STANDAR PROSEDUR OPERATIONAL

TANDA TRIAD CHUSING PADA PASIEN KRITIS

OLEH:
NIKMA
R011191040

PROGRAM STUDI ILMU KEPERAWATAN

FAKULTAS ILMU KEPERAWATAN
UNIVERSITAS HASANUDDIN
MAKASSAR
2020
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A. Definisi tekanan intra kranial

Tekanan intrakranial adalah tekanan total yang diberikan oleh otak, darah, dan CSF dalam ruang intrakranial.
Hipotesis Monroe-Kellie menyatakan jumlah volume otak intrakranial (≈80%), darah (≈10%), dan CSF (≈10%)
konstan, dan bahwa peningkatan salah satu dari ini harus diimbangi oleh penurunan yang sama di yang lain, atau
tekanan meningkat. ICP bervariasi dengan usia dan nilai normatif untuk anak-anak tidak ditetapkan dengan baik. Nilai
normal kurang dari 10 hingga 15 mm Hg untuk orang dewasa dan anak-anak yang lebih tua, 3 hingga 7 mm Hg untuk
anak kecil, dan 1,5 hingga 6 mm Hg untuk bayi cukup bulan . Nilai ICP yang lebih besar dari 20 hingga 25 mm Hg
memerlukan perawatan di sebagian besar keadaan. Nilai ICP yang bertahan lebih dari 40 mm Hg menunjukkan
hipertensi intrakranial yang parah dan mengancam jiwa .

B. Penilaian dan pemantauan tekanan intra kranial  

 Mereka yang berisiko lebih besar adalah anak-anak dengan trauma kepala, dugaan infeksi saraf, atau dugaan
lesi massa intrakranial. Tekanan yang meningkat biasanya bermanifestasi sebagai sakit kepala, muntah, lekas marah,
juling, postur tonik atau sensorium yang memburuk. Namun gejalanya tergantung pada usia, penyebab, dan evolusi ICP
yang meningkat. Pemantauan dimulai dengan penilaian dan pemeliharaan jalan nafas, fungsi pernapasan dan sirkulasi.
Prioritas segera adalah mencari tanda-tanda herniasi yang berpotensi mengancam jiwa. Jika tanda-tanda ini hadir maka
langkah-langkah untuk mengurangi tekanan intrakranial harus segera dilakukan.

Cushing'striad (bradikardia, hipertensi dan pernapasan tidak teratur) adalah tanda akhir dari herniasi sehingga
perlu juga dilakukan penilaian terhadap triad chusing ini. Adapun pedoman untuk triad chusing ini dicakupkan pada
pemeriksaan tanda- tanda vital sebagai berikut :
 Standar Operasional Prosedur (SOP)
Pemeriksaan nadi, pernapasan, tekanan darah dan suhu

Definisi Tanda Vital

Merupakan cara yang cepat dan efisien untuk memantau kondisi klien atau mengidentifikasi masalah dan
mengevaluasi respon klien terhadap intervensi. Tanda vital meliputi suhu, denyut nadi, pernapasan dan tekanan
darah.
Tujuan
Pengukuran tanda vital memberi data untuk menentukan status kesehatan klien yang lazim (data dasar), seperti
respon terhadap stres fisik dan psikologis, terapi medis dan keperawatan, perubahan tanda vital dan menandakan
perubahan fungsi fisiologis. Perubahahn pada tanda vital dapat juga menandakan kebutuhan dilakukannya
intervensi keperawatan dan medis
Indikasi/waktu pelaksanaan
1. Ketika klien masuk ke fasilitas perawatan kesehatan
2. Di rumah sakit atau fasilitas perawatan pada jadwal rutin sesuai program dokter atau standar praktik institusi.
3. Sebelum dan sesudah prosedur bedah
4. Sebelum dan sesudah prosedur diagnostik invasif
5. Sebelum dan setelah pemberian medikasi yang mempengaruhi Kardiovaskuler, pernafasan dan fungsi kontrol
suhu.
6. Ketika kondisi umum fisik klien berubah
7. Sebelum dan setelah intervensi keperawatan yang mempengaruhi tanda vital.
8. Ketika klien melaporkan gejala non-spesifik disters fisik.

Pengukuran Nadi

Langkah

Tahap Pra-interkasi A. Persiapan Alat dan Bahan

1. Jam tangan dengan jarum penunjuk detik
2. Stetoskop
3. Kapas alkohol
4. Pena dan lembar dokumentasi

Tahap Orientasi B. Perkenalkan diri

C. Jelaskan tujuan prosedur
D. Jelaskan cara mengukur nadi. Anjurkan klien untuk rilekls
dan tidak bicara. (jika klien baru melakukan kegiatan aktif,
tunggu 5 sampai 10 menit

