1) Head injuries are a common cause of disability and death in children and can range from mild to severe. Increased intracranial pressure following head trauma can lead to secondary brain injury.
2) The goal in managing increased intracranial pressure is to maintain adequate cerebral perfusion pressure through treatments aimed at lowering intracranial pressure such as hyperventilation, mannitol, and sedation/analgesia while supporting mean arterial pressure.
3) Intracranial pressure monitoring can help guide management and detect events that may require intervention to prevent herniation and optimize cerebral oxygen delivery.
Nursing management client with Increased intracranial pressure ( ICP)ANILKUMAR BR
The rigid cranial vault contains brain tissue (1,400 g), blood (75 ml), and CSF (75 ml)
The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP.
ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm hg.
The Monro-kellie hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others.
Increased ICP is a syndrome that affects many patients with acute neurologic conditions.
This is because pathologic conditions alter the relationship between intracranial volume and pressure.
Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies.
A description of brain trauma focusing on psychiatric complications
Types of TBI, epidemiology, aetiology, evaluation, investigations,
It also explores basal skull fractures.
The neuropsychiatric sequelae are described including diffuse axonal injuries, hydrocephalus, neurotransmitter changes, specific mental illness (depression, mania, PTSD, substance abuse, sleep, and psychosis)
Nursing management client with Increased intracranial pressure ( ICP)ANILKUMAR BR
The rigid cranial vault contains brain tissue (1,400 g), blood (75 ml), and CSF (75 ml)
The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP.
ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm hg.
The Monro-kellie hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others.
Increased ICP is a syndrome that affects many patients with acute neurologic conditions.
This is because pathologic conditions alter the relationship between intracranial volume and pressure.
Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies.
A description of brain trauma focusing on psychiatric complications
Types of TBI, epidemiology, aetiology, evaluation, investigations,
It also explores basal skull fractures.
The neuropsychiatric sequelae are described including diffuse axonal injuries, hydrocephalus, neurotransmitter changes, specific mental illness (depression, mania, PTSD, substance abuse, sleep, and psychosis)
Management of hypoxic ischemic encephalopathy (HIE) by Sunil Kumar Dahasunil kumar daha
Please find the power point on Management of hypoxic ischemic encephalopathy (HIE) . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Debate: Neurocritical Care Improves Outcomes in Severe TBISMACC Conference
Martin Smith and Mark Wilson debate whether neurocritical care improves outcomes in severe TBI.
Martin argues in favour of neurocritical care.
He concedes that longstanding and established practices are not as efficacious or innocuous as previously believed.
Very few specific interventions have been shown to improve outcomes in large randomised controlled trials. With the possible exception of avoidance of hypotension and hypoxaemia, most are based on analysis of physiology and pathophysiology.
Further, the substantial temporal and regional pathophysiological heterogeneity after TBI means that some interventions may be ineffective, unnecessary, or even harmful in certain patients at certain times.
Martin however, contends that improved understanding of pathophysiology and advances in neuromonitoring and imaging techniques have led to more effective and individualised treatment strategies. Ultimately, this has led to improved outcomes for patients.
In particular, the sole goal of identifying and treating intracranial hypertension has been superseded by a focus on the prevention of secondary brain insults. This is done by using a systematic, stepwise approach to maintenance of adequate cerebral perfusion and oxygenation.
Similarly, multimodal neuromonitoring also gives clinicians confidence to withhold potentially dangerous therapy. Particuarly in those with no evidence of brain ischemia/hypoxia or metabolic disturbance.
Mark Wilson on the other hand argues there is no benefit in neurocritical care following severe TBI.
The New England Journal of Medicine has published several articles that demonstrate no benefit from classic neurotrauma interventions (ICP monitoring, cooling, decompression). This is because factors such as ICP and CPP associate with bad outcomes by association rather than causation.
This debate will demonstrate that critical care just complicates things. Evidently, it is high time for the randomised trial between the very best neurocritical care and NOB therapy (Naso-pharyngeal, Oxygen and a Blanket).
Join Martin and Mark as they discuss the pros and cons of neurocritical care in the management of severe TBI.
