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Mannitol is a monosaccharide which is easy to produce and stable in solution.

It is used clinically in
doses ranging from 0.25 to 1.5 g/kg body weight. Solutions of 10% mannitol (osmolality 596
mOsm/kg) and 20% mannitol (osmolality 1,192 mOsm/kg) are commonly available for clinical use.
Cerebral effects
Mannitol does not cross the blood brain barrier so an elevated plasma osmolality due to a infusion of
hypertonic mannitol is effective in removing fluid from the brain. This is called 'mannitol
osmotherapy'. In the past other hypertonic solutions (eg hypertonic urea solution) have been used
and currently in some places hypertonic glycerol solutions are available as an alternative to
mannitol.
Mannitol infusions are useful to acutely decrease elevated intracranial pressure due to an intracranial
space occupying lesion. A typical use would be in a patient with an intracerebral haematoma due to
an acute traumatic head injury. The effect is rapid in onset (minutes) but only temporary (as the
mannitol is excreted) but its use buys time for urgent definitive therapy (eg surgical evacuation of
the haematoma and surgical haemostasis). A typical dose in an adult would be 0.5-1.5g/kg
administered as the 20% solution.
Repeated doses of mannitol have less effect and as some slowly enters the brain, rebound
intracranial hypertension is a risk. As the blood-brain barrier is probably disrupted in damaged areas
of the brain, mannitol may be both less effective here and also more may enter the brain at these
places. However, the therapeutic effect of mannitol is not dependent on a specific action at damaged
areas of the brain but rather on a global effect in decreasing intracranial fluid volume and
intracranial pressure so this has little relevance for a first dose of mannitol and especially if
definitive surgical treatment is successful. Much more problematical is use of repeated doses of
mannitol in ICU patients with traumatic intracranial hypertension in whom there is no surgically
correctable cause; such use is usually futile.
The brain cells also compensate for the presence of continued hypertonicity by the intracellular
production of 'idiogenic osmoles'. The effect is to increase intracellular tonicity and allow brain cell
volume to return towards normal presumably with improvement of intracellular functions despite
the continued hypertonicity.
Use of mannitol infusions is common intraoperatively in some neurosurgical procedures. The aim is
to decrease intracranial pressure and produce a 'slack brain' to facilitate surgical access.
Mannitol does not cross cell membranes so the cell volume of most other cells in the body is also
decreased.
Renal effects
In the renal glomeruli, mannitol is freely filtered. It is not secreted or reabsorbed by the tubules. In
the doses used clinically it retains water with it in the tubule and causes an 'osmotic diuresis'.
Consequently, mannitol is classified as an 'osmotic diuretic'. The high flow of retained tubule fluid
tends to have a flushing effect and washes fluid and solutes from the kidney. This effect is useful
clinically in management of rhabdomyolysis. The aim is to 'wash' the myoglobin out of the tubules
and prevent it precipitating there with obstruction and development of acute renal failure. The effect
of mannitol for this use is aided by maintenance of adequate intravascular volume and by urinary
alkalinisation (by administration of IV sodium bicarbonate).
Intravascular volume effects
Attention to intravascular volume status is important during any clinical use of mannitol. Initially,
the tissue dehydrating effect will increase intravascular volume with the risk of precipitating volume
overload and hypertension and/or acute congestive heart failure. Subsequently, the diuretic effect
may result in hypovolaemia (and hypernatraemia). Frusemide (a loop diuretic) may be a useful
adjunct in some cases to minimise the initial hypervolaemia.
Other effects
The increased intravascular water volume decreases the red cell concentration (decreased
haematocrit) with a resultant decrease in blood viscosity. This may improve flow and oxygen
delivery to some areas.
Mannitol has free radical scavenging properties and these may contribute to its therapeutic effects
(though this has not so far been established).
Solusi manitol hipertonik digunakan secara klinis untuk:
Cerebral dehidrasi - untuk menurunkan tekanan intrakranial