Tahap Kerja Nadi Perifer

A. Cuci tangan
B. Pilih titik nadi. Biasanya yang digunakan adalah nadi radialis
C. Posisikan klien dengan nyaman.
Jika klien telentang, letakkan tangan bawah menyilangi dada
bawah atau di samping tubuh dengan pergelangan tangan sedikit
fleksi dan telapak tangan menghadap ke bawah. Jika klien
duduk, tekuk siku 90° dan sokong lengan bawah pada kursi.
Fleksikan sedikit pergelangan tangan dengan telapak tangan
menghadap ke bawah
D. Letakkan ujung dua atau tiga jari pertama di atas alur sekitar
bagian radial dengan tidak terlalu kuat. Penggunaan ibu jari
dikontraindikasikan
E. Bila nadi teratur, kaji selama 30 detik kemudian hasilnya
dikalikan 2. Bila tidak teratur, kaji selama 60 detik penuh.
F. Kaji frekuensi, irama dan volume nadi
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G. Bantu klien kembali pada posisi nyaman

H. Catat hasil pada lembar dokumentasi
I. Cuci tangan
Nadi Apikal
1. Jaga privasi
2. Cuci tangan
3. Bersihkan earpiece dan diafragma stetoskop dengan kapas
alkohol bila diperlukan
4. Pada klien dengan posisi telentang atau duduk, turunkan
selimut dan buka pakaian untuk memaparkan strenum dan
bagian kiri dada
5. Letakkan diafragma stetoskop pada impuls apikal dan
dengarkan bunyi jantung normal S1 dan S2 yang terdengar
seperti lup-dub
6. Apabila bunyi jantung teratur, hitung denyut jantung selama
3o detik kalikan 2. Bila tidak teratur, hitung selama 60 detik
7. Kaji frekuensi, irama dan kekuatan denyut jantung
8. Bantu klien kembali ke posisi nyaman dan bantu rapikan
pakaian bila perlu.
9. Catat hasil pada lembar dokumentasi
10. Cuci tangan

Tahap Terminasi 1. Rapikan alat

2. Evaluasi perasaan klien
3. Berpamitan dengan klien

Pengukuran pernapasan

Langkah

Tahap Pra-interaksi A. Persiapan Alat dan Bahan

1. Jam tangan dengan detik
2. Pena dan lembar dokumentasi

Tahap Orientasi B. Perkenalkan diri

C. Jelaskan tujuan prosedur
D. Jelaskan cara pengukuran pernapasan. Bila klien sedang aktif
tunggu 5 sampai 10 menit

Tahap Kerja E. Pasang tirai

F. Cuci tangan
G. Posisikan klien secara nyaman. Duduk atau berbaring dengna
bagian kepala tempat tidur ditinggikan 45 sampai 60 derajat
H. Pastikan gerakan dada klien dapat terlihat. Buka pakaian dari
dada bila perlu
I. Letakkan tanganklien pada posisi rileks yang tidak
menghalangi pandangan terhadap dada klien, atau letakkan
tangan perawata langsung di atas abdomen
J. Observasi siklus pernapasan penuh
K. Jika irama teratur hitung selama 30 detik kalikan 2. Hitung
selama 60 detik bila irama tidak teratur atau pada bayi atau anak
kecil
L. Kaji frekuensi da irama pernapasan
M. Posisikan kembali klien pada posisi yang nyaman
 N. Cuci tangan
O. Catat hasil pada lembar dokumentasi

Tahap Terminasi P. Rapikan alat

Q. Evaluasi perasaan klien
R. Berpamitan dengan klien

Pengukuran Tekanan Darah

Langkah

Tahap Pra-interaksi A. Persiapan Alat dan Bahan

1. sfigmomanometer
2. katung dan manset
3. stetoskop
4. pena dan lembar dokumentasi

Tahap Orientasi B. perkenalkan diri

C. jelaskan tujuan prosedur
D. jelaskan cara pengukuran darah. Anjurkan klien untuk
menghindari kafein dan merokok 30 menit sebelum pengkajian

Tahap Kerja E. pilih manset sesuai ukuran

F. pastikan ruangan tenang
G. cuci tangan
H. posisikan klien dengan nyaman. Duduk atau berbaring,
posisikan beban lengan atas (sokong bila diperlukan) pada
setinggi jantung dengan telapak menghadap atas
I. gulung lengan baju pada bagian atas lengan
J. palpasi arteri brakialis. Letakkan manset 2,5 cm di atas nadi
brakialis
K. dengan manset masih kempis, pasang manset dengan rata dan
pas sekeliling lengan atas.
L. Letakkan manometer sejajar mata. Pengamat tidak boleh
lebih jauh dari 1 meter.
M. Palapsi arteri radialis atau brakialis dengan ujung jari dari
satu tangan sambil menggembungkan manset dengan cepat
sampai tekanan 30 mmHg di atas titik di manadenyut tidak
teraba
N. Kempiskan manset dan tunggu 30 detik
O. Letakkan earpiece stetoskop pada telinga dan pastikan bunyi
jelas.
P. Letakkan diafragma pada arteri brakialis dengan kontak
langsung pada kulit
Q. Tutup katup balon tekanan searah jarum jam sampai kencang
R. Gembungkan manset 30 mmHg di atas tekanan sistolik yang
dipalpasi
S. Dengan perlahan lepaskan dengan kecepatan 2 smapai 3
mmHg per detik
T. Catat titik pada manometer saat bunyi jelas yang pertama
terdengar
U. Lanjutkan mengempiskan manset, catat dimana titik muffled
atau dampened timbul
V. Kempiskan manset dengan segera hingga tuntas
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W. Bantu klien kembali pada posisi nyaman

