Head Trauma Mark Bromley PGY2 Jason Lord FRCPC
Head Trauma
Mark Bromley PGY2
Jason Lord FRCPC
• Physiology• Concussion Mild TBI
• Epidural Hematoma• Subdural Hematoma• Traumatic SAH• Contusion• Skull Fractures
• ED Approach to Head Trauma• Severe Head Injury – Mgmt
• How to Read a Head CT Brain Death
Pathophysiology
Cerebral Blood Flow
• CBF is maintained @ MAP of 60-150 mm Hg
• Hypertension, alkalosis, and hypocarbia promote cerebral vasoconstriction
• Hypotension, acidosis, and hypercarbia cause cerebral vasodilation
Hypotension
Cerebral Blood Flow
• In Trauma, ↑ CBF with a disrupted BBB → vasogenic edema
• CBF α CPP• CPP = MAP – ICP • CBF is constant when CPP is 50-160 mm Hg
• If CPP < 40 mm Hgo Øautoregulation of CBF ↓CBF tissue ischemia
Monro-Kellie Doctrine
• Cranial vault is a fixed volume …any change in the contents either o displaces the normal contents or o raises the pressure inside the skull
• The cranial vault is normally filled by three thingso brain o bloodo cerebral spinal fluid.
• If a person were to have a brain tumor:o it displaces one of the normal components (i.e. ↓spinal fluid) o ↑ICP
Direct Injury
• head is struck by an object or its motion is arrested by another object
• skull initially bends inward at the point of contact (coup)
• some energy is transmitted to the brain by shock waves that travel distant to the site of impact or compression
Indirect Injury
• cranial contents are set into motion by forces other than the direct contact of the skull with another object
• acceleration-deceleration injury • as brain moves within the skull, bridging subdural
vessels are strained (subdural hematomas) • shear and strain injuries (diffuse axonal injury or
concussion)• intracranial content movement abruptly arrested
(contrecoup)• penetrating injury - pressure waves can damage
structures distal to the path of the missile.
Primary Injury
• mechanical irreversible damage that occurs at the time of head trauma: o brain lacerations, hemorrhages, contusions, and
tissue avulsions o 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 Brain Injury
• intracellular and extracellular derangements (metabolic, ischemic, ion shifting)
• All currently used acute therapies for TBI are directed at reversing or preventing secondary injury
Secondary Brain Injury
• Neurologic outcome is influenced by the extent and degree of secondary brain injury
• Hypotension (sBP < 90 mm Hg) reduces cerebral perfusion (ischemia and infarction)
• Hypoxia (PO2 < 60 mm Hg)o apnea caused by brainstem compression or injuryo partial airway obstructiono injury to the chest wall that interferes with normal
respiratory excursiono pulmonary injury that reduces effective oxygenation
Secondary Brain Injury
• Anemia (reduced oxygen-carrying capacity of the blood) o Increased mortality when Hct < 30%
• Other potential reversible causes of secondary injury in head injury include hypercarbia, hyperthermia, coagulopathy, and seizures
Case• 17 ♂ playing soccer
…was “headed” by another playero No LOCo Pulled from game – kept getting beateno Progressive confusiono Amnestic of the event
• Now GCS 15
• No Focal Neurologic findings
o ?Imagingo ?Follow-up
Note: Minor Head Injury is defined as a witnessed loss of consciousness, definite amnesia, or witness disorientation in a patient with a GCS 13-15.
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.
Concussion and Mild TBI
Concussion
“grossly normal structural neuroimaging”
Signs: GCS 13-15 at 30 min post injury Symptoms: confusion and amnesia +/- LOC
↓focus ↓orientation slurred speech / poor coordination emotional
Course: resolution of symptoms follows a sequential course
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 o GCS <15 o Abnormal CT scan: intracranial bleeding, cerebral edema o Seizures o Abnormal INR PTT
• His Dad take you aside and says there’s a big tourney on the weekend with scouts flying in to watch.
…can he play?
Return to play• Rest until all symptoms have resolved• Graded program of exertion• > 1 day at each level is needed • If any symptoms appear, patients drop back to the previous
asymptomatic level and try again after 24 h
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.
