دمج شباتر البالغين .....

Assessment of the
Abdomen
Learning objective
At the end of this session the student will able
to:
1. Identify function of gastrointestinal system .
2. Identify path of digestion.
3. Define phases of digestion.
4. Enumerate the parts of gastrointestinal.
5. Explain the physical assessment of
abdomen
Function of Digestive System
Produces various chemicals to

break down the food.
Filters out harmful substances.
Gets rid of solid wastes.
Path of Digestion
Mouth
Pharynx
Esophagus
Stomach
Small Intestine
Large Intestine
Anus
Digestion
The chemical breakdown of complex
biological molecules into simplest form by
digestive enzyme .
– Lipids to fatty acids
– Proteins to individual amino acids
– Carbohydrates into simple sugars

N.B: Digestive enzymes: are special
proteins that help break up large
molecules of food into very tiny
molecules that can be absorbed and
used by the cells in the form of
nutrition.
Phases of Digestion
Ingestion
Movement
Digestion
Absorption
Further digestion
Egestion :removal of
digestive waste.
The Digestive Tract
A long muscular tube
is approximately 28
feet with many
sections and areas.
Begins with the

mouth and ends with
the anus.
Parts of the Digestive
Tract
– Mouth
– Pharynx
– Esophagus
– Stomach
– Small Intestine
– Large Intestine
– Rectum
– Rectal canal and anus
Accessory Parts
Organs that are not in the digestive tract but
helps in the digestion
– Teeth
– Tongue
– Salivary glands
– Liver
– Gall bladder
– Pancreas
Mouth
Functions:
– Food enters in the mouth or oral
cavity
– Tasting
– Mechanical breakdown of food
– Secretion of (salivary amylase) by
salivary glands
Structures in the mouth that aids in
digestion:
Teeth : cut, tear, crush and grind food.
Salivary glands : produce and secrete

saliva into the oral cavity:
– Parotid (beneath the cheeks)
– Submaxillary (below the jaw bone)

–Sublingual (below the tongue)
 saliva moistens the food and contains

enzymes (ptyalin or salivary
amylase) that begins digestion of
starch into smaller polysaccharides.
• Tongue
– Mixes and rolls food into tiny mashed up
bits (Bolus) ‫قطع صغيرة مهروسة‬
– Pushes the bolus toward the pharynx and

into the esophagus when swallowing.
Taste buds‫براعم التذوق‬: it is located on the
tongue and at the back of the mouth
- Are sensitive to substance that are sweet,
sour, bitter and salty ‫حساس لمادة حلوة وحامضة‬
‫ومرة ومالحة‬
ّ
Fig. 21.7
Mechanism of Swallowing
Swallowing is a coordinated activity of the
tongue, soft palate, pharynx and esophagus.
Phases :
– Food is pushed into the pharynx by the
tongue. (voluntary)
– Tongue blocks the mouth
– Soft palate closes off the nose
– Larynx (Adam’s Apple) rises so the

Epiglottis (a flap of tissue) can close
the opening of the trachea.
Pharynx
It is a musculomembranous passage that leads
from the nose and mouth to the esophagus.
The passage of food from the pharynx into the

esophagus is the second stage of swallowing.
When food is being swallowed, the larynx is
closed off from the pharynx to keep food from
getting into the respiratory tract.
Esophagus
A straight muscular tube that is about 10 inches
(25 cm) long which connects the mouth with the
stomach
Food takes about 4 to 8 seconds as it passes
through to the stomach.
Its walls contain smooth muscles that contracts
in wavy motion (Peristalsis).
Peristalsis propels food and liquid slowly
down the esophagus into the stomach.
Cardiac Sphincter (ring-like valve) relaxes to
allow food into the stomach.
Peristalsis
Stomach
J-shaped muscular sac
Has inner folds (rugae) that increases the surface

area of the stomach.
Food is mixed with gastric juices (hydrochloric acid

and enzymes) secreted by the stomach walls.
HCL helps break down food and kills bacteria that

came along with the food.
Stomach
Stomach
Pepsin – major enzyme; converts proteins into
peptides in the presence of HCL.
Mucus – lubricates food and protects the gastric

lining from strong digestive juices.
Converts the bolus into a liquid (chyme) after

4 hrs of mechanical and chemical digestion
Chyme passes through the pyloric sphincter

into the small intestine.
Movements in Stomach
Small Intestine
Long (20 ft), coiled ‫ملفوفة‬tube beneath the
stomach.
Has three parts:
 Duodenum : upper part; about 10 inch;
connected to the stomach. where the
digestive juices from the pancreas and the
liver combine with chyme making it thin and
watery.
 Jejunum : about 8 ft
 Ileum : about 12 ft
Sites of greatest amount of digestion and
absorption
Takes about 4 – 8 hrs to complete its journey.
Mucosa (inner wall) – secretes several
enzymes that acts on the food.
Where the pancreatic enzymes are emptied
into.
Digested nutrients are absorbed through
intestinal walls.
Absorbed materials cross the mucosa into the
blood then other parts of the body for storage
or further chemical change.
Peristalsis moves the undigested food to the
large intestine
Movement in small intestine:
Mixing: Segmental contraction that occurs in small intestine

Secretion: Lubricate, liquefy, digest
Digestion: Mechanical and chemical
Absorption: Movement from tract into circulation or lymph
Elimination: Waste products removed from body
Pancreas
The pancreas is a long, tapering organ lying
behind the stomach.
The head of the gland lies in the curve of the
small intestine near the pyloric valve. The
body of the pancreas extends to the left
toward the spleen.
Produces a juice that contains enzymes
(amylase and insulin) to break down
carbohydrates, fats and protein.
Secretes the juice into the duodenum through
the pancreatic duct.
Liver
– Largest organ of the body
– It is located in the upper part of the

abdomen with its larger (right) lobe to the
right of the midline. It is just under the
diaphragm and above the lower end of the
stomach.
Functions
blood detoxification
protein, hormone and biochemical's
synthesis and production
major role in metabolism (synthesis and
breakdown of small and complex
molecules)
glycogen storage
decomposition of red blood cells
Stores vitamins A,D,E,K
cont,
– Produces bile (watery, greenish substance)
– Secretes bile to the gall bladder via the

hepatic duct and cystic duct .
– Part of the digestive, circulatory and

excretory systems.
– Removes excess amino acids from the body

Gall bladder
- The gallbladder is a dark green sac.
– Stores bile in between meals.
– Secretes bile to the duodenum through
the bile duct during mealtime.
Bile contains bile salts, pigments,
cholesterol and phospholipids.
Bile is an emulsifier NOT an enzyme.
Emulsifier – dissolves fat into the

watery contents in the intestine.
Liver, Gallbladder, Pancreas, and Duct System
Fig. 21.20
Large Intestine ( colon)
 larger diameter, but shorter (5 ft)
The cecum, located on the lower right side of the

abdomen, is the first portion of the large intestine
into which food is emptied from the small intestine.
Colon divided into ( ascending colon, transverse

colon and descending colon) The last portion
makes an S curve (sigmoid) toward the center and
posterior of the abdomen and ends in the rectum
Large intestine ( colon)
Water is absorbed from the undigested
food making the waste harder until it
becomes solid.
Waste stays for 10 – 12 hours.
Appendix hangs on the right side of the

large intestine.
Large Intestine
The rectum and anus
The rectum: is about 5 inches long and follows the
curve of the sacrum and coccyx until it bends back
into the short anal canal.
The anus: is the external opening at the lower end of

the digestive system. It is kept closed by a strong
sphincter muscle.
The rectum receives feces and periodically expels

this material through the anus is called defecation.
Nursing Assessment
A- History : Take history from patients about:
1. Dietary history
- The number of meals ate per day.
- Meal times.
- Food restrictions or special diets followed.
- appetite status e.g. (increased, decreased

or no appetite)
2. Bowel patterns history; especially a
change in bowel patterns, can provide
clues that will aid in the diagnosis of the
problem
(1) Frequency of bowel movements.
(2) Use of laxatives and/or enemas.
(3) Changes in bowel habits.
(4) Stool Description.
(a) Constipation.
(b) Diarrhea.
(c) Blood in stool.
(d) Mucous in stool.
(e) Black, tarry stools.
(f) Pale or clay colored stools.
(g) Foul smelling stools.
(h) Pain with stool.
Subjective data
Take present history about any digestive
complain such as:
- Vomiting , diarrhea, constipation, nausea,

indigestion , heartburn, epigastria pain and
weight loss.
- Ask patient about the factors increase or

decrease these complain.
B- Physical assessment
Inspection
Palpation
Percussion
Auscultation
Examination of the abdomen
Position : the patient is resting in a supine
position, knees slightly flexed to relax the
abdominal muscles.
In order to facilitate the referencing of location,

the abdomen is viewed as four quadrants or
nine regions. The quadrant division is the most
commonly used by nursing personnel.
Inspection
Perform a brief, general head-to-toe visual inspection
of the patient.
1. The height and weight within normal range for the

patient's age and body type
2. Observe the skin for the following:
Color (pale, gray, ruddy, jaundiced).
Bruises, lesion ,rashes and turgor and moisture.
Edema. ‫ الطفح الجلدي‬، ‫ اآلفات‬، ‫الكدمات‬

3. Examine the mouth and throat.
Look at the lips, tongue, and mucous membranes,

noting abnormalities such as cuts, sores, or
discoloration.
Observe the condition of the teeth. Note any

discolored, cracked, chipped, loose, or missing teeth.
Observe the gums. they healthy and pink.
Note the patient's breath for unusual odors (fruity,

foul, alcohol, and so forth).
4. Abdominal contour : flat, rounded,
scaphoid
 Inspect for masses ,enlarged organs

,symmetry .
5. The umbilicus : observe its contour and

location , and any inflammation or bulges
suggesting a hernia
Auscultation
Auscultate the abdomen. Move the
stethoscope in a symmetrical pattern, listening
in all four quadrants.
a. Listen for bowel sounds. The best location is

below and to the right of the umbilicus.
Describe the sounds heard according to

location, frequency, and character of the
sound.
Auscultation of Bowel
Sounds
Absent : No BS for 5 min
Hypoactive : less than

5/min
Active : 5-30 per min
Hyperactive : > 30 /min
52
Bowel sound may be :
 Increased in diarrhea or early intestinal

obstruction
 Decreased as in peritonitis
b. Listen for Abdominal bruit and friction rub:
 If the patient has high blood pressure , listen in
the epigastrium and in each upper quadrant for
bruit.
 Listen for bruit over the aorta, the iliac arteries,

and the femoral arteries, bruit confined to
systole are common and don’t signify occlusive
disease
 Hepatic bruit suggests carcinoma of the
liver
 Friction rub are grating sounds with

respiratory variation. They indicate
inflammation of the peritoneal surface of
an organ . Listen over liver and spleen for
friction rubs
Palpation
Palpation is used to detect muscle, tenderness,
and masses.
Gently palpate the abdomen, moving in a

symmetrical pattern and covering all four
quadrants.
Right Upper Quadrant (RUQ):
Note: liver, gallbladder, duodenum, right
kidney and hepatic flexure of colon
Right Lower Quadrant (RLQ):
Note: cecum, appendix (in case of female,
right ovary & tube)
Left Lower Quadrant (LLQ):
Note: sigmoid colon (in case of female, left
ovary & tube)
Cont,
Left Upper Quadrant (LUQ)
Note: stomach, spleen, left kidney,
pancreas (tail), splenic flexure of colon
Epigastric Area
Note: stomach, pancreas (head and body),
aorta
Abdomen
Sites of Referred Abdominal Pain
Palpation
N.B: Please note the following:
A normal kidney is not palpable
A normal liver edge may be palpable
A palpable spleen is considered enlarged
The aorta may be palpable. When it is
wide, think about an abdominal aortic
aneurysm (an excessive localized
enlargement of an artery caused by a
weakening of the artery wall).
Percussion
Place one hand on the area to be
examined and with First one or two fingers
of the other hand, strike the hand resting
on the abdomen
When find dullness to percussion on the left

side, think about abnormalities, such as an
enlarged spleen.
Percussion helps to assess the amount
and distribution of gas in the abdomen and
identify possible masses that are solid or
fluid filled
Percuss the abdomen lightly in all four

quadrants
Note any large dull areas may indicate

mass or enlarged organ
References
Bickley, L. & Szilagyi, P. Bates’ Guide to
Physical Examination and History Taking
(9th ed.). Philadelphia: Lippincott. Health
assessment text: (2007). ISBN-13: 978-0-
7817-8519-8
Intestinal obstruction
Definition
• Intestinal obstruction is blockage of the inside of the intestines
by an actual mechanical ; functional obstruction; or temporary.
• This blockage prevent the normal flow of intestinal contents
through the intestinal tract

Causes
1. Mechanical obstruction
• An intraluminal obstruction or a mural obstruction from pressure on
the intestinal walls occurs. Example :
Intussusception , tumors and neoplasm , stenosis, strictures,
adhesions, hernias and abscesses

Mechanical obstruction
Intussusception
Intussuception
One part of the intestine slips into another
Part located below it
Result in
The intestinal lumen becomes narrowed
Intussusception, valvulus; hernia

Volvulus
Bowel twists and turns on itself •
Result in
Intestinal lumen becomes obstructed. Gas and fluid •
accumulate in the trapped bowel
Obstruction due to tumor
A tumor that exists within the wall of the intestine
extends into the intestinal lumen, or a tumor outside
the intestine causes pressure on the wall of the
intestine
Result in Intestinal lumen becomes partially obstructed;
if the tumor is not removed, complete obstruction
results
Obstruction due to tumor

Obstruction due to adhesions
Loops of intestine become adherent to areas that heal slowly or scar

after abdominal surgery
Result in
• After surgery, adhesions produce a kinking of an intestinal loop

Adhesions
Obstruction due to hernia

Protrusion of intestine through a weakened area in the abdominal
muscle
Result in
• Intestinal flow may be completely obstructed. Blood flow to the area
may be obstructed as well
2. Functional obstruction
The intestinal musculature cannot propel the contents along the •

bowel.
Examples: muscular dystrophy, endocrine disorder (DM) •

3. Temporary obstruction
The blockage can be temporary and the result of the manipulation of •
the bowel during surgery

Intestinal Obstruction
Obstructions are further classified as complete or partial.
• A complete obstruction is acute and may cause vomiting, abdominal pain,

and septic shock
• Partial obstruction may cause chronic diarrhea and weight loss by

disrupting intestinal motility and allowing overgrowth of the normal
intestinal flora.
Intestinal Obstruction
Clinical signs vary and depend on:
1. The location of the obstruction,
2. The duration of the obstruction, and
3. The integrity of the intestinal wall.

Small Bowel Obstruction
Pathophysiology
•Intestinal contents, fluid and gas accumulate

above the intestinal obstruction
•The abdominal distention and retention of

fluid reduce the absorption of fluids and
stimulate more gastric secretion.
Pathophysiology
• With increasing distention, pressure within the

intestinal lumen increases, causing a decrease in
venous arteriolar capillary pressure.
• This cause edema, congestion, necrosis and rupture

or perforation of the intestinal wall, lead to
peritonitis.
Pathophysiology
• Reflux vomiting may be caused by abdominal

distention.
• Vomiting results in a loss of hydrogen ions and

potassium from the stomach, leading to a reduction
of chlorides and potassium in the blood and to
metabolic alkalosis
Pathophysiology
•Dehydration and acidosis develop from loss
of water and sodium
•The patient may develop hypovolemic shock

Clinical Manifestation
• The initial symptom is usually crampy pain that is wavelike and

colicky.
• The patient may pass blood and mucus, but no fecal matter and no
flatus.
• Vomiting
If the obstruction is complete:
a. The peristaltic waves initially become extremely vigorous and

eventually assume a reverse direction.
b. The intestinal contents propelled toward the mouth instead of

toward the rectum.
If the obstruction is in the ileum:
Fecal vomiting occur
a. First, the patient vomits the stomach contents

b. Then vomits the bile stained contents of the
duodenum and the jejunum
c. Finally, darker, fecal like contents of the ileum
signs of dehydration become evident
a. Intense thirst
b. Drowsiness
c. Generalized malaise
d. Aching and a parched tongue and
mucous membranes
abdominal distention
o The lower the obstruction is in the GI tract,

the more marked the abdominal distention.
o Hypovolemic shock occurs from dehydration

and loss of plasma volume.
Assessment and Diagnostic
Findings
1. Clinical signs & symptoms
2. Abdominal X-ray
Show abnormal quantities of gas, fluid
or both in the bowel.
3. CBC
Findings
4. Barium contrast, radiographic studies,

either of the upper gastrointestinal
tract or via a barium enema
Medical Management
1. Correcting fluid and electrolyte

imbalances
2. IV fluids are given while carefully
monitoring serum electrolyte
concentrations, vital signs and urine
output.
Medical Management
3. Insetting nasogastric tube and applying

suction to remove air and fluid.
4. In case of adhesions, Surgery is often

necessary to break the bands of adhesions
5. If a hernia, can be manually reduced

Medical Management
6. If bowel infarction or gangrene has

occurred, intestinal resection and
antibiotics are needed.
Nursing Management
1. Maintaining the function of the

nasogastric tube
2. Assessing and measuring the nasogastric

output, consistency, type, color, amount
and pH of drainage.
Nursing Management
3.Careful observation of fluid and electrolyte

balances is of primary importance's
4. Strict records of intake and output, daily weights,

vital signs and serum electrolyte concentration
Nursing Management
5. Monitoring nutritional status and assessing improvement
• Return of normal bowel sounds
• Decreased abdominal distention
• Improvement in abdominal pain and tenderness
• Passage of flatus or stool

Nursing Management
6. The nurse reports

• Discrepancies in intake and output.
• Worsening of pain or abdominal distention
• Increased nasogastric output
7. If no improvement prepare the patient for
surgery .
Medical Management
Large Bowel Obstruction
Pathophysiology
As in small bowel obstruction
• Obstruction in the large bowel can

lead to sever distention and
perforation unless some gas and fluid
can flow back through the ileal valve
Pathophysiology
• If the blood supply is cut off in the colon, necrosis may occur.
• In the large intestine, dehydration occurs more slowly than in the small
intestine because the colon can absorb its fluid contents and can distend
to a size considerably beyond its normal full capacity.