X. Cuci tangan
Y. Catat hasil pada lembar dokumentasi

Tahap Terminasi Z. Rapikan alat

AA. Evaluasi perasaan klien
BB. Berpamitan dengan klien

Pengukuran Suhu

Langkah

Tahap Pra Interaksi A. Persiapan Alat dan Bahan

1. Termometer
2. Sarung tangan
3. Tissue
4. Kassa
5. Pelumas
6. Bengkok
7. Pulpen
8. Lembar dokumentasi
B. Ketika mengukur suhu oral, tunggu 20 sampai 30 menit
sebelum mengukur suhu, jika klien merokok atau makan atau
minum yang panas atau dingin

Tahap Orientasi C. Perkenalkan diri

D. Menjelaskan tujuan prosedur
E. Menjelaskan bagaimana cara mengukur suhu

Tahap Kerja Suhu Oral

1. Cuci tangan
2. Gunakan sarung tangan
3. Untuk termometer kaca, bila disimpan dalam larutan
desinfektan, cuci dengan air dingin sebelum digunakan
4. Siapkan termometer dengan derajat di bawah 35,5 °C atau
turn on pada termometer elektri
5. Ambil tisu lembut dan lap bagian pentolan termometer
dengan gerakan rotasi. Buang tisu.
6. Minta klien membuka mulut kemudian letakkan ujung
termometer di bawah lidah klien pada sublingual
7. Minta klien menutup mulut
8. Tunggu 3-5 menit atau sampai berbunyi pada termomter
elektrik
9. Ambil termometer dan lepasakan serta buang pembungkus
plastik dan baca hasilnya
10. Lap termometer dengan tisu alkohol kemudian keringkan
dengan kassa. Simpan kembali pada tempatnya
11. Lepaskan dan buang sarung tangan
12. Cuci tangan
13. Catat pada lembar dokumentasi
Suhu Rektal
1. Pasang tirai
2. Cuci tangan
3. Gunakan sarung tangan
4. Lakukan langkah 3-5 seperti sebelumnya
5. Posisikan klien secara sim dengan fleksi kaki bagian atas.
6. Minta klien menurunkan celana dengan hanya memaparkan
area anus atau anal
7. Beri pelumas secukupnya di atas tisu. Lumasi termometer.
8. Dengan tangan non-dominan, regangkan bokong untuk
memaparkan anus
9. Minta klien untuk bernapas perlahan dan rileks
10. Masukkan termometer ke dalam anus, 2,5 – 3,5 cm untuk
dewasa atau 1,2 – 2,5 cm untuk anak-anak. Jangan mendorong
paksa termometer, bila terasa tahanan, tarik segera termometer.
11. Biarkan termometer selama 3 menit atau sampai berbunyi
pada termometer digital
12. Keluarkan termometer dengan hati hati. Lap sekresi dengan
tisu dengan gerakan rotasi daria arah jari ke pentolan. Buang tisu
13. Baca hasilnya.
14. Lap area anal untuk membuang pelumas atau feses
15. Bantu klien kembali pada posisi nyaman
16. Lap termometer dengan tisu alkohol atau basuh dengan air
hangat bersabun, cuci dengan air dingin kemudian keringkan.
17. Buang sarung tangan. Cuci tangan
18. Catat hasil pada lembar dokumentasi
Suhu Aksilla
1. Pasang tirai
2. Cuci tangan
3. Gunakan sarung tangan
4. Posisikan klien secara nyaman, duduk atau berbaring
5. Singkirkan pakaian pada lengan
6. Keringkan daerah aksilla dengan kassa
7. Lakukan langkah 3-5 seperti sebelumnya
8. Letakkan termometer di tengah aksilla, turunkan lengan
menjepit termometer dan letakkan tangan menyilang pada dada
klien.
9. Biarkan termometer 5-10 menit atau sampai berbunyi pada
termometer digital
10. Ambil termometer. Lap dengan tisu dengan gerakan rotasi
11. Baca hasilnya
12. Lap termometer dengan tisu alkohol, lalu keringkan dengan
kassa
13. Bantu klien memasang pakaiannya kembali
14. Buang sarung tangan. Cuci tangan
15. Catat hasil pada lembar dokumentasi
Suhu Timpani
1. Cuci tangan
2. Gunakan sarung tangan
3. Posisikan klien secara nyaman, dengan kepala berpaling ke
satu sisi, menjauhi perawat
4. Siapkan termometer timpani, pasang pembungkis plastik
sekali pakai
5. Tarik cuping telinga ke arah atas dan belakang pada orang
dewasa atau ke arah bawah dan belakang pada anak-anak
6. Arahkan termometer secara perlahan ke sisi anterior menuju
gendang telinga dengan gerakan memutar sampai masuk
7. Tekan tombol aktifkan
8. Tunggu sampai termometer berbunyi atau muncul tanda
cahaya pada termometer
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9. Ambil termometer secara perlahan. buang pembungkus

plastiknya.
10. Baca hasilnya
11. Buang sarung tangan. Cuci tangan
12. Catat hasilnya pada lembar dokumentasi

