Andrew W. Asimos, MD Treating Elevated ICP in the TBI Patient.

Andrew W. Asimos, MD

Treating Elevated ICP in Treating Elevated ICP in the TBI Patientthe TBI Patient


Andrew Asimos, MDAndrew Asimos, MDDirector of Emergency Stroke CareDirector of Emergency Stroke CareNeuroscience and Spine InstituteNeuroscience and Spine Institute

Carolinas Medical Center, Charlotte, NCCarolinas Medical Center, Charlotte, NC

Adjunct Associate Professor, Department of Emergency MedicineAdjunct Associate Professor, Department of Emergency MedicineUniversity of North Carolina School of Medicine at Chapel HillUniversity of North Carolina School of Medicine at Chapel Hill


Attending PhysicianAttending PhysicianEmergency MedicineEmergency Medicine

Carolinas Medical CenterCarolinas Medical CenterDepartment of Emergency MedicineDepartment of Emergency Medicine

Charlotte, NCCharlotte, NC



Session ObjectivesSession Objectives

• Present a relevant patient case

• State key clinical questions

• Outline the procedure for treating elevated ICP


A Clinical CaseA Clinical Case


Clinical HistoryClinical History• 18 year old male non-helmeted skateboarder,

struck his head on driveway• Closest L1TC one hour by helicopter• Being taken to non-trauma center ED• Prehospital care: IV, O2 via NRB mask,

monitor• Intermittently combative• Attempting immobilization


Physical ExamPhysical Exam• 98.8 100/60 110 12 pulse ox 95%• Gen: Intermittently agitated• Head: Scalp abraisions, soft tissue

selling over R temporal-parietal region, hemotympanum

• Face: Several abrasions • Eyes: 4 mm, equal, reactive


Physical ExamPhysical Exam• Chest: BSBE, no crepitus

• Cardiac: Tachycardia without murmur

• Abd: Soft, FAST negative

• Pelvis: Stable to compression

• Ext: No long bone deformity, abrasions


Neurologic ExamNeurologic Exam• Motor: Withdraws to painful stimuli,

no posturing, no pathological reflexes

• Eyes: Open to painful stimuli, PERL

• Verbal: Perseverating speech

• Sensory: No sensory level


Provisional DiagnosisProvisional Diagnosis

• Moderate to Severe TBI– GCS Score ≈ 9-10


Key Clinical QuestionsKey Clinical Questions• In the setting of acute TBI, what are the clinical signs

and symptoms of increased ICP?• What imaging findings suggest impending herniation

syndrome in the TBI patient?• How should patients with suspected increased ICP in

the setting of TBI be managed?• What are the roles for the following therapies in the

setting of suspected increased ICP: mannitol, hyperventilation, steroids, seizure prophylaxis, and skull trephination?


Initial CTInitial CT


Treating Elevated ICP inTreating Elevated ICP inthe TBI Patientthe TBI Patient : :

Key Clinical ConceptsKey Clinical Concepts


ICP Detection PearlsICP Detection Pearls

• VS don’t change until late in the clinical course of increased ICP and herniation

• Signs and symptoms of increased ICP in TBI– GCS score of 8 or less– Decreased level of consciousness– Cranial nerve findings

• Eye exam is key

– CT scans showing ventricle or cistern abnormalities, or midline shift


Eye Examination in Suspected Eye Examination in Suspected Increased ICPIncreased ICP

Pupillary Findings Clinical Significance

Unilaterally dilated Ipsilateral lesion, increased ICP

6th nerve palsy May be first sign of ICP rise

Loss of upward gaze Increased ICP compressing pretectal area against the posterior tentorial incisura

Midposition and fixed Sympathetic and parasympathetic failure at the midbrain

Extremely miotic pupils Pontine lesion or narcotic overdose

Bilaterally dilated and poorly responsive

Sympathetic overactivity from catecholamines or anticholinergic medications

Bilaterally fixed & dilated Markedly elevated ICP or brain death

Papilledema Rarely present in the acute phase of TBI


Brain HerniationBrain Herniation

• Cranial contents compartmentalized by a layering of dura mater– Folding dura forms distinct brain

compartments• Falx cerebri – separates 2 hemispheres• Tentorium cerebelli – separates

infratentorial structures from supratentorial structures

• Expansion of IC contents limited by skull and these compartments


Transtentorial HerniationTranstentorial Herniation

• Brain traverses tentorium at the level of the incisura

• Divided into– Descending

• Largest category• Mass effect in the cerebrum pushes supratentorial brain

through incisura to the posterior fossa

– Ascending• Mass effect in posterior fossa leads to brain extending

through the incisura in an upward


Central Transtentorial HerniationCentral Transtentorial Herniation

• Causes– Diffuse and severe TBI swelling– Centrally located, supratentorial masses

• Thalamic hemorrhage– Lesions of the frontal, parietal, & occipital

lobes• Downward movement of the

diencephalon and rostral midbrain through the tentorial notch


Diagnosing Central Transtentorial Diagnosing Central Transtentorial HerniationHerniation