Ginjal Perlindungan - untuk melindungi terhadap perkembangan gagal ginjal karena diuresis osmotik
dalam beberapa situasi klinis (misalnya dengan rhabdomyolysis)
Hipertonisitas menyebabkan gerakan pasif air di seluruh hambatan lipid dalam menanggapi gradien
osmotik.
Manitol adalah monosakarida yang mudah untuk memproduksi dan stabil dalam larutan. Hal ini
digunakan secara klinis dalam dosis berkisar antara 0,25 sampai 1,5 g / kg berat badan. Solusi dari 10%
manitol (osmolalitas 596 mOsm / kg) dan 20% manitol (osmolalitas 1.192 mOsm / kg) biasanya
tersedia untuk penggunaan klinis.
Efek serebral
Manitol tidak melewati sawar darah otak sehingga osmolalitas plasma meningkat karena infus manitol
hipertonik efektif dalam menghilangkan cairan dari otak. Ini disebut 'osmoterapi manitol'. Dalam solusi
masa lalu hipertonik lainnya (misalnya larutan urea hipertonik) telah digunakan dan saat ini di
beberapa tempat solusi gliserol hipertonik tersedia sebagai alternatif untuk manitol.
Infus manitol berguna untuk menurunkan tekanan intrakranial akut tinggi karena ruang menempati lesi
intrakranial. Sebuah penggunaan yang khas akan pada pasien dengan hematoma intraserebral karena
cedera kepala akut traumatis. Efeknya adalah cepat onset (menit) tetapi hanya sementara (sebagai
manitol yang diekskresikan) namun penggunaannya membeli waktu untuk terapi definitif mendesak
(misalnya evakuasi bedah hematoma dan hemostasis bedah). Dosis yang khas pada orang dewasa akan
0.5-1.5g / kg diberikan sebagai solusi 20%.
Dosis berulang manitol memiliki efek kurang dan beberapa perlahan memasuki otak, rebound
hipertensi intrakranial adalah risiko. Sebagai penghalang darah-otak mungkin terganggu di daerah yang
rusak dari otak, manitol mungkin keduanya kurang efektif di sini dan juga lebih mungkin masuk ke
otak di tempat-tempat ini. Namun, efek terapi manitol tidak tergantung pada tindakan tertentu di daerah
yang rusak dari otak tetapi lebih pada efek global dalam penurunan volume cairan intrakranial dan
tekanan intrakranial jadi ini memiliki sedikit relevansi untuk dosis pertama manitol dan terutama jika
definitif bedah pengobatan berhasil. Jauh lebih problematis adalah penggunaan dosis berulang manitol
pada pasien ICU dengan hipertensi intrakranial traumatik di antaranya tidak ada pembedahan penyebab
diperbaiki; penggunaan tersebut biasanya sia-sia.
Sel-sel otak juga mengimbangi kehadiran terus hipertonisitas oleh intraseluler produksi 'osmoles
idiogenic'. Efeknya adalah untuk meningkatkan tonisitas intraseluler dan memungkinkan volume sel
otak untuk kembali ke keadaan normal mungkin dengan peningkatan fungsi intraseluler meskipun
hipertonisitas terus.
Penggunaan infus manitol umum intraoperatif di beberapa prosedur bedah saraf. Tujuannya adalah
untuk menurunkan tekanan intrakranial dan menghasilkan 'otak slack' untuk memfasilitasi akses bedah.
Manitol tidak lintas membran sel sehingga volume sel yang paling sel-sel lain dalam tubuh juga
menurun.
Efek ginjal
Dalam glomeruli ginjal, manitol yang bebas disaring. Hal ini tidak disekresikan atau diserap kembali
oleh tubulus. Dalam dosis yang digunakan secara klinis mempertahankan air dengan itu di tubulus dan
menyebabkan 'diuresis osmotik'. Akibatnya, manitol diklasifikasikan sebagai 'diuretik osmotik'. Aliran
tinggi cairan tubulus ditahan cenderung memiliki efek pembilasan dan mencuci cairan dan zat terlarut
dari ginjal. Efek ini secara klinis bermanfaat dalam pengelolaan rhabdomyolysis. Tujuannya adalah
untuk 'mencuci' mioglobin keluar dari tubulus dan mencegahnya mempercepat sana dengan obstruksi
dan perkembangan gagal ginjal akut. Pengaruh manitol untuk penggunaan ini dibantu oleh
pemeliharaan volume intravaskular yang memadai dan oleh alkalinisasi urin (dengan pemberian IV
natrium bikarbonat).
Efek volume intravaskular
Perhatian terhadap status volume intravaskular penting dalam setiap penggunaan klinis manitol.
Awalnya, efek jaringan dehidrasi akan meningkatkan volume intravaskular dengan risiko pencetus
kelebihan beban volume dan hipertensi dan / atau gagal jantung kongestif akut. Selanjutnya, efek
diuretik dapat menyebabkan hipovolemia (dan hipernatremia). Frusemide (loop diuretik) dapat menjadi
tambahan yang berguna dalam beberapa kasus untuk meminimalkan hipervolemia awal.
Efek lainnya
Peningkatan volume air intravaskular menurun konsentrasi sel darah merah (hematokrit menurun)
dengan penurunan resultan viskositas darah. Hal ini dapat meningkatkan aliran dan pengiriman oksigen
ke beberapa daerah.
Manitol memiliki sifat radikal bebas dan ini dapat menyebabkan efek terapeutik (meskipun ini belum
sejauh ini telah ditetapkan).
'Fluid Physiology' by Kerry Brandis -from http://www.anaesthesiaFluid Physiology