1. Rapikan alat
2. Evaluasi perasaan klien
3. Berpamitan dengan klien

Tahap terminasi
DOI 10.1007/s12098-010-0190-2
SYMPOSIUM ON PICU PROTOCOLS OF AIIMS
Management of Raised Intracranial Pressure
Naveen Sankhyan & K. N. Vykunta Raju &
Suvasini Sharma & Sheffali Gulati
Received: 3 August 2010 / Accepted: 18 August 2010 / Published online: 7 September 2010
# Dr. K C Chaudhuri Foundation 2010
Abstract Appropriate management of raised intracranial
pressure begins with stabilization of the patient and
simultaneous assessment of the level of sensorium and the
cause of raised intracranial pressure. Stabilization is
initiated with securing the airway, ventilation and circula-
tory function. The identification of surgically remediable
conditions is a priority. Emergent use of external
ventricular drain or ventriculo-peritoneal shunt may be
lifesaving in selected patients. In children with severe
coma, signs of herniation or acutely elevated intracranial
pressure, treat- ment should be started prior to imaging or
invasive monitoring. Emergent use of hyperventilation and
mannitol are life saving in such situations. Medical
management involves careful use of head elevation,
osmotic agents, and avoiding hypotonic fluids. Appropriate
care also includes avoidance of aggravating factors. For
refractory intracranial hypertension, barbiturate coma,
hypothermia, or decom- pressive craniectomy should be
considered.
Keywords Coma . Critically ill child . Intracranial
hypertension . Traumatic brain injury
Introduction
Raised intracranial pressure (ICP) is a common neurolog-
ical complication in critically ill children. The cause may
be
N. Sankhyan : K. N. Vykunta Raju : S. Sharma : S. Gulati
(*)
Child Neurology Division, Department of Pediatrics, All India
Institute of Medical Sciences,
New Delhi 110029, India
e-mail: sheffaligulati@gmail.com
either an increase in brain volume, cerebral blood flow, or
cerebrospinal fluid (CSF) volume. Despite its high inci-
dence, there are few systematically evaluated treatments of
intracranial hypertension. Most management recommenda-
tions are based on clinical experience and research done in
patients with traumatic brain injury.
Intracranial Pressure: Normal Values
Intracranial pressure is the total pressure exerted by the
brain, blood and CSF in the intracranial vault. The
Monroe- Kellie hypothesis states the sum of the
intracranial volumes of brain (≈80%), blood(≈10%), and
CSF(≈10%) is constant, and that an increase in any one of
these must be offset by an equal decrease in another, or
else pressure increases. The ICP varies with age and
normative values for children are not well established.
Normal values are less than 10 to 15 mm Hg for adults
and older children, 3 to 7 mm Hg for young children, and
1.5 to 6 mm Hg for term infants [1]. ICP values greater
than 20 to 25 mm Hg require treatment in most
circumstances. Sustained ICP values of greater than
40 mm Hg indicate severe, life-threatening intracranial
hypertension [2].
Cerebral Pressure Dynamics
Cerebral perfusion pressure (CPP) is a major factor that
affects cerebral blood flow to the brain. CPP measurement
is expressed in millimeters of mercury and is determined by
measuring the difference between the mean arterial
pressure (MAP) and ICP (CPP = MAP – ICP). It is
apparent from the formula that, CPP can reduce as a result
of reduced MAP or raised ICP, or a combination of
these two. CPP
a
measurements aid in determining the amount of blood
volume present in the intracranial space. It is used as an
important clinical indicator of cerebral blood flow and
hence adequate oxygenation. Normal CPP values for
children are not clearly established, but the following
values are generally accepted as the minimal pressure
necessary to prevent ischemia: adults CPP>70 mm Hg;
children CPP>50–60 mm Hg; infants/toddlers CPP> 40–
50 mm Hg [3].
Causes of Raised ICP
The various causes of raised ICP (Table 1) can occur
individually or in various combinations. Based on the
Monroe-Kellie hypothesis, raised ICP can result from
increase in volume of brain, blood, or CSF. Frequently it is
a combination of these factors that result in raised ICP. The
causes of raised ICP can also be divided into primary or
secondary depending on the primary pathology. In primary
causes of increased ICP, normalization of ICP depends on
rapidly addressing the underlying brain disorder. In second-
ary causes of raised ICP the underlying systemic or
extracranial cause has to be managed.
Table 1 Causes of raised intracranial pressure
Increased brain volume
Intracranial space occupying lesions
Brain tumors
Brain abscess
Intracranial hematoma
Intracranial vascular malformation
Cerebral edema
Encephalitis (viral, inflammatory)
Meningitis
Hypoxic ischemic encephalopathy
Traumatic brain injury
Hepatic
encephalopathy Reye’s
syndrome Stroke
Reye’s syndrome
Increase in CSF volume
Hydrocephalous
Choroids plexus palpilloma
Increased blood volume
Vascular malformations
Cerebral venous thrombosis
Meningitis, encephalitis
Assessment and Monitoring
Identify children at risk for raised ICP (Table 1). Those at
greater risk are children with head trauma, suspected
neuroinfections, or suspected intracranial mass lesions.
Raised pressure usually manifests as headache, vomiting,
irritability, squint, tonic posturing or worsening sensorium.
However the symptoms depend on the age, cause, and
evolution of the raised ICP.
Initial Assessment
As with any sick child, one begins with assessment and
maintenance of the airway, breathing and circulatory
function. An immediate priority is to look for potentially
life threatening signs of herniation (Table 2). If these signs
are present then measures to decrease intracranial pressure
should be rapidly instituted. Cushing’s triad (bradycardia,
hypertension and irregular breathing) is a late sign of
herniation.