• Progressive rostrocaudal deterioration of brainstem function1. Compression of diencephalic structures causes lethargy,

apathy, or confusion2. Loss of upward gaze due to compression of the diencepahlic

pretectal area against the posterior tentorial incisura3. Extensor plantar responses, paratonia, ipsilateral

decortication, contralateral decerebration4. Pupils dilate to midposition because of sympathetic and

parasympathetic dysfuction5. Hyperventilation6. Decerebrate rigidity7. Autonomic dysregulation

• VS do not change until late


Uncal HerniationUncal Herniation

• Associated with supratentorial masses and masses in the temporal fossa– Subdural or epidural hematoma, large MCA stroke,

temporal lobe tumor

• Medial portion of the temporal lobe (uncus) displaces over the tentorial notch

• Causing compression of– Ipsilateral oculomotor nerve and brainstem

compression– Occasionally the ipsilateral PCA


Diagnosing Uncal HerniationDiagnosing Uncal Herniation• Classically, a stepwise progression

1. Early clinical sign is dilatation of the ipsilateral pupil– Compression of the parasympathetic fibers traveling on the periphery of

the third nerve2. Loss of the light reflex, ipsilateral ptosis, “down and out” eye

– Patient may be surprisingly alert3. Contralateral hemiparesis

– Compression of the ipsilateral cerebral peducle against the free edge of the tentorium

– Rarely ipsilateral hemiparesis (Kernohan’s phenomenon)4. Consciousness deteriorates

– Midbrain compession, sometimes associated hemorrhage, with compromise of the ascending portion of the RAS

5. Bilateral pupillary dilation• Changes in VS may not occur until just prior to fatal herniation

– Respiratory changes and bradycardia


Descending Transtentorial Descending Transtentorial Herniation Herniation

Clinical Findings Imaging Findings Complications

•Ipsilateral dilated pupil

•Contralateral hemiparesis

•Ipsilateral hemiparesis if Kernohan’s Notch is present (false localizer)

•Contralateral temporal horn widening

•Ipsilateral ambient cistern widening

•Ipsilateral prepontine cistern widening

•Uncus extending into the suprasellar cistern

•Occipital infarct from posterior cerebral artery compression

•Durette hemorrhage


Imaging Findings of Descending Imaging Findings of Descending Transtentorial Herniations Transtentorial Herniations


Imaging Findings of Uncal Imaging Findings of Uncal HerniationHerniation

Usual six pointed star appearance of the suprasellar cistern

Truncated suprasellar cistern on the ipsilateral

side of the herniation


Right Uncal HerniationRight Uncal Herniation


Descending Transtentorial Shift to Descending Transtentorial Shift to the Leftthe Left


Durette Hemorrhage:Durette Hemorrhage:A Complication of Descending Transtentorial HerniationA Complication of Descending Transtentorial Herniation


Featured Procedures or ProtocolsFeatured Procedures or Protocols

• Treatment protocol for the management of elevated intracranial pressure (ICP)

• Skull trephination for the management of suspected uncal herniation due to an expanding epidural hematoma


Elevated ICP Therapy:Elevated ICP Therapy: The ProcedureThe Procedure


BTF Guidelines for the Management BTF Guidelines for the Management of Severe Traumatic Brain Injuryof Severe Traumatic Brain Injury

Management andPrognosis of SevereTraumatic Brain Injury

Brain Trauma Foundation, Inc, American Association of Neurological Surgeons. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.


BTF TBI Treatment GuidelinesBTF TBI Treatment Guidelines

• Head Injury Guidelines Task Force (AANS)– Initial draft 2000, revision due 2006

• Key Concept– Evidence based TBI treatment guidelines

exist and are widely available

Brain Trauma Foundation, Inc, American Association of Neurological Surgeons. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.


Elevated ICP Rx ProcedureElevated ICP Rx Procedure

• Evaluate globally all resuscitation needs


Initial ManagementInitial Management

• No Standards or Guidelines• Options

– Complete and rapid physiologic resuscitation

– No specific treatment for intracranial hypertension in the absence of signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial explanations

Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe

Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.


Hypoxia and Hypotension in TBIHypoxia and Hypotension in TBI

Outcome % Insult # Pts % Total G-M S-V Dead

Total 717 100 43 20 37

Neither 308 43 54 19 27

Hypoxia 161 22 51 22 28

Hypotension 82 11 33 17 50

Both 166 23 21 22 57

Chesnut RM et al. Chesnut RM et al. J TraumaJ Trauma 34(2):216-22, 1993 Feb. 34(2):216-22, 1993 Feb.




