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Management of
patient with
increased Intracranial
Pressure
Prepared by
SALMAN HABEEB
CONTENTS OF SKULL
• SKULL IS RIGID CLOSED STRUCTURE
CONTAINS
1- the brain and interstitial fluid- 78%;
2- intravascular blood-12%
3- the CSF -10%
INTRACRANIAL
PESSURE
• ICP IS THE TOTAL PRESSURE EXERTED BY
THE THREE COMPONENTS WITHIN THE
SKULL
• IT IS THE HYDROSTATIC FORCE MEASURED
IN THE BRAIN CSF COMPARTMENT
• MONRO-KELLIE HYPOTHSIS STATES THAT
SKULL IS A RIGID STRUCTURE IF THE
VOLUME OF THE ANY THREE COMPONENTS
INCREAESES THE VOLUME FROM ANOTHER
COMPONENT IS DISPLACED , THE TOTAL
INTRACRANIAL VOLUME WILL NOT CHANGE
Normal compensatory
mechanisms
• ALTERATION CSF VOLUME- INCRESED ABSORPTION
DECREASED
PRODUCTION
DISPLACEMENT TO
SUBARACHNOID SPACE
ALTERATION IN BLOOOD VOLUME- VASOCONSTRICTION
VASODILATION
TISSUE BRAIN VOLUME- DISTENTION OF DURAL
• These compensatory mechanisms are to
maintain a relatively constant amount of
cerebral blood flow to meet the metabolic
needs of the brain tissue
• Cerebral blood flow is the amount of blood in
millimeters passing through 100g of brain
tissue in 1minute
• Under normal conditions, the cerebral blood
flow ranges between 50 and 60mL per 100g
brain per minute
• It makes approximately 700 to 850mL blood
per minute for the whole brain and accounts
for about 20% of the total cardiac output.
• The brain uses 20% of the body’s oxygen
and 25% of the glucose
Increased intracranial
pressure
• Increased ICP is a life threatening situation that
results from an increase in any or all of three
components within the skull
(brain, CSF , blood )
• Brain edema is the common cause for elevated
intracranial pressure
Causes of brain edema
Space-Occupying Lesions
Intracerebral hemorrhage
Epidural hemorrhage
Subdural hemorrhage
Tumor
Abscess
CEREBRAL INFECTIONS
• MENINGITIS
• ENCEPHALITIS
BRAIN SURGERY
VASCULAR INSULT
• Anoxic and ischemic episodes
• Cerebral infarction (thrombotic and embolic)
TOXIC or METABOLIC ENCEPHALOPATHIES
• Lead or arsenic poisoning
• Hepatic encephalopathy
• Uremic encephalopathy
HYDROCEPHALUS
CEREBRAL EDEMA
• VASOGENIC CEREBRAL EDEMA
• CYTOTOXIC CEREBRAL EDEMA
• INTERSTITIAL CEREBRAL EDEMA
VASOGENIC CERBRAL
EDEMA
• IT IS CAUSED BY CHANGES IN ENDOTHELIAL
LINING OF CEREBRAL CAPILLARIES
• THESE CHANGES ALLLOW LEAKAGE OF
MACROMOLECULES FROM THE CAPILLARIES INTO
SURROUNDING EXTRAVASCULAR SPACE
• BRAIN TUMOURS, ABSCESSES AND INGESTED
TOXINS COMMON CAUSES
CYTOTOXIC CEREBRAL
EDEMA
• IT RESULTS FROM LOCAL DISRUPTION OF THE
FUNCTIONAL OR MORPHOLOGICAL INTEGRITYOF CELL
MEMBRANE
• IT DEVELOPS FROM DESTRUCTIVE LESIONS OR
TRAUMA TO BRAIN TISSUE RESULTING IN CEREBRAL
HYPOXIA
• MOST OFTEN IN GREY MATTER OF BRAIN
INTERSTITIAL
CEREBRAL EDEMA
• It is the result of periventricular diffusion of
ventricular CSF in a patient with uncontrolled
hydrocephalus
Mechanism of elevated
ICP
CRANIAL INSULT
TISSUE EDEMA
ELEVATED ICP
COMPRESSION OF BLOOD VESSELS
DECREASED CEREBRAL BLOOD FLOW
DECREASED O2 WITH DEATH OF BRAIN CELLS
FURTHER INCREASE IN EDEMA AROUND NECROTIC TISSUE
FURTHER ELEVATION IN ICP WITH COMPRESSION OF
BRAIN
STEM AND RESPIRATORY CENTER
ACCUMULATION OF CO2
VASODIALATION
INCREASED ICP RESULTING FROM INCREASED BLOOD
FLOW
CLINICAL
MANIFESTATION
CHANGE IN LEVEL OF CONSCIOUSNESS
• SENSITIVE AND RELIABLE INDICATOR OF
NEUROLOGIC STATUS
• IT RESULTS FROM IMPAIRED CERBRAL PERFUSION
AFFFECTING CEREBRAL CORTEX AND RAS
CHANGE IN VITAL SIGNS
• INDICATE INCREASED PRESURE ON THE THALAMUS,
HYPOTHALAMUS, PONS AND MEDULLA
• MANIFESTED AS CUSHINGS TRIAD
ELEVATED SYSTOLIC BP
BRADYCARDIA
WIDENING OF PULSE PRESSURE
• CHANGE IN BODY TEMPERATURE HYPOTHALAMUS
AFFECTED
OCCULAR SIGNS
• COMPRESSION OF CRANIAL NERVE (111)- PUPILLARY
