Raised intra cranial pressure

RAISED ICT IS AN IMPORTANT ONE IN CASE OF CVAs THERE MAY BE FALSE LOCALISING SIGNS//

3. PIVOTAL ROLE IN CRITICAL CARE PIVOTAL ROLE IN CRITICAL CARE
MANAGEMENTMANAGEMENT
RAISED INTRACRANIAL PRESSURERAISED INTRACRANIAL PRESSURE

4. INTRODUCTIONINTRODUCTION
What is intracranial pressure?What is intracranial pressure?
Pressure within the cranial cavity (within a rigid structure) Pressure within the cranial cavity (within a rigid structure)
Skull /cranialvault exerted by the intracranial contentsSkull /cranialvault exerted by the intracranial contents.

5. Normal Intracranial PressureNormal Intracranial Pressure
5 – 15 mmHg in adult at rest5 – 15 mmHg in adult at rest
<20mmHg usually in most
In recumbent posture – 8mmHg or 110 mmH
2
0
Zero in standing posture due to transmission of CSF column Zero in standing posture due to transmission of CSF column
to the lumbar region.to the lumbar region.

6. A View of CSFA View of CSF
11
0 0
function of CSF in mechanical one – water jacket.(1500gm of function of CSF in mechanical one – water jacket.(1500gm of
brain tissue brain tissue  50gm in CSF) 50gm in CSF)
Average intracranial volume is 1700ml
Volume of brain is 1200-1400ml
CSF Volume 70 – 160ml (104ml-mean)
Spinal subarachanoid space 10-20ml of CSFSpinal subarachanoid space 10-20ml of CSF
Average rate of CSF formation is
◦21-22 ml/hr
◦0.35ml/min
◦500ml/day
◦renewed 4 or 5 times daily

7. Main site of formation of CSF – choroid plexure floor of the Main site of formation of CSF – choroid plexure floor of the
lateral, third, fourth ventriclelateral, third, fourth ventricle
Blood brain barrier – is formed byBlood brain barrier – is formed by
◦Endothelium of the choroidal, brain capillaries
◦Plasma membrane, adventitia of these vessels, pericapillary foot Plasma membrane, adventitia of these vessels, pericapillary foot
processes of astrocytesprocesses of astrocytes
◦CSF has “sink action” Davson’s term
◦CSF third circulation by “WILLIAM HARVEY” (Blood, Lymph)CSF third circulation by “WILLIAM HARVEY” (Blood, Lymph)

8. Raised ICPRaised ICP
Part of compartmental syndrome
Persistent elevation of > 20mmHg for > 10min is Persistent elevation of > 20mmHg for > 10min is
raised ICP raised ICP
> 30mmHg – poor prognosis> 30mmHg – poor prognosis..

9. MONRO – KELLIE DOCTRINEMONRO – KELLIE DOCTRINE
An increase in the volume of any one of the three
components brain, blood, CSF must be at the expense
of the other two beyond the autoregulation.
Brain is least compressible among the three.Brain is least compressible among the three.
Cerebral blood flow is autoregulatedCerebral blood flow is autoregulated
Autoregulation persist until cerebral prefusion pressure Autoregulation persist until cerebral prefusion pressure
is in range of 60-160 mmHgis in range of 60-160 mmHg
If CPP <60mmHg -- If CPP <60mmHg -- ¯¯CBFCBF

10. CUSHING TRIADCUSHING TRIAD
HypertensionHypertension
BradycardiaBradycardia
Irregular respirationIrregular respiration
Later phenomenon of raised ICTLater phenomenon of raised ICT

11. Intracranial Pressure causesIntracranial Pressure causes
Intracranial MassesIntracranial Masses
Blockage of CSFBlockage of CSF
HaemorrhageHaemorrhage
Hypertensive encephalopahtyHypertensive encephalopahty
Venous Sinus thrombosisVenous Sinus thrombosis
HyperadrenalismHyperadrenalism
Attitude sicknessAttitude sickness
TetracyclineTetracycline
Vit-A intoxicationVit-A intoxication

