some impairment of ocular motility by thisstage, some degree of exophoria ispresent in most people when they are not completelyawake.However, examining oculocephalicresponses by rotating the head usually willdisclose eye movement problems
Infection most often related to duration of catheter placement , infection rate significantly increased after 5 days of palcement.
find a reduction in CSF and systemic infection in the group that received prolonged antibiotic prophylaxis. It should be noted that infections that develop in patients who receive prolonged or broad-spectrum antibiotic prophylaxis, or both, for EVD placement are often caused by more virulent microorganisms such as Candida and gram-negative organisms.[32-34] Currently, the “Guidelines for the Management of Severe Traumatic Brain Injury” does not recommend antibiotic prophylaxis for EVD placement/catheterization.significantly reduce bacterial adhesion versus controls in vitro and in animal models. In one randomized controlled trial, Zabramski and coworkers showed that a catheter impregnated with minocycline and rifampin reduced the infection rate significantly from 9.4% to 1.3
The percussion wave is the most constant in amplitude and derives from pulsations in large intracranial arteries. The tidal wave has a more variable shape and is thought to arise from brain elastance. The tidal wave and the dicrotic wave are separated by the dicrotic notch, which corresponds to the dicrotic notch in the arterial pulse waveform.
it is possible to insert the probe into a region with pathology as well.t is possible to insert the ICP monitor even in patients with severely compressed ventricles or those with a significant midline shift.
The most significant problem of the Camino fiberoptic device is zero drift. The device is first zeroed to atmospheric pressure (usually at room temperature) and then inserted into the brain parenchyma. Recalibration cannot be performed unless the transducer is removed from the patient, zeroed, and then reinserted. Zero drift then occurs over time, which will lead to an erroneous ICP reading. According to the manufacturer, the drift for the first 24 hours should be only 2 mm Hg and then should be 1 mm Hg for the first 5 days. However, clinical studies have shown that the daily drift is significantly larger than the manufacturer's specification. Daily drift rates of 0.5 to 3.2 mm Hg have been reported, and the maximal drift reported in most studies is usually greater than 20 mm Hg (positive or negative).[41,43-45] In most clinical series, recalibration was often needed, and this was often discovered when the clinical picture did not match the ICP reading or a negative ICP reading appeared on the monitor., However, there has been no report of erroneous ICP reading resulting in clinical mismanagement, such as missing an enlarging mass lesion
Prevention or treatment of factors that may aggravate or precipitate intracranial hypertension is a cornerstone of neurologic critical care. Specific factors that may aggravate intracranial hypertension include obstruction of venous return (head position, agitation), respiratory problems (airway obstruction, hypoxia, hypercapnia), fever, severe hypertension, hyponatremia, anemia, and seizures
WITH ELEVATION MAP REDUCED AND ICP ALSO REDUCED HENCE CBF IS CONSTANT.J Trauma. 2004 Oct;57(4):687-93; discussion 693-5.Decompressivelaparotomy to treat intractable intracranial hypertension after traumatic brain injury
which may be needed to improve oxygenation, can increase ICP by impeding venous return and increasing cerebral venous pressure and ICP, and by decreasing blood pressure leading to a reflex increase of cerebral blood volume.
Fever increases metabolic rate by 10% to 13% per degree Celsius
. If the decision is made to treat systemic hypertension, the choice of antihypertensive agent is important. Vasodilating drugs, such as nitroprusside, nitroglycerin, and nifedipine, can be expected to increase ICP and may reflexively increase plasma catecholamines, which may be deleterious to the marginally perfused injured brain. Sympathomimetic-blocking antihypertensive drugs, such as β-blocking drugs (labetalol, esmolol) or central acting α-receptor agonists (clonidine), are preferred because they reduce blood pressure without affecting the ICP. Agents with a short half-life have an advantage when the blood pressure is labile.
