Head Trauma

Sean Caine

Stefan Da Silva

Normal Physiology Pathophysiology Concussion Mild TBI Epidural Hematoma Subdural Hematoma Traumatic SAH Contusion Skull Fractures ED Approach to Head Trauma Severe Head Injury – Mgmt

Objectives

Anatomy

Normal Physiology Intracranial vault

Fixed internal volume of 1400-1700 mL

Contents include: Brain Parenchyma – 80% Cerebrospinal fluid – 10% Blood – 10%

Normal Physiology The Brain

SEMISOLID structure Weighs 1400 g (3 lbs)

CSF 100-150 mL Produced primarily by the choroid plexus at 20mL/hr or 500

mL/day Resorbed via arachnoid granulations into venous system

Intravascular blood 100-150mL Volume of blood determined by cerebral blood flow (CBF)

Monro-Kellie Doctrine Originally described over 150 yrs ago

Recognizing the skull to be a “rigid box” ICP is a function of the volume of its three components: Brain Blood CSF

Monro-Kellie Doctrine

Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC (Ed), Williams and Wilkins 1996. p. 646; figure 18.1.

Monro-Kellie Doctrine

Smith ER, Sepideh AH. Evaluation and management of intracranial pressure in adults. UpToDate. Last updated October 1, 2008.

Cerebral Blood Flow CBF = (CAP – CVP) ÷ CVR

↓CVR and ↑ CBF Hypotension, acidosis, and hypercarbia cause

cerebral vasodilation

↑CVR and ↓CBF Hypertension, alkalosis, and hypocarbia promote

cerebral vasoconstriction

Cerebral Blood FlowAutoregulation CBF is constant when CPP is 50-160 mmHg

CPP=MAP-ICP

Normal ICP is 5-15 mmHg

If CPP < 40 mm Hg Øautoregulation of CBF ↓CBF tissue ischemia

Cerebral Blood Flow

Smith ER, Sepideh AH. Evaluation and management of intracranial pressure in adults. UpToDate. Last updated October 1, 2008.

Ischemia

Hypertensive Encephelopathy

Cerebral Edema

Pathophysiology

Direct Injury “direct” contact of head with object

skull initially bends inward at the point of contact (coup) Local trauma Skull fractures Penetrating trauma

some energy is transmitted to the brain by shock waves that travel distant to the site of impact or compression

VERY RARELY OCCURS IN ISOLATION!

Indirect Injury acceleration-

deceleration injury in absence of direct contact with skull Concussion

(contrecoup) DAI subdural hematomas Injury distal to

penetrating head trauma

Primary Injury mechanical irreversible damage that occurs at the

time of head trauma: brain lacerations, hemorrhages, contusions, and tissue

avulsions mechanical cellular disruption and microvascular injury

No specific intervention exists to repair or reverse primary brain injury

Public health interventions aimed at reducing the occurrence of head trauma

Secondary Insults Complicated series of reactions neurochemical,

neuroanatomic, and neurophysioligical initiated at the time of injury

All currently used acute therapies for TBI are directed at reversing or preventing secondary injury

Therefore the cornerstone to ED mngmt of TBI…

DEFENCE!!!

Secondary Brain Insults Neurologic outcome is influenced by the extent and

degree of secondary brain insults

Hypotension (sBP < 90 mm Hg) reduces cerebral perfusion (ischemia and infarction)

Hypoxia (PO2 < 60 mm Hg) apnea caused by brainstem compression or injury partial airway obstruction injury to the chest wall that interferes with normal respiratory

excursion pulmonary injury that reduces effective oxygenation

Secondary Insults Anemia (reduced oxygen-carrying capacity

of the blood) Increased mortality when Hct < 30%

Other potential reversible causes of secondary injury in head injury include hypercarbia, hyperthermia, coagulopathy, and seizures

Case 1 18 yo male presents with headache, nausea,

vomiting x 3 over 12 hours Mother states “there is a virus going around school” Star player on high school team At game last night sat out 3rd quarter after getting

his “bell rung” Returned to game for 4th quarter despite not feeling

well

Case 1 On exam:

Vitals BP: 118/70 HR: 101 RR: 14 T: 36.4

Neuro GCS: 15

Physical exam otherwise unremarkable

Concussion and Mild TBI

Concussion Definition:

“Exposure to a blunt force or acceleration deceleration injury AND any period of transient

confusion, disorientation, impaired consciousness, loss of consciousness for less

than 30 minutes, and any period of dysfunction of memory (amnesia) associated with the event,

neurological or neuropsychological dysfunction”

Practice parameter: The Management of Concussion in Sports (Summary Statement). Report on Quality Standards Subcommittee. Neurology 1997; 48:581-585.

