GI tract Visualization http://nursinglectures.blogspot.com

GIT Visualization Barium Swallow- UGIS Pretest: written consent, NPO the night Intratest: administer barium orally, then followed by X-ray Post-test: Laxative for constipation, increased fluids, assess for intestinal obstruction , warn that stool is light colored!

Barium Swallow- UGIS

Pretest: written consent, NPO the night

Intratest: administer barium orally, then followed by X-ray

Post-test: Laxative for constipation, increased fluids, assess for intestinal obstruction , warn that stool is light colored!

GIT Visualization Barium Enema- LGIS Pretest: Informed consent, NPO the night, Enema the morning Intratest: Position on LEFT side, administer enema, then X-ray follow Post-test: Cleansing enema , Laxative for constipation, assess for intestinal obstruction

Barium Enema- LGIS

Pretest: Informed consent, NPO the night, Enema the morning

Intratest: Position on LEFT side, administer enema, then X-ray follow

Post-test: Cleansing enema , Laxative for constipation, assess for intestinal obstruction

macky

Barium Enema

GIT Visualization Esophagogastroscopy Pretest: Informed consent, NPO for 8 hours, warn that gag reflex is abolished Intratest: Position on LEFT side during scope insertion Post-test: NPO until gag returns. Monitor for complications

Esophagogastroscopy

Pretest: Informed consent, NPO for 8 hours, warn that gag reflex is abolished

Intratest: Position on LEFT side during scope insertion

Post-test: NPO until gag returns. Monitor for complications

GIT Visualization Anoscopy, proctoscopy, proctosigmoidoscopy, colonoscopy Pretest: Consent, NPO, and enema administration the morning Intratest: Position on the LEFT side during scope insertion Post-test: Monitor for complications

Anoscopy, proctoscopy, proctosigmoidoscopy, colonoscopy

Pretest: Consent, NPO, and enema administration the morning

Intratest: Position on the LEFT side during scope insertion

Post-test: Monitor for complications

macky

Gallbladder Oral cholescystogram PTC ERCP Ultrasound

Oral cholescystogram

PTC

ERCP

Ultrasound

IV Cholecystogram X-ray visualization of the gallbladder after administration of contrast media intravenously Pre-test: Allergy to iodine and sea-foods Intra-test: ensure patent IV line Post-test: increase fluid intake to flush out the dye, Assess for delayed hypersensitivity reaction to the dye like chills and N/V

X-ray visualization of the gallbladder after administration of contrast media intravenously

Pre-test: Allergy to iodine and sea-foods

Intra-test: ensure patent IV line

Post-test: increase fluid intake to flush out the dye, Assess for delayed hypersensitivity reaction to the dye like chills and N/V

macky

Oral Cholecystogram X-ray visualization of the gallbladder after administration of contrast media Done 10 hours after ingestion of contrast tablets Done to determine the patency of biliary duct

X-ray visualization of the gallbladder after administration of contrast media

Done 10 hours after ingestion of contrast tablets

Done to determine the patency of biliary duct

macky

Endoscopic retrograde cholangiopancreatography Examination where a flexible endoscope is inserted into the mouth and via the common bile duct and pancreatic duct to visualize the structures Iodinated dye can also be injected after for the x-ray procedure

Examination where a flexible endoscope is inserted into the mouth and via the common bile duct and pancreatic duct to visualize the structures

Iodinated dye can also be injected after for the x-ray procedure

Endoscopic retrograde cholangiopancreatography Pre-test: consent, NPO for 12 hours, Allergy to sea-foods, Atropine sulfate Intra-test: Gag reflex is abolished, Position on LEFT side Post-test: NPO until gag reflex returns, Position side lying and monitor for perforation and hemorrhage

Pre-test: consent, NPO for 12 hours, Allergy to sea-foods, Atropine sulfate

Intra-test: Gag reflex is abolished, Position on LEFT side

Post-test: NPO until gag reflex returns, Position side lying and monitor for perforation and hemorrhage

Percutaneous Transhepatic Cholangiogram Under fluoroscopy, the bile duct is entered percutaneously and injected with a dye to observe filling of hepatic and biliary ducts

Under fluoroscopy, the bile duct is entered percutaneously and injected with a dye to observe filling of hepatic and biliary ducts

macky

Ultrasound of the liver, gallbladder and pancreas Consent MAY be needed Place patient on NPO!!! Laxative may be given to decrease the bowel gas

Consent MAY be needed

Place patient on NPO!!!

Laxative may be given to decrease the bowel gas

HIATAL HERNIA Protrusion of the esophagus into the diaphragm thru an opening Two types- Sliding hiatal hernia (most common) and Axial hiatal hernia ASSESSMENT Heartburn Regurgitation Dysphagia 50%; without symptoms DIAGNOSTIC TEST Barium swallow and fluoroscopy. NURSING INTERVENTIONS Provide small frequent feedings AVOID reclining for 1 hour after eating Elevate the head of the head on 8 –inch block Provide pre-op and post-op care

HIATAL HERNIA

Protrusion of the esophagus into the diaphragm thru an opening

Two types- Sliding hiatal hernia (most common) and Axial hiatal hernia

ASSESSMENT

Heartburn

Regurgitation

Dysphagia

50%; without symptoms

DIAGNOSTIC TEST

Barium swallow and fluoroscopy.

NURSING INTERVENTIONS

Provide small frequent feedings

AVOID reclining for 1 hour after eating

Elevate the head of the head on 8 –inch block

Provide pre-op and post-op care

Hiatal hernia – X-ray Hiatal hernia

Sliding Hiatal Hernia Causes: Muscle weakness in the esophageal hiatus: Aging process Congenital muscle weakness Obesity Trauma Surgery Prolonged increases in intra-abdominal pressure

Sliding Hiatal Hernia

Causes:

Muscle weakness in the esophageal hiatus:

Aging process

Congenital muscle weakness

Obesity

Trauma

Surgery

Prolonged increases in intra-abdominal pressure

Sliding Hiatal Hernia

Paraesophageal / Rolling Hernias Cause: anatomic defect.

Paraesophageal / Rolling Hernias

Cause: anatomic defect.

Management Medications Antacids Antiemetics Histamine Receptor Antagonist Gastric Acid Secretion Inhibitor AVOID; These drugs lowers the LES (lower esophageal sphincter) pressure: Anticholinergics Xanthine derivatives Ca-channel blockers Diazepam

Management

Medications

Antacids

Antiemetics

Histamine Receptor Antagonist

Gastric Acid Secretion Inhibitor

AVOID; These drugs lowers the LES (lower esophageal sphincter) pressure:

Anticholinergics

Xanthine derivatives

Ca-channel blockers

Diazepam

GASTROESOPHAGEAL REFLUX DISEASE

Gastro-esophageal reflux (GERD) Backlow incompetent LES May mimic ANGINA or MI ASSESSMENT (for GERD) Heartburn Dyspepsia Regurgitation Epigastric pain Dysphagia Ptyalism

Gastro-esophageal reflux (GERD)

Backlow

incompetent LES

May mimic ANGINA or MI

ASSESSMENT (for GERD)

Heartburn

Dyspepsia

Regurgitation

Epigastric pain

Dysphagia

Ptyalism

Diagnostic test Endoscopy or barium swallow Gastric ambulatory pH analysis

Diagnostic test

Endoscopy or barium swallow

Gastric ambulatory pH analysis

NURSING INTERVENTION Provide small frequent feedings AVOID reclining for 1 hour after eating Elevate the head of the head on 8 –inch block Provide pre-op and post-op care

NURSING INTERVENTION

Provide small frequent feedings

AVOID reclining for 1 hour after eating

Elevate the head of the head on 8 –inch block

Provide pre-op and post-op care

Gastritis

Conditions of the Stomach GASTRITIS Inflammation of the gastric mucosa May be Acute or Chronic Etiology: Acute- bacteria, irritating foods, NSAIDS, alcohol Etiology: Chronic- Ulceration, bacteria, Autoimmune disease, diet, alcohol, smoking

GASTRITIS

Inflammation of the gastric mucosa

May be Acute or Chronic

Etiology: Acute- bacteria, irritating foods, NSAIDS, alcohol

Etiology: Chronic- Ulceration, bacteria, Autoimmune disease, diet, alcohol, smoking

Conditions of the Stomach PATHOPHYSIOLOGY OF Gastritis Insults  cause gastric mucosal damage  inflammation, hyperemia and edema  superficial erosions  decreased gastric secretions, ulcerations and bleeding

PATHOPHYSIOLOGY OF Gastritis

Insults  cause gastric mucosal damage  inflammation, hyperemia and edema  superficial erosions  decreased gastric secretions, ulcerations and bleeding

Conditions of the Stomach ASSESSMENT (Acute) Dyspepsia Headache Anorexia Nausea/Vomiting ASSESSMENT (Chronic) Pyrosis Singultus Sour taste in the mouth Dyspepsia N/V/anorexia Pernicious anemia

ASSESSMENT

(Acute)

Dyspepsia

Headache

Anorexia

Nausea/Vomiting

ASSESSMENT (Chronic)

Pyrosis

Singultus

Sour taste in the mouth

Dyspepsia

N/V/anorexia

Pernicious anemia

Conditions of the Stomach DIAGNOSTIC PROCEDURE EGD- to visualize the gastric mucosa for inflammation Low levels of HCl Biopsy to establish correct diagnosis whether acute or chronic

DIAGNOSTIC PROCEDURE

EGD- to visualize the gastric mucosa for inflammation

Low levels of HCl

Biopsy to establish correct diagnosis whether acute or chronic

Conditions of the Stomach NURSING INTERVENTIONS 1. Give BLAND diet 2. Monitor for signs of complications like bleeding, obstruction and pernicious anemia 3. Instruct to avoid spicy foods, irritating foods, alcohol and caffeine

NURSING INTERVENTIONS

1. Give BLAND diet

2. Monitor for signs of complications like bleeding, obstruction and pernicious anemia

3. Instruct to avoid spicy foods, irritating foods, alcohol and caffeine

Conditions of the Stomach NURSING INTERVENTIONS 4. Administer prescribed medications- H2 blockers, antibiotics, mucosal protectants 5. Inform the need for Vitamin B12 injection if deficiency is present

NURSING INTERVENTIONS

4. Administer prescribed medications- H2 blockers, antibiotics, mucosal protectants

5. Inform the need for Vitamin B12 injection if deficiency is present

Gastritis

Acute Gastritis Chronic Gastritis

macky PEPTIC ULCER DISEASE

Conditions of the Stomach PEPTIC ULCER DISEASE An ulceration of the gastric and duodenal lining Gastric ulcer and Duodenal ulcer Most common Peptic ulceration: anterior part of the upper duodenum

PEPTIC ULCER DISEASE

An ulceration of the gastric and duodenal lining

Gastric ulcer and Duodenal ulcer

Most common Peptic ulceration: anterior part of the upper duodenum

Conditions of the Stomach PATHOPHYSIOLOGY of PUD Disturbance in acid secretion and mucosal protection Increased acidity or decreased mucosal resistance  erosion and ulceration

PATHOPHYSIOLOGY of PUD

Disturbance in acid secretion and mucosal protection

Increased acidity or decreased mucosal resistance  erosion and ulceration

Duodenal Ulcer Gastric Ulcer Pain occurs 90 min to 3h after meals; wakes up patient midnight to 3 AM Commonly pain occurs within a short time of food intake Relieved by food, antacids and H2 blockers; is not associated with vomiting (if atypical features occur think of complications) High gastric acid levels Commonly accompanied by nausea, vomiting with food intake and a variable response to medications Low gastric acid levels H. pylori +++ H. pylori +++ Does not represent a malignancy Malignancy + Usually not accompanied by a high complication rate 25% will be accompanied by significant bleeding; higher mortality and morbidity