[PubMed] reported of patients with severe anemia presenting with symptoms of increased ICP and signs of papilledema, which resolve with treatment of the anemia The mechanism is thought to be related to the marked increase in CBF that is required to maintain cerebral oxygen delivery when anemia is severe.
Although a disadvantage of this therapy is that the neurologic examination cannot be monitored closely, the sedatives and muscle relaxants can be interrupted once a day, usually before morning rounds, to allow neurologic assessments.
Myopathy is associated with the use of neuromuscular blocking agents, particularly in combination with corticosteroids . Polyneuropathy has been observed in patients with sepsis and multiple organ failure. Prolonged neuromuscular blockade is seen in patients with multiple organ failure especially with kidney and liver dysfunction
If these premises be true, it does not then appear very conceivable
how any portion of the circulating fluid can ever be withdrawn from
within the cranium, without its place being simultaneously occupied
by some equivalent; or how anything new or exuberant can be
intruded without an equivalent displacement.
- George Kellie
To discuss the physiologic mechanisms that maintain
normal intracranial pressure
To discuss pathological and clinical features of raised
To discuss the monitoring and management of raised
Understanding of the CSF circulation — MAGENDIE who
described a small foramen in the floor of the fourth ventricle 175
ALEXANDER MONRO &GEORGE KELLIE((1823-24,
Scotland) ) defined closed box concept
(1846) - BURROW - The concept of reciprocal
volume changes between blood and CSF to account for
the changes in ICP.
(early 20th century) - WEED - An understanding of
raised ICP encompasses an analysis of both
intracranial volume and craniospinal compliance
1866 Lyden measures ICP via trephine
1866 Knoll produces graphic CSF pressure
1870 Duret observes deleterious effects of
injecting fluid in to dogs skulls
1891 QUINKE introduced LP allowing CSF
sampling & measurement
1900 CUSHING describes the classic Triad seen
with severely elevated ICP
1960 LUNDBERG introduced long term
continuous ICP monitoring via an
indwelling intraventricular catheter.
(1972) -MARIO BROCK organised the first
International Symposium on Intracranial Pressure in
• (1987) - MARMAROU published his studies on
intracranial compliance in the head injured and
described the pressure volume index (PVI).
Definition: The pressure that is exerted on to the
brain tissue by external forces, such as cerebrospinal
fluid (CSF) and blood.
Normal ICP: adults: 10-15 mm Hg / 135-200 mm of
children: 3-7 mm Hg
infants: 1.5-6 mm Hg
neonates: <-2 mm Hg
Principle buffers in the brain: CSF & to a lesser extent,
venous blood volume as they are connected to low
CSF: spinal subarachnoid space [through foramen
Venous blood: Jugular veins, Emissary veins.
Brain can distort in a plastic fashion
allows some compensation
Can result in secondary hydrocephalus
Compensatory mechanisms can accommodate an
additional 100-120 ml in the intracranial volume
the summarized volume of the intracranial
components (brain tissue, blood, CSF) is constant.
Inrease of any of them is possible only at the expense
of the other two, and inceases the intracranial
Vintracranial vault = Vbrain + Vblood + Vcsf
The brain is essentially non-compressible
Any increase in intracranial volume decreases CSF
CSF - primarily displaced into the spinal
Blood - venoconstriction of CNS capacitance
vessels displaces blood in jugular venous system
Exhaustion of compensation
Once these limited homeostatic mechanisms are
exhausted additional small increases in intracranial
volume produce marked elevations in ICP
Raised ICP may decrease CBF resulting in vicious
ICP mm Hg
ICP controlled due
Autoregulation of cerebral blood flow
Automatic alteration in diameter of cerebral blood
vessels to maintain constant blood flow to brain
Cerebral autoregulation is a mechanism whereby over wide
range, large changes in systemic BP produce only small
changes in CBF, Due to autoregulation.