• The symptom may develop and progress relatively

slowly.
• Constipation may be the only symptom for days, If the
obstruction in the sigmoid or rectum.
• The abdomen becomes markedly distended, loops of
large bowel become visibly outlined through the
abdominal wall.
• Crampy lower abdominal pain
• Finally fecal vomiting develops.
• Symptoms of shock may develop.

Assessment and diagnostic
finding
• Symptom
• X-ray studies (flat and upright) show

distended colon
• Barium studies are contraindicated.

Medical Management
• A colonoscopy and decompress the bowel

• A cecostomy
• Surgical opening is made into the cecum.
• May be performed for patients who are poor
surgical risks and urgently need relief from
the obstruction.
Medical Management
A cecostomy
Medical Management
• A rectal tube may be used to decompress an

area that is lower in the bowel
• Temporary or permanent clostomy may be
necessary
• An ileoanal anastomosis may be performed if it
is necessary to remove the entire large colon.
Nursing Management
Vital signs
• Patients with bowel obstruction are likely to exhibit signs of

hypovolaemic shock as it becomes increasingly difficult to maintain
homeostasis because of dehydration caused by :
• nausea and vomiting and
• the shift of fluid into the bowel.

Nursing Management
Nurses need to monitor vital signs closely and

respond appropriately to changes in the following
1. Temperature – this can denote deterioration or

aggravation of the inflammatory process leading
to sepsis. This can be as a result of perforation of
the bowel.
Nursing Management
Vital signs
2. Pulse – tachycardia in this instance can be

linked to the compensatory mechanism
associated with hypovolaemia as the heart
attempts to circulate the lower blood volume
and is also associated with sepsis
Nursing Management
3. Respiration – this is increased as the heart

and lungs work together to oxygenate the
small volume of circulating blood and
remove excess carbon dioxide from the
blood. Acidosis may develop.
Nursing Management
4. Blood pressure – there will be hypotension

related to the low circulatory volume.
Nursing Management
Oxygen saturation – to monitor the amount

of oxygen binding to the haem. Oxygen
therapy is usually necessary to ensure
adequate oxygenation and tissue
perfusion.
Nursing Management
Urine output – to ensure renal perfusion is

maintained. As hypovolaemia occurs,
blood is diverted to the essential organs
to ensure their continued perfusion.
Nursing Management
Increasing abdominal distension and pain –

this can be a sign of peritonitis and
perforation of the bowel demonstrating a
deteriorating clinical condition.
Nursing Management
Pain
• Pain It is essential that good pain management is

achieved to enable the patient to be prepared for
surgery.
• Several different preparations can be used to help

treat pain during the pre-operative period. Morphine
are common
Nursing Management
• Note: morphine increases nausea and

vomiting as it stimulates the chemoreceptor
trigger zone in the brain. Therefore it is
important to use regular antiemetics.
• Morphine also has the advantage of lowing
down gut motility
Nursing Management
2. Hyoscine butylbromide can be useful in controlling the

colicky, spasmodic-type pain associated with bowel
obstruction as it encourages the smooth muscle to relax.
3. Octreotide can also reduce the amount of fluid that enters

the gut in bowel obstruction, thus helping to relieve some
of the pain associated with abdominal distension
Nursing Management
Dehydration and fluid and electrolyte balance
During bowel obstruction, especially small bowel obstruction, fluid levels

can quickly rise within the gut. This is because reduced peristalsis
causes the bowel to dilate and rapidly lose its function of absorbing
water and minerals, which in turn affects fluid and electrolyte balance.
Nursing Management
• Hourly monitoring of fluid balance is an essential part

of nursing care because diminished absorption of
fluid can affect haemodynamic stability quickly and
hypovolaemia can occur rapidly.
Nursing Management
• Urine output can provide a valuable

indication of fluid balance in patients who
would be expected to have a general healthy
renal function
Nursing Management
• Nurses need to be able to identify the normal range for urea

and electrolyte results and then consider the physiological
aspects to hypovolaemia.
• When a patient’s urea and electrolyte results are raised, and

when read in conjunction with the haematocrit, the blood is
concentrated and the patient is hypovolaemic or dehydrated
Nursing Management
Nausea and vomiting
• Cyclizine and prochlorperazine can be used to treat

nausea in patients with bowel obstruction as they act
centrally on the chemoreceptor trigger zone and the
vomiting centre.
Dr Neveen Adel Amer
Hernia
Definition
 Hernia is a protrusion of a viscus
through an abdominal opening or a
weakened area in the wall of the
cavity
Hernia
Causes
1. Defect in the integrity of the
muscle wall
 Weakened collagen
 Widened spaces
Hernia
Causes
 Increased intraabdominal pressure
 Pregnancy
 Obesity
 Abdominal distention
 Ascites
 Heavy lifting or
 Coughing
Hernia
Hernia
Inguinal hernia
these hernias are divided into two different
types:
1. Direct and
2. Indirect.
 Both occur in the groin area but they have
slightly different origins.
 Both of these types of hernias can similarly
appear as a bulge in the inguinal area.
Hernia
Inguinal hernia
Distinguishing between the direct and indirect hernia.
Indirect inguinal hernia
 An indirect inguinal hernia may occur at any age.
 It is a sac formed from the peritoneum that contains

a portion of the intestine.
 The hernia pushes downward at an angle into the

inguinal canal.
 It usually follows the pathway that the testicles

made during pre birth development.
 It descends from the abdomen into the scrotum.

Hernia
2. Direct inguinal hernia:
in contrast to indirect inguinal hernia
 The direct hernia tends to occur in the middle-
aged and elderly
 It pass through a weak point in the abdominal

wall.
 It rarely protrude into the scrotum.

Hernia
Hernia
Direct inguinal hernia:
indirect inguinal hernia:

Hernia
3. A femoral hernia
 The femoral canal is the path

through which the femoral artery,
vein, and nerve leave the abdominal
cavity to enter the thigh
Hernia
3. A femoral hernia
 It occurs below the inguinal ligament as a bulge
 It occurs more frequently in women.
 It is at risk of becoming irreducible (not able to be

pushed back into place) and strangulated.
Hernia
3. A femoral hernia
Hernia
4. Umbilical hernia:
 It may be a congenital or acquired
 Congenital hernia appear in infancy. It occurs when
the rectus muscle is weak or the umbilical opening
fails to close after birth.
 Acquired umbilical hernias directly result from

increased intra abdominal pressure.
 Umbilical hernias can appear later in life or in

women who are having or have had children.
Hernia
Hernia
Hernia
5. Incisional hernia:
 Abdominal surgery causes a flaw in the
abdominal wall.
 This flaw can create an area of weakness where
a hernia may develop.
 This occurs after 2-10% of all abdominal
surgeries, although some people are more at
risk.
 Even after surgical repair, incisional hernias
may return.
Hernia
5. Incisional hernia
Hernia
Hernia Symptoms
 The signs and symptoms of a hernia can range from

noticing a painless lump to the painful, tender,
swollen protrusion of tissue that you are unable to
push back into the abdomen—an incarcerated
strangulated hernia.
Hernia
Hernia Symptoms
Reducible
 When the contents of the hernia sac can be replaced

into the abdominal cavity by gentle pressure.
Irreducible
 When hernia cannot be reduced or placed back into

the abdominal cavity
Hernia
Strangulated
 When the blood supply to the herniated

segment of the bowel is cut off by pressure from
the hernial ring
 Signs of strangulation are abdominal

distention, nausea, vomiting, pain, fever and
tachycardia
Hernia
Self-Care at Home
 In general, all hernias should be repaired unless
severe preexisting medical conditions make surgery
unsafe.
 Trusses and surgical belts or bindings may be

helpful in holding back the protrusion of selected
hernias when surgery is not possible or must be
delayed.
Hernia
Self-Care at Home
 Avoid activities that increase intra-

abdominal pressure (lifting,
coughing, or straining) that may
cause the hernia to increase in size.
Surgical treatment
Herniorrhaphy
 Is the surgery of choice for hernia
repair
Hernioplasty
 Is performed less frequently but can
be performed in conjunction with a
herniorrhaphy.
Surgical treatment
Herniorrhaphy
 During a herniorrhaphy, the surgeon
makes an abdominal incision and
replaces the contents of the hernial
sac into the abdominal cavity before
closing the opening
Surgical treatment
Hernioplasty
 When a hernioplasty is performed, the
surgeon reinforces the weakened muscle
wall with mesh, or wire.
The surgeon may perform surgery through a
laparoscope instead of using the open
surgical method.
Hernia
Post-operative Complications include the following:
 Recurrence (most common)
 Urinary retention
 Wound infection
 Fluid build-up in scrotum (called hydrocele
formation)
 Nerve irritation
 Scrotal hematoma (bruise)
 Testicular damage on the affected side
(rare)
Nursing Management
Assessment
 The nurse inspects the abdomen when

the client is lying and standing
 If the hernia is reducible, it may
disappear when the patient is lying flat.
 The nurse asks the patient to strain and
observes for bulging
Nursing Management
Assessment
 Auscultates the abdomen for active
bowel sounds.
 Absent bowel sounds may indicate
obstruction and strangulation.
Nursing Management
Assessment
To palpate the hernia
 Inserting a finger in the ring and noting any
changes when the patient coughs.
 The nurse never forces the hernia to reduce ,
this maneuver can cause strangulated
intestine to rupture.
Nursing Management
 Teach patient that A truss is a pad made
with firm material
 It is held in place over the hernia with a
belt to help keep the abdominal contents
from protruding into the hernial sac.
Intervention
 The patient usually applies the truss

before arising.
 Teach the patient to assess the skin
under the truss daily and to protect it
with a light layer of powder.
Nursing Management
In the immediate postoperative period
 The surgeons generally allow patients to return to
their usual activities , with avoidance of straining
and lifting from 2 to 6 weeks (depend on site and
extent of repair).
 The nurse instruct the patient about symptom to be
reported, including fever, chills, wound drainage,
redness or separation of the incision, and
increasing incisional pain
Nursing Management
Post-operative Care
 A fluid intake at least 1500 to 2500 ml/day prevents
dehydration and maintains urinary function
 If the patient cannot void, the surgeons order
catheterization
Nursing Management
Post-operative Care
 avoid coughing .
 To promote lung expansion, the nurse encourage
deep breathing and frequent turning
 In inquinal hernia, the physician often orders a
scrotal support and ice bags applied to the
scrotum to prevent swelling
Nursing Management
Post-operative Care
 The nurse encourages early ambulation on the day
of surgery if it is not contraindicated by scrotal
swelling.
 Ambulation helps promote comfort and a feeling of
wellbeing and decrease the risk of postoperative
complication.
Nursing Management
Post-operative Care
 The patient experience difficulty voiding .
Techniques to stimulate voiding, such as allowing
water to run
 Careful monitoring of intake and output
 Carefully palpates the abdomen for distention
 A fluid intake at least 1500 to 2500 ml/

Gastro-Esophageal
Reflux Disease
DR. Nevin Adel Amer

Overview
 Anatomy and physiology
 Definition of GERD
 Phathophysiology
 Clinical manifistations
 Diagnostic tests
 Medical management
 Nursing management
Anatomy and physiology
 Esophagus
 Mucus-lined, muscular tube that carries food from the
mouth to stomach.
 Begins at the base of the pharynx and ends about
4cm below the diaphragm.
 Its ability to transport food and fluid is facilitated by
the upper esophageal sphincter (hypophrengeal) and
the lower esophageal sphincter (gastroesophageal).
 There is no serosal layer of the esophagus.
GERD
 Some degree of esophageal reflux (back-
flow of gastric and dudenal contents into
the esophagus) is normal in both adults
and children.
 GERD is the excessive reflux.
Pathophysiology
 Normally, Lower Esophageal Sphincter (LES)
creates enough pressure around the lower end
of the esophagus to close it. So, gastric content
don’t back up into the esophagus.
 Reflux occurs when LES pressure is deficient or
the pressure of the stomach exceed LES
pressure
 When this happens, the LSE relaxes.
Pathophysiology
 Common causes
 Incompetent lower esophageal sphincter
 Pyloric stenosis
 Motility disorder
Pathophysiology
The acidity of gastric content and amount of
time in contact with esophageal mucosa
are related to the degree of mucosal
damage.
 Esophageal ulcer and esophagitis may
result
Clinical Manifestations
 Pyrosis (Burning sensation in the esophagus).
 Dyspepsia (indigestion).
 Regurgitation.
 Dysphagia or odynophagia (pain on swallowing)
 Hypersalivation.
 Esophagitis.
findings
 Endoscopy
findings
 Barium swallow
 To evaluate the damage
to the esophgeal
mucosa.
findings
 Ambulatory 12- to 36-hour
esophageal pH monitoring
 to evaluate the degree of acid reflux
findings
 Bilirubin monitoring (bilitec)
 To measure bile reflux patterns
Medical Management
 Health Education
 Diet
 Low fat diet
 Avoid caffeine, tobacco, beer, milk, foods
containing peppermint or spearmint, and
carbonated beverage.
 Avoid eating or drinking 2 hours before bed
time.
Medical Management
 Health Education
 Maintain body weight.
 Avoid tight-fitting clothes.
 Elevate the head of the bed on 15-20cm
blocks.
 Elevate the upper body on pillow.
Medical Management
 Medications
 Antacids or H2 receptor antagonist.
 famotidine, nizatidine, or rantidine
 Proton pump inhibitors
 Lanzoprazole, esomeprazole, or rabeprazole.
 Prokinetic agents
 Bethanecol, dompridone, and meetoclopramide.
Medical Management
 Surgical intervention
 Nissen fundoplication
(wrapping of a portion of the gastric fundus around the
sphincter area of esophagus)
Nursing management
Assessment Nursing Objective Intervention evaluation
diagnosis
Pt complains Impaired -Pt not to Teach -Pt has no
of pyrosis tissue have pyrosis patient to more
integrity R/ for after 8 hrs. avoid foods pyrosis
T -Pt is able to that cause -Pt knows
esophageal verbalize pain and or the
exposure to knowledge of can necessity
gastric acid necessity increase lifestyle
lifestyle acid changes
changes with secretion.
24 hours of
discharge
from the
hospital
Nursing management
diagnosis
- Pt complains Risk of Pt won’t Teach the pt -No more
of recurrent aspiration show signs to: regurgitation
regurgitation R/T of aspiration -Elevate the s, according
recurrent within 8 HOB while to the pt
regurgitation hours in bed
- Pt shows
signs of -Eat small
uncomforting. frequent
meals.
-Not to eat
or drink 2
hours
before bed
time
Nursing management
diagnosis
- Pt complains Acute pain Pain will be -Assure that - Pain score
of pain 8 on R/T tissue relieved pt is taking became 2
scale exposed to within 8 his out of 10
gastric hours medication
-Pt shows
content on time
signs of Teach
uncomfort patient to
avoid foods
that cause
pain and or
can
increase
acid
secretion
Nursing management
diagnosis
-Pt has weight Imbalance Pt will -Explain the -No more
loss nutrition R/T achieve importance weigh loss
-Pt state that decrease adequate of adequate during the
he is not intake caloric and nutrition daily
eating so he’ll nutritional -Teach the weighting
not feel intake pt about the -Pt receiving
pyrosis. diet which and
doesn’t adequate
cause caloric diet
esophagus as followed
irritation by Dietitian
Summary
 GERD is an excessive reflux may occur because
of a incompetent lower esophageal sphincter,
pyloric stenosis, or a motility disorder.
 symptoms may include pyrosis, dyspepsia,
regurgitation.
 Management starts with health education, then
medications, and the last option will be the
surgical interventions
 Nurses play a significant role in providing care
for patients with GERD.
Thanks
 Peptic ulcer disease (PUD) is a break in the continuity of
the esophageal, gastric, or duodenal mucosa. PUD occur in
any part of gastrointestinal (GI) tract that comes in contact
with hydrochloric acid and pepsin.

