CLIENT PROFILE

HOSPITAL. : Caraga Regional Hospital

NAME OF PATIENT. : Patient “P”
AGE. : 11 years old
SEX. : Female
BIRTHDATE. : April 10, 2012
NATIONALITY. : Filipino
EDUCATIONAL ATTAINMENT. : Elementary Level
ADDRESS. : P2, Villafranca, Gigaquit, SDN
RELIGION. : Roman Catholic
HEIGHT. : 141cm
WEIGHT. : 29kgs

ADMISSION DATA

ADMITTING DUE DATE I TIME : September 6 , 2023 / 12: 37 PM

ADMITTING PHYSICIAN. : Janna Beatriz A. Marcon, M.D.
CHIEF COMPLAINT. : intermittent Ferer & 2 months
ADMITTING DIAGNOSIS. : T/ C Rheumatic FEVER;
R/O SEPSIS

BRIEF HISTORY OF PRESENT ILLNESS:

2 months PTC; onset of intermittent fever associated with joint pains no other S /sx. Persistent
prompted consult at OPD and was advised admission.

REVIEW OF SYSTEM

GENERAL PHYSICAL SURVEY

Patient lies on bed wearing black shirt and red pants. Patient shows presence of weary eyes,
she’s been experiencing unexplained or on going headache sometimes. Patient stands 141cm
and weighs 29 kg. Her BMI is 14.59,which is underweight. Vital signs are the following:
Temperature of 36.4°c; Pulse rate of 116 bpm; Respiratory rate of 22 cpm.
Physical Assessment- Pedia
Skin, Hair, Nails Assessment
Skin
Upon inspection, the patient is healthy with no different color and invisible skin turgor.

Hair and Scalp

The patient,s hair is black and long,evenly distributed. Healthy and clean hair, no presence of
dandruff observed, and no lice were noted.

Nails
Trimmed nails, thick but blueish in color upon inspection.

Head and Neck Assessment

The patient’s head and face are symmetrical and round. No presence of lumps, masses or
lesions was noted upon palpation. Pulses are present at both carotid arteries located at the left
and right side of the neck below the jaw.

Eye Assessment
The sclera of the patient is white. Her pupil is black and equal in size and reactive to light.
Blinking is symmetrical. But weary eyes in appearance were observed.

Ear Assessment
Ears are equal in size and similar in appearance. The auricles are symmetrical and uniform in
color with her facial skin. No presence of discharges was noted,but slightly clean and can not
hear due to a strong side effects of medication.

Nose and Sinuses Assessment

Upon inspection, nasal flaring is not observed. The patient’s nose appeared symmetric and like
the color of her face. No presence of discharges was noted. No nodules, masses, or pain were
noted during palpation.

Mouth and Pharynx Assessment

The patient’s lips were pale. No lesions or inflammation were noted on her gums. The tongue is
symmetrical but pale was noted during the inspection. She can move her tongue from side to
side up and down. Tonsils are present without edema, enlargement, or inflammation.

Cardiac Assessment
The patient’s blood pressure is 80/60mmHg. The midclavicular line in the 5 th intercostal space is
flat. The heart rate is 116 beats per minute upon auscultation.

Peripheral Vascular System Assessment

Arms are equal in size and symmetrical. Skin is warm to touch. Radial and brachial pulses are
palpable upon palpation. Legs upon inspection, the lower extreme ties of the patient are
symmetrical in length. No scars were noted, but unable to walk due to joint pain. Femoral,
popliteal, posterior tibial pulses are palpable.

Thorax and Lung Assessment

Anterior chest upon inspection, patient does not feel difficulty during inhalation and exhalation.
Upon palpation, no tenderness was noted. Patient respiratory rate is 22cycle per minute. The
chest expansion is symmetrical, no thorax deformities or masses, upon palpation.
Abdominal Assessment
Upon inspection, the patient abdomen is flat, symmetrical with no bulging, swelling,
discouloration. Skin intact.Bowel sound are absent upon auscultation.

Musculoskeletal Assessment
No deviation, inflammation, or bony deformities. Can move shoulders and head to right and left
without difficulty.

Genitourinary- Reproductive Assessment

No presence of pain during urination as verbalized by the patient. Patient’s verbalized
frequency of urination, voiding every hour.

