Mine - Assignment in RLE50

A.
DIABETES MELLITUS
I. Brief Background of the Disease
A chronic, progressive disease characterized by the body’s inability to

metabolize carbohydrates, fats, and proteins, leading to hyperglycemia. Diabetes
is a disease in which the body doesn't produce or properly use insulin. Insulin is a
hormone produced in the pancreas, an organ near the stomach. Insulin is
needed to turn sugar and other food into energy. When you have diabetes, your
body either doesn’t make enough insulin or can’t use its own insulin as well as it
should, or both. This causes sugars to build up too high in your blood.
Diabetes mellitus is defined as a fasting blood glucose of 126 milligrams

per deciliter (mg/dL) or more. “Pre-diabetes” is a condition in which blood
glucose levels are higher than normal but not yet diabetic. People with pre-
diabetes are at increased risk for developing type 2 diabetes, heart disease and
stroke, and have one of these conditions: (1) impaired fasting glucose (100 to
125 mg/dL); and (2) impaired glucose tolerance (fasting glucose less than 126
mg/dL and a glucose level between 140 and 199 mg/dL two hours after taking an
oral glucose tolerance test). Furthermore, this disease condition classified into
two: (a) Type 1 DM; and (b) type 2 DM.
II. Etiologic Factor/ Agent
Type 1 DM
Previously called IDDM or juvenile-onset diabetes mellitus, is

characterized by destruction of pancreatic beta cells, leading to absolute insulin
deficiency. It occurs in males similar to that in females with the condition
commonly seen among African Americans, Hispanic Americans, Asian
Americans, and Native Americans than in whites. It is inherited as a
heterogenous, multigenic trait. Environmental factors such as viruses appear to
trigger an autoimmune process that destroys beta cells.
Type 2 DM
Previously called NIDDM or adult-onset diabetes mellitus, is a disorder

involving both genetic and environmental factors. It is most common type of
diabetes mellitus, affecting 90% of all people who have disease. It is the leading
cause of new blindness in adults 20-74 years of age and is the leading cause of
chronic renal failure, accounting for about 40% of new cases. Likewise, half th
number of nontraumatic amputations in the US. Obesity is a risk factor,
accounting 85% of all people with type 2 diabetes mellitus. It is unclear whether
impaired tissue sensitivity to insulin or impaired insulin secretion is the primary
defect in this type of DM.
III. Medical Management
It includes restoring and maintaining blood glucose levels to as near

normal as possible by balancing diet, exercise, and the use of oral hypoglycemic
agents or insulin.
Promote Proper Nutrition. The general goal of dietary management is to help

clients with diabetes mellitus improve metabolic control by making changes in
nutrition habits which includes (1) improving blood glucose and lipid levels, (2)
providing consistency in day-to-day food intake (for type 1), (3) facilitating weight
management (for type 2), (4) providing adequate nutrition for all stages of life. It
is not necessary tyo give up alcoholic beverages among clients with DM, but
health care providers must be aware of the potential adverse effects of alcohol
specific to diabetes mellitus and teach the clients accordingly. Alcohol
consumption must then be evaluated and measured strictly. Specific artificial
sweeteners may be helpful to consume desired caloric intake which include
fructose, sorbitol, and xylitol which cause less elevation of the blood sugar. Non-
nutritive sweeteners which do no cause caloric and blood glusoce elevation may
be taken by the patient with DM such as saccharine, aspartame, and sucralose.
Promote Regular Physical Activity. Physical activity lowers down the blood
glucose level by increasing carbohydrate metabolism, fosters weight reduction
and maintenance, increases insulin sensitivity, increases high-density lipoprotein
(HDL) levels, decreases triglyceride levls, lowers blood pressure, and reduces
stress and tension.
Administer Medications
Oral antidiabetics. Major classes include sulfonylureas, biguanides,

meglitinides, thiazolidinediones, alpha-glucosidase inhibitors, incrtin mimetics,
and amylinomimetics. Many oral medications are aimed at only one aspect of the
underlying pathogenesis of type 2 DM, tus, multiple medications are often
needed to achive optimal glycemic control.
Insulin Therapy. For type 1 DM, they don’t produce enough insulin to sustain life
thus; they are depending to exogenous insulin administration on a daily basis. In
contrast, clients with type 2 DM may need no to take insulin for adequate glucose
control, especially in times of stress or illness.
IV. Nursing Management
(1) Assessment. The client may have a decrease pulses and may look pale and
may manifest cold clammy feet not to mention, the client may have thick brittle
nails and numbness and tingling of feet.
Diagnosis. Ineffective peripheral tissue perfusion related to decreased arterial
flow
Planning. Within 8 hours of nursing intervention the patient will be able to
understand the disease condition, demonstrate awareness of safety factors and
proper foot care, and maintain adequate hydration to maximize perfusion.
Intervention. Elevate feet when up in chair. Avoid long periods with feet in
dependent position to minimize interruption of blood flow and reduce venous
pooling. Instruct client to avoid constricting clothing and socks and fitting shoes.
Compromised circulation and decreased pain sensation may precipitate or
aggravate tissue breakdown.Reinforce safety precautions regarding use of
heating pads, hot water bottles or soaks. Heat causes vasodilation and
decreases sensation of pain.
Evaluation. Within 8 hours of nursing intervention the patient demonstrate ways
of proper foot care.
(2) Assessment. The client may present reddened areas, decreased peripheral,
circulation, bed immobility, and may even have edema.
Diagnosis. Risk for Impaired skin Integrity related to prolonged bedrest, edema,
decreased tissue perfusionClient will maintain skin integrity.
Intervention. Inspect skin, noting bony prominences, and presence of edema,
physical immobility, and areas of altered circulation. Provide gentle massage
around reddened or blanched areas to improve blood flow and circulation.
Encourage frequent position change. Assist with ROM to improve blood flow
increasing perfusion. Provide frequent skin care; minimize contact with moisture
or secretions because excessive dryness and or moisture damages skin and
hastens skin breakdown. Check fit for shoes and slippers, and change as needed
to decrease risk of pressure on feet.
Planning. After nursing intervention, the patient will be free from wounds.
(3) Assessment. The client may have a decreased appetite, weight loss,
increased thirst and urination, muscle weakness, refusal to eat related to anxiety
for possible increase in glucose.
Diagnosis. Risk for imbalanced nutrition: less than body requirements related to
hypermetabolic state
Planning. After nursing intervention the patient will be able to demonstrate
maintenance of desired weight or progressive weight, and experience no signs of
malnutrition.
Intervention. Weigh the patient ot have baseline data and determine if the
patient has lose weight or not. Divide feeding to small frequent feedings. Give the
client nutritious foods like vegetables and fruits, less carbohydrates and fats.
Avoid sweets, sodas and alcoholic beverages. Encourage intake of vitamin
supplements. Promote pleasant, relaxing environment for the client to enhance
his appetite.
Evaluation. After nursing intervention the patient presented no signs of
malnutrition and the patient cooperated to the food regimen.
V. Pathophysiology (please refer to the next page)
VI. Bibliography
Medical – Surgical Nursing (Clinical Management for Positive Outcomes) 8th

Edition by Joyce M. Black and Jane Hokanson Hawks. 2008
B. ACUTE GASTROENTERITIS
Gastroenteritis (also known as gastric flu or stomach flu, although

unrelated to influenza) is inflammation of the gastrointestinal tract, involving both
the stomach and the small intestine and resulting in acute diarrhea. It can be
transferred by contact with contaminated food and water. The inflammation is
caused most often by an infection from certain viruses or less often by bacteria,
their toxins, parasites, or an adverse reaction to something in the diet or
medication. Current death rates have come down significantly to approximately
1.5 million deaths annually in the year 2000, largely due to the global introduction
of oral rehydration therapy and is a leading cause of death among infants and
children under 5.
At least 50% of cases of gastroenteritis due to foodborne illness are

caused by norovirus. Another 20% of cases, and the majority of severe cases in
children, are due to rotavirus. Other significant viral agents include adenovirus
and astrovirus.
Risk factors include consumption of improperly prepared foods or

contaminated water and travel or residence in areas of poor sanitation. It is also
common for river swimmers to become infected during times of rain as a result of
contaminated runoff water.
Clinical Manifestations:
• Low grade fever to 100°F (37.8°C)

• Nausea with or without vomiting
• Mild to moderate diarrhea
• Crampy and painful abdominal bloating
More serious symptoms include:
• Blood in vomit or stool

• Vomiting more than 48 hours
• Fever higher than 101°F (40°C)
• Swollen abdomen or abdominal pain
• Dehydration that is manifested by weakness, lightheadedness, decreased
and concentrated urination, dry skin and poor turgor, and dry lips and
mouth.
Gastroenteritis has many causes. Viruses and bacteria are the most
common.
Viruses and bacteria are very contagious and can spread through
contaminated food or water. In up to 50% of diarrheal outbreaks, no specific
agent is found. The infection can spread from person to person because of
improper handwashing following a bowel movement or handling a soiled diaper.
Gastroenteritis caused by viruses may last one to two days. However,

some bacterial cases can continue for a longer period of time.
Viruses
Norovirus - Fifty to seventy percent of cases of gastroenteritis in adults are

caused by the noroviruses (genus Norovirus, family Caliciviridae. This virus is
highly contagious and spreads rapidly. Norovirus is the most common cause of
gastroenteritis in the United States.
Noroviruses can be transmitted and infect individuals by
o contaminated food and liquids,
o touching objects contaminated with norovirus and then placing the hands
or fingers in the mouth,
o direct contact with an infected individual (for example, exposure to

norovirus when caring or sharing foods, drinks, eating utensils with an
affected individual, and
o exposure to infected individuals and objects in daycare centers and

nursing homes.
Norovirus is often in the news when cruise ship passengers contract the virus,
which causes gastroenteritis.
Rotavirus - According to the CDC, "Rotavirus was also the leading cause
of severe diarrhea in U.S. infants and young children before rotavirus vaccine
was introduced for U.S. infants in 2006. Prior to that, almost all children in the
United States were infected with rotavirus before their 5th birthday. Each year in
the United States in the pre-vaccine period, rotavirus was responsible for more
than 400,000 doctor visits; more than 200,000 emergency room visits; 55,000 to
70,000 hospitalizations; and 20 to 60 deaths in children younger than 5 years of
age."
Other viruses that cause gastrointestinal symptoms include:
• Adenoviruses - This virus most commonly causes respiratory illness;

however, other illnesses may be caused by adenoviruses such as
gastroenteritis, bladder infections, and rash illnesses.
• Parvoviruses - The human bocavirus (HBoV), which can cause gastroenteritis

belongs to the family Parvoviridae.
• Astroviruses - Astrovirus infection is the third most frequent cause of

gastroenteritis in infants.
Bacteria
Bacteria may cause gastroenteritis directly by infecting the lining of the

stomach and intestine. Some bacteria such as Staphylococcus aureus produce a
toxin that is the cause of the symptoms. Staph is a common type of food
poisoning.
Escherichia coli infection can cause significant complications. E. coli

O157:H7 (one type of the bacteria) can cause complications in approximately
10% of affected individuals (for example, kidney failure in children [hemolytic-
uremic syndrome or HUS), bloody diarrhea, and thrombotic thrombocytopenic
purpura (TTP) in the elderly.
Salmonella, Shigella and Campylobacter
Salmonella, Shigella and Campylobacter are also common causes of illness.
• Salmonella is contracted by ingesting the bacteria in contaminated food or

water, and by handling poultry or reptiles such as turtles that carry the germs.
• Campylobacter occurs by the consumption of raw or undercooked poultry

meat and cross-contamination of other foods. Infants may contract the
infection by contact with poultry packages in shopping carts. Campylobacter
is also associated with unpasteurized milk or contaminated water. The
infection can be spread to humans by contact with infected stool of an ill pet
(for example, cats or dogs). It is generally not passed from human to human.
• Shigella bacteria generally spreads from an infected person to another
person. Shigella are in diarrheal stools of infected individuals while they are
ill, and for up to one to two weeks after contracting the infection. Shigella
infection also may be contracted from eating contaminated food, drinking
contaminated water, or swimming or playing in contaminated water (for
example, wading pools, shallow play fountains). Shigella can also be spread
among men who have sex with men.
Clostridium difficile
Clostridium difficile (C difficile) bacteria may overgrow in the large intestine

after a person has been on antibiotics for an infection
Other risk factors for C difficile infection are hospitalization, individuals 65

years of age or greater, and existing chronic medical conditions.
Parasites and Protozoans
These tiny organisms are less frequently responsible for intestinal

irritation. A person may become infected by one of these by drinking
contaminated water. Swimming pools are common places to come in contact
with these parasites. Common parasites include. Giardia is the most frequent
cause of waterborne diarrhea, causing giardiasis. Often, people become infected
after swallowing water that has been contaminated by animal feces (poop). This
may occur by drinking infected water from river or lakes but giardia may also be
found in swimming pools, wells and cisterns. Cryptosporidium (Crypto) is a
parasite that lives in the intestine of affected individuals or animals. The infected
individual or animal sheds the Cryptosporidium parasite in the stool. Crypto may
also be found in food, water, soil, or contaminated surfaces (swallowing
contaminated recreational water, beverages, uncooked food, unwashed fruits
and vegetables, touching contaminated surfaces such as bathroom fixtures, toys,
diaper pails, changing tables, changing diapers, caring for an infected individual
or handling an infected cow or calf). Those at risk for serious disease are
individuals with weakened immune systems.
III. Mode of Transmission
Acute gastroenteritis is predominantly spread via the faecal-oral route.

