Module Neurotrauma

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Traumatic Brain Injury and Traumatic Brain Injury and increased ICPincreased ICP

Intracranial HematomasIntracranial Hematomas

Spontaneous Subarachnoid Spontaneous Subarachnoid HemorrhageHemorrhage

Herniation SyndromesHerniation Syndromes

Traumatic Brain Traumatic Brain Injury and Injury and

Increased ICPIncreased ICP

Practically Practically speaking, the brain speaking, the brain

is protected by a is protected by a rigid case, within rigid case, within which there is which there is no no

“extra” space“extra” space..

The Cranial VaultThe Cranial Vault Skull (holds three things)Skull (holds three things)

BrainBrain BloodBlood Cerebro-Spinal Fluid (CSF)Cerebro-Spinal Fluid (CSF)

An increase in any one of these three An increase in any one of these three “compartments” displaces the other two.“compartments” displaces the other two.

The principle buffer in the system is CSF.The principle buffer in the system is CSF. Only small volume increases can be Only small volume increases can be

tolerated before intracranial pressure tolerated before intracranial pressure (ICP) begins to rise.(ICP) begins to rise.

The Monroe-Kellie The Monroe-Kellie DoctrineDoctrine

Increase in one constituent Increase in one constituent necessitates a compensatory necessitates a compensatory decrease in the volume of another decrease in the volume of another constituent.constituent.

ComplianceCompliance

Because the three constituents that Because the three constituents that take up residence within the cranial take up residence within the cranial vault are housed within a relatively vault are housed within a relatively rigid container, small increases in rigid container, small increases in volume can drastically increase the volume can drastically increase the intracranial pressureintracranial pressure

This is the concept of This is the concept of compliancecompliance.. Compliance = change in volume/change Compliance = change in volume/change

in pressurein pressure

Normal Cerebral Normal Cerebral MetabolismMetabolism

Brain tissue relies on aerobic metabolism – Brain tissue relies on aerobic metabolism – gets starved for oxygen very quickly gets starved for oxygen very quickly because it has no real backup energy because it has no real backup energy reserve.reserve.

Normal cerebral metabolism requires a Normal cerebral metabolism requires a blood flow of approximately 50 blood flow of approximately 50 mL/100g/min.mL/100g/min.

Serious neurological deficits begin to occur Serious neurological deficits begin to occur at 20 mL/100g/min.at 20 mL/100g/min.

Prolonged Cerebral Blood Flow > 12 Prolonged Cerebral Blood Flow > 12 mL/100g/min. results in cerebral infarction.mL/100g/min. results in cerebral infarction.

MAP and ICPMAP and ICP

MAP = “Mean Arterial Pressure”MAP = “Mean Arterial Pressure” Defined as: [(2 x DBP) + (SBP)]/3Defined as: [(2 x DBP) + (SBP)]/3 This is literally the average arterial This is literally the average arterial

blood pressure over a single cardiac blood pressure over a single cardiac cycle.cycle.

ICP = “Intra-Cranial Pressure”ICP = “Intra-Cranial Pressure” 15 mmHg is getting into the upper 15 mmHg is getting into the upper

limits of normal in you and me.limits of normal in you and me. MAP – ICP = CPPMAP – ICP = CPP

Cerebral Perfusion Cerebral Perfusion PressurePressure

Cerebral Perfusion Pressure is key to Cerebral Perfusion Pressure is key to brain tissue survival.brain tissue survival.

CPP = MAP – ICPCPP = MAP – ICP This takes measurable physiologic This takes measurable physiologic

parameters into account to determine if parameters into account to determine if the individual is able to adequately the individual is able to adequately oxygenate brain tissue. It is the net oxygenate brain tissue. It is the net pressure of blood delivery to the brain.pressure of blood delivery to the brain.

In a normal adult, CPP is generally In a normal adult, CPP is generally regulated between 70 and 90 mmHg (can regulated between 70 and 90 mmHg (can be more or less).be more or less).