CPP would have to drop below 40 in a normal brain before
CBF would be impaired,
Cerebral perfusion pressure (CPP)
Pressure needed to ensure blood flow to the brain
CPP = MAP – ICP
Normal is 70 to 100 mm Hg
<50 mm Hg is associated with ischemia and neuronal
The critical parameter for brain function and survival is
not actually ICP, rather it is adequate cerebral blood
flow (CBF) to meet CMR02 demands
Cerebral Blood Flow
Net increase in water content of both intracellular &
extracellular compartment of cerebral tissue
Vasogenic edema : neoplasms, hematomas, abscesses
Cytotoxic edema : hypoxia/ischemia
Interstitial edema : obstructive hydrocephalus—.
Definition of herniation
Herniation of brain
tissue from one
by calvarial and /or dural
boudaries) to another.
SEVEN MAJOR PATTERNS OF BRAIN SHIFT
(PLUM AND POSNER ‘S CLASSIFICATION)
lateral displacement of the
occurs when an expanding
lesion presses the cerebral
against the falx.
Ipsilateral anterior cerebral
artery (ACA) infarction as
ACA is entrapped under
LATERAL DISPLACEMENT OF THE
Occurs when an
expanding mass lesion
pushes the diencephalon
displacement of the
calcified pineal gland
This lateral displacement is
roughly correlated with the
degree of impairment of
Coma due to impairment
of the ascending arousal
system at the
Pituitary stalk may
become partially avulsed,
Downward displacement of the midbrain or pons
Stretches the medial perforating branches of the
Pressure and Push of
tonsils against FM
closing of 4th ventricle
can occur suddenly
Upward brainstem herniation
Rapidly expanding post.
Vermis and midbrain
Compressing the dorsal
midbrain ,blood vessels
and the cerebral
Impaired upgaze , LOC
• Headache - usually frontal and classically worse after lying down.
• Vomiting - classically early morning, and without associated nausea.
• Blurred vision.
• Tense fontanelle in infants.
• Depressed conscious state.
• Cushing'striad: hypertension, bradycardia,apnoea.
• Pupillary changes: uni or bilateral pupillary dilation.
• VI nerve palsy (false localising sign).
• Papilloedema - may not be present if increase in ICP is of recent onset (< 24 hrs).
CLINICAL FEATURES OF
ACTIVATION OF ANS
& VAGUS NERVE
Indications for ICP monitoring
Trauma and ICH are the two prime indications for ICP monitoring.
The classic indication is in the patient in a coma with a Glasgow Coma
Scale score of 8 or less.
Perioperative ICP monitoring :undergone tumor or arteriovenous
malformation resection and are at risk for cerebral edema with an
inability to follow a clinical neurological examination.
Selected non neurosurgical cases where risk of raised ICP.
Ideal ICP monitor
• Nils Lundberg outlined the basic requirements for an
• Minimal trauma during placement
• Negligible risk for infection
• No CSF leakage, easy to handle, reliable
• Able to continue to function during various diagnostic
and therapeutic procedures
American National Standard for Intracranial Pressure
Monitoring Devices, specifies that
ICP monitoring device should have
A pressure range between 0 and 100 mm Hg,
Accuracy of 2 mm Hg in the range of 0 to 20 mm Hg
Maximal error of 10% in the range of 20 to 100 mm Hg
External Ventricular Drain
An external ventricular drain (EVD), or
ventriculostomy drain, connected to an external strain
gauge is currently the “gold standard” for measuring
Serves also as a therepeutic device
Accurate placement of an EVD may be difficult.
In some patients, it is simply not possible to place an
Complications include malposition(4-20%)
And infection (8.8%)
Factors affecting the complications with
VENUE OF PLACEMENT
PROPHYLACTIC CATHETER EXCHANGE
PROPHYLACTIC ANTIBIOTIC USE
The ICP waveforms recorded with
. Left ventricular
the cardiac component.