12. Cerebral or Extracerebral massCerebral or Extracerebral mass
◦Tumor
◦Massive infraction with edema
◦Contusion
◦Parenchymal
◦SDH : EDH
◦Abscess

13. General Brain Swelling General Brain Swelling
◦Anoxia, Acute hyponatremia
◦A hepatic failure
◦Hypertensive encephalopathy
◦Reye syndrome
­­Venous PressureVenous Pressure
◦Heart Failure
◦Obs. Of superior mediastinum Jugular veins
◦Cerebral vein thrombosis

14. Obstruction to flow and absorption of CSFObstruction to flow and absorption of CSF
◦Hydrocephalus
◦Meningitis – usual cause
◦If at absorption surface – the ventricles remain normal in size.
­­Volume of CSFVolume of CSF
◦Meningits ; SAH
­­CSF production CSF production
◦Choroid plexus tumors
◦In children hydrocephalus

15. TYPES OF CEREBRAL EDEMATYPES OF CEREBRAL EDEMA
CytotoxicCytotoxic
◦Cerebral swelling  cellular engorgement  neuron, glia
◦Is due to ischemia
Vasogenic edemaVasogenic edema
◦Accumalation of extracellular fluid
◦Defective BBB
◦Leaky capillaries
◦Seen in metastases, gliomas, meningiomas

16. Changes in CRANIUMChanges in CRANIUM
Sub falcine hermation Sub falcine hermation
◦Shift of cingulate gyrus of one hemisphere under the
falxcerebri to contra lateral side.
◦Septum pellucidum may shift from midline.
Uncal HerniationUncal Herniation
Tentorial – Mid brainTentorial – Mid brain
Tonsillar – Foramen magnumTonsillar – Foramen magnum

17. CLINICAL FEATURESCLINICAL FEATURES
HeadacheHeadache
Worse in early morning,
lying down
Increased on coughing,
straining, bending
Improves through the day,
ambulation
Associated with vomiting
Relieved by analgesia
Dull ache
Often mild

18. Reason : Reason :
◦ relative hypercarbic, hypoxia state during sleep may be relative hypercarbic, hypoxia state during sleep may be
responsible for exacerbation on waking upresponsible for exacerbation on waking up
◦Compression of pain sensitive vascular structuresCompression of pain sensitive vascular structures

19. Clinical Signs of herniation
Brain stem compression
Loss of pupillary activity
Impairment of eye movements
Hyperventilation
Motor posturing flexion or extension
Herniation is often is rapidly fatal

20. Vomiting with / without NauseaVomiting with / without Nausea
◦Projectile
◦Due to irritation of the vagal nuclei in the floor of fourth
ventricle by the ­ICP
◦Relieves headache Temporarily
Double vision, Blurred visionDouble vision, Blurred vision
◦Due to III, VI CN palsies
Frontal Lobe Frontal Lobe
◦Personality changes
◦Unsteadiness of gait
◦Incontinence of urine

21. Right side hemiplegia, garbled speech – dominant temporal Right side hemiplegia, garbled speech – dominant temporal
lobelobe.
Lethargy, drowsiness
Unconsciousness – COMAUnconsciousness – COMA
Papilloedema – due to CSF shunted into optic nerve sheaths,
may be the only sign of increased CSF / increased ICP
Arterial hypertensionArterial hypertension
FeverFever

23. InvestigationsInvestigations
CT Scan with Contrast
MRI with ContrastMRI with Contrast
◦Except cerebral abscess
Technetium brain scan – destructive skull vault, skull base lesionsTechnetium brain scan – destructive skull vault, skull base lesions
EEG – Cerebral abscess, focal slow waves seenEEG – Cerebral abscess, focal slow waves seen
Skull Film- not useful in hemispherical tumors
Routine tests Routine tests
Angiography, volumetric MRI
Lumbarpuncture only after imaging
Biopsy

