Peritonitis And Other Git Complications

Presentation by : Group 1 PERITONITIS and other GIT complications ..

PREPARED BY; 1.Nur Syafiqah Bt Kamaruzaman(08DIN0050) 2.Haryani Jakarsi (08DIN0086) 3.Nabilah Bt Abu Samah (08DIN0021) 4.Nur Izzati Bt Ismail (08DIN0028) 5.Warsana A/P Bonsi (08DIN0412)

A &E

DEPT

Mr. Tan m/60yrs

C/O

You’ve been diagnosed with..

PERITONIT IS

FINALLY..

DEFINITION OF PERITONITIS •

dominal organs. The membrane supports the abdominal organs and

vPeritonitis is a serious disorder caused by an inflammation of the peritoneum, most often due to bacterial infection. v vIt is a life threatening illness which is often associated with various abdominal disorders and is routinely assessed for in all client with

LOCATION OF PERITONEUM

PERITONEUM

TYPES OF PERITONITIS • Primary peritonitis • usually caused by liver disease. Fluid builds up in the abdomen, creating a prime environment for the growth of bacteria.

• • Secondary peritonitis • caused by other conditions that allow bacteria, enzymes, or bile into the peritoneum from a hole or tear in the gastrointestinal or biliary tracts. Such tear can be caused by pancreatitis, a ruptured appendix, stomach ulcer, Crohn's disease, or diverticulitis. Peritoneal dialysis, which uses the blood vessels in the peritoneum to filter waste from your blood when your kidneys are not able to

CAUSES OF PERITONITIS 1. Infected peritonitis

vPerforation of a hollow viscus is the most common cause of peritonitis. E.g perforation of the distal oesophagus, of the stomach of the duodenum of the remaining intestine (e.g. appendicitis, diverticulitis, inflammatory bowel disease (IBD), intestinal infarction,colorectal carcinoma, meconium peritonitis). Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body, perforation by an endoscope or catheter, and anastomotic leakage. In most cases of perforation of a hollow viscus, mixed bacteria are isolated; the most common agents include Gram-negative bacilli (e.g. Escherichia coli) and anaerobic bacteria (e.g. Bacteroides fragilis).

CAUSES OF PERITONITIS 2.Disruption of the peritoneum vIt occurs even in the absence of perforation of a hollow viscus, may also cause infection simply by letting microorganisms into the peritoneal cavity. Examples include trauma, surgical wound, continuous ambulatory peritoneal dialysis, intra-peritoneal

CLINICAL MANIFESTATIONS

INVESTIGATIONS 1.X-RAYS 2. Plain abdominal X-ray may reveal dilated, oedematous intestines, although it is mainly useful to look for pneumoperitoneum (free air in the peritoneal cavity), which may also be visible on chest X-rays.

2. PHYSICAL EXAMINATION The 1. abdomen is hard and painful. There are no bowel movements or sounds.

3. BLOOD TESTS To check for which bacteria are responsible. 4. LAPAROSCOPY A slender tube is inserted through an abdominal incision and the insides examined.

5. PERITONEAL LAVAGE If reasonable doubt still persists, an exploratory peritoneal lavage may be performed (e.g. in cases of trauma, in order to look for white blood cells, red blood cells, or bacteria).

6. PARACENTASIS In patients with ascites, a diagnosis of peritonitis is achieved via paracentesis (abdominal tap): more than 250 polymorphonucleate cells per μL is considered diagnostic. In addition, Gram stain and culture of the peritoneal fluid can determine the microrganism responsible and determine their sensibility to antimicrobial agents.

PATHOPHYSIOLOGY Peritoneal infected Inflammatory reaction at walls of localised area

Increase capillary permeabili

Vascular dilatation

hyperemia Fluid shift

Decrease circulatory volume

Peristalsis slow caused abdominal distension

PERITONITIS

Bacteremia

Septicemia

NURSING CARE PLAN 1 Alteration in comfort : pain related to abdominal distension

Date:25.10.2009 Time:8.15 am Nursing Problem : Alteration in comfort : pain related to abdominal distension . Supporting Data:1)Patient verbalized that he in pain at the abdomen . 2)Patient face looked pale 3)Patient blood pressure 140/80mmHg, pulse 70 4) Patient choose number 6 out of 10 from pain scale which is consider as moderate pain. Goal : Patient’s pain will be reduced 1-2 hours after nursing interventions carried out and during hospitalization .