Neurologic Assessment
Patient “P” awake and conscious with eyes open and looking at the examiner. She’s not
responds sometimes due to, cannot hear us because of the strong side effects of antibiotic
intake. She shows expressions relevant to her mood. Patient “P” ii conscious, oriented, and
aware of place, time, and people.
 GENOGRAM

HYPERTENSIO CYSTS DIABET

SURGER HEALTHY TIS
N
Y

HEALTH
Y

GRANDFATHER

GRANDMOTHER

MOTHER

FATHER

PATIENT

-BROTHER

SISTER
 ANATOMY AND PATHOPHYSIOLOGY OF RHEUMATIC FEVER

The heart is a fist-sized organ that pumps blood throughout your body. It’s the primary organ of your
circulatory system.

The heart is an organ made up mostly of muscle, and it plays a vital role in keeping you and your body
healthy and strong.

The human heart is one the most important organs of the body that is essential for survival. It is part of
the circulatory system, which is the body system that carries blood and other substances to and from
the heart. The other main parts of the circulatory system are blood vessels, which include veins, arteries,
and capillaries. And the heart beats automatically because it’s controlled by the autonomic nervous
system. In 24 hours, your heart averages about 115,000 beats per day!

So how does the heart work exactly? Well, the heart consists of left and right ventricles at the bottom
and left and right atriums at the top. Blood pushes through the atriums into the ventricles on each side
of the heart through little “gates” every time the heart beats. These gates basically help ensure the
blood flows in the right direction. The blood travels through the different vessels throughout the rest of
the body.

You can think of blood vessels as little train tracks that carry blood to different parts of the body. The
trip for a single drop of blood throughout the body takes only about a minute.

Blood carries oxygen, food, minerals, and vitamins as well, and all these things help your body move,
grow, and make repairs. In fact, they even help you think!

The stuff in your blood that the body doesn’t need gets set out as waste through the lungs, kidneys, and
liver. To keep your heart healthy, there are a few things you can do. Exercising will help strengthen the
muscles of your heart. Eating fruits and vegetables also helps keep your arteries clear. Drinking plenty of
water is also essential because water makes up about 83% of the heart. If you don’t have enough water,
your heart can become less and less healthy.

Finally, remember to move around. Moving around helps both your body and your mind.
 PATHOPHYSIOLOGY

Predisposing Factors:
Precipitating Factors:
Age: 11 years old ► Strep throat infection
Gender: Female ►Joint pain
Family history of surgical
infection

Rheumatic Fever
Causes: Risk Factors:
►Strep throat ►Environment
►Impetigo Causative Agent: ►Genetic Host
►Sinusitis Group A streptococcus ►Undernutrition
►Ear infection ►Age
►Crowded areas

Signs and Symptoms:

Mode of Transmission:
●Fever
●Fatigue ●Airborne droplets
●Arthritis ●Hand contact w/nasal
●Chest pain discharge
●Contaminated objects
●Contaminated food

Affected organs:
●Joints ●Skin
●Heart ●CNS

Signs and Symptoms

Joints CNS
►Migratory polyathritis ►Sydenham chorea

Heart Skin
►Carditis ►Subcutaneous nodules
►Heart failure ►Erythema marginatum
►Heart murmurs

Diagnostic test
●Modified Jones criteria
●Testing for GAS (culture,rapid
strep test or antistreptolycin O and
anti-Dnase B titers
●ECG
●Echocardiography w/ Doppler
●Erythrocyte sedimentation
rate(ESR)
●C-reactive protein(CRP)level

Medication/Treatment
●Antibiotic
●Aspirin
●Cortecosteroids
 If Treated: If left Untreated:
●Medications ●Rheumatic Heart
●Good Hygiene Disease occur
●Early Detection ●Required Surgery
●Prevent Further

DEATH

LEGEND:
Disease Process
Clinical Manifestations
If Treated
If Left Untreated
Death
Narrative:

Rheumatic fever is a nonsuppurative, acute inflammatory complication of group A streptococcal

pharyngeal infection, causing combinations of arthritis, carditis, subcutaneous nodules,
erythema marginatum, and chorea. Diagnosis is based on applying the modified Jones criteria
to information gleaned from history, examination, and laboratory testing. Treatment includes
aspirin or other nonsteroidal anti-inflammatory drugs, corticosteroids during severe carditis,
and antimicrobials to eradicate residual streptococcal infection and prevent reinfection.

