Treating Elevated ICP in the TBI Patient

Andrew Asimos, MD Director of Emergency Stroke Care Neuroscience and Spine Institute Carolinas Medical Center, Charlotte, NC Adjunct Associate Professor, Department of Emergency Medicine University of North Carolina School of Medicine at Chapel Hill 54 1 54

Attending Physician Emergency Medicine Carolinas Medical Center Department of Emergency Medicine Charlotte, NC 54 1 54

Session Objectives Present a relevant patient case State key clinical questions Outline the procedure for treating elevated ICP 54 2 54

A Clinical Case

Clinical 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 54 3 54

Physical 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 54 3 54

Physical Exam Chest: BSBE, no crepitus Cardiac: Tachycardia without murmur Abd: Soft, FAST negative Pelvis: Stable to compression Ext: No long bone deformity, abrasions 54 3 54

Neurologic Exam Motor: Withdraws to painful stimuli, no posturing, no pathological reflexes Eyes: Open to painful stimuli, PERL Verbal: Perseverating speech Sensory: No sensory level 54 3 54

Provisional Diagnosis Moderate to Severe TBI GCS Score ≈ 9-10

Key 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? 54 2 54

Initial CT

Treating Elevated ICP in the TBI Patient : Key Clinical Concepts

ICP 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 Increased 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 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 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 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 Herniation Progressive rostrocaudal deterioration of brainstem function Compression of diencephalic structures causes lethargy, apathy, or confusion Loss of upward gaze due to compression of the diencepahlic pretectal area against the posterior tentorial incisura Extensor plantar responses, paratonia, ipsilateral decortication, contralateral decerebration Pupils dilate to midposition because of sympathetic and parasympathetic dysfuction Hyperventilation Decerebrate rigidity Autonomic dysregulation VS do not change until late

Uncal 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 Herniation Classically, a stepwise progression Early clinical sign is dilatation of the ipsilateral pupil Compression of the parasympathetic fibers traveling on the periphery of the third nerve Loss of the light reflex, ipsilateral ptosis, “down and out” eye Patient may be surprisingly alert Contralateral hemiparesis Compression of the ipsilateral cerebral peducle against the free edge of the tentorium Rarely ipsilateral hemiparesis (Kernohan’s phenomenon) Consciousness deteriorates Midbrain compession, sometimes associated hemorrhage, with compromise of the ascending portion of the RAS Bilateral pupillary dilation Changes in VS may not occur until just prior to fatal herniation Respiratory changes and bradycardia

Descending Transtentorial 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 Transtentorial Herniations

Imaging Findings of Uncal Herniation Usual six pointed star appearance of the suprasellar cistern Truncated suprasellar cistern on the ipsilateral side of the herniation

Right Uncal Herniation

Descending Transtentorial Shift to the Left

Durette Hemorrhage: A Complication of Descending Transtentorial Herniation

Featured 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: The Procedure

BTF Guidelines for the Management of Severe Traumatic Brain Injury Management and Prognosis of Severe Traumatic 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 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 Procedure Evaluate globally all resuscitation needs 54 2 54

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

Elevated ICP Rx Procedure Evaluate globally all resuscitation needs Do not provide prophylactic osmotherapy Only with clinical deterioration Do not use prophylactic hyperventilation 54 2 54

Mannitol Standards Guidelines 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 Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

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

Mannitol 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.

Elevated ICP Rx Procedure Evaluate globally all resuscitation needs Do not provide prophylactic osmotherapy Only with clinical deterioration Do not use prophylactic hyperventilation 54 2 54

Hyperventilation Standards Guidelines 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 Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

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

Elevated ICP Rx Procedure Evaluate globally all resuscitation needs Do not provide prophylactic osmotherapy Only with clinical deterioration Do not use prophylactic hyperventilation Consider seizure prophylaxis 54 2 54

Seizure Prophylaxis Standards Guidelines Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate is not recommended for preventing late post-traumatic seizures Guidelines None Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

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

Elevated ICP Rx Procedure Evaluate globally all resuscitation needs Do not provide prophylactic osmotherapy Only with clinical deterioration Do not use prophylactic hyperventilation Consider seizure prophylaxis Do not use steroids 54 2 54

Steroids Standards Guidelines Options The use of steroids is not recommended for improving outcome or reducing ICP in patients with severe TBI Guidelines None Options Brain Trauma Foundation, Inc, AANS. Guidelines for the Management of Severe Traumatic Brain Injury. New York (NY): Brain Trauma Foundation, Inc.; 2000. 165 p.

Steroids 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 Decompression 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 Need

Emergent Cranial Decompression: The Procedure 4 cm vertical incision External auditory canal is key landmark Three cm superior to zygoma Two cm anterior to ear

Emergent Cranial Decompression: The 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

Emergent Cranial Decompression: The Procedure 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

Emergent Cranial Decompression: The Procedure 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 Patient Outcome

ED 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 54 3 54

Patient Outcome Hematoma evacuated without difficulty Three day ICU stay Minimal cognitive deficits on hospital discharge No motor deficits 54 3 54

Treating Elevated ICP in the TBI Patient : A 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

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