophageal junction |
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Hiatal Hernia
Gerontologic Considerations |
↑Incidence with age
• Medications commonly taken by older patients can ↓ LES pressure • LES may become less competent with aging • First indications may be esophageal bleeding or respiratory complications |
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GERD
Etiology and Pathophysiology |
Obesity is a risk factor
• Pregnant women are at increased risk • Cigarette and cigar smoking can contribute to GERD • Hiatal hernia is a common cause of GERD |
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GERD
Clinical Manifestations |
Symptoms of GERD
– Heartburn (pyrosis) • Most common clinical manifestation • Burning, tight sensation felt beneath the lower sternum and spreads upward to throat or jaw • Felt intermittently • Relieved by milk, alkaline substances, or water – Dyspepsia • Pain or discomfort centered in upper abdomen – Noncardiac chest pain • More common in older adults Regurgitation – Effortless return of food or gastric contents from stomach into esophagus or mouth – Described as hot, bitter, or sour liquid coming into the mouth or throat |
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GERD
Clinical Manifestations |
Individual may also
report – Wheezing – Coughing – Dyspnea – Hoarseness – Sore throat – Lump in throat – Choking – Regurgitation • Gastric symptoms such as – Early satiety, postmeal bloating, nausea, and vomiting – Related to delayed gastric emptying |
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GERD
Complications |
Related to direct local effects of gastric acid
on esophageal mucosa – Esophagitis • Inflammation of esophagus • Frequent complication • Other risk factors include hiatal hernia, chemical irritation • Repeated exposure—esophageal stricture – Resulting in dysphagia Barrett’s esophagus • Replacement of normal squamous epithelium with columnar epithelium • Precancerous lesion • Diagnosed in 10% to 15% of patients with chronic reflux • Signs and symptoms: None to perforation • Must be monitored every 1 to 3 years by endoscopy |
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GERD
Complications |
Respiratory
– Due to irritation of upper airway by secretions • Cough, Bronchospasm, Laryngospasm – Potential for asthma, bronchitis, and pneumonia • Dental erosion – From acid reflux into mouth – Especially posterior teeth |
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GERD
Diagnostic Studies |
History and PE
• Barium swallow – Can detect protrusion of gastric fundus • Upper GI endoscopy – Useful in assessing LES competence – Degree of inflammation, scarring, strictures Biopsy and cytologic specimens – Differentiate carcinoma from Barrett’s esophagus • Esophageal manometric (motility) studies – Measure pressure in esophagus and LES • Radionuclide tests – Detect reflux of gastric contents – Rate of esophageal clearance |
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GERD
Diagnostic Studies |
Monitoring pH
– Laboratory or 24-hour ambulatory – Determine esophageal pH using specially designed probes • High-dose proton pump inhibitor treatment for 2 weeks can be used as a first step in diagnosis of GERD |
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GERD
Collaborative Care • Drug therapy |
Histamine (H2)-receptor blockers
• Decrease secretion of HCl acid • Reduce symptoms and promote esophageal healing in 50% of patients • Side effects uncommon – Pepcid, Zantac, Tagamet – Acid protective • Used for cytoprotective properties – Sucralfate (Carafate)Proton pump inhibitors (PPI) • Decrease gastric HCl acid secretion • Promote esophageal healing in 80% to 90% of patients • May be beneficial in ↓ esophageal strictures • Headache: Most common side effect – Prilosec, Nexium, Aciphex – Antacids • Quick but short-lived relief • Neutralize HCl acid • Taken 1 to 3 hours after meals/bedtime – Maalox, Mylanta |
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GERD
Collaborative Care • Drug therapy (cont’d) |
Cholinergic
• Increase LES pressure • Improve esophageal emptying • Increase gastric emptying • Negative: Stimulate HCl acid secretion – Bethanechol (Urecholine) – Prokinetic drugs • Promote gastric emptying • Reduce risk of gastric acid reflux – Metoclopramide (Reglan |
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GERD
Collaborative Care • Surgical |
Surgical therapy
– Necessary if • Conservative therapy fails • Hiatal hernia present • Esophageal stricture and stenosis • Chronic esophagitis • Bleeding – Reduce reflux of gastric contents by enhancing integrity of LES – Most performed laparoscopically – Nissen fundoplication |
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GERD
Gerontologic Considerations |
↑ Incidence with age
• Medications commonly taken by older patients can ↓ LES pressure • LES may become less competent with aging • First indications may be esophageal bleeding or respiratory complications |
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Gastritis
|
Inflammation of gastric mucosa
• One of most common problems affecting the stomach • Result of a breakdown in gastric mucosal barrier • Stomach tissue unprotected from autodigestion by HCl acid and pepsinTissue edema results • Disruption of capillary walls – With loss of plasma into gastric lumen – Possible hemorrhage |
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Gastritis
Etiology and Pathophysiology |
Risk factors
– Drugs • Direct irritating effect on gastric mucosa • Aspirin, NSAIDs, and corticosteroids – Microorganisms • Helicobacter pylori – Important cause of chronic gastritis – Promotes breakdown of gastric mucosal barrier • Staphylococcus organisms – Environmental factors • Radiation, smoking – Pathophysiologic conditions • Burns, renal failure, sepsis – Other factors • Psychologic stress, NG tube – Diet • Alcohol, spicy food |
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Gastritis
Clinical Manifestations |
Anorexia
– Nausea – Vomiting – Epigastric tenderness – Feeling of fullness – Hemorrhage • Common with alcohol abuse • May be only symptom |
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Liver Review
|
Largest internal organ
Located in RUQ 1500 ml blood flow through Q minute Blood supply from hepatic artery and hepatic portal vein Performs 400 functions Affects every system in the body Deoxification (ETOH, opiods, sedatives) Forms prothrombin and some clotting factors Bilirubin metabolism Converts the bilirubin from destroyed RBCs to a water soluble form that can be excreted |
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Liver Function- 3 Catergories
|
Storage
Protection Metabolism (400 functions in three categories) |
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Storage- Function
|
Stores of several minerals and vitamins
Copper Iron Magnesium Vitamin B 12 and B 6, Folic Acid Niacin Fat soluble vitamins A, D, E, and K |
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Protection- Function
|
Phagocytic Kupffer’s cells
(specialized liver cells) Engulfs harmful bacteria Engulfs anemic RBC Also, detoxifies potentially harmful compounds (drugs, chemicals, ETOH) |