A first episode of acute rheumatic fever (ARF) can occur at any age but occurs most often
between 5 years and 15 years of age, which are the peak years of age for streptococcal
pharyngitis. ARF is uncommon before 3 years and after 21 years. However, preceding
symptomatic pharyngitis is recognized in only about two-thirds of patients with ARF. Group A
streptococcal (GAS) pharyngitis is the etiologic precursor of acute rheumatic fever, but host and
environmental factors are important. GAS M proteins share epitopes (antigenic-determinant
sites that are recognized by antibodies) with proteins found in synovium, heart muscle, and
heart valve, suggesting that molecular mimicry by GAS antigens from rheumatogenic strains
contributes to arthritis, carditis, and valvular damage. Genetic host risk factors include the
D8/17 B-cell antigen and certain class II histocompatibility antigens. Undernutrition,
overcrowding, and lower socioeconomic status predispose to streptococcal infections and
subsequent episodes of rheumatic fever. Remarkably, although GAS infections of both the
pharynx and of other areas of the body (skin and soft-tissue structures, bones or joints, lungs,
and bloodstream) may cause poststreptococcal glomerulonephritis, nonpharyngitis GAS
infections do not lead to ARF.
The reason for this distinct difference in complications resulting from infection by the same
organism is not well understood. The joints, heart, skin, and central nervous system (CNS) are
most often affected. Pathology varies by site.
Joints
Joint involvement manifests as nonspecific synovial inflammation, which if biopsied sometimes
shows small foci resembling Aschoff bodies (granulomatous collections of leukocytes, myocytes,
and interstitial collagen). Unlike the cardiac findings, however, the abnormalities of the joints
are not chronic and do not leave scarring or residual abnormalities ("ARF licks the joints but
bites the heart").
Heart
Cardiac involvement manifests as carditis, typically affecting the heart from the inside out, i.e.,
valves and endocardium, then myocardium, and finally pericardium. It is sometimes followed
years to decades later by chronic rheumatic heart disease, primarily manifested by valvular
stenosis, but also sometimes by regurgitation, arrhythmias, and ventricular dysfunction.
In acute rheumatic fever, Aschoff bodies often develop in the myocardium and other parts of
the heart. Fibrinous nonspecific pericarditis, sometimes with effusion, occurs only in patients
with endocardial inflammation and usually subsides without permanent damage. Characteristic
and potentially dangerous valve changes may occur. Acute interstitial valvulitis may cause
valvular edema.
In chronic rheumatic heart disease, valve thickening, fusion, and retraction or other
destruction of leaflets and cusps may occur, leading to stenosis or insufficiency. Similarly,
chordae tendineae can shorten, thicken, or fuse, worsening the regurgitation of damaged
valves or causing the regurgitation of an otherwise unaffected valve. Dilation of valve rings may
also cause regurgitation.

The rheumatic valvular disease most commonly involves the mitral and aortic valves. The
tricuspid and pulmonic valves are seldom if ever affected in isolation.

In acute rheumatic fever, the most common cardiac manifestations are:

●Mitral regurgitation
●Pericarditis
●Sometimes aortic regurgitation
In chronic rheumatic heart disease, the most common cardiac manifestations are :
●Mitral stenosis
●Aortic regurgitation (often with some degree of stenosis)
●Perhaps tricuspid regurgitation (often along with mitral stenosis)

Skin
Subcutaneous nodules appear indistinguishable from those of juvenile idiopathic arthritis (JIA),
but biopsy shows features resembling Aschoff bodies. Erythema marginatum differs
histologically from other skin lesions with similar macroscopic appearance, eg, the rash of
systemic JIA, immunoglobulin A–associated vasculitis (formerly called Henoch-Schönlein
purpura), erythema chronicum migrans, and erythema multiforme. Perivascular neutrophilic
and mononuclear infiltrates of the dermis occur.

CNS
Sydenham chorea, the form of chorea that occurs with ARF, manifests in the CNS as
hyperperfusion and increased metabolism in the basal ganglia. Increased levels of antineuronal
antibodies have also been shown.

An initial episode of symptoms of rheumatic fever occurs typically about 2 to 3 weeks after the
streptococcal infection. Manifestations typically involve some combination of the joints, heart,
skin, and CNS.