Concussion Or more simply put:

“Any trauma-induced alteration in mental status”

Practice parameter: The Management of Concussion in Sports (Summary Statement). Report on Quality Standards Subcommittee. Neurology 1997; 48:581-585.

Odds Ratio for Specific Clinical Findings and Positive Head CT

Smits et al.

OR (95% CI)

Ibanez et al

OR (95% CI)

Fabbri et al.

OR (95% CI)

Signs of basilar skull fracture

14 (8-22) 11 (6-23) 10 (6-16)

Vomiting 3 (2-4) 4 (2-7) 5 (3-8)

Posttraumatic seizure 3 (1-10) 2 (0.25-17) 8 (6-12)

GCS 14 2 (1-3) 7 (4-14) 19 (14-26)

Neurological deficits 2 (1-3) 7 (2-25) 19 (13-28)

Anticoagulation 2 (1-4) 4 (3-7) 8 (3-9)

Dangerous Mechanism 2 (1-4) 3 (2-4)

Loss of consciousness 2 (1-3) 7 (4-11) 2 (2-3)

Posttraumatic amnesia 1.7 (1-2) 3 (2-5) 8 (6-12)

Headache 1.4 (1-2) 3 (2-6)

Intoxication 1 (0.6-2) 1 (0.3-3)

Age>65 2 (1-3) 2 (1-3)

Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical Policy: Neuroimaging and ydecisionmaking in adult mild brain injury in the acute setting, in ACEP and CDC Clinical Policy. 2008.

Signs of basilar skull fracture

14 (8-22)

Vomiting 3 (2-4)

Posttraumatic seizure 3 (1-10)

GCS 14 2 (1-3)

Neurological deficits 2 (1-3)

Anticoagulation 2 (1-4)

Dangerous Mechanism 2 (1-4)

Loss of consciousness 2 (1-3)

Canadian CT Head Rule

Inclusion Criteria (must have all of the following) Blunt head trauma resulting in LOC, definite amnesia, or witnessed disorientation Initial ED GCS = 13-15 Injury occurred within 24 hrs

Exclusion Criteria <16 yrs old Minimal head injury No clear hx of trauma as primary event (ie syncope or seizure) Penetrating or depressed skull fracture Acute focal neuro deficit Seizure prior to being assessed Bleeding disorder or anticoagulant use Second assessment Pregnant

Canadian CT Head RuleHigh Risk (for neurological intervention) GCS <15 2 h after injury Suspected open or depressed skull fracture Any sign of basal skull fracture

hemotympanum, ‘racoon’ eyes, CSF oto/rhinorrhea, Battle’s sign Vomiting > 2 episodes Age > 65 years

Medium risk (for brain injury on CT) Amnesia before impact > 30 min Dangerous mechanism

Pedestrian vs MVA, ejected from MVA, fall from 3 ft or 5 stairs

Design: prospective cohort study ( June 2000-December 2002). 9 EDs. 2707 adults blunt head trauma → witnessed LOC, disorientation, or definite amnesia and a

GCS 13-15. The CCHR and NOC were compared in a subgroup of 1822 adults with minor head injury and GCS 15.

Outcomes Neurosurgical intervention and clinically important brain injury evaluated by CT and a structured follow-up telephone interview.

Results Among 1822 patients with GCS 15, 8 (0.4%) required neurosurgical intervention and 97 (5.3%) had clinically important brain injury. NOC and the CCHR both had 100% sensitivity CCHR was more specific (76.3% vs 12.1%, P.001) (neurosurgical intervention) ↓ CT rates (52.1% vs 88.0%, P.001)

Conclusion For patients with minor head injury and GCS score of 15, the CCHR and the NOC have equivalent high sensitivities for need for neurosurgical intervention and clinically important brain injury, but the CCHR has higher specificity for important clinical outcomes than does the NOC, and its use may result in reduced imaging rates.

His Dad takes you aside and mentions that a big game is coming up with US College Scouts.…can he play?

Case continued…

Return to PlayGraded program of exertion > 24 hrs at each level is needed If any symptoms appear starts back to the previous asymptomatic

level

McCrory P, Johnston K, Meeuwisse W, Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague 2004. Br J Sports Med 2005;39(4):196-204.