8.5 Infusion of Hypertonic Mannitol Solutions

As part of intensive treatment of traumatic brain injury, intracranial pressure (ICP) should be controlled when the cerebral p
greater than 20mmHg. Intracranial hypertension occurs in approximately 40% of all patients with severe traumatic brain injury.
important than control of ICP per se. Measures to increase mean arterial pressure should be instituted prior to starting more com

There are several methods for controlling ICP. These are usually applied in a stepwise fashion to achieve control, where poss
injured patient is tracheal intubation with a cuffed tube. This protects and maintains the airway and allows for maximal oxygena
Ventilation

Carbon dioxide dilates the cerebral blood vessels, increasing the volume of blood in the intracranial vault and therefore increasin
kPa / 30mmHg).
Previously, hyperventilation was used routinely to maximally reduce PaCO2. No studies have shown
this to improve outcome in these patients. Additionally, transcranial doppler (TCD) assessment and
positron emission tomography (PET) shows this can induce significant constriction of cerebral vessels
and this increase in cerebral vascular resistance may reduce cerebral blood flow to below the ischaemic
threshold. One study has shown an improvement in long-term outcome when hyperventilation is not
used routinely.
Consequently hyperventilation should be used only for short periods when immediate control of ICP is
necessary. For example in the patient who has an acute neurological deterioration prior to CT scanning
and surgical intervention. Hyperventilation should not take the PaCO2 level to below 3.5-4 kPa as there
is minimal beneficial effect on ICP below this level.
Occasionally hyperventilation may be necessary for longer periods in patients with persistently high
ICPs who have not responded to other treatment modalities. These patients may benefit from more
intensive neuromonitoring such as jugular venous oxygen saturation and transcranial doppler
assessments to ensure cerebral perfusion is not being compromised at the expense of ICP. Persistent
hyperventilation should not be used in the first 24 hours and preferably not within the first 5 days
following brain injury.
Intravenous fluid therapy
Patients with severe brain injury should be kept normovolaemic. Previous regimens recommending that
patients be kept 'dry' have essentially been discarded as there is significant risk of both hypotensive
episodes (leading to a fall in cerebral perfusion) and systemic inflammatory respinse syndrome (SIRS)
or multiple organ failure (MOF) leading to failure of oxygenation and ventilation. Dehydration has
little effect on cerebral oedema.
Free water (as dextrose solutions) should NOT be administered. This will decrease plasma osmolality
and so increase the water content of brain tissue (the blood brain barrier acting as a semipermeable
membrane). Elevated blood sugar levels are associated with a worsening of neurologic injury after
episodes of global cerebral ischaemia. Ischaemic brain metabolises glucose to lactic acid, lowering
tissue pH and potentially exacerbating ischaemic injury.
Hypertonic solutions and osmotic diuretics such as mannitol will have the opposite effect. This
mechanism requires an intact blood brain barrier. If this is damaged, as may be the case following
injury, low molecular weight, osmotically active particles may leak into the cerebral interstitium. In this
case mannitol may have no effect in reducing brain water content, and maintenance of the colloid
oncotic pressure in the vessels by administration of colloids, plasma proteins or other high molecular
weight compounds may, theoretically, be of benefit. However in practice, colloids offer little benefit
over crystalloid solutions.
There has been considerable interest in the use of hypertonic crystalloid solutions for the treatment of
hypovolaemia in the presence of intracranial hypertension. Animal studies have proven the efficacy of
hypertonic solutions in reversing shock, and sometimes in controlling ICP. Clinical trials suggest that
survival after severe brain injury (GCS<9) may be improved with hypertonic solutions. However those
injuries leading to a breakdown in the blood brain barrier show little or worsened response to

hypertonic fluid administration.