Joints
Migratory polyarthritis is the most common manifestation of acute rheumatic fever, occurring
in about 35 to 66% of children; it is often accompanied by fever. "Migratory" means the
arthritis appears in one or a few joints, resolves but then appears in others, thus seeming to
move from one joint to another. Joints become extremely painful and tender; these symptoms
are often out of proportion to the modest warmth and swelling present on examination (this is
in contrast to the arthritis of Lyme disease, in which the examination findings tend to be more
severe than the symptoms).

Ankles, knees, elbows, and wrists are usually involved. Shoulders, hips, and small joints of the
hands and feet also may be involved, but almost never alone. If vertebral joints are affected,
another disorder should be suspected.

Arthralgia-like symptoms may be due to nonspecific myalgia or tenodynia in the periarticular

zone; tenosynovitis may develop at the site of muscle insertions. Joint pain and fever usually
subside within 2 weeks and seldom last > 1 month.

Heart
Carditis can occur alone or in combination with pericardial rub, murmurs, cardiac enlargement,
or heart failure. In the first episode of acute rheumatic fever, carditis occurs in about 50 to 70%.
Patients may have high fever, chest pain, or both; tachycardia is common, especially during
sleep. Although the carditis of ARF is considered to be a pancarditis (involving the endocardium,
myocardium, and pericardium), valvulitis is the most consistent feature of ARF, and if it is not
present, the diagnosis should be reconsidered. The diagnosis of valvulitis has classically been
made by auscultation of murmurs, but subclinical cases (ie, valvular dysfunction not manifested
by murmurs but recognized on echocardiography and Doppler studies) may occur in cases of
ARF.
Heart murmurs are common and, although usually evident early, may not be heard at initial
examination; in such cases, repeated clinical examinations as well as echocardiography are
recommended to determine the presence of carditis. Mitral regurgitation is characterized by an
apical pansystolic blowing murmur radiating to the axilla. The soft diastolic blow at the left
sternal border of aortic regurgitation, and the presystolic murmur of mitral stenosis, may be
difficult to detect. Murmurs often persist indefinitely. If no worsening occurs during the next 2
to 3 weeks, new manifestations of carditis seldom follow. ARF typically does not cause chronic,
smoldering carditis. Scars left by acute valvular damage may contract and change, and
secondary hemodynamic difficulties may develop in the myocardium without persistence of
acute inflammation.
Pericarditis may be manifested by chest pain and a pericardial rub.
Heart failure caused by the combination of carditis and valvular dysfunction may cause dyspnea
without rales, nausea and vomiting, a right upper quadrant or epigastric ache, and a hacking,
nonproductive cough. Marked lethargy and fatigue may be early manifestations of heart failure.

Skin
Cutaneous and subcutaneous features are uncommon and almost never occur alone, usually
developing in a patient who already has carditis, arthritis, or chorea.
Subcutaneous nodules, which occur most frequently on the extensor surfaces of large joints
(eg, knees, elbows, wrists), usually coexist with arthritis and carditis. Fewer than 10% of
children with acute rheumatic fever have nodules. Ordinarily, the nodules are painless and
transitory and respond to treatment of joint or heart inflammation.
Erythema marginatum is a serpiginous, flat or slightly raised, nonscarring, and painless rash.
Fewer than 6% of children have this rash. The rash usually appears on the trunk and proximal
extremities but not the face. It sometimes lasts < 1 day. Its appearance is often delayed after
the inciting streptococcal infection; it may appear with or after the other manifestations of
rheumatic inflammation.

CNS
Sydenham chorea occurs in about 10 to 30% of children. It may develop along with other
manifestations but frequently arises after the other manifestations have subsided (often
months after the acute streptococcal infection) and thus may be overlooked as an indicator of
acute rheumatic fever. Onset of chorea is typically insidious and may be preceded by
inappropriate laughing or crying. Chorea consists of rapid and irregular jerking movements that
may begin in the hands but often becomes generalized, involving the feet and face.