Take Home – Concussion • Players should not be allowed to return to play in
the current game or practice • Players should not be left alone, and regular
monitoring for deterioration is essential during the initial few hours after injury
• Return to play must follow a medically supervised series of steps
• Players should never return to play while symptoms persist
Case• 20 year-old ♂ university student • presents after a morning game of baseball in which he
collided with another player• Brief LOC …meanwhile she bled profusely from the chin • When he recovered, she offered him a ride to the
emergency room, which he declined, saying "it's just a bump on the head"
• He returned to his room and told his roommates the story, and remained lucid through the morning.
• After lunch → restless with a severe HA → seizure.
• OE: ↓LOC R pupil dilated
Epidural Hematoma
Epidural Hematoma
• Usually due to arterial injury o trauma to the skull base → tearing of middle meningeal arteryo 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
• Blow to the head fractures the temporal bone and ruptures branches of the middle meningeal artery, lies outside the dura.
• The ruptured artery then leaks blood between the inner skull and the dura.
• The increasing volume of blood strips the dura from the inside of the skull, forming, in effect, a large blood blister which pushes against the brain as it expands.
• The hematoma may strip the dura from the bone as far as the sutures of the skull.
• This stripping of the dura from the calvarium may be part of the reason for the severe headache.
Epidural Hematoma - Hx
• Mean age 20-30 years
• Caused by MVC, Falls, Assaultso 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
o hematoma expansion o elevated intracranial pressureo brain herniation
• Operativeo Craniotomy and hematoma evacuationo Burr Hole
• Non-Operativeo Close observationo 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
o < 30 cm3
o < 15-mm thicknesso < 5-mm midline shift (MLS) in patients o with a GCS > 8 o w/o focal deficit
…non-operative mgmt with serial CTs and close neurological observation in a neurosurgical center
Epidural - ?Surgical
Case
• 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 o 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%
Case• 51 ♂ MVC – single vehicle at highway
speeds off road and into a tree
• ?LOC
• GCS 8 (scene) 8 (now)
Subarachnoid Hemorrhage
Traumatic SAH
• TSAH is defined as blood within the CSF and meningeal intima o 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 o ↓GCS → SAHo 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
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 o depressed segment is > 5mm below inner
table o gross contamination, o dural tear with pneumocephaluso underlying hematoma
• Craniectomy o underlying brain is damaged and swollen
?CSF Leak
• 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
• 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. Spontaneous
3. To voice
2. To pain
1. None
Verbal Responses (V)5. Oriented
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
1. None
Motor response (M)6. Obeys commands
5. Localizes pain
4. Withdraws from pain
3. Abnormal flexion
2. Abnormal extension
1. None
*Developed for evaluation of head trauma 6 hours post injury Deceased and rocks have GCS 3
Emergent Management of Closed Head Injury
Case
• 22 ♀ bicycle vs truck
• LOC
• Agitated at the scene
• GCSo Opens eyes to paino Withdraws o Sounds – no inteligible words
2
4
2
Outline• Airway• Avoid Hypoxia • Avoid Hypotension
• Brain Specific Therapieso Positiono Hyperventilationo Mannitolo Hypertonic Salineo 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
o 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
o Lidocaine 1.5-2 mg/kg IV o Rocuronium 0.06 - 0.1 mg/kg (defasciculating dose) o Fentanyl 3 ug/kg IVP
• Prevent Vagally stimulated bradycardiao Atropine 0.01 mg/kg IV (Minimum dose: 0.1 mg)
• Sedation o Etomidate 0.3 mg/kg IVP OR o Thiopental (Pentothal) 4 mg/kg IVP (IF BP stable) ORo Propofol 2mg/kg IVP ORo Midazolam 0.1mg/kg (max 5mg) IVP
• Apply cricoid pressure • Muscle relaxants
o Succinylcholine 1.5 mg/kg IV OR o 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
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
• 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
desaturation occurs rapidly below SpO2 of 90–92%
AVOID HYPOTENSION
010
203040
50607080
90100
none early late both
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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)o doubles mortality*o ↑ 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?o Enough to maintain CBFNormally (MAP 60-150 mmHg and ICP ~10 mmHg)o CPP is normally between 70 and 90 mmHgo <70 mmHg for a sustained period → ischemic injury
• Outside of the limits of autoregulationo ↑ MAP raises CPP o ↑ ICP lowers CPP
Blood pressure control
• BP should maintain CPP>60 mmHg o pressors can be used safely without further ↑ ICP
…in the setting of sedation → ?iatrogenic ↓BPo Hypertension should generally not be treated
• Avoid CPP <60 mmHg oro normalization of BP in chronic HTN
…the autoregulatory curve has shifted to the right
Case
• Asymetric Pupils – L fixed and dilated
• What is happening?