During inspiration ,
there is a fall in ICP and
rise in ICP during
waveform of highest
frequency consist of as
many as five smaller
the percussion wave
the tidal wave (W2)
the dicrotic wave (W3)
Lundberg's classification of ICP
A waves or plateau waves
Lundberg N: Continuous
recording and control of
ventricular fluid pressure in
neurosurgical practice. Acta
Scand 1960; 36(Suppl 49):1-
A WAVES or PLATEAU WAVES
Steep raise in ICP to 50-80 mm Hg
Duration 2-20 minutes
Result of an increase in cerebrovascular blood
volume due to vasodilation.
Plateau waves are a normal compensatory
response to decreases in CPP
Lundberg B waves
Short elevations of A modest nature (10 to 20 mm hg)
that occur at A frequency of 0.5 to 2 hz/S
Thought to relate to vasodilation secondary to
respiratory fluctuations in paco2
Questionable clinical significance
Are more rapid sinusoidal fluctuations occurring
approximately every 10 seconds
Corresponding to traube-hering-mayer fluctuations in
Fiberoptic devices for ICP monitoring in which the
catheter tip measures the amount of light reflected off
a pressure-sensitive diaphragm .
The most widely studied fiberoptic device is the
Camino fiberoptic ICP monitoring device (Integra
Neuroscience, Plainsboro, NJ).
Ease of insertion.
low complication rate
(breakage or dislocation)
The subarachnoid screw (bolt)
A subdural screw or bolt is a hollow screw that is
inserted through a hole drilled in the skull. It is placed
through dura mater.
This allows the sensor to record from inside the
Does not penetrate the brain.
Lower risk of infection than
the intraventricular catheter
It is easier to place.
It is unable to drain CSF
The accuracy is questionable.
It has a microchip
pressure sensor at
the tip of a flexible
nylon cable that
electricity based on
can be placed in various
compartments, including the
ventricle, parenchyma, and
using an Air-Pouch mounted
in the tip region of a dual
One lumen transmits the
pressure to the Brain-
Pressure Monitor. The second
lumen is used for drainage of
To measure compliance, the monitor injects a small
amount of air into the air balloon pouch and measures
the pressure response to this change in volume
Noninvasive Intracranial Pressure
optic nerve sheath diameter (ONSD), which can be
measured by ultrasound, correlates with ICP.
demonstrated a strong linear relationship between
ONSD and ICP.
But the critical value of ONSD for detecting elevated
ICP (ICP >20 mm Hg) is different in the various
studies, thus limiting its potential use at this time
venous ophthalmodynamometry, which measures
venous opening pressure (VOP), to calculate ICP.
Drawback -requires dilation of the pupil to perform
Both ONSD and VOP measurement can be performed
only intermittently and therefore can be used just as a
screening tool for ICP elevation rather than as a
Tympanic membrane displacement gives an idea of
Cochlear fluid pressure acts as a surrogate for ICP.
But less accurate.
Measuring ICP based also on changes in patterns of
blood flow velocity in the intracranial arteries, which
can be assessed by transcranial Doppler.
Delay in visual evoked potentials.
Intracranial hypertension secondary to traumatic brain
Traumatically induced masses: epidural or subdural
hematomas, hemorrhagic contusions, foreign body,
and depressed skull fractures
Hyperemia owing to vasomotor paralysis or loss of
Hypoventilation that leads to hypercarbia with
subsequent cerebral vasodilation
Goals of therapy
Maintain ICP at less than 20 to 25 mm Hg.
Maintain CPP at greater than 60 mm Hg by
maintaining adequate MAP.