Cerebral MetabolismCerebral Metabolism In the uninjured brain, the arterioles regulate In the uninjured brain, the arterioles regulate

CBF to the brain over MAPs ranging from 50-CBF to the brain over MAPs ranging from 50-150 mmHg.150 mmHg.

Outside of this range, the arterioles lose the Outside of this range, the arterioles lose the ability to autoregulate, and blood flow becomes ability to autoregulate, and blood flow becomes dependent upon blood pressure (this is called dependent upon blood pressure (this is called pressure-passive flow).pressure-passive flow).

MAPs less than 50 run risk of ischemia due to MAPs less than 50 run risk of ischemia due to decreased blood flow, while MAPs greater than decreased blood flow, while MAPs greater than 150 causes excess CBF that can contribute to 150 causes excess CBF that can contribute to increased intracranial pressure.increased intracranial pressure.

Autoregulation is impaired in the injured brainAutoregulation is impaired in the injured brain..

Cerebral Cerebral AutoregulationAutoregulation

Summing that up - Summing that up -

Normal anatomy implies a fixed space Normal anatomy implies a fixed space in skull where small increase in volume in skull where small increase in volume causes large increase in pressure.causes large increase in pressure.

Perfusion of brain tissue is impaired by Perfusion of brain tissue is impaired by anything that’s taking up space or anything that’s taking up space or decreasing blood delivery to the tissue.decreasing blood delivery to the tissue.

Normal autoregulation processes that Normal autoregulation processes that help the brain maintain homeostasis help the brain maintain homeostasis are impaired after injury.are impaired after injury.

The TRAUMATIC neuro The TRAUMATIC neuro examexam

When dealing with “Emergency” When dealing with “Emergency” neurological evaluation, you MUST neurological evaluation, you MUST MUST MUST MUST MUST MUST MUST MUST MUST KNOWKNOW the concept of the Glascow Coma the concept of the Glascow Coma Scale!!!!!!!Scale!!!!!!!

Clinical Assessment: Clinical Assessment: GCSGCS

Diagnostic ImagingDiagnostic Imaging This is a great way to get past the This is a great way to get past the

handicap of having a relatively inflexible handicap of having a relatively inflexible surface to evaluate.surface to evaluate.

Often provides you the information you Often provides you the information you need to ANTICIPATE a problem or need to ANTICIPATE a problem or PREVENT its occurrence before it PREVENT its occurrence before it becomes clinically apparent.becomes clinically apparent.

Newer diagnostic imaging modalities Newer diagnostic imaging modalities have REVOLUTIONIZED management of have REVOLUTIONIZED management of intracranial pathology (the benefit to intracranial pathology (the benefit to traumatic brain injury is immeasurable)!traumatic brain injury is immeasurable)!

““Reading head films 101”Reading head films 101”

#1 – Identify the modality#1 – Identify the modality #2 – Orient yourself#2 – Orient yourself #3 – Describe what you see; don’t #3 – Describe what you see; don’t

just try to find what’s abnormaljust try to find what’s abnormal #4 – Pay attention to symmetry!#4 – Pay attention to symmetry! #5 – Pay attention to proportion#5 – Pay attention to proportion

The CT ScanThe CT Scan

The CT scan single-The CT scan single-handedly handedly revolutionized the revolutionized the landscape for head-landscape for head-trauma.trauma.

Allows Allows quick quick evaluation of evaluation of intracranial space intracranial space (and skull).(and skull).

Good for Good for acuteacute eval. eval. ““Fancy X-ray”Fancy X-ray”

Traumatic Brain InjuryTraumatic Brain Injury

Two general types of injury:Two general types of injury: Primary – represents the direct result of the Primary – represents the direct result of the

initial trauma.initial trauma. FractureFracture Cerebral contusionCerebral contusion Vascular disruptionVascular disruption

Secondary – results from the evolution of the Secondary – results from the evolution of the initial injury or complications. (This is what we initial injury or complications. (This is what we aim to minimize)aim to minimize)

Hypoxia and ischemiaHypoxia and ischemia Cerebral edemaCerebral edema Intracranial hypertension (ICH)Intracranial hypertension (ICH)

Cerebral IschemiaCerebral Ischemia

This is the mechanism that underlies This is the mechanism that underlies “secondary” injury to the brain.“secondary” injury to the brain.