A peptic ulcer may arise at various locations:
Stomach (called gastric ulcer)
Duodenum (called duodenal ulcer)
Esophagus (called esophageal ulcer)
causes
 A major causative factor (60% of gastric and up to 90% of
duodenal ulcers) is chronic inflammation due to
Helicobacter pylori.
 Emotional stress.
 Ulcers can also be caused or worsened by drugs such as

Aspirin and other NSAIDs.
 Chronic gastritis.
 Smoking cigarettes and using tobacco and alcohol which

increase HCL secretion.
• Overuse of laxatives is also known to cause peptic
ulcers.
• A family history is often present in duodenal
ulcers, especially when blood group O is also
present.
Clinical manifestations:
• Abdominal pain
• Bloating and abdominal fullness
• Nausea and lots of vomiting
• Loss or increase appetite and weight loss or gain
• Hematemesis (vomiting of blood); this can occur due to bleeding
directly from a gastric ulcer, or from damage to the esophagus
from severe/continuing vomiting or melena (tarry, foul-smelling
feces due to oxidized iron from hemoglobin)
• Constipation or diarrhea may occur.
Diagnosis:
1- An esophagogastroduodenoscopy (EGD), a
form of endoscope, also known as a gastroscopy, is
carried out on patients in whom a peptic ulcer is
suspected. By direct visual identification, the location
and severity of an ulcer can be described. Moreover,
if no ulcer is present, EGD can often provide an
alternative diagnosis.
 The diagnosis of Helicobacter pylori can be made by:
 Direct culture from an EGD biopsy specimen; this is difficult

to do, and can be expensive. Most labs are not set up to
perform H. pylori cultures;
 Measurement of antibody levels in blood (does not require

EGD). It is still somewhat controversial whether a positive
antibody without EGD is enough to warrant eradication
therapy;
 Physical health: problems of the musculoskeletal and/or
nervous system can have negative affect on body movement.

Osteoporosis and osteoarthritis are examples for conditions that
can damage the skeletal system leading to impaired mobility.
Disorders of the nervous system that impair movement occur
less frequently but are often more serious. Parkinson's disease,
multiple sclerosis, central nervous system tumors, cerebral
vascular accidents, and spinal cord injuries can leave muscle
groups weakened, paralyzed, spastic, or flaccid.
Complications:
 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.
 Perforation (a hole in the wall).

 Penetration is when the ulcer continues into adjacent
organs such as liver and pancreas.
 Scarring and swelling due to ulcers causes narrowing in

the duodenum and gastric outlet obstruction. Patient often
presents with severe vomiting.
Comparison between duodenal ulcer & Gastric
ulcer
feature Duodenal Gastric
Age 30 – 60 years Usually 50 and over
gastric one.
incidence - It is most 80% of cases. - 15% of cases.
Pain - - Pain occurs 2-3 hours after meal, - Pain occurs after 0.5-1 hour after
often awakened between 1-2 am. eating. Rarely occur at night.
Vomiting Vomiting uncommon - Vomiting common

Bleeding Hematemesis less, but melena more Hemorrhage more likely to occur.
common than hematemesis. Hematemesis more than melena.
Gastric Secretion - Hyper-secretion of HCL Decreased secretion
Weight Weight gain Weight loss
Pain relived by Frequent meals Vomiting.
ingestion of food does not help but
sometimes increase it
Malignancy possibility occasionally rare
Perforation possibility more less

Medical management:
 Younger patients with ulcer-like symptoms are
often treated with antacids or an H2 antagonist
(Tagemet, Zantac) before EGD is undertaken.
Medical management:
 Bismuth compounds may actually reduce or even clear
organisms.
 When H. pylori infection is present, the most effective

treatments are combinations of 2 antibiotics (e.g.
Clarithromycin, Amoxicillin, Tetracycline, Metronidazole)
and 1 proton pump inhibitor (PPI), sometimes together
with a bismuth compound.
Medical management:
 In complicated, treatment-resistant cases, 3
antibiotics (e.g. amoxicillin + clarithromycin +
Metronidazole) may be used together with a PPI and
sometimes with bismuth compound.
 In the absence of H. pylori, long-term higher dose
PPIs is often used.
 7-Since the widespread use of PPI's in the 1990s,

surgical procedures (like "highly selective
vagotomy") for uncomplicated peptic ulcers
became out of date
Dietary modification
 To avoid oversecretion of acid and hyper motility in GIT by:
 Avoiding extreme temperature or over stimulation from

consumption of meat extracts, alcohol, coffee, and
smoking and other caffeinated beverage and diet rich in
milk and cream.
 Regular eating pattern to neutralize acid.
 Small frequent feeding.
 Eat foods that can be tolerated and avoids those that

produce pain.
• To avoid oversecretion of acid and hyper motility in GIT by:
• Avoiding extreme temperature or over stimulation from
consumption of meat extracts, alcohol, coffee, and
smoking and other caffeinated beverage and diet rich in
milk and cream.
• Regular eating pattern to neutralize acid.
• Small frequent feeding.
• Eat foods that can be tolerated and avoids those that
produce pain.
Nursing process
• To avoid oversecretion of acid and hyper motility in GIT by:
• Avoiding extreme temperature or over stimulation from
consumption of meat extracts, alcohol, coffee, and smoking
and other caffeinated beverage and diet rich in milk and
cream.
• Regular eating pattern to neutralize acid.
• Small frequent feeding.
• Eat foods that can be tolerated and avoids those that
produce pain.
Nursing process
I-Assessment
 Ask the patient to describe the pain and methods used to
relive it.
 Ask patient to list his/ her usual food intake for 72 hours
to describe food habits as speed of eating, regularity of
meals preference of spicy foods, use of seasoning, use of
caffeinated beverage and coffee.
 Assess vital signs and report tachycardia and hypotension
may indicate anemia from GIT bleeding.
 The stool is tested for occult blood.
II-Nursing diagnosis
 Acute Pain R/T effect of gastric acid secretion of
damaged tissue.
 Imbalanced nutrition R/T changes in diet
 Anxiety R/T coping with an acute disease.
 Knowledge deficit about prevention of symptoms and
management of the condition.
III-Nursing intervention:
1. Relieve pain
 Administer medication as prescribed.
 Avoid aspirin, foods and beverages that contain caffeine as coffee and tea.
 Encourage to learn relaxation techniques
 Regular meals.
2-Teaching dietary self management:
 Assume semi recumbent position during meal time, after
meal lie down for 20-30 minutes.
 Fluids are discouraged with meals but may given 1 hour
before or 1 hour after mealtime.
 CHO intake should be kept low, sucrose and glucose are
avoided
2-Teaching dietary self management:
 Antispasmodic as prescribed help to delaying the emptying
of the stomach.
 Small and frequent meal should be eaten
 Dietary supplements as vitamin B12 and iron may be
prescribed.
3-Reduce anxiety
 assess what the patient knows about the disease
 allow patient to express fear.
 explanation about diagnosis, treatment, medication.
 good interaction between patient and nurse.
 Encourage the family to participate in patient care and

emotional support.
4. Patient teaching
 Instruct patient about importance of continuing taking

medication even after S&S have decreased.
 Instruct patient to avoid certain medications and foods

that increase S&S.
 Instruct patient about eating diet at regular times and in a

relaxed setting.
 avoid smoking
 rest and stress reduction

2. Monitoring and managing potential
complications:
 Hemorrhage which is the most common complications.
It occurs in about 15% of patients. It may be manifested
by Hematemesis or Melena.
 The vomited blood may be bright red or it can have a

coffee ground appearance (dark) from the oxidation
of hemoglobin
 The nurse should assess patient for bleeding as
dizziness, nausea which may precedes bleeding,
monitor vital signs, and monitor hemoglobin and
Hematocrite level and record hourly urinary output to
detect anuria or oliguria
Management consists of
 rapidly replace the blood lost.
 stopping the bleeding and stabilize the patient
 Infusion of saline or lactated ringers and blood

product
 insert NG tube to remove blood clot and acid,

prevent nausea and vomiting and provide a mean
to monitor further bleeding.
 Insert urinary catheter to monitor urinary out put

 Administer O2 therapy.
 place patient in recumbent position with leg elevated to

prevent hypotension or to prevent aspiration from
vomiting so place him/ her on the left side.
B-Perforation and penetration:
 perforation: is the erosion of the ulcer through the

gastric serosa into the peritoneal cavity without warning. It
requires immediate surgery. Its signs and symptoms
include( sudden and sever upper abdominal pain which
may be referred to shoulder especially right because of
irritation of the phrenic nerve in the diaphragm, vomiting
and collapse, tender and rigid abdomen, hypotension and
tachycardia indicating shock.
 penetration: is the erosion of the ulcer through the gastric serosa into
adjacent structures such as pancreas and biliary tract. Its symptoms include:
back and epigastric pain that not relived by medication. It requires immediate
surgery.
Prepared by
Dr/ Nevin Adel Amer

Diabetes Mellitus
 Diabetes mellitus is a group of metabolic diseases
characterized by elevated levels of glucose in the blood
(hyperglycemia) resulting from directs in insulin
secretion, insulin action, or both.
Pancreas
 Pancreas consists of 2 types of tissues:-
1. Acini (exocrine part): secrete digestive juices into
duodenum.
2. Islets of langerhans (endocrine part): secrete
hormones directly into blood.
Insulin Hormone
 Insulin is a hormone secreted from beta cell of
pancreas, control glucose level in the blood by
regulating the production and storage of glucose
ACTIONS
1- On CHQ metabolism (hypoglycemic)
 ↑ glucose transport across the cell membranes of
skeletal muscles, heart, adipose tissue through
stimulation of facilitated diffusion (the only
hypoglycemic H in the body)
 ↑ glucose utilization inside the cells.
Insulin Hormone
 2- On protein metabolism (anabolic)
 Insulin stimulate protein synthesis and inhibits protein
catabolism
 3- On fat metabolism (Upogenic)
 Insulin stimulate lipogenesis as it stimulate
glucose utilization as a source of energy →↓ fat
utilization.
 insulin inhibits lipolysis as it inhibits lipase
enzyme →↓ F.A release into blood
Insulin Hormone
 On potassium metabolism
 Insulin causes K+ to enter the cells with a resultant
lowering of the ECF K+; concentration
Blood glucose regulation (homeostasis)
 The fasting blood glucose is 70-126 mg/dl. This
concentration increases up to 140 mg/dl during the
first hour after meal
 The feedback system for control of blood glucose
returns the glucose concentration very rapidly to the
fasting level within 2 hours after the last carbohydrate
absorption.
 In starvation, the glycogenolytic and gluconeogenic
function of the liver provides glucose that is required
to maintain the fasting blood glucose level
Risk Factors for Diabetes mellitus
 Family history diabetes.
 Obesity
 Race/ethnicity (e.g, African Americans, Hispanic
Americans, Native Americans Asian Americans, Pacific
Islanders)
 Age > 45 years
 Previously identified impaired fasting glucose or impaired
glucose tolerance.
 Hypertension (>140/90mm Hg)
 HDL cholesterol level <35mg/dl and or triglyceride level
>250mg/dl
 History of gestational diabetes.
Clinical manifestations
 3 Ps (Polyuria, Polydipsia, polyphagia).
 Other symptoms include fatigue and weakness
sudden vision changes, tingling or numbness in hand
or feet, dry skin, skin lesions or wounds that are slow
to heal, and recurrent infections.
 The onset of type 1 diabetes may also be associated
with sudden weight loss or nausea, vomiting, or
abdominal pains, if DKA has developed.
Classification of Diabetes
 There are several different types of diabetes mellitus;
they may differ in cause, clinical course, and
treatment. The major classifications of diabetes are:
 Type 1 diabetes (previously referred to as insulin-
dependent diabetes mellitus).
 Type 2 diabetes (previously referred to as non-
insulin-dependent diabetes mellitus).
 Gestational diabetes mellitus.
 Diabetes mellitus associated with other conditions or
syndromes
Table: Classification of Diabetes Mellitus and
Related Glucose Intolerances
Diagnostic Findings
FASTING BLOOD SUGAR (FBS)
Adult: Serum and plasma: 70-126 mg/dl.
Nursing Implications with Rationale
• Patient should be fasted 6-8 hours before test except for water.
• Hold morning insulin and drugs until blood specimen is taking.
• Record on the laboratory slip if the client has been taking daily
cortione preparations, thiazides, or loop diuretics.
two hour postprandial blood sugar
 Adult: Serum or plasma : <140 mg/dl/2 h. Blood :
<120mg/dl/2h
 Elderly: serum: < 160mg/dl/2 h. Blood :
<140mg/dl/2h
Glucose tolerance test-
 The test may be indicated when there is a familial
history of diabetes, in women having babies weighing
10 Ib or more, in persons having extensive. Surgery or
injury and in person with obesity problems.
 Hgb A1C: long-term measure of glucose control that is
a result ofglucose attaching to hemoglobin for the life
of the rbc (120 days).
Urine Testing for Ketones:-
 Ketones in the urine signal that control of type 1
diabetes is deteriorating.
 The most commonly used method to detect ketonuria
is to use a urine dipstick .The reagent pad on the strip
turns a purplish color when ketones are present.
Diabetes Management
 The main goal of diabetes treatment is to normalize
insulin activity and blood glucose levels to reduce the
development of vascular and neuropathic
complications.
There are five components of diabetes
management.
 Nutrition
 Exercise
 Monitoring
 Pharmacology
 Education
Nutritional Management
 Nutrition, diet, and weight control are the foundation
of diabetes management. Nutritional management of
the diabetic patient includes the following goals
 Providing all the essential food constituents

(eg.vitamins, minerals) necessary for optimal
nutrition while meeting energy needs
 Achieving and maintaining a reasonable weight.

Nutritional Management
 Preventing wide daily fluctuations in blood glucose
levels, with blood glucose levels as close to normal as is
safe and practical to prevent or reduce the risk for
complications
 Decreasing serum lipid levels, if elevated, to reduce
the risk for macrovascular disease.
Nutritional tips:-
 The patient must fix the time & amount of daily food
to allow matching of insulin / tablet regime to diet.
 Reduce the rate of carbohydrate absorption to avoid
glycaemic peaks.
 Avoid simple sugars, as they are rapidly absorbed.
 Carbohydrates should be taken as starches & other
complex sugars.
 Consumption of fibre-rich foods causes slowing of
sugar absorption.
 Use foods with low glycaemic index.
 Advice frequent, relatively small meals i.e. 3 main
meals & 3 snacks in between meals:
 Caloric Requirements
 Calorie-controlled diets are planned by first
calculating the individual's energy needs and caloric
requirements based on the patient's age, gender,
height, and weight. An activity element is then
factored in to provide the actual number of calories
required for weight maintenance.
 N.B: To promote a 1-to 2-pound weight loss per week,
500 to 1.000 calories are subtracted from the daily
total.
 The calories are distributed into carbohydrates,
proteins, and fats, and a meal plan is then developed.
 Specify the caloric needs to maintain desired
body weight
 For obese patient: 1000 - 1500 Kcal/day.
 For elderly patient: 1500 - 2000 Kcal/day.
 For young active patient: 2000 - 3000 Kcal/day.
 Adjust proportion of food elements to avoid
atherosclerosis
 50: 60% of calories from carbohydrates
 20: 30% of calories from fats.
 20% of calories from proteins.
 carbohydrates
 The goal of the diabetic diet is to emphasize the
intake of complex carbohydrates especially those
high in fiber, such as whole grain breads, cereals
pastas and beans than simple carbohydrates as
sugar. This type of diet plays a role in lowering
total cholesterol and LDL (low density lipoprotein)
in the blood .Increasing fiber in the diet may also
improve blood glucose levels, leading to decrease
in the need for exogenous insulin.
 fats
 The recommendations regarding fat content of the
diabetic diet include both reduction in the total
percentage of calories from fat sources and
limitation of the amount of saturated fats to 10 %
of total calories .In addition, limitation of total
intake of dietary cholesterol to less than 300 mg /
day is recommended.
 Protein
 The meal plan may include the use of some non
animal source of protein (eg, legumes and whole
grains) to help reduce saturated fat and cholesterol
intake.
 Requirements increase for children and during
pregnancy.
 Prevented Food
 Sugar- all type of honey- Jam- Fruit Juice- Alcohol
drinks- butter - Ice Cream- Peanuts.
 Non Favorable food
 Kidney- Liver- Meat fat- Sausage- Brain- duck- goose-
Pigeon
2-Exercise
 Exercise is extremely important in managing diabetes because
of its effects on lowering blood glucose and reducing
cardiovascular risk factors by increasing the uptake of glucose
by body muscles and by improving insulin utilization.
 It also improves circulation and muscle tone and useful in
diabetes in relation to losing weight, easing stress, and
maintaining a feeling of well-being.
 Exercise also alters blood lipid levels, increasing levels of high-
density lipoproteins and decreasing total cholesterol and
triglyceride levels.
2-Exercise
 The exact amount of food needed varies from person
to person and should be determined by blood glucose
monitoring. Some patients find they do not require a
pre-exercise snack if they exercise within I to, 2 hours
after a meal. Other patients may require extra food
regardless of when they exercise.
 To avoid post exercise hypoglycemia, especially after
strenuous or prolonged exercise, the patient may need
to eat a snack at the end of the exercise session and
monitor the blood glucose level before, during, and
after the exercise period.
2-Exercise
 The patient should be instructed to always carry
simple sugar such as hard candy to take it for
symptomatic hypoglycemia and also should carry
identification band.
 Avoiding trauma to the lower extremities is especially
important in the patient with numbness related to
neuropathy.
 Use proper foot wear and avoid exercises in extreme
hot or cold and Inspect feet after exercise.
3-Monitoring Glucose Levels
and ketones
 Blood glucose monitoring is a cornerstone of diabetes
management, and self-monitoring of blood glucose
(SMBG) levels by patients has dramatically altered
diabetes care. Frequent SMBG enables people with
diabetes to adjust the treatment regimen to obtain
optimal blood glucose control. This allows for
detection and prevention of hypoglycemia and
hyperglycemia and plays a critical role in normalizing
blood glucose levels, which in turn may reduce the risk
of long-term diabetic complications.
3-Monitoring Glucose Levels
and ketones
Frequency of SMBG
 For most patients who require insulin, SMBG is
recommended one to four times daily (usually before
meals and at bedtime).
 Patients not receiving insulin may be instructed to
assess their blood glucose levels at least (three times
per week, including a 2-hour postprandial test).
 Testing urine for glucose and ketones is also a self-
monitoring test that aid patient in treatment
Pharmacologic
Therapy:
Insulin therapy:-
Indications of insulin
 IDDM
 Diabetic ketoacidosis and lactic acidosis
 NIDDM:
 If there is no response to diet and oral
antidiabetics
 If there is critical episodes e.g. operations, stress,
infections, ischemia, trauma and pregnancy
Types of insulin preparations:-
Type of insulin onset duration indication
Rapid acting 10-15 4-6 hrs Used for rapid reduction of glucose
level
Short acting ½ - 1hr 4 – 6 hrs Usually administered 20 -30 min