There is no single best fluid for patients with traumatic brain injury, but isotonic crystalloids are widely
used and have good scientific basis. Normal saline or lactated RInger's solution should be the standard
resuscitation fluid until further studies show a clear benefit from other therapies. Regardless of the fluid
type chosen, normovolemia must be maintained and episodes of hypotension avoided.
Mannitol
Mannitol, a 6-carbon sugar, is widely used in head injury management, though it has never been
subjected to a randomised control trial against placebo and the methods and timing of administration
vary widely. It is an osmotic diuretic and can have significant beneficial effects on ICP, cerebral blood
flow and brain metabolism. Mannitol has two main mechanisms of action. Immediately after bolus
administration it expands circulating volume, decreases blood viscosity and therefore increases cerebral
blood flow and cerebral oxygen delivery.
Its osmotic properties take effect in 15-30 minutes when it sets up an osmotic gradient and draws water
out of neurons. However after prolonged administration (continuous infusion) mannitol molecules
move across into the cerebral interstitial space and may exacerbate cerebral oedema and raise ICP.
Mannitol itself directly contributes to this breakdown of the blood brain barrier.
Mannitol is therefore best used by bolus administration where an acute reduction in ICP is necessary.
For example the patient with signs of impending herniation (unilateral dilated pupil / extensor
posturing) or with an expanding mass lesion may benfit from mannitol to acutely reduce ICP during the
time necessary for CT scanning and/or operation.
Mannitol is wholly excreted in the urine and causes a rise in serum urine and osmolality. Patients with
poor renal perfusion (shock), sepsis, receiving nephrotoxic drugs or with a serum osmolality over
320mOsm are at risk of acute tubular necrosis. Hypolaemia should be avoided with the infusion of
isotonic fluids as necessary.
Sedation and anaesthesia
All but the most severely brain injured patients (GCS 3) will require anaesthesia for intubation. The
cardiovascular responses to intubation induce a rise in ICP which is exaggerated in those patients on
the cusp of the pressure-volume curve. Rapid sequence intubation is probably the safest method of
establishing an airway in these patients.
Continuing sedation will be necessary in most patients to allow adequate ventilation and to prevent
coughing or fighting the ventilator. Ensuing valsalva-type maneuvers cause sharp rises in intracranial
pressure. Which agents are used to achieve sedation is probably less important. However short acting
preparations will allow finer control of the depth of anaesthesia and faster recovery from sedation.
Agents with a longer duration of action such as diazepam may be best administered by intravenous
bolus as required rather than by constant infusion to avoid build-up of active metabolites.
Sedation is not analgesia, and pain requirements must be addressed to provide a quiet, comfortable
patient. Adequate analgesia will also reduce the requirements for sedation and neuromuscular blockade.
The use of neuromuscular blocking agents is not routinely required for continued ventilation. However
some patients whose high sedative requirements lead to adverse cardiovascular effects may benefit
from pharmacologic paralysis.

trauma.org 5:1 2000


Previously, hyperventilation was used routinely to maximally reduce PaCO2. No studies have shown
this to improve outcome in these patients. Additionally, transcranial doppler (TCD) assessment and
positron emission tomography (PET) shows this can induce significant constriction of cerebral vessels

and this increase in cerebral vascular resistance may reduce cerebral blood flow to below the ischaemic
threshold. One study has shown an improvement in long-term outcome when hyperventilation is not
used routinely.
Consequently hyperventilation should be used only for short periods when immediate control of ICP is
necessary. For example in the patient who has an acute neurological deterioration prior to CT scanning
and surgical intervention. Hyperventilation should not take the PaCO2 level to below 3.5-4 kPa as there
is minimal beneficial effect on ICP below this level.
Occasionally hyperventilation may be necessary for longer periods in patients with persistently high
ICPs who have not responded to other treatment modalities. These patients may benefit from more
intensive neuromonitoring such as jugular venous oxygen saturation and transcranial doppler
assessments to ensure cerebral perfusion is not being compromised at the expense of ICP. Persistent
hyperventilation should not be used in the first 24 hours and preferably not within the first 5 days
following brain injury.
Intravenous fluid therapy
Patients with severe brain injury should be kept normovolaemic. Previous regimens recommending that
patients be kept 'dry' have essentially been discarded as there is significant risk of both hypotensive
episodes (leading to a fall in cerebral perfusion) and systemic inflammatory respinse syndrome (SIRS)
or multiple organ failure (MOF) leading to failure of oxygenation and ventilation. Dehydration has
little effect on cerebral oedema.
Free water (as dextrose solutions) should NOT be administered. This will decrease plasma osmolality
and so increase the water content of brain tissue (the blood brain barrier acting as a semipermeable
membrane). Elevated blood sugar levels are associated with a worsening of neurologic injury after
episodes of global cerebral ischaemia. Ischaemic brain metabolises glucose to lactic acid, lowering
tissue pH and potentially exacerbating ischaemic injury.
Hypertonic solutions and osmotic diuretics such as mannitol will have the opposite effect. This
mechanism requires an intact blood brain barrier. If this is damaged, as may be the case following
injury, low molecular weight, osmotically active particles may leak into the cerebral interstitium. In this
case mannitol may have no effect in reducing brain water content, and maintenance of the colloid
oncotic pressure in the vessels by administration of colloids, plasma proteins or other high molecular
weight compounds may, theoretically, be of benefit. However in practice, colloids offer little benefit
over crystalloid solutions.
There has been considerable interest in the use of hypertonic crystalloid solutions for the treatment of
hypovolaemia in the presence of intracranial hypertension. Animal studies have proven the efficacy of
hypertonic solutions in reversing shock, and sometimes in controlling ICP. Clinical trials suggest that
survival after severe brain injury (GCS<9) may be improved with hypertonic solutions. However those
injuries leading to a breakdown in the blood brain barrier show little or worsened response to
hypertonic fluid administration.
There is no single best fluid for patients with traumatic brain injury, but isotonic crystalloids are widely
used and have good scientific basis. Normal saline or lactated RInger's solution should be the standard
resuscitation fluid until further studies show a clear benefit from other therapies. Regardless of the fluid
type chosen, normovolemia must be maintained and episodes of hypotension avoided.
Mannitol
Mannitol, a 6-carbon sugar, is widely used in head injury management, though it has never been
subjected to a randomised control trial against placebo and the methods and timing of administration
vary widely. It is an osmotic diuretic and can have significant beneficial effects on ICP, cerebral blood
flow and brain metabolism. Mannitol has two main mechanisms of action. Immediately after bolus
administration it expands circulating volume, decreases blood viscosity and therefore increases cerebral
blood flow and cerebral oxygen delivery.
Its osmotic properties take effect in 15-30 minutes when it sets up an osmotic gradient and draws water