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Metabolism- Function
|
Fat metabolism
Converts fatty acid into energy & ketones Produces bile CHO metabolism Converts glucose to glycogen for storage Protein metabolism Amino acids and ammonia Ammonia – Urea- Excreted via kidneys Synthesizes blood protein (albumin/globulin) |
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Hepatitis
|
Inflammation of the liver
Viral hepatitis (acute or chronic) Most common cause- Types of infectious viral hepatitisA, B, C, D, E, F- very uncommon/ Controversial, G- very uncommon |
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Hepatitis
Etiology |
Causes
A, B, C, D, E, and G virus Cytomegalovirus Epstein-Barr virus Herpes virus Coxsackievirus Rubella virus |
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Pathophysiology of Hepatitis
Acute Infection |
Liver becomes enlarged and congested
with inflammatory cells, lymphocytes, and fluid. Liver damage mediated by Cytotoxic cytokines Natural killer cells Liver cell damage results in hepatic cell necrosis |
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Pathophysiology of Hepatitis
Acute Infection |
Liver becomes distorted as result of
widespread inflammation, necrosis, and heptaocellular regeneration. Proliferation and enlargement of Kupffer cells Inflammation of the periportal areas may interrupt bile flow Cholestasis may occur The increase in pressure with the portal circulation, interfering with blood flow. Liver cells can regenerate with time and if no complications occur- resume their normal appearance and function |
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Hepatitis
Clinical Manifestations |
Acute phase
Lasts from 1 to 4 months May be icteric (symptomatic) or anicteric Physical exam may reveal hepatomegaly, lymphadenopathy and splenomegaly During incubation, symptoms include Malaise Anorexia Fatigue Nausea Occasional vomiting Abdominal discomfort Headache Low-grade fever Arthralgias Skin rashes |
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Hepatitis
Clinical Manifestations |
Urine darkens due to excess bilirubin being
excreted If bilirubin cannot flow out of liver, stool will be light or clay-colored Jaundice Results when bilirubin diffuses into tissues Pruritus can accompany jaundice Accumulation of bile salts beneath the skin When jaundice occurs, fever subsides Liver usually enlarged and tender Convalescent phase Begins as jaundice is disappearing Lasts weeks to months Major complaints Malaise Easy fatigability |
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Hepatitis A Virus (HAV)
Etiology |
Transmitted fecal–oral route, parenteral
(rarely) RNA virus Frequently occurs in small outbreaks 61,000 cases occur annually in the United States 10 million cases occur worldwide Nearly universal during childhood in developing countries Hepatitis A virus (HAV) Found in feces 2 or more weeks before the onset of symptoms and up to 1 week after the onset of jaundice Present in blood briefly No chronic carrier state |
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Hepatitis A Virus (HAV)
Etiology |
Hepatitis A virus (HAV)
Anti-HAV immunoglobulin M (IgM) Appears in the serum as the stool becomes negative for the virus Detection of IgM anti-HAV indicates acute hepatitis Anti-HAV immunoglobulin G (IgG) IgG anti-HAV: Indicator of past infection Presence of IgG antibody provides lifelong immunity |
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Hepatitis B Virus (HBV)
Etiology |
DNA virus
Transmission of HBV-Transmission occurs when infected blood/body fluids enter the body Sexually transmitted disease More infectious than HIV Can live on a dry surface for 7 days Kissing/sharing food items may spread the virus via saliva Perinatally by mothers infected Percutaneously (IV drug use) |
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Hepatitis B Virus (HBV)
Etiology |
Hepatitis B virus
Presence of hepatitis B surface antibodies Indicates immunity from HBV vaccine Past HBV infection With chronic infection, liver enzyme values may be normal or 15% to 25% of chronically infected persons die from chronic liver disease 30% of patients with HBV are asymptomatic |
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Hepatitis C virus (HCV)
Etiology |
RNA virus
Transmitted percutaneously Risk factors IV drug use Most common mode of transmission in United States and Canada Blood transfusions Transmission <1 per 1 million blood transfusions High-risk sexual behavior Hemodialysis Occupational exposure Perinatal transmission |
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Hepatitis C virus (HCV)
Statistics |
Approximately 170 million people are infected
with the hepatitis C virus (HCV) About 30,000 new cases diagnosed annually 8000 to 10,000 people in the United States die each year from complications of end-stage liver disease 2nd to HCV About 30% to 40% of HIV-infected patients also have HCV 80% of patients with acute HCV will be asymptomatic Up to 10% of patients with HCV cannot identify a source Additional data needed regarding risk of body piercings, tattooing, and intranasal drug use in transmission of HCV |
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Hepatitis D virus (HDV)
Etiology |
Also called delta virus
Defective single-stranded RNA virus Cannot survive on its own Requires the helper function of HBV to replicate |
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Hepatitis
Complications |
Most patients with acute viral hepatitis
recover completely with no complications Overall mortality rate <1% Chronic hepatitis Cirrhosis Hepatocellular carcinoma Fulminant hepatitis Results in severe impairment or necrosis of liver cells and potential liver failure Develops in small percentage of patients Occurs because of Complications of hepatitis B Toxic reactions to drugs and congenital metabolic disorders |
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Jaundice
|
Caused by diseased liver cells
Obstruction of bile duct Bile absorbed into blood Skin, mucous membranes and sclera stained Urine becomes orange and foamy Stools light colored or clay colored Puritis |
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Jaundice
|
A deposition of bile pigment due to an
abnormally elevated concentration of bilirubin Seen when serum bilirubin > 2.5 mg/dL Causes Excessive destruction of RBCs Bilirubin is the final breakdown product of hemeglobin Caused By Diseased Liver Cells Hepatocellular Obstruction Of Bile Duct Extrahepatic obstructive |
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Hepatitis
Diagnostic Studies |
History
Physical assessment findings Hepatic tenderness Hepatomegaly Splenomegaly Palpable liver Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) g-Glutamyl transpeptidase (GGT) Alkaline phosphatase Prothrombin time Biopsy If diagnosis is in doubt Chronic hepatitis |
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Hepatitis
Diagnostic Studies |
Serum proteins
Serum bilirubin Urinary bilirubin Urinary urobilinogen Sonograms (Fibroscan) Determining degree of liver scarring |
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Hepatitis
Diagnostic Studies Hep C |
Hepatitis C