Neurological Assessment
After the initial stabilization, a thorough history and clinical
examination is performed to determine the possible etiology
and further course of management. Pupillary abnormalities
and abnormalities in ocular movements as determined by
sponta- neous, dolls eye or cold caloric testing are important
clues to the localization of brainstem dysfunction. The
examination of fundus is focused on detection of
papilledema, keeping in mind that its absence does not rule
out raised ICP. The motor system examination focuses on
identifying posturing or flaccidity due to raised ICP or focal
deficits. Findings on the general physical and systemic
examination may provide clues to the underlying cause for
raised ICP (e.g. jaundice/hepatomegaly in hepatic
encephalopathy, rash in viral encephalitis etc.).
Neuroimaging
The imaging study of choice for the patient with raised
intracranial pressure presenting to the emergency room is a
computed tomography (CT) scan. A contrast study is
helpful to identify features of infection (meningeal en-
hancement, brain abscess etc.) and tumors. If CT scan is
normal, and the patient has clinical features of raised ICP,
then an MRI with MR venogram must be obtained once the
patient is stabilized. MRI can pick up early stroke, venous
thromboses, posterior fossa tumors and demyelinating
lesions which might be missed on CT.
Invasive ICP Monitoring
ICP monitoring is used mainly to guide therapy, such as
in determining when to drain CSF or administer
Indian J Pediatr (2010) 77:1409–1416
Table 2 Clinical recognition of herniation syndromes
Type of herniation
Subfalcine herniation (medially, of the cingulate gyrus)
Central transtentorial
Lateral transtentorial (downward and medially of uncus
and parahippocampal gyrus)
Upward Transtentorial (upward of the cerebellar
vermis and midbrain)
Transforaminal (downward of cerebellar tonsils and
medulla)
a
Clinical signs of potentially reversible brain herniation
mannitol or sedation. In addition, invasive monitoring
allows for observation of the shape, height, and trends
of individual and consecutive ICP waveforms that may
reflect intracranial compliance, cerebrovascular status
and cerebral perfusion. Guidelines for ICP monitoring
are available for traumatic brain injury [4]. ICP
monitoring is indicated for a patient with Glasgow Coma
Scale (GCS) score of 3–8 (after resuscitation) with either
an abnormal admission head CT or motor posturing and
hypotension [4]. The role and benefit of ICP monitoring
in other conditions such as subarachnoid hemorrhage,
hydrocephalus, intracranial infections, and Reyes syn-
drome remains unclear. Also, the availability of this
modality is limited. In other brain injuries, such as
hypoxic and ischemic injuries, monitoring ICP has not
been shown to improve outcome [5].
Management of Intracranial Hypertension
The goal for patients presenting with raised ICP is to identify
and address the underlying cause along with measures to
reduce ICP (Fig. 1, Table 3). It is important not to delay
treatment, in situations where identifying the underlying
cause will take time. When elevated ICP is clinically evident,
the situation is urgent and requires immediate reduction in
ICP. Avoidance of factors aggravating or precipitating raised
ICP is an important goal for all children with intracranial
hyperten- sion. The availability of ICP monitors is not
universal and should not come in the way of emergent
therapy.
ABCs
The assessment and management of the airway, breathing
and circulation (ABCs) is the beginning point of manage-
ment. Early endotracheal intubation should be considered
141
Clinical manifestations
Impaired consciousness, monoparesis of the contralateral lower extremitya
Impaired consciousness, abnormal respirations, symmetrical small reactivea or
midposition fixed reactive pupils, decorticatea evolving to decerebrate posturing
Impaired consciousness, abnormal respirations, third nerve palsya (unilateral dilated
pupil, ptosis), hemiparesisa
Prominent brainstem signs, downward gaze deviation, upgaze palsy, decerebrate
posturing
Impaired consciousness, neck rigidity, opisthotonus, decerebrate rigidity, vomiting,
irregular respirations, apnea, bradycardia
for those children with GCS <8, evidence of herniation,
apnea or have inability to maintain airway. Intubation
should proceed with administration of medications to blunt
the ICP during the procedure. Suggested medications are
lidocaine, thiopental and a short-acting non depolarizing
neuromuscular blockade agent (e.g.vecuronium, atracu-
rium) [6]. Appropriate oxygenation should be ensured. If
there is evidence of circulatory failure, fluid bolus should
be given. Samples should be drawn for investigations as
suggested by history.
Positioning
Mild head elevation of 15–30° has been shown to reduce
ICP with no significant detrimental effects on CPP or
CBF [7]. The child’s head is positioned midline with the
head end of the bed elevated to 15–30° to encourage
jugular venous drainage [7]. Sharp head angulations and
tight neck garments or taping should be avoided [8]. One
has to ensure that the child is euvolemic and not in shock
prior to placing in this position [6].
Hyperventilation
Decreasing the PaCO2 to the range of 30–35 mm of Hg, is
an effective and rapid means to reduce ICP [6, 9].
Hyperventilation acts by constriction of cerebral blood
vessels and lowering of CBF. This vasoconstrictive effect
on cerebral arterioles lasts only 11 to 20 h because the pH
of the CSF rapidly equilibrates to the new PaCO 2 level.
Moreover, aggressive hyperventilation can dramatically
decreases the CBF, causing or aggravating cerebral ische-
mia [10, 11]. Hence, the most effective use of hyperven-
tilation is for acute, sharp increases in ICP or signs of
impending herniation [12].
141 Indian J Pediatr (2010) 77:1409–1416