It all comes back around to Cerebral It all comes back around to Cerebral Perfusion Pressure.Perfusion Pressure. Remember that you’ve got two opposing Remember that you’ve got two opposing

forces – the mean arterial pressure forces – the mean arterial pressure “pushing” oxygenated blood into brain “pushing” oxygenated blood into brain tissue, and intracranial pressure pushing tissue, and intracranial pressure pushing back.back.

CPP = MAP - ICPCPP = MAP - ICP

Bottom LineBottom Line You need adequate CPP to maintain viable You need adequate CPP to maintain viable

brain tissue. brain tissue. Once past the primary injury, secondary Once past the primary injury, secondary

injury sets in as the volume of any one (or injury sets in as the volume of any one (or more) of the three constituents starts to more) of the three constituents starts to increase and cerebral ischemia occurs.increase and cerebral ischemia occurs.

ICP begins to rise relatively quickly once ICP begins to rise relatively quickly once the extra volume increases (especially the extra volume increases (especially beyond ~100 cc’s.)beyond ~100 cc’s.)

Generally, 60 – 70 mmHG is the target CPP Generally, 60 – 70 mmHG is the target CPP for patients with TBI.for patients with TBI.

It is thought that ICP should be treated It is thought that ICP should be treated once it hits a threshhold of 20 mmHg.once it hits a threshhold of 20 mmHg.

Symptoms and Signs of Symptoms and Signs of Elevated ICPElevated ICP

TriadTriad Headache, nausea, vomitingHeadache, nausea, vomiting

Cranial nerve palsiesCranial nerve palsiesPapilledemaPapilledema

Usually from a more chronic processUsually from a more chronic process

Vital sign changesVital sign changes Cushing’sCushing’s

Arterial hypertension and bradycardiaArterial hypertension and bradycardia

Respiratory changesRespiratory changes

PapilledemaPapilledema Swelling of the optic Swelling of the optic

nerve head with nerve head with engorgement of the engorgement of the retinal veinsretinal veins

Presence almost Presence almost always indicates always indicates raised intracranial raised intracranial pressure.pressure.

Management of Elevated Management of Elevated ICP:ICP:

Airway/ventilator Airway/ventilator supportsupport

Maintain Maintain adequate CPPadequate CPP

Osmotic diuresisOsmotic diuresisHypertonic salineHypertonic salineSedation/Sedation/analgesiaanalgesia

HypothermiaHypothermiaNeuromuscular Neuromuscular blockadeblockade

Barbiturate Barbiturate comacoma

Glycemic controlGlycemic controlCSF drainageCSF drainageCraniectomyCraniectomy

Therapeutic Therapeutic Modalities for Modalities for

Reduction of ICPReduction of ICP

Intracranial Intracranial HematomasHematomas

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Epidural HematomaEpidural Hematoma

Typically younger patientsTypically younger patients Patients may present with Patients may present with

alterations in consciousness, alterations in consciousness, headache, nausea/vomiting, etc.headache, nausea/vomiting, etc.

Evidence of trauma: Contusion, Evidence of trauma: Contusion, laceration, or bony step-off may be laceration, or bony step-off may be observed on the head (should have observed on the head (should have high clinical suspicion).high clinical suspicion).


““Classic presentation”: Impact on Classic presentation”: Impact on side of head with “lucid interval,” side of head with “lucid interval,” then CT scan demonstrating biconvex then CT scan demonstrating biconvex (lenticular – “lens shaped”) hematoma (lenticular – “lens shaped”) hematoma causing brain compression and causing brain compression and midline shift.midline shift.

Deterioration can be rapid. Deterioration can be rapid. Prognosis is generally excellent if Prognosis is generally excellent if

managed aggressively!!!managed aggressively!!! Mortality estimated as high as 20%!Mortality estimated as high as 20%!