Transmission is facilitated through contaminated food (particularly raw shellfish),
water (including ice) and person to person contact. Aerosols are thought to be
important in the transmission of norovirus and it is also known to persist on
certain contaminated surfaces such as carpets for weeks
IV. Medical Management
Home care. Clear fluids are appropriate for the first 24 hours to maintain
adequate hydration. They should be given oral rehydration solutions such as
Pedialyte for pediatric patients or commercially prepared oral rehydration
solution. For homemade ORS, mix 2 tablespoons of sugar (or honey) with ¼
teaspoon of table salt in 1 liter (1 qt) of clean or previously boiled water.
Hospitalization. Hydration through intravenous line. Replacement of fluid losses

volume per volume.Encourage small, frequent feedings. After 24 hours without
vomiting , begin to offer soft bland foods such as the BRAT diet, which includes
bananas, rice, applesauce without sugar, toast, pasta, and potatoes
The most common antibiotics that are used in the treatment are clindamycin (for
example, Cleocin), fluoroquinolones (for example, levofloxacin [Levaquin'],
ciprofloxacin [Cipro, Cirpo XR, Proquin XR]), penicillins, and cephalosporins.
V. Nursing Management
(1) Assessment. The patient may manifest sunken eyeballs, poor skin turgor
and pain scale 0f 8/10. Alteration of the vital signs may be noticeable as follows
BP: 170/100mmHg, PR: 82bpm, RR: 40cpm, and Temp: 36.7.
Diagnosis. Deficient fluid Volume related to active fluid volume loss
Planning. After 8hrs of nursing interventions, the patient fluid and blood volume
will return to normal.
Intervention. Monitor and record every 2hrs. or as necessary until stable then
monitor and record vital signs because tachyycardia, dyspnea, or hypotension
may indicate fluid deficit or electrolyte imbalance. Measure I/O q 4hrs. record and
report significant changes include urine & stool. low urine output 7 high specific
gravity indicates hypovolemia. Administer fluids, blood or blood products or
plasma expanders to replace fluids & whole blood loss and facilitate fluid
movement into intravascular space. Assess skin turgor and oral mucous
membrane q 4hrs. to check for dehydration
Evaluation. After 8hrs of having interventions, the patient’s fluid and blood
volume return to normal as evidenced by table V/s.
(2) Assessment: The client may experience abdominal cramping, loose bowel
movement with yellowish watery stool, nausea & vomiting, increase bowel
sounds/ peristalsis.
Diagnosis. Diarrhea related to infectious process
Planning. Within 1-2 days of nursing care and interventions the patient will be
free to diarrhea
Intervention. Auscultate the abdomen For presence Location & characteristics
of bowel sounds. Discuss to the patient the different causative factors and
rationale for treatment regimen for the education for the patient. Restrict solid
food intake to allow the bowel rest & reduce intestinal workload. Provide for
changes in dietary foods to allow foods that precipitate diarrhea. Limit caffeine,
High fiber foods and fatty foods to prevent gastric irritation.
Evaluation. After 1-2 days of nursing interventions, the patient shall be free of
diarrhea as evidenced by re-established and maintained normal bowel
movement, reduced in frequency of stools and stool returned to its normal
consistency
(3) Assessment. The patient may have an increased body temperature of more
than 37.5C.
Diagnosis. Hyperthermia related to dehydration as evidenced by increase in
body temperature higher than normal range.
Planning. After the nursing care plan, the client will be able to demonstrate
temperature within normal range, be free of chills.
Intervention. Monitor patient temperature (degree and pattern); note shaking
chills/profuse diaphoresis. Monitor environmental temperature; limit/add bed
linens as indicated. Provide tepid sponge baths; avoid use of alcohol.
VI. Pathophysiology (please refer to the next page)
VII. Bibliography.

wikipedia.com
scibd.com
C. ACUTE PYELONEPHRITIS
Acute pyelonephritis is a potentially organ- and/or life-threatening infection

that characteristically causes some scarring of the kidney with each infection and
may lead to significant damage to the kidney (any given episode), kidney failure,
abscess formation (eg, nephric, perinephric), sepsis, or sepsis
syndrome/shock/multiorgan system failure. More than 250,000 cases occur in the
United States each year (1995 estimate), and approximately 200,000 patients
require hospitalization (1997 data). Wide variation exists in the clinical
presentation, severity, options, and disposition of acute pyelonephritis.
Diagnosing and managing acute pyelonephritis is not always

straightforward. In the age range of 5-65 years, it typically presents in the context
of a symptomatic (eg, dysuria, frequency, urgency, gross hematuria, suprapubic
pain) urinary tract infection (UTI) with classic upper urinary tract symptoms (eg,
flank pain, back pain) with or without systemic symptoms (eg, fever, chills,
abdominal pain, nausea, vomiting) and signs (eg, fever, costovertebral angle
tenderness) with or without leukocytosis. However, it can present with
nonspecific symptoms.
A number of studies using immunochemical markers have shown that

many women, who initially present with lower tract symptoms, actually
have pyelonephritis. This group of young women is often identified when short-
course therapy for uncomplicated cystitis fails. In the extremes of age, the
presentation may be so atypical that pyelonephritis is not in the differential
diagnosis. In the infant, the presentation may be feeding difficulty or fever. In the
elderly, the presentation may be mental status change or fever. Acute
pyelonephritis is complex, and there is no consistent set of signs and symptoms
that are both sensitive and specific for the diagnosis; therefore, clinicians must
maintain a high index of suspicion
Most cases of "community-acquired" pyelonephritis are due to bowel

organisms that enter the urinary tract. Common organisms are E. coli (70-80%)
and Enterococcus faecalis. Hospital-acquired infections may be due to coliforms
and enterococci, as well as other organisms uncommon in the community
(e.g. Klebsiella spp., Pseudomonas aeruginosa). Most cases of pyelonephritis
start off as lower urinary tract infections, mainly cystitis and prostatitis.
E. coli can invade the superficial umbrella cells of the bladder to form
Intracellular Bacterial Communities (IBCs), which can mature into biofilms. These
Biofilm-producing e. coli are resistant to antibiotic therapy and immune system
responses, and present a possible explanation for the recurrence of UTIs,
including Pyelonephritis. [2]
Risk is increased in the following situations:
• Mechanical: any structural abnormalities to the kidneys and the urinary

tract, vesicoureteral reflux (VUR) especially in young children, calculi (kidney
stones), urinary tract catheterisation, urinary tract stents or drainage
procedures (e.g. nephrostomy), pregnancy, neurogenic bladder (e.g. due to
spinal cord damage, spina bifida or multiple sclerosis) and prostate disease
(e.g. benign prostatic hyperplasia) in men
• Constitutional: diabetes mellitus, immunocompromised states
• Behavioural: change in sexual partner within the last year, spermicide use
• Positive family history (close family members with frequent urinary tract
infections)
As practically all cases of pyelonephritis are due to bacterial

infections, antibiotics are the mainstay of treatment. Mild cases may be treated
with oral therapy, but generally intravenous antibiotics are required for the initial
stages of treatment. The type of antibiotic depends on local practice, and may
include fluoroquinolones (e.g. ciprofloxacin), beta-lactam
antibiotics (e.g. amoxicillin or acephalosporin), trimethoprim (alone or in
combinaiton with sulfamethoxazole). Aminoglycosides are generally avoided due
to their toxicity, but may be added for a short duration.[1]
All acute cases with spiking fevers and leukocytosis should be admitted to
the hospital for IV fluids hydration and IV antibiotic treatment
immediately. ciprofloxacin IV 400 mg every 12 hours is the first line treatment of
choice. Alternatively, ampicillin IV 2g every 6 hours plus gentamicin IV 1 mg/kg
every 8 hours also provide excellent coverage. If the patient is
pregnant, ampicillin/gentamicincombination is the treatment of choice,
as ciprofloxacin is contraindicated. During the course of antibiotic treatment,
serial white blood count and temperature should be closely monitored. Typically,
the IV antibiotics should be continued till the patient is afebrile for at least 24 to
48 hours, then equivalent oral antibiotic agents can be given for a total of 2-week
duration of treatment.[4]
Intravenous fluids may be administered to compensate for the reduced

oral intake, insensible losses (due to the raised temperature)
and vasodilation and to maximize urine output. If the patient is septic secondary
to an obstructing stone, percutaneous nephrostomy is indicated for source
control.
In recurrent infections, additional investigations may identify an underlying

abnormality. Occasionally, surgical intervention is necessary to reduce chances
of recurrence. If no abnormality is identified, some studies suggest long-
term preventative (prophylactic) treatment with antibiotics, either daily or
after sexual intercourse.[5] In children at risk of recurrent UTIs, meta-analysis of
the present literature indicates that not enough studies have been performed to
conclude prescription of long-term antibiotics have a net positive benefit.
[6]
Ingestion of cranberry juice has been studied as a prophylactic measure; while
studies are heterogeneous, many suggest a benefit.[7]
Some recommend other nutritional approaches to prevent recurrence of

UTIs. Increasing fluid intake, consuming cranberry juice, blueberry juice, and
fermented milk products containing probioticbacteria, have been shown to inhibit
adherence of bacteria to the epithelial cells of the urinary tract.[8]
(1) Assessment. The client may verbalize reports of pain, guarding of body part
and changes in vital signs
Diagnosis. Acute pain related to acute inflammation of renal tissues
Planning. Within 1 hr of nursing intervention, the patient will reduce pain
sensation and maintain, report pain is relieved, and restore normal vital signs.
Intervention: Assess for pain using pain scale for baseline data; Teach patient
relaxation techniques and diversion, imagery and distraction to minimize
sensation of pain; Provide comfort measures such as touch therapy,
repositioning, use of cold/heat packs to promote non-pharmacological pain
management.
Evaluation. Within1 hr, the patient experienced relief of pain and comfort.
(2) Assessment. The client may have a body temperature of >38 degree
celcius; skin warm to touch; flushed skin; tachycardia; abnormal increased of
respiratory rate of >12 – 24cpm; chills; flushed skin.
Diagnosis. Hyperthermia related to inflammatory process secondary to infection
in the urinary tract.
Planning. After 10-15 min. of nursing intervention, the patient will be able to
restore normal body temperature for about 36.0-37.5
Intervention. Assess the vital signs for baseline data. Do tepid sponge bath to
reduce the heat in the body.Wear loose cotton clothing to ventilate the body and
let the heat disperse. Instruct client to increase fluid intake to hydrate the body
and cool down from within.
Evaluation. Within 10-15mins. Of nursing intervention, the patient achieved the
normal body temperature.
(3) Assessment. The client may experience dysuria and urgency and frequency
to void
Diagnosis. Impaired Urinary Elimination related to inflammation and irritation of
the bladder mucosa secondary to infection.
Planning. Within 8 hours of nursing intervention the patient will achieve normal
elimination pattern or participate in measures to correct or compensate for the
defects.
Intervention. Assess intake and output to determine kidney function. Increase
fluid intake to help maintain renal function and to flush away bacteria. Assist with
toileting to facilitate voiding. Instruct client to avoid sodas and spicy foods
because this might irritate the urinary tract.
Evaluation. Within 8 hours of nursing intervention, the patient achieved normal
elimination pattern.
VII. Bibliography
Wikipedia.com