Several tests available Antibodies to HCV are not protective May be indicator of chronic disease Anti-HCV antibody test by immunoassay If positive Confirmatory testing must be done Six genotypes and 50 subtypes of HCV Genotyping: Important role in managing infection One of the strongest predictors of response to therapy and influences duration of treatment Should be determined before drug therapy started |
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Hepatitis
Collaborative Care |
Prevention
Hepatitis A Hepatitis A vaccine Preexposure prophylaxis IM in deltoid Immune globulin (IG) Pre/post exposure Temporary passive immunity Hepatitis B Immunization Most effective method Part of routine vaccination schedules for newborns, adolescents, and adults in major risk groups Recombivax HB, Engerix-B |
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Hepatitis
Collaborative Care |
Hepatitis B
Immunization (cont’d) Recombinant DNA using HBsAg Promotes synthesis of specific antibodies against hepatitis B Series of three IM injections given at 0–1–6 month intervals More than 95% effective |
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Hepatitis
Collaborative Care |
Prevention
Hepatitis B Hepatitis B immune globulin (HBIG) Used for postexposure with vaccine Contain antibodies to HBV Should be given within 24 hours of exposure |
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Hepatitis
Collaborative Care |
Prevention
Hepatitis C No vaccine to prevent HCV CDC does not recommend IG or antiviral agents for postexposure prophylaxis |
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Hepatitis
Collaborative Care |
No specific treatment or therapy for
acute viral hepatitis Most patients can be managed at home Emphasis on resting the body and receiving adequate nutrients |
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Hepatitis
Collaborative Care |
Drug therapy
No specific drug therapies Support therapy Antiemetics Dimenhydrinate (Dramamine) Trimethobenzamide (Tigan) Phenothiazines should not be used If requires sedative or hypnotic, diphenhydramine (Benadryl) or chloral hydrate may be used |
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Hepatitis
Collaborative Care |
Drug therapy for chronic hepatitis B
Focused on Viral load Liver enzyme levels Rate of disease progression Rate of drug-resistant HBV Long-term goals Prevention of cirrhosis and liver cancer Not all patients respond to current therapeutic regimensDrug therapy for chronic hepatitis B -Interferon Multiple effects on viral replication cycle Must be administered subcutaneously Side effects: Flu like symptoms, depression, hair thinning, diarrhea, insomnia Nucleoside analogs When active viral replication exists Inhibit viral DNA synthesis Lamivudine (Epivir) Taken for 1 year |
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Hepatitis
Collaborative Care |
Drug therapy for chronic hepatitis C
Directed at eradicating virus Reducing viral load Decreasing progression of disease Treatment Pegylated -interferon with ribavirin (Rebetol, Copegus) Ribavirin side effects: Anemia, anorexia, cough, rash, pruritus, dyspnea, insomnia, teratogenicity |
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Hepatitis
Collaborative Care |
Nutritional therapy
No special diet Vitamins (B-complex and vitamin K) Low-fat Adequate calories |
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CIRRHOSIS:
Degeneration of Liver Tissue |
A chronic progressive
disease characterized by destruction of liver cells and the replacement of connective tissue by scar tissue and fibrous bands |
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Hepatitis
Clinical Manifestations |
Almost all cases of hepatitis A resolve
Absence of jaundice does not mean recovery General considerations Not all patients with hepatitis virus have jaundice Termed anicteric hepatitis |
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TYPES OF CIRRHOSIS
|
Alcoholic (Laënnec’s,
portal, fatty) Also known as portal, nutritional or fatty Most common type Associated with longterm alcohol use Alcohol has a toxic effect on the liver liver inflammation Post-necrotic Necrosis from infections Often a complication of acute viral hepatitis May follow exposure to industrial or chemical hepatotoxins Post-necrotic Necrosis from infections Often a complication of acute viral hepatitis May follow exposure to industrial or chemical hepatotoxins |
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TYPES OF CIRRHOSIS
|
Biliary/Obstructive
A result of chronic biliary obstruction, bile stasis, inflammation or diffuse hepatic fibrosis Cardiac Also known as vascular Associated with rsided heart failure Venous congestion anoxia cell necrosis |
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Etiology
|
Exact factors are not clearly defined
There may be a genetic component Cause varies with the type of cirrhosis Chronic infection with hepatitis B virus is a common cause as is long-term alcohol use |
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|
Diagnosis of Cirrhosis
|
Symptoms
LFTs X-ray – hepatomegaly UGI – varices CT – ascites EGD – varices Liver scan – masses, hepatic thickening |
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|
Manifestations of cirrhosis
|
Elevated liver
enzymes: AST (SGOT) ALT (SGPT) ALP GGT Decreased Serum protein Serum albumin Other elevated liver function tests (LFTs): LDH Bilirubin Prothrombin time (PT) (INR) Partial Thromboplastin time (APTT or PTT) Globulins Ammonia |
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|
Symptoms
|
Early
Mild RUQ pain (progressively worsens) GI symptoms Anorexia Indigestion Dyspepsia Weight loss N/V (may be bloody) Diarrhea/constipation Flatulence Fatigue even with light exertion Generalized weakness Fever Increased bleeding, petechiae, ecchymosis Dry skin Palmar erythema Spider angiomas Nose, cheeks, upper thorax, shoulders |
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Cirrhosis
Clinical Manifestations |
Jaundice
Decreased ability to conjugate and excrete bilirubin by liver cells Functional derangement of liver cells Compression of bile ducts by overgrowth of connective tissue Minimal or severe depending on liver damage Late stages of cirrhosis Patient will usually be jaundiced Pruritus from accumulation of bile salts Skin lesions Due to increase in circulating estrogen from liver’s inability to metabolize steroid hormones Spider angiomas Small dilated blood vessels with bright red center and spiderlike branches Nose, cheeks, upper trunk, neck, shoulders Palmar erythema Red area on palms of bands that blanches with pressure |
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Cirrhosis
Clinical Manifestations |
Endocrine disorders
Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver Damaged liver is unable to metabolize these hormones and various manifestations occur Alteration in hair distribution due to estrogen Hyperaldosterism Sodium retention/potassium loss |
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Cirrhosis
Clinical Manifestations |
Hematologic disorders
Splenomegaly From backup of blood from portal vein Bleeding tendencies Decreased production of hepatic clotting factors Peripheral neuropathy Dietary deficiencies of thiamine, folic acid, and vitamin B12 |