Nursing interventions:

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1.

Assess patient’s level of pain by asking patient whether the pain is mild , moderate or severe using pain scale and site of pain. •® As a baseline data and to plan proper nursing interventions to reduce pain •I-I assessed my patient’s level of pain using pain scale 1-10 and he choose 6-7 that moderate pain at the •

abdomen .

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2)Monitor vital signs especially blood pressure and pulse rate . •®Elevated blood pressure and pulse indicate patient’s in pain •I-I had monitored my patient’s vital signs especially blood pressure and pulse rate • •

3) Position patient to semi flower’s position as indicated . ® to keep patient comfortable and to reduce diaphragmatic irritation and abdominal tension . I-I had position my patient to a semi fowler’s and ensure my patient is comfortable .

4) Teach patient deep breathing exercises . •® deep breathing exercise may relax the muscle by divertional therapy and reduce pain . •I-I thought my patient to do deep breathing exercise when his condition was alert and I encouraged him to perform when he feels the pain •

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5) Provide call bell near to patient. ® To get nurses help when necessary. I-I put the call bell near to the patient and ask him to press if needed help.

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6)Inform doctor if patient’s pain still persist

® for further management •I-I didn’t informed doctor because my patient’s pain has reduced . •

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7)Administer medication as ordered by doctor such as Antiemetics hydroxyzine (vistaril) . •® hydroxyzine (vistaril) is for reduces nausea and vomiting . •I-I administer hydroxyzineto my patient and explain to his for pain management.  •

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Date:25.10.09 •Time:10.15 am •

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Evaluation :Patient’s pain reduce after 2 hour nursing intervention carried out.

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Supporting Data:1)Patient’s verbalized that pain is reduce. • 2)Patient’s vital signs stable :BP: 120/80 mmHg and Pulse 86 bpm •

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NURSING CARE PLAN 2 Fluid volume deficit related to active fluid loss

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Date/time : 25.10.2009 @ 0900 hours

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Nursing Diagnosis : Fluid Volume Deficit Related To Active Fluid Loss such as Vomiting.

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Supporting Data : pt c/o vomit x4. • pt look pale, poor skin turgor, dry mucous membranes. •

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Goal : patient will be improved fluid balance within 2 hours after nursing intervention given during hospitalization.

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Nursing intervention : •1) Monitor vital signs, noting presence of hypotension (including postural changes) •® As a baseline data for further intervention. •I I assess patient condition such as vital signs and patient look pale, poor skin turgor, and dry mucous skin membrane. •

2) Maintain accurate I/O chart. •® Reflects hydration status. •I I record accurately his input and output in •

3) Observe skin/mucous membrane dryness, turgor. •® Hypovolemia, fluid shifts, and nutritional deficits contribute to poor skin turgor, taut edematous tissues. •I I assess his condition and its show that he had poor skin turgor and dry mucous membrane. •

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4) Encourage patient to drink more water. •® To rehydrate fluid loss from body. •I I give patient mineral water and advice him to •

5) Provide and maintain IV replacement therapy as ordered. •® Use of IV replacement is based on the degree of dehydration, ongoing losses, insensible water loss and electrolyte results. •I I maintain and make sure the drip is on the right regime. •

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6) Compare admission weight to preadmission weight, take daily weight. •® The degree of dehydration can be determined by the percentage of weight loss. Daily weights aid in determining progress toward rehydration. •I I compare his weight from his on admission to this day and his weight decreased 2kg. •

7) Report patient condition to the Dr if patient condition still persist. •® For further intervention. •I I report patient condition to Dr when he did round. •

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Date/Time : 25.10.2009 @ 1000 hours

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Evaluation : Patient will be remain hydrated within 2 hours after nursing intervention given and during hospitalization.

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Evidence : Patient more comfortable, improved skin turgor, dry mucous membrane.

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Signature : STN VZ.