DUODENAL / GASTRIC ULCER Age: 30-60 M:F: 2-3:1 80%- duodenal Hypersecretion of HCL (+) weight gain Pain occurs 2-3 p.c .; often awakened between 1-2 am; ingestion of food relieves pain 50 and over 1:1 15% GU N-hyposecretion of HCl Weight loss Pain occurs ½ hrs pc ; rarely occurs at night; relieved by vomiting ; ingestion of food does not help, sometimes inc pain

Age: 30-60

M:F: 2-3:1

80%- duodenal

Hypersecretion of HCL

(+) weight gain

Pain occurs 2-3 p.c .; often awakened between 1-2 am; ingestion of food relieves pain

50 and over

1:1

15% GU

N-hyposecretion of HCl

Weight loss

Pain occurs ½ hrs pc ; rarely occurs at night; relieved by vomiting ; ingestion of food does not help, sometimes inc pain

DUODENAL / GASTRIC ULCER DU Vomiting uncommon Hge less common; melena more common More likely to perforate Malignancy rare Risk factors: a. H. pylori b. Alcohol/Smoking c. Cirrhosis d. Stress GU Vomiting common Hge more likely; hematemesis more common Occasionally Risk factors a. H. pylori b. Gastritis c. Alcohol/Smoking d. NSAIDs e. Stress

DU

Vomiting uncommon

Hge less common; melena more common

More likely to perforate

Malignancy rare

Risk factors:

a. H. pylori

b. Alcohol/Smoking

c. Cirrhosis

d. Stress

GU

Vomiting common

Hge more likely; hematemesis more common

Occasionally

Risk factors

a. H. pylori

b. Gastritis

c. Alcohol/Smoking

d. NSAIDs

e. Stress

PUD Laboratory: CBC Endoscopy Gastric acid analysis UGIS

Laboratory:

CBC

Endoscopy

Gastric acid analysis

UGIS

Medical management Supportive Drug therapy Nursing Interventions: Administer medications as ordered Provide nursing care for the client with ulcer surgery. Prepare the client for diagnostic procedure for barium swallow and EGD.

Medical management

Supportive

Drug therapy

Nursing Interventions:

Administer medications as ordered

Provide nursing care for the client with ulcer surgery.

Prepare the client for diagnostic procedure for barium swallow and EGD.

Provide client teaching and discharge planning Prepare the patient for surgery if warranted. Usually, the indication includes- unresponsive ulcer healing for 12-16 weeks, life-threatening hemorrhage and perforation.

Provide client teaching and discharge planning

Prepare the patient for surgery if warranted. Usually, the indication includes- unresponsive ulcer healing for 12-16 weeks, life-threatening hemorrhage and perforation.

Ulcer Surgery

Ulcer Surgery Surgery is performed when peptic ulcer disease does not respond to medical management. Types Vagotomy: Antrectomy: Pyloroplasty: Gastroduodenostomy (Billroth I): Gastrojejunostomy (Billroth II): Gastrectomy: removal of 60%-80% of the stomach Esophagojejunostomy (total gastrectomy): removal of the entire stomach with a loop of jejunum anastomosed to the esophagus

Ulcer Surgery

Surgery is performed when peptic ulcer disease does not respond to medical management.

Types

Vagotomy:

Antrectomy:

Pyloroplasty:

Gastroduodenostomy (Billroth I):

Gastrojejunostomy (Billroth II):

Gastrectomy: removal of 60%-80% of the stomach

Esophagojejunostomy (total gastrectomy): removal of the entire stomach with a loop of jejunum anastomosed to the esophagus

Nursing Interventions Relieving pain Reducing anxiety Maintaining optimal nutritional status Monitoring and managing potential complications Hemorrhage Perforation and penetration Pyloric obstruction

Relieving pain

Reducing anxiety

Maintaining optimal nutritional status

Monitoring and managing potential complications

Hemorrhage

Perforation and penetration

Pyloric obstruction

Conditions of the Stomach SURGICAL PROCEDURES FOR PUD Post-operative Nursing management 1. Monitor VS 2. Post-op position: FOWLER’S 3. NPO until peristalsis returns 4. Monitor for bowel sounds 5. Monitor for complications of surgery

SURGICAL PROCEDURES FOR PUD

Post-operative Nursing management

1. Monitor VS

2. Post-op position: FOWLER’S

3. NPO until peristalsis returns

4. Monitor for bowel sounds

5. Monitor for complications of surgery

Conditions of the Stomach Post-operative Nursing management 6. Monitor I and O, IVF 7. Maintain NGT 8. Diet progress: clear liquid  full liquid  six bland meals 9. Manage DUMPING SYNDROME

Post-operative Nursing management

6. Monitor I and O, IVF

7. Maintain NGT

8. Diet progress: clear liquid  full liquid  six bland meals

9. Manage DUMPING SYNDROME

DUMPING SYNDROME A group of unpleasant vasomotor and GI symptoms caused by rapid emptying of gastric content into the jejunum. Associated with the presence of hyperosmolar chyme

DUMPING SYNDROME

A group of unpleasant vasomotor and GI symptoms caused by rapid emptying of gastric content into the jejunum.

Associated with the presence of hyperosmolar chyme

Early signs and symptoms (5 to 30 minutes p.c.). Weakness, tachycardia, dizziness, diaphoresis, pallor, feeling of fullness or discomfort. Nausea and explosive diarrhea Rapid emptying of hypertonic food from the stomach Distention of the jejunum causing early symptoms Fluid shift from the bloodstream into the jejunum Decreased blood volume Shock – like manifestations

Early signs and symptoms (5 to 30 minutes p.c.). Weakness, tachycardia, dizziness, diaphoresis, pallor, feeling of fullness or discomfort. Nausea and explosive diarrhea

Rapid emptying of hypertonic food from the stomach

Distention of the jejunum causing early symptoms

Fluid shift from the bloodstream into the jejunum

Decreased blood volume

Shock – like manifestations

Late signs and symptoms (2 to 3 hrs. p.c.) Sudden hyperglycemia Increased insulin secretion Reactive HYPOGLYCEMIA

MANAGEMENT OF DUMPING SYNDROME Eat in a low fowler’s position Lie down after a meal (left side) Moderate fat, high protein diet. Fats slows down gastric motility, proteins increase colloidal osmotic pressure and prevents shifting of plasma

MANAGEMENT OF DUMPING SYNDROME

Eat in a low fowler’s position

Lie down after a meal (left side)

Moderate fat, high protein diet. Fats slows down gastric motility, proteins increase colloidal osmotic pressure and prevents shifting of plasma

MANAGEMENT OF DUMPING SYNDROME Small frequent feedings Limit carbohydrates, no simple sugars Give fluids 1 hr before and after meals Avoid very hot and cold foods and beverages Anticholinergic or antispasdomic medications are given

Small frequent feedings

Limit carbohydrates, no simple sugars

Give fluids 1 hr before and after meals

Avoid very hot and cold foods and beverages

Anticholinergic or antispasdomic medications are given

Inflammatory Bowel Disease: Crohns and Ulcerative colitis

CHRONIC INFLAMMATORY BOWEL DISORDERS A.Regional ENTERITIS (Crohn’s Disease) B. Ulcerative Colitis Transmural Mucous ulceration Ileum/ascending colon Rectum/ lower colon Cause Unknown Unknown Jewish Familial Environmental Jewish Emotional stress Age 20-30 years 40-60 years 15-40 years Bleeding  ; stool with pus and mucus Severe; stool with blood, pus and mucus

Transmural

Mucous ulceration

Ileum/ascending colon

Rectum/ lower colon

Unknown

Unknown

Jewish

Familial

Environmental

Jewish

Emotional stress

20-30 years

40-60 years

15-40 years

 ; stool with pus and mucus

Severe; stool with blood, pus and mucus

Perianal involvement Severe Mild Fistulas Common Rare Rectal involvement 20% 100% Diarrhea 5-6 soft stool/ day 20-30 watery stool/ day Abdominal pain + +

Severe

Mild

Common

Rare

20%

100%

5-6 soft stool/ day

20-30 watery stool/ day

+

+

Weight loss + + Intervention TPN Steriods Azulfidine (Sulfasalazine) Ileostomy Colectomy Diet TPN Steriods Azulfidine (Sulafasalazine) Ileostomy/ Proctocolectomy

+

+

TPN

Steriods

Azulfidine (Sulfasalazine)

Ileostomy

Colectomy

Diet

TPN

Steriods

Azulfidine (Sulafasalazine)

Ileostomy/

Proctocolectomy

Nursing Interventions for Crohn’s and UC Maintain NPO during the active phase Monitor for complications like severe bleeding, dehydration, electrolyte imbalance Monitor bowel sounds, stool and blood studies Restrict activities Administer IVF, electrolytes and TPN if prescribed

Nursing Interventions for Crohn’s and UC

Maintain NPO during the active phase

Monitor for complications like severe bleeding, dehydration, electrolyte imbalance

Monitor bowel sounds, stool and blood studies

Restrict activities

Administer IVF, electrolytes and TPN if prescribed

Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and vegetables especially SPINACH, pepper, alcohol and caffeine.

Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and vegetables especially SPINACH, pepper, alcohol and caffeine.

Diet progression- clear liquid  LOW residue, high protein diet Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/ iron-supplements

Diet progression- clear liquid  LOW residue, high protein diet

Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/ iron-supplements

macky Crohn’s Disease: Anatomic Distribution Small bowel alone (33%) Colon alone (20%) Ileocolic (45%) Least Most Freq of involvement

Pathophysiology of IBD - pt. 1 macky fbg06

Pathophysiology of IBD - pt. 2 macky fbg06

APPENDICITIS

Appendicitis Inflammation of the vermiform appendix that prevents mucus from passing into the cecum

Appendicitis

Inflammation of the vermiform appendix that prevents mucus from passing into the cecum

PATHOPHYSIOLOGY Obstruction of the appendix lumen Mucosal inflammation and bacterial proliferation Increased intra-luminal Pressure Lymphoid swelling Decreased venous drainage Thrombosis Bacterial invasion Abscess Gangrene Perforation (24 to 36 hours) Peritonitis

Assessment findings Acute abdominal pain that usually starts in the epigastric or umbilical region Mc Burney’s Point initially intermittent then become steady and severe over a short period. Appendicitis “signs” Rebound tenderness Psoas sign (lateral position with right hip is palpated) Rovsing’s sign (right quadrant pain when the left is palpated) Obturator sign (pain on external rotation of the right thigh)

Assessment findings

Acute abdominal pain that usually starts in the epigastric or umbilical region

Mc Burney’s Point

initially intermittent then become steady and severe over a short period.

