Details of CSF dynamics and ICP along with ICP management for Neurology and Neurosurgery Residents

1. CSF FLOW DYNAMICS AND ICP
WITH MANAGEMENT
DR SAMEEP KOSHTI

2. Normal ICP
• The upper limit of normal ICP in adults and older children
• 15 mm Hg, (usual range is 5 to 10 mm Hg)
• Transient physiologic changes resulting from coughing or sneezing often produce
• pressures exceeding 30 to 50 mm Hg, but ICP returns rapidly to baseline levels.
• ICP can be measured by low-volume displacement transducers
• in the intraventricular, intraparenchymal, subdural, or epidural spaces.

3. • The ICP waveform is normally pulsatile and can be divided into three major
components.
• Cardiac activity/Pulse
• Left ventricular contraction
• more recent analysis has implicated the high-compliance venous blood vessels responsible for
transmission of pulse.

4. • The Respiratory Pulse
• during the respiratory cycle,
• Generated by pressure changes in the thoracic and abdominal cavities.
• During inspiration,
• there is a fall in arterial blood pressure and an increase in pressure gradient from cerebral veins to central
venous capacitance vessels.
• This gradient drives cerebral venous return, which is therefore increased on inspiration, with a concomitant
drop in cerebral blood volume.
• Mechanical ventilation and intrathoracic alter the ICP waveform.

5. If the ICP waveform at a higher chart speed,
• the waveform of highest frequency can be
seen to consist of as many as five smaller
peaks.
• Three of these are relatively constant
the percussion wave (W1),
the tidal wave (W2), and
the dicrotic wave (W3)
• 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,

6. PHYSICAL PRINCIPLES
• ICP is synonymous with CSF pressure and is defined as
• the pressure that must be exerted against a needle introduced into the CSF space to just
prevent escape of fluid .
• Pressure (P) is defined as force (F) per unit area (A).
• Unit :
• either millimeters of water (mm H2O) or
• millimeters of mercury (mm Hg).
• mmHG = mm H2O/13.6
• The SI unit for pressure is the pascal (Pa), which is defined as 1 newton (N)/square meter;
• 1 kilopascal (kPa) = 7.5 mm Hg or 102 mm H2O.

7. • In actual fact,
• three different pressures contribute to steady state dynamics ICP:
• atmospheric pressure,
• therefore absolute ICP varies with altitude
• hydrostatic pressure, and
• The contribution of hydrostatic pressure depends on the weight of fluid and tissue above the point
of measurement, divided by the cross-sectional area at that level.
• For example, lumbar CSF pressure is greater in the sitting position compared with the lateral
decubitus position
• increasing degrees of head-down tilting further increase the contribution of hydrostatic pressure.
• filling pressure.
• by the
• Volume of the intracranial contents : blood, brain, CSF, and any pathologic masses. and the
• Elastance : the pressure change per unit of volume change.
• Compliance is the inverse of elastance, and both measures are useful for understanding the
physiology of ICP.

8. STEADY STATE DYNAMICS -- ICP
• In the absence of disease,
• baseline ICP and
• the amplitude of the pulsatile components of ICP remain constant.
• Skull should be considered a rigid container of noncompressible elements.
• ICP therefore depends on the relative constancy of total volume inside the skull,
contributed to by CSF, blood, and brain tissue.
• Equation for ICP:
• Vcsf + Vblood +Vbrain +Vother = Vintracranial (CONSTANT)
• The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue,
and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or the
Monro–Kellie hypothesis.

9. • The Monro–Kellie hypothesis:
• states that
• “the cranial compartment is incompressible and that the volume inside the cranium is
fixed.
• The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume
equilibrium, such that any increase in volume of one of the cranial constituents must be
compensated by a decrease in volume of another.”
• The principal buffers for increased volumes
• include CSF and,
• to a lesser extent, blood volume.
• These buffers respond to increases in volume of the remaining intracranial
constituents.
• e.g. increase in lesion volume (e.g., epidural hematoma) will be compensated by the
downward displacement of CSF and venous blood.

11. CSF CIRCULATION
• Formation:
• the choroid plexuses of the lateral, third, and fourth ventricles;
• Some originates from the ependymal cells lining the ventricles (Contribution ranges from
50-100%)
• from the brain substance through the perivascular spaces.
• Production rate :
• produced continuously at a rate of about 0.5 (0.2-0.7) mL per minute and
• with a total volume of about 150 mL
• this corresponds to a turnover time of about 5 hours.
• rates of CSF production follow a diurnal variation, with peak production rates in the late
evening and early morning
• The circulation is aided by :
• the arterial pulsations of the choroid plexuses and
• by the cilia on the ependymal cells lining the ventricles.