Second Impact Syndrome Rare event

High mortality rate

Rapid/fulminant cerebral edema from second impact before brain fully recovers

Post-concussive syndrome Prevalence:

80% are symptom free at 6 weeks 15% with symptoms at 1 yr

Common symptoms: H/A, dizziness, decreased concentration, memory problems,

sleep disturbances, irritability, fatigue, visual disturbances, judgement problems, depression, anxiety

Virtually clinically indistinguishable from PTSD Require F/U with sports med/neuropsych

Recurrent Concussions Strong evidence that recurrent concussions

are more significant/severe than initial one

Young age is a risk factor

Associated with diminished cognitive function, slower recovery times, prolonged disability

Special Considerations: Mild TBI in presence of coagulopathy Increased risk for poor outcome

>80% mortality for ICH in pts with elevated INR

Smaller studies suggest that >70% pts with elevated INR deteriorated after a normal CT

Mngmt: Correct INR with FFP, vitamin K in context of ICH Admit and observe pts with elevated INR (> 2) and normal

CT

Observation and disposition Observation is recommended for 24 hours after a mild TBI

because of the risk of intracranial complications

Hospital admission is recommended for patients at risk for immediate complications from head injury GCS <15 Abnormal CT scan: intracranial bleeding, cerebral edema Seizures Abnormal INR PTT

F/U with sports med/urgent neuro with PPCS>3weeks

Take Home – Concussion Players should not be allowed to return to

play in the current game or practice Players should not be left alone to monitor

for deterioration Return to play must follow a medically

supervised series of steps Players should never return to play while

symptoms persist

Case 2 28 year-old ♂ brought in by EMS

Found outside the Cecil Tavern

“I was just standing outside minding my own f***ing business smoking when two a**holes came up asked me for a cigarette and then cracked me across the head with a baseball bat”

Bystanders state the was a brief LOC lasting ~5 min

EMS suspect he is intoxicated. Smells of booze. Slurred speech. Disshevelled. Confused. Often mumbling and eyes drifting close but rousable/

Case 2 O/E:

AVSS GCS: 14 Right temporal swelling/boggy scalp

Within minutes of sharing his colourful story… Difficult to rouse Right fixed and dilated pupil

Epidural Hematoma

Epidural Hematoma Usually due to arterial injury

trauma to the skull base → tearing of middle meningeal artery

results in hemorrhage

Occasionally anterior cranial fossa → rupture of the anterior meningeal artery vertex → dural arteriovenous fistula

In ~15 % of cases, injury to one of the dural sinuses, or the confluence of sinuses in the posterior cranial fossa, is the source of hemorrhage

Epidural-Pathophysiology Typically fraature of temporal bone ruptures

branches of the middle meningeal artery

Expanding hematoma limited by dural attachment at sutures

This stripping of the dura from the calvarium may

be part of the reason for the severe headache.

PterionPterion

Epidural Hematoma - Hx Mean age 20-30 years Caused by MVC, Falls, Assaults

Skull # present 75-95% of the time

Transient LOC with a “lucid interval”

Symptoms: HA, N/V, drowsiness, confusion, aphasia, seizures, and hemiparesis

Epidural Hematoma - Imaging Head CT – fast, simple

“lens-shaped” pattern

collection is limited by dural attachments at cranial sutures

Epidural - Management Neurologic emergency

hematoma expansion elevated intracranial pressure brain herniation

Operative Craniotomy and hematoma evacuation Burr Hole

Non-Operative Close observation serial brain imaging

hematoma enlargement neurologic deterioration

An EDH > 30 cm3 should be surgically evacuated regardless of the patient's GCS

GCS < 9 with anisocoria → evacuation ASAP An EDH

< 30 cm3

< 15-mm thickness < 5-mm midline shift (MLS) in patients with a GCS > 8 w/o focal deficit

…non-operative mgmt with serial CTs and close neurological observation in a neurosurgical center

Surgical Indications for EDH

Case 3 83 ♀ presents with confusion Gradually increasing over the past week No history of trauma

GCS: 14 CN: ii-xii normal – no focal findings Urine + nitrates/leuks –epithelials CT Head

Subdural Hematoma

Subdural Hematoma SDHs form b/w the dura and the brain Usually they are caused by the movement of the brain

relative to the skull acceleration-deceleration injuries

Common in patients with brain atrophy (EtOH or elderly)

Superficial bridging vessels traverse greater distances than in patients with no atrophy (more likely to rupture with rapid movement of the head)

Occurs in ~30% of patients with severe head trauma slow bleeding of venous structures delays clinical signs

Acute SDH 24 hours post trauma ↓ LOC; lucid interval: 50% - 70% → ↓mentation

Subacute SDH symptomatic 24h - 2 wks post injury CT: hypodense or isodense lesion

absence of sulci

shift

contrast detection of isodense lesions

Chronic SDH >2 weeks post trauma Hemiparesis or Weakness: ~45% ↓LOC: ~50%

What type of ICH is this? Why?