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Cirrhosis
Complications Portal hypertension |
Characterized by
Increased venous pressure in portal circulation Splenomegaly Ascites Large collateral veins Esophageal varices Systemic hypertensionPrimary mechanism is the increased resistance to blood flow through the liver Persistent pressure in portal vein Causes dilation of veins of portal venous system |
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Cirrhosis
Complications Esophageal varices |
dilated esophageal veins
Complex of tortuous veins at lower end of esophagus Develop in areas where collateral and systemic circulations communicate Prone to bleeding Chemical irritants Mechanical trauma pressure in esophagusContain little elastic tissue and are fragile Bleeding esophageal varices Most life-threatening complication of cirrhosis 80% of variceal hemorrhages |
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Cirrhosis
Complications Gastric varices |
Located in upper portion of stomach
20% of variceal hemorrhages |
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|
Cirrhosis
Complications Peripheral edema and ascites |
Edema
Colloidal oncotic pressure from impaired liver synthesis of albumin Portacaval pressure from portal hypertension Occurs as ankle/presacral edemaAscites Accumulation of serous fluid in peritoneal or abdominal cavity Abdominal distention with weight gain Common manifestation of cirrhosis |
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|
Cirrhosis
Collaborative Care Ascites |
High-carbohydrate, low-Na+ diet
(2 g/day) Diuretics Paracentesis Removes fluid from abdominal cavity Temporary measurePeritoneovenous shunt Continuous reinfusion of ascitic fluid from the abdomen to the vena cava Not first-line therapy Complications—thrombosis, infection, fluid overload, DIC |
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Cirrhosis
Complications Encephalopathy (hepatic coma) |
Also known as portal system encephalopathy
Most probable cause is ammonia levels Precipitating factors High protein diet Infections Hypovolemia Hypokalemia Constipation Drugs: hypnotics, opioids, sedatives, analgesics, diureticsGoal: Decrease ammonia formation Sterilization of GI tract with antibiotics (e.g., neomycin) Lactulose (Cephulac) traps NH3 in gut Cathartics/enemas |
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|
Cirrhosis
Complications Hepatorenal syndrome |
Hepatorenal syndrome
Progressive oliguric renal failure Left untreated, median survival of less than 2 weeks Treatment aimed at Improving liver function Maintaining blood volume Maintaining cardiac output Dialysis Medications such as octreotide, albumin, and dopamine |
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Cirrhosis Complications
|
Internal hemorrhoids
Occur because of the dilation of the mesenteric veins and rectal veins Caput medusae Ring of varices around the umbilicusJaundice Hepatocellular disease Intrahepatic obstruction Coagulation defects ¯ absorption of vitamin K due to ¯ bile ¯ clotting factors |
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Cirrhosis Nutritional Therapy
|
Diet for patient without complications
High in calories (3000 kcal/day) CHO Moderate to low fat Protein restriction rarely justified Protein supplements if protein-calorie malnutrition Low-sodium diet for patient with ascites and edema |
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|
Cirrhosis
Collaborative Care |
Nonsurgical procedure
Transjugular intrahepatic portosystemic shunt (TIPS) Tract (shunt) between systemic and portal venous system Used to redirect portal blood flow Decreases portal venous pressure and decompresses varices |
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Cirrhosis
Collaborative Care |
Surgical procedures
Used more in emergency situations Portacaval shunt Decreases bleeding episodes Does not prolong life; patient dies of hepatic encephalopathy Distal splenorenal shunt (Warren shunt) Leaves portal venous flow intact Incidence of hepatic encephalopathy With time blood flow to liver |
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Nursing Diagnoses
Alteration in Thought Processes (Liver failure) |
Hepatic coma/encephalopathy
LOC changes Later signs: Asterixis (liver flap) Fetor hepaticus Convulsions and coma |
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|
Rx for Increased Ammonia
(NH3) |
Low protein or no protein diet
Lactulose (Cephulac) Neomycin High cleansing enema Neuro assessments Protect from injury |
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Nursing Management
Nursing Implementation Bleeding varices |
Bleeding varices
Close observation for signs of bleeding Balloon tamponade care Explanation of procedure Check for patency Position of balloon verified by x-ray Deflation of balloon q8–12h Lumens labeledBalloon tamponade (cont’d) Saline lavage/NG suction to remove blood Monitor for complications Most common—aspiration pneumonia Scissors at bedside Semi-Fowler’s position Oral/nasal care |
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Nursing Management
Nursing Implementation Hepatic encephalopathy |
Hepatic encephalopathy
Maintain safe environment Assess carefully Level of responsiveness Sensory and motor abnormalities Fluid/electrolyte imbalances Acid–base balance Effect treatment measuresNeurologic status q2h Prevention of constipation Limit physical activity Control hypokalemia Ensure proper nutrition |
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Liver Cancer
Two types |
Hepatocellular – primary liver cancer
Male > female 30 to 70% also have cirrhosis Risk factors Trauma Nutritional deficiences Exposure to carcinogens eg thorium dioxide, Aspergillus Metastatic – frequently from esophagus, stomach, colon, rectum, breast, lung, and malignant melanoma |
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When caring for a pt. with hepatic
encephalopathy, the nurse may give enemas, provide a low-protein diet, and administer Lactulose in order to |
b. decrease amount of serum ammonia
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Liver cancer
|
Usually fatal within 6 months
Symptoms initially Epigastric or RUQ pain Fatigue Anorexia Weight loss |
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Liver Cancer
Later Sx and Tx |
Later symptoms
Jaundice Ascites Bleeding Encephalopathy Treatment Surgery if a single lobe is involved Cryosurgical ablation of the liver Chemotherapy |
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Gallbladder
|
Pear-shaped sac
Inferior side of the liver Concentrates and stores bile Releases bile to small intestine |
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Bile
|
Digestive fluid that breaks down fats
into fatty acids Aids in the absorption of fat-soluble vitamins Contains mostly cholesterol, bile salts and bilirubin |
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Gallbladder Disease
|
Two most common problems with the
gallbaldder and biliary tree Cholelitiasis – stone formation Cholecyctitis – inflammation Acute Chronic |
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Cholelithiasis