Appendicitis “signs”

Rebound tenderness

Psoas sign (lateral position with right hip is palpated)

Rovsing’s sign (right quadrant pain when the left is palpated)

Obturator sign (pain on external rotation of the right thigh)

Nursing Interventions Administer antibiotics/ antipyretics as ordered prevent perforation of the appendix; don’t give enemas or cathartics or use heating pad

Nursing Interventions

Administer antibiotics/ antipyretics as ordered

prevent perforation of the appendix; don’t give enemas or cathartics or use heating pad

Surgical procedure= APPENDECTOMY If appendicitis ruptured (peritonitis): with penrose drains; Position: semi-fowler’s position to localize inflammation within the pelvic area Resume all normal activities within 2 to 4 weeks In addition to routine post-op care Monitor NG tube (usually with low suction) Monitor penrose drains Position in semi-fowler’s or lying on right side to facilitate drainage Administer antibiotics as ordered

Surgical procedure= APPENDECTOMY

If appendicitis ruptured (peritonitis): with penrose drains; Position: semi-fowler’s position to localize inflammation within the pelvic area

Resume all normal activities within 2 to 4 weeks

In addition to routine post-op care

Monitor NG tube (usually with low suction)

Monitor penrose drains

Position in semi-fowler’s or lying on right side to facilitate drainage

Administer antibiotics as ordered

DIVERTICULITIS

DIVERTICULITIS Diverticulum is outpouching of the mucosal lining of the GI tract, commonly in the colon. Diverticula/ diverticulosis are multiple outpouching Diverticulitis is acute inflammation and infection commonly caused by trapped fecal material and bacteria Causes: Low fiber diet, chronic constipation and obesity

DIVERTICULITIS

Diverticulum is outpouching of the mucosal lining of the GI tract, commonly in the colon.

Diverticula/ diverticulosis are multiple outpouching

Diverticulitis is acute inflammation and infection commonly caused by trapped fecal material and bacteria

Causes: Low fiber diet, chronic constipation and obesity

Low fecal volume in the colon Increased intraluminal pressure Decreased muscle strength in the colon wall Herniation/Outpoutching of mucous membrane Entrapment of fecal material and bacteria Inflammation and infection Scarring Abscess Bleeding Perforation Peritonitis Decreased muscle strength in the colon wall

CONDITIONS OF THE LARGE INTESTINE ASSESSMENT findings for D/D 1. Left lower Quadrant pain 2. Flatulence 3. Bleeding per rectum 4. nausea and vomiting 5. Fever 6. Palpable, tender rectal mass

ASSESSMENT findings for D/D

1. Left lower Quadrant pain

2. Flatulence

3. Bleeding per rectum

4. nausea and vomiting

5. Fever

6. Palpable, tender rectal mass

CONDITIONS OF THE LARGE INTESTINE NURSING INTERVENTIONS 1. Maintain NPO during acute phase 2. Provide bed rest 3. Administer antibiotics, analgesics like meperidine (morphine is not used) and anti-spasmodics 4. Monitor for potential complications like perforation, hemorrhage and fistula 5. Increase fluid intake

NURSING INTERVENTIONS

1. Maintain NPO during acute phase

2. Provide bed rest

3. Administer antibiotics, analgesics like meperidine (morphine is not used) and anti-spasmodics

4. Monitor for potential complications like perforation, hemorrhage and fistula

5. Increase fluid intake

CONDITIONS OF THE LARGE INTESTINE NURSING INTERVENTIONS 6. Avoid gas-forming foods or HIGH-roughage foods containing seeds, nuts to avoid trapping 7. introduce soft, high fiber foods ONLY after the inflammation subsides 8. Instruct to avoid activities that increase intra-abdominal pressure

NURSING INTERVENTIONS

6. Avoid gas-forming foods or HIGH-roughage foods containing seeds, nuts to avoid trapping

7. introduce soft, high fiber foods ONLY after the inflammation subsides

8. Instruct to avoid activities that increase intra-abdominal pressure

INTESTINAL OBSTRUCTION

CONDITIONS OF THE LARGE INTESTINE DIAGNOSTIC STUDIES 1. If no active inflammation, COLONOSCOPY and Barium Enema 2. CT scan is the procedure of choice! 3. Abdominal X-ray

DIAGNOSTIC STUDIES

1. If no active inflammation, COLONOSCOPY and Barium Enema

2. CT scan is the procedure of choice!

3. Abdominal X-ray

Intestinal Obstruction 2 Types: Mechanical Functional

2 Types:

Mechanical

Functional

Small Bowel Obstruction Intestinal contents, fluid, gas accumulate above the IO abdominal distention & retention of fluid absorption of fluids stimulates more gastric secretion pressure w/n intestinal lumen venous & arteriolar capillary pressure edema, congestion rupture

Intestinal contents, fluid, gas accumulate above the IO abdominal distention & retention of fluid absorption of fluids stimulates more gastric secretion pressure w/n intestinal lumen venous & arteriolar capillary pressure edema, congestion rupture

Nursing Assessment Crampy abdominal pain wavelike and colicky (+) blood and mucus; (-) fecal (-) flatus (+) vomiting Obstruction complete reverse peristalsis Ileal obstruction fecal vomiting Distended abdomen Signs of DHN

Crampy abdominal pain wavelike and colicky

(+) blood and mucus; (-) fecal (-) flatus

(+) vomiting

Obstruction complete reverse peristalsis

Ileal obstruction fecal vomiting

Distended abdomen

Signs of DHN

Medical Management NGT IVF Surgery

NGT

IVF

Surgery

LARGE BOWEL OBSTRUCTION

PERITONITIS

Peritonitis Local or generalized inflammation of part or all of the parietal and visceral surfaces of the abdominal cavity. Initial response: edema, vascular congestion, hypermotility of the bowel and outpouring plasma-like fluid from the extracellular, vascular and interstitial compartments into the peritoneal space. .

Peritonitis

Local or generalized inflammation of part or all of the parietal and visceral surfaces of the abdominal cavity.

Initial response: edema, vascular congestion, hypermotility of the bowel and outpouring plasma-like fluid from the extracellular, vascular and interstitial compartments into the peritoneal space.

.

Later response: abdominal distention leading to respiratory compromise, hypovolemia results in decreased urinary output. Intestinal motility gradually decrease and progresses to paralytic ileus

Later response: abdominal distention leading to respiratory compromise, hypovolemia results in decreased urinary output.

Intestinal motility gradually decrease and progresses to paralytic ileus

Inflammation Adhesions Abscess Intestinal Obstruction Fluid shift into abdominal cavity (300-500 ml.)  Peristalsis Bowel distended with gas & fluid Hypovolemia Electrolyte imbalance Dehydration Shock Pathophysiology

Hypovolemia

Electrolyte imbalance

Dehydration

Shock

Medical Management Fluid, colloid and electrolyte O2 therapy Antibiotics Surgery

Medical Management

Fluid, colloid and electrolyte

O2 therapy

Antibiotics

Surgery

Nursing Management Position on side with knees flexed Monitor VS; I and O Observe drainage SIGNS THAT PERITONITIS IS IMPROVING: 1. temperature 2. pulse 3. softening of the abdomen 4. (+) bowel sounds (+) bowel movement 5. (+) flatus

Position on side with knees flexed

Monitor VS; I and O

Observe drainage

SIGNS THAT PERITONITIS IS IMPROVING:

1. temperature

2. pulse

3. softening of the abdomen

4. (+) bowel sounds (+) bowel movement

5. (+) flatus

Nursing Interventions Assess respiratory status for possible distress. Assess characteristics of abdominal pain and changes overtime. Administer medications as ordered. Perform frequent abdominal assessment. Monitor and maintain fluid and electrolyte balance; monitor for sings of septic shock. Maintain patency of NG or intestinal tubes. Place client in Fowler’s position to localize peritoneal contents. Provide routine pre-and post-op care if surgery ordered.

Nursing Interventions

Assess respiratory status for possible distress.

Assess characteristics of abdominal pain and changes overtime.

Administer medications as ordered.

Perform frequent abdominal assessment.

Monitor and maintain fluid and electrolyte balance; monitor for sings of septic shock.

Maintain patency of NG or intestinal tubes.

Place client in Fowler’s position to localize peritoneal contents.

Provide routine pre-and post-op care if surgery ordered.

HEMORRHOIDS

HEMORRHOIDS These are dilated blood vessels beneath the lining of the skin in the anal canal Two types of Hemorrhoids exist External Hemorrhoids: occur below the anal sphincter Internal Hemorrhoids: occur above the anal sphincter Causes Chronic constipation Pregnancy Obesity Prolonged sitting and standing Wearing constricting clothes Disease conditions like liver cirrhosis, RSCHF (right-sided CHF)

HEMORRHOIDS

These are dilated blood vessels beneath the lining of the skin in the anal canal

Two types of Hemorrhoids exist

External Hemorrhoids: occur below the anal sphincter

Internal Hemorrhoids: occur above the anal sphincter

Causes

Chronic constipation

Pregnancy

Obesity

Prolonged sitting and standing

Wearing constricting clothes

Disease conditions like liver cirrhosis, RSCHF (right-sided CHF)

Assessment Constipation in an effort to prevent pain or bleeding associated with defecation. Anal pain. Rectal bleeding (usually bright red-hematochezia) Internal hemorrhoids may prolapse, usually painless. External hemorrhoids are usually painful.

Assessment

Constipation in an effort to prevent pain or bleeding associated with defecation.

Anal pain.

Rectal bleeding (usually bright red-hematochezia)

Internal hemorrhoids may prolapse, usually painless. External hemorrhoids are usually painful.

Nursing Management High fiber diet, liberal fluid intake Bulk laxatives Hot Sitz Bath; warm compress, witch hazel cream can be applied to decrease size. Local anesthetic application- Nupercaine.

Nursing Management

High fiber diet, liberal fluid intake

Bulk laxatives

Hot Sitz Bath; warm compress, witch hazel cream can be applied to decrease size.

Local anesthetic application- Nupercaine.

Surgery Hemorrhoidectomy Sclerotheraphy (5% phenol in oil) Cryosurgery Rubber-band ligation; done only if hemorrhoids are INTERNAL Pre-op Care Low residue diet to reduce the bulk of stool. Stool softeners.

Surgery

Hemorrhoidectomy

Sclerotheraphy (5% phenol in oil)

Cryosurgery

Rubber-band ligation; done only if hemorrhoids are INTERNAL

Pre-op Care

Low residue diet to reduce the bulk of stool.

Stool softeners.

Post –op Care Promotion of comfort Analgesics as prescribed Post-op position: Side-lying position or prone position Hot sitz bath 12-24 hours post-op to promote comfort and hasten healing Promotion of elimination Stool softeners are given as prescribed. Analgesic before initial defecation Encourage the client to defecate as soon as the urge occurs Enema as prescribed, using small-bore rectal tube

Post –op Care

Promotion of comfort

Analgesics as prescribed

Post-op position: Side-lying position or prone position

Hot sitz bath 12-24 hours post-op to promote comfort and hasten healing

Promotion of elimination

Stool softeners are given as prescribed.

Analgesic before initial defecation

Encourage the client to defecate as soon as the urge occurs

Enema as prescribed, using small-bore rectal tube

Anal Fissure An elongated laceration between the anal canal and the perianal skin. Anal Absess Results from the obstruction of gland ducts in the anorectal region by feces, leading to infection. Anal Fistula Involves development of an abnormal communication between the anal canal and skin outside the anus. Caused by rupture and drainage of an abscess.

Anal Fissure

An elongated laceration between the anal canal and the perianal skin.

Anal Absess

Results from the obstruction of gland ducts in the anorectal region by feces, leading to infection.

Anal Fistula

Involves development of an abnormal communication between the anal canal and skin outside the anus.

Caused by rupture and drainage of an abscess.