Case 4

51 ♂ MVC – single vehicle at highway speeds off road and into a tree

?LOC GCS 8 (scene) 8 (now)

Traumatic Subarachnoid Haemorrhage

Traumatic SAH TSAH is defined as blood within the CSF and

meningeal intima results from tears of small subarachnoid vessels

detected on the first CT scan in up to 33% of patients with severe TBI (incidence of 44% in all cases of severe head trauma)

incidence of skull fractures and contusions ↓GCS → SAH SAH → ↓Outcome

Traumatic SAH

Øcontrast CT: density in basilar cisterns

density interhemispheric fissures/sulci

prognosis reasonable cerebral vasospasm → cerebral ischemia

Chicken vs Egg Did this patient lose consciousness while driving

because of spontaneous SAH and subsequently crash his car, or did the patient sustain head injury from the motor vehicle accident causing traumatic SAH?

cerebral angiogram to exclude an underlying aneurysm or vascular malformation

Diffuse Axonal Injury

Diffuse Axonal Injury Definition: prolonged traumatic coma not caused by mass

lesions, ischemic insults, or nontraumatic etiologies

Typically coma persisting > 6h

CT often normal classic finding are small petechial hemorrhages adjacent to

third ventricle, within the corpus collosum, or internal capsule

Most common CT finding in severe head injury

Diffuse Axonal Injury Mild DAI

Coma 6-24 h 1/3 will demonstrate

decorticate or decerebrate posturing

15% mortality Most recover with mild or no

permanent deficits

Mod DAI Coma > 24h Abnormal posturing Severe posttraumatic

amnesia Moderate cognitive deficit 25% mortality

Severe DAI Majority due to MVA Autonomic dysfunction

(tachycardia, HTN, irreg resps)

Majority die Others are severely disabled

or persistent vegetative satate

SKULL FRACTURES

Linear skull fracture low-energy blunt trauma over a wide surface area

of the skull. Full thickness through bone …of little significance except

when it runs through a vascular channel, venous sinus groove suture

Then, it may cause epidural hematoma venous sinus thrombosis and occlusion sutural diastasis

Fractures Greater than 3 mm in width Widest at the center and

narrow at the ends Runs through both the outer

and the inner lamina of bone, hence appears darker

Usually over temporoparietal area

Usually runs in a straight line Angular turns

Sutures Less than 2 mm in width Same width throughout Lighter on x-rays compared

with fracture lines At specific anatomic sites Does not run in a straight

line Curvaceous

Basilar skull fracture Petrous temporal bone: CSF otorrhea and bruising over mastoids (Battle

sign) Anterior cranial fossa: CSF rhinorrhea and bruising below eyes (raccoon

eyes) Longitudinal temporal bone → ossicular chain disruption and conductive

deafness Facial palsy, nystagmus, and facial numbness are 2’ to VII, VI, and V CN palsy

Transverse temporal bone: VIII CN palsy and labyrinth injury → nystagmus, ataxia, and permanent neural hearing loss

Occipital condylar fracture: coma and have other associated c-spine injuries

Vernet syndrome or jugular foramen syndrome is involvement of IX, X, and XI CN → difficulty in phonation, aspiration and ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.

Depressed Skull Fracture Elevation

depressed segment is > 5mm below inner table gross contamination, dural tear with pneumocephalus underlying hematoma

Craniectomy underlying brain is damaged and swollen

CSF Oto/rhinorrhea Dab fluid on a tissue paper, a clear ring of wet tissue beyond the blood

stain, called a "halo" or "ring" sign

ED Approach to Head Trauma

Focused Hx Mechanism LOC Seizure? Ambulatory at scene GCS at scene

Focused Physical ABC’s ATLS protocol GCS Signs of external injury Pupils Check Ears/Nose Extremities - movement

Glasgow Coma Scale*

Eye Opening (E)4. Spontaneous3. To voice2. To pain1. None

Verbal Responses (V)5. Oriented4. Confused3. Inappropriate words2. Incomprehensible sounds1. None

Motor response (M)6. Obeys commands5. Localizes pain4. Withdraws from pain3. Abnormal flexion2. Abnormal extension1. None

*Developed for evaluation of head trauma 6 hours post injury Deceased and rocks have GCS 3

Emergent Management of Closed Head Injury

Case 6 22 ♀ bicycle vs truck LOC Agitated at the scene GCS

Opens eyes to pain Withdraws on left and localizes on right Sounds – no inteligible words

2

5

2

Outline Airway Avoid Hypoxia Avoid Hypotension

Brain Specific Therapies Position Hyperventilation Mannitol Hypertonic Saline Cooling

Indications for ICP Monitoring Surgical Management

Airway Capture it!

How you do it probably does not have a great effect on neurological outcome unless you cause hypoxemia or hypotension

There is little evidence-based medicine to guide the choice of agents

Intubation – Indications* Coma (i.e. GCS 8) or significantly deteriorating LOC Loss of protective laryngeal reflexes Copious bleeding into mouth Respiratory arrhythmia Ventilatory insufficiency

clinical decision - not necessarily requiring ABG Bilateral mandibular fracture Any facial injury compromising airway Seizures Any other injury that requires ventilation/intubation

*Eastern Association For The Surgery of Trauma, 2003; NICE guidelines, 2003

Case Paramedics state his GCS “…was 7 or 8 at

the scene”

Should they have intubated?