before meals may taking with
combination with long acting
Intermediate 2 –4 hrs 6 – 20 hrs Usually taken after food

acting
Long -acting 6-8hrs 20-30hrs Used primarily to control fasting

glucose level
Types of insulin preparations:-
 general, the short acting insulin are expected to cover
meals immediately after the injection, while the
intermediate are expected to cover subsequent meals,
and the long acting provide a relatively constant level
of insulin and control primarily the fasting glucose
level.
Route of administration
 Mainly SC (all preparations)
 In emergency regular insulin is given by IV infusion.
 Special routes:
 Intranasal route by the adjuvants cause mucosal
irritation.
 Intraperitoneal route is used in IDDM patients with
end-stage renal failure treated by ambulatory
peritoneal dialysis.
 Infusion pump either open loop ('delivers insulin at a
constant rate) or closed loop (delivers insulin
according to blood glucose level).
2- Insulin regimens
 After calculation of units needed per day. 2/3 dose to
be given in the morning and 1/3 dose at the evening. In
the morning (before breakfast), give 2/3 the dose of
intermediate type (NPH) and 1/3 the amount of rapid
type (regular). In the evening (before dinner), give 1/2
the dose of intermediate type and the other of rapid
type. N.B: 1- In elderly patients and those needing
more than 30 units / day, a single injection of a long
acting insulin is suitable.
2- Insulin regimens
 In some cases, a mixture of short- and intermediate-
acting insulin may be given in the morning. Further
doses of short-acting insulin are given before lunch
and the evening meal and an evening dose of
intermediate-acting insulin is given at bedtime.
 A regimen of multiple injections of short-acting
insulin before the main meals, with an appropriate
dose of an intermediate-acting insulin given at
bedtime, may be used.
Complications of insulin
therapy (Adverse effects):
 Hypoglycemia
 Hypersensitivity reactions (insulin allergy
 Insulin
 Transient generalized edema: may occur in the early
treatment of under nourished patients.
 Hypokalemia
 Local allergic reactions
 Lipodystrophy: It is a depressed area at the site of
injection due to atrophy of adipose tissue after
repeated injections.
 Hypertrophy: It is a proliferation of fatty tissue due to
Recommendations for insulin
therapy
 Insulin absorption depends on the areas of injection.
Injection in the abdominal wall results faster
absorption.
 Unopened vials of insulin should be stored in the
refrigerator but not be frozen. An opened vial that is
being used daily should be stored at room
temperature.
Oral Antidiabetic drugs
 Sulphonylureas
 Biguanides
 Glucosidase inhibitors
 Thiazolidinediones
Instructions with oral
antidiabetic agents:-
 Patients must understand that oral agents are
prescribed as an addition to other treatment
modalities, such as blood glucose monitoring and
exercise.
 Use of oral antidiabetic medications may need to be
halted temporarily and insulin prescribed if
hyperglycemia develops that is attributable to
infection, trauma, or surgery.
 In time, oral antidiabetic agents may no longer be
effective in controlling diabetes because of decline in
function of beta cells. In such cases, the patient is
treated with insulin.
Instructions with oral
antidiabetic agents:-
 Approximately half of all patients who initially use oral
antidiabetic agents eventually require insulin.
 Because mechanisms of action vary (Fig. 41-5), effects
may be enhanced with the use of multidose, multiple
medications. Use of multiple medications with
different mechanisms of action is very common today.
A combination of oral agents with insulin, usually
glargine at bedtime, has also been used frequently as a
treatment for some patients with type 2 diabetes.
46
OutLines
 Introduction
 Definition
 Types
 stages
 Etiology and risk factors:
 Pathophysiology
 Clinical manifestation
 Diagnosis
 Complications
 Management
 Nursing care plan of the medical client
Anatomy Of The Liver
Functions of The Liver
 Glucose Metabolism
 After a meal, glucose is taken up from the portal venous blood
by the liver and converted into glycogen, which is stored in
the hepatocytes.
 Subsequently, the glycogen is converted back to glucose and
released as needed into the bloodstream to maintain normal
levels of blood glucose.
Protein Metabolism
 T he liver also plays an important role in protein
metabolism. It synthesizes almost all of the plasma
proteins including albumin and blood clotting
factors.
 Ammonia Conversion
 Use of amino acids from protein for
gluconeogenesis results in the formation of
ammonia as a byproduct. The liver converts this
metabolically generated ammonia into urea.
Ammonia produced by bacteria in the intestines is
also removed from portal blood for urea synthesis.
In this way, the liver converts ammonia, a potential
toxin, into urea, a compound that can be excreted
in the urine.
 Fat Metabolism
 The liver is also active in fat metabolism. Through
action of bile secretions on the intestine to facilitate
lipid metabolism and absorption of fat soluble
metabolisms.
 Vitamin and Iron Storage

 Vitamins A, B, and D and several of the B-complex
vitamins are stored in large amounts in the liver.
Certain substances, such as iron and copper, are
also stored in the liver. Because the liver is rich in
these substances, liver extracts have been used for
therapy for a wide range of nutritional disorders.
 Bile Formation
 Bile is continuously formed by the hepatocytes and
collected in the canaliculi and bile ducts.
 Bile is collected and stored in the gallbladder and is
emptied into the intestine when needed for digestion..
 Bilirubin Excretion
 Hepatocytes remove bilirubin from the blood and
chemically modify it through conjugation to
glucuronic acid, which makes the bilirubin more
soluble in aqueous solutions. The conjugated
bilirubin is secreted by the hepatocytes into the
adjacent bile canaliculi and is eventually carried in
the bile into the duodenum.
 In the small intestine, bilirubin is converted into
urobilinogen, which is in part excreted in the feces
and in part absorbed through the intestinal
mucosa into the portal blood.
Definition
 Liver Cirrhosis
Cirrhosis is a chronic disease characterized by
replacement of normal liver tissue with diffuse fibrosis
that disrupts the structure and function of the liver.
Causes of Cirrhosis
 Chronic hepatitis B
 Chronic hepatitis C
 Alcohol
 Bilharzias
 Mal nutrition
 Other:
o Haemochromatosis
o Non-alcoholic fatty liver disease
o Primary biliary cirrhosis
o Sclerosing cholangitis
o Autoimmune hepatitis
o Cystic fibrosis...
Major types of cirrhosis:
There are three types of cirrhosis or scarring of the liver:

 Alcoholic cirrhosis, in which the scar tissue
characteristically surrounds the portal areas. This is most
frequently due to chronic alcoholism and is the most
common type of cirrhosis.
 Postnecrotic cirrhosis, in which there are broad bands of
scar tissue as a late result of a previous bout of acute viral
hepatitis.
 Biliary cirrhosis, in which scarring occurs in the liver
around the bile ducts. This type usually is the result of
chronic biliary obstruction and infection (cholangitis); it is
much less common than the other two types.
Pathophysiology liver cirrhosis
nutritional alcohol
deficiency consumption
exposure to infectious
certain chemicals schistosomiasis
Sbstance
destroyed liver
cells
necrosis liver cells
scar tissue
Loss liver function

Clinical Manifestations
 The manifestations to categorize the

disorder into two main presentations.
1-Compensated cirrhosis
2- Decompensated
Clinical Manifestations of Cirrhosis
A-Compensated
o Intermittent mild fever
o Vascular spiders
o Palmar erythema (reddened palms)
o Unexplained epistaxis
o Ankle edema
o Vague morning indigestion
o Flatulent dyspepsia
o Abdominal pain
o Firm, enlarged liver
o Splenomegaly
B-Decompensated
o Ascites
o Jaundice
o Weakness
o Muscle wasting
o Weight loss
o Continuous mild fever
o Clubbing of fingers
o Purpura (due to decreased platelet count)
o Spontaneous bruising
o Epistaxis
o Hypotension
o Sparse body hair
o White nails
o Gonadal atrophy
Liver Enlargement
 Early in the course of cirrhosis, the liver tends to be

large and its cells loaded with fat.
 The liver is firm and has a sharp edge noticeable on
palpation.
 Abdominal pain may be present because of recent,
rapid enlargement of the liver, producing tension on
the fibrous covering of the liver (Glisson’s capsule).
 Later in the disease, the liver decreases in size as scar
tissue contracts the liver tissue. The liver edge, if
palpable, is nodular.
Assessment and Diagnostic Findings
There are many diagnostic tests that may provide information
about liver function.
 Serum globulin level rises.
 Enzyme tests indicate liver cell damage: serum alkaline
phosphatase, AST, ALT, and GGT levels increase, and the
serum cholinesterase level may decrease.
 Bilirubin tests are performed to measure bile excretion or bile
retention; elevated levels can occur with cirrhosis and other
liver disorders.
 Prothrombin time is prolonged.
 Ultrasound scanning is used to measure the
difference in density of parenchymal cells and scar
tissue.
 CT, MRI, and radioisotope liver scans give
information about liver size and hepatic blood
flow and obstruction.
 Diagnosis is confirmed by liver biopsy.
 Arterial blood gas analysis may reveal a
ventilation– perfusion imbalance and hypoxia.
Complications
 Ascites
 Hepatorenal syndrome
 Variceal hemorrhage
 Hepatic encephalopathy
 Hepatocellular carcinoma
Ascites
 Accumulation of fluid within the peritoneal cavity
 Most common complication of cirrhosis

 Assessment of ascites
 Grading
 Grade 1 — mild; Detectable only by US
 Grade 2 — moderate; Moderate symmetrical distension of the
abdomen
 Grade 3 — large or gross ascites with marked abdominal distension

Ascites
 Treatment aimed at the underlying cause of the hepatic
disease and at the ascitic fluid itself
 Paracetasis for sever ascites that cannot be controlled by
medications
 Dietary sodium restriction
 Limiting sodium intake to 88 meq (2000 mg) per day

Ascites
 The most successful therapeutic regimen is the
combination of single morning oral doses of
Spironolactone and Furosemide, beginning with 100 mg
and 40 mg
 Two major concerns with diuretic therapy for cirrhotic
ascites:
 Overly rapid removal of fluid
 Progressive electrolyte imbalance

Infection and Peritonitis
 Bacterial peritonitis may develop in cirrhotic patient
with ascites in the absence of an intra-abdominal
source of infection or an abscess. This condition is
referred to as spontaneous bacterial peritonitis.
Bacteremia is believed to be the most likely route of
infection. Clinical signs may be absent; paracentesis
may be necessary for diagnosis. Antibiotic therapy is
effective in the treatment and prevention of recurrent
episodes of spontaneous bacterial peritonitis.
Portal Obstruction
 These late manifestations are due partly to chronic
failure of liver function and partly to obstruction of the
portal circulation.
 Practically all the blood from the digestive organs is
collected in the portal veins and carried to the liver.
 Because a cirrhotic liver does not allow the blood free
passage, it backs up into the spleen and the GI tract
and these organs become the seat of chronic passive
congestion; that is, they are stagnant with blood and
thus cannot function properly.
 Indigestion and altered bowel function result.
Gastrointestinal Varices
 The obstruction to blood flow results in the formation
of collateral blood vessels in the GI system and shunting
of blood from the portal vessels into blood vessels with
lower pressures.
 The esophagus, stomach, and lower rectum are
common sites of collateral blood vessels.
 These distended blood vessels form varices or
hemorrhoids, depending on their location .Because
these vessels were not intended to carry the high
pressure and volume of blood imposed by cirrhosis,
they may rupture and bleed.
Hepatorenal syndrome
 acute renal failure coupled with advanced hepatic
disease (due to cirrhosis or less often metastatic tumor or
severe alcoholic hepatitis)
 characterized by:
 Oliguria
 benign urine sediment
 very low rate of sodium excretion
 progressive rise in the plasma creatinine concentration
Hepatorenal Syndrome
 Reduction in GFR often clinically masked
 Prognosis is poor unless hepatic function improves
 Nephrotoxic agents and overdiuresis can precipitate
HRS
Jaundice
 When the bilirubin concentration in

the blood is abnormally elevated, all
the body tissues, including the sclerae
and the skin, become yellow-tinged or
greenish-yellow
Edema
Another late symptom of cirrhosis is edema, which is
attributed to chronic liver failure. A reduced plasma
albumin concentration predisposes the patient to the
formation of edema. Edema is generalized but often
affects lower extremities, upper extremities, and the
presacral area. Facial edema is not typical.
Overproduction of aldosterone occurs, causing
sodium and water retention and potassium excretion.
Vitamin Deficiency and Anemia
Because of inadequate formation, use, and storage of

certain vitamins (notably vitamins A, C, and K), signs
of their deficiency are common, particularly
hemorrhagic phenomena associated with vitamin K
deficiency. Chronic gastritis and impaired GI function,
together with inadequate dietary intake and impaired
liver function, account for the anemia often associated
with cirrhosis. The anemia and the patient’s poor
nutritional status and poor state of health result in
severe fatigue, which interferes with the ability to carry
out routine daily activities.
Mental Deterioration
Additional clinical manifestations include

deterioration of mental function with impending
hepatic encephalopathy and hepatic coma.
Neurologic assessment is indicated and includes the
patient’s general behavior, cognitive abilities,
orientation to time and place, and speech patterns.
Medical management
Drug Therapy
 There is no specific drug therapy for cirrhosis
 Drugs are used to treat symptoms and complications of advanced liver
disease
 For example,
 Antacids are prescribed to decrease gastric distress and minimize the
possibility of GI bleeding.
 Vitamins and nutritional supplements promote healing of damaged
liver cells and improve the general nutritional status.
 Potassium-sparing diuretics (spironolactone [Aldactone], triamterene
[Dyrenium]) may be indicated to decrease ascites, if present; these
diuretics are preferable to other diuretic agents because they minimize
the fluid and electrolyte changes common with other agents.
Medical management
Nutritional Therapy
 Diet for patient without complications:
 High in calories
  CHO
 Moderate to low fat
 Amount of protein varies with degree of liver damage
 Low sodium diet for patient with ascites and edema
Nursing Management:
Assessment
 Assessment the onset of symptoms and the
history of precipitating factors, particularly long-
term alcohol abuse, as well as dietary intake and
changes in the patient’s physical and mental
status.
 Assessment The patient’s past and current patterns
of alcohol use (duration and amount) .
 It is also important to document any exposure to
toxic agents encountered in the workplace or
during recreational activities.
Assessment
 The nurse assesses the patient’s mental status through the
interview and other interactions with the patient;
orientation to person, place, and time is noted.
 The patient’s ability to carry out a job or household activities
provides some information about physical and mental
status.
 The patient’s relationships with family, friends, and
coworkers may give some indication about incapacitation
secondary to alcohol abuse and cirrhosis.
 Abdominal distention and bloating, GI bleeding, bruising,
and weight changes are noted.
 The nurse assesses nutritional status, which is of major
importance in cirrhosis, by daily weights and monitoring of
plasma proteins, transferrin, and creatinine levels.
Nursing Diagnosis
Based on all the assessment data, the patient’s major
nursing diagnosis may include the following:
 Activity intolerance related to fatigue, general
debility, muscle wasting, and discomfort
 Imbalanced nutrition, less than body requirements,
related to chronic gastritis, decreased GI motility, and
anorexia
 Impaired skin integrity related to compromised
immunologic status, edema, and poor nutrition.
 Risk for injury and bleeding related to altered clotting
mechanisms
Potential Complications
 Based on assessment data, potential complications
may include:
 Bleeding and hemorrhage
 Ascities
 Portal hypertension
 Hepatic encephalopathy
 Fluid volume excess
Planning and Goals
The goals for the patient may include