out of neurons. However after prolonged administration (continuous infusion) mannitol molecules
move across into the cerebral interstitial space and may exacerbate cerebral oedema and raise ICP.
Mannitol itself directly contributes to this breakdown of the blood brain barrier.
Mannitol is therefore best used by bolus administration where an acute reduction in ICP is necessary.
For example the patient with signs of impending herniation (unilateral dilated pupil / extensor
posturing) or with an expanding mass lesion may benfit from mannitol to acutely reduce ICP during the
time necessary for CT scanning and/or operation.
Mannitol is wholly excreted in the urine and causes a rise in serum urine and osmolality. Patients with
poor renal perfusion (shock), sepsis, receiving nephrotoxic drugs or with a serum osmolality over
320mOsm are at risk of acute tubular necrosis. Hypolaemia should be avoided with the infusion of
isotonic fluids as necessary.
Sedation and anaesthesia
All but the most severely brain injured patients (GCS 3) will require anaesthesia for intubation. The
cardiovascular responses to intubation induce a rise in ICP which is exaggerated in those patients on
the cusp of the pressure-volume curve. Rapid sequence intubation is probably the safest method of
establishing an airway in these patients.
Continuing sedation will be necessary in most patients to allow adequate ventilation and to prevent
coughing or fighting the ventilator. Ensuing valsalva-type maneuvers cause sharp rises in intracranial
pressure. Which agents are used to achieve sedation is probably less important. However short acting
preparations will allow finer control of the depth of anaesthesia and faster recovery from sedation.
Agents with a longer duration of action such as diazepam may be best administered by intravenous
bolus as required rather than by constant infusion to avoid build-up of active metabolites.
Sedation is not analgesia, and pain requirements must be addressed to provide a quiet, comfortable
patient. Adequate analgesia will also reduce the requirements for sedation and neuromuscular blockade.
The use of neuromuscular blocking agents is not routinely required for continued ventilation. However
some patients whose high sedative requirements lead to adverse cardiovascular effects may benefit
from pharmacologic paralysis.

trauma.org 5:1 2000


Mendelow AD, Teasdale GM, Russell T et al. Effect of mannitol on cerebral blood flow and
cerebral perfusion pressure in human head injury. J Neurosurg 63:43-48, 1985
Muizelaar JP, Lutz HA, Becker DP et al. Effect of mannitol on ICP and CBF and correlation with
pressure autoregulation in severely head injured patients. J Neurosurg 61:700-706, 1984
Rosner MJ, Coley I. Cerebral perfusion pressure: a hemodynamic mechanism of mannitol and the
pre-mannitol hemogram. Neurosurg 21:147-156, 1987
Cruz J, Miner ME, Allen SJ et al. Continuous monitoring of cerebral oxygenation in acute brain
injury: injection of mannitol during hyperventilation. J Neurosurg 73:725-730, 1990
Cold GE. Cerebral blood flow in acute head injury. Acta Neurochir S49:18-21, 1990
Kaufmann AM, Cardozo E. Aggravation of vasogenic cerebral edema by multiple dose mannitol. J
Neurosurg 77:574-589, 1992
Schwartz ML, Tator CH, Rowed DW. The University of Toronto head injury treatment study: A
prospective randomised comparison of pentobarbital and mannitol. Can J Neurol Sci 11:434-440,
1984

