CHAPTER II

THEORITICAL BACKGROUND

2.1 Theotical Review Of head injury

2.1.1 Anatomy And Physiologi Of Brain

Gambar 2. 1 Anatomy of Brain

(Sumber: http//tfakhrizalspd. Wordpress.com, diakses tanggal 15 juni 2010 pukul 20.00 Wita)

Otak dibagi dua bagian yaitu otak besar dan otak besar (serebrum) dan otak kecil

(serebelum). Otak besar terdiri dari lobous frontalis, lubos parientalis, lobus

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oksipitalis dan lobus temporalis. Permukan otak bergelombang dan berlekuk-lekuk

membentuk seperti sebuah lekukan yang disebut girus (Muttaqin, 2008: 26)

Ada 4 macam lobus otak besar terdiri dari :

Lobus Frontal

Lobus frontal merupakan lobus terbesar yang terletak pada fosa anterior. Area ini

mengontrol perilaku individu, membuat keputusan, kepribadian, dan menahan diri.

Lobus Pariental

Lobus Parieal disebut juga lobus sensorik. Area ini menginterpretasikan sensasi rasa

yang tidak berpengaruh adalah bau. Lobus pariental mengatur individu untuk

mengetahui posisi dan letak bagian tubuhnya.

Lobus Temporal

Lobus temporal berfungsi mengintegrasikan sensasi pengecap, penciuman

pendengaran dan memori jangka pendek.

Lobus Oksipitalis

Lobus oksipitalis terletak pada lobus posterior hemisfer serebri. Bagian ini

bertanggung jawab menginterprestasikan penglihatan.

2.2 Definition

Menurut A. Grace dan Neil R. borley (2007:71) cedera kepala merupakan proses

dimana terjadi trauma langsung terhadap kepala yang menyebabkan kerusakan

tengkorak dan otak.

Arif Muttaqin (2008:280) cedera kepala merupakan suatu gangguan traumatic dari

fungsi otak yang di sertai atau tanpa disertai perdarahan dalam subtansi otak tanpa di

ikuti terputusnya kontinuitas otak.

Fransisca B. Batticaca (2008:96) Trauma atau cedera kepala juga dikenal sebagai

cedera otak adalah gangguan fungsi normal otak karena trauma tumpul maupun

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trauma tajam. Deficit neurologi terjadi karena robeknya substansia alba, iskemia,

dan pengaruh massa karena hemoragik, serta edema serebral di sekitar jaringan otak.

Head injury can be defined as any alteration in mental or physical functioning

related to a blow to the head. Loss of consciousness does not need to occur. The

severity of head injuries is most commonly classified by the initial postresuscitation

Glasgow Coma Scale (GCS) score, which generates a numerical summed score for

eye, motor, and verbal abilities. Traditionally, a score of 13-15 indicates mild injury,

a score of 9-12 indicates moderate injury, and a score of 8 or less indicates severe

injury. In the last few years, however, some studies have included those patients

with scores of 13 in the moderate category, while only those patients with scores of

14 or 15 have been included as mild. Concussion and mild head injury are generally

synonymous (Stein SC. Minor head injury: 13 is an unlucky number. J Trauma. Apr

2001;50(4):759-60).

A head injury is any trauma that leads to injury of the scalp, skull, or brain. The

injuries can range from a minor bump on the skull to serious brain injury.

Head injury is classified as either closed or open (penetrating). A closed head injury

means you received a hard blow to the head from striking an object, but the object

did not break the skull.

An open, or penetrating, head injury means you were hit with an object that broke

the skull and entered the brain. This usually happens when you move at high speed,

such as going through the windshield during a car accident. It can also happen from

a gunshot to the head (Heegaard WG, Biros MH. Head. In: Marx J. Rosen’s

Emergency Medicine: Concepts and Clinical Practice. 7th ed. St. Louis, Mo: Mosby;

2009:chap. 38.).