 Increased participation in activities
 Improvement of nutritional status
 Improvement of skin integrity
 Decreased potential for injury
 Improvement of mental status
 Absence of complications.
Nursing Interventions:
1) Promoting rest:
 The patient with active liver disease requires rest and other
supportive measures to permit the liver to reestablish its
functional ability.
 If the patient is hospitalized, weight and fluid intake and
output are measured and recorded daily.
 The nurse adjusts the patient's position in bed for maximal
respiratory efficiency, which is especially important if ascites
is marked because it interferes with adequate thoracic
excursion.
 Oxygen therapy may be required in liver failure to oxygenate
the damaged cells and prevent further cell destruction.
1) Promoting rest:
 Rest reduces the demands on the liver and increases the
liver's blood supply. Because the patient is susceptible
to the hazards of immobility, efforts to prevent
respiratory, circulatory, and vascular disturbances are
initiated. These measures may help prevent such
problems as pneumonia, thrombophlebitis, and
pressure ulcers.
 When nutritional status improves and strength
increases, the nurse encourages the patient to increase
activity gradually. Activity and mild exercise, as well as
rest, are planned.
 Provide diet high in carbohydrates with protein intake
consistent with liver function. Administer
supplemental vitamins (A, B complex, C, and K).
Improving Nutritional Status:
 Assess dietary intake and nutritional status through diet history and diary,
daily weight measurements and laboratorydata.
 Provide diet high in carbohydrates with protein intake consistent with liver
function.
 Assist patient in identifying low-sodium foods.
 Elevate the head of the bed during meals.
 Provide oral hygiene before meals and pleasant environment for meals at
meal time.
 Provide attractive meals and an aesthetically pleasing setting at meal time.
 Eliminate alcohol.
 Apply an ice collar for nausea.
 Administer medications prescribed for nausea, vomiting, diarrhea, or
constipation.
 Encourage increased fluid intake and exercise if the patient reports
constipation.
 The patient with cirrhosis who has no ascites or
edema and exhibits no signs of impending hepatic
coma should receive a nutritious, high-protein diet
if tolerated.
 Supplemented by vitamins of the B complex and
others as indicated (including vitamins A, C, K. and
folic acid). Because proper nutrition is so important,
the nurse makes every effort to encourage the
patient to eat.
 Small, frequent meals are tolerated well than three large meals.
 Patients with prolonged or severe anorexia, or those who are vomiting or
eating poorly for any reason, may receive nutrients enterally or
parenteral nutrition.
 Patients with fatty stools (steatorrhea) should receive water-soluble
forms of fat-soluble vitamins A, D, and E (Aquasol A, D, and E).
 Folic acid and iron are prescribed to prevent anemia.
 If the patient shows signs of impending or advancing coma, the amount
of protein in the diet is decreased temporarily.
 In the absence of hepatic encephalopathy, a moderate-protein, high-
calorie intake is provided, with protein foods of high biologic value.
 A high-calorie intake should be maintained, and supplemental vitamins
and minerals should be provided (eg, oral potassium if the serum
potassium level is normal or low and if renal function is normal).
Providing Skin Care:
 Providing careful skin care is important because of
subcutaneous edema, the patient's immobility,
jaundice, and increased susceptibility to skin
breakdown and infection.
 Assess degree of discomfort related to pruritus and
edema.
 Note and record degree of jaundice and extent of
edema.
 Keep patient’s fingernails short and smooth.
 Provide frequent skin care; avoid use of soaps and
alcohol-based lotions.
Providing Skin Care:
 Massage every 2 hours with emollients; turn every 2 hours
 Initiate use of alternating-pressure mattress or low air loss bed.
 Recommend avoiding use of harsh detergents.
 Assess skin integrity every 4–8 hours. Instruct patient and family
in this activity.
 Restrict sodium as prescribed to minimizes edema formation.
 Perform range of motion exercises every 4 hours; elevate
edematous extremities whenever possible.
 It is important to avoid irritating soaps
 The use of adhesive tape to prevent trauma to the skin.
 Lotion may be soothing to irritated skin; the nurse takes
measures to minimize scratching by the patient.
Reducing risk of injury:
 Assess level of consciousness and cognitive level.
 Provide safe environment (pad side rails, remove obstacles in
room, prevent falls).
 Provide frequent surveillance to orient patient and avoid use
of restraints.
 Replace sharp objects (razors) with safer items.
 Observe each stool for color, consistency, and amount.
 Be alert for symptoms of anxiety, epigastric fullness,
weakness, and restlessness.
 Test each stool and emesis for occult blood.
 Observe for hemorrhagic manifestations: ecchymosis,
epistaxis, petechiae, and bleeding gums.
Reducing risk of injury:
 Record vital signs at frequent intervals, depending on
patient acuity (every1–4 hours).
 Keep patient quiet and limit activity.
 Assist physician in passage of tube for esophageal
balloon tamponade, if its insertion is indicated.
 The nurse instructs the patient to ask for assistance to
get out of bed.
 Because of the risk for bleeding from abnormal
clotting, the patient should use an electric rather than
a safety razor.
 A soft-bristle toothbrush will help to minimize
bleeding gums, pressure applied to all venipuncture
sites will help to minimize bleeding.
Monitoring and Managing Potential Complications:
Bleeding and Hemorrhage
 Precautionary measures include protecting the patient with
padded side rails, Applying pressure to injection sites
 Avoiding injury from sharp objects.
 The nurse observes for melena and assesses stools' for blood
(signs of possible internal bleeding).
 Vital signs are monitored regularly.
 Precautions are taken to minimize rupture of esophageal
varices for avoiding further increases in portal pressure.
 Dietary modification and appropriate use of stool softeners
may help prevent straining during defecation.
 The nurse closely monitors the patient for GI bleeding and
keeps readily available equipment (Sengstaken-Blakemore
tube), IV fluid and medications needed to treat hemorrhage
from esophageal and gastric varices.
Management ascities
 Ascities is a problematic because as more fluid retained, it
push up on the diaphragm, thereby impairing the patient's
breathing pattern. Nursing assessment of respiratory
status through respiratory rate, breath sound and arterial
blood gases monitoring is critical
 Frequent monitoring of abdominal girths and daily weight
alerts the nurse to fluid accumulation. Abdominal girths
should be measured at the level of the umbilicus
 Positioning the patient in a semi fowler's position allows
for free diaphragm movement. Frequent deep breathing
and coughing exercise and changes in position are
important for the prevention of this complication
Management ascities
 Ascites is manage through bed rest , low sodium diet, fluid restriction,
and diuretic therapy. Diuretic must be administered cautiously , because if
the intravenous volume is depleted quickly , acute renal failure may be
induced. Closed monitoring of serum creatinine level , BUN level, and
urine output is important for the early detection of this potential
complication.
 Careful monitoring of electrolyte balance, particularly serum potassium
and sodium, is also important in diuretic administration
 Paracentesis is a medical therapy for ascites , in which ascetic fluid is
withdrawn through percutaneous need aspiration . Close monitoring of
vital signs during this procedure is necessary, especially as fluid is with
drawn. Major complications include sudden loss off intravascular pressure
(decreased blood pressure) and tachycardia. One to two liters of fluid is
generally withdrawn at one time in ordered to prevent this complication.
Nurse should document the amount, color, and character of peritoneal
fluid obtained. Also, a specimen of the fluid is sent to the laboratory for
analysis.
Hepatic Encephalopathy
 Hepatic encephalopathy and coma, possible complications of
cirrhosis,
 Monitoring is an essential nursing function to identify early
deterioration in mental status.
 The nurse monitors the patient's mental status closely and
reports changes so that treatment of encephalopathy can be
initiated promptly.
 Because electrolyte disturbances can contribute to
encephalopathy, serum electrolyte levels are carefully
monitored and corrected if abnormal.
 Oxygen is administered if oxygen desaturation occurs.
 The nurse monitors for fever or abdominal pain, which may
signal the onset of bacterial peritonitis or other infection.
Fluid Volume Excess
 Monitoring intake and output
 Monitoring daily weight changes
 Monitoring changes in abdominal girth
 Assessment edema formation
 Close assessment of the cardiovascular and respiratory status is
key for the nurse caring for patients with this disorder.
 Administering diuretics,
 Implementing fluid restrictions,
 Enhancing patient positioning can optimize pulmonary function.
 Fluid retention may be noted in the development of ascites and
lower extremity swelling and dyspnea.
 Patients are also monitored for nocturia and, later, oliguria as
these states indicate increasing severity of liver function.
Promoting Home and Community-Based
Care:
Teaching Patients Self-Care

 During the patient's hospital stay, the nurse and other
health care providers prepare the patient with cirrhosis
for discharge, focusing on dietary instruction.
Nutritional Guidelines for Liver
cirrhosis
General guidelines
 Total calories 35-40kcal/kg/day
 60 - 70 percent carbohydrates - primarily
complex carbohydrates, such as pasta and
whole-grain breads.
 20-30 percent protein - only lean animal
protein and/or vegetable protein.
 10 - 20 percent polyunsaturated fat.
General guidelines
 8-12 glasses of water per day.
 1,000 to 1500 milligrams of sodium per day
 Avoidance of excessive amounts of vitamins and
minerals, especially vitamin A, vitamin B3, and iron.
 No alcohol
 Avoidance of processed food.
 Liberal consumption of fresh organic fruits and
vegetables.
 Avoidance of excessive caffeine consumption - no
more than 1-3 cups of caffeine-containing beverages
per day.
 Vitamin D and calcium supplement.
cirrhosis
 PROTEIN
 Protein intake must be adjusted in accordance with a
person's body weight and the degree of liver damage
present.
 Approximately 0.8 grams of protein per kilogram of body
weight is recommended in the diet each day for someone
with stable liver disease.
 People with unstable liver disease or decompensated
cirrhosis need to lower the percentage of protein content
in their diets so that it falls between approximately 10 to 15
%.
 They need to eat only vegetable sources of protein.
PROTEIN
 A diet high in animal protein ( which typically

contains alot of ammonia) may precipitate an episode
of encephalopathy among these people.
 Vegetarian diets, on the other hand, have a low
ammonia content and have been shown to be much
less likely than animal protein diets to induce
encephalopathy.
 It is important to keep in mind that some popular
weight-loss diets involve the consumption of a very
high animal protein content. People with cirrhosis are
advised to avoid any such diets.
cirrhosis
Energy
 Give glucose to cover 50 % - 60 % of non-protein
energy requirements.
 Reduce glucose infusion rate to 2–3 g kg in case of
hyperglycemia and use consider the use of i.v. insulin.
 Use lipid emulsions with a content of n-6 unsaturated
fatty acids lower than in traditional pure soybean oil
emulsions.
cirrhosis
Amino acids
 Provide amino acids at 1.2–1.5 g kg.
 Micronutrients Give water soluble vitamins and trace
elements daily from the first day of PN.
 In alcoholic liver disease, administer vitamin B1 prior
to starting glucose infusion to reduce the risk of
Wernicke’s encephalopathy.
 In acute or subacute liver failure, provide amino acids
at 0.8–1.2 g kg
cirrhosis
FAT
 Fats are the body's most efficient means for storing excess
energy. It is important for people with liver disease to
minimize their fat intake by avoiding foods that are high in
fat content. Excess fat can result in a fatty liver or
nonalcoholic steatohepatitis (NASH).
 As a general rule, no more than 30% of a person's caloric
intake should come from fat.
 While it is important to eat as little fat as possible, because
people need some fat in order to properly absorb the four
fat-soluble vitamins A,D,E, and K. Without some fat, these
vitamins may become deficient in the body.
cirrhosis
 Carbohydrates
 People with liver disease should strive for a diet
consisting of approximately 60 - 70 % carbohydrates,
with complex carbohydrates ( starches and fibers)
predominating.
 A well-balanced diet will include at least 400 grams of
carbohydrates. If there are too few carbohydrates in a
person's diet, this will likely result in excessive protein
and fat intake
cirrhosis
Iron (Fe)
 There are two types of dietary iron. Heme, or animal
iron (red meat) ,is well absorbed from the
diet. Nonheme, or plant iron ( spinach), is poorly
absorbed into the body
 The average American consumes about 10 - 20 mg of
iron per day.
 In order to increase the absorption of plant iron into
the body a vitamin C supplement should be consumed
at the same time.
cirrhosis
Calcium
 If calcium supplementation is taken, it should be limited to
no more than 1000-2000 milligrams /day, and should be
taken with a vitamin D supplement (which is usually
included in the calcium tablet).
Low Sodium Diet
 2000- 2400 mg Sodium/ day
 <200 mg/ serving or 700 mg/ meal
 Replace salt shaker with herb shaker
 Stock kitchen with fresh unprocessed foods
 Avoid eating out- eat in!
cirrhosis
Magnesium
350 mg. Doses larger than 400 mg may cause stomach problems
and diarrhea
Phosphorus
1000 mg. doses larger than 250 mg may cause stomach problems for
sensitive individuals
Potassium
3500 mg. Large doses may cause stomach upsets, intestinal
problems or heart rhythm disorder
Fluid Intake
 Avoid overhydration usually 6-8 cups/day is adequate (48-64 oz)
 Suck on ice chips, candy or gum rather than guzzling water
 If low serum sodium is an issue, may need a fluid restriction
 Avoid dehydration however-can lead to renal problems
Self-Care
Clients with cirrhosis are managed at home unless
they encounter complications or are in the end stage of
the disease process. Hence it is important to teach
them how to maintain adequate nutrition, to alternate
rest and activity, and to avoid hepatotoxic substances.
Refer the client to the appropriate agency or support
group for assistance with alcohol cessation.
Thyroid Gland
T h y ro id g la n d
By the end of the lecture; the students will be able to

• Expla in mech a n ism o f fun ctio n o f th y ro id g la n d .
• List sig n s a n d sy mpto ms o f h y po a n d h y perth y ro id ism.
• Differen tia te between d ifferen t ty pes o f th y ro id d y sfun ctio n .
Thyroid Gland
• Thyroid gland is a butterfly-shaped organ
located in the lower neck anterior to the
trachea
• It consists of two lateral connected by an
isthmus
• The blood flow to the thyroid is very high (
about 5 ml/min/g of thyroid), about five
times the blood flow to the liver. This reflect
the metabolic activity of the thyroid gland
Thyroid Gland
Thyroid Gland
Thyroid hormone
Two separate hormone produced by the

thyroid gland make up thyroid hormone :
throxine and triiodothyronine. T4 contains
four iodine atomes in each molecule and T3
contains only three
Thyroid Gland
Thyroid hormone
• Thyroxine (T4) accounts for about 90% of

the hormone secreted from the thyroid.
• Most of the T4 that is secreted is converted

into T3 by the liver and kidneys.
Thyroid Gland
Regulation of Thyroid Function
• The secretion of T3 and T4 is under the
control of thyroid stimulating hormone (TSH
or Thyrotropin) from the anterior pituitary
gland.
• In turn the release of TSH is determined by the
level of thyroid hormones in the blood.
(negative feedback)
Thyroid Gland
Throtropin – releasing hormone (TRH),
secreted by the hypothalamus, exerts a
modulating influence on the release of TSH
from the pituitary.
Thyroid Gland
Thyrotropin releasing hormone (TRH) from
the hypothalamus stimulates the pituitary
gland to secrete thyroid-stimulating
hormone (TSH). TSH stimulates the thyroid
to produce thyroid hormone (T3 and T4).
High circulating levels of T3 and T4 inhibit
further TSH secretion and thyroid hormone
production through a negative feedback
mechanism.
Thyroid Gland
Function of thyroxine and triiodothyronine
1. Control the cellular metabolic activity
2. Influence cell replication
3. Important in brain development
4. Normal growth
Thyroid Gland
Calcitonin
Calcitonin, or thyrocalcitonin, is another

important hormone secreted by the thyroid
gland. It is secreted in response to high
plasma levels of calcium, and reduces the
plasma level of calcium by increasing its
deposition in bone.
Calcitonin hormone by thyroid
Thyroid Function
• Consequently, hypo or hyperthyroidism
may
result from:
• A defect in the target gland or
• Disturbance in the secretion of TSH or