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PREVENTIONS Peritonitis focused on prompt recognition and treatment of condition that lead to perforation of abdominal viscera or any condition that release bacteria or chemicals into peritoneum cavity. üIntake of fiber diet üLaxative üEnema ~can help prevent appendicitis or diverticulitis.

PREVENTIONS vIf patient receiving peritoneal dialysis, you can help avoid peritonitis by cleaning the area around the catheter with antiseptic and washing hands before touching the catheter. vPre-operative and postoperative antibiotics therapy are also being use to help in preventing peritonitis as and early treatment of GI inflammatory conditions.

PEPTIC ULCER

APPENDICIT IS

IBS

GASTROENTRIT IS

CA COLON

GASTRIT IS

CHOLELITHIA SIS

GERD

CHOLELITHIASIS (39) Pancreas: Acute hemorrhagic pancreatitis.

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DEFINITION • Cholelithiasis is the presence of one or more calculi (gallstones) in the gallbladder. • • Gallstones tend to be asymptomatic.

MANIFESTATION CHOLELITHIASIS S Pain Abrupt onset •

Severe, steady •Localized to epigastrium and RUQ of abdomen •May radiate to back, right scapula, and shoulder •Last 30 minutes to 5 hours •

Associated symptoms

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Nausea, vomiting

Complications

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Cholecystitis •Common bile duct obstruction with possible jaundice and liver damage •Common duct obstruction with pancreatitis

RISK FACTOR OF CHOLELITHIASIS

ü Age ü Family history of cholelithiasis ü Race or ethnicity ü Obesity, hyperlipidemia ü Rapid weight loss ü Female gender; use of oral contraceptives ü Biliary stasis: pregnancy, fasting, prolonged parenteral nurition ü Disease or condition: cirrhosis; ileal disease or resection; sickle cell anemia; glucose intolerance

Treatment Of Cholelithiasis Medical options Ø Cholelithiasis can be dissolved by oral ursodeoxycholic acid, but it may be required that the patient takes this medication for up to two years. Ø Sometimes can be relieved by endoscopic retrograde sphincterotomy (ERS) following endoscopic retrograde cholangiopancreatography (ERCP). Ø Can be broken up using a procedure called lithotripsy (Extracorporeal Shock Wave Lithotripsy), which is a method of concentrating ultrasonic shock waves onto the stones to break them into tiny pieces. •

Surgical options

1. Open cholecystectomy: This procedure is performed via an incision into the abdomen (laparotomy) below the right lower ribs. Recovery typically consists of 3–5 days of hospitalization, with a return to normal diet a week after release and normal activity several weeks after release. 2. Laparoscopic cholecystectomy: This procedure, introduced in the 1980s,is performed via three to four small puncture holes for a camera and instruments. Postoperative care typically includes a same-day release or a one night hospital stay, followed by a few days of home rest and pain medication. Laparoscopic cholecystectomy patients can generally resume normal diet and light activity a week after release, with some decreased energy level and minor residual pain continuing for a month or two. The procedure also has the benefit of reducing operative complications such as bowel perforation and vascular injury.

IRRITABLE BOWEL SYNDROME

IRRITABLE BOWEL SYNDROME (IBS)

DEFINITION … • Known as spastic bowel or functional colitis . • Motility disorder with no identifiable organic cause . • ( Medical-Surgical Nursing ,critical thinking in client care, Fourth Edition : Priscilla LeMone,RN,DSN,FAAN . Karen Burke,RN,MS(page : 762) ) •

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ETIOLOGY • Unknown. • Psychosocial factors : • * distress • * anxiety • * Physical abuse • * Depression • * Sleep disturbances

• Physiologic factors : * Constipation * various genetic * abdominal discomfort * environmental factor

GASTROENTERITIS

DEFINITION OF GASTROENTERITIS Is an inflammation of the stomach and small intestine. Enteritis may be caused by a bacteria, viruses, parasites, or toxins. •

The infectious organism usually enters the body in contaminated water or food. For this reason, gastroenteritis often is called “food poisoning”.