Diagnosis of Rheumatic Fever

●Modified Jones criteria (for initial diagnosis)
●Testing for GAS (culture, rapid strep test, or antistreptolysin O and anti-DNase B titers)
●ECG Echocardiography with Doppler
●Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level

A preceding streptococcal infection is suggested by a recent history of pharyngitis and is

confirmed by one or more of the following:
●Positive throat culture
●Increased or preferably rising antistreptolysin O titer
●Positive rapid GAS antigen test in a child with clinical manifestations suggestive of
streptococcal pharyngitis
Recent scarlet fever is highly suggestive. Throat cultures and rapid strep antigen tests are often
negative by the time ARF manifests, whereas titers of antistreptolysin O and anti-DNase B
typically peak 3 to 6 weeks after GAS pharyngitis. About 80% of children with ARF have a
significantly elevated antistreptolysin O titer; if an anti-DNase B antibody level is also done, the
percentage with confirmed GAS infection is higher, especially if acute and convalescent samples
are tested.
Joint aspiration may be needed to exclude other causes of arthritis (eg, infection). The joint
fluid is usually cloudy and yellow, with an elevated white blood cell (WBC) count composed
primarily of neutrophils; culture is negative. Complement levels are usually normal or slightly
decreased, compared with decreased levels in other inflammatory arthritides.
ECG is done during the initial evaluation. Serum cardiac marker levels are obtained; normal
cardiac troponin I levels exclude prominent myocardial damage. ECG abnormalities such as PR
prolongation do not correlate with other evidence of carditis. Only 35% of children with ARF
have a prolonged PR interval; higher-degree heart block may occur but is uncommon. Other
ECG abnormalities may be due to pericarditis, enlargement of ventricles or atria, or
arrhythmias.
Echocardiography can detect evidence of carditis even in patients without apparent murmurs
and is recommended for all patients with confirmed or suspected ARF. Echocardiography is also
used to detect subclinical carditis in patients with apparently isolated Sydenham chorea and to
monitor the status of patients with recurrences of carditis or chronic rheumatic heart disease.
However, not all echocardiographic abnormalities represent rheumatic carditis; isolated trivial
valvar regurgitation or trivial pericardial effusion may be a nonspecific finding.
ESR and serum CRP are sensitive but not specific. The ESR is typically > 60 mm/hour. CRP is
typically > 30 mg/L (> 285.7 nmol/L) and often > 70 mg/L (> 666.7 nmol/L); because it rises and
falls faster than ESR, a normal CRP may confirm that inflammation is resolving in a patient with
prolonged ESR elevation after acute symptoms have subsided. In the absence of carditis, ESR
usually returns to normal within 3 months. Evidence of acute inflammation, including ESR,
usually subsides within 5 months in uncomplicated carditis. The WBC count reaches 12,000 to
20,000/mcL (12 to 20 × 109/L) and may go higher with corticosteroid therapy.

Treatment of Rheumatic Fever

●Antibiotics
●Aspirin
●Sometimes corticosteroids
The primary goals of rheumatic fever treatment are eradication of group A streptococcal
infection, relief of acute symptoms, suppression of inflammation, and prophylaxis against
future infection to prevent recurrent heart disease. For general management, patients should
limit their activities if they have symptoms of arthritis, chorea, or heart failure. In the absence
of carditis, no physical restrictions are needed after the initial episode subsides. In
asymptomatic patients with carditis, strict bed rest has no proven value, despite its traditional
usage.

Antibiotic treatment
Although poststreptococcal inflammation is well developed by the time ARF is detected, a 10-
day course of oral penicillin or amoxicillin, or a single injection of benzathine penicillin, is used
to eradicate any lingering organisms and prevent reinfection. For specific regimens, see
treatment of streptococcal pharyngitis. Antibiotic prophylaxis is continued as described below.
Aspirin and other anti-inflammatory drugs
Aspirin controls fever and pain and should be given to all patients with arthritis and/or mild
carditis. Although aspirin has been used for many decades, there are surprisingly few data from
controlled trials to define the optimal dosing schedule. Salicylate toxicity is the limiting factor to
aspirin therapy and is manifested by tinnitus, headache, or hyperpnea; it may not appear until
after 1 week of therapy. Salicylate levels are measured only to manage toxicity. Enteric-coated,
buffered, or complex salicylate molecules provide no advantage. For patients with minimal to
mild carditis, there are no controlled data to suggest that adding prednisone to aspirin therapy
speeds resolution of illness or prevents rheumatic heart disease.
Other nonsteroidal anti-inflammatory drugs (NSAIDs) have been reported in small trials to be
effective; naproxen (7.5 to 10 mg/kg orally 2 times a day) is the most studied. However, other
NSAIDs have few advantages over aspirin, especially in the first week of therapy when salicylism
is uncommon. Acetaminophen is not effective for symptoms of acute rheumatic fever.
Prednisone 1 mg/kg orally 2 times a day (up to 60 mg/day) is recommended instead of aspirin
for patients with moderate to severe carditis (as judged by a combination of clinical findings,
presence of cardiac enlargement, and possibly by severely abnormal echocardiography results).
If inflammation is not suppressed after 2 days or for severe heart failure, an IV corticosteroid
pulse of methylprednisolone succinate (30 mg/kg IV once a day, maximum 1 g/day, for 3
successive days) may be given. Oral corticosteroids typically are given for 2 to 4 weeks and then
tapered over another 2 to 3 weeks. Aspirin should be started during the corticosteroid taper
and continued for 2 to 4 weeks after the corticosteroid has been stopped. Aspirin dose is the
same as above. Inflammatory markers such as Erythrocyte sedimentation rate and C-reactive
protein may be used to monitor disease activity and response to treatment. Recurrences of
mild cardiac inflammation (indicated by fever or chest pain) may subside spontaneously; aspirin
or corticosteroids should be resumed if recurrent symptoms last longer than a few days or if
heart failure is uncontrolled by standard management (eg, diuretics, angiotensin-converting
enzyme inhibitors, beta-blockers, inotropic agents).