Conditions of the Accessory Organs

The Gallbladder Conditions of the Accessory organs

CONDITION OF THE GALLBLADDER Cholecystitis Inflammation of the gallbladder Can be acute or chronic

Cholecystitis

Inflammation of the gallbladder

Can be acute or chronic

CONDITION OF THE GALLBLADDER Cholecystitis Acute cholecystitis usually is due to gallbladder stones

Cholecystitis

Acute cholecystitis usually is due to gallbladder stones

CONDITION OF THE GALLBLADDER Cholecystitis Chronic cholecystitis is usually due to long standing gall bladder inflammation

Cholecystitis

Chronic cholecystitis is usually due to long standing gall bladder inflammation

Cholelithiasis Formation of GALLSTONES in the biliary apparatus

Formation of GALLSTONES in the biliary apparatus

Predisposing FACTORS “ F” Female Fat Forty Fertile Fair

“ F”

Female

Fat

Forty

Fertile

Fair

macky

Pathophysiology Supersaturated bile, Biliary stasis Stone formation Blockage of Gallbladder Inflammation, Mucosal Damage and WBC infiltration

Supersaturated bile, Biliary stasis

Stone formation

Blockage of Gallbladder

Inflammation, Mucosal Damage and WBC infiltration

CONDITION OF THE GALLBLADDER ASSESSMENT findings for cholecystitis 1. Indigestion, belching and flatulence 2. Fatty food intolerance

ASSESSMENT findings for cholecystitis

1. Indigestion, belching and flatulence

2. Fatty food intolerance

CONDITION OF THE GALLBLADDER ASSESSMENT findings for cholecystitis 3. Epigastric pain that radiates to the scapula or localized at the RUQ 4. Mass at the RUQ

ASSESSMENT findings for cholecystitis

3. Epigastric pain that radiates to the scapula or localized at the RUQ

4. Mass at the RUQ

CONDITION OF THE GALLBLADDER ASSESSMENT findings for cholecystitis 5. Murphy’s sign 6. Jaundice 7. dark orange and foamy urine

ASSESSMENT findings for cholecystitis

5. Murphy’s sign

6. Jaundice

7. dark orange and foamy urine

CONDITION OF THE GALLBLADDER DIAGNOSTIC PROCEDURES 1. Ultrasonography- can detect the stones 2. Abdominal X-ray 3. Cholecystography

DIAGNOSTIC PROCEDURES

1. Ultrasonography- can detect the stones

2. Abdominal X-ray

3. Cholecystography

CONDITION OF THE GALLBLADDER DIAGNOSTIC PROCEDURES 4. WBC count increased 5. Oral cholecystography cannot visualize the gallbladder 6. ERCP: reveals inflamed gallbladder with gallstone

DIAGNOSTIC PROCEDURES

4. WBC count increased

5. Oral cholecystography cannot visualize the gallbladder

6. ERCP: reveals inflamed gallbladder with gallstone

CONDITION OF THE GALLBLADDER NURSING INTERVENTIONS 1. Maintain NPO in the active phase 2. Maintain NGT decompression

NURSING INTERVENTIONS

1. Maintain NPO in the active phase

2. Maintain NGT decompression

CONDITION OF THE GALLBLADDER NURSING INTERVENTIONS 3. Administer prescribed medications to relieve pain. Usually Demerol (MEPERIDINE) Codeine and Morphine may cause spasm of the Sphincter  increased pain. Morphine cause MOREPAIN

NURSING INTERVENTIONS

3. Administer prescribed medications to relieve pain. Usually Demerol (MEPERIDINE)

Codeine and Morphine may cause spasm of the Sphincter  increased pain. Morphine cause MOREPAIN

CONDITION OF THE GALLBLADDER 4. Instruct patient to AVOID HIGH- fat diet and GAS-forming foods 5. Assist in surgical and non-surgical measures 6. Surgical procedures- Cholecystectomy, Choledochotomy, laparoscopy

4. Instruct patient to AVOID HIGH- fat diet and GAS-forming foods

5. Assist in surgical and non-surgical measures

6. Surgical procedures- Cholecystectomy, Choledochotomy, laparoscopy

CONDITION OF THE GALLBLADDER PHARMACOLOGIC THERAPY Analgesic- Meperidine Chenodeoxycholic acid= to dissolve the gallstones Antacids Anti-emetics

PHARMACOLOGIC THERAPY

Analgesic- Meperidine

Chenodeoxycholic acid= to dissolve the gallstones

Antacids

Anti-emetics

CONDITION OF THE GALLBLADDER Post-operative nursing interventions 1. Monitor for surgical complications 2. Post-operative position after recovery from anesthesia- LOW FOWLER’s

Post-operative nursing interventions

1. Monitor for surgical complications

2. Post-operative position after recovery from anesthesia- LOW FOWLER’s

CONDITION OF THE GALLBLADDER Post-operative nursing interventions 3. Encourage early ambulation 4. Administer medication before coughing and deep breathing exercises 5. Advise client to splint the abdomen to prevent discomfort during coughing

Post-operative nursing interventions

3. Encourage early ambulation

4. Administer medication before coughing and deep breathing exercises

5. Advise client to splint the abdomen to prevent discomfort during coughing

CONDITION OF THE GALLBLADDER Post-operative nursing interventions 6. Administer analgesics, antiemetics, antacids 7. Care of the biliary drainageor T-tube drainage 8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed

Post-operative nursing interventions

6. Administer analgesics, antiemetics, antacids

7. Care of the biliary drainageor T-tube drainage

8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed

T-tube

Cholecystectomy/ Choledochostomy/ Choledochotomy

Cholecystectomy/Choledochostomy/Choledochotomy Open Cholecystectomy: Choledochostomy: Laparoscopic Cholecystectomy Choledochotomy:

Cholecystectomy/Choledochostomy/Choledochotomy

Open Cholecystectomy:

Choledochostomy:

Laparoscopic Cholecystectomy

Choledochotomy:

Pancreatitis

Pancreatic secretions 1. Bicarbonate- to neutralize the acidic chyme from the stomach 2. Pancreatic amylase- for carbohydrate digestion

1. Bicarbonate- to neutralize the acidic chyme from the stomach

2. Pancreatic amylase- for carbohydrate digestion

Pancreatic secretions 3. Pancreatic lipase- for fat digestion 4. Trypsin and chymotrypsin- for protein digestion

3. Pancreatic lipase- for fat digestion

4. Trypsin and chymotrypsin- for protein digestion

macky

Fig. 16.22 macky

CONDITION OF THE PANCREAS Pancreatitis Inflammation of the pancreas Can be acute or chronic

Pancreatitis

Inflammation of the pancreas

Can be acute or chronic

CONDITION OF THE PANCREAS Pancreatitis Etiology and predisposing factors Alcoholism Hypercalcemia Trauma Hyperlipidemia

Pancreatitis

Etiology and predisposing factors

Alcoholism

Hypercalcemia

Trauma

Hyperlipidemia

CONDITION OF THE PANCREAS Pancreatitis Etiology and predisposing factors Biliary tract disease - cholelithiasis Bacterial disease PUD Mumps

Pancreatitis

Etiology and predisposing factors

Biliary tract disease - cholelithiasis

Bacterial disease

PUD

Mumps

CONDITION OF THE PANCREAS PATHOPHYSIOLOGY of acute pancreatitis Self-digestion of the pancreas by its own digestive enzymes principally TRYPSIN

PATHOPHYSIOLOGY of acute pancreatitis

Self-digestion of the pancreas by its own digestive enzymes principally TRYPSIN

CONDITION OF THE PANCREAS PATHOPHYSIOLOGY of acute pancreatitis Spasm, edema or block in the Ampulla of Vater  reflux of proteolytic enzymes  auto digestion of the pancreas  inflammation

PATHOPHYSIOLOGY of acute pancreatitis

Spasm, edema or block in the Ampulla of Vater  reflux of proteolytic enzymes  auto digestion of the pancreas  inflammation

CONDITION OF THE PANCREAS PATHOPHYSIOLOGY of acute pancreatitis Autodigestion of pancreatic tissue Hemorrhage, Necrosis and Inflammation KININ ACTIVATION will result to increased permeability Loss of Protein-rich fluid into the peritoneum HYPOVOLEMIA

PATHOPHYSIOLOGY of acute pancreatitis

Autodigestion of pancreatic tissue

Hemorrhage, Necrosis and Inflammation

KININ ACTIVATION will result to increased permeability

Loss of Protein-rich fluid into the peritoneum

HYPOVOLEMIA

CONDITION OF THE PANCREAS ASSESSMENT findings 1. Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake 2. Abdominal guarding

ASSESSMENT findings

1. Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake

2. Abdominal guarding

CONDITION OF THE PANCREAS ASSESSMENT findings 3. Bruising on the flanks and umbilicus 4. N/V, jaundice 5. Hypotension and hypovolemia 6. Signs of shock

ASSESSMENT findings

3. Bruising on the flanks and umbilicus

4. N/V, jaundice

5. Hypotension and hypovolemia

6. Signs of shock

CONDITION OF THE PANCREAS DIAGNOSTIC TESTS 1. Serum amylase and serum lipase 2. Ultrasound 3. WBC 4. Serum calcium 5. CT scan 6. Hemoglobin and hematocrit

DIAGNOSTIC TESTS

1. Serum amylase and serum lipase

2. Ultrasound

3. WBC

4. Serum calcium

5. CT scan

6. Hemoglobin and hematocrit

CONDITION OF THE PANCREAS NURSING INTERVENTIONS 1. Assist in pain management. Usually, Demerol is given . Morphine is AVOIDED 2. Assist in correction of Fluid and Blood loss

NURSING INTERVENTIONS

1. Assist in pain management. Usually, Demerol is given . Morphine is AVOIDED

2. Assist in correction of Fluid and Blood loss

CONDITION OF THE PANCREAS NURSING INTERVENTIONS 3. Place patient on NPO to inhibit pancreatic stimulation 4. NGT insertion to decompress distention and remove gastric secretions 5. Maintain on bed rest

NURSING INTERVENTIONS

3. Place patient on NPO to inhibit pancreatic stimulation

4. NGT insertion to decompress distention and remove gastric secretions

5. Maintain on bed rest

CONDITION OF THE PANCREAS NURSING INTERVENTIONS 7. Position patient in SEMI-FOWLER’s to decrease pressure on the diaphragm 8. Deep breathing and coughing exercises 9. Provide parenteral nutrition

NURSING INTERVENTIONS

7. Position patient in SEMI-FOWLER’s to decrease pressure on the diaphragm

8. Deep breathing and coughing exercises

9. Provide parenteral nutrition

CONDITION OF THE PANCREAS NURSING INTERVENTIONS 10. Introduce oral feedings gradually- HIGH carbo, LOW FAT 11. Maintain skin integrity 12. Manage shock and other complications

NURSING INTERVENTIONS

10. Introduce oral feedings gradually- HIGH carbo, LOW FAT

11. Maintain skin integrity

12. Manage shock and other complications

Damage to pancreatic cells Inflammation Edema of the Pancreas and Pancreatic duct Obstruction to the Flow of Pancreatic Enzyme Activation of Pancreatic Enzymes inside Pancreas AUTODIGESTION of the Pancreas Fatty Necrosis, Ulceration, Hemorrhage, Infection Pathophysiology

CHRONIC PANCREATITIS NURSING ASSESSMENT: Abdominal pain LUQ mass Steatorrhea and foul smelling stools Weight loss Muscle wasting Jaundice S/Sx DM

NURSING ASSESSMENT:

Abdominal pain

LUQ mass

Steatorrhea and foul smelling stools

Weight loss

Muscle wasting

Jaundice

S/Sx DM

NIRSING INTERVENTION Diet: fat/CHON limited Avoid heavy meals/alcohol Supplemental vitamins Pancreatic enzyme Insulin

NIRSING INTERVENTION

Diet: fat/CHON limited

Avoid heavy meals/alcohol

Supplemental vitamins

Pancreatic enzyme

Insulin

Notify MD: increased steatorrhea, abdominal distention, cramping, and skin breakdown

Notify MD: increased steatorrhea, abdominal distention, cramping, and skin breakdown

Hepatitis

Hepatitis Infectious inflammation of the liver parenchyma caused by bacteria, viruses and other microorganisms. Viral hepatitis is caused by systemic viral infections that predominantly affect the hepatocytes and cause an increase in transaminases. ALT is excreted mainly by the hepatocytes whereas AST may be excreted anywhere in the GI tract in addition to the liver. ALT is specific for hepatocyte damage; thus in viral hepatitis ALT>AST, unlike ethanol heapatitis which the opposite is true. Viral hepatitis is one of the three causes of transaminase elevation>1,000 (the other two being toxins- acetaminophen and shock liver). Cirrhosis can develop as a result of chronic hepatitis that occurs with hepatitis B and C. Fulminatic hepatic failure with massive hepatic necrosis is rare but can occur with all viral hepatitides. Viral hepatitides are caused by RNA viruses, except hepatitis B, which are caused by DNA virus. There is wide spread inflammation of the liver tissue with liver cell damage due to hepatic cell degeneration and necrosis; proliferation and enlargement of the Kuppfer cells; inflammation of the perportal areas (may cause interruption of the bile flow).