• Do not provide prophylactic osmotherapy– Only with clinical deterioration

• Do not use prophylactic hyperventilation


MannitolMannitol

• Standards– There are insufficient data to support a

treatment standard for the use of mannitol

• Guidelines– Mannitol is effective for control of raised ICP

after severe head injury– Effective doses range from 0.25 g/kg body

weight to 1 gm/kg body weight




MannitolMannitol

• Options– The indications for the use of mannitol prior

to ICP monitoring are signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial explanations

– Avoid hypovolemia by fluid replacement

• Intermittent boluses may be more effective than continuous infusion




MannitolMannitol

• Appropriate dosing range in the ED is 0.25-1.4 g/kg administered “wide open”

• The Cochrane Review concludes high-dose mannitol (1.4 g/kg) appears to be preferable to conventional-dose mannitol in the pre-operative management of patients with acute intracranial hematomas

Roberts I et al. Mannitol for acute traumatic brain injury. Cochrane Injuries Group Cochrane Database of Systematic Reviews 2005.





• Do not use prophylactic hyperventilation– Only with clinical deterioration


HyperventilationHyperventilation

• Standards– In the absence of increased ICP, chronic prolonged

hyperventilation therapy (PaCO2 <25 mm Hg) should be avoided after severe traumatic brain injury

• Guidelines– The use of prophylactic hyperventilation (PaCO2

<35 mm Hg) therapy during the first 24 hours after severe traumatic brain injury should be avoided because it can compromise CPP during a time when CBF is reduced




HyperventilationHyperventilation

• Options– Hyperventilation therapy may be necessary

for brief periods• When there is acute neurologic deterioration

– For longer periods if there is intracranial hypertension refractory to sedation, paralysis, cerebrospinal fluid drainage, and osmotic diuretics








• Consider seizure prophylaxis


Seizure ProphylaxisSeizure Prophylaxis

• Standards– Prophylactic use of phenytoin,

carbamazepine, phenobarbital or valproate is not recommended for preventing late post-traumatic seizures

• Guidelines– None




Seizure ProphylaxisSeizure Prophylaxis

• Options– It is recommended as a treatment option that

anticonvulsants may be used to prevent early post-traumatic seizures in patients at high risk for seizures following head injury

– Phenytoin and carbamazepine have been demonstrated to be effective in preventing early post-traumatic seizures

– Available evidence does not indicate that prevention of early post-traumatic seizures improves outcome following head injury








• Consider seizure prophylaxis

• Do not use steroids


SteroidsSteroids

• Standards– The use of steroids is not recommended for

improving outcome or reducing ICP in patients with severe TBI

• Guidelines– None

• Options– None




SteroidsSteroids

• Conclusions– In the absence of a meta-analysis, we

feel most weight should be placed on the result of the largest trial

– The increase in mortality with steroids in this trial suggest that steroids should no longer be routinely used in people with traumatic head injury

Alderson P, Roberts I. Corticosteroids for acute traumatic brain injury. Cochrane Injuries Group Cochrane Database of Systematic Reviews 2005.


Indications for Emergent Cranial Indications for Emergent Cranial DecompressionDecompression

• To evacuate extradural hematomas• To reverse clinical signs of tentorial

herniation• Rapid, progressive neurologic

deterioration• Timely inavailability of a

neurosurgeon


Gather Up What You will NeedGather Up What You will Need


• 4 cm vertical incision

• External auditory canal is key landmark– Three cm superior

to zygoma– Two cm anterior to

ear

Emergent Cranial Decompression:Emergent Cranial Decompression:The ProcedureThe Procedure



• Retract the scalp and galea

• May hit the superficial temporal artery

• Cut through the temporal fascia and temporal muscle

• Retract with a Weitlaner retractor



• Drill a hole, enlarge with a Burr

• Careful as the inner table is perforated

• Epidural hematoma will likely have a jelly consistency

• Middle meningeal artery is deep to clot

• Foramen spinosum transmits middle meningeal artery



• Be prepared to replace blood loss

• If no CT prior and bilateral fixed pupils or no clot, consider repeating on contra-lateral side


ED Treatment and ED Treatment and Patient OutcomePatient Outcome


ED Patient ManagementED Patient Management• Patients RSI’d, paralyzed and sedated for emergenct

CT scanning• CT scan indicates a right temporal epidural

hematoma• Aeromedically evacuated to a L1TC• On arrival to L1TC, right pupil noted to be dilated,

ABG on arrival with pCO2 39• Bolused with 1.4 gm/kg Mannitol• Ventilatory rate increased, TV unchanged• Emergently taken to OR for hematoma evacuation


Patient OutcomePatient Outcome• Hematoma evacuated without difficulty

• Three day ICU stay

• Minimal cognitive deficits on hospital discharge

• No motor deficits


Treating Elevated ICP in the Treating Elevated ICP in the TBI PatientTBI Patient : :

A RetrospectiveA Retrospective


Treating Elevated ICP

in the TBI Patient • Know the clinical and CT signs of

elevated ICP• Know the treatment guidelines• If a neurosurgical intervention is

anticipated, know its relative availability• If a heroic procedure is the only option,

know its basic steps, gather required equipment, and utilize any consultants possible


Questions??Questions??

[email protected]@ferne.org

Andrew W. Asimos, MD Treating Elevated ICP in the TBI Patient.

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