Smith HP, Kelly DL, McWhorter JM et al. Comparison of mannitol regimens in patients with
severe head injury undergoing intracranial monitoring. J Neurosurg 65:820-824, 1986MCQ
Sebagai bagian dari perawatan intensif cedera otak traumatis, tekanan intrakranial (ICP) harus
dikontrol ketika tekanan perfusi serebral (CPP) turun di bawah 70mmHg dan / atau ICP lebih
besar dari 20 mmHg. Hipertensi intrakranial terjadi pada sekitar 40% dari semua pasien dengan
cedera otak traumatis yang parah. Pemeliharaan tekanan perfusi serebral yang memadai lebih
penting daripada kontrol ICP per se. Langkah-langkah untuk meningkatkan tekanan arteri ratarata harus dilembagakan sebelum memulai metode yang lebih kompleks kontrol ICP.
Ada beberapa metode untuk mengendalikan ICP. Ini biasanya diterapkan secara bertahap untuk
mencapai kontrol, mana mungkin. Prasyarat mutlak bagi pasien berpotensi parah cedera otak
adalah intubasi trakea dengan tabung diborgol. Ini melindungi dan memelihara jalan napas dan
memungkinkan untuk oksigenasi maksimal dan kontrol ventilasi.
Ventilasi
Karbon dioksida melebarkan pembuluh darah otak, meningkatkan volume darah di lemari besi
intrakranial dan karena itu meningkatkan ICP. Pasien harus berventilasi untuk normocapnia
(PaCO2 4.0 kPa / 30mmHg).
Sebelumnya, hiperventilasi digunakan secara rutin untuk mengurangi maksimal PaCO2. Tidak
ada penelitian telah menunjukkan ini untuk meningkatkan hasil pada pasien ini. Selain itu,
doppler transkranial (TCD) tomography penilaian dan positron emission (PET) menunjukkan
ini dapat menyebabkan penyempitan pembuluh otak yang signifikan dan peningkatan resistensi
pembuluh darah otak dapat mengurangi aliran darah otak ke bawah ambang batas iskemik.
Satu studi telah menunjukkan peningkatan dalam hasil jangka panjang ketika hiperventilasi
tidak digunakan secara rutin.
Akibatnya hiperventilasi harus digunakan hanya untuk periode singkat ketika kontrol langsung
dari ICP diperlukan. Misalnya pada pasien yang memiliki kerusakan neurologis akut sebelum
CT scan dan intervensi bedah. Hiperventilasi tidak harus mengambil tingkat PaCO2 ke bawah
3,5-4 kPa karena ada minimal efek menguntungkan pada ICP di bawah tingkat ini.
Kadang-kadang hiperventilasi mungkin diperlukan untuk waktu yang lebih lama pada pasien
dengan ICPs tetap tinggi yang tidak menanggapi terapi lainnya. Pasien-pasien ini mungkin
mendapat manfaat dari neuromonitoring lebih intensif seperti penilaian saturasi oksigen dan
transkranial doppler vena jugularis untuk memastikan perfusi serebral tidak sedang terganggu
dengan mengorbankan ICP. Hiperventilasi Persistent tidak boleh digunakan dalam 24 jam
pertama dan sebaiknya tidak dalam 5 hari pertama setelah cedera otak.
Terapi cairan intravena
Pasien dengan cedera otak parah harus disimpan normovolaemic. Rejimen sebelumnya
merekomendasikan bahwa pasien tetap 'kering' telah dasarnya telah dibuang karena ada risiko
yang signifikan dari kedua episode hipotensi (yang mengarah ke penurunan perfusi serebral)
dan sindrom respinse inflamasi sistemik (SIRS) atau kegagalan organ multiple (MOF)
menyebabkan kegagalan oksigenasi dan ventilasi. Dehidrasi memiliki sedikit efek pada edema
serebral.
Air bebas (sebagai solusi dekstrosa) harus tidak diberikan. Hal ini akan menurunkan osmolalitas
plasma dan meningkatkan kadar air jaringan otak (blood brain barrier bertindak sebagai
membran semipermeabel). Kadar gula darah tinggi yang terkait dengan memburuknya cedera
neurologis setelah episode iskemia serebral global. Otak iskemik memetabolisme glukosa
menjadi asam laktat, menurunkan pH jaringan dan berpotensi memperburuk cedera iskemik.
Larutan hipertonik dan diuretik osmotik seperti manitol akan memiliki efek sebaliknya.
Mekanisme ini membutuhkan penghalang darah otak utuh. Jika ini rusak, yang mungkin
menjadi kasus setelah cedera, berat molekul rendah, osmotik partikel aktif dapat bocor ke
interstitium otak. Dalam hal ini manitol mungkin tidak berpengaruh dalam mengurangi kadar