12. • From the fourth ventricle  the median aperture and the lateral foramina of
the lateral recesses of the fourth ventricle  the subarachnoid space 
cerebellomedullary cistern and pontine cisterns  flows superiorly through the
tentorial notch of the tentorium cerebelli  inferior surface of the cerebrum 
• Some superiorly to lateral aspect of each cerebral hemisphere
• Some inferiorly in the subarachnoid space around the spinal cord and cauda equina.
• Here,the fluid is at a dead end,and its further circulation relies on the pulsations of the
spinal arteries and the movements of the vertebral column, respiration, coughing, and the
changing of the positions of the body.

13. • CSF ABSORPTION:
1. The main sites: arachnoid villi (Together called arachnoid granulations) that project into the dural venous
sinuses, especially the superior sagittal sinus.
• The arachnoid granulations increase in number and size with age and tend to become calcified with advanced age.
2. into the venous sinuses
• occurs when the cerebrospinal fluid pressure exceeds the venous pressure in the sinus.
• (not true vice versa as Arachnoid villi tubules closes in case of raised venous pressure and act as valves).
3. Some directly into the veins in the subarachnoid space,
4. Lymphatics draining CSF
1. Some possibly escapes through the perineural lymph vessels of the cranial and spinal nerves.
2. Lymphatics in arterial walls
3. Olfactory lymphatic system
5. Glyphatic system for solute clearance
6. Parenchymal absorption by capillaries
• Because the production of cerebrospinal fluid from the choroid plexuses is constant, the rate of
absorption of cerebrospinal fluid through the arachnoid villi controls the cerebrospinal fluid pressure.
• CSF reabsorption cease at CSF pressures of less than 5 mm Hg.

14. GLYMPHATIC PATHWAY
• fluid enters the parenchyma from perivascular Virchow-Robin spaces propelled by
artery pulsation.
• Nedergaard and colleagues have described
• The periarterial pathway for propelling the fluid into the parenchyma that is regulated by glial
surface aquaporin channels.
• the “glymphatic” system clearance mechanism
• increases in function with sleeping
• disturbed in
• brain trauma and in
• dementia in which amyloid clearance is decreased.
• Dysfunction of this lymphatic system may lead to
• forms of parenchymal edema.
• This system, combined with the dural, perivascular, and olfactory lymphaticsystems,
constitutes the brain's mechanism of clearance.

16. Parenchymal absorption by capillaries
• The existence of parenchymal absorption more easily explains the stable ventricle
configuration in a child with arrested hydrocephalus,even with an apparent
complete aqueduct stenosis.
• Changes in CSF parenchymal absorption with age
• also help explain the late onset of symptoms in patients with longstanding
hydrocephalus, as seen in adult-onset congenital hydrocephalus.
• wherein aqueductal stenosis is compensated by parenchymal absorption for many years.

20. GENERAL PHYSIOLOGY OF CSF
• In the adult, out of the typically 1500-mL intracranial space is occupied by
• 87 % -the brain,
• 9% by compartmental CSF (ventricles, cisterns, and subarachnoid space), and
• 4% by blood.
• Ventricular CSF volume  7.49 mL to 70.5 mL, (mean of 31.9 mL)
• CSF, in general, has a
• higher sodium, chloride, and magnesium concentration than in a plasma filtrate.
• The concentrations of potassium, calcium, urea, and glucose are lower.
• The overall osmolality is, however, similar.
• Current thinking therefore holds that a simple filtration process is modified by
energy-dependent secretion and reabsorption processes.

21. MODEL FOR CSF DYNAMICS

22. • The rate of formation of fluid (If)
• constant
• independent of the pressure that has to be pumped against.
• Minimally affected in case of raised ICP
• The fluid enters a compliant storage space,
• which can expand to accommodate the added volume, and
• represented by an element (C)
• decreases its compressibility with increasing volume ( much like the resistance offered by a
rubber balloon at maximal inflation.)
• Resistance (Ro) = (total resistance to the outflow of the CSF) comprises
• of the CSF channels/pathway (upto the arachnoid villi)
• of the villi proper
• under normal conditions remains fixed and independent of ICP.
• The final element of this model is the dural sinus pressure (Pd). Fluid crossing the arachnoid
villi must overcome this exit pressure.