• What would you like to do?
Herniation
1) The brain squeezes under the falx cerebri in cingulate herniation 2)The brainstem herniates caudally3) The uncus and the hippocampal gyrus herniate into the tentorial notch 4)The cerebellar tonsils herniate through the foramen magnum in tonsillar herniation.
• Uncus can squeeze the third cranial nerve which controls ipsilateral parasympathetic input to the eye o pupillary dilatation o deviation of the eye to "down and out"
Brain Specific Therapies
Position• Maximize venous outflow from the head
o ↓ excessive flexion or rotation of the neck o avoid restrictive neck tapingo minimize stimuli that could induce Valsalva (i.e. suctioning)
• Position the head above the heart (30o) o head elevation may lower CPP
Hyperventilation
• Once a mainstay for treatment of ↑ICP
• Concerns about cerebral ischemia o 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
0m
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00
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in6
0
0m
l/1
00
g/m
in6
0
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
Mannitol
Benefits:o Plasma expanding effecto Reduces hematocrit and viscosityo ↑ cerebral blood flowo Osmotic effect creates a fluid gradient out
of cells. This osmotic effect initially decreases intracellular edema, thus decreases ICP
Mannitol
• Drawbacks:o Osmotic diuresiso HYPOTENSIONo May accumulate in the brain and result is a
“reverse osmotic shift” potentially increasing ICP
o Acute renal failure
Mannitol
Indications: (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)
Hypertonic Saline
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;28:1136-1143Dose: 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
o There are no clear guidelines o ? 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 criteriao 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 analysiso Two reviewers o Relative risks and 95% confidence intervals (95%CI) were calculated
• Main resultso 10 eligible RCTs, 2036 participantso (RR) for early seizure prevention was 0.34 (95%CI 0.21, 0.54)o ↓ risk of early seizures by 66% o 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' conclusionso Prophylactic anti-epileptics reduce early seizures o No reduction in late seizures o No effect on death and neurological disabilityo 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.
Blood Glucose
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.
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
Brain Tissue pH and Blood GlucoseB
rain
pH
Glucose0 5 10 15 20
6
6.5
7
7.5
Brain p
H
Steroids
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
Cooling
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.”
Therapeutic Hypothermia:Experimental Evidence
NABIS:H I
AIM
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
NABIS:H I Outcomes
56.85 56.01
27.92 26.59
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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
Therapeutic Hypothermia: Cardiac Arrest
Hypothermia Treatment Window
Future Directions
ER physician’s role in brain death
• Hope Programhttp://iweb.calgaryhealthregion.ca/hope
Questions?
Acknowledgements
Dr. Jason LordDr. David Zygun
How to Read a Head CT
How to Read a Head CT• Has assumed a critical role in the daily practice
of Emergency Medicine for evaluating intracranial emergencies
• Most practitioners have limited experience with interpretation
• In many situations, the Emergency Physician must initially interpret and act on the CT without specialist assistance
Trauma CT• Is there evidence of hemorrhage?
o Within the ventricleso Within the subdural spaceo Within the subarachnoid spaceo Within the epidural space
• Is there mass effect?o Effacement of sulci
• Is there cerebral edema?o Small ventricleso Small basilar cisternso General effacement of cortical sulcio Diffuse loss of grey-white differentiation
• Is there local loss of grey-white differentiation?o Infarction/Inflammation/Tumor
• Is there Hydrocephalus?o Communicating vs non-communicating
• Have the cisterns been scrutinized for hemorrhage and size?• Is there evidence of infarction?• Is there calcification?• Have the midline structures been examined?• Have all images been analyzed?