DILATION
• FIXED UNILATERAL DILATED PUPIL – HERNIATION OF
THE BRAIN
• OPTIC- BLURRED VISION, DIPLOPIA
• TROCHLEAR, ABDUCENS - EYE MOVEMENTS
MIDLINE SHIFT OF BRAIN
DECREASE IN MOTOR
FUNCTION
• CONTROLATERAL HEMIPARESIS OR
HEMIPLEGIA
• DECORTICATION- INTERRUPTION OF
VOLUNTARY MOTOR CORTEX
• DECEREBRATION- DISRUPTION OF MOTOR
FIBERS IN THE MIDBRAIN AND BRAIN STEM
• IT is a state of severe hyperextension and spasticity in
which an individual's head, neck and spinal column enter
into a complete "bridging" or "arching" position
• Opisthotonusposition
HEADACHE
• COMPRESSION OF OTHER
INTRACRANIAL STRUCTURES
• CONTINOUS, WORSE IN THE
MORNING
VOMITING
• PROJECTILE TYPE
• COMPRESSION TO CTZ( VOMITING CENTER)
DIAGNOSTIC STUDIES
• HISTORY COLLECTION AND PHYSICAL EXAMINATION
• COMPUTED TOMOGRAPHY
• MAGNETIC RESONANCE IMAGING
• ELECTROENCEPHALOGRAM
• POSITRON EMISSION TOMOGRAPHY
• MEASUREMENT OF ICP
• LP?
Measurement of ICP
• ICP should be monitored in patients admitted with Glasgow
coma scale (GCS) 8or less and an abnormal CT or MRI
• NORMAL ICP 5-15 mm hg/10 to 20cm H2O
• METHODS
EPIDURAL
SUBDURAL
SUBARACHNOID
INTRAPARENCHYMAL
VENTRICULAR
• GOLD STANDARD – VENTRICULOSTOMY
• A Specialized catheter is inserted into right
lateral ventricle and coupled to an external
transducer
This technique
• directly measures pressure inside ventricles,
• facilitates removal or sampling of CSF
• for intraventricular drug administration
• Direct visualization of the height of the CSF column
generated outside the body or through its
measurement by an external transducer
• CSF drainage
using a closed system, elevations in ICP are
controlled by removal of CSF by gravity drainage and
by adjusting the height of drip chamber and drainage
bag relative to ventricular reference point
oTypically a point 15 cm above ear canal
the drainage bag is placed
oRaising the height diminishes the drainage
and vice versa
oNormal adult CSF production- 20-30ml/hr
oTotal CSF volume- 90-150ml
COMPLICATIONS
• Tentorial herniation
mass lesion in the cerebrum forces the brain to
herniate downward through the opening created by
the brain stem
• Uncal herniation
lateral and downward herniation
• Cingulateherniation
It occurs when there is lateral displcement of
brain tissue beneath the falx cerebrai
MANAGEMENT
GOALS
• Identifying and treating the underlying cause
of increased ICP
• Maintaining adequate perfusion and
oxygenation to the brain
DRUG THERAPY
Administer INJ.mannitol 25%
• It acts in TWO ways
1. Plasma expansion
2. Osmotic effect
• It have an immediate plasma expanding effect that reduces
the hematocrit and blood viscosity there by increasing CBF
and cerbral oxygenation
• It creates a vascular osmotic gradient , that will results to
move the fluid from tissues to blood vessels
• Corticosteriods( dexamethasone, dexona)
It will help to improve the neuronal function
Inhibit the synthesis of prostaglandins thereby
preventing formation of inflammatory mediators
• Barbiturates ( Thiopental, pentobarbital )
It will decrease in cerebral metaabolism and subsequent
decrease in ICP
• Antiepileptics( phenytoin)
As seizure prophylaxis
• H2 receptor antagonists or proton pump inhibitors
Prevent gastric ulcers and bleeding
Hyperventilation therapy
• In the past aggressive hyperventilation was one of
the important treatment modality
• It will decrease the C02 level in the blood
PaCO2 less than 25 mm Hg
• Brief periods of less aggressive hyperventilation
therapy is useful
PaCO2 30-35 mm Hg
REDUCING CSF AND INTRACRANIAL BLOOD
VOLUME
• CSF drainage is frequently performed because the
removal of CSF with a ventriculostomy drain may
dramatically reduce ICP and restore cerebral
perfusion pressure.