Avoid factors that aggravate or precipitate elevated
Indications to treat IC-HTN
ICP '" 20-25 mm Hg
Ropper AH :Raised ICP in neurological disesases Sem neurology 4:397-400,1984
Bullock R,Chesnut R M,Cliflon G, eral.: Guidelines for tbe management or
severe head injury, The Brain Trauma Foundation (New York), The American
ASliociation of Neurological Surgeons The Joint Section of Neu· rotrauma and
Critical Care, 1995
General care to minimize intracranial
Optimizing cerebral venous outflow
Blood pressure control
Treatment of anemia
Sedation and analgesia
Optimizing cerebral venous
Head end elevation to 30-450 reduces the ICP 1 by
Enhancing the venus outflow
Promoting CSF displacement and
Reducing MAP at carotids
Efeect is immediate
1Neurosurgery. 2004 Mar;54(3):593-7;
Effects of head posture on cerebral hemodynamics: its influences on
intracranial pressure, cerebral perfusion pressure, and cerebral
Avoid hypoxia (PaO2 <60mmhg or O2 sat< 90%)
Ventilate to normocarbia( avoid prophylactic
Optimal respiratory management is crucial for control
Mechanical ventilation also can have adverse effects on
Adjusting ventilator settings ( PEEP)
potent vasodilator and Fever-induced dilation of
cerebral vessels can increase CBF and may increase
worsens neurologic injury 1.
1.Jones PA, Andrews PJD, Midgley S, et al. Measuring the burden of
secondary insults in head-injured patients during intensive care. J
Neurosurg Anesth. 1994;6:4–14.
Blood pressure control
Avoid hypotension –normalize intravascular volume.
Use pressors if needed.
Control hypertension if present.
Treatment of anemia
It is reported of patients with severe anemia
presenting with symptoms of increased ICP and signs
of papilledema, which resolve with treatment of the
anemia 1 .
Biousse V, Rucker JC, Vignal C, et al. Anemia and papilledema. Am J
Seizures can increase cerebral metabolic rate and ICP.
Control of seizures found to increase the outcome in
severe traumatic brain injury.
Lee ST, Lui TN, Wong CW, et al. Early seizures after severe closed head
injury. Can J Neurol Sci. 1997;24:40–3.
Sedation and analgesia
Agitation and pain may significantly increase blood
pressure and ICP.
Light sedation and good analgesia
Schwab, S. et al. "Moderate Hypothermia in the
Treatment of Patients with Severe Middle Cerebral
Artery Infarction." American Heart Association. July 31,
1998, pg. 2461-2466
Measures for refractory
Heavy sedation and paralysis
Heavy sedation and paralysis
Intracranial hypertension caused by agitation,
posturing, or coughing can be prevented by sedation
and nondepolarizing muscle relaxants that do not
alter cerebrovascular resistance.
morphine and lorazepam for analgesia/sedation and
cisatracurium or vecuronium as a muscle relaxant.
Can minimize these complications by
Limiting the use and dose
Measuring creatine phosphokinase daily
Stopping thedrug daily to evaluate response.
isolated from the secretions of the plant flowering ash
and called manna after its resemblance to the Biblical
Today, mannitol is commercially produced by catalytic
hydrogenation of fructose, sucrose (invert sugar), or
Schwarz, 1994; Ojamo et al., 2000
An osmotic diuretic
alcohol of the 6C sugar mannose
confined to the extracellular space
only slightly metabolized and rapidly excreted by the
Mannitol induces diuresis by elevating the osmolarity of
the glomerular filtrate and thereby hindering tubular
reabsorption of water.
Excretion of sodium and chloride is also enhanced
Time to action 1-5min, peak at 20-60min; ICP returns to
baseline by 4hours
Mannitol osmotherapy in brain
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'.
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.
Blood viscosity autoregulation of
Influences intracranial compliance: hence
improvement in neurological status can occur despite
little measurable effect on ICP.
autoregulation is mediated through alterations in the
level of adenosine in response to oxygen availability
changes in cerebral tissue.
The decrease in blood viscosity after mannitol
administration leads to an improved oxygen transport
to the brain.
. When autoregulation is intact, more oxygen leads to
decreased adenosine levels, resulting in
The decrease in resistance to flow from the decreased
blood viscosity is balanced by increased resistance
from vasoconstriction, so that CBF remains the same
A test dose of mannitol should be given prior to
instituting therapy for patients with marked oliguria or
those believed to have inadequate renal function.