Hepatitis

Infectious inflammation of the liver parenchyma caused by bacteria, viruses and other microorganisms.

Viral hepatitis is caused by systemic viral infections that predominantly affect the hepatocytes and cause an increase in transaminases. ALT is excreted mainly by the hepatocytes whereas AST may be excreted anywhere in the GI tract in addition to the liver. ALT is specific for hepatocyte damage; thus in viral hepatitis ALT>AST, unlike ethanol heapatitis which the opposite is true. Viral hepatitis is one of the three causes of transaminase elevation>1,000 (the other two being toxins- acetaminophen and shock liver). Cirrhosis can develop as a result of chronic hepatitis that occurs with hepatitis B and C. Fulminatic hepatic failure with massive hepatic necrosis is rare but can occur with all viral hepatitides. Viral hepatitides are caused by RNA viruses, except hepatitis B, which are caused by DNA virus.

There is wide spread inflammation of the liver tissue with liver cell damage due to hepatic cell degeneration and necrosis; proliferation and enlargement of the Kuppfer cells; inflammation of the perportal areas (may cause interruption of the bile flow).

Viral Hepatitis A Single-stranded RNA virus transmitted via fecal-oral route predominantly. Poor hygiene or contaminated food and shellfish increase risk of transmission. There is no transplacental transmission. It carries the risk of fulminant hepatitis. There is incubation period: 15-45 days. Viral Hepatitis B Hepatitis B is caused by a DNA virus, identified in all body fluids, blood, saliva, synovial fluid, breast milk, ascites, cerebral spinal fluid, etc. Transmitted by blood and body fluids (saliva, semen, vaginal secretions): often from contaminated needles among IV drug abusers; intimate/ sexual contact. Hepatitis B accounts for 50% of cases of fulminant hepatitis. In an adult who develops acute hepatitis B, there is approximately 10% chance that it will progress into chronic hepatitis; in the neonate the chance is 90% for chronic hepatitis. Incubation period is very long: 1-6 months.

Viral Hepatitis A

Single-stranded RNA virus transmitted via fecal-oral route predominantly. Poor hygiene or contaminated food and shellfish increase risk of transmission. There is no transplacental transmission. It carries the risk of fulminant hepatitis. There is incubation period: 15-45 days.

Viral Hepatitis B

Hepatitis B is caused by a DNA virus, identified in all body fluids, blood, saliva, synovial fluid, breast milk, ascites, cerebral spinal fluid, etc. Transmitted by blood and body fluids (saliva, semen, vaginal secretions): often from contaminated needles among IV drug abusers; intimate/ sexual contact. Hepatitis B accounts for 50% of cases of fulminant hepatitis. In an adult who develops acute hepatitis B, there is approximately 10% chance that it will progress into chronic hepatitis; in the neonate the chance is 90% for chronic hepatitis. Incubation period is very long: 1-6 months.

Viral Hepatitis C This is caused by a single-stranded RNA virus that is generally transmitted predominantly by blood products. Currently it is the most common hepatitis among IV drug abusers and in prisons. Before 1990 it accounted for 90% of transfusion hepatitis. Risk for sexual transmission is present but much lower that with hepatitis B (<5%). Perinatal transmission is 5%, needlestick transmission is 5-10% and risk of hepatocellular carcinoma is 1-4% in cirrhotics. Incubation is 2 weeks- 6 months. There is a high risk of progression to chronic form (70-80%). It is associated with extrahepatic manifestations commonly: mixed cryoglobulinemia and polyarteritis nodosa.

Viral Hepatitis C

This is caused by a single-stranded RNA virus that is generally transmitted predominantly by blood products. Currently it is the most common hepatitis among IV drug abusers and in prisons. Before 1990 it accounted for 90% of transfusion hepatitis. Risk for sexual transmission is present but much lower that with hepatitis B (<5%). Perinatal transmission is 5%, needlestick transmission is 5-10% and risk of hepatocellular carcinoma is 1-4% in cirrhotics. Incubation is 2 weeks- 6 months. There is a high risk of progression to chronic form (70-80%). It is associated with extrahepatic manifestations commonly: mixed cryoglobulinemia and polyarteritis nodosa.

Viral Hepatitis D Caused by an RNA virus that affects either simultaneously with hepatitis B or as a super-infection in a person with chronic hepatitis B. Hepatitis D infection cannot occur unless there is current and ongoing replication of the hepatitis B virus. Overall this infection carries the highest risk among acute viral hepatitis for fulminant disease; the risk is even greater in super-infection. Predominantly seen in patients exposed to blood products (drug addicts and hemophiliacs). If anti-HBs antibodies are present, then that person is immune to hepatitis B and D. Viral Hepatitis E Similar to hepatitis A with fecal or oral transmission, there is no chronic form. The risk of fulminant disease has been described mainly in preganant patients.

Viral Hepatitis D

Caused by an RNA virus that affects either simultaneously with hepatitis B or as a super-infection in a person with chronic hepatitis B. Hepatitis D infection cannot occur unless there is current and ongoing replication of the hepatitis B virus. Overall this infection carries the highest risk among acute viral hepatitis for fulminant disease; the risk is even greater in super-infection. Predominantly seen in patients exposed to blood products (drug addicts and hemophiliacs). If anti-HBs antibodies are present, then that person is immune to hepatitis B and D.

Viral Hepatitis E

Similar to hepatitis A with fecal or oral transmission, there is no chronic form. The risk of fulminant disease has been described mainly in preganant patients.

Assessment findings Preicteric stage Anorexia, nausea and vomiting, fatigue, constipation or diarrhea, weight loss. Right upper quadrant discomfort, hepatomegaly, splenomegaly, lymphadenopathy. Icteric stage Fatigue, weight loss, light-colored stools, dark urine. Continued heapatomegaly with tenderness, lymphatomegaly, splenomegaly Jaundice, pruritus. Posticteric stage Fatigue, but an increased sense of weel-being, hepatomegaly gradually decreasing

Assessment findings

Preicteric stage

Anorexia, nausea and vomiting, fatigue, constipation or diarrhea, weight loss.

Right upper quadrant discomfort, hepatomegaly, splenomegaly, lymphadenopathy.

Icteric stage

Fatigue, weight loss, light-colored stools, dark urine.

Continued heapatomegaly with tenderness, lymphatomegaly, splenomegaly

Jaundice, pruritus.

Posticteric stage

Fatigue, but an increased sense of weel-being, hepatomegaly gradually decreasing

Pathophysiology of Viral Hepatitis There is Diffuse Inflammatory Infiltration of Hepatic Tissue with Mononuclear Cells and local, spotty or single cell necrosis Preicteric (prodromal phase)- lasts for 1 week. Assessment: Elevated temperature and chills, nausea and vomiting, dyspnea, anorexia (the major manifestation) headache, arthralgia, tenderness in RUQ, weakness, general malaise, weight loss, hepatomegaly and lymphadenopathy. Icteric Phase: Starts with the onset of jaundice, it reaches its intensity in 2 weeks and lasts from 4 to 6 weeks= worsening of anorexia, anausea and vomiting, dyspnea, weakness and malaise and liver tenderness increases. Posticteric Phase: Begins with the disappearance of jaundice, normally lasts for several weeks up to 4

Pathophysiology of Viral Hepatitis

There is Diffuse Inflammatory Infiltration of Hepatic Tissue with Mononuclear Cells and local, spotty or single cell necrosis

Preicteric (prodromal phase)- lasts for 1 week. Assessment: Elevated temperature and chills, nausea and vomiting, dyspnea, anorexia (the major manifestation) headache, arthralgia, tenderness in RUQ, weakness, general malaise, weight loss, hepatomegaly and lymphadenopathy.

Icteric Phase: Starts with the onset of jaundice, it reaches its intensity in 2 weeks and lasts from 4 to 6 weeks= worsening of anorexia, anausea and vomiting, dyspnea, weakness and malaise and liver tenderness increases.

Posticteric Phase: Begins with the disappearance of jaundice, normally lasts for several weeks up to 4

Decrease Ammonia formation Restrict protein in the diet Duphalac (lactulose) Neomycin sulfate Tap water or NSS enema Avoid sedatives and paracetamol. Avoid ASA. Avoid Hypokalemia

Decrease Ammonia formation

Restrict protein in the diet

Duphalac (lactulose)

Neomycin sulfate

Tap water or NSS enema

Avoid sedatives and paracetamol.

Avoid ASA.

Avoid Hypokalemia

Diagnostic tests All 5 types of hepatitis SGPT, SGOT or AST, alkaline, phosphatase, bilirubin, ESR: all increased (preicteric) Leukocytes, lymphocytes, neutrophils: all decreased (pericteric) Prolonged PT Hepatitis A Hepatits A virus (HAV) in stool before onset of disease Anti-HAV (IgM): positive in acute infection; indicating a recent exposure. Anti-HAV (IgG) appears soon after onset of jaundice; indicates previous exposure and life-long immunity.

Diagnostic tests

All 5 types of hepatitis

SGPT, SGOT or AST, alkaline, phosphatase, bilirubin, ESR: all increased (preicteric)

Leukocytes, lymphocytes, neutrophils: all decreased (pericteric)

Prolonged PT

Hepatitis A

Hepatits A virus (HAV) in stool before onset of disease

Anti-HAV (IgM): positive in acute infection; indicating a recent exposure.

Anti-HAV (IgG) appears soon after onset of jaundice; indicates previous exposure and life-long immunity.

Hepatitis B HBsAG (surface antigen): positive, develops 4-12 weeks after injection (in the acute phase. Anti-HBsAG: negative in 80% of cases. If positive alone, indicates prior immunity via vaccination. If core antibody (anti-HBc) is also present his point toward a previous infection and immunity. Anti-HBc: associated with infectivity, develops 2-16 weeks after infection HBeAg: associated with infectivity and disappears before jaundice Anti-HBe: present in carriers, represents low jaundice Hepatitis C Antibody to hepatitis C (anti-HCV) is usually posititve. HCV RNA polymerase chain reaction is the most sensitive way to detect hepatitis C

Hepatitis B

HBsAG (surface antigen): positive, develops 4-12 weeks after injection (in the acute phase.

Anti-HBsAG: negative in 80% of cases. If positive alone, indicates prior immunity via vaccination. If core antibody (anti-HBc) is also present his point toward a previous infection and immunity.