air otak, dan pemeliharaan tekanan onkotik koloid di kapal dengan pemberian koloid, protein
plasma atau senyawa dengan berat molekul tinggi lain mungkin, secara teoritis, menjadi
manfaat. Namun dalam prakteknya, koloid menawarkan sedikit keuntungan atas solusi
kristaloid.
Ada minat yang cukup besar dalam penggunaan solusi kristaloid hipertonik untuk pengobatan
hipovolemia dengan adanya hipertensi intrakranial. Penelitian pada hewan telah membuktikan
keampuhan larutan hipertonik dalam membalikkan shock, dan kadang-kadang dalam
mengendalikan ICP. Uji klinis menunjukkan bahwa kelangsungan hidup setelah cedera otak
berat (GCS <9) dapat ditingkatkan dengan larutan hipertonik. Namun mereka cedera yang
menyebabkan gangguan dalam sawar darah otak menunjukkan sedikit atau memburuk
menanggapi pemberian cairan hipertonik.
Tidak ada cairan terbaik tunggal untuk pasien dengan cedera otak traumatis, tetapi kristaloid
isotonik yang banyak digunakan dan memiliki dasar ilmiah yang baik. Normal saline atau
larutan Ringer laktat harus cairan resusitasi standar sampai penelitian lebih lanjut
menunjukkan manfaat yang jelas dari terapi lain. Terlepas dari jenis cairan yang dipilih,
normovolemia harus dijaga dan episode hipotensi dihindari.
Mannitol
Manitol, gula 6 karbon, banyak digunakan di kepala manajemen cedera, meskipun belum
pernah mengalami percobaan terkontrol secara acak terhadap plasebo dan metode dan waktu
administrasi bervariasi. Ini adalah diuretik osmotik dan dapat memiliki efek menguntungkan
yang signifikan pada ICP, aliran darah otak dan metabolisme otak. Manitol memiliki dua
mekanisme utama aksi. Segera setelah pemberian bolus itu mengembang volume sirkulasi,
mengurangi kekentalan darah dan karena itu meningkatkan aliran darah otak dan pengiriman
oksigen serebral.
Sifat osmotik yang berlaku di 15-30 menit ketika mendirikan gradien osmotik dan menarik air
keluar dari neuron. Namun setelah pemberian berkepanjangan (infus) molekul manitol bergerak
melintasi ke dalam ruang interstitial otak dan dapat memperburuk edema serebral dan
meningkatkan ICP. Manitol sendiri langsung memberikan kontribusi untuk pemecahan ini
sawar darah otak.
Oleh karena itu yang terbaik manitol digunakan oleh administrasi bolus mana pengurangan
akut di ICP diperlukan. Misalnya pasien dengan tanda-tanda herniasi yang akan datang
(unilateral dilatasi pupil / ekstensor sikap) atau dengan lesi massa berkembang dapat benfit dari
manitol untuk mengurangi akut ICP selama waktu yang diperlukan untuk CT scan dan / atau
operasi.
Manitol sepenuhnya diekskresikan dalam urin dan menyebabkan peningkatan serum urin dan
osmolalitas. Pasien dengan perfusi miskin ginjal (shock), sepsis, menerima obat nefrotoksik atau
dengan osmolalitas serum lebih 320mOsm beresiko nekrosis tubular akut. Hypolaemia harus
dihindari dengan infus cairan isotonik yang diperlukan.
Sedasi dan anestesi
Semua tetapi pasien paling parah cedera otak (GCS 3) akan membutuhkan anestesi untuk
intubasi. Tanggapan kardiovaskular untuk intubasi menginduksi kenaikan ICP yang berlebihan
pada pasien-pasien di puncak kurva tekanan-volume. Intubasi urutan cepat mungkin metode
yang paling aman mendirikan saluran napas pada pasien ini.
Melanjutkan sedasi akan diperlukan pada kebanyakan pasien untuk memungkinkan ventilasi
yang memadai dan untuk mencegah batuk atau melawan ventilator. Berikutnya Valsava-jenis
manuver menyebabkan kenaikan tajam dalam tekanan intrakranial. Yang agen yang digunakan
untuk mencapai sedasi mungkin kurang penting. Namun persiapan akting singkat akan
memungkinkan kontrol yang lebih baik dari kedalaman anestesi dan pemulihan lebih cepat dari
sedasi. Agen dengan durasi yang lebih lama dari tindakan seperti diazepam dapat terbaik