From the definition above can be concluded that head injury is a traumatic disruption

of brain function that causes damage to the skull and is the leading cause of death.

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2.3 Etiology

Menurut Arif muttaqin (2008: 271) penyebab cedera kepala adalah adanya

trauma pada kepala meliputi trauma oleh benda/serpihan tulang yang

menembus jaringan otak.

Sedangkan menurut Cholik Harun dan Saifu Nurhidayah (2009:49) etiology cedera

kepala adalah: kecelakaan lalu lintas, jatuh, pukulan, kejatuhan benda, cedera lahir

dan luka tembak.

It can be concluded etiology of head injury is a direct trauma to the head or was

injured at birth.

Menurut Arif Mansjoer, (2002: 3) cedera kepala dapat diklasifikasikan berdasarkan

mekanisme terjadinya, tingkat keparahan dan marfologi cedera.

a. Mekanisme terjadinya cedera

1. Trauma tumpul

a) Kecepatan tinggi contohnya tabrakan.

b) Kecepatan rendah contohnya terjatuh, dipukul

b. Tingkat keparahan cedera

Berdasarkan tingkat keparahan cedera kepala, dapat dinilai dari Glaslow Coma

Scale (GCS):

1) Cedera kepala ringan :

a) Skor skala koma Glaslow 14-15 (radar penuh, atentif, dan orientatif)

b) Tidak ada intoksikasi alcohol atau obat terlarang

c) Klien dapat mengeluh nyeri kepala dan pusing

d) Klien dapat menderita abrasi, laserasi, atau hematoma kulit kepala

e) Tidak adanya criteria cedera sedang-berat

2) Cedera kepala sedang :

a) Skor skala koma Glaslow 9-13 (konkusi, letargi, atau stupor)

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b) Konkusi

c) Amnesia pasca trauma

d) Muntah

e) Tanda kemungkinan fraktur cranium (tanda Battle, mata rabun,

hematimpanum, otorea atau rinorea cairan serebrospinal)

f) Kejang

3) Cedera kepala berat :

a) Skor skala koma Glaslow 3-8 (koma)

b) Penurunan derajat kesadaran secara progresif

c) Tanda neurologis fokal

d) Cedera kepala panetrasi atau teraba fraktur depresi cranium

c. Moorfologi cedera

1. Fraktur tengkorak

a) Cranium: linear atau stelatum, depresi atau non depresi, terbuka atau

tertutup.

b) Basis dengan atau tanpa kebocoran cairan serebrospinal dengan atau

tanpa kelumpuhan nervus VII.

2. Lesi intracranial

a) Focial: epidural, subdural, intraserebral.

b) Difus: konkusi ringan, konkusi klasik, cedera aksonal difus.

c) Tidak ada kehilangan kesadaran (misalnya konkusi)

d) Tidak ada intoksikasi alcohol atau obat terlarang

e) Klien dapat mengeluh nyeri kepala dan pusing

f) Klien dapat menderita abrasi, laserasi atau hematoma kulit kepala

g) Tidak adanya criteria cedera sedang-berat

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Menurut Arif Muttaqin, (2006: 124). Tipe trauma kepala adalah:

1. Trauma kepala terbuka

Kerusakan otak dapat terjadi bila tulang tengkorak masuk ke dalam jaringan otak

dan melukai atau merobek durameter yang menyebabkan CSF merembes.

Kerusakan saraf otak dan jaringan otak.

2. Trauma kepala tertutup

Dapat mengakibkan kondisi komosio, kontosio, hematom epidural, hematom

subdural, hematom intracranial.