SIGNS & SYMPTOMS OF GASTROENTERITIS Nausea Vomiting Diarrhea Mild fever Severe abdominal cramp

GASTROINTESTINAL EFFECTS Anorexia, nausea, and vomiting. Abdominal pain and cramping. Borborygmi diarrhea

GENERAL EFFECTS Malaise, weakness, and muscle aches. Headache. Dry skin and mucous membrane. Poor skin turgor. Orthostatic hypotension, tachycardia. Fever.

COLORECTAL CANCER

EFINITION OF COLORECTAL CANCE Colorectal cancer, also called colon cancer or large bowel cancer, includes cancerous growths in the colon, rectum and appendix. Many colorectal cancers are thought to arise from adenomatous polyps in the colon. These mushroomshaped growths are usually benign, but some may develop into cancer over time. The majority of the time, the diagnosis of localized colon cancer is through colonoscopy. Therapy is usually through surgery, which in many cases is followed by chemotherapy.

RISK FACTORS OF CA COLON

1. Age: risk of developing cancer increases with age. 2.History of cancer: Individuals who have previously been diagnosed and treated for colon cancer are at risk for developing colon cancer in the future. Women who have had cancer of the ovary, uterus, or breast are at higher risk of developing colorectal cancer. 3. Smoking. Smokers are more likely to die of colorectal cancer than non-smokers. 4. Diet. Studies show that a diet high in red meat and low in fresh fruit, vegetables, poultry and fish increases the risk of colorectal cancer.

SYMPTOMS OF CA COLON LOCAL SYMPTOMS Feeling of incomplete defecation Diarrhea or constipation Reduction in diameter of stool Malena stool CONSTITUTIONAL SYMPTOMS •iron deficiency anaemia •fatigue, •palpitations •pallor •weight loss, •a decreased appetite

METASTASIS SYMPTOMS ~ca colon most commonly spreads to liver and cause: Jaundice Abdominal pain

GASTRO - ESOPHAGEAL REFLUX DISEASE ( GERD )

DEFINITION OF Gastroesophageal refluxGERD disease (GERD), gastric reflux disease, or acid reflux disease is defined as chronic symptoms or mucosal damage produced by the abnormal reflux in the esophagus. This is commonly due to transient or permanent changes in the barrier between the esophagus and the stomach. This can be due to incompetence of the lower esophageal sphincter, transient lower esophageal sphincter relaxation, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia. Respiratory and laryngeal manifestations of GERD are commonly referred to as extraesophageal reflux disease (EERD).

Heart burn

Trouble swallowing (dysphag

Signs and Symptoms of GERD

Nausea

Regurgitation

Excessive salivatio

Pain with swallowing (odynophagia)

TREATMENTS OF Lifestyle modifications GERD Dietary modification

The following may exacerbate the symptoms of GERD: 1. Coffee and alcohol stimulate gastric acid secretion. Taking these before bedtime especially can cause evening reflux. 2. Antacids based on calcium carbonate (but not aluminum hydroxide) were found to actually increase the acidity of the stomach. However, all antacids reduced acidity in the lower esophagus, so the net effect on GERD symptoms may still be positive.

3. Foods high in fats and smoking reduce lower esophageal sphincter competence, so avoiding these may help. Fat also delays stomach emptying. Eating within 2–3 hours before bedtime. Large meals. Having smaller, more frequent meals reduces GERD risk, as it means there is less food in the stomach at any one time. 4. Carbonated soft drinks with or without sugar. 5.Chocolate and peppermint should be avoided.

Positional therapy •Sleeping on the left side has been shown to reduce nighttime reflux episodes in patients.

Medications •Proton pump inhibitors •Gastric H2 receptor blockers •Antacids

Surgical treatments for GERD •The standard surgical treatment is the Nissen fundoplication . In this procedure the upper part of the stomach is wrapped around the LES to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia. The procedure is often done laparoscopically. When compared to medical management laparoscopic fundoplication had better results at 1 year. An obsolete treatment is vagotomy ("highly selective vagotomy"), the surgical removal of vagus nerve branches that innervate the stomach lining.

PEPTIC ULCER DISEASE

DEFINITION •peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer disease, is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely painful.