For more like this, head to our podcast page. #CodaPodcast
Enumerates the effect of different anesthetic agents on the CNS and compares their relative efficacy and safety in providing good outcome in neuroanesthesia
Management of hypoxic ischemic encephalopathy (HIE) by Sunil Kumar Dahasunil kumar daha
Please find the power point on Management of hypoxic ischemic encephalopathy (HIE) . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Debate: Neurocritical Care Improves Outcomes in Severe TBISMACC Conference
Martin Smith and Mark Wilson debate whether neurocritical care improves outcomes in severe TBI.
Martin argues in favour of neurocritical care.
He concedes that longstanding and established practices are not as efficacious or innocuous as previously believed.
Very few specific interventions have been shown to improve outcomes in large randomised controlled trials. With the possible exception of avoidance of hypotension and hypoxaemia, most are based on analysis of physiology and pathophysiology.
Further, the substantial temporal and regional pathophysiological heterogeneity after TBI means that some interventions may be ineffective, unnecessary, or even harmful in certain patients at certain times.
Martin however, contends that improved understanding of pathophysiology and advances in neuromonitoring and imaging techniques have led to more effective and individualised treatment strategies. Ultimately, this has led to improved outcomes for patients.
In particular, the sole goal of identifying and treating intracranial hypertension has been superseded by a focus on the prevention of secondary brain insults. This is done by using a systematic, stepwise approach to maintenance of adequate cerebral perfusion and oxygenation.
Similarly, multimodal neuromonitoring also gives clinicians confidence to withhold potentially dangerous therapy. Particuarly in those with no evidence of brain ischemia/hypoxia or metabolic disturbance.
Mark Wilson on the other hand argues there is no benefit in neurocritical care following severe TBI.
The New England Journal of Medicine has published several articles that demonstrate no benefit from classic neurotrauma interventions (ICP monitoring, cooling, decompression). This is because factors such as ICP and CPP associate with bad outcomes by association rather than causation.
This debate will demonstrate that critical care just complicates things. Evidently, it is high time for the randomised trial between the very best neurocritical care and NOB therapy (Naso-pharyngeal, Oxygen and a Blanket).
Join Martin and Mark as they discuss the pros and cons of neurocritical care in the management of severe TBI.
For more like this, head to our podcast page. #CodaPodcast
Enumerates the effect of different anesthetic agents on the CNS and compares their relative efficacy and safety in providing good outcome in neuroanesthesia
Stroke or Cerebrovascular incident, is defined as an abrupt onset of a neurological deficit that is attributable to a focal vascular cause.
The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain
Defines intracranial pressure, cerebral perfusion pressure and mean arterial pressure. Depict formula for caculating ICP, CPP& MAP. Enumerate both pathological and non- pathological causes for increased ICP. Explain Monroe Kellie hypothesis, pathophysiology of increase Intracranial pressure medical, surgical and nursing management of Increased intracranial pressure.
Edward Fohrman | Anesthetic Considerations for Intracranial TumorsEdward Fohrman
Read Edward Fohrman's thoughts on Anesthetic considerations for intracranial tumors. Edward is the Founder and CEO of Fohrman Anesthesia.
Read more at EdwardFohrman.com
Nursing management of the client with increased intracranial pressureANILKUMAR BR
The rigid cranial vault contains brain tissue (1,400 g), blood (75 mL), and CSF (75 mL)
The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP.
ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm Hg. Increased ICP is a syndrome that affects many patients with acute neurologic conditions.
This is because pathologic conditions alter the relationship between intracranial volume and pressure. Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumours, subarachnoid haemorrhage, and toxic and viral encephalopathies
1. ICP & Head Trauma
Sophia R. Smith, MD
WRAMC
November 2, 2005
2. Introduction
• Head injuries are one of the most common
causes of disability and death in children.
• The Centers for Disease Control and
Prevention (CDC) estimates that more
than 10,000 children become disabled
from a brain injury each year.
• Head injuries can be defined as mild as a
bump to severe in nature.