Anti-HBc: associated with infectivity, develops 2-16 weeks after infection

HBeAg: associated with infectivity and disappears before jaundice

Anti-HBe: present in carriers, represents low jaundice

Hepatitis C

Antibody to hepatitis C (anti-HCV) is usually posititve.

HCV RNA polymerase chain reaction is the most sensitive way to detect hepatitis C

Nursing Interventions Promote adequate nutrition. Administer anti-emetics as ordered, 30 minutes before meals to decrease occurrence of nausea and vomiting Provide small, frequent meals of a high-carbohydrate, moderate- to high-protein, high vitamin, high- calorie intake Avoid very hot or very cold foods Ensure rest/ relaxation: plan schedule for rest and activity periods, organize nursing care to minimize interruption. Monitor/ relieve pruritus Administer corticosteroids are ordered. Institute isolation procedures are required: pay special attention to good hand-washing technique and adequate sanitation. In hepatitis A administer immune serum globulin (ISG) early to exposed individuals as ordered.

Nursing Interventions

Promote adequate nutrition.

Administer anti-emetics as ordered, 30 minutes before meals to decrease occurrence of nausea and vomiting

Provide small, frequent meals of a high-carbohydrate, moderate- to high-protein, high vitamin, high- calorie intake

Avoid very hot or very cold foods

Ensure rest/ relaxation: plan schedule for rest and activity periods, organize nursing care to minimize interruption.

Monitor/ relieve pruritus

Administer corticosteroids are ordered.

Institute isolation procedures are required: pay special attention to good hand-washing technique and adequate sanitation.

In hepatitis A administer immune serum globulin (ISG) early to exposed individuals as ordered.

In hepatitis B Screen donors for HBsAg. Use disposable needles an syringes. Instruct client/ others to avoid sexual intercourse while disease is active. Administer ISG to exposed individuals as ordered. Administer hepatitis B immunoglobulin (HBIG) as ordered to provide temporary and passive immunity to exposed individuals. To produce active immunity, administer hepatitis B vaccine to those individuals at high risk. In non-A, non-B: use disposable needles and syringes; ensure adequate sanitation. Provide client teaching and discharge planning concerning Importance of avoiding alcohol Avoidance of persons with known infections Balance of activity and rest periods Importance of not donating blood Dietary modifications Recognition and reporting of signs of inadequate convalescence: anorexia, jaundice, increasing liver tenderness/ discomfort. Techniques/ importance of good personal hygiene

In hepatitis B

Screen donors for HBsAg.

Use disposable needles an syringes.

Instruct client/ others to avoid sexual intercourse while disease is active.

Administer ISG to exposed individuals as ordered.

Administer hepatitis B immunoglobulin (HBIG) as ordered to provide temporary and passive immunity to exposed individuals.

To produce active immunity, administer hepatitis B vaccine to those individuals at high risk.

In non-A, non-B: use disposable needles and syringes; ensure adequate sanitation.

Provide client teaching and discharge planning concerning

Importance of avoiding alcohol

Avoidance of persons with known infections

Balance of activity and rest periods

Importance of not donating blood

Dietary modifications

Recognition and reporting of signs of inadequate convalescence: anorexia, jaundice, increasing liver tenderness/ discomfort.

Techniques/ importance of good personal hygiene

General Preventive Measures Hand washing by all persons Feces, urine, blood and other fluids are considered potentially infectious and should be disposed properly. Contaminated needles and other equipment that comes in contact with infected blood and body fluids, disposable and non-disposable needles, syringes and other equipment used in patient care must be handled with great care; discarded in appropriate containers. Preventive Measures Used with Persons with Known Hepatitis For clients with known hepatitis A, enteric precautions should be implemented For clients with Hepatits B; non-A, non-B hepatitis; blood and body fluid precaution should be observed Instruct clients with viral hepatitis not to donate blood. Advise client with acute hepatitis B; non-A, non-B hepatitis or delta hepatitis not to have intimate sexual contact during the period of infection.

General Preventive Measures

Hand washing by all persons

Feces, urine, blood and other fluids are considered potentially infectious and should be disposed properly.

Contaminated needles and other equipment that comes in contact with infected blood and body fluids, disposable and non-disposable needles, syringes and other equipment used in patient care must be handled with great care; discarded in appropriate containers.

Preventive Measures Used with Persons with Known Hepatitis

For clients with known hepatitis A, enteric precautions should be implemented

For clients with Hepatits B; non-A, non-B hepatitis; blood and body fluid precaution should be observed

Instruct clients with viral hepatitis not to donate blood.

Advise client with acute hepatitis B; non-A, non-B hepatitis or delta hepatitis not to have intimate sexual contact during the period of infection.

Summary of Collaborative Management in Viral Hepatitis Promotion of rest to relieve fatigue Maintenance of food and fluid intake 3,000 ml/day of fluids for fever and vomiting; monitor I and O, weight Well-balanced diet; encourage fruit juices and carbonated beverages Fats may need to be restricted Alcoholic beverages should be avoided Prevention of injury Prolonged prothrombin time leads leads to bleeding tendencies Monitor urine and stools for fresh or old blood; the skin for petechiae Monitor prpthrombin time, hematocrit and hemoglobin Plan so that all blood samples are collected at one time to avoid several punctures Avoid parenteral injections, if possible

Summary of Collaborative Management in Viral Hepatitis

Promotion of rest to relieve fatigue

Maintenance of food and fluid intake

3,000 ml/day of fluids for fever and vomiting; monitor I and O, weight

Well-balanced diet; encourage fruit juices and carbonated beverages

Fats may need to be restricted

Alcoholic beverages should be avoided

Prevention of injury

Prolonged prothrombin time leads leads to bleeding tendencies

Monitor urine and stools for fresh or old blood; the skin for petechiae

Monitor prpthrombin time, hematocrit and hemoglobin

Plan so that all blood samples are collected at one time to avoid several punctures

Avoid parenteral injections, if possible

Apply pressure to injection sites and venipuncture sites for minutes Advise client to use soft toothbrush or swabs Administer vitamin K as ordered Provision of comfort measures Relaxing baths, bakrubs, fresh linens and quiet dark environment Relieve pruritus through the following measures: Use of cool, light, non- restrictive clothing Use of soft, dry, clean bedding, use of warm baths Application of emollient creams and lotions to dry skin Maintenance of cool environment Administration of antihistamines as ordered Use of diversional activities, e.g. reading, TV and radio

Apply pressure to injection sites and venipuncture sites for minutes

Advise client to use soft toothbrush or swabs

Administer vitamin K as ordered

Provision of comfort measures

Relaxing baths, bakrubs, fresh linens and quiet dark environment

Relieve pruritus through the following measures:

Use of cool, light, non- restrictive clothing

Use of soft, dry, clean bedding, use of warm baths

Application of emollient creams and lotions to dry skin

Maintenance of cool environment

Administration of antihistamines as ordered

Use of diversional activities, e.g. reading, TV and radio

Cirrhosis of the Liver

LIVER Normal Function 1. Stores glycogen 2. Synthesizes proteins 3. Synthesizes globulins 4. Synthesizes Clotting factors 5. Secreting bile 6. Converts ammonia to urea 7. Stores Vitamims and minerals 8. Metabolizes estrogen

Liver function test: AST aspartate aminotransferase formerly SGOT 4.8 - 19 U/L ALT alanine aminotransferase formerly SGPT 2.4 - 7 U/L highly specific

Liver function test:

AST aspartate aminotransferase formerly SGOT 4.8 - 19 U/L

ALT alanine aminotransferase formerly SGPT 2.4 - 7 U/L highly specific

Liver Biopsy

Jaundice a symptom of a disease yellow pigmentation of the skin due to accumulation of bilirubin pigment usually observed first in the sclera kernicterus (brain) fatal

a symptom of a disease

yellow pigmentation of the skin

due to accumulation of bilirubin pigment

usually observed first in the sclera

kernicterus (brain) fatal

Hemolytic Jaundice due to: rapid RBC destruction increased in indirect, unconjugated or B2 due to transfusion reaction or EBF

due to:

rapid RBC destruction increased in indirect, unconjugated or B2

due to transfusion reaction or EBF

Obstructive Jaundice due to: biliary atresia inflammation of the biliary tract tumors cholestatic agent total bilirubin is increased bile is dammed into the liver and reabsorbed into the circulatory s/sx: deep orange, foamy urine dark tea colored urine clay colored stool severe itchiness steatorrhea

due to:

biliary atresia

inflammation of the biliary tract

tumors

cholestatic agent

total bilirubin is increased

bile is dammed into the liver and reabsorbed into the circulatory

s/sx:

deep orange, foamy urine

dark tea colored urine

clay colored stool

severe itchiness

steatorrhea

Hepatic Jaundice due to: Diseased liver (hepatitis or cirrhosis) Inability of the liver to clear normal amount of bilirubin from the blood Increased bilirubin and albumin

due to:

Diseased liver (hepatitis or cirrhosis)

Inability of the liver to clear normal amount of bilirubin from the blood

Increased bilirubin and albumin

Jaundice Management: Control pruritus calamine baking soda NaHCO3 Antihistamine Soothing baths Drug Cholestyramine = it binds bile salts in the intestine and eliminated via feces. Look for the cause and manage it

Control pruritus

calamine

baking soda

NaHCO3

Antihistamine

Soothing baths

Drug

Cholestyramine = it binds bile salts in the intestine and eliminated via feces.

Look for the cause and manage it

Cirrhosis of the Liver Chronic, progressive disease characterized by inflammation, fibrosis and degeneration of the liver parenchymal cells Destroyed liver cells are replaced by scar tissue, resulting in architectural changes and malfunction of the liver

Cirrhosis of the Liver

Chronic, progressive disease characterized by inflammation, fibrosis and degeneration of the liver parenchymal cells

Destroyed liver cells are replaced by scar tissue, resulting in architectural changes and malfunction of the liver

Types Laennec’s cirrhosis: associated with alcohol abuse and malnutrition Biliary cirrhosis: associated with biliary obstruction Post necrotic cirrhosis Cardiac cirrhosis

Types

Laennec’s cirrhosis: associated with alcohol abuse and malnutrition

Biliary cirrhosis: associated with biliary obstruction

Post necrotic cirrhosis

Cardiac cirrhosis

Pathogenesis: repeated destruction of hepatic cell  scar tissue formation (fibrotic)  regeneration of liver cell follows  another destruction will occur  cycle (scarring and regeneration) will be repeated until hepatocytes becomes fibrotic and liver function is compromised

repeated destruction of hepatic cell  scar tissue formation (fibrotic)  regeneration of liver cell follows  another destruction will occur  cycle (scarring and regeneration) will be repeated until hepatocytes becomes fibrotic and liver function is compromised

Pathophysiology Alcohol abuse Leonnec’s Cirrhosis Malnutrition Infection Postnecrotic Cirrhosis Drugs Biliary Obstruction- Biliary Cirrhosis RSCHF- Cardiac Cirrhosis Destruction of HEPATOCYTES FIBROSIS/SCARRING Obstruction of blood flow Increase Pressure in the venous and sinusoidal channels Fatty infiltration FIBROSIS/SCARRING PORTAL HYPERTENSION } }

Assessment of Liver Cirrhosis Portal HPN and the consequences are: Hepatomegaly = initially then the liver shrinks in size as fibrosis replaces the liver parenchyma Splenomegaly = due to increased backpressure of the blood Caput medusae (dilated veins over the abdomen) Spider angioma (telangiectasia / dilated capillaries over the face and the anterior trunk) = due to increased estrogen. Palmar erythema . This is also due to estrogen level in males.