Fig. 1 Algorithmic approach to Child with signs/symptoms of raised ICP

a child with raised ICP

Immediate Measures*

. Maintain airway and adequate ventilation and circulation Head end elevation-15-

.
Ongoing care Sedation and analgesia Avoid noxious stimuli Control fever
Prevention and treatment of seizures

Maintain euglycemia
Hyperventilation: (target PCO2 : 30-35mm Hg ) To be used in emergent situations like herniation to bridge more definitive therapy. No
No hyotonic fluid infusions Maintain Hb above 10gm%
Surgical intervention

Evacuation of hematoma

Neuroimaging : Suggestive of surgically remediable“Yes”

cause; hydrocephalous,
CSF diversionlarge hematoma, etc

Decompressive craniectomy

“No” or delay

Osmotherapy**

BP Normal: Mannitol Hypotension, Hypovolemia Serum osmolality >320 mOsm/kg, Renal failure: Hypertonic Saline

Other options;***

.Heavy sedation and paralysis

.Barbiturate coma
.Hypothermia
Special situations

. Steroids: Intracranial tumors with perilesional edema, neurocysticercosis with high lesion load, ADEM, pyomeningitis,TBM, Abscess

. Acetazolamide: Hydrocephalus, Benign intracranial, high altitude illness

(*- May be initiated immediately after brief evaluation if situation is urgent. Measures also used in children awaiting surgical/radiologial
procedures, ** -Preferable to monitor ICP, ***- undertake only with ICP monitoring)