TRF
Thyroid Function
Goiter
• Enlargement of the thyroid gland, which
often visible on the anterior part of the neck.
Goitre is caused by various hypothyroid and
hyperthyroid conditions
• May be very large compressing the
esophagus and interfering with swallowing
(dysphagia)
• Or cause pressure on trachea
Thyroid Function
Goiter
Hypothyrodism
Definition
• Is a disorder in which levels of
thyroid hormones are
decreased.
Hypothyroidism
Hypothyroidism
Results from subnormal levels of thyroid
hormone. It can range from mild form to
myxedema (advanced form).
Myxedema refers to accumulation of
mucopolysaccharides in subcutaneous and
other interstitial tissues
Myxedema
Hypothyroidism
Causes
• Autoimmune thyroiditis (Hashimoto’s
disease), in which the immune system
attacks the thyroid gland.
• Hyperthyroidism treated by radioiodine,
surgery, or antithyroid medication.
• Iodine deficiency and iodine excess
Hypothyroidism
Types
• Primary hypothyroidism
Dysfunction of the thyroid gland itself
• Central hypothyroidism
The thyroid dysfunction is caused by
failure of pituitary gland, the
hypothalamus, or both
Hypothyroidism
Types
• Pituitary or secondary hypothyroidism
entirely pituitary disorder
• Hypothalamic or tertiary hypothyroidism
the disorder is present in hypothalmus
resulting in inadequate secretion of TSH
because of decreased stimulation by TRH
• Cretinism
Hypothyroidism is present at birth
Hypothyroidism
Cretinism
Hypothyroidism
is present at birth
Hypothyroidism
Early symptom include:
• Fatigue
Makes it difficult for a person to complete a
full day’s work or participate in usual
activities
• Hair loss brittle nails and dry skin are
reported
• Numbness and tingling of the fingers
Hypothyroidism
Early symptom include:
• Menstrual disturbances such as

menorrhagia or amenorrhea
Hypothyroidism
Sever hypothyroidism result in
• Subnormal temperature and pulse rate,
the patient often complains of being cold
even in a warm temperature
• Gain weight without an increase in food
intake
• The skin become thickened because of an
accumulation of mucopolysaccharides in
the subcutaneous tissues
Hypothyroidism
Advanced hypothyroidism result in
• Personality and cognitive changes
characteristics of dementia
• Inadequate ventilation and sleep apnea
• Myxedema coma, the patient become
hypothermic and unconscious
Hypothyroidism
Medical Management
Thyroid hormone replacement
Synthetic levothyroxine (synthroid or

levothroid) is the preferred medicine .
The dose is based on the patient’s serum
TSH concentration
Hypothyroidism
Medical Management
Supportive therapy
1. Measured arterial blood gases to determine
carbon dioxide retention and to guide the use of
assisted ventilation to combat hypoventilation.
2. Measure oxygen saturation by pulse oximetry
3. Application of external heat is avoided because it
increase oxygen requirement and may lead to
vascular collapse
Hypothyroidism
Medical Management
Supportive therapy
4. If hypoglycemia is evident, concentrated

glucose may be prescribed to provide
glucose without precipitating fluid
overload
Hypothyroidism
Medical Management
Supportive therapy
Nursing Alert
The nurse monitor for myocardial ischemia or
infarction, which may occure in response
to therapy in patient with sever, long
standing hypothyroidism or myxedema
coma
Hypothyroidism
Medical Management
Supportive therapy
The nurse must be alert for signs of
angina, especially during early phase of
treatment, if detected , the administration
of thyroid hormone must be discontinued
immediately.
Hypothyroidism
Medical Management
Supportive therapy
Later, when it can be resumed safely,

thyroid hormone replacement should be
prescribed cautiously at a lower dosage
and under the close observation.
Hypothyroidism
Medical Management
Complications: medication interaction
1. Thyroid hormone may increase blood glucose
levels.
2. The effect of thyroid hormone may increased by
phenytoin and tricyclic antidepressants
3. Thyroid hormone may increase digitalis ,
anticoagulants, this requiring carful observation
and assessment by the nurse for side effects of
these agents
4. Bone loss may occur
Hypothyroidism
Medical Management
Complications: medication interaction
5. Sever untreated hypothyroidism is
characterized by an increased
susceptibility to all hypnotic and sedative
agents. Because they are likely to cause
respiratory depression, which can easily
be fatal because of decreased respiratory
reserve and alveolar hypoventilation.
Hypothyroidism
Nursing Management
Modifying activity
1. pt’s experience decreased energy and
moderate to sever lethargy, so the patient
become at risk to develop complication of
immobility
2. The nurse role is to assist in the pt’s
hygiene and encourage him to participate
in activity according to his tolerance
Hypothyroidism
Nursing Management
Monitoring physical status
1. Monitor vital signs and cognitive level
closely to detected signs of deteroration
that resulted from metabolic rate
exceeding the ability of the cardiovascular
and pulmonary system to respond.
Hypothyroidism
Nursing Management
Promoting physical comfort
1. The patient often experience and extreme intolerance to
cold, even if the room temperature feels comfortable or
hot.
a. provide extra clothing and blankets
b. protect patient from cold and draft
c. Avoid using of heating pads and electric blankets
because of:
- The risk of peripheral vasodilatation and
- The patient may be burned from this item because of
delayed responses and decreased of mental status
Hypothyroidism
Nursing Management
Return of normal bowel function (prevent constipation)
1. Encourage increased fluid intake within limits of
fluid restriction
2. Provide food high in fiber
3. Instruct patient about foods with high water
content
4. Encourage increased mobility within patient’s
exercise tolerance
5. Encourage patient to use laxatives
Hypothyroidism
Nursing Management
Treated myxedema and myxedema coma
1. Monitor patient for increasing severity of
sign and symptoms of hypothyroidism
• Decreased level of consciousness , dementia
• Decreased vital signs (BP, RR, T,)
• Increasing difficulty in a wakening or
arousing patient.
Hypothyroidism
Nursing Management
Treated myxedema and myxedema coma
2. Assist in ventilatory support if respiratory
depression and failure occur
3. Administer prescribed medications (e.g
thyroxine) with extreme caution
4. Turn and reposition patient at intervals
5. Avoid use of hypnotic, sedative and analgesic
agents.
Hyperthyroidism
Hyperthyroidism
Hyperthyroidism (Graves’ disease)
Excessive secretion of thyroid hormone
• Sometimes is referred to as thyrotoxicosis)
• Nervousness , hyperxcitable, irritable, and
apprehensive
• They canot sit quietly
• They suffer from palpitations and
• Their pulse is abnormally rapid at rest as well as
on excertion
Hyperthyroidism
• They tolerate heat poorly and perspire unusually

freely
• The skin is flushed continuously, with a

characteristic salmon colour, and is likely to warm,
soft and moist
• Patients may exhibit exophthalmos (bulging eyes)

Hyperthyroidism
Exophthalmos
Hyperthyroidism
• Increased appetite and dietary intake
• Progressive weight loss
• Abnormal muscular fatigbility and weakness

(difficulty in climbing stairs and rising from
a chair)
Hyperthyroidism
• Basis of symptoms
• Increase in serum T4 and an increased

123I or 125I uptake by thyroid
Hyperthyroidism
Medical Management
• Three forms of treatment are avaulable for
treating hyperthyroidism and controlling
excessive thyroid activity
1. Irradiation involving the administration of
radioisotope 123I for destructive effect on the
thyroid gland.
2. Pharmacotherapy as antithyroid medication
3. Surgery , with removal of most of thyroid gland
Hyperthyroidism
Nursing Management
Improving Nutritional status
• Provide several well balanced meals of
small size, even up to six meals a day
(because the patient appetite is increased)
• Select foods and fluids to replace fluid lost
through diarrhoea ( that result from
increased peristalsis) and diaphoresis
Hyperthyroidism
Nursing Management
Improving Nutritional status
• Highly seasoned food and stimulants such
as cola and alcohol should be discouraged.
• Encouraged high calorie, high protein diet
• Provide a quite atmosphere during
mealtimes to aid in digestion.
• Monitor patient’s weight and dietary
intake to monitor nutritional status
Hyperthyroidism
Nursing Management
Maintaining normal body temperature
The patient with hyperthyroidism frequently
finds a normal room temperature too
warm because of an exaggerated
metabolic rate and heat production.
• The environment should be maintained at
a cool, comfortable temperature and
bedding and clothing changed as needed
Hyperthyroidism
Nursing Management
Maintaining normal body temperature
Provide cool baths and cool or cold fluids

Hyperthyroidism
Nursing Management
Monitoring and Managing potential
complication
Monitor the patient for signs and symptom of
thyroid strom
• Monitor cardiac and respiratory function
by measuring:
• Vital signs and cardiac output, ECG, arterial blood
gases and pulse oximetry
Hyperthyroidism
Nursing Management
Monitoring and Managing potential complication
• Administer of oxygen to prevent hypoxia , to

improve tissue oxygenation and to meet the high
metabolic demands
• Administer IV fluid to maintain blood glucose

levels and to replace lost fluids
Hyperthyroidism
Nursing Management
Monitoring and Managing potential

complication
• Antithyriod medications (methimazole)

may be prescribed to reduce thyroid
hormone levels
Hyperthyroidism
Nursing Management
Care of eyes
• If the patient experiences eye changes the

patient need instructions about correct
instillation of eye drops or ointment
prescribed to so the the eyes and protect the
exposed cornea
Dialysis
Definition
Dialysis is used to remove fluid and uremic waste
products from the body when the kidneys cannot do
so.
Methods of therapy include
 Hemodialysis
 Continuous renal replacement therapy
 Peritoneal dialysis
Indication of dialysis
 Patients with edema that does not respond to
treatment
 Hepatic coma
 Hyperkalemia
 Hypercalcemia
 Hypertension
 Uremia.
Type of dialysis
 Acute dialysis
 Chronic dialysis.
Acute dialysis
Acute dialysis is indicated when there is
 A high and rising level of serum potassium
 Fluid overload
 Impending pulmonary edema
 Increasing acidosis
 Pericarditis
 It may also be used to remove certain medications or
other toxins (poisoning or medication overdose) from
the blood.
Chronic dialysis
Chronic or maintenance dialysis is indicated in
 Chronic renal failure,
 Fluid overload not responsive to diuretics and fluid

restriction, and a general lack of well-being.
 An urgent indication for dialysis in patients with

chronic renal failure is pericardial friction rub.
Hemodialysis
Most dialyzers, or artificial kidneys contain
thousands of tiny cellophane tubules
that act as semipermeable membranes.
The blood flows through the tubules,
while a solution (the dialysate) circulates
around the tubules. The exchange of
wastes from the blood to the dialysate
occurs through the semipermeable
membrane of the tubules
Dialysate solution
 Dialysate, is a solution
made up of all the
important electrolytes in
their ideal extracellular
concentrations and has
the same chemical
composition as the blood
except for urea and waste
products,
FIGURE 1 Hemodialysis system. (A) Blood from an artery is pumped
into (B) a dialyzer where it flows through the cellophane tubes, which act
as the semipermeable membrane (inset). The dialysate, which has the
same chemical composition as the blood except for urea and waste
products, flows in around the tubules. The waste products in the blood
diffuse through the semipermeable membrane into the dialysate.
Principles of Hemodialysis
Diffusion
Osmosis
Ultrafiltration
Diffusion
 The toxins and wastes in the blood are removed by
diffusion—that is, they move from an area of higher
concentration in the blood to an area of lower
concentration in the dialysate.
Osmosis
 Excess water is removed from the blood by
Osmosis ,the water moves from an area of
higher solute concentration (the blood) to
an area of lower solute concentration (the
dialysate bath)
Ultrafiltration
 Is defined as water moving under high pressure to an
area of lower pressure. This process is much more
efficient at water removal than osmosis. Ultrafiltration
is accomplished by applying negative pressure or a
suctioning force to the dialysis membrane.
 Because patients with renal disease usually cannot
excrete water, this force is necessary to remove fluid to
achieve fluid balance.
Subclavian, Internal Jugularand Femoral
Catheters
 Immediate access to the patient’s circulation for acute
hemodialysis is achieved by inserting a double-lumen or
multilumen catheter into the subclavian, internal
jugular, or femoral vein.
 Although this method of vascular access involves some

risk (eg, hematoma, pneumothorax, infection,
thrombosis of the subclavian vein, and inadequate
flow), it can be used for several weeks.
Fistula
 A more permanent access, known as a fistula, is
created surgically (usually in the forearm) by joining
(anastomosing) an artery to a vein, either side to side
or end to side.
 Needles are inserted into the vessel to obtain blood
flow adequate to pass through the dialyzer. The arterial
segment of the fistula is used for arterial flow and the
venous segment for reinfusion of the dialyzed blood.
 The fistula takes 4 to 6 weeks to mature before it is
ready for use. This gives time for healing and for the
venous segment of the fistula to dilate to accommodate
two large-bore (14- or 16-gauge) needles.
Fistula
FIGURE 3 An internal arteriovenous fistula

(top) is created by a side to-side anastomosis
of the artery and vein. A graft (bottom) can
also be established between the artery and
vein.
Graft
 An arteriovenous graft can be created by
subcutaneously interposing a biologic, semibiologic,
or synthetic graft material between an artery and vein.
 Usually, a graft is created when the patient’s vessels are
not suitable for a fistula.
 Grafts are usually placed in the forearm, upper arm, or
upper thigh. Infection and thrombosis are the most
common complications of arteriovenous grafts.
Complications of Hemodialysis
 Disturbances of lipid metabolism
(hypertriglyceridemia) .
 Heart failure
 Coronary heart disease
 Angina pain
 Stroke
 Peripheral vascular insufficiency .
 Anemia
 Lack of energy and drive
 Loss of interest
 Hypotension
 Painful muscle cramping
 Air embolism , thrombotic embolism
 Dialysis dis equillibrium
 Disturbed calcium metabolism leads to renal
osteodystrophy that produces bone pain and fractures.
 Fluid overload associated with heart failure
 Malnutrition
 Infection
 Dialysis disequilibrium results from cerebral fluid
shifts. Signs and symptoms include headache, nausea
and vomiting, restlessness, decreased level of
consciousness, and seizures. It is more likely to occur in
acute renal failure or when blood urea nitrogen levels
are very high (exceeding 150 mg/dL).
 Use of erythropoietin (Epogen) before the start of
dialysis has been shown to have a significant effect on
hematocrit values for the first 19 months after starting
dialysis.
Pharmacologic Therapy
 Patients require medications (eg, cardiac glycosides, antibiotic
agents, antiarrhythmic medications, antihypertensive agents) are
monitored closely to ensure that blood and tissue levels of these
medications are maintained without toxic accumulation.
 In patients receiving dialysis, all medications and their dosages

must be carefully evaluated.
 The patient must know when and when not to take the medication.
For example, if an antihypertensive agent is taken on a dialysis day,
a hypotensive effect may occur during dialysis, causing
dangerously low blood pressure.
Nutritional and Fluid Therapy
 Diet is an important factor for patients on hemodialysis because of the
effects of uremia.
Goals of nutritional therapy for patients on hemodialysis
 To minimize uremic symptoms and fluid and electrolyte imbalances
 To maintain good nutritional status through adequate protein, calorie,
vitamin, and mineral intake.
 To enable the patient to eat a palatable and enjoyable diet.
 Restricting dietary protein decreases the accumulation of nitrogenous
wastes, reduces uremic symptoms, and may even postpone the initiation
of dialysis for a few months.
 Restriction of fluid is also part of the dietary prescription because fluid
accumulation may occur, leading to weight gain, heart failure, and
pulmonary edema.
 With the initiation of hemodialysis, the patient’s dietary
intake usually still requires some restriction of dietary
protein, sodium, potassium, and fluid intake.
 Protein intake is restricted to about 1 g/kg ideal body weight
per day; therefore, protein must be of high biologic quality
and consist of the essential amino acids. Examples of foods
high in biologic protein content include eggs, meat, milk,
poultry, and fish.
 Sodium is usually restricted to 2 to 3 g/day; fluids are
restricted to an amount equal to the daily urine output
plus 500 mL/day.
 Potassium restriction (average 1.5 to 2.5 g/day) depends
on the amount of residual renal function and the frequency of
dialysis
Nursing Management
Protecting the vascular access
 The nurse assesses the vascular access for patency and takes
precautions to ensure that the extremity with the vascular
access is not used for measuring blood pressure o for
obtaining blood specimens; tight dressings, restraints, or
jewelry over the vascular access are to be avoided as well.
 The bruit, or “thrill,” over the venous access site must be

evaluated at least every 8 hours.
Protecting the vascular access
 When blood flow is reduced through the access for
any reason (hypotension, application of blood
pressure cuff or tourniquet), the access can clot or
become infected.
 The nurse observes the patient for signs and
symptoms of infection, such as redness, swelling,
drainage from the site, and fever.
 Patients with renal disease are more prone to
infection; therefore, infection control measures
must be used for all procedures.
Taking Precautions During Intravenous
Therapy
 When the patient needs intravenous therapy, the rate
of administration must be as slow as possible and
should be strictly controlled by a volumetric infusion
pump.
 Accurate intake and output records are essential.

Monitoring Symptoms Of Uremia
 As metabolic end products accumulate, uremic
symptoms worsen. Patients whose metabolic rate
accelerates (those on corticosteroid medications or
parenteral nutrition, those with infections or bleeding
disorders, those undergoing surgery) accumulate
waste products more quickly and may require daily
dialysis. These same patients are more likely to
experience complications than other dialysis patients.
Controlling Electrolyte Levels And Diet
 Electrolyte alterations are common, and potassium changes
can be life threatening.
 All intravenous solutions and medications to be
administered are evaluated for their electrolyte content.
Serum laboratory values are assessed daily.
 If blood transfusions are required, they may be administered
during hemodialysis, if possible, so that excess potassium
can be removed.
 Dietary intake must also be monitored.
 With the initiation of hemodialysis, the patient’s dietary intake usually
still requires some restriction of dietary protein, sodium, potassium, and
fluid intake.
 Protein intake is restricted to about 1 g/kg ideal body weight per day;
therefore, protein must be of high biologic quality and consist of the
essential amino acids to prevent poor protein use and to maintain a
positive nitrogen balance. Examples of foods high in biologic protein
content include eggs, meat, milk, poultry, and fish.
 Sodium is usually restricted to 2 to 3 g/day; fluids are restricted to an
amount equal to the daily urine output plus 500 mL/day. The goal for
hemodialysis patients is to keep their interdialytic (between dialysis
treatments) weight gain under 1.5 kg.
 Potassium restriction (average 1.5 to 2.5 g/day) depends on the
amount of residual renal function and the frequency of dialysis
Management of complications
Skin care
 Keeping the skin clean and well moisturized using
bath oils, super fatted soap, and creams or lotions
helps to promote comfort and reduce itching.
 Teaching the patient to keep the nails trimmed to
avoid scratching and excoriation and to rub lotion into
the skin instead of scratching also promotes comfort.
Monitoring Blood Pressure
Managing hypertension
 Many dialysis patients receive some form of
antihypertensive therapy and require intense teaching
about its purpose and adverse effects.
 Antihypertensive agents must be withheld on dialysis
days to avoid hypotension due to the combined effect of
the dialysis and the medication.
 Maintaining strict fluid and sodium control.
Preventing Infection
 Preventing and controlling infection are essential
because the incidence of infection is high. Infection of
the vascular access site and pneumonia are common.
 Assess Clinical manifestations of infection include shaking

chills, fever, rapid heartbeat and respirations (tachycardia and
tachypnea), and either an increase or a decrease in WBCs
CONTROL OF INFECTION
• Measure patient’s temperature q4h; consult physician
for elevations >37.8° C (100'' F).
• Assess and document condition of indwelling IV sites

and other catheter sites q8h.
• Be alert to swelling, erythema, tenderness, and drainage.