23. • CSF pressure (ICP) = (If × Ro) + Pd.
• Steady-state ICP:
• proportional to three parameters:
• (1) the rate of CSF formation,
• (2) the resistance to CSF absorption, and
• (3) the dural sinus pressure.
• When these parameters remain constant, ICP is unchanged,
• the compliance element does not actively participate in ICP regulation.
• An increase in
• CSF formation,
• outflow resistance, or
• venous pressure at the site of fluid absorption
• can alter this dynamic equilibrium and result in elevated ICP.
• Product of (If × Ro) contributes 10% and Pd (Dural sinus pressure) contributes remainder 90%.
• Both are independent of each other.
• With this distribution, it is concluded:
• the outflow resistance:
• would have to increase markedly to cause a significant rise in the ICP.
• sagittal sinus pressure (Pd)
• Much smaller elevations caused by venous sinus obstruction would be transmitted directly to the CSF system, thus raising resting ICP.

24. PULSATION MODEL OF COMMUNICATING HYDROCEPHALUS
• In the new concept,
• the flow of the arterial pulsations into the cranium is considered to be sequential,
• beginning from the large subarachnoid arteries at the skull base to the small arterioles in the
parenchyma.
• Pulsations are dissipated into the subarachnoid CSF and into the choroidal arteries and ventricular CSF.
• The bulk flow of blood that remains after the pulsations have been filtered out continues
through the capillary pathways and represents a windkessel mechanism.
• Most important, this model provides an alternative view to the “bulk flow
theory” causing ventricular enlargement.
• Increased impedance to pulsations in the subarachnoid space increases pulsations in the
blood flow to the choroidal arteries and the choroid plexus, thereby increasing the
pulsations in the ventricular CSF.
• The ventricular pulsations exceed those in the subarachnoid space, and it is theorized that
a transmantle pulse pressure gradient and subsequent ventricular expansion result.
• Future work will focus on demonstrating that this model accounts for the pathologic
changes seen in communicating hydrocephalus

25. Cerebral Blood flow
• The mean normal adult CBF is 53 mL/100 g per minute.

26. NON STEADY STATE DYNAMICS
• Many pathologic states, such as hematoma, tumor, hydrocephalus, and cerebral
edema,
• are associated with changes in intracranial volume, which can, in turn, cause elevated ICP.
1. The most common clinical cause of raised ICP is traumatic brain injury,
• the pathology of which encompasses several possible VOTHERS.
• Brain edema contributes extra volume to the intracranial contents in the form of water.
• intracerebral collections of blood in extradural, subdural, subarachnoid, or
intraparenchymal .
• Furthermore, trauma may induce changes in VBLOOD as a result of disrupted autoregulation
and hyperemia.

27. • 2.ANEURYSMAL RUPTURE AND SAH
• ICP to rise instantaneously,
• and as ICP approaches the mean arterial blood pressure, (ICP= MAP)
• bleeding slows,
• And ultimately  cerebral perfusion pressure is critically low.
• Due to
• intraparenchymal blood collection, increased CBV, and a strong vasomotor reaction to the ensuing injury.
• 3.Brain tumors
• slowly increasing VOTHER, so  compensatory changes can occur.
• Hemorrhage into the body of a tumor
• in a system that is already compensated and therefore dynamically stressed can have disastrous results.
And sudden rise in ICP.
• Also, prolonged periods of increased hydrostatic pressure (such as lying down)
• substantial increases in ICP
• This phenomenon, coupled with the diurnal variation in CSF secretion,
• underlie the early morning headaches and nausea experienced by these patients.

28. • 4.hydrocephalus,
• an impaired CSF drainage system causes CSF accumulation.
• Increases Vcsf
• 5.IIH
• The cause of elevated ICP in idiopathic intracranial hypertension is not known,
• CSF production and drainage have been implicated as the cause.
• 6.Meningitis can influence ICP in several patterns,
• blocking CSF drainage pathways or
• by stimulating marked cerebral edema.
• 7.Arteriovenous malformation
• significant increase in VBLOOD
• If hameorrhage occurs  VOTHER

29. • 8.BRAIN EDEMA
• Def: an increase in the brain tissue water content
• contributes to VOTHER or VBRAIN.
• cytotoxic : intracellular water accumulation
• Vasogenic : extracellular water accumulation
• Assoc. with an open blood-brain barrier and fluid leakage.
• First, for brain tissue water to rise, even under cytotoxic conditions, water has to enter the tissue from
an external source, the most likely of which is blood vessels. Therefore, even cytotoxic edema has a
“vasogenic” origin.
• It is the pathologic cause and the final site of edema accumulation that must distinguish these
phenomena.
• ICP in Idiopathic NPH
• According to guidelines:
• the lumbar pressures : range from 60 to 240 mm H2O.