Epidural HematomaEpidural Hematoma Epidural Hematomas – 90% seen in head Epidural Hematomas – 90% seen in head

trauma with a skull fracture that crosses trauma with a skull fracture that crosses a portion of the a portion of the middle meningeal middle meningeal artery/veinartery/vein..

Middle meningeal artery is torn Middle meningeal artery is torn approximately 2/3approximately 2/3rdsrds of the time. of the time.

Blood which collects in the epidural Blood which collects in the epidural space is limited by the intracranial space is limited by the intracranial sutures, where the dural membrane is sutures, where the dural membrane is closely adherent to the inside of the closely adherent to the inside of the calvarium.calvarium.


Skull FractureSkull Fracture

Epidural Hematoma Epidural Hematoma (underneath skull (underneath skull

fracture)fracture)


Generally, treatment is surgical.Generally, treatment is surgical. Can sometimes manage Can sometimes manage smallsmall EDHs EDHs

conservatively if they are asymptomatic conservatively if they are asymptomatic (but you still MUST get these patients (but you still MUST get these patients to a Neurosurgeon so that if the EDH to a Neurosurgeon so that if the EDH evolves or clinical picture worsens they evolves or clinical picture worsens they can receive immediate treatment.can receive immediate treatment.

What really hurts these patients is What really hurts these patients is delay in diagnosis, delay in transfer, delay in diagnosis, delay in transfer, i.e. anything that delays treatment!!!i.e. anything that delays treatment!!!



Subdural HematomaSubdural Hematoma

Come in three different “flavors”:Come in three different “flavors”: AcuteAcute SubacuteSubacute ChronicChronic

Don’t be fooled!!! Acute to Chronic Don’t be fooled!!! Acute to Chronic SDHs are different clinical entities!SDHs are different clinical entities!

Acute Subdural Acute Subdural HematomaHematoma

About twice as common (or more) as EDHs.About twice as common (or more) as EDHs. Major difference compared to EDH – magnitude Major difference compared to EDH – magnitude

of primary injury is usually much higher in acute of primary injury is usually much higher in acute SDH (mortality is HIGHER!).SDH (mortality is HIGHER!).

Two most common causes of Acute SDH:Two most common causes of Acute SDH: Accumulation of blood around parenchymal lacerationAccumulation of blood around parenchymal laceration Tearing of surface/bridging vessels from acceleration-Tearing of surface/bridging vessels from acceleration-

deceleration during violent head motiondeceleration during violent head motion Mechanism of injury: “brain rattles inside head.”Mechanism of injury: “brain rattles inside head.” Much higher risk in patients on anticoagulation!Much higher risk in patients on anticoagulation!

Acute SDHsAcute SDHs

Typically an older patient who suffers Typically an older patient who suffers some type of head injury (or suspected some type of head injury (or suspected injury) and gets a CT scan in the ER.injury) and gets a CT scan in the ER.

Radiographically, what you typically Radiographically, what you typically see is a HYPER-dense CRESCENT-see is a HYPER-dense CRESCENT-shaped fluid collection that CROSSES shaped fluid collection that CROSSES SUTURE LINES!!! SUTURE LINES!!!

Associated parenchymal bleeding, Associated parenchymal bleeding, even subarachnoid blood is not an even subarachnoid blood is not an uncommon finding.uncommon finding.

Acute SDHAcute SDH

30-day mortality is between 50 and 30-day mortality is between 50 and 80%!80%!

Dramatic difference between Dramatic difference between mortality of EDH and Acute SDH is mortality of EDH and Acute SDH is secondary to the magnitude of secondary to the magnitude of primary brain injury, which is primary brain injury, which is typically much greater in the setting typically much greater in the setting of Acute SDH than EDH.of Acute SDH than EDH. Also they are usually older patients.Also they are usually older patients.