24. SPECIFIC INVESTIGATIONSSPECIFIC INVESTIGATIONS
Invasive intracranial pressure monitoring
Extradural <1%, baseline drift
Subdural
Intraparenchymal, accurate 1%, breakage
Intraventricular can also be used for drainage, increased
inflammation rate
Cisternography
Transfontametry
Transcranial doppler flow velocity

25. IMMEDIATE MEASURES IMMEDIATE MEASURES
Rapidly effective areRapidly effective are
Elevate head end by 30-45Elevate head end by 30-45
00
– straight head position – straight head position
◦Head elevation - Head elevation - ¯¯JVP, JVP, ¯¯venous outflowvenous outflow
◦Sharp head angulation - avoidedSharp head angulation - avoided
Hyperventilation – Acute lowering of ICPHyperventilation – Acute lowering of ICP
◦16-20 cycles / min (ventilated) / Ambu bag by face mask16-20 cycles / min (ventilated) / Ambu bag by face mask
◦Action < 30minAction < 30min
◦Diminishes in 1-3 hrDiminishes in 1-3 hr
◦Tapered over 6-12 hrTapered over 6-12 hr
◦Sudden cessationSudden cessation leads to increased ICPleads to increased ICP

26. Hyperventilation should be such that Hyperventilation should be such that PCoPCo
22 < 30mmHg < 30mmHg
If < 25mmHg – exacerbate cerebral ischemia by causing If < 25mmHg – exacerbate cerebral ischemia by causing
excessive vasoconstrictionexcessive vasoconstriction..
MannitolMannitol
◦Biphasic actionBiphasic action
◦¯¯ICP by cerebral dehydrating effectICP by cerebral dehydrating effect
◦RAPID infusion is imp.RAPID infusion is imp.
◦¯¯ Brain volume – by osmotic gradientBrain volume – by osmotic gradient
◦Osmotic diuretic – free water clearanceOsmotic diuretic – free water clearance

27. 20% mannitol 1g/kg loading dose20% mannitol 1g/kg loading dose
Every 4-6hrs @ 0.25 – 0.5g/kgEvery 4-6hrs @ 0.25 – 0.5g/kg
It should be given over 10minIt should be given over 10min
Action in 10-20min lasts for 3-6 hrsAction in 10-20min lasts for 3-6 hrs

28. ◦Disadvantages:Disadvantages:
Congestive cardiac failure – due to volume contractionCongestive cardiac failure – due to volume contraction
Hypokalemia– serum electrolytes every 6hrsHypokalemia– serum electrolytes every 6hrs
HyperosmolarityHyperosmolarity
ATN ATN
Sudden rebound increased ICPSudden rebound increased ICP
Normal saline (0.9%) should be givenNormal saline (0.9%) should be given
No action if > 315m osm/kg , maintain <300 or <280No action if > 315m osm/kg , maintain <300 or <280
Drainage of CSF Drainage of CSF
◦ 5-10ml of CSF to be removed5-10ml of CSF to be removed
Use of steroids Use of steroids
◦ Dexamethasone 4-6mg 6Dexamethasone 4-6mg 6
thth
Hrly Hrly

29. Neurosurgical procedures
Craniotomy
Ventriculostomy
Placement of ICP monitor

30. ICP monitors
Ventricular monitors
External drainage can be done
High infection rate
Increased after 5 days
Intraparenchymal
It is fibroptic , acurate, 1% infectgion, inflexible, Breakage
Epiudural Transudes
Superficial to dura
<1% infection
Baseline drift (>5-10mmHg)


31. Normal Intracranial Pressure 50-200cmH2O (4-15mmHg)
Jugular venous pressure is normally principle determinant of
ICP

32. Initially as volume is added to the intracranial space, minimal increase
in pressure occurs – Highly compliant nature of intra cranial contents
¯
As intracranial volume increases CSF is displaced through foramen
magnum blood is displaced from compressed brain tissue
¯
Loss of compliance
¯
Further increase in intracranial volume leads to dramatic elevation of
ICP