Nutritional therapy
• All patients must have their nutritional needs met
regardless of their state of consciousness or health
• Adequate fluid volume should be maintained
POSITIONING
• Head position: Maintain head in midline
position at above 30 degrees to improve
cerebral venous drainage; lower cerebral
blood volume (CBV) will lower ICP.
Surgical decompression
• Surgical decompression is indicated for
clear-cut mass lesions amenable to removal,
i.e. tumor, epidural bleed, large contusion. For
refractory elevated ICP without a surgical
lesion, there may be a role for a
decompressive craniectomy. Especially if
done early after the initial insult, it may
improve functional outcomes of patients.
NURSING
MANAGEMENT
• ASSESSMENT
NEUROLOGICAL ASSESSMENT
GLASGOW COMA SCALE
MIN SCORE- 3
MAX SCORE- 15
GCS below 8- indicative of coma
NURSING DIAGNOSIS
• Ineffective tissue perfusion (cerebral) related to reduction
of arterial blood flow and cerebral edema as evidenced by
CPP<60 mm hg, GCS score <8, altered mental status,
changes in mental status
INTERVENTIONs
• maintain hemodynamic parameters within
normal range
• Calculate and monitor CPP
• Monitor neurologic status
• Maintain input and output chart
• Administer medication
• Administer oxygen
• Decreased intracranial adaptive capacity related to
decreased cerebral perfusion as evidenced by ICP More
than 20 mm of hg, elevated systolic pressure, bradycardia
and widened pulse pressure
Interventions
• Monitor vital signs, ICP and neurologic status
• Position the head end of the bed 30 degree or more
• Maintain normothermia
• Give sedatives
• Administer osmotic diuretics
• Decrease stimuli in patients environment

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Management of patient with increased intracranial pressure

  • 1. Management of patient with increased Intracranial Pressure Prepared by SALMAN HABEEB
  • 2. CONTENTS OF SKULL • SKULL IS RIGID CLOSED STRUCTURE CONTAINS 1- the brain and interstitial fluid- 78%; 2- intravascular blood-12% 3- the CSF -10%
  • 3. INTRACRANIAL PESSURE • ICP IS THE TOTAL PRESSURE EXERTED BY THE THREE COMPONENTS WITHIN THE SKULL • IT IS THE HYDROSTATIC FORCE MEASURED IN THE BRAIN CSF COMPARTMENT • MONRO-KELLIE HYPOTHSIS STATES THAT SKULL IS A RIGID STRUCTURE IF THE VOLUME OF THE ANY THREE COMPONENTS INCREAESES THE VOLUME FROM ANOTHER COMPONENT IS DISPLACED , THE TOTAL INTRACRANIAL VOLUME WILL NOT CHANGE
  • 4.
  • 5.