Acute adverse haemodynamic effects
- variable effects on BP following a bolus of mannitol
- the acute vasodilatory effect of mannitol
decrease in plasma pH
release of ANP
histamine release from basophils
direct impairment of contractile properties of vascular
Dehydration and Electrolyte Disturbances
- osmotic diuretics result in excess net free water
- sodium imbalance
- other electrolytes imbalance :potassium, phosphate
- cardiac arrhythmias and neuromuscular
complications are common
- definition is any unexpected rise in ICP after the
administration of osmotherapy
- explanation : due to penetration of osmotically active
particles into the brain, their accumulation creating an
osmotic gradient favouring movement of water into
the brain, and oedema formation
other possible mechanisms
rapid volume depletion stemming from overzealous
administration of osmotic diuretics
overly rapid administration of hypotonic fluids to
patients after a prolonged period of hyperosmolar
in the former case, volume depletion sets the stage for
hyperviscosity and haemodynamic compromise leading
to reactive cerebral hyperaemia
- in the latter case, a CNS adjusted to the hyperosmolar
state is suddenly exposed to plasma of reduced
•Opens the BBB, and mannitol that has crossed the
BBB may draw fluid into the CNS which can aggravate
vasogenic cerebral edema'''. It should be tapered to
prevent ICP rebound"
• Corticosteroids + phenytoin + mannitol may cause
hyperosmolar nonketotic state wit
•High doses of mannitol carries the risk of acute renal
•Large doses prevents diagnosing DI
Cautions with mannitol
Used systemically and orally to decrease the
Not metabolically inert. Partially metabolised
to CO2 and water.
Oral Glycerol decreases the ICP in 30-60min.
DOSAGE: 1.2gm/kg, maintainence 0.5-1gm/kg
every 3-4 hrs
IV Preparation: 10% glycerol in 0.4 N saline
Complications: Hemolysis, hemoglobinuria,
renal failure and hyperosmolar coma.
the addition of glycerol to mannitol avoids rebound
edema likely to be observed with the intravenous
administration of only mannitol.
This comnbination stiategy is able to enlance the
diffusion of water from cerebrospinal fluid back into
plasma by elevating the osmolality of the plasma
ICP reduction best with 23.4 % saline
10%, 7.2% and 3% have also been used
Dosage of 3% saline 1-2ml/kg Q12h. over 5
ICP reduction best with 23.4 % saline but ill-
has a clear advantage over mannitol in hypovolemic
and hypotensive patients.
Qureshi et al. Critical Care Medicine, 26(3) (1998) Use of hypertonic (3%)
saline/acetate infusion in the treatment of cerebral edema: Effect on
intracranial pressure and lateral displacement of the brain
Mechanism of action:
Membrane stabilizing effect helps in preserving
Direct vasodilatation of pial vessels
Reduction of blood viscosity due to enhancement
of the intravascular volume
Rapid absorption of cerebrospinal fluid
Restoration of the normal membrane potentials
Local dehydration of brain tissue
Induce constriction of cerebral arteries by alkalinizing
Reduction in cerebral blood volume decreases ICP.
hyperventilation (HPV) to pco2. " 30-35 mm Hg
Used only for
short periods for acute neurologic deterioration
or chronically for documented IC-HTN
unresponsive to sedation, paralytics, CSF drainage
and osmotic therapy
do not use prophylactically
avoid aggressive hyperventilation (pCO<25 mm
Used in conjunction with mannitol to treat raised
Furosemide works synergitically with mannitol
remove free water
appropriate in patients with fluid overload
decreases CSF production
decreases edema in pathological areas(disrupted
oncodiuretic therapy: albumin infusion followed by
furosemide (no hyperosmolality or hypernatremia)
Dexamethasone is the most widely used
Steroids are effective in reducing ICP in tumors.
No proven benefit in Head injured patients.
In cerebral ischemia they may worsen outcome
direct steroid toxicity
increase glucose levels which increases
lactic acid levels.