Komosio/geger otak dengan tanda-tanda :

1. Cedera kepala ringan

2. Disfungsi neurologis sementara dan dapat pulih kembali

3. Hilang kesadaran sementara, kurang dari 10-20 menit

4. Tanpa kerusakan otak permanen

5. Muncu gejala nyeri kepala, pusing, muntah

6. Disorientasi sementara

7. Tidak ada gejala sisa

8. Tidak ada terapi khusus

Komosio cerebri memar otak, dengan tanda-tanda :

1. Ada memar otak

2. Perdarahan kecil local/difus dengan gejala adanya gangguan local kecil dan

adanya perdarahan, gejala :

Gangguan kesadaran lebih lama

Kelainan neurologic positif

Reflek patologik, positif, lumpuh, konvulsi

Amnesia retrograde lebih nyata

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2.4 Patofisiogi

Mekanisme cedera memegang peranan yang sangat besar dalam menentukan berat

ringannya konsekuensi patofisiologi dari trauma kepala. Cedera percepatan

(aselerasi) terjadi jika benda yang sedang bergerak membentur kepala yang diam,

seperti trauma akibat pukulan benda tumpul, atau karena kena lemparan benda

tumpul. Cedera perlambatan (deselerasi) adalah bila kepala membentur objek yang

secara relative tidak bergerak, seperti badan mobil atau tanah. Kedua kekuatan ini

mungkin terjadi secara bersamaan bila terdapat gerakan kepala tiba-tiba tanpa

kontak langsung, seperti yang terjadi bila posisi badan diubah secara kasar dan

cepat. Kekuatan ini biasa dikombinasi dengan perubahan posisi rotasi pada kepala

yang menyebabkan trauma regangan dan robekan pada substansi alba dan batang

otak.

Cedera primer yang terjadi pada waktu benturan, menyebabkan memar pada

permukaan otak, laselerasi substansi alba, cedera robekan atau hemoragi. Sebagai

akibatnya, terjadi cedera sekunder yang menyebabkan berkurangnya kemampuan

autoregulasi serebral pada area cedera bahkan tidak ada sama sekali. Akbatnya

terjadi hyperemia (peningkatan volume darah) pada area peningkatan permeabilitas

kapiler, serta vasolidasi arterial, menimbulkan peningkatan isi intracranial dan

akhirnya meningkatkan tekanan intracranial. Beberapa kondisi yang dapat

menyebabkan cedera otak sekunder meliputi hipoksia, hiperkarbia, dan hipotensi.

Ketiga hal tersebut menyebabkan penurunan kesadaran, sesak nafas dan pusing.

Penurunan kesadaran mengakibatkan perubahan persepsi sensori, gangguan nutisi

dan gangguan personal hygiene. Pusing dapat mengakibatkan gangguan perfusi

jaringan dan keterbatasan aktivitas. Sedang sesak nafas menyebabkan pola nafas

menjadi tidak efektif. (Hudak, 2002:226)

Classification of head injury: minor head injury GCS 15-13, loss of concsiousness

less than 30 minutes, moderate head injury: GCS between 9-12loss of concsiousness

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between 30 minute until 24 hours and mayor head injury: GCS between 3-8, loss of

concsiousness more than 24 hours

2.5 Sign And Symptom

Menurut Cholik harun Rosjidi dan Saiful Nurhidayah (2009:56) gejala cedera kepala

adalah; pasien sadar akan mengeluh nyeri kepala, muntah bersifat projektif,

kesadaran menurun, perubahan tipe pernafasan, tekanan darah menurun, bradikardi,

suhu tubuh yang sulit di kendalikan.

Menurut Tarwoto, et. al (2007:285) secara umum tanda dan gejala pada cedera

kepala meliputi ada atau tidaknya fraktur tengkorak, tingkat kesadaran dan

kerusakan jaringan otak.

Menurut Fransisca B. Batticaca, (2008: 96)

Gejala-gejala yang timbul bergantung pada jumlah dan distribusi cedera otak. Nyeri

yang menetap atau setempat, biasanya menunjukkan adanya fraktur, sehingga

penegakkan diagnosis dapat dilakukan dengan pemeriksaan foto tengkorak. Fraktur

dasar tengkorak cenderung melintas sinus paranasal pada tulang prontal atau lokasi

tengah telinga di tulang temporal, perdarahan sering terjadi dari hidung, faring, atau

telinga dan darah terlihat di bawah konjungtiva. Suatu area ekomosis mungkin

terlihat di atas mastoid.