D. CEREBROVACULAR ACCIDENT
A stroke, previously known medically as a cerebrovascular accident

(CVA), is the rapidly developing loss of brain function(s) due to disturbance in
the blood supply to the brain. This can be due toischemia (lack of blood flow)
caused by blockage (thrombosis, arterial embolism), or a hemorrhage (leakage
of blood).[1] As a result, the affected area of the brain is unable to function,
leading toinability to move one or more limbs on one side of the body, inability
to understand or formulate speech, or an inability to see one side of the visual
field.
A stroke is a medical emergency and can cause

permanent neurological damage, complications, and lead to death. It is the
leading cause of adult disability in the United States and Europe and it is the
second leading cause of death worldwide. Risk factors for stroke
include advanced age, hypertension (high blood pressure), previous stroke
or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette
smoking and atrial fibrillation.[2] High blood pressure is the most important
modifiable risk factor of stroke.
An ischemic stroke is occasionally treated in a hospital

with thrombolysis (also known as a "clot buster"), and some hemorrhagic strokes
benefit from neurosurgery. Treatment to recover any lost function is stroke
rehabilitation, ideally in a stroke unit and involving health professions such
as speech and language therapy, physical therapy and occupational therapy.
Prevention of recurrence may involve the administration of antiplatelet drugs
such as aspirin and dipyridamole, control and reduction of hypertension, and the
use of statins. Selected patients may benefit from carotid endarterectomyand the
use of anticoagulants.
Thrombotic stroke. In thrombotic stroke a thrombus (blood clot) usually forms

around atherosclerotic plaques. Since blockage of the artery is gradual, onset of
symptomatic thrombotic strokes is slower. A thrombus itself (even if non-
occluding) can lead to an embolic stroke (see below) if the thrombus breaks off,
at which point it is called an "embolus." Two types of thrombosis can cause
stroke:
• Large vessel disease involves the common and internal
carotids, vertebral, and the Circle of Willis. Diseases that may form
thrombi in the large vessels include (in descending incidence):
atherosclerosis, vasoconstriction (tightening of the
artery), aortic, carotid or vertebral artery dissection, various inflammatory
diseases of the blood vessel wall (Takayasu arteritis, giant cell
arteritis,vasculitis), noninflammatory vasculopathy, Moyamoya
disease and fibromuscular dysplasia.
• Small vessel disease involves the smaller arteries inside the brain:
branches of the circle of Willis, middle cerebral artery, stem, and arteries
arising from the distal vertebral and basilar artery. Diseases that may form
thrombi in the small vessels include (in descending
incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood
vessel as a result of high blood pressure and aging) and fibrinoid
degeneration (stroke involving these vessels are known as lacunar
infarcts) and microatheroma (small atherosclerotic plaques).
• Sickle cell anemia, which can cause blood cells to clump up and block
blood vessels, can also lead to stroke. A stroke is the second leading killer
of people under 20 who suffer from sickle-cell anemia.[19]
Embolic stroke. An embolic stroke refers to the blockage of an artery by
an arterial embolus, a travelling particle or debris in the arterial bloodstream
originating from elsewhere. An embolus is most frequently a thrombus, but it can
also be a number of other substances including fat (e.g. from bone marrow in
a broken bone), air, cancer cells or clumps of bacteria (usually from
infectious endocarditis).
Because an embolus arises from elsewhere, local therapy solves the

problem only temporarily. Thus, the source of the embolus must be identified.
Because the embolic blockage is sudden in onset, symptoms usually are
maximal at start. Also, symptoms may be transient as the embolus is partially
resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation)
but may originate from elsewhere in the arterial tree. In paradoxical embolism,
a deep vein thrombosis embolises through anatrial or ventricular septal defect in
the heart into the brain.
Cardiac causes can be distinguished between high and low-risk:
• High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic

disease of the mitral or aortic valve disease, artificial heart valves, known
cardiac thrombus of the atrium or ventricle, sick sinus syndrome,
sustained atrial flutter, recent myocardial infarction, chronic myocardial
infarction together with ejection fraction <28 percent,
symptomatic congestive heart failure with ejection fraction <30
percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic
endocarditis, infective endocarditis, papillary fibroelastoma, left atrial
myxoma and coronary artery bypass graft (CABG) surgery
• Low risk/potential: calcification of the annulus (ring) of the mitral valve,

patent foramen ovale (PFO), atrial septal aneurysm, atrial septal
aneurysm with patent foramen ovale, left ventricular aneurysm without
thrombus, isolated left atrial "smoke" on echocardiography (no mitral
stenosis or atrial fibrillation), complex atheroma in the ascending aorta or
proximal arch
Systemic hypoperfusion. Systemic hypoperfusion is the reduction of blood flow

to all parts of the body. It is most commonly due to cardiac pump failure
from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of
myocardial infarction, pulmonary embolism, pericardial effusion, or
bleeding. Hypoxemia (low blood oxygen content) may precipitate the
hypoperfusion. Because the reduction in blood flow is global, all parts of the brain
may be affected, especially "watershed" areas - border zone regions supplied by
the major cerebral arteries. A watershed stroke refers to the condition when
blood supply to these areas is compromised. Blood flow to these areas does not
necessarily stop, but instead it may lessen to the point where brain damage can
occur. This phenomenon is also referred to as "last meadow" to point to the fact
that in irrigation the last meadow receives the least amount of water.
Venous thrombosis. Cerebral venous sinus thrombosis leads to stroke due to
locally increased venous pressure, which exceeds the pressure generated by the
arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking
of blood into the damaged area) than other types of ischemic stroke.
Intracerebral hemorrhage. Generally occurs in small arteries or arterioles and is
commonly due to hypertension, intracranial vascular malformations
(including cavernous angiomas or arteriovenous malformations), cerebralamyloid
angiopathy, or infarcts into which secondary haemorrhage has occurred.[2] Other
potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug
use (e.g. amphetamines orcocaine). The hematoma enlarges until pressure from
surrounding tissue limits its growth, or until it decompresses by emptying into
the ventricular system, CSF or the pial surface. A third of intracerebral bleed is
into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days,
higher than ischemic stroke or even the very deadly subarachnoid hemorrhage
(which, however, also may be classified as a type of stroke).
Anticoagulation drugs. Oral anticoagulants such as warfarin have been the

mainstay of stroke prevention for over 50 years. However, several studies have
shown that aspirin and antiplatelet drugs are highly effective insecondary
prevention after a stroke or transient ischemic attack. Low doses of aspirin (for
example 75–150 mg) are as effective as high doses but have fewer side effects;
the lowest effective dose remains unknown.
Thienopyridines (clopidogrel, ticlopidine) "might be slightly more effective" than
aspirin and have a decreased risk of gastrointestinal bleeding, but they are more
expensive.]Their exact role remains controversial. Ticlopidine has more skin
rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.
[61]
Dipyridamole can be added to aspirin therapy to provide a small additional
benefit, even though headache is a common side effect. Low-dose aspirin is also
effective for stroke prevention after sustaining a myocardial infarction. Except for
in atrial fibrillation, oral anticoagulants are not advised for stroke prevention —
any benefit is offset by bleeding risk.
In primary prevention however, antiplatelet drugs did not reduce the risk of
ischemic stroke while increasing the risk of major bleeding. Further studies are
needed to investigate a possible protective effect of aspirin against ischemic
stroke in women.
Surgery. Surgical procedures such as carotid endarterectomy or

carotid angioplasty can be used to remove significant atherosclerotic narrowing
(stenosis) of the carotid artery, which supplies blood to the brain. There is a large
body of evidence supporting this procedure in selected cases. Endarterectomy
for a significant stenosis has been shown to be useful in the secondary
prevention after a previous symptomatic stroke. Carotid artery stenting has not
been shown to be equally useful. Patients are selected for surgery based on age,
gender, degree of stenosis, time since symptoms and patients'
preferences. Surgery is most efficient when not delayed too long —the risk of
recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after
5 years, but endarterectomy reduces this risk to around 5%. The number of
procedures needed to cure one patient was 5 for early surgery (within two weeks
after the initial stroke), but 125 if delayed longer than 12 weeks.
Screening for carotid artery narrowing has not been shown to be a
useful screening test in the general population. Studies of surgical intervention
for carotid artery stenosis without symptoms have shown only a small decrease
in the risk of stroke. To be beneficial, the complication rate of the surgery should
be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by
avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die
due to the surgery itself, and 89 will remain stroke-free but would also have done
so without intervention.
(1) Assessment. The client may have slurred speech, right eye dilated, ↓ in
muscle strength, GCS of E= 3, V=2, M=4, with poor muscle tone on the right and
left hand and foot, limited ROM on the right hand and foot(only able to carry out
passive ROM on this area), unable to carry out activities without assistance such
as feeding and changing clothes, difficulty in chewing and swallowing, with pale
nail beds, level 3 physical mobility
Diagnosis. Ineffective cerebral tissue perfusion r/t interruption of blood flow in
the brain secondary to presence of subacute infarcts of the right basal ganglia.
Planning. Within 8 hours of nursing intervention, the patient will be able to
manifest improved nail beds from pale to pinkish, manifest a normal papillary
response and lacunar infarct of the left basal ganglia of the brain and improved
physical mobility from level 3 to level 2 and improved GCS scale.
Intervention. Establish rapport to the patient and S. O.’s. Monitor V/S every 30
minutes. Evaluate pupils, noting size, shape and equity. Elevate HOB (15
degrees) and maintain head or neck in midline. Provide quiet and restful
atmosphere. Reposition pt every 2 hours. Patient in comfortable position. Provide
support on affected body part such as pillows and assistance to do ADL’s as
needed.Provide safety precautions by raising up the side rails. Encourage the
patient and S.O.’s to avoid sedentary lifestyle such as drinking liquor, smoking,
improper exercise and too much fatty foods.
Evaluation. After 8 hours of nursing intervention, goal was met as evidenced by
patient having an improved nail beds from pale to pinkish in color and patient
having a normal papillary response.
(2) Diagnosis. Impaired physical mobility r/t subacute infarcts of the right basal
ganglia and lacunar infarct of the left basal ganglia of the brain.
Planning. After 8 hours of nursing intervention, the patient will be able to
participate in performing ADL’s with minimal assistance from others, do active
and passive ROM exercise on the right side of his body within physical limitations
after hours of sleep and have an adequate rest and sleep of about 4-5 hours.
Intervention. Establish rapport to the patient and S. O.’s. Assess and determine
factors that contribute to physical immobility. Determine degree of immobility &
muscle strength. Assist patient in comfortable position. Provide support on
affected body parts such as pillow. Provide safety precautions by raising up the
side rails. Provide environment free from noise and disturbances. Change
position every 2 hours and possibly more often if placed on the affected part.
Massage pressure points after each position changes. Assist in performing ADL.
Assist in performing ROM exercise after hours of sleep & within physical
limitations. Encourage the pt and S.O.’s to avoid sedentary lifestyle such as
drinking liquor, smoking, improper exercise and too much fatty foods.
Evaluation. After 8 hours of nursing intervention, goal was met as evidenced by
patient participated in performing ADL’s with minimal assistance, patient having
an active and passive ROM exercise within physical limitations after hours of
sleep, and patient having an adequate sleep of 4 hours.
(3) Assessment: For Client’s not changing of IV site within 24-36hrs.