Osmotherapy in ICP [13]. For this reason, when it is time to stop

Mannitol
Mannitol has been the cornerstone of osmotherapy in
raised ICP. However, the optimal dosing of mannitol is not
known. A reasonable approach is to use an initial bolus of
0.25–1 g/kg (the higher dose for more urgent reduction of
ICP) followed by 0.25–0.5 g/kg boluses repeated every 2–
6 h as per requirement. Attention has to be paid to the fluid
balance so as to avoid hypovolemia and shock. There is
also a concern of possible leakage of mannitol into the
damaged brain tissue potentially leading to “rebound” rises
mannitol, it should be tapered and its use should be limited
to 48 to 72 h. Apart from hypotension, rebound rise in ICP,
mannitol can also lead to hypokalemia, hemolysis and
renal failure.
Hypertonic Saline
Hypertonic saline has a clear advantage over mannitol in
children who are hypovolemic or hypotensive. Other
situations where it may be preferred are renal failure or
serum osmolality >320 mosmol/Kg. It has been found
effective in patients with serum osmolality of up to
Indian J Pediatr (2010) 77:1409–1416
Table 3 Summary of measures to reduce intracranial pressure
1 Assessment and management of ABC’s (airway, breathing,
circulation)
2 Early intubation if; GCS <8, Evidence of herniation, Apnea,
Inability to maintain airway
3 Mild head elevation of 15–30° (Ensure that the child is
euvolemic)
4 Hyperventilation: Target PaCO2: 30–35 mm Hg (suited for acute,
sharp increases in ICP or signs of impending herniation)
5 Mannitol: Initial bolus: 0.25–1 g/kg, then 0.25–0.5 g/kg, q 2–6 h
as per requirement, up to 48 h
6 Hypertonic Saline: Preferable in presence of Hypotension,
Hypovolemia, Serum osmolality >320 mOsm/kg, Renal failure,
Dose: 0.1–1 ml/kg/hr infusion, Target Na +−145–155 meq/L.
7 Steroids: Intracranial tumors with perilesional edema,
neurocysticerocosis with high lesion load, ADEM,
pyomeningitis, TBM, Abscess
Acetazolamide: Hydrocephalous, benign intracranial, high
altitude illness
8 Adequate sedation and analgesia
9 Prevention and treatment of seizures: use Lorazepam or
midazolam followed by phenytoin as initial choice.
10 Avoid noxious stimuli: use lignocaine prior to ET suctioning
[nebulized (4% lidocaine mixed in 0.9% saline) or intravenous
(1–2 mg/kg as 1% solution) given 90 sec prior to suctioning]
11 Control fever: antipyretics, cooling measures
12 Maintenance IV Fluids: Only isotonic or hypertonic fluids
(Ringer lactate, 0.9% Saline, 5% D in 0.9% NS), No
Hypotonic fluids
13 Maintain blood sugar: 80–120 mg/dL
14 Refractory raised ICP:
• Heavy sedation and paralysis
• Barbiturate coma
• Hypothermia
• Decompressive craniectomy
360 mosmol/Kg [14]. Concerns with its use are bleeding,
rebound rise in ICP, hypokalemia, and hyperchloremic
acidosis, central pontine myelinolysis, acute volume over-
load, renal failure, cardiac failure or pulmonary edema
[15– 17]. Despite these concerns, current evidence suggests
that hypertonic saline as currently used is safe and does not
result in major adverse effects [18]. In different studies the
concentration of hypertonic saline used has varied from
1.7% to 30% [18]. The method of administration has also
varied and hence, evidence based recommendations are
difficult. It would be reasonable to administer hypertonic
saline as a continuous infusion at 0.1 to 1.0 mL/kg/hr, to
target a serum sodium level of 145–155 meq/L [19, 20].
Serum sodium and neurological status needs to be closely
monitored during therapy. When the hypertonic saline
therapy is no longer required, serum sodium should be
slowly corrected to normal values (hourly decline in serum
sodium of not more than 0.5 meq/L) to avoid
complications
141
associated with fluid shifts [6]. Monitoring of serum
sodium and serum osmolality should be done every 2–4 h
till target level is reached and then followed up with 12
hourly estimations. Under careful monitoring, hypertonic
saline has been used for up to 7 days [21].
Other Agents
Acetazolamide (20–100 mg/kg/day, in 3 divided doses,
max 2 g/day) is a carbonic anhydrase inhibitor that reduces
the production of CSF. It is particularly useful in patients
with hydrocephalous, high altitude illness and benign
intracranial hypertension. Furosemide (1 mg/kg/day,
q8hrly), a loop diuretic has sometimes been administered
either alone or in combination with mannitol, with variable
success [22, 23]. Glycerol is another alternative osmotic
agent for treatment of raised ICP. It is used in the oral (1.5
g/kg/day, q4–6hrly) or intravenous forms. Given
intravenously, it reduces ICP with effect lasting for about
70 min without any prolonged effect on serum osmolality
[24]. Glycerol readily moves across the blood brain barrier
into the brain. Though not proven, there is concern of
rebound rise in ICP with its use.
Steroids
Glucocorticoids are very effective in ameliorating the
vasogenic edema that accompanies tumors, inflammatory
conditions, infections and other disorders associated with
increased permeability of blood brain barrier, including
surgical manipulation [25]. Dexamethasone is the preferred
agent due to its very low mineralocorticoid activity (Dose:
0.4–1.5 mg/kg/day, q 6 hrly) [26]. Steroids are not
routinely indicated in individuals with traumatic brain
injury [27]. Steroids have not been found to be useful and
may be detrimental in ischemic lesions, cerebral malaria
and intracranial hemorrhage [26, 28, 29].
Sedation and Analgesia
Raised ICP is worsened due to agitation, pain, and patient-
ventilator asynchrony [8]. Adequate analgesia, sedation
and occasionally neuromuscular blockade are useful
adjuvant in the management of raised ICP. Appropriate
Analgesia and sedation is usually preferred over
neuromuscular blockade, as it is quickly reversible and
allows for neurological monitoring. For sedation it is
preferable to use agents with minimal effect on blood
pressure. Short acting benzodiaze- pines (e.g. midazolam)
are useful for sedation in children. If the sedatives are not
completely effective, then a neuro- muscular blocking
agent (e.g. Pancuronium, atracurium, vecuronium) may be
required.
141