Methods: Before–After system wide controlled clinical trial conducted in 17 cities. Adult patients who had experienced major trauma in a BLS phase and a subsequent ALS phase (during which paramedics were able to perform intubation and administer fluids and drugs intravenously). The primary outcome was survival to hospital discharge.

Results: Survival did not differ overall (81.1% ALS v. 81.8% among those in the BLS; p=0.65) Among patients with GCS < 9, survival was ↓ with ALS (50.9% v. 60.0%; p=0.02) The adjusted odds of death for the advanced life-support v. basic life-support phases were non-significant

(1.2, 95% confidence interval 0.9–1.7; p=0.16)

Interpretation: The OPALS Major Trauma Study showed that systemwide implementation of full advanced life-support programs did not decrease mortality or morbidity for major trauma patients. We also found that during the ALS phase, mortality was greater among patients with GCS < 9.

Airway Preparation and Preoxygenation Prevent ICP rise

Lidocaine 1.5-2 mg/kg IV Rocuronium 0.06 - 0.1 mg/kg (defasciculating dose) Fentanyl 3 ug/kg IVP

Prevent Vagally stimulated bradycardia Atropine 0.01 mg/kg IV (Minimum dose: 0.1 mg)

Sedation Etomidate 0.3 mg/kg IVP OR Thiopental (Pentothal) 4 mg/kg IVP (IF BP stable) OR Propofol 2mg/kg IVP OR Midazolam 0.1mg/kg (max 5mg) IVP Ketamine (2 mg/kg) IV

Muscle relaxants Succinylcholine 1.5 mg/kg IV OR Rocuronium 0.6 mg/kg IV

Airway - Intubation Lidocaine (1.5 to 2 mg/kg IV push)

…may ↓ cough reflex, HTN response, ICP

Succinylcholine – fasciculations ↑ICP premedicate w a subparalytic dose of a nondepolarizing agent

Etomidate (0.3 mg/kg IV) good effect on ICP ↓CBF and metabolism minimal adverse effects on BP Minimal respiratory depressant effects

Ketamine May increase ICP Anaes and animal studies indicate no increased ICP

Methods: Medline literature search was undertaken for evidence of the effect of succinylcholine (SCH) on the intracranial pressure (ICP) of patients with acute brain injury and whether pretreatment with a defasciculating dose of competitive neuromuscular blocker is beneficial in this patient group.

Conclusions: Studies were weak and small

For those patients suffering acute TBI the authors could find no studies that investigated the issue of pretreatment with defasciculating doses of competitive neuromuscular blockers and their effect on ICP in patients given SCH.

SCH caused ↑ ICP for patients undergoing neurosurgery for brain tumours with elective anaesthesia and that pretreatment with defasciculating doses of neuromuscular blockers reduced such increases. ?impact on outcome.

Background: laryngeal instrumentation and intubation is associated with a marked, transient rise in ICP.

Methods: A literature search was carried out to identify studies in which intravenous lidocaine was used as a pretreatment for RSI in major head injury. Any link to an improved neurological outcome was also sought.

Results: No evidence was found to support the use of intravenous lidocaine as a pretreatment for RSI in patients with head injury and its use should only occur in clinical trials.

Case 7 22 ♀ with presumed CHI Now intubated.

What are your priorities?

AVOID HYPOXEMIA

Volume 40(5) May 1996 pp 764-767

Hypoxemia and Arterial Hypotension at the Accident Scene in Head Injury

Stocchetti, Nino MD; Furlan, Adriano MD; Volta, Franco MD Design: Prospective, observational study.

Materials and Methods: Arterial Hbo2 was measured before tracheal intubation at the accident scene in 49 consecutive patients with head injuries. Arterial

pressure was measured using a sphygmomanometer.

Main Results: Mean arterial saturation was 81% (SD 24.24); mean arterial systolic pressure was 112 mm Hg (SD 37.25). Airway obstruction was detected in 22 cases. Twenty-seven patients showed an arterial saturation lower than 90% on the scene, and 12 had a systolic arterial pressure of less than 100 mm Hg. The

outcome was significantly worse in cases of hypotension, desaturation, or both.

Conclusions: Hypoxemia and shock are frequent findings on patients at the accident scene. Hypoxemia is more frequently detected and promptly corrected, while arterial hypotension is more difficult to control. Both insults may have a significant impact on outcome

Methods: 846 cases of severe TBI (GCS ≤ 8) were analyzed retrospectively to clarify the effects of multiple factors on the prognosis of patients.