30. Intracranial Pressure-Volume Relationship
A,
• shows how
compliance
changes as
greater volumes
are added.
• The CSF system
is in the phase of
spatial
compensation at
point ‘a’
• compared with
spatial
decompensation
at point ‘b’
B,
• used as a
description of
intracranial
compliance.

31. Contd..
• Curve of P-V graph:
• The normal pressure volume curve is hyperbolic.
• Above 50 mm Hg, and as ICP approaches mean arterial pressure,
• the curve tends to flatten again; thus, the complete curve is not hyperbolic but rather
sigmoid.
• Compliance:
• The reciprocal of the slope of this curve (ΔV/ΔP) represents the compliance of the system,
• which is maximal in the period of spatial compensation
• Another method :
• plot ICP logarithmically against volume, which gives a straight line
• Its slope is the pressure-volume index (PVI),
• the calculated volume in milliliters needed to raise ICP by a factor of 10
• In normal adults, PVI is 25 to 30 mL
• When compliance is reduced by a pathologic process, PVI diminishes, and therefore small volume changes
result in much greater pressure changes.
• < 13 mL are considered clearly abnormal.
• normal infants have PVIs below 10 mL, and the adult PVI of 25 mL is reached at around 14 years of age.

33. • Although the brain occupies 80% of the intracranial space,
• this volume is effectively available for compensation only when increases in VOTHER occur
slowly.
• With more rapid changes, brain shifts and herniations are more likely to occur.
• Although blood and CSF occupy less of the intracranial space,
• their total volume can be reduced more rapidly.

34. Effects of raised ICP
• CPP = MAP – ICP
• If ICP increases, CPP falls; and
• if the lower limit of autoregulation (50-70 mmHg) is exhausted, CBF will begin to fall.

35. Signs and symptoms of raised ICP
• cardinal symptoms :
• headache,
• vomiting, and
• Papilledema
• is a reliable and objective measure of raised ICP, with good specificity.
• Varying degrees of cranial nerve palsies may arise as a result of pressure on
brainstem nuclei (particularly abducens palsies).

36. Contd..
• The Cushing response, defined as arterial hypertension and bradycardia,
• arises as a result of either generalized central nervous system ischemia or
• local ischemia due to pressure on the brainstem.
• Bradycardia
• mediated by the vagus nerve and can occur independently of hypertension.
• Abnormal respiration
• Cheyne-Stokes respiration arises from damage to the diencephalic region, and
• sustained hyperventilation occurs in patients with dysfunction of the midbrain and upper pons.
• Midpontine lesions cause slow respiration;
• pontomedullary lesions result in ataxic respirations;
• upper medullary lesions cause rapid, shallow breathing; and
• with greater medullary involvement, ataxic breathing predominates.

37. HERNIATION SYNDROMES
1. Central herniation – central syndrome
• structures involved from rostral to caudal
• Diencephalic
• change in behavior or
• even loss of consciousness.
• alters respiration, causing interruptions of sighing, yawning, or pausing;
• Cheyne-Stokes respiration may appear.
• Pupils become small, with a poor reactivity to light.
• A unilateral lesion can cause
• contralateral hemiparesis, with
• ipsilateral paratonia and decorticate responses.
• With progressive midbrain involvement,
• respiration becomes tachypneic, and
• the pupils fall into a midline fixed position.
• Internuclear ophthalmoplegia may arise, and
• motor :
• bilateral decerebrate posturing.
• Pons involvement:
• respiration remains rapid and shallow.
• Motor examination:
• flaccid extremities with bilateral extensor plantar responses.
• Medullary involvement:
• respiration slows and becomes irregular with prolonged sighs or gasps.
• As hypoxia ensues, the pupils dilate, and brain death follows shortly thereafter.