Diagnois. Risk for infection r/t prolonged catheterization
Planning. Within 8hr. shift of nursing interventions, the patient will demonstrate
proper hand washing as well as the significant others, verbalize understanding
about the sign and symptoms of infection and when to report these to the
physician or nurse, and able to identify what food he must eat as well as able to
increase his fluid intake at the range of 8-10 glasses of water.
Intervention. Monitor and teach the pt. to the signs of infection, Encouraged
the pt. to wash hands before contact with the patient, Encourage intake of
protein- and calorie-rich foods. Encourage fluid intake of 2000 ml to 3000 ml of
water per day.
Evaluation. After 8hr. shift of nursing interventions, the patient was demonstrate
proper hand washing as well as the significant others, verbalize understanding
about the sign and symptoms of infection and when to report these to the
physician or nurse, and able to identify what food he must eat as well as able to
increase his fluid intake at the range of 8-10 glasses of water
V. Pathophysiology (please refer to the next page)
VI. Bibliography: Medical – Surgical Nursing (Clinical Management for Positive

Outcomes) 8th Edition by Joyce M. Black and Jane Hokanson Hawks. 2008
E. HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy is caused by disorders that affect the liver. These

include disorders that reduce liver function (such as cirrhosis or hepatitis) and
conditions in which blood circulation does not enter the liver. The exact cause of
hepatic encephalopathy is unknown.
An important job of the liver is to change toxic substances that are either
made by the body or taken into the body (such as medicines) and make them
harmless. However, when the liver is damaged, these "poisons" may build up in
the bloodstream.
Ammonia, which is produced by the body when proteins are digested, is

one of the harmful substances that is normally made harmless by the liver. Many
other substances may also build up in the body if the liver is not working well.
They can cause damage to the nervous system.
Hepatic encephalopathy may occur suddenly in people who previously

had no liver problems when damage occurs to the liver. More often, the condition
is seen in people with chronic liver disease.
The causes of Hepatic Encephalopathy may include:
• excessive nitrogen load

• electrolyte or metabolic imbalance like hyponatremia
• overuse of drugs that may damage the liver
• other infections that may have damaged the liver like urinary tract infection,
spontaneous bacterial peritonitis
• surgeries that may have caused progression of a liver disease
• impaired liver function due to cirrhosis or hepatitis
• liver failure
• Identify and Treat Precipitating Causes-protein restrictions to keep protein

level to a minimum
• Reduce Nitrogenous Wastes (Ammonia) in the Blood and Bacteria in the
Colon-administration of neomycin and lactulose to reduce bacteria in
gastrointestinal tract
• Maintain Fluid Volume Balance-monitor IV fluids and monitor possible risk for
fluid deficit due to third space movement of fluids
(1) Assessment. The client may feel generalized weakness, and may report
exertional discomfort/dyspnea. Furthermore, BP might shows increasing of more
than 90 – 120/ 60 – 80 mm Hg.
Diagnosis. Activity intolerance related to fatigue, anemia from poor nutrition and
bleeding, ascites, dysponea from pressure of ascites to diaphragm, muscle
wasting
Planning. Within 8 hours of thorough nursing intervention, the client will be able
to use identified techniques to enhance activity tolerance.
Intervention. Alternate rest & activity, Monitor hemoglobin and hematocrit to rule
out any bleeeding. Assist with daily living activities to conserve energy.
Administer iron supplements or blood transfusion as ordered to treat anemia.
Assist with measures to decrease edema and ascities to increase the lung
capacity.
Evaluation. After 8 hours of thorough nursing intervention, the client will be able
to use identified techniques to enhance activity tolerance.
(2) Assessment. Breakage of the first line of defense, presence of wound.

Diagnosis. Ineffective protection related to decrease filtering of bacteria by liver
and impaired synthesis of clotting factors.
Planning, Within 8 hours of thorough nursing intervention, the client will be free
from any form injury.
Intervention. Monitor for manifestations of hemorrhage. Provide assistance with
ambulation and activities of daily living. Use small-gauge needles for injections
and apply prolonged pressure after injection. Recommend soft – bristle
toothbrush. Teach to avoid vigorous blowing of nose or straining at stool.
Administer vitamin K as ordered. Follow infection control procedures
(3) Assessment. BMI less than in his required height and weight. May report
loss of weight, as well generalized weakness.
Diagnosis. Imbalanced nutrition: less than body requirements related to
impaired utilization and storage of nutrients from vomiting
Planning. Demonstrate progressive weight gain toward goal.
Intervention. Weigh daily. Provide oral hygiene before meals. Administer
antiemetic as ordered. Provide small and frequent meals. Determine food
preferences and assist in selection of those that contain low or no protein and
low salt. Prevent constipation
Evaluation. After thorough nursing intervention the client, demonstrate
progressive weight gain toward goal.
VII. Bibliography
• http://www.scribd.com/doc/11001524/Hepatic-Encephalopathy-and-Coma-and-
End-Stage-Renal-Dse
• http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001347
• Medical Surgical Nursing by Black
F. LIVER CIRHHOSIS
Cirrhosis is an irreversible result of various disorders that damage liver

cells over time. Eventually, damage becomes so extensive that the normal
structure of the liver is distorted and its function is impaired. The disease process
often takes the following path:
Scarring. The main damage in cirrhosis is triggered by scarring (fibrosis)

that occurs from injuries due to alcohol, viruses, or other assaults. The scar
tissue and other changes in liver cells gradually replace healthy liver tissue and
act like small dams to alter the flow of blood and bile in and out of the liver.
Altered Blood and Bile Flow. The changes in blood and bile flow have
significant consequences, with both the liver and other organs responding to the
altered flow:
• The spleen overproduces nitric oxide, a chemical that causes blood

vessels in the spleen to widen (dilate).
• The small blood vessels and bile ducts in the liver itself, however,
narrow ( constrict ). (Blood vessels in other organs, including the
kidney, also narrow.)
• Blood flow coming from the intestine into the liver is slowed by the
narrow blood vessels. It backs up through the portal vein and seeks
other routes.
• Enlarged, abnormally twisted and swollen veins called varicesform

in the stomach and lower part of the esophagus in order to
compensate for the backup blood.
• Bilirubin also builds up in the bloodstream, resulting in jaundice, a

yellowish cast in the skin and eyes, as well as dark-colored urine.
• Fluid buildup also occurs in the abdomen (called ascites ), and

swelling in the legs is common.
Alcoholic liver disease once was considered to be the predominant cause

of cirrhosis in the United States. Hepatitis C has emerged as the nation's leading
cause of both chronic hepatitis and cirrhosis.
Many cases of cryptogenic cirrhosis appear to have resulted from
nonalcoholic fatty liver disease (NAFLD). When cases of cryptogenic cirrhosis
are reviewed, many patients have one or more of the classical risk factors for
NAFLD: obesity, diabetes, and hypertriglyceridemia.1 It is postulated that
steatosis may regress in some patients as hepatic fibrosis progresses, making
the histologic diagnosis of NAFLD difficult.
Up to one third of Americans have NAFLD. About 2-3% of Americans

have nonalcoholic steatohepatitis (NASH), where fat deposition in the hepatocyte
is complicated by liver inflammation and fibrosis. It is estimated that 10% of
patients with NASH will ultimately develop cirrhosis. NAFLD and NASH are
anticipated to have a major impact on the United States' public health
infrastructure over the next decade.
Most common causes of cirrhosis in the United States
• Hepatitis C (26%)
• Alcoholic liver disease (21%)
• Hepatitis C plus alcoholic liver disease (15%)
• Cryptogenic causes (18%)
• Hepatitis B, which may be coincident with hepatitis D (15%)
• Miscellaneous (5%)
Miscellaneous causes of chronic liver disease and cirrhosis
• Autoimmune hepatitis
• Primary biliary cirrhosis
• Secondary biliary cirrhosis (associated with chronic extrahepatic bile duct
obstruction)
• Primary sclerosing cholangitis
• Hemochromatosis
• Wilson disease
• Alpha-1 antitrypsin deficiency
• Granulomatous disease (eg, sarcoidosis)
• Type IV glycogen storage disease
• Drug-induced liver disease (eg, methotrexate, alpha methyldopa,
amiodarone)
• Venous outflow obstruction (eg, Budd-Chiari syndrome, veno-occlusive
disease)
• Chronic right-sided heart failure
• Tricuspid regurgitation
Common modes of transmission in developing countries are:

• perinatal (from mother to baby at birth)
• early childhood infections (in apparent infection through close
interpersonal contact with infected household contacts)
• unsafe injections practices
• blood transfusions
• sexual contact
In many developed countries (e.g. those in Western Europe and North
America), patterns of transmission are different than those mentioned above.
Today, the majority of infections in these countries are transmitted during young
adulthood by sexual activity and injecting drug use. HBV is a major infectious
occupational hazard of health workers.
HBV is not spread by contaminated food or water, and cannot be spread
casually in the workplace.
The virus incubation period is 90 days on average, but can vary from
about 30 to 180 days. HBV may be detected 30 to 60 days after infection and
persist for widely variable periods of time.
Generally, liver damage from cirrhosis cannot be reversed, but treatment

could stop or delay further progression and reduce complications. A healthy diet
is encouraged, as cirrhosis may be an energy-consuming process. Close follow-
up is often necessary. Antibiotics will be prescribed for infections, and various
medications can help with itching. Laxatives, such aslactulose, decrease risk of
constipation; their role in preventing encephalopathy is limited.
Treating underlying causes. Alcoholic cirrhosis caused by alcohol abuse is

treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis
involves medications used to treat the different types of hepatitis, such as
interferon for viral hepatitis and corticosteroids for autoimmune hepatitis.
Cirrhosis caused by Wilson's disease, in which copper builds up in organs, is
treated withchelation therapy (e.g., penicillamine) to remove the copper.
Preventing further liver damage. Regardless of underlying cause of cirrhosis,

alcohol and paracetamol, as well as other potentially damaging substances, are
discouraged. Vaccination of susceptible patients should be considered
for Hepatitis A and Hepatitis B.
Preventing complications
Ascites. Salt restriction is often necessary, as cirrhosis leads to accumulation of

salt (sodium retention). Diuretics may be necessary to suppress ascites.
Esophageal variceal bleeding. For portal hypertension, propranolol is a

commonly used agent to lower blood pressure over the portal system. In severe
complications from portal hypertension, transjugular intrahepatic
portosystemic shunting is occasionally indicated to relieve pressure on the
portal vein. As this can worsen encephalopathy, it is reserved for those at low
risk of encephalopathy, and is generally regarded only as a bridge to liver
transplantation or as a palliative measure.
Hepatic encephalopathy. High-protein food increases the nitrogen balance, and

would theoretically increase encephalopathy; in the past, this was therefore
eliminated as much as possible from the diet. Recent studies show that this
assumption was incorrect, and high-protein foods are even encouraged to
maintain adequate nutrition.[18]
Hepatorenal syndrome. The hepatorenal syndrome is defined as a urine

sodium less than 10 mmol/L and a serum creatinine > 1.5 mg/dl (or 24
hour creatinine clearance less than 40 ml/min) after a trial of volume expansion
without diuretics.[19]
Spontaneous bacterial peritonitis. Cirrhotic patients with ascites are at risk

of spontaneous bacterial peritonitis.
Decompensated cirrhosis. In patients with previously stable cirrhosis,

