head trauma sean caine stefan da silva. normal physiology pathophysiology concussion mild tbi...
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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