Fraktur dasar tengkorak dicurigai ketika cairan serebrospinal (CSS) keluar dari

telinga (otore serebrospinal). Keluarnya CSS merupakan masalah serius karena

dapat menyebabkan infeksi seperti meningitis, jika organisme masuk kedalam basis

kranii melalui hidung, telinga, atau sinus melalui robekan pada dura meter. Laserasi

atau kontusio otak ditnjukkan oleh CSS yang mengandung darah.

We know that signs, symptoms of head injury is that there is a skull fracture and

changes in vital signs and a decreased level of consciousness.

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2.6 Treatment

Menurut Tarwonto,et.al (2007:280) pengobatan pasien cedera kepala adalah:

Diuretik, Antikonvulsan, Kortikosteroid, Antagonis histamin, Antibiotik.

Menurut Cholik Harun Rosjidi dan Saiful Nurhidayat (2009:97) obat yang sering

digunakan adalah: Manitol intravena, Steroid, Terapi koma serta Antipiretik untuk

mencegah demam

We understand that treatment to head injury are diuretics, anticonvulsants,

corticosteroids, and antibiotics.

2.7 Diagnostic Examination

Menurut Arif Muttaqin (2008:284) pemeriksaan diagnostik pada pasien cedera

kepala adalah: CT scan (dengan/tanpa kontras)/MRI: Celebral Angiograpy, Serial

EEG, BEAR: PET, Kadar elektrolit Rontgen thorak 2 arah, thoaksentetis, analisa gas

darah

Menurut Tarwoto,et.al (2007:288) tes diagnostik untuk pasien cedera kepala adalah:

Foto tengkorak: mengetahui adanya fraktur tengkorak, Foto servikal: mengetahui

adanya fraktur servikal, CT-scan / MRI, serum alkohol dan serum obat, Pemeriksaan

obat dalam urine

From that definition we know the diagnostic examinations to head injury are CT-

scan, EKG, electrolyte level and x-ray

2.8 Prognosis

Menurut Pierce A.Grace dan Neil R.Borley (2007:93) Prognosis yang berhubungan

dengan derajat kesadaran saat tiba di rumah sakit adalah: jika GCS saat tiba maka

mortalitasnya 1%, 8-12 : 5%, dan kurang dari 8 : 40%

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Menurut dr. George,at,al (2009:19) pasien dengan GCS yang rendah pada 6-24 jam

setelah trauma, prognosisnya lebih buruk dari pada pasien dengan GCS 15

The conclusion of the prognosis is a client with low GCS experiencing a high

mortality.

2.9 Complication

Komplikasi yang terjadi pada cedera kepala menurut Tarwoto,et,al (2007:290)

adalah: Kejang, pnemonia, perdarahan gastrointestinal, disritmia jantung, kerusakan

kontrol respirasi.

Komplikasi cedera otak menurut Cholik harun rosjidi dan Saiful Nurhidayah

(2008:84) adalah: edema pulmonal, kejang, kebocoran cairan serebrosfinal.

It can be concluded that the complications of head injury is seizures, bleeding,

pulmonary edema, damage control respiration.

2.10 Theoritical Review Of Nursing

Assesment

Menurut Arif muttaqin (2008: 276-277)

Keadaan Umum

Pada keadaan cedera kepala umumnya mengalami penurunan kesadaran (cedera

kepala ringan/cedera otak ringan, GCS 13-15, cedera kepala sedang GCS 9-12,

cedera kepala berat/cedera otak berat, bila GCS kurang atau sama dengan 8) dan

terjadi perubahan pada tanda-tanda vital.