decompensation may occur due to various causes, such
as constipation, infection (of any source), increased alcohol
intake, medication, bleeding from esophageal varices or dehydration. It may
take the form of any of the complications of cirrhosis listed above.Patients with
decompensated cirrhosis generally require admission to hospital, with close
monitoring of the fluid balance, mental status, and emphasis on adequate
nutrition and medical treatment – often
with diuretics, antibiotics, laxatives and/or enemas, thiamine andoccasionally
steroids, acetylcysteine and pentoxifylline. Administration of saline is
generally avoided as it would add to the already high total body sodium content
that typically occurs in cirrhosis.
(1) Assessment. The client may present anasarca, weight gain, altered
electrolyte level, oliguria, and may have altered vital signs like temperature of
37.3C, Heart Rate of 89; Respiratory Rate of 20cpm and BP of 120/80mm Hg.
Diagnosis. Fluid volume excess related to compromised regulatory mechanism.
Planning. Within 8 hours of rendering nursing care, the patient will demonstrate
stabilized fluid volume and decreased edema.
Intervention. Measure intake and output, weigh daily, and note weight gain more
than 0.5 kg/day, Assess respiratory status, noting increase d respiratory rate,
dyspnea, Monitor blood pressure, Auscultate lungs, noting diminished/absent of
breath sounds and developing adventitious sounds, Assess degree of
peripheral/dependent edema, Measure abdominal girth, and Encourage bed rest
when ascites is present. Reflects circulating volume status. Positive balance/
weight gain often reflects continuing fluid retention. Indicative of pulmonary
congestion. Blood pressure elevation usually associated with fluid volume excess
but may not occur because fluid shifts out of the vascular space.Increasing
pulmonary congestion may result consodilation, impaired gas exchange, and
complications.Fluid shifts into tissues as a result of sodium and water retention,
decreased albumin, and increased antidiuretic hormone. Reflects accumulation
of fluid resulting from loss of plasma proteins or fluids into peritoneal space. May
promote recumbency-induced dieresis. To control edema and ascites.
Evaluation. After 8 hours of nursing interventions, the patient was able to
demonstrate stabilized fluid volume and decreased edema.
(2) Assessment. The client may present facial grimace, with pain scale of 6/10,
irritable, with guarding behavior, with massive ascites
Diagnosis. Acute pain and discomfort related to enlarged tender liver and as
cites as evidenced by facial grimace and pain scale of 6/10.
Planning. After 8 hours of rendering nursing care, the patient will be able to
demonstrate diversional activities lessen pain.
Intervention. Maintain bed rest when the patient experiences abdominal
discomfort. Observe record, and report presence and character of pain and
discomfort. Reduce sodium and fluid intake if prescribed. Teach patient
diversional activities such as deep breathing exercises and provide reading
materials. Prepare patient and assist with paracentesis.
Evaluation. Within 8 hours of nursing intervention, patient seen doing the
diversional activities instructed and patient’s pain lessened from 6/10 to 4/10.
(3) Assessment. The client may use of accessory muscles when breathing, with
labored breathing (shallow breathing), RR- 29 cycles per minute.
Diagnosis. Impaired Gas Exchange r/t accumulation of fluid in pleural space
secondary to underlying physiologic condition.
Planning. Within 8 hours of giving effective nursing intervention and health
teaching, the patient will be able to know positioning techniques that improve
ventilation.
Intervention. Position client in either semi-fowlers position or side lying position.
Encourage client to cough as tolerated. Monitor respiratory rate, depth, and
effort, including use of accessory muscles, nasal flaring, and thoracic or
abdominal breathing. Monitor client’s behavior and mental status for onset of
restlessness, agitation, confusion and in the late stages, extreme lethargy.
Observe for cyanosis in skin: note especial color of tongue and oral mucous
membrane.
Evaluation. Within 8 hours of giving effective nursing intervention and health
teaching, the patient was able to know positioning techniques that improve
ventilation
VII. Bibliography

Scribd.com
G. TYPHOID FEVER
Typhoid fever, also known as typhoid, is a common worldwide illness,

transmitted by the ingestion of food or water contaminated with the feces of an
infected person, which contain the bacterium Salmonella enterica enterica,
serovar Typhi. The bacteria then perforate through the intestinal wall and are
phagocytosed by macrophages. The organism is a Gram-negative short bacillus
that is motile due to its peritrichous flagella. The bacterium grows best at 37°C /
98.6°F – human body temperature. This fever received various names, such as
gastric fever, abdominal typhus, infantile remittant fever, slow fever, nervous
fever, pythogenic fever, etc. The name of "typhoid" was given by Louis in 1829,
as a derivative from typhus. The impact of this disease falls sharply with the
application of modern sanitation techniques. Typhoid fever is a bacterial disease,
caused by Salmonella typhi. Symptoms usually develop 1–3 weeks after
exposure, and may be mild or severe. They include high fever, malaise,
headache, constipation or diarrhea, rose-colored spots on the chest, and
enlarged spleen and liver. Healthy carrier state may follow acute illness. Typhoid
fever can be treated with antibiotics. However, resistance to common
antimicrobials is widespread. Healthy carriers should be excluded from handling
food.
• Salmonella typhi
It is transmitted through the ingestion of food or drink contaminated by the

feces or urine of infected people. Typhoid fever transmission takes place when a
person eats food or drinks beverages that have been handled by a person
shedding the Salmonella typhi bacteria. The bacteria are also transmitted when
sewage contaminated with Salmonella typhi gets into water used for drinking or
washing food. Typhoid fever transmission is most common in areas of the
developing world, including parts of Asia, Africa, and Latin America.

A vaccine is available but is generally reserved for people traveling to
underdeveloped countries where significant exposure may occur. Strict attention
to food and water precautions while traveling to such countries is the most
effectivepreventive method. AntibioticResistance is increasing:
First-Line: Fluoroquinolones
• Alternative antibiotics (resistance is common)
 Chloramphenicol
 Amoxicillin
 Trimethoprim-Sulfamethoxazole (Septra)
(1) Assessment. The client may have increase in body temperature higher than
normal range ( 38.7 C), flushed skin, warm to touch, increased respiratory rate
(38 cpm), tachycardia (133 bpm).
Diagnosis. Hyperthermia related to presence of infection
Planning. Within 30 mins of nursing care and intervention, the client will be able
to demonstrate temperature within normal range and be free of chills, Experience
no associated complications
Intervention. Monitor client temperature—degree and pattern. Note shaking
chills or profuse diaphoresis. Monitor environmental temperature. Limit or add
bed linens, as indicated. Provide tepid sponge baths. Avoid use of alcohol.
Room temperature and linens should be altered to maintain near-normal body
temperature. Tepid sponge baths may help reduce fever. Note: Use of
ice water or alcohol may cause chills, actually elevating temperature. Antipyretics
reduce fever by its central action on the hypothalamus. F ever should be
controlled in clients who are neutropenic or asplenic. However, fever may be
beneficial in limiting growth of organisms and enhancing autodestruction of
infected cells.
Evaluation. Within 30 mins of nursing care and interventions, the client was able
to demonstrated temperature within normal range and be free of chills and
experienced no associated complications.
(2) Assessment. The client may have hyperactive Bowel sound, defecates four
times liquid stools per day, abdominal Pain ( scale of 6/10)
Diagnosis. Diarrhea related to infectious process
Planning Within 8 hours of nursing care and intervention, the client will be able
to reestablish and maintain normal pattern bowel functioning, verbalized
understanding of causative factors and rationale for treatment regimen and
demonstrate appropriate behaviors to assist with resolution of causative factors.
Intervention. Restrict solid fluid intake, as indicated , Limit caffeine and high
fiber : avoid milk and fruits as appropriate. Encourage oral intake of fluids
bouillon, or commercial preparations as appropriate.
Evaluation. After thorough nursing care and intervention, the client was able to
reestablish and maintain normal pattern bowel functioning and verbalized
understanding of causative factors and rationale for treatment regimen and
demonstrate appropriate behaviors to assist with resolution of causative factors
(3) Assessment. The client may be lethargic, lack of energy, disinterest in

surroundings
Diagnosis. Fatigue related to poor physical condition
Planning. Within 8 hours of nursing care and interventions, the client will be able
to report improved sense of energy, identify basis of fatigue and individual areas
of control, participate in recommendation treatment program.
Intervention. Establish realistic activity goals with client and encourage forward
movement. Plan interventions to allow individually adequate rest periods.
Schedule activities for periods when client has the most energy. Provide
diversional activities and avoid overstimulation.
Evaluation. After 8 hours of nursing care and interventions, the client was able
to report improved sense of energy and identified basis of fatigue and individual
areas of control as well as participated in recommendation treatment program
VII. Bibliography

H. DENGUE HEMORRHAGIC FEVER
Dengue fever also known as breakbone fever, is an acute febrile

infectious disease caused by the dengue virus. Typical symptoms include
headache, a characteristic skin rash, and muscle and joint pains; in a small
proportion the disease progresses to life-threatening complications such as
dengue hemorrhagic fever (which may lead to severe hemorrhage) and dengue
shock syndrome (where a very low blood pressure can cause organ dysfunction).
Dengue is usually transmitted by the mosquito Aedes aegypti, and rarely

Aedes albopictus. The virus exists in four different types, and an infection with
one type usually gives lifelong immunity to that type, but only short-term immunity
to the others. There is currently no available vaccine, but measures to reduce the
habitat and the number of mosquitoes, and limiting exposure to bites, are used to
decrease the incidence of dengue.
The rate of infection has increased dramatically over the last 50 years,
with around 50–100 million people being infected yearly. A global disease,
dengue is currently endemic in more than 110 countries. Early descriptions of the
condition date from 1779, and its viral cause and the transmission were
elucidated in the early 20th century. Dengue has become a worldwide problem
since the Second World War.
Dengue virus is flavivirus genus from flaviviridae family. This virus is a

RNA virus ecosahedral shaped, have infectious Envelope vertebrata including
human intermediaries with mosquito and can result in fatal . Aedis aegypti
mosquitoes transmit dengue virus between humans.

Dengue viruses are transmitted to humans through the bites of infective
female Aedes mosquitoes. Mosquitoes generally acquire the virus while feeding
on the blood of an infected person. After virus incubation for eight to 10 days, an
infected mosquito is capable, during probing and blood feeding, of transmitting
the virus for the rest of its life. Infected female mosquitoes may also transmit the
virus to their offspring by transovarial (via the eggs) transmission, but the role of
this in sustaining transmission of the virus to humans has not yet been defined.
Infected humans are the main carriers and multipliers of the virus, serving
as a source of the virus for uninfected mosquitoes. The virus circulates in the
blood of infected humans for two to seven days, at approximately the same time
that they have a fever; Aedes mosquitoes may acquire the virus when they feed
on an individual during this period.
• Dengue fever is usually a self-limited illness, and only supportive care is