dikelola oleh bolus intravena yang dibutuhkan bukan oleh infus konstan untuk menghindari
penumpukan metabolit aktif.
Sedasi tidak analgesia, dan persyaratan sakit harus diatasi untuk memberikan tenang, nyaman
pasien. Analgesia yang memadai juga akan mengurangi kebutuhan untuk sedasi dan blokade
neuromuskular.
Penggunaan agen memblokir neuromuskuler tidak secara rutin diperlukan untuk ventilasi terus.
Namun beberapa pasien yang tinggi penenang persyaratan menyebabkan efek kardiovaskular
yang merugikan dapat mengambil manfaat dari kelumpuhan farmakologis..com
Hypoglycemia and hyperglycemia need to be identified and treated early in the evaluation. Not only
can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal
ischemia. Administration of glucose in hypoglycemia produces profound and prompt improvement,
while insulin should be started for patients with stroke and hyperglycemia. Ongoing studies will help to
determine the optimal level of glycemic control.[2]
Hyperthermia is infrequently associated with stroke but can increase morbidity. Administration of
acetaminophen, by mouth or per rectum, is indicated in the presence of fever (temperature >100.4 F
[38 C]).
Supplemental oxygen is recommended when the patient has a documented oxygen requirement. To
date, there is conflicting evidence whether supernormal oxygenation improves outcome.
Optimal blood pressure targets remain to be determined. Many patients are hypertensive on arrival.
American Stroke Association guidelines have reinforced the need for caution in lowering blood
pressures acutely.
In the small proportion of patients with stroke who are relatively hypotensive, pharmacologically
increasing blood pressure may improve flow through critical stenoses.
Serial monitoring and interventions when necessary early in the clinical course and eventual stroke
rehabilitation and physical and occupational therapy are the ideals of management. (See Table 2,
below.)
In patients with transient ischemic attacks (TIAs), failure to recognize the potential for near- term
stroke, failure to perform a timely assessment for stroke risk factors, and failure to initiate primary and
secondary stroke prevention exposes the patient to undue risk of stroke and exposes clinicians to
potential litigation. TIAs confer a 10% risk of stroke within 30 days, and one half of the strokes
occurring after a TIA, occurred within 48 hours
Tujuannya agar pengelolaan akut pasien stroke adalah untuk menstabilkan pasien dan untuk
menyelesaikan evaluasi awal dan penilaian, termasuk pencitraan dan laboratorium penelitian, dalam
waktu 60 menit dari kedatangan pasien. [1] (Lihat Tabel 1, di bawah ini.) Keputusan Kritis fokus pada
kebutuhan untuk intubasi, kontrol tekanan darah, dan penentuan risiko / manfaat untuk intervensi
trombolitik.
Hipoglikemia dan hiperglikemia perlu diidentifikasi dan diobati dini dalam evaluasi. Tidak hanya dapat
keduanya menghasilkan gejala yang menyerupai stroke iskemik, tetapi mereka juga dapat
memperburuk iskemia saraf yang sedang berlangsung. Administrasi glukosa dalam hipoglikemia
menghasilkan peningkatan yang mendalam dan cepat, sementara insulin harus dimulai untuk pasien
stroke dan hiperglikemia. Studi yang sedang berlangsung akan membantu untuk menentukan tingkat
optimal kontrol glikemik. [2]
Hyperthermia yang jarang berhubungan dengan stroke tetapi dapat meningkatkan morbiditas.
Administrasi acetaminophen, melalui mulut atau rektum, ditunjukkan dengan adanya demam (suhu>
100,4 F [38 C]).

Oksigen dianjurkan bila pasien memiliki kebutuhan oksigen didokumentasikan. Sampai saat ini, ada
bukti yang bertentangan apakah oksigenasi supernormal meningkatkan hasil.
Target tekanan darah yang optimal tetap ditentukan. Banyak pasien hipertensi pada saat kedatangan.
Pedoman American Stroke Association telah memperkuat perlunya kehati-hatian dalam menurunkan
tekanan darah akut.
Dalam sebagian kecil dari pasien stroke yang relatif hipotensi, farmakologi meningkatkan tekanan
darah dapat meningkatkan aliran melalui stenosis kritis.
Serial monitoring dan intervensi bila diperlukan pada awal perjalanan klinis dan rehabilitasi stroke
akhirnya dan terapi fisik dan pekerjaan adalah cita-cita manajemen. (Lihat Tabel 2, di bawah ini.)
Pada pasien dengan serangan iskemik transient (TIA), gagal untuk mengenali potensi stroke jangka
dekat-, kegagalan untuk melakukan penilaian tepat waktu untuk faktor risiko stroke, dan gagal untuk
memulai pencegahan stroke primer dan sekunder menghadapkan pasien untuk tidak semestinya risiko
stroke dan menghadapkan dokter untuk potensi litigasi. TIA memberi risiko 10% stroke dalam waktu
30 hari, dan satu setengah dari stroke terjadi setelah TIA, terjadi dalam waktu 48 jam