Riwayat Penyakit Sekarang

Adanya riwayat trauma yang mengenai kepala akibat dari kecelakaan lalu lintas,

jatuh dari ketinggian, dan trauma langsung ke kepala. Pengkajian yang didapat

meliputi tingkat kesadaran (GCS <15), konvulsi, muntah, takipnea, sakit kepala,

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wajah simetris atau tidak, lemah, luka dikepala, paralisis, akumulasi secret pada

saluran pernafasan, adanya liquor dari hidung dan telinga, serta kejang,. Adanya

penurunan atau perubahan pada tingkat kesadaran dihubungkan dengan perubahan di

dalam intracranial, keluhan perubahan perilaku juga umum terjadi. Sesuai

perkembangan penyakit, dapat terjadi letargi, tidak responsive, dan koma. Perlu

ditanyakan pada klien atau kelurga yang mengantar klien (bila klien tidak sadar)

tentang penggunaan obat-obatan adiktif dan penggunaan alcohol yang sering terjadi

pada beberapa klien yang suka ngebut-ngebutan.

Riwayat Penyakit Dahulu

Pengkajian yang perlu ditanyakan meliputi adanya riwayat hipertensi, riwayat cedera

kepala sebelumnya, diabetes mellitus, penyakit jantung, anemia, penggunaan obat-

obatan antikoagulan, aspirin, vasodilator, obat-obat adiktif, konsumsi alcohol

berlebihan.

Riwayat Penyakit Keluarga

Mengkaji adanya anggota generasi terdahulu yang menderita hipertensi dan diabetes

mellitus.

According to Tarwoto,el,al (2007)

Activity and Rest

Symtoms: Weakness, fatique, loss of balance.

Signs: A change of conciousness, way of walking was straight

1. Circulation

Symptoms: Hypertension, Badycardia, Tachycardia

2. Ego Integrity

Symptoms: Change in behavior or personality

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Signs: Anxiety, irritability, confusion, and depression

3. Elimination

Symptoms: Incontinence of bledder/bowel or malfunctioning of food/fluid,

nausea, vomiting, and experiencing changes in appette

Signs: vomiting, swallowing disorders cough, spit out, dysphagia

4. Neurosensori

Symptoms: loss of consciousness while, hearing loss, changes in vision, loss of

some field of vision, taste disturbances

Signs: a changes of consciousness can be up to coma, altered mental status, loss

of sensing and hearing, loss of sensation in part of the body, difficulty in

determining the position of the body

5. Pain

Symptoms: headache with an intensity and a different location, usually long

Signs: interesting response to the excitatory severe pain, anxiety, could not rest

6. Respiratory

Signs: changes in breathing pattern, Wheezing, stridor, ronchi, wheezing

7. Security

Symptoms: New Trauma/trauma due to accidents

Signs: A fracture/dislocation, visual disturbances, skin lacerations, discoloration,

such as raccoon eye, batle marks around the ears (a sign of taruma), presence of

fluid flow (drainage from the ear/nose dating cerebrospinal (CSS) muscle tone is

lost.

o Social Interaction

Signs: Afasia motorik or sensory without meaning talking, repeatly. It can be

concluded that data on the patients studied are: The identity of the patient and

responsible, a history of past events, history of head injury incidence, the use

of alcohol and drugs and themain complaints of clients.

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Than we uderstand that data on patients are: The identity of the patient and

responsible, a history of previous disease, history of head injury incidence, the

use of alcohol and drugs and the main complaints of clients.

2.11 Diagnosis And Nursing Intervention

According to Doengoes, M, E (2006) Nursing Care Plan

1. Acute pain related to tissue trauma secondary muscle spasma rifleks.

a. Explain and help clients with pain relief measures and non-invasive

nonfarmakologi .

Rational: the approach by using relaxation and other nonfarmakologi showed

effectiveness in reducing pain.

b. Teach relaxation techniques to reduce muscle tension frame, which can reduce

pain intensity and also increase relaxation massage.