33. CEREBRL PERFUSION PRESSURE
Important determinant of CBF
CPP = MABP – ICP
In presence of auto regulation, CBF is maintained at a constant level
across a wide range of CPP ( 50-150mmHg)
In presence of injury auto regulation impaired
CBF directly proportional to CPP
CPP should be maintain 70-120mmHg
<70mmHg secondary hypoxic ischemic damage
> 120mmHg break through hyperperfusion

34. ICP WAVEFORMS
Effects of systemic arterial, venous pressure on intracranial
contents
Initial offered deflection systemic arterial pressure wave
two types
Lundberg A waves
Plateau waves – Dangerous elevation of ICP 20-80mmHg

35. Global Hypokinesia
Lundberg B waves
Less amplitude 20mmHg
1-5minutes
Less Dangerous
Marker of abnormal auto regulation

36. Respiration pattern
No localizing value
Depressed inspiration - Severe Coma
Cheyne stokes respiration – Hyperventilation & Apnea,
Bihemispheric lesions, Metabolic encephalopathy, stable
breathing pattern,
Doesnot imply impending respiratory arrest

Hyperventilation – Systemic diseases , Meatabolic acidosi,
Hepatic encephalopathy,
Central neurogenic hyperventilation, CNS Lymphoma, Brain
stem damage

37. Localizing value
Apneustic breathing – Prolonged inspirtory phase, apnea –
pontine damage
Cluster breathing , shallow hyperventilation, cerebellar
damage
Ataxic (biot’s ) breathing – irregular choatic , medullary
respiratory centre, apnea

39. What is Kernohans notch?
What is lymphatic blood supply of brain?
What is Queckenstedt test?
Where is megalencephaly seen?
What are late signs of late intracranial pressure?
Where is hyperventilation useful?

40. GENERALIZED TREATMENTGENERALIZED TREATMENT
Sedation, Paralysis – needs intubation
◦Morphine IV 2.5mg every hrlyMorphine IV 2.5mg every hrly
◦Fenatanyl IV 50mg/mlFenatanyl IV 50mg/ml
25-100mg IVP –rapid control25-100mg IVP –rapid control
Infusion 4mg/250ml NS @ 5ml /hrInfusion 4mg/250ml NS @ 5ml /hr
◦Propofol IV 10mg/ml – reversiblePropofol IV 10mg/ml – reversible
5-50mcg/kg/min5-50mcg/kg/min

41. BP management BP management
◦if CPP > 120mmHgif CPP > 120mmHg
◦if ICP > 20mmHgif ICP > 20mmHg
◦maintainmaintain CPP > 70mmHg by treatment of hypertension CPP > 70mmHg by treatment of hypertension
◦Labetalol IV 5mg/ml - Labetalol IV 5mg/ml - aa1 1 bb1 blocker 20 – 80 mg every 1 blocker 20 – 80 mg every
10-20minutes10-20minutes
◦Nicardpine IV 25mg / 250 ml Ns @5ml /HrNicardpine IV 25mg / 250 ml Ns @5ml /Hr
◦Increase BP by Dopamine 800mg/500ml NS Increase BP by Dopamine 800mg/500ml NS

42. Seizures Seizures
◦Iv.Phenytoin 25mg/min slowlyIv.Phenytoin 25mg/min slowly
◦Iv. Diazepam resp.depressionIv. Diazepam resp.depression
◦Iv.LorazepamIv.Lorazepam
◦TheopentalTheopental
FeverFever
◦Acetaminophem 650mg every 4hrlyAcetaminophem 650mg every 4hrly
◦Indomethacin 25 mg every 6hrlyIndomethacin 25 mg every 6hrly

43. Blood glucose – Between 70-140mg/dlBlood glucose – Between 70-140mg/dl
NaNa
++
> 140mmol/L > 140mmol/L
Avoid fluid overload, dehydrationAvoid fluid overload, dehydration
High caloric feeds High caloric feeds
Hyperosmolar isovolemia neededHyperosmolar isovolemia needed
Foley’s catheterFoley’s catheter