Mechanism of action:
Reduction in CSF production
Membrane stabilization & restoration of BBB
Reduction in ICP secondary to antiedema
Improves CSF bulk outflow at arachnoid villi
Dexamehtasone 10mg loading dose
Barbiturate protect brain from anoxic, ischemic
and vasogenic cerebral edema.
Useful in reducing ICP resistant for other
methods of treatment.
Mechanism of action:
Uncouples brain metabolism and CBF
Reduces CMRO2 permitting tolerance of a
degree of ischemia or anoxia => lower demand
for CBF =>reduces the CBV and hence reduces
Free radical scavenger
Dosage: 10mg/kg adminstered over 30min.
followed by 1-5mg/kg to maintain a serum
concentration of 3.5 – 4.5mg/100ml or 10 – 20min
of burst suppression
Major disadvantage: Hypotension, (treated with
dopamine), myocardial depression
Administration in ICU with arterial line BP and
Euvolemia to be ensured
Pressor support if required
Causes a decrease in ICP by reducing the CMRO2
and depression of metabolic requirements.
Body temp has to to be reduced to 32.8deg. Fall in
ICP was average of 45% to a maximum of 80%..
Moderate hypothermia can help to control critically
elevated ICP values in severe space-occupying
edema after MCA stroke and may improve clinical
outcome in these patients1.
At 27deg C: cardiac arrhythmias
Problems during rewarming: seizures, drowsiness,
Resection of mass lesions
Acute epidural and subdural hematomas , brain
abscess, tension pneumocephalus and tumors etc
need to be removed
Works immediately by
removal of CSF
long-term benefit by
allowing edema fluid to
drain into the ventricular
External decompression: Decompressive
Reports suggest that decompressive craniectomy
effectively reduces ICP in most (85%) patients with
intracranial hypertension refractory to
conventional medical treatment
Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive craniectomy for
malignant swelling due to severe head injury. J Neurosurg. 2006;104:469–79.
Polin RS, Shaffrey ME, Bogaev CA, et al. Decompressive bifrontal craniectomy in the treatment
of severe refractory posttraumatic cerebral edema. Neurosurgery. 1997;41:84–92.
Brain oxygenation measured by tissue PO2 and blood
flow estimated by middle cerebral artery flow velocity
also are usually improved after decompressive
Stiefel MF, Heuer GG, Smith MJ, et al. Cerebral oxygenation following
decompressive hemicraniectomy for the treatment of refractory intracranial
hypertension. J Neurosurg. 2004;101:241–7.
Bor-Seng-Shu E, Hirsch R, Teixeira MJ, et al. Cerebral hemodynamic changes
gauged by transcranial Doppler ultrasonography in patients with posttraumatic
brain swelling treated by surgical decompression. J Neurosurg. 2006;104:93–100.
Subdural/ subgaleal hygroma
Enhancement of brain edema with fresh
Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive
craniectomy for malignant swelling due to severe head injury. J Neurosurg.
1. Youmans Neurological Surgery, 6th Edition
By H. Richard Winn, Md
2. Plum And Posner’s Diagnosis Of Stupor And Coma
3. Neurosurgery By, Setti S. Rengachary, Robert H.
4. Goodman & Gilman's The Pharmacological Basis Of
Therapeutics - 11th Ed. (2006)
1. first systematic recording of ICP done by
d) all of the above
2. the level of CPP under which CBF would impair is
3.The territory of infarcts seen in uncal herniation
4. The limiting factor for therapy barbiturate is
d)all the above
5.Factor associated with incidence of infection in EVD
a)insertion of IVC in neuro intensive care unit
c)use of steroids
6.most significant problem of fiberoptic ICP monitor
7.best method of ICP monitor in patients with massive
edema with slit ventricles
8.the best method of ICP monitor in coagulopathy
9.During mannitol administration , to prevent renal
failure the serum osmolality should be below
a)320 m osm
d)250 m osm
10.the minimum diametre of decompressive
craniectomy flap is
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