|
Formation of gallstones in the
gallbladder Exact pathology is unclear Formed from the solid parts of bile Pigmented – 1/3 of stones Cholesterol – 2/3 of stones Cause problems when they block the flow of bile |
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Cholelithiasis- Risk factors
|
Age - increased with age
Gender – women > men estrogen level pregnancy (especially multiparity) oral contraceptives postmenopausal therapy (HRT) Obesity Cirrhosis |
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Cholelithiasis- Risk factors
|
Sedentary lifestyle
Diet High cholesterol, low fiber Low calorie or liquid protein diet Diabetes mellitus Cholesterol-lowering drugs -decreases cholesterol in blood but increases amount of cholesterol in the bile |
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|
“General Rule”
|
Female
Fair Fat Forty Fertile Age not an absolute |
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Manifestations of Cholelithasis
|
Tenderness in RUQ,
epigastrium, or both May radiate to the midback between scapulae (BOA’s sign) Nausea/Vomiting Jaundice Clay-colored stools |
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Diagnosis-Cholelithasis
|
CBC & LFTs
Ultrasonography – best diagnostic test X-ray Cholangiogram HIDA Scan ERCP (Endoscopic retrograde cholangiopancreatography) |
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|
Medical Management- Chole
|
Nutritional therapy (first choice)
Low fat Smaller, more frequent meals Pharmacology – Bile acid therapy UDCA – chenodeoxycholic acid CDCA – ursodeoxycholic acid Opioids – Demerol (No morphine- Why?) |
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|
Medical Management -Chole
|
Antispasmotics - Bentyl
Antiemetics – Tigan Cholestyramine resin - Questran Cholesterol solvents: MTBE (rarely used) Prevent Dehydration |
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Surgical Mgmt - Chole
|
Endoscopic**
Surgery – remove stone, and/or gall bladder Laproscopic Abdominal (open) (traditional) possible t-tube (drains bile from body until swelling decreases) Lithotripsy – use of sound waves to dissolve stonesReport bile drainage > 1000 ml/day Bile salts Bile may be collected and given back to the patient via NG Given synthetic bile salts (Decholin) Never irrigate, aspirate, or clamp T-tube without an order |
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Gallbladder Surgery
|
Nursing Care
Manage pain- Fowler’s position Discharge- usually 7-10 days Bloody drainage- normal for 1-2 hours Greenish-brown drainage- after 2 hours Usually 400ml in 1st 24 hours 200ml per 24 hours after |
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Post-operative Care- chole
|
Medications
Pain management – Demerol Antiemetics Care for drains and incision Surgical drain – usually out within 24 to 48 hrs T-tube – may stay in for 6 weeks Diet Low fat at least initially |
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Cholecystitis
|
Inflammation of the
gallbladder Empyema (pus) Usually caused by cholelithiasis 90% with acute cholecystitis |
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|
Cholecystitis
|
Conditions that
Affect the regular filling or emptying of the gallbladder Decrease blood flow to the gallbladder Conditions include Trauma, inadequate blood supply, prolonged anesthesia and surgery, adhesions, edema, tumors, long-term fasting, prolonged dehydration, prolonged immobility, excessive opioid use |
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|
Cholecystitis- n/v, lab, med mgmt
|
Signs/Symptoms
Intolerance to fatty food N/V Murphy’s Sign RUQ pain and tenderness Lab Work Increased WBC Increased serum amylase Medical Management Antibiotics IVF Cholecystectomy NG tube to decompress |
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Gallbladder Cancer
|
Uncommon, highly fatal
Females > Male Difficult to treat Insidious onset Symptoms similar to chronic cholecystitis Often found working up suspected cholecystitis |
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|
Uncommon, highly fatal
Females > Male Difficult to treat Insidious onset Symptoms similar to chronic cholecystitis Often found working up suspected cholecystitis |
Pancreas secretes:
Bicarbonate Digestive enzymes trypsin (protein) amylase (CHO) lipase (fats) Insulin |
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Pancreatitis
|
Inflammation due to autodigestion
(digestion of the pancreas by its own enzymes - trypsin). Toxic enzymes released may damage blood vessels, vital organs ie lungs, heart Acute or chronic |
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|
Etiology
|
Most common causes
Biliary tract disease with gallstones obstructive pancreatitis Excessive alcohol injestion Iatrogenic – secondary to manipulation during biliary tract, pancreas, gastric, & duodenal proceduresOther factors Oral birth control pills Viral infection Pancreatic obstruction eg tumor Toxicity related to medications eg opioids, thiazides |
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|
Acute Pancreatitis
Definition |
An acute inflammatory process of the
pancreas Degree of inflammation varies from mild to edema to severe necrosis |
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Acute Pancreatitis
|
Often due to early activation of the
digestive enzymes Activate in pancreas instead of intestine Pathological processes Lipolysis Protolysis Necrosis of blood vessels Inflammation |
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Chronic Pancreatitis
|
A progressive destructive disease
Remissions and exacerbations Inflammation to fibrosis to pancreatic insufficiency to decreased function Usually the result of repeated episodes of acute pancreatitis |
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|
Pacreatitis secondary to blockage - Manifestations
|
Sudden severe pain in middle to left
upper abdomen Sudden onset, intense, continuous Radiates to back, left flank, left shoulder Pain is worse when walking and lying supine Pain is relieved by sitting and leaning forward |
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|
Pacreatitis secondary to blockage - Manifestations
|
Fever, sweating
N & V Tachycardia Hypotension Generalized jaundice Rigid abdomen Ecchymosis Malaise, weaknessFever, sweating N & V Tachycardia Hypotension Generalized jaundice Rigid abdomen Ecchymosis Malaise, weaknessFever, sweating N & V Tachycardia Hypotension Generalized jaundice Rigid abdomen Ecchymosis Malaise, weaknessFever, sweating N & V Tachycardia Hypotension Generalized jaundice Rigid abdomen Ecchymosis Malaise, weaknessAbdominal tenderness Less intense in chronic Weight loss ¯ or absent bowel sounds Cullen’s sign (umbilicus) Turner’s sign (flank bruising) |
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|
Pancreatitis Lab Findings
|
Lab tests
Elevated amylase Often 3 times normal value Peaks in 24 hr; falls to normal by 3 to 4 days Elevated lipase More specific test for the diagnosis Rises after 48 hr; remains elevated for 2 weeks Amylase and lipase may be normal or only moderately elevated in chronic pancreatitis Serum glucose Often elevated in both acute and chronic formsElevated WBC in acute pancreatitis Elevated ALT 3 times normal or greater Decreased Ca++ and Mg+ If there is fat necrosis Elevated bilirubin is common in chronic form |