Minimization of Stimulation
Attempt must be made to reduce the number of elective
interventions that are likely to be painful or excessively
stimulating. Lidocaine instilled endotracheally has been
shown to prevent the endotracheal suctioning-induced
ICP increase and CPP reduction in adults with severe
traumatic brain injury [30]. It is recommended to instil
lidocaine at body temperature, slowly, and through a fine
tube advanced into the endotracheal tube within its length
(avoid direct contact with the mucosa) [30]. Lidocaine can
be given in nebulized (usually 4% lidocaine mixed in
0.9% saline) or intravenous forms (1–2 mg/kg as 1%
solution given 90 sec prior to suctioning) for the same
purpose [9].
Fluids
The main goal of fluid therapy is to maintain euvolemia,
normoglycemia and prevent hyponatremia. Children with
raised ICP should receive fluids at a daily maintenance
rate, as well as fluid boluses as indicated for hypovole-
mia, hypotension, or decreased urine output. Mainte-
nance fluids usually consist of normal saline with daily
requirements of potassium chloride based on body
weight. All fluids administered must be isotonic or
hypertonic (e.g. Ringer lactate, normal saline) and
hypotonic fluids must be avoided (e.g. 0.18% saline in
5% dextrose, Isolyte P) [7]. Hyponatremia is to be
avoided and if it occurs, must be corrected slowly.
Blood Glucose
Blood glucose must be maintained between 80–120 mg/dL
in a child with raised ICP [7]. Studies in children with
traumatic brain injury have shown that hyperglycemia is
associated with poor neurological outcome and increased
mortality [31]. On the other hand, hypoglycemia is known
to induce a systemic stress response and cause disturbances
in CBF, increasing the regional CBF by as much as 300%
in severe hypoglycaemia. Hypoglycemia can also lead to
neuronal injury and therefore, should be managed
aggressively.
Temperature Regulation
Maintaining normothermia is important to prevent compli-
cations of temperature fluctuations. This is achieved by
frequent measurements of body temperature and correcting
any fluctuations using antipyretics, and assisted cooling or
heating per needed.
Indian J Pediatr (2010) 77:1409–1416
Prevention and Treatment of Seizures
Children with significant head injury and neuroinfections are
at risk for seizures. Seizures can increase CBF and cerebral
blood volume leading to increased ICP. They can also
increase the metabolic needs of the brain and predispose to
ischemia [6]. Seizures, if clinically evident, must be treated.
Given the lack of studies in children and in patients with non
traumatic raised ICP, evidence based recommendation
regarding prophylactic anti-epileptic therapy are not possible.
But it is reasonable, and a common practice is to use
prophylactic anticonvulsants for short term in children with
raised ICP, unless indicated otherwise [6, 26]. If available, it
is prudent to use continuous electroencephalography (EEG)
to identify subclinical seizure activity in children with
increased risk for seizures.
Anemia
Theoretically, anemia would increase CBF and secondarily
raise ICP. There have been case reports of patients with
severe anemia presenting with symptoms of raised ICP
and papilledema [32]. Though not rigorously studied, it is
common practice to maintain hemoglobin above 10 g/dL
in patients with traumatic brain injury and raised ICP.
Surgical Therapy
Cerebrospinal Fluid Drainage CSF drainage using a
external ventricular drainage (EVD) or
ventriculoperitoneal shunt provides for an immediately
effective means to lower ICP. In addition EVD provides a
method for continuously monitoring ICP. CSF drainage is
particularly useful in the presence of hydrocephalus. But it
may be considered even in children without hydrocephalus.
Its effectiveness in lowering ICP has been shown to be
comparable to intravenous mannitol or hyperventilation
[33]. However, it is of limited utility in diffuse brain edema
with collapsed ventricles.
Resection of Mass Lesions Surgery should be undertaken
when a lesion amenable to surgical intervention is
identified as the primary cause of raised ICP. Common
situations where this neurosurgical intervention is
preferentially employed are acute epidural or subdural
hematomas, brain abscess, or brain tumors.
Target of Therapy
When facilities for ICP monitoring are available, the
management is tailored to maintaining an adequate CPP
Indian J Pediatr (2010) 77:1409–1416
(i.e. Children >50–60, infants/toddlers >40–50 mm Hg)
and lower ICP to acceptable levels (i.e. <20 mm Hg for
children older than 8 yrs, <18 for 1–8 yrs, and <15 mm
for infants).
Other Therapies for Refractory Raised ICP
Barbiturates
Use of barbiturates is generally reserved for cases with
refractory raised ICP. Thiopentone can be used for this
purpose and the dosing of the drug is adjusted to a target
ICP as monitored on an ICP monitor. The drug is titrated
to a 90% burst suppression (2–6 bursts per minute) using
an EEG monitor. Monitoring a child in barbiturate coma
should include EEG, ICP monitoring, invasive hemody-
namic monitoring (arterial blood pressure, central venous
pressure, SjvO2) and frequent assessment of oxygenation
status. The complication rate of barbiturate therapy is high
and includes hypotension, hypokalemia, respiratory com-
plications, infections, hepatic dysfunction and renal dys-
function [34].
Hypothermia
Evidence from carefully conducted studies in adults and
children does not show any improvement in the neurologic
outcome in head injured patients with the use of
therapeutic hypothermia [35, 36]. However, studies do
suggest a lowered ICP during the hypothermia therapy in
children [35, 37]. So, in children with refractory raised
ICP, controlled hypothermia may be considered.
Decompressive Craniectomy On rare occasions when all
other measures fail, decompressive craniectomy with
duraplasty may be valuable procedure. Reports of its use
in children with traumatic brain injury have shown benefit
[38, 39]. It may offer an alternative treatment option in
uncontrolled ICP refractory to other measures.
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