38. Uncal herniation – Uncal syndrome
• often begins with
• 3rd nerve compression:
• a unilaterally dilated and poorly reactive pupil,
• then fully dilate with external oculomotor ophthalmoplegia.
• Midbrain compression ensues,
• consciousness may be impaired,
• followed by contralateral decerebrate posturing.
• On occasion, posturing or hemiparesis may occur ipsilateral to the lesion as a result of pressure on the
contralateral cerebral peduncle on the edge of the tentorium cerebelli (KERNOHAN’s Notch and
PHENOMENON)
• Further progression:
• extensor plantar response appears bilaterally,
• along with dilation of the contralateral pupil.
• Finally, patients will develop
• hyperpnea,
• midposition pupils,
• impaired oculovestibular response, and
• bilateral decerebrate rigidity.
• From this point, progression is as for the central syndrome.

39. SUBFALCINE HERNIATIONS

40. ICP MONITORING
• Intracranial hypertension is found in 40% to 60% of severe head injuries
• Data from the Traumatic Coma Data Bank have shown that the
• proportion of hourly ICP recordings above 20 mm Hg is highly significant in predicting outcome.
• Used in :
• Brain trauma
• Reye’s syndrome and other causes of fulminant hepatic failure
• In the case of intracranial tumors
• After trauma in adults, guidelines for ICP monitoring include :
• a GCS : 3-8
• an abnormal CT HEAD
• If CT HEAD Normal : two or more of the following should prompt monitoring anyway:
• age older than 40 years,
• unilateral or bilateral motor posturing, or
• systolic blood pressure below 90 mm Hg.
• GCS>8
• If CT Head : significant mass lesions or treatment is required for associated injuries.

41. ICP MEASUREMENT METHODS
1. “Ventriculostomy” coupled with a pressure transducer remains the “gold standard
• Adv:
• Access to CSF for dynamic testing and
• drainage to control ICP
• Disadv:
• catheter placement can be difficult when the ventricles are small or shifted from the midline,
• risk of infection rises in ventriculostomies after 5 days (<10 %)
• less than 2% hemorrhagic complications
2. the subarachnoid bolt,
3. epidural transducer,
4. Subdural catheter
5. fiberoptic microtransducer.
• The bolt and epidural transducer,
• less invasive,
• Less accurate
• Fiberoptic catheter-transducers
• cannot be recalibrated externally;
• Good accuracy
• easy to place, and
• the complication rate is low because of their small size and lack of fluid coupling.

42. • There is no uniform agreement about the critical level of ICP beyond which
treatment is mandatory.
• Saul and Ducker demonstrated benefits by
• treating ICP above 15 mm Hg compared with a group of patients treated for ICP above 25 mm Hg.
• Marmarou and colleagues
• calculated the ICP threshold most predictive of 6-month outcome by logistic regression.
• The threshold that correlated best was 20 mm Hg, and this is the current level at which most centers
begin treatment.
• Current opinion now regards CPP as the critical parameter that should be
monitored in concert with ICP.

44. VCSF MANAGEMENT
• If CSF diversion is required:
1. temporary external drainage
• (ventriculostomy),
• Helps to know whether permanent internal drainage would be beneficial or not.
2. temporary internal drainage
• (ventriculosubgaleal shunt),
• with a short side arm opening into the subgaleal space, which is dissected at the time of surgery.
• provides continuous ventricular decompression for several weeks to months without the need for
percutaneous aspiration of the reservoir.
3. permanent internal drainage
• (ventriculoperitoneal shunt,
• ventriculoatrial shunt, or
• third ventriculostomy)
• Alternative to VP shunt in certain situations without the potential risks inherent in standard
ventriculoperitoneal shunting.

45. Contd…
• Adjunctive therapy with medications such as :
1. ACETAZOLAMIDE,
• Reductions of CSF production by 16% to 66% have been achieved.
• has a cerebral vasodilator effect,
• which may transiently worsen intracranial hypertension, and so
• its use is contraindicated in patients with closed head injury.
2. FUROSEMIDE, and
3. CORTICOSTEROIDS
• can transiently decrease CSF production.
• Synergistic action
• When acetazolamide is combined with furosemide.