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|
Radiology studies- pancreatitis
|
CT
MRI ERCP Only definitive diagnostic test in chronic is identification of calcification of pancreatic tissue in a biopsy |
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|
Pancreatitis Lab Finding
|
Elevated
Amylase Peaks in 24 hr; falls to normal by 48-82 hrs Lipase Rises after 48 hr; remains elevated for 5-7 days Serum Glucose Often elevated WBC in acute pancreatitis Potential 3rd spacing of fluid |
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|
Complications of Acute
|
Jaundice
Transient hyperglycemia Coagulation defects Left lung pleural effusions Atelectasis and pneumonia Shock Multi-system organ failure |
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|
Complications of Chronic
|
Fat malabsorption steatorrhea,
weight loss and muscle wasting Jaundice Ascited LUQ mass ?? Pseudocyst or abscess |
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|
Medical Management
|
Decrease stimulation of pancreatic enzymes
NPO with TPN, IV hydration Possible NG tube Medicate for pain Meperidine (thought to be the drug of choice) Morphine Both may cause the Sphincter of Oddi to constrict Medications to decrease acidity and decrease secretin Anticholinergics - Bentyl Antacids – histamine blocker eg Zantac Somatostatin (octreotide) |
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Chronic Management
|
Analgesics
Enzyme replacements – do not mix with protein foods Donnazyme (pancreatin) Pancrelipase (cotazym, Pancrease) Insulin therapy |
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|
Surgical Management
|
Not usually indicated
May be done if there is an abscess or pseudocyst May be done if the is a biliary tract obstruction |
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|
Discharge Teaching: Diet
|
Bland diet
Increase CHO (450gm), protein (120 gm) Decrease fat to decrease pancreatic stimulation (< 50 grams/day) Avoid stimulants ie large meals, ETOH, caffeine May give 6 small feedings per day May need supplemental fat-soluble vitamins May need pancreatic enzyme replacements Needs to be taught to watch for Continued N&V, pain Frothy/foul smelling stools (steatorrhea) Presence of fat in the stool Fever > 2 days |
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|
Pancreatic Cancer
|
4th leading cause of death
by cancer Cause unknown Can be primary or metastasis Low 5 year survival rate Possible risk factors Smoking (2X the incidence if > 2 ppd) High fat diet, diet high in meat or both Exposure to chemicals ie benzidine, coke Chronic pancreatitis and diabetes may increase risk |
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|
Pancreatic cancer Manifestations
|
Abdominal pain: dull, aching
Anorexia Fast weight loss Nausea Jaundice if starts in the head of pancreas may obstruct common bile duct |
|
|
Pancreatic cancer - Lab test
|
increased amylase, lipase, alk phos, bilirubin, CEA, CA 19-9
|
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|
Dx Test Pancreatic cancer
|
CT, biopsy, ERCP***
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|
Mgmt of Pancreatic cancer
|
Medical – if a poor surgical candidate
Chemotherapy Radiation Pain Management Morphine Nutritional support Psychological support (poor prognosis) Surgery Pancreatectomy Whipple (radical pancreaticoduodenectomy) |
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|
Post op care pancreatic cancer
|
Monitor GI drainage
NG, drainage tubes May develop fistulas due to breakdown of anastomosis sites Biliary, pancreatic, or gastric Position – Semi-Fowler’s Monitor fluid and electrolyte status Monitor glucose levels |
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|
OSTEOPROSIS
POROUS BONE OR FRAGILE BONE DISEASE |
Chronic and progressive
Low bone mass and structural deterioration of bone tissue Cost 13 billion a year Silent because it robs bone of resources over time Bone can no longer with stand normal mechanical stress8 times more common in women Women have lower intake of calcium from 15 to 50 Women have lower bone mass due to smaller frame Bone absorption begins earlier in women Pregnancy and lactation depletes stores |
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|
Risk factors
|
Age- around 30 y/o
Gender- women >50 Ethnicity- Caucasian and Asian women Bone structure and body weight- petite/thin Family history Prior hx fracture/bone break Meds (ie prednisone) |
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|
Osteoporosis
|
Bone is continually deposited by
osteoblasts and reabsorbed by osteoclasts called remodeling Osteoporosis- bone reabsorption exceeds bone deposits Most common in the spine, hips and wrists Drug interactions Antiseziure meds, heparin, thyroid, steroids Fractures of the spinal vertebrae produce loss of height and kyphosis First signs is pain or spontaneous fractures |
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|
Tests
|
Bone mineral density tests
QUS- quantitative ultrasound measures bone density with sound waves on the heel, knee or shin DEXA-dual energy x-ray absorptiometry, measures bone density in the spine, hips and forearm, can be used over time to track bone density loss |
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|
Management- Osteoporosis
|
Proper nutrition
Calcium supplementation 1000mg/day premenopausal, 1500 for post Need also Vitamin D No smoking or ETOH Exercise Prevention of fractures |
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|
DRUG THERAPY
|
Biophosphonates
Inhibit osteoclast mediated bone resorption increasing Bone mineral density Fosmax, Aredia, ACtonel, Bonefos, Skelid, Boniva Calcitonin Inhibits osteoclast bone resorption, can be IM, SQ or nasallly HRT for low heart risk patients Inhibits osteoclast activity, leading to decreased reabsorption |
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Arthritis
|
A general term used to describe a
condition where a joint is damaged and painful Two most common types Osteoarthritis Rheumatoid |
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|
Osteoarthritis, sometimes called
degenerative joint disease or osteoarthrosis |
most
common form of arthritis. Osteoarthritis occurs when cartilage in your joints wears down over time |
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|
Risk factors - osteoarthritis
|
older age, sex women>men, bone deformities, joint injuries, obesity, certain occupations, other diseases (gout, RA)
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|
Treatment - Osteoarthritis
|
There's no known cure for
osteoarthritis, but treatments can help to reduce pain and maintain joint movement Medications Acetaminophen NSAIDS Tramadol Narcotic pain medications Cortisone injections Artificial synovial Fluid |
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|
Surgical and other treatments- osteoarthritis
|
Viscosupplementation:Injections of
hyaluronic acid derivatives (Hyalgan, Synvisc) may offer pain relief by providing some cushioning Joint replacement Realigning bones Fusing Bones |