Consult physician for any of these findings.
• Catheter and drain tips may be cultured when
removed by cutting the tip of the catheter or drain
(using aseptic technique) and placing the cut portion
in a sterile container to be taken to the laboratory for
culture.
• Record volume appearance, color and odor of urine.
Be alert for sings of urinary infections
 Auscultate lung fields every 8 hrs, noting presence of
ronchi, crackles and decrease breath sounds.
 Careful hand hygiene is imperative; facemasks may be
worn by hospital staff and visitors to reduce the risk for
transmitting infectious agents.
 Strict aseptic technique must be used while performing
any invasive procedure or providing wound care.
Meeting psychosocial needs
 Dialysis alters the lifestyle of the patient and family.
 The nurse needs to give the patient and family the

opportunity to express feelings of anger and concern over the
limitations that the disease and treatment impose and over
possible financial problems and job insecurity.
 Counseling and psychotherapy may be necessary.
 The nurse helps the patient to identify safe, effective coping
strategies to cope with these ever-present problems and fears.
‫صدق هللا العظيم‬
Chronic renal
failure
By
A.L/ Nevin Adel Amer
• Introduction
• Risk Factors
• Causes of CRF
• Stages of chronic renal disease
• Signs and Symptoms of Chronic Renal Failure
• Assessment and Diagnostic Findings
• Complications of chronic renal failure
• Medical Management
• Nutritional Therapy
• Other Therapy: Dialysis
• Nursing Management
 Chronic renal failure, or ESRD, is a progressive, irreversible
deterioration in renal function in which the body’s ability to
maintain metabolic and fluid and electrolyte balance fails,
resulting in uremia or azotemia (retention of urea and other
nitrogenous wastes in the blood).
 Age > 60 years
 Race or ethnic background
 African-American
 Hispanic
 American Indian
 Asian
 History of exposure to chemicals/toxins
 Cigarette smoking
 Heavy metals
 Family history of chronic kidney disease

Causes of CRF
 Diabetic Nephropathy
 Vascular Disease
 Polycystic Kidney Disease/ Genetics
 Obstructive nephropathy
 chronic glomerular Disorders/ Glomerulonephritis
• recurring pyelonephritis (kidney infection)
• autoimmune disorders such as systemic lupus erythematosus

Stage 1the normal stage of renal function:-
 GFR>70 ml/min, BUN<6.5 mmol/L, Scr<110 umol/L
Stage 2: Reduced renal reserve,
 It is Characterized by a 40% to 75% loss of nephron function.

The patient usually does not have symptoms because the
remaining nephrons are able to carry out the normal functions
of the kidney.
 GFR 50-70 ml/min, 6.5 <BUN< 9 mmol/L, 110 <Scr< 178

umol/L.
stage 3:- azotemic stage
 Renal insufficiency occurs when 75% to 90% of nephron

function is lost. At this point the kidney loses its ability to
concentrate urine and anemia develops. The patient may report
polyuria and nocturia.
 GFR<50 ml/min,BUN>9 mmol/L, Scr>178 umol/L there may

be slight fatigue, anorexia and anemia
Stage 4:- uremic stage
 End-stage renal disease (ESRD), the final stage of chronic renal

failure, occurs when there is less than 10% nephron function
remaining. All of the normal regulatory, excretory, and hormonal
functions of the kidney are severely impaired. ESRD is evidenced by
elevated creatinine and blood urea nitrogen levels as well as
electrolyte imbalances.
 GFR<25 ml/min,BUN>20 mmol/L, Scr>445 umol/L a constellation

of uremic syndrome may appear in this stage
 Once the patient reaches this point, dialysis is usually indicated.

Many of the symptoms of uremia are reversible with dialysis.
Every body system is affected by the uremia of chronic renal failure,
Neurologic
 Weakness and fatigue; confusion; inability to concentrate;
disorientation; tremors; seizures; asterixis; restlessness of legs;
burning of soles of feet; behavior changes
Integumentary
• Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis;
purpura; thin, brittle nails; coarse, thinning hair
Cardiovascular
• Hypertension; pitting edema (feet, hands, sacrum); periorbital
edema; pericardial friction rub; engorged neck veins; pericarditis;
pericardial effusion; pericardial tamponade; hyperkalemia;
hyperlipidemia
Pulmonary
• Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic

pain; shortness of breath; tachypnea; Kussmaul-type respirations;
uremic pneumonitis; “uremic lung”
Gastrointestinal
• Ammonia odor to breath (“uremic fetor”); metallic taste; mouth

ulcerations and bleeding; anorexia, nausea, and vomiting; hiccups;
constipation or diarrhea; bleeding from gastrointestinal tract
Hematologic
 Anemia; thrombocytopenia
Reproductive
 Amenorrhea; testicular atrophy; infertility; decreased libido
Musculoskeletal
 Muscle cramps; loss of muscle strength; renal osteodystrophy;

bone pain; bone fractures; foot drop
•
Assessment and diagnostic finding
History-taking, Look for

 Family history of renal disease
 Personal history of diabetes, hypertension, atheromatous
disease.
 Recurrent upper urinary tract infections, uropathy, stones.
 Systemic disease or autoimmune disease or Gout
 proteinuria, haematuria .
 Chronic or intermittent use of potentially nephrotoxic drugs:
 Exposure to toxic substances at work: lead, cadmium.
Investigation
1- blood tests
 Serum protein electrophoresis
 Serum creatinine and BUN levels increase.
 Fasting blood glucose.
 ABG to assess for acidosis
 CBC to assess anemia
 Serum calcium and serum phosphorus
2. Urine tests
 Quantitative urine microscopy and cytology performed on fresh urine to detect and
quantify haematuria , leukocyturia or to look for casts.
 24h proteinuria(combined with determination of 24 h creatininuria, which validates the

quality of the 24-hurine sample
 Glomerular Filtration Rate.

Imaging
 Renal ultrasound: kidney size, asymmetry, irregular margins,

large polycystic kidneys, nephrocalcinosis, stones,
hydronephrosis, cyst, tumour.
 Bladder ultrasound: abnormalities of the lower urinary tract,
 Plain abdominal film: stones, arterial calcification

Complications of chronic renal failure
Potential complications of chronic renal failure that concern the
nurse and that necessitate a collaborative approach to care include
the following:
• Hyperkalemia due to decreased excretion, metabolic acidosis,
catabolism, and excessive intake (diet, medications, fluids)
• Hyperkalemia can be diagnosed by Plasma K>5.5mmol/L
• And ECG changes
• Pericarditis, pericardial effusion, and pericardial tamponade due
to retention of uremic waste products and inadequate dialysis
• Hypertension due to sodium and water retention an malfunction of
the renin–angiotensin–aldosterone system
• Anemia due to decreased erythropoietin production, decreased
RBC life span, bleeding in the GI tract from irritating toxins, and
blood loss during hemodialysis
• Bone disease and metastatic calcifications due to retention of
phosphorus, low serum calcium levels, abnormal vitamin D
metabolism, and elevated aluminum levels
Medical Management
All factors that contribute to ESRD and all factors that are reversible
(eg, obstruction) are identified and treated.
Management is accomplished primarily with medications and diet
therapy, although dialysis may also be needed to decrease the level of
uremic waste products in the blood.
• Complications can be prevented or delayed by administering
prescribed antihypertensives, erythropoietin (Epogen), iron
supplements, phosphate-binding agents, and calcium
supplements.
• Dietary intervention is necessary with deterioration of renal
function and includes careful regulation of protein intake, fluid
intake to balance fluid losses, sodium intake to balance sodium
losses, and some restriction of potassium. At the same time,
adequate caloric intake and vitamin supplementation must be
ensured by Adequte intake of calories(30-35kcal/kg/d)
• Protein is restricted because urea, uric acid, and organic acids—
the breakdown products of dietary and tissue proteins—
accumulate rapidly in the blood when there is impaired renal
clearance Protein restriction (0.5-0.8mg/kg/d).
• The allowed protein must be of high biologic value (dairy
products, eggs, meats). High-biologic-value proteins are those
that are complete proteins and supply the essential amino acids
necessary for growth and cell repair.
• Usually, the fluid allowance is 500 to 600 mL more than the
previous day’s 24-hour urine output.
• Calories are supplied by carbohydrates and fat to prevent wasting.
Vitamin supplementation is necessary because a protein-restricted
diet does not provide the necessary complement of vitamins.
• Additionally, the patient on dialysis may lose water-soluble
vitamins from the blood during the dialysis treatment.
• Low phosphate diet(600-1000mg/d)
The patient with chronic renal failure requires astute nursing care to
avoid the complications of reduced renal function and the stresses
and anxieties of dealing with a life-threatening illness. Examples of
potential nursing diagnoses for these patients include the following:
• Nursing Diagnosis: Excess fluid volume related to decreased
urine output, dietary excesses, and retention of sodium and water
• Goal: Maintenance of ideal body weight without excess fluid
Assess fluid status:
a. Daily weight
b. Intake and output balance
c. Skin turgor and presence of edema
d. Distention of neck veins
e. Blood pressure, pulse rate, and rhythm
f. Respiratory rate and effort
Limit fluid intake to prescribed volume.
Identify potential sources of fluid:
a. Medications and fluids used to take medications: oral and
intravenous
b. Foods
Explain to patient and family rationale for restriction.
Assist patient to cope with the discomforts resulting from fluid
restriction.
Provide or encourage frequent oral hygiene.
Nursing Diagnosis: Imbalanced nutrition; less than body requirements related
to anorexia, nausea, vomiting, dietary restrictions, and altered oral mucous
membranes
Goal: Maintenance of adequate nutritional intake

1. Assess nutritional status:
a. Weight changes
b. Laboratory values (serum electrolyte, BUN, creatinine, protein, transferrin,

and iron levels)
1. Assess patient’s nutritional dietary patterns:
a. Diet history
b. Food preferences
c. Calorie counts
1. Assess for factors contributing to altered nutritional intake:
a. Anorexia, nausea, or vomiting
b. Diet unpalatable to patient
c. Depression
d. Lack of understanding of dietary restrictions
1. Provide patient’s food preferences within dietary restrictions.
2. Promote intake of high biologic value protein foods: eggs,
dairy products, meats.
 Encourage high-calorie, low-protein, low-sodium, and low-
potassium snacks between meals.
 Alter schedule of medications so that they are not given

immediately before meals.
 Explain rationale for dietary restrictions and relationship to

kidney disease and increased urea and creatinine levels.
 Provide written lists of foods allowed and suggestions for
improving their taste without use of sodium or potassium.
 Provide pleasant surroundings at meal-times.
 Weigh patient daily.
 Assess for evidence of inadequate protein intake:
a. Edema formation
b. Delayed healing
c. Decreased serum albumin levels

Nursing Diagnosis: Deficient knowledge regarding condition and treatment
Goal: Increased knowledge about condition and related treatment

 Assess understanding of cause of renal failure, consequences of renal failure,
and its treatment:
a. Cause of patient’s renal failure
b. Meaning of renal failure
c. Understanding of renal function
d. Relationship of fluid and dietary restrictions to renal failure
e. Rationale for treatment (hemodialysis, peritoneal dialysis,

transplantation)
 Provide explanation of renal function and consequences of
renal failure at patient’s level of understanding and guided by
patient’s readiness to learn.
 Assist patient to identify ways to incorporate changes related to

illness and its treatment into lifestyle.
 Provide oral and written information as appropriate about:
a. Renal function and failure
b. Fluid and dietary restrictions
c. Medications
d. Reportable problems, signs, and symptoms
e. Follow-up schedule
f. Community resources
g. Treatment options
Nursing Diagnosis: Activity intolerance related to fatigue, anemia, retention of
waste products, and dialysis procedure
Goal: Participation in activity within tolerance

 Assess factors contributing to fatigue:
a. Anemia
b. Fluid and electrolyte imbalances
c. Retention of waste products
d. Depression
 Promote independence in self-care activities as tolerated; assist if fatigued.
 Encourage alternating activity with rest.
 Encourage patient to rest after dialysis treatments.

Nursing Diagnosis: Disturbed self-esteem related to dependency, role
changes, change in body image, and change in sexual function
Goal: Improved self-concept
 Assess patient’s and family’s responses and reactions to illness and

treatment.
 Assess relationship of patient and significant family members.
 Assess usual coping patterns of patient and family members.

 Encourage open discussion of concerns about changes
produced by disease and treatment:
a. Role changes
b. Changes in lifestyle
c. Changes in occupation
d. Sexual changes
e. Dependence on health care team
 Explore alternate ways of sexual expression other than sexual

intercourse.
 Discuss role of giving and receiving love, warmth, and
affection.
Collaborative Problems: Hyperkalemia; pericarditis, pericardial
effusion, and pericardial tamponade; hypertension; anemia;
bone disease and metastatic calcifications
 Goal: Patient experiences an absence of complications
Hyperkalemia
 Monitor serum potassium levels and notify physician if level

greater than 5.5 mEq/L.
 Assess patient for muscle weakness, diarrhea, ECG changes

(tall-tented T waves and widened QRS).
Pericarditis, Pericardial Effusion, and Pericardial Tamponade
 Assess patient for fever, chest pain, and a pericardial friction rub (signs of
pericarditis) and, if present, notify physician.
 If patient has pericarditis, assess for the following every 4 hours:
a. Paradoxical pulse > 10 mm Hg
b. Extreme hypotension
c. Weak or absent peripheral pulses
d. Altered level of consciousness
e. Bulging neck veins
 Prepare patient for cardiac ultrasound to aid in diagnosis of pericardial effusion

and cardiac tamponade.
 If cardiac tamponade develops, prepare patient for emergency pericardiocentesis.

 Hypertension
• Monitor and record blood pressure as indicated.
• Administer antihypertensive medications as prescribed.
• Encourage compliance with dietary and fluid restriction

therapy.
• Teach patient to report signs of fluid overload, vision

changes, headaches, edema, or seizures.
Anemia
• Monitor RBC count, hemoglobin, and hematocrit levels as

indicated.
• Administer medications as prescribed, including iron and

folic acid supplements, Epogen, and multivitamins.
• Avoid drawing unnecessary blood specimens.
• Teach patient to prevent bleeding: avoid vigorous nose

blowing and contact sports, and use a soft toothbrush.
 Administer blood component therapy as indicated.

 Bone Disease and Metastatic Calcifications
• Administer the following medications as prescribed:

phosphate binders, calcium supplements, vitamin D
supplements.
• Monitor serum lab values as indicated (calcium,

phosphorus, aluminum levels) and report abnormal findings
to physician.
• Assist patient with an exercise program.

Acute Renal Failure
ACUTE RENAL
FAILURE
Acute Renal Failure
ACUTE RENAL FAILURE

introduction
 Acute renal failure (ARF) is a sudden and almost complete loss of kidney
function (decreased GFR) over a period of hours to days.
 ARF manifests with oliguria, anuria, or normal urine volume.
 Oliguria (less than 400 mL/day of urine) is the most common clinical
situation seen in ARF; anuria (less than 50 mL/day of urine) and normal
urine output are not as common.
 Regardless of the volume of urine excreted, the patient with ARF
experiences rising serum creatinine and BUN levels and retention of
other metabolic waste products (azotemia) normally excreted by the
kidneys.
Causes of ARF
1. Prerenal Failure
a) Volume depletion resulting from:
 Hemorrhage.
 Renal losses (diuretics, osmotic diuresis)
 Gastrointestinal losses (vomiting, diarrhea, nasogastric
suction)
b) Impaired cardiac efficiency resulting from:
 Myocardial infarction
 Heart failure
 Dysrhythmias
 Cardiogenic shock
c) Vasodilatation resulting from:
Acute Renal Failure
 Sepsis
 Anaphylaxis
 Antihypertensive medications or other medications that cause
vasodilation
2. Intrarenal Failure
a) Prolonged renal ischemia resulting from:
 Pigment nephropathy (associated with the breakdown of blood
cells containing pigments that in turn occlude kidney structures)
 Myoglobinuria (trauma, crush injuries, burns)
 Hemoglobinuria (transfusion reaction, hemolytic anemia)
b) Nephrotoxic agents such as:
 Aminoglycoside antibiotics (gentamicin, tobramycin)
 Radiopaque contrast agents
 Heavy metals (lead, mercury)
 Solvents and chemicals (ethylene glycol, carbon tetrachloride,
arsenic)
 Nonsteroidal anti-inflammatory drugs (NSAIDs)
 Angiotensin-converting enzyme inhibitors (ACE inhibitors)
c) Infectious processes such as:
 Acute pyelonephritis
 Acute glomerulonephritis
3. Postrenal Failure
a) Urinary tract obstruction, including:
 Calculi (stones)
Acute Renal Failure
 Tumors
 Benign prostatic hyperplasia
 Strictures
 Blood clots
Pathophysiology of ARF
 Although the pathogenesis of ARF and oliguria is not always
known, many times there is a specific underlying problem.
Some of the factors may be reversible if identified and treated
promptly, before kidney function is impaired.
 This is true of the following conditions that reduce blood flow
to the kidney and impair kidney function: (1) hypovolemia; (2)
hypotension; (3) reduced cardiac output and heart failure; (4)
obstruction of the kidney or lower urinary tract by tumor,
blood clot, or kidney stone; and (5) bilateral obstruction of the
renal arteries or veins.
 If these conditions are treated and corrected before the kidneys
are permanently damaged, the increased BUN and creatinine
levels, oliguria, and other signs may be reversed.
 Although renal stones are not a common cause of ARF, some
types may increase the risk for ARF. Some hereditary stone
diseases, primary struvite stones, and infection-related
urolithiasis associated with anatomic and functional urinary
Acute Renal Failure
tract anomalies and spinal cord injury may cause recurrent

bouts of obstruction as well as crystalspecific damage to
tubular epithelial cells and interstitial renal cells.
Clinical phases of ARF:
a) Initiation phase
b) Oliguria phase
c) Diuresis phase
d) Recovery phase
1. The initiation period
 begins with the initial insult and ends when oliguria develops.
2. The oliguria period
 is accompanied by a rise in the serum concentration of
substances usually excreted by the kidneys (urea, creatinine,
uric acid, organic acids, and the intracellular cations
 The minimum amount of urine needed to rid the body of
normal metabolic waste products is 400 mL.
 In this phase uremic symptoms first appear and life-
threatening conditions such as hyperkalemia develop.
3. the diuresis period.
 the third phase, the patient experiences gradually increasing
urine output, which signals that glomerular filtration has
started to recover.
Acute Renal Failure
 Laboratory values stop rising and eventually decrease.