Rational: will the blood circulation so that the needs of O2 by the network will

met and will reduce the pain.

c. Teach distraction for acute pain.

Rational: the pain is to distract the fun stuff.

d. Give a break when the pain the pain and give a comfortable position such as

when sleeping, a small pillow place behind it.

Rational: break will relax all of network so that it will increase the comfort

e. Increase knowledge of the causes of pain in connect some pain will last a long

time.

Rational: the knowledge that will help reduce the pain felt. And can help

develop client adherence to therapeutic plan.

f. Observation of the client’s pain and motor responses, 30 minute after

administration of analgesic drugs to assess theireffectiveness as will as every 1-

2 hour after a maintenance action for 1-2 days.

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Rational: optimal assessment will provide objective data the nurse to prevent

possible complications and appropriate intervention.

g. Collaboration with physicians, giving analgesics.

Rational: analgesic block the path of pain, so pain will be reduced

2. Nutrition less than body requirements related to changes in the ability to digest

food, increased metabolic needs.

a. Independent

Evaluate client’s ability to eat

Rational: the client with a tacheostomy tube may be difficult to eat, but the

client with endotracheal tube or hose can use mag diet parenteral member.

b. Observation/body weigh if possible.

Rational: signs of weigh loss (7-10%) and lack of nutritional intake to support

the problem catabolism, giycogen content in muscle, and sensitivity to the

ventilator.

c. Monitor the state of the decreased muscle subcutaneous fat loss.

Rational: showing lack of muscle energy and reduce the function of respiratory

muscles.

d. Note the oral intake if indicated, encourage clients to eat.

Rational: apetite is usually dimished and incoming nutrients were reduced,

encourage clients to choose food that are liked to eat (when the recommended).

e. Provide snacks and soft

Rational: prevent the occurrace of fatigue, facilitate the entery of food, and

prevent disorders of the stomach.

f. Review the gastroentistinal system including bowel sound, record changes and

the gut such as nausea, vomiting, observed changes in bowel movement, such as

diarrhea, constipation.

Rational: the function of gastrointestinal system are very important to include

food. Ventilator can cause bloating in the stomach and gastric beeding.

g. Collaboration

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Adjust diet according to a given client situation.

Rational: a diet high in calories, protein, carbohydrates are needed for

installation ventilator to maintain the function of the mscles of respiration,

carbohydrates can be reduced and increased use of fat to prevent the production

of CO2 and setting the rest of the respiration.

h. Encourage fluids 2500cc/day for hert problems do not occur

Rational: prevent dehydration due to the use of a ventilator during the

unconscious and prevent constipation.

i. Perform laboratory tests are indicated as serum, BUN/creatine and glucose

Rational: provides precise information about the state of the nutrients it needs

clients.

3. Ineffective breating pattern related to respiratory depression in the center of the

brain.

a. Calculate the patient’s breathing a minute.

Rational: rapid breathing of the patient may cause respiratory alkalosis and

breathing slowly increase the pressure Pa Co2 and cause respiratory acidosis.

b. Check the mouthing tube.

Rational: to provide adequate ventilation in the delivery of tidal volume.

c. Observation ratio of inspiration in inspiratory phase is usually 2 times longer

than inspiration.

d. Check the ventilator hose every time (15 minutes).

Rational: obstruction can lead to inadequate drainage and cause the volume of

air distribution is inadequate

e. Consider the patient’s state of humidity and temperature of dehydration can

drain the secretions/fluids so that the lungs becomes thick and increase the risk

of infection.

4. Disruption of brain tissue perfusion in relation to brain edema.

a. Monitor and record neurological status using the GCS.

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Rational: eye-opening reflex recovery determines the level of consciousness,

motor response determines the capability to respond to external stimuli and

indications of a good state of consciousness.

b. Monitor vital signs.