Results: Worse outcomes were strongly correlated (p < 0.05) with GCS score, age,

pupillary response and size, hypoxia, hyperthermia, and high intracranial pressure (ICP).

Even a single O2 sat reading < 90% was associated with a significantly worse outcome

Conclusions: These findings indicate that prevention of hypoxia, control of high ICP, and prevention of hyperthermia may improve outcome in patients with TBI

AVOID HYPOTENSION

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Timing of hypotension (SBP < 90 mmHg)

Traumatic Coma Data Bank 1991

Favourable outcome

Unfavourable outcome

Hypotension Single occurrence of ↓BP (SBP<90mmHg)

doubles mortality* ↑ disability in survivors of head injury*

↑duration and ↑ frequency = ↓ prognosis**

*Chesnut et al., 1993; Management and Prognosis of Severe Traumatic Brain Injury, 2000

**Schierhout and Roberts, 2000

Hypotension

Mean Arterial Pressure What is adequate?

Enough to maintain CBFNormally (MAP 60-150 mmHg and ICP ~10 mmHg) CPP is normally between 70 and 90 mmHg <70 mmHg for a sustained period → ischemic injury

Outside of the limits of autoregulation ↑ MAP raises CPP ↑ ICP lowers CPP

Blood pressure control BP should maintain CPP>60 mmHg

pressors can be used safely without further ↑ ICP

…in the setting of sedation → ?iatrogenic ↓BP Hypertension should generally not be treated

Avoid CPP <60 mmHg or normalization of BP in chronic HTN

…the autoregulatory curve has shifted to the right

Case 8 Asymetric Pupils – L fixed and dilated

What is happening? What would you like to do?

Herniation Syndromes

Uncal Most common Temporal lobe uncus forced

through tentorial hiatus Compression of CN III causing

ipsilateral: Anisocoria Impaired EOM Sluggish pupil (EARLY) Fixed and dilated (LATE)

Contralateral Babinski’s Bilateral decorticate posturing

(LATE)

Anterior view of transtentorial herniation caused by large epidural hematoma. Skull fracture overlies hematoma. (From Rockswold GL: Head injury. In Tintinalli JE et al [eds]: Emergency Medicine. New York, McGraw-

Hill, 1992, p 915.)

Herniation Syndromes

Kernohan’s notch syndrome Contralateral cerebral

peduncal forced against opposite endge of tentorium

~25% of uncal herniations

Motor signs ipsilateral to the dilated pupil

Anterior view of transtentorial herniation caused by large epidural hematoma. Skull fracture overlies hematoma. (From Rockswold GL: Head injury. In Tintinalli JE et al [eds]: Emergency Medicine. New York, McGraw-

Hill, 1992, p 915.)

Herniation Syndromes

Central Transtentorial Bilateral rostrocaudal

deterioration Early

Bilateral motor weakness Pinpoint pupils (<2mm) Increased muscle tone Bilateral Babinski’s

Later Midpoint fixed pupils Decorticate → decerebrate Irregular resps

http://download.imaging.consult.com/ic/images/S1933033208702313/gr8-midi.jpg (Accessed May 12, 2009)

Herniation Syndromes

Cerebellotonsillar 70% mortality Medullary compression by

cerebellar tonsils Sudden respiratory and CV

collapse Pinpoint pupils Flaccid quadriplegia

http://scielo.isciii.es/img/revistas/neuro/v18n3/5_img_1ab.jpg (Accessed May 12,

2009)

Herniation Syndromes

Upward Transtentorial

Expanding posterior fossa lesion Pinpoint pupils Downward conjugate

gaze

http://download.imaging.consult.com/ic/images/S1933033208702313/gr10-midi.jpg

Brain Specific Therapies

Position Maximize venous outflow from the head

↓ excessive flexion or rotation of the neck avoid restrictive neck taping minimize stimuli that could induce Valsalva (i.e. suctioning)

Position the head above the heart (30o) head elevation may lower CPP

Hyperventilation Once a mainstay for treatment of ↑ICP Concerns about cerebral ischemia

difficult to demonstrate

Outcome worse with hyperventilation in some studies of head injury

Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial

Methods: RCT normal ventilation PaCO2 35Hg

hyperventilation PaCO2 25Hg hyperventilation plus THAM

Outcome: GCS at 3/6/12 months

Results:Those in the 25 mm Hg group did worse

Muizelaar et. al. 1991

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Acute head injury (6 hrs post impact)Areas in red show regions with rCBF < 20 ml/100g/min)

(Coles et al. Crit Care Med 2002)

PaCO2: 25 mmHgPaCO2: 38 mmHg

Mannitol

Benefits: Plasma expanding effect Reduces hematocrit and viscosity ↑ cerebral blood flow Osmotic effect creates a fluid gradient out of

cells. This osmotic effect initially decreases intracellular edema, thus decreases ICP

Mannitol Drawbacks:

Osmotic diuresis HYPOTENSION May accumulate in the brain and result is a

“reverse osmotic shift” potentially increasing ICP Acute renal failure

MannitolIndications: (prior to ICP monitoring)

1. Signs of transtentorial herniation2. Progressive neurological deterioration

not attributable to extra-crainal complications

Dose: 0.25 – 1g/kg IV bolusAvoid hypovolemia

(foley recommended)

Hyperosmotic agents Mannitol effective through non- osmotic effects

Problems with big fluid shifts from diuresis

Increasing interest in use of hypertonic saline (3-24%)

? more effective with fewer side effects.