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|
Other tx for osteoarthritis
|
Rest often, exercise, lose weight, use heat/cold to manage pain, otc creams, assistive devices, acupuncture, ginger, glucosamine and chondroitin, Avocado-soybean unsaponifiables (ASUs), Tai chi and yoga
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|
Rheumatoid Arthritis
|
The second most common connective
tissue disease The most destructive to the joint Chronic, progressive systemic inflammatory process Primarily affects the synovial joints Onset is characterized by synovitis |
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|
RA- Pathological Joint Changes
|
Early changes
Synovium thickens hyperemic Fluid accumulates in joint space Pannus forms Fibrous adhesions, body ankylosis and calcifications Etiology Probably a combination of genetic and environmental factors Possibly autoimmune |
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|
RA- Assessments/Manifestations
|
Joint
Pain, warmth, redness, limited motion, deformities Stiffness Lasts more than 30-60 min. Fatigue Anorexia, weight loss Systemic Manifestations |
|
|
RA- Systemic manifestations
|
Osteoporosis
Anemia Weight loss (2 to 3 pounds) Subcutaneous nodules Peripheral neuropathy, parasthesias Vasculitis Pericarditis Sjögren’s syndrome Renal disease |
|
|
RA- Laboratory Findings
|
No single test to confirm: anemia, increase erythrocyte sed rate, increased c-reactive protein, presence of rheumatoid factor, synovial fluid-increased WBC count, increase antinuclear antibody titer, increase WBC's
|
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|
RA- Diagnosis Criteria
|
Four of seven must be present
Morning stiffness in and around joints > 1 hr Arthritis of 3 or more areas simultaneously Arthritis of at least 1 area in a wrist, MCP or PIP joint Symmetric arthritis involving the same joint areas Rheumatoid nodules Serum positive rheumatoid factor Radiologic changes typical of RA on hand and wrist X-rays |
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|
RA-Management Goals
|
Relieve pain and
inflammation Preserve joint function Facilitate healing |
|
|
RA- Management
|
Rest/Exercise
Joint protection, Splints Daily heat/cold therapy to relieve stiffness Immersion in paraffin “glove” Well balanced diet Omega 3 fatty acids to ¯ inflammation Vitamins A, C, E Psychological Support |
|
|
RA- Medical Management
|
Anti-inflammatory agents
Salicylates – drug of choice for pain and inflammation ASA – 12 to 18 tabs daily in divided doses Sulfasalazine (Azulfadine) NSAIDS May take 6 to 8 weeks to determine efficacy COX-2 inhibitors (celecoxib – Celebrex) Disease-modifying agents To slow the disease or produce a disease remission Plaquenil (hydroxychloroquine) Antimalarial agent Retinal toxicity Cytotoxic agents Methotrexate weekly Immuran Cytoxan |
|
|
RA- Medical Management
|
Gold salts
Gold sodium thiomalate (Myochrysine) Use test dose Weekly injection is painful SE: rash, blood dyscrasias, renal involvement Oral gold preparation Ridura – taken daily Steroids – chronic use Deltasone (prednisone) Can be used short-term Long-term use associated with DM, infections, fluid and electrolyte imbalance, HTN, osteoporosis, glaucoma |
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|
RA- Medical Management
|
Tumor Necrosis Factor Blockers
Enbrel (etanercept) - SQ 2X per week Infliximab (Remicade) - IV over several hours Adalimumab (Humaria) – SQ weekly Minocycline A form of the antibiotic tetracycline Low incidence of adverse effects Analgesics Tylenol Darvon Darvocet-N |
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|
Invasive treatments for RA
|
Plasmapheresis (to remove circulating
antibodies) Arthroplasty Arthroscopy Synovectomy – remove damaged tissue Arthrodesis – joint fusion Total joint replacements |
|
|
Arthroplasty
|
Arthroplasty: refers to repair or refashioning
tissues within a joint Tissues replaced include Bones Cartilage Synovium Ligaments Tendons |
|
|
Reasons for Arthroplasty
|
Relieve restrictive movements of a joint
Relieve pain Remove loose or torn tissues (ligaments, cartilage or calcium) Reshape one or both bone ends to make a joint perform more smoothly Remove overgrown, hypertrophied tissues |
|
|
Joint Replacement
|
Almost any joint in the body can
be replaced Basic means to anchor prostheses Cemented Porous Hybrid (hip) Femoral component cemented Hip socket is not |
|
|
Post-operative Management (THR) total hip replacement
|
At risk for injury: dislocation
Maintain slight abduction Avoid hip flexion > 90 degrees HOB not elevated more than 70 degrees Activity CPM usually at 0-30 degrees 00B pm or next day With cemented prosthesis, partial wt-bearing With porous, only toe-touch wt. bearing for 6 wks. |
|
|
Post-operative Management (THR) total hip replacement
|
At risk for injury: infection
Monitor incision and any drain sites Monitor vital signs Alteration in comfort Possible PCA At risk for altered tissue perfusion Excessive postop blood loss? Neurovascular assessments DVT potential Monitor for Nausea/vomiting Neurovascular changes Pulses, warmth, color, capillary refill, pain, movement, and sensation |
|
|
Discharge Instructions (THR)
|
Activities: Dos and Don’ts
Notify provider If operative site reddens If there is any drainage If there is an increase in pain If they run a fever Prophylactic antibiotics before dental or other invasive procedures |
|
|
TKR
|
More exercise than
THR CPM usually at 0-60 degrees Quad setting exercises** NO abduction pillow Compression dressing at first |
|
|
Osteomyelitis
|
An infection of the bone
and bone marrow Can affect any bone in the body Usually caused by a staph infection Still a common problem Avoid if at all possible!! |
|
|
Types of Osteomyelitis
|
Acute - Less than 4 weeks
More common in children and older adults Often from an infection in another part of the body or the result of penetrating trauma Long bones are a common site Chronic – More than 4 weeks Adults with compromised vascular supply are at greatest risk Advanced age and concurrent disease may prolong the course of the infection |
|
|
Sx of Osteomyelitis
|
Pain in the bone
Constant, localized, pulsing sensation, increases with movement Common with chronic Local swelling and warmth Less common with chronic Nausea Fever – 101o Less common with chronicGeneral discomfort Drainage of pus through the skin Common with chronic |
|
|
Osteomyelitis Diagnostic Findings
|
Lab tests: increased wbc, ESR, + culture
Radiological studies: Bone scan, MRI, Bone biopsy-definitive diagnose |
|
|
Osteomyelitis Medical Management
|
IV antibiotics
Long-term – (8-10 weeks) Possibly hyperbaric oxygen Pain management Bed rest Irrigation of wound |
|
|
Osteomyelitis Surgical Management
|
Debridement of
necrotic or infected bone Bone grafts Amputation |
|
|
Possible Complications- osteomyelitis
|
heal
Permanent stiffness in a nearby joint Loosening of implanted joint Fracture Amputation |
|
|
Ankle Sprains
|
Occur when ligaments are stretched/torn
Most common athletic injury 85% occur on outside of ankle joint Symptoms vary depending on severity Type I - ligament stretched Type II - some fibers torn Type III - entire ligament torn |
|
|