Antibiotic prophylaxis
Antistreptococcal prophylaxis should be maintained continuously after the initial episode of
acute rheumatic fever to prevent recurrences. Antibiotics taken orally are slightly less effective
as those given by injection. However, with the oral route, painful injections are avoided, and
clinic visits and observation for postinjection reactions are not needed. The optimal duration of
antistreptococcal prophylaxis is uncertain. Children without carditis should receive prophylaxis
for 5 years or until age 21 (whichever is longer).
 NURSING CARE PLAN 1
Assessment:

Subjective Cues:
“Nagbalik-balik ija hilanat ug pirme nagluja”,as verbalized by the SO.
Objective Cues:
- Fatigue
- Warm skin
V/S taken as follows:
Temp: 38.2C
PR: 130 bpm
RR: 27bpm
BP: 80/60mmHg
02sat: 99%
Diagnosis:
Hyperthermia related to inflammatory process, as evidenced by increasing body temperature

Planning:

After 8 hours of sufficient nursing intervention patient’s core temperature will decrease to 37.5
and maintain it.
Intervention:
Independent:
- Monitor core temperature by appropriate route (Rectal and tympanic route) ; To ensure the
accurate temperature of the patient and to monitor it.
- Monitor Heart rate and rhythm and respiration; To record the abnormalities of his status.
- Monitor and report all sources of fluid losses; To avoid dehydration of the patient.
- Monitor respirations.
- Monitor blood pressure, noting hypotension.
Dependent:
-Administer chlorpromazine or diazepam as ordered by the doctor; To avoid Shivers and
siezures.
-Administer antipyretics, orally or rectally as ordered by the doctor; To avoid liver failure into
pedias.
-Provide supplemental oxygens; to offset increased oxygen demans and consumption.
Collaboration:
Provide High calorie diet, enteral nutrition, or parenteral nutrition ; To meet increased
metabolic demands
Evaluation:
After 8 hours of sufficient nursing interventions the patient’s core temperature was decreased
to 37.5 and maintin it.

NURSING CARE PLAN 2

Assessment:
Subjective:
“Sakit ako mga joints” as verbalized by the patient.
Objective:
- Pain scale: 7/10
- Warm skin
V/S taken as follows:
Temp: 38.2C
PR: 130bpm
RR: 27bpm
BP: 80/70mmHg
02sat: 99%

Diagnosis:

Acute pain on joints related to migratory inflammation of joints.

Planning:
After 8 hours of sufficient nursing intervention patient will report that pain is relieved with
relief on its face and will be scaled to 2/10.
Interventions:
Independent:
-Monitor skin color and temperature and vital signs; which are usually altered in acute pain.
-Determine factors in client’s lifestyle; that can affect responses to analgesics.
-Provide Comfort measures ( Hot and Cold compress) To ease the pain of the patient.
Identify ways to avoid or minimize pain.
Dependent:
- Administer analgesics as indicated to maximun dosage; To maintain acceptable level of pain.
- Note clients attitude toward pain and use of pain medications; Client may have beliefs
restricting use of medications.
Collaboration:
Collaborate in treatment of underlying condition or disease processes causing
Evaluation:
After 8 hours of sufficient nursing intervention patient was reported that pain is relieved and
was be scaled to 2/10.