Outcome with Na+; survival with Na+ 180 mmol/l!

Munar et al. J Neurotrauma 2000. 17:41-51. Horn et al. Neurol Res 1999;21: 758-64

Quereshi et al. J Trauma 1999;47:659-65. Simma et al. Crit Care Med 1998;26:1265-70.

Clark & Kochanek. Crit Care Med 1998;26:1161-2.Doyle et al. J Trauma 2001; 50: 367-383.

Petersen et al. Crit Care Med 2000;28:1136-1143

Dose: 2-4 ml/Kg 5% NaClMax Na+ ~ 160 mmol/lMax osmol ~ 325 mOsm/l

Methods: Consecutive patients with clinical TTH treated with 23.4% saline (30 to 60mL) were included in a retrospective cohort. Factors associated with successful reversal of TTH were determined.

Results: 76 TTH events. In addition to 23.4% saline, TTH management included hyperventilation (70% of events), mannitol (57%), propofol (62%), pentobarbital (15%), ventriculostomy drainage (27%), and decompressive hemicraniectomy (18%). Reversal of TTH occurred in 57/76 events (75%). Reversal of TTH was predicted by a 5 mmol/L rise in serum sodium concentration (p 0.001) or an absolute serum sodium of 145 mmol/L (p 0.007) 1 hour after 23.4% saline. Adverse effects included transient hypotension in 13 events (17%); no evidence of central pontine myelinolysis was detected on post-herniation MRI (n 18). Twenty-two patients (32%) survived to discharge, with severe disability in 17 and mild to moderate disability in 5.

Conclusion: Treatment with 23.4% saline was associated with rapid reversal of transtentorial herniation (TTH) and reduced intracranial pressure, and had few adverse effects. Outcomes of TTH were poor, but medical reversal may extend the window for adjunctive treatments.

Case The R2 ER resident on NSx asks what you

think his chances are of putting in a EVD?

What are the indications for ICP monitoring?

Antiepileptic therapy

Antiepileptic therapy Seizure incidence

12% blunt trauma 50% penetrating head injury

Seizures can contribute to Hypoxia, Hypercarbia Release of excitatory neurotransmitters ↑ICP

Anticonvulsant therapy → if seizing

Prophylaxis There are no clear guidelines ? high-risk mass lesions

Anti-epilepticAcute Treatment Lorazepam (0.05-0.15 mg/kg IV, over 2-5 min - max 4 mg)

Diazepam (0.1 mg/kg, up to 5 mg IV, Q10 min - max20 mg)

Prophylaxis phenytoin (13 to 18 mg/kg IV) fosphenytoin (13 to 18 phenytoin equivalents/kg)

Selection criteria All randomised trials of anti-epileptic agents, in which study participants had a clinically defined acute

traumatic head injury of any severity. Trials in which the intervention was started more than eight weeks after injury were excluded.

Data collection and analysis Two reviewers Relative risks and 95% confidence intervals (95%CI) were calculated

Main results 10 eligible RCTs, 2036 participants (RR) for early seizure prevention was 0.34 (95%CI 0.21, 0.54) ↓ risk of early seizures by 66% Seizure control in the acute phase did not show ↓ mortality (RR = 1.15; 95%CI 0.89, 1.51) ↓ death/disability (RR = 1.28; 95%CI 0.90, 1.81)

Authors' conclusions Prophylactic anti-epileptics reduce early seizures No reduction in late seizures No effect on death and neurological disability Insufficient evidence is available to establish the net benefit of prophylactic treatment at any time after

injury.

Seizure Prophylaxis in Severe Head Trauma  

Indications* Depressed skull fracture    Paralyzed and intubated patient    Seizure at the time of injury    Seizure at ED presentation    Penetrating brain injury    Severe head injury (GCS ≤8)    Acute subdural hematoma    Acute epidural hematoma    Acute intracranial hemorrhage    Prior Hx of seizures

*Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed.

Steroids Beneficial in tumors Decreases cerebral edema Many reasonable sized RCTs that have

failed to show benefit. Some have shown mild benefits in

subgroup analysis Not recomended

On Injuries of the Head 400 B.C.E

“…a man will survive longer in winter than in summer, whatever be the part of the head in which the wound is situated.”