3. Prevalence of Pediatric Trauma
• Trauma is the leading cause of death in infants
and children
• Trauma is the cause of 50% of deaths in people
between 5 and 34 years of age
• Motor vehicle related accidents account for 50%
of pediatric trauma cases
• $16 billion is spent annually caring for injuries to
children less than 16 years of age
4. Traumatic Brain Injury
Primary Brain Injury Secondary Brain
Injury
Results from what has • Physiologic and
occurred to the brain biochemical events
at the time of the which follow the
injury primary injury
7. Factors that Effect Secondary
Brain Injuries
• Blood Pressure
• Oxygenation
• Temperature
• Control of Blood Glucose
• Fluid Volume Status
• Increased Intracranial Pressure
8. SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY
diffuse axonal
BBB inflammation injury
disruption apoptosis
necrosis
edema
formation
Brain trauma ischemia
energy failure
cytokines
Eicosanoids
Acetyl polyamines Calcium
endocannabinoids Choline ROS
Shohami, 2000
Green – pathophysiological processes; Yellow – various mediators
9. Anatomy of the cranium
• There are various brain contents that are
localized within a rigid structure.
– Cranium
• The cranial vault contents include:
– The brain
– The cerebral spinal fluid
– The cerebral blood
10. Cerebral Spinal Fluid
• CSF
– 150 cc in adults at all times
•Children slightly less
– Produced by choroid plexus – 20 cc/hr
– CSF is absorbed into venous system at
the subarachnoid villi
11. Cerebral blood and brain
• Cerebral blood
– Sum of blood in capillaries, veins, and arteries
• Brain
– 80% of the total intracranial volume
• All of these contents are maintained @ a
balanced pressure referred to as intracranial
pressure (ICP)
12. Monro-Kellie Doctrine
• The ICP within the skull is directly related
to the volume of the contents.
– Defined as the Monro-Kellie Doctrine
– This doctrine states that any increase in
volume of the contents within the brain must
be met with a decrease in the other cranial
contents.
15. Cerebral Blood Flow
• CBF is directly linked to the metabolic
requirements of the brain.
• As the brain metabolic activity increases,
CBF increases
– Vasodilatation of cerebral vessels
– Increase in cerebral blood volume
– Consequent increase in ICP
16. Cerebral blood flow
• CBF maintained when MAP range is
50mmHg to 150mmHg
– Cerebral auto regulation
• As BP increase baroreceptors sense event
and cerebral arteries vasoconstrict CBF
maintained with a CBV decrease
• As BP decrease cerebral arteries dilate to
increase flow CBV increase
17. Auto regulation
• This process is lost in pathological states
– Esp. Head trauma
– CBF decreases linearly to MAP below range
• Results is ischemia (strokes) to brain regions
– CBF increases linearly to MAP above auto
regulation range
• HTN encephalopathy as CBV and ICP increase
18.
19. Mediators of CBF
• Local and global mediators of CBF and
metabolism are important.
– Hypoxia and pH are most important
– As local paO2 decreases, CBF increases
– CBF is affected by pH (and its surrogate
pCO2)
20. Blood: Cerebral Blood Flow
The brain has the ability
to control its blood
supply to match its
metabolic requirements
Chemical or metabolic
byproducts of cerebral
metabolism can alter
blood vessel caliber and
behavior
21. Studies of hyperventilation &
ICP
• This relationship has been well studied as
a therapeutic option in particular
intentional hyperventilation to lower
cerebral blood flow and thus intracranial
pressure.
• No longer a practice
– Modest hyperventilation
22. On call
• So, you are in the ER on your first
night of call and the next thing you
know you get your very first trauma
patient.
• How do you evaluate?
25. Glascow Coma Scale
Eye Opening
Spontaneous 4
To Voice 3
To Pain 2
None 1
Best Verbal
Oriented 5
Confused 4
Inappropriate Words 3
Incomprehensible Sounds 2
None 1
Best Motor
Obeys Commands 6
Localizes Pain 5
Withdraws to Pain 4
Flexion to Pain 3
Extension to Pain 2
None 1
26.
27. Severe TBI
• Indications for Intubation
– GCS< 8
– Fall in GCS of 3
– Unequal pupils
– Inadequate respiratory effort or
significant lung/chest injury
– Loss of gag
– apnea
28. Treatment
• Intubation.
– Pretreatment with lidocaine 1
mg/kg IV may prevent rise in
intracranial pressure (ICP).
29. Treatment
• Hyperventilation
– to maintain PO2 >90 torrs, PCO2 30 to 32 torrs.