  • 6. Normal compensatory mechanisms • ALTERATION CSF VOLUME- INCRESED ABSORPTION DECREASED PRODUCTION DISPLACEMENT TO SUBARACHNOID SPACE ALTERATION IN BLOOOD VOLUME- VASOCONSTRICTION VASODILATION TISSUE BRAIN VOLUME- DISTENTION OF DURAL
  • 7. • These compensatory mechanisms are to maintain a relatively constant amount of cerebral blood flow to meet the metabolic needs of the brain tissue • Cerebral blood flow is the amount of blood in millimeters passing through 100g of brain tissue in 1minute • Under normal conditions, the cerebral blood flow ranges between 50 and 60mL per 100g brain per minute
  • 8. • It makes approximately 700 to 850mL blood per minute for the whole brain and accounts for about 20% of the total cardiac output. • The brain uses 20% of the body’s oxygen and 25% of the glucose
  • 9. Increased intracranial pressure • Increased ICP is a life threatening situation that results from an increase in any or all of three components within the skull (brain, CSF , blood ) • Brain edema is the common cause for elevated intracranial pressure
  • 10. Causes of brain edema Space-Occupying Lesions Intracerebral hemorrhage Epidural hemorrhage Subdural hemorrhage Tumor Abscess
  • 11. CEREBRAL INFECTIONS • MENINGITIS • ENCEPHALITIS BRAIN SURGERY VASCULAR INSULT • Anoxic and ischemic episodes • Cerebral infarction (thrombotic and embolic) TOXIC or METABOLIC ENCEPHALOPATHIES • Lead or arsenic poisoning • Hepatic encephalopathy • Uremic encephalopathy HYDROCEPHALUS
  • 12. CEREBRAL EDEMA • VASOGENIC CEREBRAL EDEMA • CYTOTOXIC CEREBRAL EDEMA • INTERSTITIAL CEREBRAL EDEMA
  • 13. VASOGENIC CERBRAL EDEMA • IT IS CAUSED BY CHANGES IN ENDOTHELIAL LINING OF CEREBRAL CAPILLARIES • THESE CHANGES ALLLOW LEAKAGE OF MACROMOLECULES FROM THE CAPILLARIES INTO SURROUNDING EXTRAVASCULAR SPACE • BRAIN TUMOURS, ABSCESSES AND INGESTED TOXINS COMMON CAUSES
  • 14. CYTOTOXIC CEREBRAL EDEMA • IT RESULTS FROM LOCAL DISRUPTION OF THE FUNCTIONAL OR MORPHOLOGICAL INTEGRITYOF CELL MEMBRANE • IT DEVELOPS FROM DESTRUCTIVE LESIONS OR TRAUMA TO BRAIN TISSUE RESULTING IN CEREBRAL HYPOXIA • MOST OFTEN IN GREY MATTER OF BRAIN
  • 15. INTERSTITIAL CEREBRAL EDEMA • It is the result of periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus
  • 16. Mechanism of elevated ICP CRANIAL INSULT TISSUE EDEMA ELEVATED ICP COMPRESSION OF BLOOD VESSELS DECREASED CEREBRAL BLOOD FLOW
  • 17. DECREASED O2 WITH DEATH OF BRAIN CELLS FURTHER INCREASE IN EDEMA AROUND NECROTIC TISSUE FURTHER ELEVATION IN ICP WITH COMPRESSION OF BRAIN STEM AND RESPIRATORY CENTER ACCUMULATION OF CO2 VASODIALATION INCREASED ICP RESULTING FROM INCREASED BLOOD FLOW
  • 18. CLINICAL MANIFESTATION CHANGE IN LEVEL OF CONSCIOUSNESS • SENSITIVE AND RELIABLE INDICATOR OF NEUROLOGIC STATUS • IT RESULTS FROM IMPAIRED CERBRAL PERFUSION AFFFECTING CEREBRAL CORTEX AND RAS
  • 19. CHANGE IN VITAL SIGNS • INDICATE INCREASED PRESURE ON THE THALAMUS, HYPOTHALAMUS, PONS AND MEDULLA • MANIFESTED AS CUSHINGS TRIAD ELEVATED SYSTOLIC BP BRADYCARDIA WIDENING OF PULSE PRESSURE • CHANGE IN BODY TEMPERATURE HYPOTHALAMUS AFFECTED
  • 20. OCCULAR SIGNS • COMPRESSION OF CRANIAL NERVE (111)- PUPILLARY DILATION • FIXED UNILATERAL DILATED PUPIL – HERNIATION OF THE BRAIN • OPTIC- BLURRED VISION, DIPLOPIA • TROCHLEAR, ABDUCENS - EYE MOVEMENTS
  • 22. DECREASE IN MOTOR FUNCTION • CONTROLATERAL HEMIPARESIS OR HEMIPLEGIA • DECORTICATION- INTERRUPTION OF VOLUNTARY MOTOR CORTEX • DECEREBRATION- DISRUPTION OF MOTOR FIBERS IN THE MIDBRAIN AND BRAIN STEM
  • 23.
  • 24.
  • 25. • IT is a state of severe hyperextension and spasticity in which an individual's head, neck and spinal column enter into a complete "bridging" or "arching" position • Opisthotonusposition
  • 26. HEADACHE • COMPRESSION OF OTHER INTRACRANIAL STRUCTURES • CONTINOUS, WORSE IN THE MORNING
  • 27. VOMITING • PROJECTILE TYPE • COMPRESSION TO CTZ( VOMITING CENTER)
  • 28. DIAGNOSTIC STUDIES • HISTORY COLLECTION AND PHYSICAL EXAMINATION • COMPUTED TOMOGRAPHY • MAGNETIC RESONANCE IMAGING • ELECTROENCEPHALOGRAM • POSITRON EMISSION TOMOGRAPHY • MEASUREMENT OF ICP • LP?