Compare: EDH vs acute Compare: EDH vs acute SDHSDH

Chronic SDHsChronic SDHs

Generally occur in elderly (avg age of Generally occur in elderly (avg age of presentation is 63 yrs)presentation is 63 yrs)

Other risk factors: alcohol abuse, Other risk factors: alcohol abuse, coagulopathies, fall risk, seizures, etc.coagulopathies, fall risk, seizures, etc. Anything that impairs blood clotting, coagulation, Anything that impairs blood clotting, coagulation,

etc.etc. Patients can present any of a multitude of Patients can present any of a multitude of

different ways: TIA-type symptoms, headache, different ways: TIA-type symptoms, headache, confusion, lethargy, speech trouble, weakness, confusion, lethargy, speech trouble, weakness, etc.etc.

Often, no known history of trauma or event.Often, no known history of trauma or event.


Prevailing thought is that Chronic SDHs Prevailing thought is that Chronic SDHs evolve from small / asymptomatic acute evolve from small / asymptomatic acute SDHs. SDHs.

Blood within the subdural space causes Blood within the subdural space causes inflammatory response; fibroblasts inflammatory response; fibroblasts invade, neomembranes form, invade, neomembranes form, neovascularization occurs.neovascularization occurs.

Chronic SDHs can be very complex, multi-Chronic SDHs can be very complex, multi-lobed structures.lobed structures.

Tend to gradually get larger over time.Tend to gradually get larger over time.


On CT scans, these are CRESCENT-On CT scans, these are CRESCENT-shaped HYPO-dense lesions that cross shaped HYPO-dense lesions that cross suture lines.suture lines.

Not uncommon to see lobules within the Not uncommon to see lobules within the fluid collection.fluid collection.

Not uncommon to see subacute or even Not uncommon to see subacute or even acute blood within a chronic SDH.acute blood within a chronic SDH.

Treatment is surgical when symptomatic Treatment is surgical when symptomatic or (generally speaking) once thickness or (generally speaking) once thickness exceeds 1cm.exceeds 1cm.


Bilateral Bilateral occurrence as occurrence as often as 25% of the often as 25% of the timetime

Acute vs. Chronic SDHsAcute vs. Chronic SDHs

Radiographic difference Radiographic difference between SDH types: between SDH types:

TimeframeTimeframe Acute SDHs – hyperdense (less than Acute SDHs – hyperdense (less than

one week old)one week old) Subacute SDHs – isodense (between Subacute SDHs – isodense (between

five days and three weeks old)five days and three weeks old) Chronic SDHs – hypodense (between Chronic SDHs – hypodense (between

three weeks and 3-4 months old)three weeks and 3-4 months old)

UnderstandUnderstand

Acute SDHs, like EDHs, need to be Acute SDHs, like EDHs, need to be diagnosed immediately.diagnosed immediately. If Neurosurgery service is not available, If Neurosurgery service is not available,

these patients must be transferred to these patients must be transferred to hospital where it IS available.hospital where it IS available.

Delays in diagnosis, transfer, Delays in diagnosis, transfer, treatment, etc. can (and do) kill treatment, etc. can (and do) kill patients!patients!

Intracerebral Intracerebral hemorrhagehemorrhage

ICHICH

In adults, this is the second-most common form In adults, this is the second-most common form of stroke (~30%) and by far the most deadly.of stroke (~30%) and by far the most deadly.

Typical onset during activity, with headache; Typical onset during activity, with headache; also N/Valso N/V

Age > 55Age > 55 Hypertension (greatest association)Hypertension (greatest association) Drug useDrug use Coagulopathy, liver dysfunction, etc., all Coagulopathy, liver dysfunction, etc., all

associated with poorer outcomes.associated with poorer outcomes. ANY prior CVA increases risk ANY prior CVA increases risk 2323 times! times!