46. Vblood MANAGEMENT
• There is no absolute blood volume or CBF that is normal;
• these parameters are rather defined by the metabolic activity of the brain itself.
• For example,
• Normal brain: the mean absolute CBF of 53 mL/100 g per minute
• may be considered hyperemic in the anesthetized brain or ischemic in a portion of epileptic cortex.
• Extremes of CBF, both low and high,
• have been seen in patients with poor outcome after head injury
• Measurements of CBF performed within 6 hours of severe head trauma
• (Glasgow Coma Scale score ≤ 8) are reduced (22.5 ± 5.2 mL/l00 g per minute) and correlate well
with Glasgow Coma Scale score and eventual outcome.
• 45-65% of head injury victims will exhibit hyperemia in the 12 to 24 hours after injury.
• Increased CBF and CBV are seen in the acute encephalopathy of Reye’s syndrome
• In general, CBF tends to stabilize by 36 to 48 hours after injury.

47. Contd…
• As ICP increases,
• arteriovenous oxygen difference usually rises
• because of reductions in venous Po2 caused by greater oxygen extraction.
• CBV increases with vasodilation in response to lowered CPP or a rise in Paco2.
• TO reduce CBV
• The most efficacious methods are
1. HYPERVENTILATION
2. HEAD END ELEVATION
• Hyperventilation
• hypocapnic vasoconstriction
• moves blood from the pial circulation to the veins and sinuses.
• Reductions of the cerebral metabolic rate of oxygen are seen after trauma.
• CO2 responsivity can be preserved in the absence of pressure autoregulation, and its prolonged loss is
considered a grave sign.
• In Adults, a 1-torr change in Paco2 is associated with a 3% change in CBF.

48. Contd..
• Hyperventilation (contd..)
• induces tissue alkalosis: which can buffer the intracellular and CSF acidosis seen after severe head
injury.
• higher levels of vasoconstriction may be sufficient to produce cerebral ischemia
• Hyperventilation to a Paco2 of 25 ± 2 in patients with a Glasgow motor scale of 4 or 5 resulted in
Glasgow outcome scores at 6 months that were significantly worse than those in controls.
• Consequently, only moderate hyperventilation is necessary (32 to 35 torr), (1torr= 1mmHg) which
is thought to be sufficient to avoid ischemic effects.
• concept of “inverse steal” to explain the risk of hyperventilation-induced ischemia.
• In patients with intact or supersensitive CO2 responsivity,
• hypocapnia can lead to shunting of blood from high-resistance, maximally constricted vessels to low-resistance,
dilated vessels that lack CO2 responsivity.
• These areas may be so severely damaged;
• thus, hyperventilation may tend to redistribute blood from viable tissue into nonviable tissue.
• When possible, these investigators recommend that arteriovenous oxygen difference and CBF be monitored
along with ICP and that hyperventilation be performed cautiously in patients with evidence of cerebral ischemia.
• When hyperventilation is discontinued, it should be tapered during 24 to 48 hours. Abrupt discontinuation
can cause vasodilation as the extracellular pH falls, resulting in ICP elevations.

49. HEAD END ELEVATION
• Elevation of the head to 30 degrees
• Facilitates adequate venous drainage and
• possibly CSF drainage also.
• This degree of elevation does not alter CPP.
• In one study:
• CPP and CBF seemed unaffected by head position until the head was elevated to 60 degrees.
• Rotation of the head or flexion of the neck
• can also impair jugular venous flow and raise ICP.
• So,maintain the head in a neutral position.

50. PRINCIPLES OF ICP MANAGEMENT BY CPP MANAGEMENT
• Low CPP:
• stimulates arteriolar vasodilation, causing increases in both CBV and ICP.
• By elevation of CPP with vasopressors,
• the blood vessel will be stimulated by the mechanisms of pressure autoregulation to
vasoconstrict, consequently reducing the CBV and ICP.

51. VBRAIN MANAGEMENT
• Increases in VBRAIN occur most frequently
• as a result of cerebral edema
• Treatment is directed toward
1. removal of the cause of edema,
2. control of its propagation, and
3. enhancement of its clearance.
4. Efforts to decrease the formation of vasogenic edema
• prevention of cerebrovascular hypertension and
• appropriate choice of fluid resuscitation.

52. • Control of systemic and cerebrovascular hypertension is especially important
when intracranial hypertension exists or when cerebral autoregulation is
impaired.
• The choice of antihypertensive drugs in patients with increased ICP is important.
• nifedipine, chlorpromazine, and reserpine decreased mean arterial pressure and increased ICP, thereby
reducing CPP.
• Sodium nitroprusside is commonly used now for rapid control of blood pressure in adult critical care;
however, despite its highly efficacious action, prolonged use is not considered safe because of a risk of
cyanide ion toxicity.
• Propranolol has been shown to be
• superior to hydralazine for control of hypertension in head-injured patients
• because it decreases both cardiac demands and serum levels of epinephrine and norepinephrine.