CLASSIFICATIONS

1.Stomach (called gastric ulcer) 2. Duodenum (called duodenal ulcer) 3. Oesophagus (called Oesophageal ulcer) 4. Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

Symptoms of a peptic ulcer can be; 1. abdominal pain, 2. waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus) 3. nausea, 4. vomiting 5. loss of appetite and weight loss 6. hematemesis (vomiting of blood); 7.melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin); WEIGHT LOSS

Types of peptic ulcers:

•Type I: Ulcer along the lesser curve of stomach • •Type II: Two ulcers present - one gastric, one duodenal • •Type III: Prepyloric ulcer •Type IV: Proximal gastroesophageal ulcer •Type V: Anywhere along gastric body, NSAID induced

Complications 1.Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels. 2.Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back. 3.Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas. Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting. 4.Pyloric stenosis

APPENDICITIS

APPENDICITIS • Is the inflammation of the vermiform appendix, the small, finger-like pouch attached to the ceacum of colon. • • Usual location of appendix is right iliac region. • • Acute appendicitis is most common cause of acute inflammation in right lower quadrant. •

ETIOLOGY 1.Ulceration of the appendiceal of mucosa 2. 3.Obstruction within the colon 4. 5.Kinking of appendix 6. 7.Enlarged lymphoid follicle 8. 9.Trapped barium •

INCIDENCE 1.Occur at any age 2. 3.Peak incidence between age of age 20-30 years. 4. 5.Male and female affected equally 6. 7.Perforation more common in infants and elderly. •

PREVENTION 1.Aimed at reducing risk of obstruction or inflammation of appendiceal lumen. 2. 3.Regularity of bowel elimination pattern. 4. 5.Adequate amount of dietary intake.

CLINICAL MANIFESTATION 1. Abdominal pain – begin in epigastric area

2. 3. Nausea and vomiting

4. 5. Pain – shift to right lower quadrant within few hours

6. 7. Urge to defecate or pass flatus

8. 9. Tenderness – absent in early stage

10. 11.Temperature – usually normal sometimes slightly elevated

INVESTIGATION 1.Full blood count – WBC elevated 2. 3.X-ray – some patient show a fecal in right lower quadrant on abdominal x-ray

GASTRITIS

GASTRITIS Definition of gastritis; • Inflammation of gastric • mucosa • • • May classified as • 1. acute or • 2. chronic •

Inflamed stomach lining

ACUTE GASTRITIS • Inflammation of gastric mucosa • or submucosa after expose to local irritants •

• There are various degree of • mucosal necrosis and • inflammatory reaction.

CHRONIC GASTRITIS • The diffuse chronic inflammatory process involving the mucosal lining of stomach • May divided into 3 categories: • i) Superficial gastritis • - consist of infiltration of lamina propria by • lymphocytes and plasma cell • - it’s localized in outer area of mucosa • - superficial gastritis cause inflamed, edematous mucosa with hemorrhage

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ii) Atrophic Gastritis - occur in all layer of stomach, decreased number of fundal, parietal and seen with gastric ulcer and gastric cancer

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iii) Gastric Atrophy - refer to total loss of fundal glands, minimal inflammation and thining of gastric mucosa

ETIOLOGY ACUTE

CHRONIC

•Chronic irritant Local irritant a. Drug a. Alcohol b. Acid or alkalis b. Drug – Digitalis c. Reserpine d. Anti inflammatory agents, •Endogenous agent aspirin a. Reflux of bile e. Cytotoxics agents b. Pancreatic enzyme f. Corticosteroids c. Radiation d. Peptic ulcer disease •Bacterial Endotoxins e. Renal disease •

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Life style a. Heavy cigarette smoking b. Use of alcohol

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CLINICAL MANIFESTATIONS 1. Pain 2. 3. Epigastric discomfort 4. 5. Abdominal terndeness 6. 7. Cramps 8. 9. Indigestion 10. 11.Nausea and vomiting

PREVENTION 1.Precaution ingestion of drug 2. 3.Avoid irritating substances include drug 4. 5.Moderation use of alcohol 6.

INVESTIGATIONS 1.Full blood count 2. 3.Stool FEME 4. 5.X-ray 6. 7.Gastroscopy

IS THERE ANY QUESTIONS??

Thanks a lot for lending your ears .. From :

haryaniThanks

syafiqah

izzati

nabilah warsana