ICHICH

Four most common locations:Four most common locations: Basal Ganglia (Putamen, in particular)Basal Ganglia (Putamen, in particular) ThalamusThalamus Deep Cerebellar NucleiDeep Cerebellar Nuclei Brainstem (Pons by far)Brainstem (Pons by far)

Despite extensive study, the role of surgery Despite extensive study, the role of surgery in management of ICH is largely unclear.in management of ICH is largely unclear. Surgery never shown to improve long-term Surgery never shown to improve long-term

outcome over best medical management outcome over best medical management (Cerebellar hemorrhage is exception)(Cerebellar hemorrhage is exception)

Cerebellar ICHCerebellar ICH

Other causes of ICHOther causes of ICH

TumorTumor AVMAVM Cavernous Cavernous

malformationmalformation Etc.Etc. Angiography should Angiography should

be done, if at all be done, if at all possible, whenever possible, whenever you get a patient you get a patient younger than 55 with younger than 55 with an ICH.an ICH.

Subarachnoid Subarachnoid HemorrhageHemorrhage

The most common The most common cause of cause of Subarachnoid Subarachnoid Hemorrhage (SAH) Hemorrhage (SAH) is is TRAUMATRAUMA!!!!!!!!!!!!!!!!

Ruptured Ruptured intracranial intracranial aneurysms aneurysms responsible for 85% responsible for 85% of of spontaneousspontaneous SAH.SAH.

Aneurysmal SAHAneurysmal SAH

Aneurysms tend to occur at bifurcations Aneurysms tend to occur at bifurcations or branching points of major cerebral or branching points of major cerebral vessels along the circle of Willis.vessels along the circle of Willis.

As a general rule, 30% in the anterior As a general rule, 30% in the anterior circulation (AComm), 30% in the middle circulation (AComm), 30% in the middle circulation (ICA, MCA branching points), circulation (ICA, MCA branching points), 30% in the posterior circulation 30% in the posterior circulation (PComm), and 10% in the basilar (PComm), and 10% in the basilar circulation (Basilar bifurcation, PICA, circulation (Basilar bifurcation, PICA, etc).etc).

Spontaneous aneurysmal Spontaneous aneurysmal SAHSAH

As a general rule, Neurosurgery patients As a general rule, Neurosurgery patients don’t come any sicker than aneurysm don’t come any sicker than aneurysm ruptures.ruptures.

1/3 either don’t make it to the hospital or 1/3 either don’t make it to the hospital or don’t survive the first week after don’t survive the first week after rupture.rupture.

Of those who survive, half are left with Of those who survive, half are left with serious neurological sequelae. Morbidity serious neurological sequelae. Morbidity is high, and mortality in first six months is high, and mortality in first six months approaches 50%.approaches 50%.

Aneurysmal SAHAneurysmal SAH

Classic presentation is the sudden Classic presentation is the sudden onset of the “worst headache I’ve onset of the “worst headache I’ve ever had in my life.”ever had in my life.”

Nausea, Vomiting.Nausea, Vomiting. Decreased mental statusDecreased mental status

Can be due to acute hydrocephalus, Can be due to acute hydrocephalus, necessitating ventriculostomy/EVD necessitating ventriculostomy/EVD placementplacement

Three major complications Three major complications from aneurysmal SAHfrom aneurysmal SAH

An aneurysm can RE-bleed! Greatest risk An aneurysm can RE-bleed! Greatest risk is within first 24 hours, then drops is within first 24 hours, then drops exponentiallyexponentially

Vasospasm! This can lead to stroke. Vasospasm! This can lead to stroke. Greatest incidence of symptomatic spasm Greatest incidence of symptomatic spasm is between 4 and 10 days after ruptureis between 4 and 10 days after rupture

Hydrocephalus, communicating type. Can Hydrocephalus, communicating type. Can present even months after a bleed.present even months after a bleed. Acutely, you can have obstructive Acutely, you can have obstructive

hydrocephalus.hydrocephalus.

AneurysmsAneurysms

Much more common Much more common in the population in the population than you might thinkthan you might think Some estimates as Some estimates as

high as 10%.high as 10%. Outpatient f/u for Outpatient f/u for

incidental aneurysms incidental aneurysms is appropriate.is appropriate.