Rational: increased systolic and diastolic decline and decreased level of

consciousness and signs of increased intracranial pressure. The existence of an

irregular respiratory indications of an increase in metabolism in response to

infection.

c. Maintain the head position parallel to and not pressing.

Rational: changes in the head on one side can head to anempasis o the jugular

vena and impede cerebral blood flow, for it can increase intracranial pressure.

d. Avoid excessive coughing, vomiting, straining, keep the urine measurements

and avoid prolonged constipation.

Rational: can trigger the automatic response of intracranial pressure.

e. Observe the seizure and protect patients from injury due to seizures.

Rational: seizures occur due to irritation of the brain, hypoxia, and seizures may

increase intracranial pressure.

f. Provide O2 according to the patient’s condition.

Rational: can decrease brain hypoxia.

g. Give the indicated drugs appropriately and correctly (collaboration).

Rational: help reduce intracranial pressure in biology/chemistry such as asmotic

diuretic to draw water from brain cells so it can reduce brain edem.

5. Limitations of activities related to loss of consciousness.

a. Give assistance to meet hygiene .

Rational: personal hygiene, elimination, dressing, bathing, cleaning ayes and

nail, is a basic need for comfort that must be kept by the nurse to increase

comfortable, prevent infection and beauty.

b. Provide assistance to meet the need of nutrition and fluids.

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Rational: food and drink are daily necessities that must be met in order to

maintain the continuity of energy acquisition.

c. Provide assistance to met hygiene and environmental safety.

Rational: a clean environment can prevent infections and accidents.

d. Explain to the family of measures that can be done to keep the environment safe

and clean.

Rational: family participation is required to maintain client relationships-family.

6. High risk of disruption of skin integrity related to immobilization, inadequate

peripheral circulation.

a. Assess motor and sensory function and peripheral circulation of patient.

Rational: to establish the possibility of blisters on the skin.

b. Assess the patient’s skin palpation in depressed area

c. Give the anatomical position in attitude and use the foot for areas that standout

d. Changes the position of the patient every 2 hour

Rational: prevent the decubitus

e. Maintain cleanliness and dryness of patient.

Rational: state of moisture will facilitate the occurrence of skin damage.

f. Give the skin treatment on impaired area.

Rational: prevent the infections and inflammation.

7. Family anxiety related to patient’s crisis condition.

a. Construct a trusting relationship.

Rational: to foster relationships therapeutic between nurse and family.

b. Give explanation of all procedures and actions to be performed on patient’s.

Rational: explanation will reduce the anxiety caused by ignorance.

c. Provide opportunities for families to meet with client.

Rational: maintaining patient and family relationships.

d. Provide spiritual encouragement for the family.

Rational: religious zeal can reduce anxiety and increase the faith and

steadfastness in the face of crisis.

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2.12 Evaluation

1. Acute pain related to tissue trauma secondary muscle spasma rifleks.

Evaluation: The patient is able to demonstrate 3x24 hour pain decreased or

Disappeared.

2. Nutrition less than body requirements related to changes in the ability to digest

food, increased metabolic needs.

Evaluation: understand the importance of nutrition for the body, show weight in

accordance with the results of laboratory tests.

3. Ineffective breathing pattern related to respiratory depression in the center of the

brain.

Evaluation: The use to respiratory muscle aids did not, no cyanosis or signs of

hypoxia there was no blood and gas within normal limits.

4. Disruption of brain tissue perfusion in relation to brain edema.

Evaluation: Maintain and improve the level of awareness of motor function.

Evaluation: Stable vital signs, no increase in intracranial.

5. Limitations of activities related to loss of consciousness

Evaluation: Patien’s basic needs can be met adequately.

6. High risk of disruption of skin integrity related to immobilization, inadequate

peripheral circulation.

Evaluation: Impaired skin integrity is not happen.

7. Family anxiety related to patient’s crisis condition.

Evaluation: Family anxiety may decreased.

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