– Hyperventilation may actually increase
ischemia in at risk brain tissue if PCO2 <25 torr
by causing excessive vasoconstriction and has
fallen out of favor. Prophylactic hyperventilation for
those without increased ICP is contraindicated and
worsens outcomes.
• PEEP relatively contraindicated because reduces
cerebral blood flow.
30. Maintain normal cardiac
output.
• If hypotensive from other cause such as
multi-trauma, treat shock as usual.
• Normal saline is preferred over LR since
LR is slightly hypotonic.
• Hypertonic saline (3% or 7.5%) can be
used. Especially if you see ICP changes.
31. Maintain normal cardiac
output.
• If markedly hypertensive, consider
labetalol or nitroprusside.
• Avoid lowering the blood pressure unless
diastolic blood pressure is >120 mm Hg.
32. Diuresis
• Mannitol 1 g/kg IV over 20 minutes
induces osmotic diuresis.
– Avoid if hypotensive or have CHF/renal
failure.
• Some suggest furosemide (Lasix and
others).
– Avoid if hypotensive.
33. ICP Precautions
• Elevate head of bed 30 degrees.
• Seizure prophylaxis: Phenytoin will
reduce seizures in the first week after
injury but does not change the overall
outcome.
• Steroids are ineffective in controlling ICP
in the trauma setting.
35. Manipulation of CPP
CPP = MAP - ICP
• Maintain adequate intravascular volume
– CVP
• Increase MAP
– Utilize alpha agonist--dopamine,
phenylephrine, norepinephrine
• What is appropriate goal for children?
36. CPP for children
• Aim for a CPP of >60 mmHg
– by maintaining an adequate MAP and control
of ICP
• MAP – ICP = CPP
– Minimizing the morbidity of TBI in
children
37. Additional therapies
• Prevent hyperglycemia: exacerbates
ischemic cerebral damage
• Attention to electrolyte status. These
patients are prone to electrolyte
abnormalities due to osmotic diuresis,
cerebral salt losing states, SIADH and
diabetes insipidus
38. Manipulation of ICP
Blood
• Decrease cerebral metabolic demand
– sedation, analgesia, barbiturates
– avoid hyperthermia
– avoid seizures
• Hyperventilation
– decreases blood flow to brain
– only acutely for impending herniation
• Mannitol
39. Manipulation of ICP
Brain
• Mannitol
– dehydrate the brain, not the patient!
– monitor osmolality
• Hypertonic saline
• Decompressive craniectomy
40. ICP Monitoring
• ICU patients who have sustained head trauma,
brain hemorrhage, brain surgery, or conditions
in which the brain may swell might require
intracranial pressure monitoring.
• The purpose of ICP monitoring is to continuously
measure the pressure surrounding the brain.
42. How?
• Ventriculostomy
• Intraparenchymal fiberoptic catheter
• Subarachnoid monitor
• Useful adjuncts:
– Arterial line
– Central venous line
– Foley catheter
43. Manipulation of ICP
CSF
• External drainage
– therapeutic as well as diagnostic
– technical issues
– infectious issues
44. What to do with the
information...
• Goal: adequate oxygen delivery to maintain
the metabolic needs of the brain.
• Intracranial pressure <20
• Cerebral perfusion pressure >50-70 mm Hg
CPP=MAP-ICP
45. Indications for ICP monitoring
• Glasgow coma scale <8
• Clinical or radiographic evidence of
increased ICP
• Post-surgical removal of intracranial
hematoma
• Less severe brain injury in the setting
which requires deep sedation or
anesthesia
47. Near-infrared Spectroscopy
• Uses absorption characteristics of oxy
Hgb, deoxy Hgb, and [o] cyt aa3
• Uses the ability to penetrate the
superficial brain
• Therefore the state of oxygenation can be
determined.
• Good assessment of cerebral oxygenation
48. Transcranial Doppler US
• TCD is a noninvasive technique used to
determine cerebral blood velocity in large
intracranial arteries.
• Assessment of
– Brain death
– Reperfusion injury
– Identify regions S/P TBI that are adversely
effected
49. Cerebral Microdialysis
• Measuring the partial pressure of oxygen
of brain parenchyma and metabolites
using microdialysis
• Electrode in vulnerable brain region
measures O2 concentration
• Measures also local brain metabolism