Risk of rupture at Risk of rupture at any given time is any given time is LOWLOW

““Triple-H therapy”Triple-H therapy”

HypertensionHypertension HemodilutionHemodilution HypervolemiaHypervolemia Also, Nimotop 60mg PO q4h is Also, Nimotop 60mg PO q4h is

started immediately (for vasospasm started immediately (for vasospasm prophylaxis) and continued through prophylaxis) and continued through post-bleed day #21.post-bleed day #21.

Treatment of AneurysmsTreatment of Aneurysms

Incidentally found aneurysms do not Incidentally found aneurysms do not necessitate treatment; patients may necessitate treatment; patients may choose to seek treatment or not.choose to seek treatment or not.

Ruptured aneurysms must be Ruptured aneurysms must be treatedtreated Craniotomy and clippingCraniotomy and clipping Endovascular treatment (newer Endovascular treatment (newer

treatment modality)treatment modality)

What you can doWhat you can do

In any suspected intracranial In any suspected intracranial hemorrhage, traumatic brain injury, hemorrhage, traumatic brain injury, etc., there are some principles you etc., there are some principles you can remember and things you can can remember and things you can do…do…

LabsLabs

In addition to all of the “normal” In addition to all of the “normal” labs that are drawn in the ER labs that are drawn in the ER setting, make sure you order coags setting, make sure you order coags (PT, INR, PTT) and start to correct (PT, INR, PTT) and start to correct any existing coagulopathy any existing coagulopathy appropriately.appropriately. FFPFFP Vitamin KVitamin K PlateletsPlatelets

Blood PressureBlood Pressure Take care not to “bottom out” blood Take care not to “bottom out” blood

pressure just because it’s high. Remember, pressure just because it’s high. Remember, the body is trying to maintain CPP. the body is trying to maintain CPP. In the setting of an EDH or SDH, blindly In the setting of an EDH or SDH, blindly

reducing a patient’s BP can accelerate neural reducing a patient’s BP can accelerate neural injury.injury.

In the setting of intraparenchymal hemorrhage, In the setting of intraparenchymal hemorrhage, shoot for a BP between 140 and 160 systolic; shoot for a BP between 140 and 160 systolic; the idea is drawing a balance between the idea is drawing a balance between decreasing BP to help stop the bleeding, and decreasing BP to help stop the bleeding, and protecting the ischemic penumbra.protecting the ischemic penumbra.

Blood Pressure (cont’d)Blood Pressure (cont’d)

In the setting of a ruptured In the setting of a ruptured aneurysm, allowing a patient to be aneurysm, allowing a patient to be extremely hypertensive can extremely hypertensive can predispose to re-rupture of the predispose to re-rupture of the aneurysm.aneurysm.

Herniation Herniation SyndromesSyndromes

Remembering the “Box”Remembering the “Box”

Increased ICP contributes to Increased ICP contributes to cerebral ischemia, but remember cerebral ischemia, but remember that an expanding mass lesion that an expanding mass lesion displaces its surrounding displaces its surrounding constituents. Since the intracranial constituents. Since the intracranial volume is generally considered to be volume is generally considered to be “fixed,” past a certain point that “fixed,” past a certain point that extra volume has to go somewhere.extra volume has to go somewhere.

Pertinent Anatomy Pertinent Anatomy considering herniation considering herniation

syndromessyndromes The intracranial compartment is The intracranial compartment is

divided into 3 compartments by 2 divided into 3 compartments by 2 major dural structures, the falx major dural structures, the falx cerebri and the tentorium cerebelli. cerebri and the tentorium cerebelli. The tentorium cerebelli divides the The tentorium cerebelli divides the posterior fossa or infratentorial posterior fossa or infratentorial compartment (the cerebellum and the compartment (the cerebellum and the brainstem) from the supratentorial brainstem) from the supratentorial compartment (cerebral hemispheres). compartment (cerebral hemispheres).