Although the volume of urinary output may reach normal or
elevated levels, renal function may still be markedly abnormal.
 Because uremic symptoms may still be present, the need for
expert medical and nursing management continues.
 The patient must be observed closely for dehydration during
this phase; if dehydration occurs, the uremic symptoms are
likely to increase.
4. The recovery period
 Signals the improvement of renal function and may take 3 to
12 months.
 Laboratory values return to the patient’s normal level.
Although a permanent 1% to 3% reduction in the GFR is
common, it is not clinically significant.

1. CHANGES IN URINE
 Urine output varies (scanty to normal volume),
 hematuria may be present,
 the urine has a low specific gravity (1.010 or less, compared with a
normal value of 1.015 to 1.025).
 Patients with prerenal azotemia have a decreased amount of sodium in
the urine (below 20 mEq/L) and normal urinary sediment.
Acute Renal Failure
 Patients with intrarenal azotemia usually have urinary sodium levels

greater than 40 mEq/L with casts and other cellular debris.
 Urinary casts are mucoproteins secreted by the renal tubules when
ever inflammation is present.
2. INCREASED BUN AND CREATININE LEVELS (AZOTEMIA)

 The BUN level rises steadily dependent on the degree of catabolism
(breakdown of protein), renal perfusion, and protein intake.
 Serum creatinine rises in conjunction with glomerular damage.
 Serum creatinine levels are useful in monitoring kidney function and
disease progression.
3. HYPERKALEMIA
 With a decline in the GFR, the patient cannot excrete potassium
normally.
 Patients with oliguria and anuria are at greater risk for hyperkalemia
than those without oliguria.
 Protein catabolism results in the release of cellular potassium into the
body fluids, causing severe hyperkalemia (high serum K+ levels).
 Hyperkalemia may lead to dysrhythmias and cardiac arrest.
4. METABOLIC ACIDOSIS
 Patients with acute oliguria cannot eliminate the daily metabolic load
of acid-type substances produced by the normal metabolic processes.
 In addition, normal renal buffering mechanisms fail.
Acute Renal Failure
 This is reflected by a fall in the serum CO2-combining power and

blood pH. Thus, progressive metabolic acidosis accompanies renal
failure.
5. CALCIUM AND PHOSPHORUS ABNORMALITIES

There may be an increase in serum phosphate concentrations;
 Serum calcium levels may be low in response to decreased absorption
of calcium from the intestine and as a compensatory mechanism for
the elevated serum phosphate levels.
6. ANEMIA
Anemia inevitably accompanies ARF due to
 reduced erythropoietin production,
 uremic GI lesions,
 reduced RBC life span,
 blood loss, usually from the GI tract.
Prevention of ARF
1. Provide adequate hydration to patients at risk for dehydration:
 Surgical patients before, during, and after surgery
 Patients undergoing intensive diagnostic studies requiring fluid
restriction and contrast agents (eg, barium enema, intravenous
pyelograms), especially elderly patients who may not have
adequate renal reserve
 Patients with neoplastic disorders or disorders of metabolism (ie,
gout) and those receiving chemotherapy
Acute Renal Failure
2. Prevent and treat shock promptly with blood and fluid replacement.
3. . Monitor central venous and arterial pressures and hourly urine output of
critically ill patients to detect the onset of renal failure as early as possible.
4. Treat hypotension promptly.
5. Continually assess renal function (urine output, laboratory values) when
appropriate.
6. Take precautions to ensure that the appropriate blood is administered to the
correct patient in order to avoid severe transfusion reactions, which can
precipitate renal failure.
7. Prevent and treat infections promptly. Infections can produce progressive
renal damage.
8. Pay special attention to wounds, burns, and other precursors of sepsis.
9. Give meticulous care to patients with indwelling catheters to prevent
infections from ascending in the urinary tract.
10.Remove catheters as soon as possible.
11.To prevent toxic drug effects, closely monitor dosage, duration of use, and
blood levels of all medications metabolized or excreted by the kidneys.
Medical Management
 The objectives of treatment of ARF are to restore normal chemical
balance and prevent complications until repair of renal tissue and
restoration of renal function can take place.
 Any possible cause of damage is identified, treated, and eliminated.
 Prerenal azotemia is treated by optimizing renal perfusion, whereas
postrenal failure is treated by relieving the obstruction. Treatment of
intrarenal azotemia is supportive, with removal of causative agents,
Acute Renal Failure
Overall, medical management includes:-

 Maintaining fluid balance, avoiding fluid excesses, or possibly
performing dialysis.
 Maintenance of fluid balance is based on daily body weight, serial
measurements of central venous pressure, serum and urine
concentrations, fluid losses, blood pressure, and the clinical status of
the patient.
 The parenteral and oral intake and the output of urine, gastric
drainage, stools, wound drainage, and perspiration are calculated and
are used as the basis for fluid replacement.
 The insensible fluid lost through the skin and lungs and produced
through the normal metabolic processes is also considered in fluid
management.
 Fluid excesses can be detected by the clinical findings of dyspnea,
tachycardia, and distended neck veins.
 The lungs are auscultated for moist crackles. Because pulmonary
edema may be caused by excessive administration of parenteral fluids,
extreme caution must be used to prevent fluid overload.
 The development of generalized edema is assessed by examining the
presacral and pretibial areas several times daily.
 Mannitol, furosemide, or ethacrynic acid may be prescribed to initiate
a diuresis and prevent or minimize subsequent renal failure.
 Adequate blood flow to the kidneys in patients with prerenal causes of
ARF may be restored by intravenous fluids or blood product
transfusions.
Acute Renal Failure
 If ARF is caused by hypovolemia secondary to hypoproteinemia, an

infusion of albumin may be prescribed.
 Dialysis may be initiated to prevent serious complications of ARF,
such as hyperkalemia, severe metabolic acidosis, pericarditis, and
pulmonary edema. Dialysis corrects many biochemical abnormalities;
allows for liberalization of fluid, protein, and sodium intake;
diminishes bleeding tendencies; and may help wound healing.
 Hemodialysis, peritoneal dialysis, or any of the new continuous renal
replacement therapies may be performed.
PHARMACOLOGIC THERAPY
 Because hyperkalemia is the most life-threatening of the fluid and
electrolyte disturbances, the patient is monitored for hyperkalemia
through serial serum electrolyte levels (potassium value more than 5.5
mEq/L [5.5 mmol/L]), electrocardiogram changes (tall, tented, or
peaked T waves), and changes in clinical status.
 The elevated potassium levels may be reduced by administering
cation-exchange resins (sodium polystyrene sulfonate [Kayexalate])
orally or by retention enema. works by exchanging a sodium ion for a
potassium ion in the intestinal tract.
 Sorbitol is often administered in combination with Kayexalate to
induce a Diarrhea-type effect (it induces water loss in the GI tract).
 If a retention enema is administered (the colon is the major site for
potassium exchange), a rectal catheter with a balloon may be used to
facilitate retention if necessary. The patient should retain the resin 30
to 45 minutes to promote potassium removal.
Acute Renal Failure
 Afterward, a cleansing enema may be prescribed to remove the

Kayexalate resin as a precaution against fecal impaction.
 Because many medications are eliminated through the kidneys,
medication dosages must be reduced when a patient has ARF.
 Diuretic agents are often used to control fluid volume, but they have
not been shown to hasten the recovery from ARF.
 Low-dose dopamine (1 to 3 g/kg) is often used to dilate the renal
arteries through stimulation of dopaminergic receptors
 In patients with severe acidosis, the arterial blood gases or serum
bicarbonate levels (CO2-combining power) must be monitored
because the patient may require sodium bicarbonate therapy or
dialysis.
 If respiratory problems develop, appropriate ventilator measures must
be instituted.
 The elevated serum phosphate level may be controlled with
phosphate-binding agents (aluminum hydroxide).These agents help
prevent a continuing rise in serum phosphate levels by the GIT
NUTRITIONAL THERAPY
 ARF causes severe nutritional imbalances (because nausea and
vomiting contribute to inadequate dietary intake), impaired glucose
use and protein synthesis, and increased tissue catabolism.
 The patient is weighed daily and can be expected to lose 0.2 to 0.5 kg
(0.5 to 1 lb) daily if the nitrogen balance is negative (ie, the patient’s
caloric intake falls below caloric requirements). If the patient gains or
Acute Renal Failure
does not lose weight or develops hypertension, fluid retention should

be suspected.
 Dietary proteins are limited to about 1 g/kg during the oliguric phase
to minimize protein breakdown and to prevent accumulation of toxic
end products.
 Caloric requirements are met with high-carbohydrate meals because
carbohydrates have a protein sparing effect (ie, in a high-carbohydrate
diet, protein is not used for meeting energy requirements but is
“spared” for growth and tissue healing).
 Foods and fluids containing potassium or phosphorus (bananas, citrus
fruits and juices, coffee) are restricted.
 Potassium intake is usually restricted to 40 to 60 mEq/day, and
sodium is usually restricted to 2 g/day.
 The patient may require parenteral nutrition.
 The oliguria phase of ARF may last 10 to 20 days and is followed by
the diuretic phase, at which time urine output begins to increase,
signaling that kidney function is returning.
 Blood chemistry evaluations are made to determine the amounts of
sodium, potassium, and water needed for replacement, along with
assessment for overhydration or underhydration.
 After the diuretic phase, the patient is placed on a high-protein, high-
calorie diet and is encouraged to resume activities gradually.
Nursing Management
 The nurse has an important role in caring for the patient with ARF.
Acute Renal Failure
 In addition to directing attention to the patient’s primary disorder

(which may be a factor in the development of ARF), the nurse
monitors for complications, participates in emergency treatment of
fluid and electrolyte imbalances, assesses progress and response to
treatment, and provides physical and emotional support.
 Additionally, the nurse keeps family members informed about the
patient’s condition, helps them understand the treatments, and
provides psychological support.
 Although the development of ARF may be the most serious problem,
the nurse must continue to include in the plan of care those nursing
measures indicated for the primary disorder (eg, burns, shock, trauma,
obstruction of the urinary tract).
 Because of the serious fluid and electrolyte imbalances that can occur
with ARF, the nurse monitors the patient’s serum electrolyte levels
and physical indicators of these complications during all phases of the
disorder. Hyperkalemia is the most immediate lifethreatening
imbalance seen in ARF. Parenteral fluids, all oral intake, and all
medications are screened carefully to ensure that hidden sources of
potassium are not inadvertently administered or consumed.
 Intravenous solutions must be carefully selected according to the
patient’s fluid and electrolyte status.
 The nurse monitors fluid status by paying careful attention to fluid
intake (intravenous medications should be administered in the
smallest volume possible), urine output, apparent edema, distention of
the jugular veins, alterations in heart sounds and breath sounds, and
increasing difficulty in breathing.
Acute Renal Failure
 Accurate daily weights, as well as intake and output records, are

essential. Indicators of deteriorating fluid and electrolyte status are
reported immediately to the physician, and preparation is made for
emergency treatment.
 Hyperkalemia is treated with glucose and insulin, calcium gluconate,
or dialysis.
 Fluid and other electrolyte disturbances are often treated with
hemodialysis, peritoneal dialysis, or other continuous renal
replacement therapies.
REDUCING METABOLIC RATE

 The nurse also directs attention to reducing the patient’s metabolic
rate during the acute stage of renal failure to reduce catabolism and
the subsequent release of potassium and accumulation of endogenous
waste products (urea and creatinine).
 Bed rest may be indicated to reduce exertion and the metabolic rate
during the most acute stage of the disorder.
 Fever and infection, both of which increase the metabolic rate and
catabolism, are prevented or treated promptly.
PROMOTING PULMONARY FUNCTION

 Attention is given to pulmonary function, and the patient is assisted to
turn, cough, and take deep breaths frequently to prevent atelectasis
and respiratory tract infection.
 Drowsiness and lethargy may prevent the patient from moving and
turning without encouragement and assistance.
Acute Renal Failure
PREVENTING INFECTION
 Asepsis is essential with invasive lines and catheters to minimize the
risk of infection and increased metabolism.
 An indwelling urinary catheter is avoided whenever possible because
of the high risk for UTI associated with its use.
PROVIDING SKIN CARE

 The skin may be dry or susceptible to breakdown as a result of edema;
therefore, meticulous skin care is important.
 Additionally, excoriation and itching of the skin may result from the
deposit of irritating toxins in the patient’s tissues.
 Massaging bony prominences, turning the patient frequently, and
bathing the patient with cool water are often comforting and prevent
skin breakdown.
PROVIDING SUPPORT
 The patient with ARF requires treatment with hemodialysis,
peritoneal dialysis, or continuous renal replacement therapies to
prevent serious complications
 The purpose and rationale of the treatments are explained to the
patient and family by the physician.
 High levels of anxiety and fear, however, may necessitate repeated
explanation and clarification by the nurse.
Acute Renal Failure
 The family members may initially be afraid to touch and talk to the
patient during the procedure but should be encouraged and assisted to
do so.
 Although many of the nurse’s functions are devoted to the technical
aspects of the procedure, the psychological needs and concerns of the
patient and family cannot be ignored.
 Continued assessment of the patient for complications of ARF and of
its precipitating cause is essential.

دمج شباتر البالغين .....

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دمج شباتر البالغين .....

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Assessment of the

Produces various chemicals to

– Lipids to fatty acids

– Proteins to individual amino acids

– Carbohydrates into simple sugars

Begins with the

Teeth : cut, tear, crush and grind food.

Salivary glands : produce and secrete

– Parotid (beneath the cheeks)

– Submaxillary (below the jaw bone)

 saliva moistens the food and contains

– Pushes the bolus toward the pharynx and

– Soft palate closes off the nose

– Larynx (Adam’s Apple) rises so the

from the nose and mouth to the esophagus.

The passage of food from the pharynx into the

Has inner folds (rugae) that increases the surface

Food is mixed with gastric juices (hydrochloric acid

HCL helps break down food and kills bacteria that

Mucus – lubricates food and protects the gastric

Converts the bolus into a liquid (chyme) after

Chyme passes through the pyloric sphincter

Mixing: Segmental contraction that occurs in small intestine

– It is located in the upper part of the

– Produces bile (watery, greenish substance)

– Secretes bile to the gall bladder via the

– Part of the digestive, circulatory and

– Removes excess amino acids from the body

Bile is an emulsifier NOT an enzyme.

Emulsifier – dissolves fat into the

The cecum, located on the lower right side of the

Colon divided into ( ascending colon, transverse

Waste stays for 10 – 12 hours.

Appendix hangs on the right side of the

The anus: is the external opening at the lower end of

The rectum receives feces and periodically expels

- Food restrictions or special diets followed.

- appetite status e.g. (increased, decreased

- Vomiting , diarrhea, constipation, nausea,

- Ask patient about the factors increase or

In order to facilitate the referencing of location,

1. The height and weight within normal range for the

2. Observe the skin for the following:

Color (pale, gray, ruddy, jaundiced).

Bruises, lesion ,rashes and turgor and moisture.

Edema. ‫ الطفح الجلدي‬، ‫ اآلفات‬، ‫الكدمات‬

Look at the lips, tongue, and mucous membranes,

Observe the condition of the teeth. Note any

Observe the gums. they healthy and pink.

Note the patient's breath for unusual odors (fruity,

 Inspect for masses ,enlarged organs

5. The umbilicus : observe its contour and

a. Listen for bowel sounds. The best location is

Describe the sounds heard according to

Hypoactive : less than

Active : 5-30 per min

Hyperactive : > 30 /min

 Increased in diarrhea or early intestinal

 Listen for bruit over the aorta, the iliac arteries,

 Friction rub are grating sounds with

Gently palpate the abdomen, moving in a

When find dullness to percussion on the left