o Scout and bone windows• Will contrast be helpful?• Is the CT interpritation consistent with clinical findings
Head CT
“Blood Can Be Very Bad”
Blood Can Be Very Bad
• Blood
• Cisterns
• Brain
• Ventricles
• Bone
Blood Can Be Very Bad
• Blood
• Cisterns
• Brain
• Ventricles
• Bone
Blood Can Be Very Bad
• Blood
• Cisterns
• Brain
• Ventricles
• Bone
Blood Can Be Very Bad
• Blood
• Cisterns
• Brain
• Ventricles
• Bone
Blood Can Be Very Bad
• Blood
• Cisterns
• Brain
• Ventricles
• Bone
CT Scan Basics• A CT image is a computer-generated
picture based on multiple x-ray exposures taken around the periphery of the subject
• X-rays are passed through the subject, and a scanning device measures the transmitted radiation
• The denser the object, the more the beam is attenuated, and hence fewer x-rays make it to the sensor
CT Scan Basics• The denser the object, the whiter it is on CT
• Bone is most dense = + 1000 Hounsfield U • Air is the least dense = - 1000 Hounsfield U
CT Scan Basics: Windowing
Focuses the spectrum of gray-scale used on a particular image
•Brainstem•Cerebellum•Skull Base
–Clinoids–Petrosal bone–Sphenoid bone–Sella turcica–Sinuses
Posterior Fossa
Sagittal View
Cisterns
CT Scan
Brainstem Lateral View
2nd Key Level2nd Key Level Sagittal View
2nd Key Level
Cisterns at Cerebral Peduncles Level
CT Scan
CT Scan
3rd Key Level
Cisterns at High Mid-Brain Level
CT Scan
Ventricles
CSF Production
• Produced in choroid plexus in the lateral Ventricles Foramen of Monroe IIIrd Ventricle Acqueduct of Sylvius IVth Ventricle Lushka/Magendie
• 0.5-1 cc/min• Adult CSF volume is approx. 150 cc’s• Adult CSF production is ~ 500-700 cc/day
B is for Blood• Is blood present?
o If so, where is it?o If so, what effect is it having?
Blood becomes hypodense at approx 2 weeks
Blood becomes isodense at approx 1 week
Acute blood is bright white on CT (once it clots)
Blood becomes hypodense at approximately 2 weeks
Blood becomes isodense at approx 1 week
Acute blood is bright white on CT (once it clots)
Blood becomes hypodense at approximately 2 weeks
Blood becomes isodense at approximately 1 week
Acute blood is bright white on CT (once it clots)
Epidural Hematoma• Lens shaped• Does not cross sutures• Classically described with
injury to middle meningeal artery
• ↓ mortality if treated prior to unconsciousness (< 20%)
CT Scan
Subdural Hematoma• Typically falx or sickle-shaped• Crosses sutures• Does not cross midline• Acute subdural is a marker
for severe head injury (Mortality ~ 80%)
• Chronic subdural usually slow venous bleed and well tolerated
CT Scan
CT Scan
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage• Blood in the cisterns/cortical gyral surface
o Aneurysms responsible for 75-80% of SAHo AVM’s responsible for 4-5%o Vasculitis accounts for small proportion (<1%)o No cause is found in 10-15%o 20% will have associated acute hydrocephalus
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C is for CISTERNS
• 4 key cisternso Circummesencephalico Suprasellaro Quadrigeminalo Sylvian
((BBlood lood CCan an BBe e VVery ery BBad)ad)
Cisterns• 2 Key questions to answer regarding
cisterns:o Is there blood?o Are the cisterns open?
B is for BRAIN((BBlood lood CCan an BBe e VVery ery BBad)ad)
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Tumor
Atrophy
Abscess
Hemorrhagic Contusion
Mass Effect
Stroke
Intracranial Air
Intracranial Air
Intracranial Air
V is for VENTRICLES
((BBlood lood CCan an BBe e VVery ery BBad)ad)
BONE
If…• No blood is seen• All cisterns are present/open• The brain is symmetric
• with Normal gray-white diff • The ventricles are symmetric
• without dilation• There is no fractured bone
No Worries…
Practice CT