Assessment of Liver Cirrhosis

Portal HPN and the consequences are:

Hepatomegaly = initially then the liver shrinks in size as fibrosis replaces the liver parenchyma

Splenomegaly = due to increased backpressure of the blood

Caput medusae (dilated veins over the abdomen)

Spider angioma (telangiectasia / dilated capillaries over the face and the anterior trunk) = due to increased estrogen.

Palmar erythema . This is also due to estrogen level in males.

PORTAL HYPERTENSION Esophageal varices Fluid extravasation Ascites and edema

PORTAL HYPERTENSION

Esophageal varices

Fluid extravasation

Ascites and edema

 collateral circulation vein distention (angioma) hemorrhoids spiderangioma (red dot) palmar erythema telangiectasia (permanent) esophageal varices

 collateral circulation

vein distention (angioma)

hemorrhoids

spiderangioma (red dot)

palmar erythema

telangiectasia (permanent)

esophageal varices

Caput Medusae

ASCITES HYPOALBUMINEMIA DECREASED METABOLISM OF ALDOSTERONE

HYPOALBUMINEMIA

DECREASED METABOLISM OF ALDOSTERONE

Males (increased estrogen) will result to: Gynecomastia Decreased libido Impotence Fall of body hair Atrophy of testicles Females (Increased androgen) Hirtuism Acne Deepening of voice Virilism

Males (increased estrogen) will result to:

Gynecomastia

Decreased libido

Impotence

Fall of body hair

Atrophy of testicles

Females (Increased androgen)

Hirtuism

Acne

Deepening of voice

Virilism

Esohageal Varices

Esophageal Varices Definition: ETIOLOGY: Emergency condition ASSESSMENT findings for EV Hematemesis Melena Ascites Jaundice hepatomegaly/splenomegaly Signs of Shock

Esophageal Varices

Definition:

ETIOLOGY:

Emergency condition

ASSESSMENT findings for EV

Hematemesis

Melena

Ascites

Jaundice

hepatomegaly/splenomegaly

Signs of Shock

DIAGNOSTIC PROCEDURE Esophagoscopy to locate the bleeding site

DIAGNOSTIC PROCEDURE

Esophagoscopy to locate the bleeding site

CONDITION OF THE ESOPHAGUS NURSING INTERVENTIONS FOR EV 1. Monitor VS strictly. Note for signs of shock 2. Monitor for LOC 3. Maintain NPO

NURSING INTERVENTIONS FOR EV

1. Monitor VS strictly. Note for signs of shock

2. Monitor for LOC

3. Maintain NPO

CONDITION OF THE ESOPHAGUS NURSING INTERVENTIONS FOR EV 4. Monitor blood studies 5. Administer O2 6. prepare for blood transfusion

NURSING INTERVENTIONS FOR EV

4. Monitor blood studies

5. Administer O2

6. prepare for blood transfusion

CONDITION OF THE ESOPHAGUS INTERVENTIONS FOR EV 7. prepare to administer Vasopressin and Nitroglycerin 8. Assist in NGT and Sengstaken-Blakemore tube insertion for balloon tamponade

INTERVENTIONS FOR EV

7. prepare to administer Vasopressin and Nitroglycerin

8. Assist in NGT and Sengstaken-Blakemore tube insertion for balloon tamponade

CONDITION OF THE ESOPHAGUS NURSING INTERVENTIONS FOR EV 9. Prepare to assist in surgical management: Endoscopic sclerotherapy Variceal ligation Shunt procedures

NURSING INTERVENTIONS FOR EV

9. Prepare to assist in surgical management:

Endoscopic sclerotherapy

Variceal ligation

Shunt procedures

If bleeding esophageal varices occur: Place in semi-Fowler’s position to prevent aspiration Suction the mouth Administer vasopressin as ordered Gastric lavage with tap water (room temperature saline) as ordered. Sclerotherapy Balloon tamponade with the use of Sengstaken – Blakemore tube Variceal band ligation Portasystemic shunting Portacaval Splenorenal Mesocaval

If bleeding esophageal varices occur:

Place in semi-Fowler’s position to prevent aspiration

Suction the mouth

Administer vasopressin as ordered

Gastric lavage with tap water (room temperature saline) as ordered.

Sclerotherapy

Balloon tamponade with the use of Sengstaken – Blakemore tube

Variceal band ligation

Portasystemic shunting

Portacaval

Splenorenal

Mesocaval

Nursing Interventions Provide sufficient rest and comfort. Bed rest with bathroom privileges. Encourage gradual, progressive, increasing activity with planned rest periods. Institute measures to relieve pruritus. Bath with tepid water followed by application of an emollient lotion. Provide cool, light, nonrestrictive clothing. Keep nails short to Apply cool, moist compresses to pruritic areas. Promote nutritional intake. Small frequent feedings. Promote a high calorie, low to moderate protein, high carbohydrate, low fat diet, with supplemental vitamin therapy (vitamins A, B-complex, C, D, K and folic acid) Prevent infection Frequent turning and skin care. Reverse isolation for clients with severe leucopenia Monitor WBC.

Nursing Interventions

Provide sufficient rest and comfort.

Bed rest with bathroom privileges.

Encourage gradual, progressive, increasing activity with planned rest periods.

Institute measures to relieve pruritus.

Bath with tepid water followed by application of an emollient lotion.

Provide cool, light, nonrestrictive clothing.

Keep nails short to

Apply cool, moist compresses to pruritic areas.

Promote nutritional intake.

Small frequent feedings.

Promote a high calorie, low to moderate protein, high carbohydrate, low fat diet, with supplemental vitamin therapy (vitamins A, B-complex, C, D, K and folic acid)

Prevent infection

Frequent turning and skin care.

Reverse isolation for clients with severe leucopenia

Monitor WBC.

Monitor/prevent bleeding. Administer diuretics as ordered. Provide client teaching and discharge planning concerning. Avoidance of hepatotoxic agents ( sedatives, opiates, or OTC drugs detoxified by the liver). Avoid infections, DHN, Fever Avoidance of all alcohol. Avoidance of straining at stool, vigorous blowing of nose and coughing to decrease the incidence of bleeding.

Monitor/prevent bleeding.

Administer diuretics as ordered.

Provide client teaching and discharge planning concerning.

Avoidance of hepatotoxic agents ( sedatives, opiates, or OTC drugs detoxified by the liver).

Avoid infections, DHN, Fever

Avoidance of all alcohol.

Avoidance of straining at stool, vigorous blowing of nose and coughing to decrease the incidence of bleeding.

macky

Liver physiology and Pathophysiology macky Normal Function Abnormality in function 1. Stores glycogen = Hypoglycemia 2. Synthesizes proteins = Hypo-proteinemia 3. Synthesizes globulins =Decreased Antibody formation  risk for INFECTION 4. Synthesizes Clotting factors = Bleeding tendencies 5. Secreting bile = Jaundice and pruritus 6. Converts ammonia to urea =Hyper-ammonemia 7. Stores Vitamims and minerals =Deficiencies of Vit and min 8. Metabolizes estrogen = Gynecomastia, testes atrophy

HEPACTIC ENCEPHALOPATHY Is due to increased AMMONIA levels. The liver cannot convert ammonia by products of protein metabolism into Urea Hepatic coma The initial manifestations are BEHAVIORAL changes and MENTAL changes. Advance Stage : Asterixis – Confusion / disorientation Delirium / hallucination Fetor hapaticus

HEPACTIC ENCEPHALOPATHY

Is due to increased AMMONIA levels. The liver cannot convert ammonia by products of protein metabolism into Urea Hepatic coma

The initial manifestations are BEHAVIORAL changes and MENTAL changes.

Advance Stage :

Asterixis –

Confusion / disorientation

Delirium / hallucination

Fetor hapaticus

Summary of Collaborative Management Rest. To reduce metabolic demands of the liver. Diet Early stage High calorie, HIGH carbohydrates, LOW protein that is restricted to complete protein only, moderate fats. Late stage HIGH calorie, HIGH carbohydrates, LOW protein. Skin care Avoid trauma/injury Prevent infection

Summary of Collaborative Management

Rest. To reduce metabolic demands of the liver.

Diet

Early stage

High calorie, HIGH carbohydrates, LOW protein that is restricted to complete protein only, moderate fats.

Late stage

HIGH calorie, HIGH carbohydrates, LOW protein.

Skin care

Avoid trauma/injury

Prevent infection

Decrease Ammonia formation Restrict protein in the diet Duphalac (lactulose) Neomycin sulfate Colchicine Tap water or NSS enema Avoid sedatives and paracetamol. Avoid ASA. Avoid Hypokalemia

Decrease Ammonia formation

Restrict protein in the diet

Duphalac (lactulose)

Neomycin sulfate

Colchicine

Tap water or NSS enema

Avoid sedatives and paracetamol.

Avoid ASA.

Avoid Hypokalemia

Manage Ascites Monitor weight, intake and output, abdominal girth Restrict sodium and fluid intake Administer diuretics as ordered Initially, K – sparring diuretic Later, K- wasting diuretic Administer albumin / IV as ordered assist in paracentesis

Manage Ascites

Monitor weight, intake and output, abdominal girth

Restrict sodium and fluid intake

Administer diuretics as ordered

Initially, K – sparring diuretic

Later, K- wasting diuretic

Administer albumin / IV as ordered assist in paracentesis

Abdominal Paracentesis Withdrawal of fluid from the peritonealspace Purpose: diagnostic and therapeutic Pretest: consent, empty bladder Position: sitting Site: midway between the umbilicus and symphysis

Withdrawal of fluid from the peritonealspace

Purpose: diagnostic and therapeutic

Pretest: consent, empty bladder

Position: sitting

Site: midway between the umbilicus and symphysis

Abdominal Paracentesis Intratest: 1,500 ml maximum amount collected at one time, Monitor VS Post-test : monitor VS, bleeding complication Measure abdominal girth and weight

Intratest: 1,500 ml maximum amount collected at one time, Monitor VS

Post-test : monitor VS, bleeding complication

Measure abdominal girth and weight

COLORECTAL CANCER

COLORECTAL CANCER Cause: Unknown Predisposing factors: Age above 40 years Diet Low in fiber High in fat, protein and refined carbohydrates Obesity History of IBD, familial polyposis or colon polyps Family history of colon cancer Most common site: Rectosigmoid area (70%)

COLORECTAL CANCER

Cause: Unknown

Predisposing factors:

Age above 40 years

Diet

Low in fiber

High in fat, protein and refined carbohydrates

Obesity

History of IBD, familial polyposis or colon polyps

Family history of colon cancer

Most common site: Rectosigmoid area (70%)

Assessment Ascending (right) Colon Cancer Occult blood in stool Anemia Anorexia and weight loss Abdominal pain above umbilicus Palpable mass Distal colon/ Rectal cancer Bright rectal bleeding Changed bowel habits Constipation or Diarrhea Pencil or ribbon- shaped stool Tenesmus Sensation of incomplete bowel emptying

Assessment

Ascending (right) Colon Cancer

Occult blood in stool

Anemia

Anorexia and weight loss

Abdominal pain above umbilicus

Palpable mass

Distal colon/ Rectal cancer

Bright rectal bleeding

Changed bowel habits

Constipation or Diarrhea

Pencil or ribbon- shaped stool

Tenesmus

Sensation of incomplete bowel emptying

Duke’s Classification of Colorectal Cancer Stage A: confined to bowel mucosa, 80-90% 5 –year survival rate Stage B: invading muscle wall Stage C: lymph node involvement Stage D: metastases or locally respectable tumor, less than 5%- 5- year survival rate.