44. SPECIFIC TREATMENTSPECIFIC TREATMENT
Decompressive surgeryDecompressive surgery
◦Removal of temporal bone on non dominent side acouste neuromaRemoval of temporal bone on non dominent side acouste neuroma
ChemotherapyChemotherapy
DiureticsDiuretics
Pentobarbital coma – refractory casesPentobarbital coma – refractory cases
- may cause hypotension - may cause hypotension
- 10 -20mg /kg flaccid coma- 10 -20mg /kg flaccid coma
- EEG every 24-48hrs- EEG every 24-48hrs
HemicraniectomyHemicraniectomy

45. PROGNOSISPROGNOSIS
◦Poor Prognosis – CPP < 60mmHg > 20minPoor Prognosis – CPP < 60mmHg > 20min
◦Refractory to Pentobarbital coma
◦Motor response – to pain is imp prognostic sign flexor Motor response – to pain is imp prognostic sign flexor
responseresponse

46. Idiopathic Intracranial HypertensionIdiopathic Intracranial Hypertension
Pseudo tumor cerebriPseudo tumor cerebri
Marked papilloedemaMarked papilloedema
No increased ventricular sizeNo increased ventricular size
Obese young womenObese young women
Headache, visual blurringHeadache, visual blurring
VI cranial nerve palsyVI cranial nerve palsy
CSF Pressure increasedCSF Pressure increased
Imaging is normalImaging is normal
It is due to decreased absorption of CSFIt is due to decreased absorption of CSF
Treatment Treatment
◦Steroids , Acetazolamide, shuntingSteroids , Acetazolamide, shunting

47. Normal Pressure Hydrocephalus
Enlarged cerebral ventricles
No cortical atrophy
Dementia
Urinary incontinence
gait apraxia
CSF pressure Normal
Treatment
Lumbarpuncture
Sudden increase in pressure on infusion of normal saline
shunt

48. ICP WAVES
Lundberg A waves (Plateau waves)
Dangerous elevation of ICP
20 – 80 mmHg
5min -1hr in duration
Associated with 60mmHg CPP
Lundberg B waves
10 – 20 mmHg
1 – 5 min
Less dangerous
Intracranial compliance

49. A – Pathologic
B – Arterial
C - Respiratory

50. Step wise approach
ICP Monitor ventriculostomy versus parenchymal
Goals
ICP < 20mmHg
CPP > 60mmHg
ICP > 20-25mmHg for > 5min
Drain CSF via ventriculostomy (If in place)
Elevate head end of bed –midline head position

51. Maintain (serum osmolality < 320mosml)
Glucocorticoids
Sedation
Paralysis
Hyperventilation
Pressor therapy

52. Refractory Cases
Phentobarb coma
Hypothermia
Hyperventilation
Hemicraniectomy

68. Headings
Defination
Normal Values
Brief descripation of CSF
Autoregulation of CBF
Evaluation of raised ICP
Monas Kellie Doctrine
Cushing Traid
Changes in ICP
Changes in Cranium
Types of Cerebral Edema
Causes
Clinical features
Investigations
Teatment
ProtocolN.Pressure hydrocephalus
Idiopathic intracranial HTN
Prognosis

69. References
Harrison's Principles of Internal Medicine 18
th
edi.
Adam and Uietor’s Principles of Neurology 7
th
edi.
Cecil text book of Medicine 22
nd
edi.
On call neurology – Marshall , meych
Neurology investigations – Hugher
Kumar and clarck clinical medicine – 5
th
edi.
Oxford prionciples of critical card
API text book of medicine – 8
th
edi.
Davidson & Principles , practice of Medicine 20
th
edi.
Bailey and Love – 25
th
edi.
Klashmigton manual of clinical therapeutics
Youtube.com
Newscience.com

70. Thanks to Dr.John Israel
Prof & Head of Medicine

71. One Thing about experience ins that when you don’t
have very much
You’re apt to get a lot there is a big differences between
nearly right exactly right
Coming together is beginning
Keeping together is progress
Working together is success.
Success is where preparation and opportunity meet.