required. Acetaminophen may be used to treat patients with symptomatic
fever. Aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and
corticosteroids should be avoided.
• Patients with known or suspected dengue fever should have their platelet
count and hematocrit measured daily from the third day of illness until 1-2
days after defervescence. Patients with a rising hematocrit level or falling
platelet count should have intravascular volume deficits replaced. Patients
who improve can continue to be monitored in an outpatient setting. Patients
who do not improve should be admitted to the hospital for continued
hydration.
• Patients who develop signs of dengue hemorrhagic fever warrant closer
observation. Patients who develop signs of dehydration, such as tachycardia,
prolonged capillary refill time, cool or mottled skin, diminished pulse
amplitude, altered mental status, decreased urine output, rise in hematocrit
levels, narrowed pulse pressure, or hypotension, require admission for
intravenous fluid administration.
• Successful management of severe dengue requires careful attention to fluid
management and proactive treatment of hemorrhage. Intravascular volume
deficits should be corrected with isotonic fluids such as Ringers lactate
solution. Boluses of 10-20 mL/kg should be given over 20 minutes and may
be repeated. If this fails to correct the deficit, the hematocrit value should be
determined, and, if it is rising, limited clinical information suggests that a
plasma expander may be administered. Starch, dextran 40, or albumin 5% at
a dose of 10-20 mL/kg may be used. One recent study has suggested that
starch may be preferable because of hypersensitivity reactions to dextran. If
the patient does not improve after this, blood loss should be considered.
Patients with internal or gastrointestinal bleeding may require transfusion.
Patients with coagulopathy may require fresh frozen plasma.
• After patients with dehydration are stabilized, they usually require intravenous
fluids for no more than 24-48 hours. Intravenous fluids should be stopped
when the hematocrit level falls below 40% and adequate intravascular volume
is present. At this time, patients reabsorb extravasated fluid and are at risk for
volume overload if intravenous fluids are continued. Do not interpret a falling
hematocrit value in a clinically improving patient as a sign of internal bleeding.
• Platelet and fresh frozen plasma transfusions may be required to control
severe bleeding. A recent case report demonstrated good improvement
following intravenous anti-D globulin administration in two patients. The
authors proposed that, similarly to nondengue forms of immune
thrombocytopenic purpura, intravenous anti-D produces Fcγ receptor
blockade to raise platelet counts.
• Patients who are resuscitated from shock rapidly recover. Patients with
dengue hemorrhagic fever or dengue shock syndrome may be discharged
from the hospital when they meet the following criteria:
o Afebrile for 24 hours without antipyretics
o Good appetite, clinically improved condition
o Adequate urine output
o Stable hematocrit level
o At least 48 hours since recovery from shock
o Absence of respiratory distress
o Platelet count greater than 50,000 cells/μL
(1) Assessment. The client may feel pain with the scale of 7/10, restlessness,
facial grimace, body malaise, RR= 28 cpm, increase temp of 38.7 degree celcius
Diagnosis. Acute pain related to viral infection.
Planning. At the end of 30 minutes thorough nursing intervention the will
verbalized relief of pain as evidence by pain scale of 0-3/10, absence of facial
grimace, absence of being restless and body malaise, and vital signs within
normal range.
Intervention. Obtain client assessment of pain and use pain rating scale
appropriate for age to determine severity of pain and rule out worsening of
underlying condition.Monitor vital signs every 15 minutes until stable because
alteration from normal may indicate underlying condition. Teach deep breathing
exercise to patient to promote non-pharmacological pain management.
Encourage activity to divert attention such as reading books to divert patient’s
attention from pain. Provide calm and quite environment to promote comfort to
patient.
Evaluation. After 30 minutes of nursing intervention the goals were met as
evidence by pain scale of 3/10, absence of facial grimace, absence of being
restless and body malaise and vital signs within normal range. RR= 19 c/min,
PR= 87 b/min, Temp= 37.2 degree celsius, BP= 100/70.
(2) Assessment: The patient may have a decrease WBC of 4.8 x 10^g/L,
decreased platelet of 95 x 10^g/dL, and decreased HgB of 10.3 g/dL as well as
decreased Hct of 31 %.Positive tourniquet test with fever of 38.7 degrees
Celsius. Tachypnea of 28 c/min. Hypotension of 80/60mmHg, faint pulse,
epistaxis noted (Bloody discharge of nasal), gum bleeding, restless may be
manifested.
Diagnosis. Ineffective tissue perfusion related to decreased HgB concentration
in the blood secondary to DHF stage III grade III.
Planning. Within 8 hours nursing care and interventions, the patient will be able
to demonstrate increased tissue perfusion as individually appropriate as
evidence by V/S within normal range, Negative epistaxis, No gum bleeding,
Negative tourniquet test, and Distinct pulse.
Intervention. Monitor Vital Signs every 4 hours. Provide quiet and restful
atmosphere. Instruct to avoid tiring activities. Instruct to increase fluid intake and
avoid eating dark-colored foods and fluids which can mask bleeding. Assist
patient with range of motion exercises and encourage light ambulation. Note
blood discharge of nasal and notify physician if discharge increases.Elevate head
of bed.
Evaluation. At the end of 8 hours nursing care and interventions, goal was met.
The patient was able to demonstrate increased tissue perfusion as individually
appropriate as evidence by V/S within normal range, T= 37.3 degree Celsius,
PR=85 beats per minute, RR= 22 cycles per minute, Bp= 100/70 mmHg,
Negative epistaxis, No gum bleeding, Negative tourniquet test, and Distinct
pulse.
(3) Assessment. The patient may have alteration in his body temperature (38.7
degrees Celsius), tachypnea (28 c/min), faint pulse, flushed skin, skin warm to
touch, restless, shivering.
Diagnosis. Hyperthermia related to viral infection secondary to Dengue
Hemorrhagic In-fection stage III grade III.
Planning. Within 4 hours of nursing care and interventions, the patient will
achieve normal core temperature as evidence by V/S within normal range, BT=
36.5-37.5, PR= 60 – 80 b/min, RR= 16 – 25 c/min, BP= 90/60-120/80, distinct
pulse, normal skin color and temperature, absence of shivering, calm and relax.
Intervention. Monitor Vital Signs every 15 minutes. Wrap extremities with bath
towels, Provide Tepid Sponge B every 15 minutes. Instruct client to have bed
rest. Instruct client to increase oral fluid intake. Instruct high-calorie diet.
Evaluation. After 4 hours of nursing care and interventions, the patient was able
to achieve normal core temperature as evidence by V/S within normal range:,
BT= 36.5-37.5, PR= 60 – 80 b/min, RR= 16 – 25 c/min, BP= 90/60-120/80,
distinct pulse, normal skin color and temperature, absence of shivering, calm and
relax
VII. Bibliography

I. SEIZURE DISORDER
Almost 3 million persons in the United States live with epilepsy. Epilepsy is
a neurological condition that makes people susceptible to seizures. A seizure is a
change in sensation, awareness, or behavior brought about by a brief electrical
disturbance in the brain. Seizures vary from a momentary disruption of the
senses, to short periods of unconsciousness or staring spells, to convulsions.
Some people have just one type of seizure. Others have more than one type.
Although they appear different, all seizures have the same cause: a sudden
change in how the cells of the brain send electrical signals to each other. The
condition can be caused by anything that affects the brain, including tumors and
strokes. Sometimes epilepsy is inherited. Often, no cause can be found.
Seizures are a symptom of epilepsy. Seizures ("fits," convulsions) are
episodes of disturbed brain function that cause changes in attention or behavior.
They are caused by abnormally excited electrical signals in the brain.
A single seizure may be related to a temporary medical problem (such as
brain or tumor withdrawal from alcohol). If repeated seizures do not happen
again once this underlying problem is corrected, the person does not have
epilepsy.
A single, first seizure that cannot be explained by a temporary medical
problem has about a 25% chance of returning. After a second seizure occurs,
there is about a 70% chance of future seizures and the diagnosis of epilepsy.
Common causes of seizures (see Table 1: Seizure Disorders: Causes of

Seizures) vary by age of onset:
• Before age 2: Developmental defects, birth injuries, and metabolic disorders
• Ages 2 to 14: Idiopathic seizure disorders
• Adults: Cerebral trauma, alcohol withdrawal, tumors, strokes, and unknown
cause (in 50%)
• The elderly: Tumors and strokes
In reflex epilepsy, a rare disorder, seizures are triggered predictably by an
external stimulus, such as repetitive sounds, flashing lights, video games, or
even touching certain parts of the bod
Table 1
Causes of Seizures
Condition Examples
Autoimmune disorders Cerebral vasculitis, multiple sclerosis (rarely)
Cerebral edema Eclampsia, hypertensive encephalopathy
Cerebral ischemia or hypoxia Cardiac arrhythmias, carbon monoxide
toxicity, near drowning, near suffocation,
stroke, vasculitis
Head trauma* Birth injury, blunt or penetrating injuries
CNS infections AIDS, brain abscess, falciparum malaria,
meningitis, neurocysticercosis, neurosyphilis,
rabies, tetanus, toxoplasmosis, viral
encephalitis
Congenital or developmental abnormalities Cortical malformations, genetic disorders
(eg, fifth day fits†, lipid storage diseases such
as Tay-Sachs disease), neuronal migration
disorders (eg, heterotopias), phenylketonuria
‡
Drugs and toxins Cause seizures: Camphor, cocaine and
other CNS stimulants, cyclosporine, lead,
pentylenetetrazol, picrotoxin, strychnine,
tacrolimus
Lower seizure threshold: Aminophylline,
antidepressants (particularly tricyclics),
sedating antihistamines, antimalarial drugs,
some antipsychotics (eg, clozapine),
buspirone, fluoroquinolones, theophylline
Expanding intracranial lesions Hemorrhage, hydrocephalus, tumors
Hyperpyrexia Drug toxicity (eg, with amphetamines or
cocaine), fever, heatstroke
Metabolic disturbances Commonly, hypocalcemia, hypoglycemia,
hyponatremia
Less commonly, aminoacidurias, hepatic or
uremic encephalopathy, hyperglycemia,
hypomagnesemia, hypernatremia
In neonates, vitamin B6 (pyridoxine)
deficiency
Pressure-related Decompression illness, hyperbaric O2
treatments
Withdrawal syndromes Alcohol, anesthetics, barbiturates,
benzodiazepines
*
Posttraumatic seizures occur in 25 to 75% of patients who have brain contusion, skull
fracture, intracranial hemorrhage, prolonged coma, or focal neurologic deficits.
†
Fifth day fits (benign neonatal seizures) are tonic-clonic seizures occurring between 4
and 6 days of age in otherwise healthy infants; one form is inherited.
‡
When given in toxic doses, various drugs can cause seizures.
Classification
Seizures are classified as generalized or partial.
Generalized: In generalized seizures, the aberrant electrical discharge diffusely
involves the entire cortex of both hemispheres from the onset, and
consciousness is usually lost. Generalized seizures result most often from
metabolic disorders and sometimes from genetic disorders. Generalized seizures
include the following:
Partial seizures: In partial seizures, the excess neuronal discharge occurs in
one cerebral cortex, and most often results from structural abnormalities.
Partial seizures may be
• Simple (no impairment of consciousness)
• Complex (reduced but not complete loss of consciousness)
Partial seizures may be followed by a generalized seizure (called secondary
generalization), which causes loss of consciousness. Secondary generalization
occurs when a partial seizure spreads and activates the entire cerebrum
bilaterally. Activation may occur so rapidly that the initial partial seizure is not
clinically apparent or is very brief.
Infantile spasms are characterized by sudden flexion and adduction of the arms
and forward flexion of the trunk. Seizures last a few seconds and recur many
times a day. They occur only in the first 5 yr of life, and then are replaced by
other types of seizures. Developmental defects are usually present.
Typical absence seizures (formerly called petit mal seizures consist of 10- to
30-sec loss of consciousness with eyelid fluttering; axial muscle tone may or may
not be lost. Patients do not fall or convulse; they abruptly stop activity, and then
just as abruptly resume it, with no postictal symptoms or knowledge that a
seizure has occurred. Absence seizures are genetic and occur predominantly in
children. Without treatment, such seizures are likely to occur many times a day.
Seizures often occur when patients are sitting quietly, can be precipitated by
hyperventilation, and rarely occur during exercise. Neurologic and cognitive
examination results are usually normal.
Atypical absence seizures usually occur as part of the Lennox-Gastaut
syndrome, a severe form of epilepsy that begins before age 4 yr. They differ from
typical absence seizures as follows:
• They last longer.
• Jerking or automatic movements are more pronounced.
• Loss of awareness is less complete.
Many patients have a history of damage to the nervous system,
developmental delay, abnormal neurologic examination results, and other types
of seizures. Atypical absence seizures usually continue into adulthood.
Atonic seizures occur most often in children, usually as part of Lennox-Gastaut
syndrome. Atonic seizures are characterized by brief, complete loss of muscle
tone and consciousness. Children fall or pitch to the ground, risking trauma,
particularly head injury.
Tonic seizures occur most often during sleep. Tonic seizures occur most often
in childhood. The cause is usually the Lennox-Gastaut syndrome. Tonic
(sustained) contraction of axial muscles may begin abruptly or gradually, then
spread to the proximal muscles of the limbs. Tonic seizures usually last 10 to 15
sec. In longer tonic seizures, a few, rapid clonic jerks may occur as the tonic
phase ends.
Tonic-clonic seizures may be primarily or secondarily generalized. Primarily
generalized seizures typically begin with an outcry; they continue with loss of
consciousness and falling, followed by tonic contraction, then clonic (rapidly
alternating contraction and relaxation) motion of muscles of the extremities,
trunk, and head. Urinary and fecal incontinence, tongue biting, and frothing at the
mouth sometimes occur. Seizures usually last 1 to 2 min. There is no aura.
Secondarily generalized tonic-clonic seizures begin with a simple partial or
complex partial seizure.
Myoclonic seizures are brief, lightning-like jerks of a limb, several limbs, or the
trunk. They may be repetitive, leading to a tonic-clonic seizure. The jerks may be
bilateral or unilateral. Unlike other seizures with bilateral motor movements,
consciousness is not lost unless the myoclonic seizures progress into a
generalized tonic-clonic seizure.
Juvenile myoclonic epilepsy is an epilepsy syndrome characterized by
myoclonic, tonic-clonic and absence seizures. It typically appears during
adolescence. Seizures begin with a few bilateral, synchronous myoclonic jerks,
followed in 90% by generalized tonic-clonic seizures. They often occur when
patients awaken in the morning, especially after sleep deprivation or alcohol use.
Absence seizures may occur in 1/3 of patients.
Febrile seizures occur, by definition, with fever and in the absence of
intracranial infection; they are considered a type of provoked seizure. They affect
about 4% of children aged 3 mos. to 5 yr. Benign febrile seizures are brief,
solitary, and generalized tonic-clonic in appearance. Complicated febrile seizures
are focal, last > 15 min, or recur ≥ 2 times in < 24 h. Overall, 2% of patients with
febrile seizures develop a subsequent seizure disorder. However, incidence of
seizure disorders and risk of recurrent febrile seizures are much greater among
children with complicated febrile seizures, preexisting neurologic abnormalities,
onset before age 1 yr, or a family history of seizure disorders.
Seizures that persist after use of lorazepam and phenytoin define