Case You are doing a summer locum in Nelson, BC

Cyclist brought in by EMS

Fell off 20 ft ledge while mountain biking

No Helmet

GCS 12 on the scene

O/E HR 90 RR10 BP105/72 T36.6 GCS 10 Pupils 2 mm and reactive Left temporal scalp bogginess Obvious deformity to left wrist Cspine collar, intubated, 2 large bore IVs GCS declines to 5 despite medical therapy. Right pupil

becomes fixed and dilated. Left sided babinski’s. CT scanner is 1 h E. NeuroSx is 3 h NW. No

general surgeon in town.

ED Burr Hole - Preparation1. Type and screen, PTT,

INR2. Administer IV antiobiotics

(ie ceftriaxone)3. Shave and prep patient4. 2% lido with epi to

reduce scalp bleeding5. Place sandbag/pillow

under ipsilateral shoulder to optimize venous return from head

6. Get equipment Scalpel with 15 blade Self-retaining retractor Suction Penetrator and burr drill

bit Rangeur Hook Elevator Drain (ie Jackson-Pratt) Suture tray Bone wax

ED Burr Hole - Exposure1. 4 cm vertical incision

3cm (2 finger breadths) anterior to tragus and 2cm above zygoma

2. Divide temporalis muscle and lift it off the skull with scalpel handle

3. Insert self-retaining retractor

ED Burr Holes - Decompression1. Triangular-shaped

perforator to penetrate to inner table of skull

ED Burr Holes - Decompression2. Switch to burr bit to produce

cylindrical hole3. Leave fine rim of inner table4. Separate dura from inner table

with elevator5. Rangeur rim6. If epidural – suction our blood/clot7. If subdural, elevate dura with hook

and incise with 15 blade 8. DO NOT SUCTION THE BRAIN

TISSUE9. Place drain in small pocket of

temporalis muscle and close scalp10. Consider frontal, parietal and then

contralateral holes if no hematoma found

ED Burr Holes

ED Burr Holes Relative Indications

GCS < 8 Lateralizing signs

(anisocaria, hemiparesis) Autonomic dysfunction

(tachycardia, hypertension, irregular resps)

Refractor to medical tx Delay to surgery Phone consult and NSx

agrees

Contraindications Lack of training Coagulopathy

Complications CN Injury (ie CN VII) Infection Bleeding Unable to identify lesion

Questions?

Acknowledgements

Dr. Mark BromleyDr. Stefan Da SilvaDr. David Zygun

Brain Tissue pH and Blood GlucoseB

rain

pH

Glucose0 5 10 15 20

6

6.5

7

7.5

Brain p

H

Hyperglycemia-Induced Neuronal Injury Intracellular acidosis triggers calcium entry into

the cell, lipolytic release of cytotoxic free fatty acids and glutamate and eventually cell death

↓ glucose available to the glycolytic pathway, treatment of hyperglycemia could theoretically ↓ lactate production, ↑ pH, result in less neuronal damage, and improve patient outcome

Blood Glucose Lam et al found 43% of patients with severe brain

injury to have admission blood glucose levels above 11.1 mM

Rovlias and Kotsou showed postoperative glucose levels, independent of their relationship with GCS, significantly contributed to the prediction of the patients’ prognosis

Hyperglycemia-Induced Neuronal Injury

? increased tissue lactic acidosis Brain tissue acidosis is associated with mortality following head

injury ↑ glucose supply during incomplete ischemia may allow

continuation of anaerobic glycolysis, which would lead to accumulation of lactate and subsequently to tissue acidosis

Injured brain cells may not be able to metabolize excess or even normal levels of glucose through the oxidative pathway.

Therapeutic Hypothermia:Experimental Evidence

NABIS:H I Outcomes

56.85 56.01

27.92 26.59

0

10

20

30

40

50

60

% o

f P

atie

nts

Poor Outcome Mortality

Hypothermia Normothermia

NABIS:H I Temperature Data

30

32

34

36

38

40

0 8 16 24 32 40 48 56 64 72 80 88 96

Hours from Hospital Arrival

Tem

per

atu

re (

C)

hypo mean +1 SD -1 SD normo mean +1 SD -1 SD

Target Temp8.4 + 3 hrs

NABIS:H IAIM

To determine whether surface-induced moderate hypothermia (33.0o C), begun rapidly after severe traumatic brain injury (GCS 3-8) and maintained for 48 hours will improve outcome with low toxicity

ER physician’s role in brain death Hope Program

http://iweb.calgaryhealthregion.ca/hope

Hypothermia Treatment Window

Therapeutic Hypothermia: Cardiac Arrest