Duke’s Classification of Colorectal Cancer

Stage A: confined to bowel mucosa, 80-90% 5 –year survival rate

Stage B: invading muscle wall

Stage C: lymph node involvement

Stage D: metastases or locally respectable tumor, less than 5%- 5- year survival rate.

Guidelines for Early Detection of Colorectal Cancer Digital rectal examination yearly after age 40-45 Occult blood test yearly after age 50 Protosigmoidoscopy every 5 years after age 50, following 2 negative results of yearly examination Collaborative Management Surgery Hemicolectomy Abdomino-Perineal Resection (APR) for rectosigmoid cancer Chemotherapy Fluorouracil is the most effective drug for colorectal cancer Radiotherapy Adjuvant therapy for rectal cancer

Guidelines for Early Detection of Colorectal Cancer

Digital rectal examination yearly after age 40-45

Occult blood test yearly after age 50

Protosigmoidoscopy every 5 years after age 50, following 2 negative results of yearly examination

Collaborative Management

Surgery

Hemicolectomy

Abdomino-Perineal Resection (APR) for rectosigmoid cancer

Chemotherapy

Fluorouracil is the most effective drug for colorectal cancer

Radiotherapy

Adjuvant therapy for rectal cancer

Medical Management: chemotherapy, radiation therapy, bowel surgery Colonic surgery Pre-op care Provide psychosocial support Through bowel cleansing Diet modification Low residue diet 3 to days preop, to reduce the bulk of the stool in the colon Clear liquid diet 24 hours preop Mechanical cleansing Laxatives as ordered Cleansing enema as ordered Pharmacologic suppression of colon bacteria Neomycin sulfate tablets to reduce bacterial flora. (it is poorly absorbed in the colon, thereby enhance excretion of colonic bacteria). Vitamin C and K supplement because these are lost during repeated enema administration.

Medical Management: chemotherapy, radiation therapy, bowel surgery

Colonic surgery

Pre-op care

Provide psychosocial support

Through bowel cleansing

Diet modification

Low residue diet 3 to days preop, to reduce the bulk of the stool in the colon

Clear liquid diet 24 hours preop

Mechanical cleansing

Laxatives as ordered

Cleansing enema as ordered

Pharmacologic suppression of colon bacteria

Neomycin sulfate tablets to reduce bacterial flora. (it is poorly absorbed in the colon, thereby enhance excretion of colonic bacteria).

Vitamin C and K supplement because these are lost during repeated enema administration.

Type of Colostomies Ascending Colostomy Stoma is on the right abdomen Fecal drainage is watery Transverse (Double-Barreled) Colostomy The right stoma is also called proximal stoma; closest to the small intestine; drains semi-formed feces. The left stoma is also called distal stoma; drains mucus Transverse Loop Colostomy Has 2 openings in the transverse colon, but one stoma Indicated in IBD’s Descending and Sigmoid Colostomy Stoma on the left abdomen Fecal drainage is well-formed

Type of Colostomies

Ascending Colostomy

Stoma is on the right abdomen

Fecal drainage is watery

Transverse (Double-Barreled) Colostomy

The right stoma is also called proximal stoma; closest to the small intestine; drains semi-formed feces.

The left stoma is also called distal stoma; drains mucus

Transverse Loop Colostomy

Has 2 openings in the transverse colon, but one stoma

Indicated in IBD’s

Descending and Sigmoid Colostomy

Stoma on the left abdomen

Fecal drainage is well-formed

Post-op Care Managing the perineal wound (APR) May require up to 6 months to completely heal Wound irrigations with normal saline and absorbent dressings until wound closes . Drainage is initially copious and sero-sanguinous, to be drained at regular basis to prevent infection and abscess formation T-binder is used to secure perineal dressing Sitz baths once the patient is ambulatory Foam pads or soft pillows to promote comfort when sitting Side-lying position during sleep Stoma Monitoring The stoma is pinkish to cherry red and with slight edema for 5-7 days Dark, dusky , or brown –black stoma indicates ischemia and necrosis The stoma should protrude by ½ to ¾ inch over abdomen Flatus and fecal drainage usually begin in 3 to 6 days, as peristalsis returns Empty the pouch when it is 1/3 to ½ full of stool Loop colostomy is opened 48-72 hours post-op, with cautery at bedside.

Post-op Care

Managing the perineal wound (APR)

May require up to 6 months to completely heal

Wound irrigations with normal saline and absorbent dressings until wound closes .

Drainage is initially copious and sero-sanguinous, to be drained at regular basis to prevent infection and abscess formation

T-binder is used to secure perineal dressing

Sitz baths once the patient is ambulatory

Foam pads or soft pillows to promote comfort when sitting

Side-lying position during sleep

Stoma Monitoring

The stoma is pinkish to cherry red and with slight edema for 5-7 days

Dark, dusky , or brown –black stoma indicates ischemia and necrosis

The stoma should protrude by ½ to ¾ inch over abdomen

Flatus and fecal drainage usually begin in 3 to 6 days, as peristalsis returns

Empty the pouch when it is 1/3 to ½ full of stool

Loop colostomy is opened 48-72 hours post-op, with cautery at bedside.

Teaching for Self-care Stoma Care Gently encourage the client to look at the stoma Inform that the stoma has no touch of pain sensation Instruct to report immediately any purple or black discoloration of stoma. Cleanse the stoma initially with antiseptic Skin Care Wash the skin with warm water, pat dry. Assess skin for signs of irritation or infection When pouch seal leaks, change pouch immediately Use skin barrier to protect the peristomal skin from liquid stool e.g. karaya preparation. Skin infection caused by Candida Ablicans is treated with nystatin (Mycostatin) powder.

Teaching for Self-care

Stoma Care

Gently encourage the client to look at the stoma

Inform that the stoma has no touch of pain sensation

Instruct to report immediately any purple or black discoloration of stoma.

Cleanse the stoma initially with antiseptic

Skin Care

Wash the skin with warm water, pat dry.

Assess skin for signs of irritation or infection

When pouch seal leaks, change pouch immediately

Use skin barrier to protect the peristomal skin from liquid stool e.g. karaya preparation.

Skin infection caused by Candida Ablicans is treated with nystatin (Mycostatin) powder.

Colostomy Irrigation Initially colostomy irrigation is done to stimulate peristalsis, subsequent irrigations are done to promote evacuation of feces at a regular and convenient time Recommendation with sigmoid colostomy Initiated 5 to 7 days Post-op Done in semi-Fowler’s position; then sitting on a toilet bowl once ambulatory Use warm normal saline solution Initially, introduce 200 ml. of NSS then 500 to 1,000 ml. Subsequently Dilate stoma with lubricated gloved finger before insertion of catheter Lubricate catheter before insertion Insert 2 to 4 inches of the catheter into the stoma Height of solution is 18 inches above the stoma If abdominal cramps occur during introduction of solution, temporarily stop the flow of solution until peristalsis relaxes Allow the catheter to remain in place for 5 to 10 minutes for better cleansing effect; then remove catheter to drain for 15 to 20 minutes Clean the stoma, apply stoma, apply new pouch

Colostomy Irrigation

Initially colostomy irrigation is done to stimulate peristalsis, subsequent irrigations are done to promote evacuation of feces at a regular and convenient time

Recommendation with sigmoid colostomy

Initiated 5 to 7 days Post-op

Done in semi-Fowler’s position; then sitting on a toilet bowl once ambulatory

Use warm normal saline solution

Initially, introduce 200 ml. of NSS then 500 to 1,000 ml. Subsequently

Dilate stoma with lubricated gloved finger before insertion of catheter

Lubricate catheter before insertion

Insert 2 to 4 inches of the catheter into the stoma

Height of solution is 18 inches above the stoma

If abdominal cramps occur during introduction of solution, temporarily stop the flow of solution until peristalsis relaxes

Allow the catheter to remain in place for 5 to 10 minutes for better cleansing effect; then remove catheter to drain for 15 to 20 minutes

Clean the stoma, apply stoma, apply new pouch

Managing Odor Avoid Gas – forming and foul odor foods, e.g. dairy products, highly seasoned foods, fish, cabbage, celery, cauliflower, eggs, carbonated beverages, nuts. Rinse pouch with tepid water or weak vinegar solution Place deodorant tablet or small amount of mouthwash or a piece of charcoal into the pouch Do not use pulverized ASA- it causes irritation of the stoma and damages the colostomy appliance.

Managing Odor

Avoid Gas – forming and foul odor foods, e.g. dairy products, highly seasoned foods, fish, cabbage, celery, cauliflower, eggs, carbonated beverages, nuts.

Rinse pouch with tepid water or weak vinegar solution

Place deodorant tablet or small amount of mouthwash or a piece of charcoal into the pouch

Do not use pulverized ASA- it causes irritation of the stoma and damages the colostomy appliance.

Supporting a Positive Self-Concept Encourage to view the stoma Encourage to verbalize feelings, fears and concern about stoma Encourage to participate in colostomy care. Encourage gradually resume all usual activities Avoid tight belts or waistbands over the stoma Advise to always carry colostomy supplies when traveling Resolving grief Encourage client to express feelings of loss Explore client’s usual coping strategies for handling grief Preventing Sexual Dysfunction Explore positions that minimizes stress and pressure on the pouch Empty and clean the pouch before sexual activity Use smaller – sized pouch or pouch cover during sexual activity Use of a binder of special underwear to hold the pouch secure

Supporting a Positive Self-Concept

Encourage to view the stoma

Encourage to verbalize feelings, fears and concern about stoma

Encourage to participate in colostomy care.

Encourage gradually resume all usual activities

Avoid tight belts or waistbands over the stoma

Advise to always carry colostomy supplies when traveling

Resolving grief

Encourage client to express feelings of loss

Explore client’s usual coping strategies for handling grief

Preventing Sexual Dysfunction

Explore positions that minimizes stress and pressure on the pouch

Empty and clean the pouch before sexual activity

Use smaller – sized pouch or pouch cover during sexual activity

Use of a binder of special underwear to hold the pouch secure

Home care instructions for colostomy. Instruct the colostomy patient to change the stoma appliance as needed, to wash the stoma site with warm and mild soap every 2-3 days and to change the adhesive layer as needed. These measures will prevent irritation and excoriation . Discuss dietary restrictions and suggestions to prevent blockage of the stoma, diarrhea, flatus, and odor. Tell patient to start on low fiber diet initially and then gradually introduce fiber foods. Corn, dried beans, onions, cabbage, fish, spicy dishes and some antibiotics can cause odor. Apples, melons, avocados and cantaloupe are additional foods that can cause excessive gas. Advise to drink liberal amount of fluids especially in hot weather and diarrhea.

Home care instructions for colostomy.

Instruct the colostomy patient to change the stoma appliance as needed, to wash the stoma site with warm and mild soap every 2-3 days and to change the adhesive layer as needed. These measures will prevent irritation and excoriation .

Discuss dietary restrictions and suggestions to prevent blockage of the stoma, diarrhea, flatus, and odor. Tell patient to start on low fiber diet initially and then gradually introduce fiber foods.

Corn, dried beans, onions, cabbage, fish, spicy dishes and some antibiotics can cause odor. Apples, melons, avocados and cantaloupe are additional foods that can cause excessive gas.

Advise to drink liberal amount of fluids especially in hot weather and diarrhea.

http://nursinglectures.blogspot.com FREE NURSING LECTURES - Medical Surgical Nursing Obstetric Nursing Psychiatric Nursing Fundamentals of Nursing And many more…

FREE NURSING LECTURES - Medical Surgical Nursing

Obstetric Nursing

Psychiatric Nursing

Fundamentals of Nursing

And many more…