Strain
|
A twist, pull and/or tear of a muscle
and/or tendon Pain, muscle spasm, muscle weakness, swelling, inflammation, and cramping May have loss of muscle function Common sites: Back, hamstring muscle |
|
|
Dx and Tx
|
Symptoms
X-rays to reveal fractures, dislocations or instability CT and MRI Tx:R = rest I = ice C = compression E = elevation Analgesia Splints, casts Surgery |
|
|
Bones
|
Made of a hard matrix
of calcium and cells that manipulate that matrix Osteoblasts Build more bone Osteoclasts Remove bone |
|
|
Fracture Terms
|
1. complete
2. incomplete 3. closed 4. open a. break in skin b. no break in skin c. thru part of bone d. across entire bone |
|
|
Types of fractures
|
Compression
Burst Greenstick Spiral Simple vs compound Comminuted |
|
|
Stages of Healing
|
In young, healthy adult bones, healing takes about
6 weeks Hematoma formation Fibrin meshwork Invasion by osteoblasts Callus formation Remodeling |
|
|
Factors Promoting Bone Healing
|
Immobilization of fragments
Sufficient blood supply At risk: Fracture in head of femur Proper nutrition Exercise |
|
|
Factors Inhibiting Bone Healing
|
Extensive local trauma, edema at fracture site
Bone loss, inadequate proximity of fracture surfaces Inadequate immobilization Infection Age Corticosteroids Poor nutrition, severe lack of vitamin C |
|
|
Treatment
|
Goals
Return injured limb to maximal function Prevent complications Initial Immobilization, elevation Check peripheral pulses pain, pallor, pulse, paresthesia, paralysis, (puffiness) coolness. Pain medications |
|
|
Management
|
Later management of fractures
Closed reduction Open reduction Open reduction with internal fixation (ORIF) Fixation with rods, pins, prosthesis, plates, compression hip screw |
|
|
Complications of Fractures
|
Arterial damage
Hemorrhage Peripheral nerve damage Infection Shock Avascular necrosis DVT, PE Gas gangrene Tetanus Non-union |
|
|
Compartment Syndrome
|
Compartments are sheaths of inelastic fascia
that support and partition muscles, blood vessels, and nerves in the body Pressure with a compartment to ischemia to swelling to ischemia etc =PAIN Pressure may be external or internal External – tight, bulky dressings and casts Internal – blood or fluid collection Relieve pressure within 6 hours of the onset of symptoms ie change in 5(6) Ps Limb can become useless in 24 to 48 hours |
|
|
Treatment and Complications
|
Fasciotomy
Incision through the skin and subcutaneous tissue into the fascia Complications Infection amputation Motor weakness r/t injured nerves (not reversible) Contractures Renal failure (rhabdomyolysis) |
|
|
Fat Embolus
|
Fat Emboli - release of large fat globules which
filter into the pulmonary system and cause obstruction at the capillary membrane level Thought to be from the fat in the marrow. Pressure changes within the fx bone forces molecules of fat from the marrow into the systemic circulation A serious complication Associated with fx of long bones or multiple fractures May 12-72 hr after injury Population most affected Young men 20-40 Older men 70-80 Older client with hip fx has highest risk |
|
|
Fat Embolus Signs and symptoms
|
Often begins with
confusion, agitation Tachycardia, dyspnea, fever Petechiae ******* Neck, upper arms, and/or chest and abdomen |
|
|
Lab Tests in Fat Embolism
|
increased ESR, serum lipase
decrease in serum calcium, RBC's, and platelets |
|
|
Management of Fatty Emboli
|
Shock management
Oxygen Cough, deep breathe Medications Steroids Heparin Emotional support |
|
|
Traction
|
The application of a pulling force to part/parts of
body to provide reduction, alignment, and rest. Need pull in opposite direction (counter traction) to be effective. Three types Manual Skin Skeletal May be continuous – in the treatment of a fracture May be intermittent – in the relief of muscle spasms |
|
|
5 principles of traction
|
Maintain established line of pull
Prevent friction Maintain countertraction Maintain continuous traction unless ordered otherwise Maintain correct body alignment |
|
|
General Rules for Traction
|
The weights must hang freely
Nothing rests on the traction cord The traction cord must run smoothly through the pulleys Add or remove weights slowly and only with a doctor’s order |
|
|
Skin Traction
|
Types
Buck’s Russell Pelvic Cervical halter Grip less secure than skeletal Weight limit is 10 – 12 pounds Big concern is skin integrity Remove device every 8 hours to inspect skin |
|
|
Skeletal: applied to bone
|
Balanced suspension
Thomas ring splint with Pearson attachment Skeletal-cervical tongs Halo ring |
|
|
Casts
|
Plaster of Paris
Requires well-fitted stockingette & padding under Feels hot initially, then cool and damp Takes 24-72 hours to dry Take care not to make impressions May have rough edges and require then to be petaled – use waterproof tape May need a window – if open area under cast If swelling, may need to bivalve cast, rewrap with ace wrap |
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Plaster Casts
Do's and Don'ts |
Dos:
Keep your affected limb propped up on a pillow when resting to avoid swelling. Exercise any joints sticking out from the plaster e.g. your toes or fingers, to prevent stiffness. Do NOT: Wet your plaster. Cut your plaster yourself - come back with any problems. Stand on or rest on any hard surfaces like the back of a chair for the first two days as the plaster needs to set |
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Fiberglass Cast
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Lighter in weight
Less drying time Longer wearing More breathable More expensive Can get the outside wet Still no swimming |
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Nursing Management
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Assessment ie neurovascular checks
How to detect infection, drainage Protecting from injury Skin care No hangers, pencils etc Hair dryer on cool, turkey baster Cast care |
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Fixation Devices
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Surgical treatment of fracture
May be external or internal Purposes Immobilizes Secures |
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External Fixation
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Advantages
Minimal blood loss compared to internal Allows for earkier ambulation and exercise of the affected body part while relieving pain Maintains alignment when no other method will work Disadvantages Pin site and tract infections |
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Pin Site Care
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Pin site care (Skeletal traction)
No agreed upon procedure Clean with NS, may apply Bacitracin Monitor for drainage |
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Internal Fixation
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Used when:
Impossible to maintain desired reduction by closed methods eg cast, traction In certain fractures to permit early functional use of limb In open fractures when it is impossible to maintain length otherwise Used pins, screws, rods, plates, and prostheses Hardware may or may not be removed after the fracture is healed |
