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 micro-
organisms 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:
•

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 .
•

•
•
•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
•

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.
•

• 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 .
•

•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.


•

•Date:25.10.09
•Time:10.15 am

• Evaluation :Patient’s pain reduce after 2 hour nursing

intervention carried out.
•

•Supporting Data:1)Patient’s verbalized that pain is reduce.

• 2)Patient’s vital signs stable :BP: 120/80
mmHg and Pulse 86 bpm


 NURSING CARE PLAN 2

Fluid volume deficit related to

active fluid loss
•

• Date/time : 25.10.2009 @ 0900 hours

•

• Nursing Diagnosis : Fluid Volume Deficit

Related To Active Fluid
Loss such as Vomiting.
•

• Supporting Data : pt c/o vomit x4.

• pt look pale, poor skin turgor,
dry mucous membranes.
•

• Goal : patient will be improved fluid balance

within 2 hours after nursing
intervention given during
hospitalization.
•
 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.
•

•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.
•

•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.
•

Date/Time : 25.10.2009 @ 1000 hours

•

Evaluation : Patient will be remain

•

hydrated within 2 hours after

nursing intervention given
and during hospitalization.
•

Evidence : Patient more comfortable,

•

improved skin turgor, dry mucous

membrane.
•

Signature : STN VZ.

•
 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 APPENDICIT CA
ULCER IS COLON

IBS
GASTRIT
IS

GASTROENTRIT CHOLELITHIA GERD

IS SIS
CHOLELITHIASIS
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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 Nausea, vomiting

•

Complications •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. Post-
operative 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) )
•
 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 mushroom-
shaped 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 METASTASIS
SYMPTOMS SYMPTOMS
•iron deficiency anaemia ~ca colon most
•fatigue, commonly spreads to
•palpitations liver and cause:
•pallor Jaundice
•weight loss, Abdominal pain
•a decreased appetite
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 Excessive salivatio

Regurgitation Pain with swallowing

(odynophagia)
 TREATMENTS OF
GERD
Lifestyle modifications
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
Inflamed stomach
• 2. chronic 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
• ii) Atrophic Gastritis
• - occur in all layer of stomach,
decreased number of fundal, parietal and seen
with gastric ulcer and gastric cancer
•

• iii) Gastric Atrophy

• - refer to total loss of fundal glands,
minimal inflammation and thining of gastric
mucosa
 ETIOLOGY
ACUTE CHRONIC
•Local irritant •Chronic 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
•

Life style
•

a. Heavy cigarette smoking

b. Use of alcohol
 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 izzati

syafiqah nabilah

warsana