  • 29. Measurement of ICP • ICP should be monitored in patients admitted with Glasgow coma scale (GCS) 8or less and an abnormal CT or MRI • NORMAL ICP 5-15 mm hg/10 to 20cm H2O • METHODS EPIDURAL SUBDURAL SUBARACHNOID INTRAPARENCHYMAL VENTRICULAR
  • 30.
  • 31. • GOLD STANDARD – VENTRICULOSTOMY • A Specialized catheter is inserted into right lateral ventricle and coupled to an external transducer This technique • directly measures pressure inside ventricles, • facilitates removal or sampling of CSF • for intraventricular drug administration
  • 32. • Direct visualization of the height of the CSF column generated outside the body or through its measurement by an external transducer • CSF drainage using a closed system, elevations in ICP are controlled by removal of CSF by gravity drainage and by adjusting the height of drip chamber and drainage bag relative to ventricular reference point
  • 33. oTypically a point 15 cm above ear canal the drainage bag is placed oRaising the height diminishes the drainage and vice versa oNormal adult CSF production- 20-30ml/hr oTotal CSF volume- 90-150ml
  • 34. COMPLICATIONS • Tentorial herniation mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brain stem • Uncal herniation lateral and downward herniation • Cingulateherniation It occurs when there is lateral displcement of brain tissue beneath the falx cerebrai
  • 35. MANAGEMENT GOALS • Identifying and treating the underlying cause of increased ICP • Maintaining adequate perfusion and oxygenation to the brain
  • 36. DRUG THERAPY Administer INJ.mannitol 25% • It acts in TWO ways 1. Plasma expansion 2. Osmotic effect • It have an immediate plasma expanding effect that reduces the hematocrit and blood viscosity there by increasing CBF and cerbral oxygenation • It creates a vascular osmotic gradient , that will results to move the fluid from tissues to blood vessels
  • 37. • Corticosteriods( dexamethasone, dexona) It will help to improve the neuronal function Inhibit the synthesis of prostaglandins thereby preventing formation of inflammatory mediators • Barbiturates ( Thiopental, pentobarbital ) It will decrease in cerebral metaabolism and subsequent decrease in ICP • Antiepileptics( phenytoin) As seizure prophylaxis
  • 38. • H2 receptor antagonists or proton pump inhibitors Prevent gastric ulcers and bleeding
  • 39. Hyperventilation therapy • In the past aggressive hyperventilation was one of the important treatment modality • It will decrease the C02 level in the blood PaCO2 less than 25 mm Hg • Brief periods of less aggressive hyperventilation therapy is useful PaCO2 30-35 mm Hg
  • 40. REDUCING CSF AND INTRACRANIAL BLOOD VOLUME • CSF drainage is frequently performed because the removal of CSF with a ventriculostomy drain may dramatically reduce ICP and restore cerebral perfusion pressure.
  • 41. Nutritional therapy • All patients must have their nutritional needs met regardless of their state of consciousness or health • Adequate fluid volume should be maintained
  • 42. POSITIONING • Head position: Maintain head in midline position at above 30 degrees to improve cerebral venous drainage; lower cerebral blood volume (CBV) will lower ICP.
  • 43. Surgical decompression • Surgical decompression is indicated for clear-cut mass lesions amenable to removal, i.e. tumor, epidural bleed, large contusion. For refractory elevated ICP without a surgical lesion, there may be a role for a decompressive craniectomy. Especially if done early after the initial insult, it may improve functional outcomes of patients.
  • 44. NURSING MANAGEMENT • ASSESSMENT NEUROLOGICAL ASSESSMENT GLASGOW COMA SCALE MIN SCORE- 3 MAX SCORE- 15 GCS below 8- indicative of coma
  • 45. NURSING DIAGNOSIS • Ineffective tissue perfusion (cerebral) related to reduction of arterial blood flow and cerebral edema as evidenced by CPP<60 mm hg, GCS score <8, altered mental status, changes in mental status INTERVENTIONs • maintain hemodynamic parameters within normal range • Calculate and monitor CPP • Monitor neurologic status • Maintain input and output chart • Administer medication • Administer oxygen
  • 46. • Decreased intracranial adaptive capacity related to decreased cerebral perfusion as evidenced by ICP More than 20 mm of hg, elevated systolic pressure, bradycardia and widened pulse pressure Interventions • Monitor vital signs, ICP and neurologic status • Position the head end of the bed 30 degree or more • Maintain normothermia • Give sedatives • Administer osmotic diuretics • Decrease stimuli in patients environment