53. Fluid Resuscitation
• Choice of fluid resuscitation agent is critical.
• Aggressive correction of shock improves survival and clinical outcome;
• However, the osmolality of the blood has important implications for ICP.
• Fluid replacement :
• Isotonic fluids
• (e.g., 5% dextrose, 0.45% normal saline, 0.9% normal saline, and lactated Ringer’s solution)
• regular use,
• Hypotonic solutions have the
• potential to worsen cerebral edema.
• Hypertonic solutions in bolus doses is:
• possible therapy for elevated ICP.
• However, fluid replacement therapy with hypertonic saline has been shown to be both beneficial and
detrimental for ICP in different studies.

54. EDEMA MANAGEMENT
• Steroids
• in subarachnoid hemorrhage has no proven benefit,
• but angiographically demonstrable vasospasm can be decreased by their use.
• In cerebral ischemia,
• steroids worsen outcome either by means of a direct glucocorticoid toxicity or as a consequence of elevated
serum glucose levels, which exacerbate ischemic lactic acidosis.
• Barbiturates
• Decreases the cerebral metabolic rate of oxygen,
• thus permitting tolerance of a degree of ischemia or anoxia not otherwise acceptable on the cellular level.
• So,lowers demand for CBF, which therefore tends to lower CBV and consequently lowering of ICP.
• When CO2 responsivity was normal,
• barbiturates reduced CBF and normalized ICP in 75% of patients.
• When CO2 responsivity was reduced or absent,
• CBF was unchanged or increased, and ICP was reduced in only 20% of patients.
• Pentobarbital has proved more effective at control of ICP than phenobarbital or thiopental sodium
• But in studies they have not shown improvement in outcome.

55. • Dose:
• bolus of pentobarbital (5 to 10 mg/kg) is administered during 30 minutes,
• followed by a continuous hourly maintenance infusion of 1 to 5 mg/kg
• to achieve a serum concentration of 3.5 to 4.5 mg/100 mL or
• 10 to 20 seconds of burst suppression monitored by bedside electroencephalography.
• Complications of high dose barbiturates:
• Hypotension
• hyponatremia,
• pneumonia, and
• cardiac depression.

56. CLEARANCE OF EDEMA
• Both osmotic and loop diuretics are widely used and
• can treat both vasogenic and cytotoxic edema.
• Osmotic agents
• draws free water from the brain into the intravascular compartment along the osmotic gradient.
• prevent edema formation and to speed clearance.
• transiently increase CBF so their use in the presence of hyperemia and increased CBV may be
contraindicated.
• Agents:
• Mannitol (20%)
• Urea (30%)
• Glycerol (10%)
• Causes hemolysis and renal failure when it is administered parenterally.
• Because glycerol is metabolized,
• Effect lasts for less time than with mannitol.
• glycerol was less effective in reducing ICP.

57. MANNITOL
• usually the agent of choice.
• rapid effect on ICP,
• Also increases
• plasma volume,
• decreases hematocrit, and
• decreases blood viscosity,
• which can cause a vasoconstriction and a drop in ICP.
• The dose of mannitol is 0.25 to 1 g/kg
• Given in bolus or contious fashion
• Complications :
• are dehydration,
• electrolyte imbalance,
• renal failure.
• Caution:
• Osmolality should not exceed 320 mOsm/kg because the renal tubule can be easily injured,
• especially if other nephrotoxic drugs are used concomitantly.
• High serum level penetrates mannitol into injured brain,
• especially in areas of blood-brain barrier deficiency.
• In this case, the osmolality of brain tissue will tend to draw water into the tissue and worsen edema.

58. Loop diuretics
• Furosemide and ethacrynic acid
• can be used in conjunction with mannitol to control ICP associated with edema.
• Furosemide works synergistically with mannitol
• to remove free water and is
• most appropriate in patients with fluid overload.
• Although furosemide decreases CSF production,
• this effect probably does not contribute in lowering of ICP in the acute setting.
• S/E:
• dehydration and
• loss of potassium.

59. Hypothermia
• Lowers ICP
• Probably By depression of cerebral metabolic requirements
• coupled with a slowing of injurious cellular events (e.g., lipid peroxidation).
• Improve patient outcome at 3 and 6 months after injury.

60. THANK YOU