Pertinent Anatomy Pertinent Anatomy considering herniation considering herniation

syndromessyndromes Both the falx and the tentorium have Both the falx and the tentorium have

central openings and prominent edges central openings and prominent edges at the borders of each of these openings. at the borders of each of these openings. When a significant increase in ICP When a significant increase in ICP occurs, caused by either a large mass occurs, caused by either a large mass lesion or significant cerebral edema, the lesion or significant cerebral edema, the brain can slide through these openings, brain can slide through these openings, a phenomenon known as herniation. As a phenomenon known as herniation. As the brain slides over the free dural the brain slides over the free dural edges of the tentorium or the falx, it can edges of the tentorium or the falx, it can sustain injuies caused by the dural edge. sustain injuies caused by the dural edge.

Herniation SyndromesHerniation Syndromes

UncalUncal SubfalcineSubfalcine TonsillarTonsillar

Uncal HerniationUncal Herniation When people talk “herniation”, this is it.When people talk “herniation”, this is it. The uncus of the hippocampus is pushed The uncus of the hippocampus is pushed

across the tentorial notch into the across the tentorial notch into the posterior fossa.posterior fossa.

Clinical PresentationClinical Presentation Ipsilateral “blown pupil.”Ipsilateral “blown pupil.” Compression of ipsilateral cerebral Compression of ipsilateral cerebral

peduncle (Contralateral hemiparesis).peduncle (Contralateral hemiparesis). Compression of ipsilateral PCA (Occipital Compression of ipsilateral PCA (Occipital

infarction).infarction).

Uncal HerniationUncal Herniation Uncal herniation is Uncal herniation is

generally an acute generally an acute process.process.

Earliest consistent Earliest consistent sign: sign: unilaterally unilaterally dilating pupildilating pupil!!

Once brainstem Once brainstem involvement occurs involvement occurs (i.e. contralateral (i.e. contralateral hemiparesis, hemiparesis, respiratory respiratory compromise), damage compromise), damage may be irreversible!may be irreversible!

Uncal herniationUncal herniation

PreventingPreventing uncal herniation is the uncal herniation is the general idea behind rapid diagnosis general idea behind rapid diagnosis of EDHs and aggressive of EDHs and aggressive management.management.

Subfalcine herniationSubfalcine herniation Occurs when there is Occurs when there is

herniation of the herniation of the cingulate gyrus beneath cingulate gyrus beneath the falx.the falx.

Usually asymptomatic Usually asymptomatic unless causes ipsilateral unless causes ipsilateral (or sometimes bilateral) (or sometimes bilateral) ACA occlusion ACA occlusion (contralateral leg (contralateral leg weakness can be a weakness can be a warning that warning that transtentorial herniation transtentorial herniation is about to occur!).is about to occur!).

MOST COMMON MOST COMMON HERNIATION!HERNIATION!

Tonsillar herniationTonsillar herniation In an acute setting, In an acute setting,

the cerebellar the cerebellar tonsils “cone” tonsils “cone” through the foramen through the foramen magnum, causing magnum, causing compression of the compression of the medulla. medulla.

Leads to respiratory Leads to respiratory arrest.arrest.

Typically Typically rapidlyrapidly fatal.fatal.

INFRATENTORIALINFRATENTORIAL

Tonsillar herniationTonsillar herniation

Can occur with either supra or infra-Can occur with either supra or infra-tentorial lesions, or with elevated tentorial lesions, or with elevated ICP.ICP.

Can be precipitated by Lumbar Can be precipitated by Lumbar Puncture!Puncture!

Same type of anatomical finding Same type of anatomical finding demonstrated in patients with Chiari demonstrated in patients with Chiari malformation (but chronic rather malformation (but chronic rather than acute).than acute).

SummarySummary

This online module contained This online module contained information from four of your information from four of your “topics.”“topics.” Traumatic Brain Injury and increased Traumatic Brain Injury and increased

ICPICP Intracranial hematomasIntracranial hematomas Spontaneous Subarachnoid Spontaneous Subarachnoid

HemorrhageHemorrhage Herniation SyndromesHerniation Syndromes

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Module Neurotrauma