refractory status epilepticus. Recommendations for a 3rd anticonvulsant vary and
include phenobarbital, propofol, midazolam, and valproate. Phenobarbital 15 to
20 mg/kg IV at 100 mg/min (3 mg/kg/min in children) is given; continued seizures
require another 5 to 10 mg/kg. A loading dose of valproate 10 to 15 mg/kg IV is
an alternative. At this point, if status epilepticus has not abated, intubation and
general anesthesia are necessary. The optimal anesthetic to use is controversial,
but many physicians use propofol 15 to 20 mg/kg at 100 mg/min or pentobarbital
5 to 8 mg/kg (loading dose) followed by infusion of 2 to 4 mg/kg/h until EEG
manifestations of seizure activity have been suppressed. Inhalational anesthetics
are rarely used. After initial treatment, the cause of status epilepticus must be
identified and treated.
Drug choice for long-term treatment: For partial seizures and generalized
tonic-clonic seizures, the newer anticonvulsants (eg, clonazepam, felbamate,
lamotrigine, levetiracetam, oxcarbazepine, pregabalin, tiagabine, topiramate,
zosinamide) are no more effective than the established drugs. However, the
newer drugs tend to have fewer adverse effects and to be better tolerated.
Infantile spasms, atonic seizures, and myoclonic seizures are difficult to
treat. Valproate is preferred, followed by clonazepam. For infantile spasms,
corticosteroids for 8 to 10 wk are often effective. The optimal regimen is
controversial. ACTH 20 to 60 units IM once/day may be used. A ketogenic diet (a
very high fat diet that induces ketosis) may help but is difficult to maintain.
For juvenile myoclonic epilepsy, life-long treatment is usually
recommended. Carbamazepine , oxcarbazepine, or gabapentin can exacerbate
the seizures. For febrile seizures, drugs are not recommended unless children
have a subsequent seizure in the absence of febrile illness.
Previously, many physicians gave phenobarbital or other anticonvulsants
to children with complicated febrile seizures to prevent nonfebrile seizures from
developing, but this treatment does not appear effective, and long-term use of
phenobarbital reduces learning capacity.
For seizures due to alcohol withdrawal, drugs are not recommended.
Instead, treating the withdrawal syndrome tends to prevent seizures. Treatment
usually includes a benzodiazepine.
(1) Assessment. The client may have weakness, facial grimace, irritability,
alteration in the V/S taken as follows, T: 37.3; P: 110; R: 20; BP: 120/90
Diagnosis. Risk for trauma related to loss of large muscle coordination.
Planning.Within 8 hours of nursing interventions, the patient will be able to
demonstrate behaviors, lifestyle changes to reduce risk factors and protect self
from injury.
Intervention. Explore with the patient the various stimuli that may precipitate
seizure activity. Discuss seizure warning signs and usual seizure pattern. Keep
padded side rails up with bed in the lowest position. Evaluate need for protective
head gear. Maintain strict bed rest if prodromal signs or aura experienced. Turn
head to side or suction airway as indicated. Insert plastic bite block only if jaw are
relaxed. Cradle head, place on soft area, or assist to floor if out of bed. Reorient
patient following seizure activity.
Evaluation. After 8 hours of nursing interventions, the patient was able to
demonstrated behaviors, lifestyle changes to reduce risk factors and protect self
from injury.
(2) Assessment. Client with biochemical dysfunction, onset of seizure at anytime

for 2-3 minutes, lying on bed with no significant other watching over., no safety
measures such as raising of side rails up in case of seizure activity, deficient
knowledge about the appropriate intervention of the significant other.
Diagnosis. Risk for Injury related to onset of seizures at anytime.

Planning. After 15-20 minutes of health teaching and nursing interventions,
patient will be able to verbalize understanding of individual factors that contribute
to possibility of injury. modify environment as indicated to enhance safety.
Intervention. Provide information regarding disease/condition that may result in
increased risk for injury. Maintain bed/chair in lowest position with wheels locked
to prevent risk from falls. Monitor environment for potentially unsafe conditions
and modify as needed to prevent any injury during attacks. Identify safety
devices to promote safe physical environment and individual safety. Discuss
importance of self-monitoring of conditions/emotions that can contribute to
occurrence of injury.
Evaluation After 8 hours of nursing interventions, the patient was able to
demonstrate behaviors, lifestyle changes to reduce risk factors and protect self
from injury.
.
(3) Assessment. Client with altered level of consciousness, depressed cough
and gag reflex during seizure, situation hindering elevation of upper body during
seizure such as lying flat, and neuromuscular weakness
Diagnosis. Risk for Aspiration related to neuromuscular weakness secondary to
seizure disorder.
Planning. After 15-20 minutes of health teaching and nursing interventions,
patient will be able to identify causative/risk factors and be free of aspiration.
Intervention. Note level of consciousness/awareness of surroundings, cognitive
impairment to asses causative/contributing factors. Maintain operational suction
equipment at bed side/chair side to assist in correcting factors that can lead
aspiration during seizure attacks. Feed slowly instruct client to chew slowly and
thoroughly to assist in correcting factors that can lead to aspiration. Provide
padded tongue depressor at the patient’s bedside and to be placed by any
watcher of the patient in the mouth during seizure attacks to prevent aspiration.
Provide information about the effects of aspiration on the lungs to promote
wellness and increase awareness.
Evaluation. After 15-20 minutes of health teaching and nursing interventions,
patient was be able to identify causative/risk factors and was free of aspiration.
VII. Bibliography: Medical – Surgical Nursing (Clinical Management for Positive

Outcomes) 8th Edition by Joyce M. Black and Jane Hokanson Hawks. 2008
J. ACUTE GLOMERULONEPHRITIS

A proliferative and inflammatory change in the glomerular structure. It is
usually manifested by either a nephritic syndrome or a nephritic syndrome.
Percutaneous renal biopsy is typically used to identify the type of
glomerulonephritis, and the findings assist in planning interventions and
determining the progress. It refers to a specific set of renal diseases in which an
immunologic mechanism triggers inflammation and proliferation of glomerular
tissue that can result in damage to the basement membrane, mesangium, or
capillary endothelium.
The most common cause is postinfectious Streptococcus species (i.e

group A beta-hemolytic). Two types have been described as (1)b attributed to
serotype 12, poststreptococcal nephritis due to an upper respiratory infection
occurring primarily in the winter months, and (2) attributed to serotype 49,
poststreptococcal nephritis due to a skin infection usually observed in the
summer and fall and more prevalent in southern regions of the United States.
It aims to eliminate antigens, to alter the client’s immune balance, and to

inhibit or alleviate inflammation to prevent further renal damage and improve
kidney function. Although some clients may require initial hospitalization,
treatment is typically on an outpatient basis.
Reduce Inflammation. Plasmapheresis has been used in some research

protocols to reduce the number of antigens in certain types of glomerulonephritis,
including rapidly progressive glomerulonephritis. This intervention is usually
administered in conjunction with corticosteroids and immunosuppressive agents
(i.e. azathioprine, cyclophosphamide). The technique is designed to remove the
specific circulating antibody or mediators of the inflammatory response. Large
volumes of the client’s plasma are cyclically removed and replaced with fresh
frozen plasma through a continuous-flow blood cell separator.
Antibiotic therapy (i.e. penicillin for streptococcal organisms) is used to treat post
streptococcal glomerulonephrtitis. It is also used to prophylactically after
streptococcal infections to prevent further damage.
Maintain fluid and Electrolyte Balance. Volume overload and hypertension are
treated with diuretics, antihypertensives, and restriction of dietary sodium and
water. Common complications of fluid overload include heart failure with
pulmonary edema and increased intracranial pressure. Renal failure may
develop. Appropriate monitoring is essential and should include vital signs, intake
and output, and weight recognizing complications early facilitate prompt medical
intervention.
(1) Assessment: For any client with suspected glomerulonephritis, take a

comprehensive history that includes upper respiratory tract infection, skin
infections, scarlet fever, or a history of glomrulonephritis. Also question the client
about systemic disorders that might be present, such as SLE, scleroderma,
amyloidosis, and hypertension,. Any recent invasive procedures should also be
noted. Physical examination may reveal ascites, pleural effusion and
manifestations of heart failure with pulmonary edema. Examine the urine closely
for color, amount, and abnormal substances. In particular, microscopic analysis
of the urine can be a valuable diagnostic tool with glomerulonephritis; urinary
casts are commonly seen under high magnification. Check the client’s vital signs
closely, especially the blood pressure.
Diagnosis: if the client has a reduced appetite or an aversion to food, the
nursing diagnosis Imbalanced Nutrition: Less than Body Requirements related to
lack of appetite and increased metabolic demands is appropriate.
Outcomes: The client will maintain adequate nutritional intake, as evidenced by
no weight loss, an absence of a negative nitrogen balance, and normal
electrolytes.
Interventions: It is important to protect the kidneys while they are recovering
their function. The prescribed diet is likely to be high in calories and low in
protein. This diet is designed to avoid protein catabolism and enables the kidney
to rest because it handles fewer protein molecules and metabolites.
The degree to which protein is restricted depends on the amount excreted
in the urine and the client’s individual requirements. Sodium is also restricted,
depending on the amount of edema present. Anorexia, nausea, and vomiting
may interfere with adequate intake, requiring creative intervention on your part. A
dietician can help plan the client’s diet around these restrictions.
(2) Diagnosis: A common nursing diagnosis in glomerulonephritis is Excess fluid

Volume related to reduced urine output.
Outcomes: The client will maintain balanced intake and output, as evidenced by
no manifestations of edema or fluid overload.
Interventions: Appropriate fluid balance is important. Careful monitoring of daily
weight and intake and output helps determine the progress of the edema and
thus provides an estimate of renal function. Daily measurement of edematous
parts also provides useful, objectives data. The client’s allowable fluid intake is
based on the intake and output measurements. Fluid intake is usually restricted.
Thirst may be relieved by offering hard candies, lemon slices, or ice chips rather
than a glass of water. Assist the client to “plan” fluid distribution during the day to
make the best use of allowed fluids.
(3) Diagnosis: Another common nursing diagnosis is Fatigue related to

increased metabolic demands and anemia.
Outcome: The client will conserve energy through an adequate balance of rest
and activity, as evidenced by absence of complaints of fatigue.
Interventions: Rest is essential---- both physical and emotional. As mentioned,
activity level correlates directly with the amount of hematuria and proteinuria.
Exercise also increases catabolic activity. The allowable amount of activities
depends on the results of serial urinalyses. Bed rest interspersed with periods of
limited activity may continue for several weeks to months. Therefore the client
may need help in arranging personal matters, such as family, home job, finances,
and community responsibilities.
Encourage the client to talk about any fears pr concerns, and, if

necessary, help the client deal with the emotional reactions expected during a
long-term illness with a questionable prognosis. Only after handling these
problems can the client rest emotionally. Appropriate diversionary activities may
help the client cope with prolonged physical mobility.
V. Pathophysiology (please refer to next page)
VI. Bibliography

K. CHRONIC RENAL FAILURE

Chronic renal failure (CRF) is the progressive loss of kidney function. The
kidneys attempt to compensate for renal damage by hyperfiltration (excessive
straining of the blood) within the remaining functional nephrons (filtering units that
consist of a glomerulus and corresponding tubule). Over time, hyperfiltration
causes further loss of function.
Chronic loss of function causes generalized wasting (shrinking in size) and

progressive scarring within all parts of the kidneys. In time, overall scarring
obscures the site of the initial damage. Yet, it is not until over 70% of the normal
combined function of both kidneys is lost that most patients begin to experience
symptoms of kidney failure.
The causes of chronic renal failure include chronic glomerular disease

such as glomerulonephritis, chronic infections such as tuberculosis, vascular
diseases such as hypertension, obstructive processes such as calculi, collagen
diseases such as systemic lupus erythematosus, endocrine diseases such as
diabetic neuropathy
Regular measurements of kidney function and other laboratory tests

depending on the severity of kidney impairment. General health advice: smoking
cessation, weight loss, aerobic exercise, limiting alcohol intake, limiting sodium
intake. Avoidance of nephrotoxins, e.g. IV radiocontrast agents, NSAIDs,
aminoglycosides. Cardiovascular prophylaxis:
o For patients with 10-year risk of cardiovascular disease of greater than 20%,
consider aspirin treatment (if blood pressure is below 150/90 mm Hg) and
lipid-lowering drug therapy.
o Blood pressure monitoring: blood pressure should be measured at least
annually.
o Control of hypertension: hypertension should be tightly controlled. The
threshold for initiation of antihypertensive medication:
 If urine protein to creatinine ratio (PCR) is below 100 mg/mmol:
threshold 140/90 mm Hg, target 130/80 mm Hg.
 If urine PCR is above 100 mg/mmol: threshold 130/80 mm Hg, target
125/75 mm Hg.
• Angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker

(ARB) to be started:
o If urine PCR is above 100 mg/mmol.
o In diabetic patients with microalbuminuria.
o Serum creatinine and potassium should be checked before starting
medication, two weeks after starting, and after subsequent increases in
dose. If creatinine increases by more than 20% or there is a fall in GFR of
more than 15%, repeat creatinine, check potassium and refer for specialist
opinion on whether to stop treatment or to investigate for renal artery
stenosis.
o If hyperkalaemia is present (serum K above 6 mmol/L): stop relevant
drugs, e.g. NSAIDs and potassium-retaining diuretics; check diet and
proprietary treatments, e.g. Low Salt. If hyperkalaemia persists, the ACE
or ARB should be stopped.
(1) Assessment. The client may have venous distention, generalized edema,
fatigue, weakness, and malaise.
Diagnosis. Excess fluid volume r/t compromised regulatory mechanism (renal
failure)
Planning. Within 8 hours of Nursing interventions, the patient will display
appropriate urinary output with specific gravity / laboratory studies near normal,
stable weight, vital signs within patient’s normal range and absence of edema.
Intervention. Monitor intake and output. Weight daily at same time of the day, on
same scale, with same equipment and clothing
(2) Diagnosis. Decrease in cardiac output related to an increased cardiac load

Planning. The client would improve the cardiac output of the patient.
Intervention. Auscultation of heart and lung sounds because there is an irregular
heart frequency tachycardia. Review of hypertension for Hypertension may occur
due to disturbances in the system renin-angiotensin-aldosterone system (caused
by renal dysfunction). Assess complaints of chest pain, perhatikanlokasi, rediasi,
weight (scale 0-10) because hypertension and chronic renal failure can cause
pain.Assess the level of activity, response activity because fatigue may
accompany chronic renal failure
(3) Diagnosis: Changes in nutrition: less than the needs associated with
anorexia, nausea, vomiting
Planning. Maintain adequate nutrition inputs
Intervention. Monitor the consumption of food / fluid because identifying
nutritional deficiencies. Watch for nausea and vomiting because symptoms that
accompany the accumulation of endogenous toxins that can alter or reduce
revenue and require intervention. Give the patient a little food but often because
a smaller portion to increase the input of food. Increase visits by people closest
to during meal. Provide diversion and increase the social aspect. Give frequent
oral care to reduce the discomfort of oral stomatitis and feeling unwelcome in the
mouth that can affect food inputs.
VI. Pathophysiology ( please refer to the next page)
VII. Bibliography

L. UPPER GASTROINTESTINALBLEEDING/ BLEEDING PEPTIC ULCER
Bleeding peptic ulcer disease is characterized by ulcerations and erosions

in the mucosal linings of the gastrointestinal tract. It is acidic and painful in
nature. There are several classification of this disease according to the area or
region affected. These are as follows: stomach (gastric), duodenum (duodenal),
and esophagus (esophageal). It also has varied causes.
The most common complication of peptic ulcer disease is gastrointestinal

bleeding. It occurs when the ulcer have gone beyond arteries especially large
ones, it could be life threatening. Other complication is perforation or when the
erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or
intestinal content into the abdominal cavity. Perforation at the anterior surface of
the stomach leads to acute peritonitis, initially chemical and later bacterial
peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall
perforation leads to pancreatitis; pain in this situation often radiates to the back.
A major causative factor is chronic inflammation due to Helicobacter

pylori that colonizes the antral mucosa. The immune system is unable to clear
the infection, despite the appearance of antibodies. Thus, the bacterium can
cause a chronic active gastritis (type B gastritis), resulting in a defect in the
regulation ofgastrin production by that part of the stomach, and gastrin secretion
can either be decreased (most cases) resulting in hypo- or achlorhydria or
increased. Gastric stimulates the production of gastric acid by parietal cells and,
in H. pylori colonization responses that increase gastrin, the increase in acid can
contribute to the erosion of the mucosa and therefore ulcer formation.
Another major cause is the use of NSAIDs The gastric mucosa protects
itself from gastric acid with a layer of mucus, the secretion of which is stimulated
by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-
1), which is essential for the production of these prostaglandins. COX-2 selective
anti-inflammatories (such ascelecoxib or the since withdrawn rofecoxib)
preferentially inhibit cox-2, which is less essential in the gastric mucosa, and
roughly halve the risk of NSAID-related gastric ulceration. As the prevalence
of H. pylori-caused ulceration declines in the Western world due to increased
medical treatment, a greater proportion of ulcers will be due to increasing NSAID
use among individuals with pain syndromes as well as the growth of aging
populations that develop arthritis.
The incidence of duodenal ulcers has dropped significantly during the last
30 years, while the incidence of gastric ulcers has shown a small increase,
mainly caused by the widespread use of NSAIDs. The drop in incidence is
considered to be a cohort-phenomenon independent of the progress in treatment
of the disease. The cohort-phenomenon is probably explained by improved
standards of living which has lowered the incidence of H. pylori infections.
Although some studies have found correlations between smoking and

ulcer formation, others have been more specific in exploring the risks involved
and have found that smoking by itself may not be much of a risk factor unless
associated with H. pylori infection. Some suggested risk factors such
as diet, spice consumption and blood type, were hypothesized as ulcerogens
(helping cause ulcers) until late in the 20th century, but have been shown to be of
relatively minor importance in the development of peptic ulcers. Similarly, while
studies have found that alcohol consumption increases risk when associated
with H. pylori infection, it does not seem to independently increase risk, and even
when coupled with H. pylori infection, the increase is modest in comparison to
the primary risk factor.
Younger patients with ulcer-like symptoms are often treated

with antacids or H2 antagonists before EGD is undertaken. Bismuth
compounds may actually reduce or even clear organisms, though the warning
labels of some bismuth subsalicylate products indicate that the product should
not be used by someone with an ulcer.
Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may

also be prescribed a prostaglandin analogue (Misoprostol) in order to help
prevent peptic ulcers, which may be a side effects of the NSAIDs.
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. In complicated,
treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin +
metronidazole) may be used together with a PPI and sometimes with bismuth
compound. An effective first-line therapy for uncomplicated cases would
be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H.
pylori, long-term higher dose PPIs is often used.
Treatment of H. pylori usually leads to clearing of infection, relief of

symptoms and eventual healing of ulcers. Recurrence of infection can occur and
retreatment may be required, if necessary with other antibiotics. Since the
widespread use of PPI's in the 1990s, surgical procedures (like "highly
selective vagotomy") for uncomplicated peptic ulcers became obsolete.
Perforated peptic ulcer is a surgical emergency and requires surgical

repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop
bleeding with cautery, injection, orclipping.
(1) Assessment. The patient may cry and moan because of pain, guarding on
the abdominal area, facial grimaces, and inability to focus or concentrate.
Diagnosis. Acute abdominal pain related to gastric mucosal injury
Planning. Within 30 minutes to 1 hour, of nursing care the patient will be able to
verbalize relief of pain. Teach the client’s about relaxation techniques such as
deep breathing and meditation to facilitate reduction of pain
Intervention. Provide non-pharmacological measures such as guided imagery,
reading magazines or watching TV to provide diversion of attention from pain.b
Assess frequently the patient’s vital signs to note changes in response to pain.
Instruct client to refrain from engaging in stress producing activities to prevent
further pain caused by increase in gastric juice secretion
Evaluation. After 45 minutes of nursing care, the patient reported reduction of
pain from 10/10 to 3/10.
(2) Assessment. The client may have refusal to eat, guarding behavior on the
abdomen, sweating, eating on irregular intervals, BMI less than normal.
Diagnosis. Imbalance nutrition: less than body requirements related to refusal to
eat secondary to pain of peptic ulcer disease
Planning. Within 8 hours of nursing intervention, the patient will be able to eat
amount of food required for the day. After 2 weeks of nursing interventions, the
patient will be able to maintain adequate nutrition as evidenced by normal BMI,
Intervention. Provide small frequent feeding of high biologic value at equal
intervals to promote food intake and fuel energy. Ensure adequate hydration
to prevent dehydration that may lead to further malnutrition. Instruct patient to
increase intake of protein-rich foods for more stable energy source.
Evaluation. After 8 hours of nursing interventions, the patient was able to -eat
amount of food required for the day, After 2 weeks of nursing interventions, the
patient will be able to maintain adequate nutrition as evidenced by normal BMI
VII. Bibliography


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A.

I. Brief Background of the Disease

A chronic, progressive disease characterized by the body’s inability to

Diabetes mellitus is defined as a fasting blood glucose of 126 milligrams

II. Etiologic Factor/ Agent

Previously called IDDM or juvenile-onset diabetes mellitus, is

Previously called NIDDM or adult-onset diabetes mellitus, is a disorder

III. Medical Management

It includes restoring and maintaining blood glucose levels to as near

Promote Proper Nutrition. The general goal of dietary management is to help

Oral antidiabetics. Major classes include sulfonylureas, biguanides,

IV. Nursing Management

V. Pathophysiology (please refer to the next page)

Medical – Surgical Nursing (Clinical Management for Positive Outcomes) 8th

I. Brief Background of the Disease

Gastroenteritis (also known as gastric flu or stomach flu, although

At least 50% of cases of gastroenteritis due to foodborne illness are

Risk factors include consumption of improperly prepared foods or

• Low grade fever to 100°F (37.8°C)

More serious symptoms include:

• Blood in vomit or stool

Gastroenteritis caused by viruses may last one to two days. However,

Norovirus - Fifty to seventy percent of cases of gastroenteritis in adults are

Noroviruses can be transmitted and infect individuals by

o contaminated food and liquids,

o direct contact with an infected individual (for example, exposure to

o exposure to infected individuals and objects in daycare centers and

Other viruses that cause gastrointestinal symptoms include:

• Adenoviruses - This virus most commonly causes respiratory illness;

• Parvoviruses - The human bocavirus (HBoV), which can cause gastroenteritis

• Astroviruses - Astrovirus infection is the third most frequent cause of

Bacteria may cause gastroenteritis directly by infecting the lining of the

Escherichia coli infection can cause significant complications. E. coli

Salmonella, Shigella and Campylobacter

Salmonella, Shigella and Campylobacter are also common causes of illness.

• Salmonella is contracted by ingesting the bacteria in contaminated food or

• Campylobacter occurs by the consumption of raw or undercooked poultry

Clostridium difficile (C difficile) bacteria may overgrow in the large intestine

Other risk factors for C difficile infection are hospitalization, individuals 65

Parasites and Protozoans

These tiny organisms are less frequently responsible for intestinal

III. Mode of Transmission

Acute gastroenteritis is predominantly spread via the faecal-oral route.

IV. Medical Management

Hospitalization. Hydration through intravenous line. Replacement of fluid losses

Medical – Surgical Nursing (Clinical Management for Positive Outcomes) 8th

I. Brief Background of the Disease

Acute pyelonephritis is a potentially organ- and/or life-threatening infection

Diagnosing and managing acute pyelonephritis is not always

A number of studies using immunochemical markers have shown that

II. Etiologic Factor/ Agent

Most cases of "community-acquired" pyelonephritis are due to bowel

Risk is increased in the following situations:

• Mechanical: any structural abnormalities to the kidneys and the urinary

III. Medical Management

As practically all cases of pyelonephritis are due to bacterial

Intravenous fluids may be administered to compensate for the reduced

In recurrent infections, additional investigations may identify an underlying

Some recommend other nutritional approaches to prevent recurrence of

IV. Nursing Management

VI. Pathophysiology (please refer to the next page)

Medical – Surgical Nursing (Clinical Management for Positive Outcomes) 8th