NEUROSURGICAL

EMERGENCIES

NEUROSURGICAL EMERGENCIES

OHead injuryO HydrocephalusO BrainTumoursO Intracranial Bleeds/CVA’sO Shunt complicationsO Spinal cord InjuryO Spinal cord compression and tumours.

HEAD INJURYO Major cause of mortality and morbidity in

children.O Leading cause of death in children > 1year is

trauma.O Head injury is responsible for most trauma

deaths approximately 80%. (50% in adults)

PATHOPHYSIOLOGYOChildren are more vulnerable to

injury from head traumaO Relatively large (10% of body weight)

means increased momentum and tend to land on head with falls.

O Elastic, underdeveloped cervical ligaments and muscles are less protective.O Soft calvarium.O Large subarachnoid space (veins at increased risk of tearing)

ETIOLOGYORoad traffic accidentsSevere head injuriesOFallsUsually in children <4years and usually mildORecreational activitiesBicycle accidentsOAssaults/NAIMost head injuries in kids <1yr are from falls and NAI

ANATOMYOBRAIN

Inelastic and non compressibleHas no internal support

OCRANIUMRigid and unyielding Bony buttresses at anterior

and temporal polesOMEMBRANOUS “SLINGS”

Rhoads & Pflanzer (1996) Human Physiology p. 211

Layers of the Cranial Vault

Anatomy of the Brain www.neurosurgery.org/pubpgages/patres/anatofbrain.

BRAIN INJURY

Primary

Intracranial HTN

Mass Lesion

Secondary

Delayed cell

death

Ischaemia hypoxia,

hypotension and

hypercarbia

PRIMARY BRAIN INJURY

Primary

Focal

Coup

Contra coup

Diffuse

DAI

TRAUMATIC HEAD INJURY

ALL-NET Pediatric Critical Care Textbook Source: LifeART EM Pro (1998) Lippincott Williams & Wilkins. www.med.ub.es/All-Net/english/neuropage/trauma/head-8htm

TYPES OF PRIMARY INJURY

OFocal injuriesSkull fractureParenchymal contusionParenchymal lacerationVascular injury resulting in epidural,

subdural or parenchymal haematoma.ODiffuse injuries

Diffuse axonal injuryDiffuse vascular injury

Scalp haematomas/lacerations

OVery vascular, but generally can’t lose enough blood to cause shock or hypovolemia

OCephalohematoma – beneath periosteum (does not cross suture lines)

OSubgaleal bleed - beneath galea (crosses suture lines, often boggy)O Critical in neonate (e.g. from birth trauma)O Can lead to shock/hypovolemia

OClean and examine scalp wounds well to r/o underlying skull fracture; often staple

SKULL FRACTURES

OANY skull fracture can cause underlying ICH, but 50% of bleeds have no fracture

OSkull films are of little use - if suspect skull fracture or bleed, get non contrast CT

QuickTime™ and a decompressor

are needed to see this picture.

SKULL FRACTURESOLinear(3/4)- outpatient observation OK,

but get neurosurgical evaluation and f/u if under age 2O Can develop leptomeningeal cyst if dural

tearODepressed - require neurosurgical

evaluation possible repair if depression>skull thicknessO More often develop seizuresO Often get prophylactic AEDs

OBasilar (Battle’s sign, haemotympanum, raccoon eyes) - head CT with inpatient observation, neurosurgical evaluation.

Case 1

OA 2 year-old comes in after falling approximately 3 feet from her parent’s bed. The CT scan shows the following:

What is your diagnosis?1. Epidural hematoma2. Subdural hematoma3. Diffuse axonal injury4. Contusion

Subdural

Subdural HematomaOMore common than

epidural in childrenOTears in parasagittal

bridging veinsOConcave shapeOOften associated with

more diffuse shear injury

O Immediate surgical tx if pt is unconscious and has subdural bleed

OSuspect NAI

Case 2

OA 5 year old girl falls from a second story window. You find the following on CT scan:

What is your diagnosis?

1. Epidural hematoma2. Subdural hematoma3. Diffuse axonal injury4. Contusion

Epidural Hematoma

Epidural HematomaOCaused by tears of

meningeal vesselsOConvex shapeOOften associated bone

fracture (up to 75%)OTypically few hours of

lucidity followed by rapid deterioration

ONeed close observation and often surgical evacuation

OGood prognosis if recognized and treated

SUBDURAL VS. EPIDURAL

LifeArt: Williams & Wilkinshttp://www.lifeart.com

SUBDURAL HEMATOMA

WebPath: University of Utahhttp://www-medlib.med.utah.edu

EPIDURAL HEMATOMA

WebPath: University of Utahhttp://www-medlib.med.utah.edu/

SUBDURAL vs EPIDURAL HEMATOMA

OEPIDURALO Requires linear

forceO Associated with

skull fracture and torn artery. Brain often uninjured

O “Lucid” interval common

O Common in accidental trauma

OSUBDURALO Requires

significant rotational forces

O Associated with brain injury and torn bridging veins

O Neurologic symptoms from the start

O Common in infants with NAI.

Cerebral Contusion

OOccur at the site of blunt traumaOUsually have loss of consciousnessOCan be very small/mild or large,

resulting in significant symptoms (cerebral edema, increased ICP)

OOften associated with intracranial hematomas or skull fractures

Intracerebral Haemorrhage

ORare in Paediatric population.OUsually frontal or temporal lobeOCan be bilateral(countracoup injury)OCan act as mass lesions and cause

intracranial hypertensionOCT-Hyperdense/mixedOMRI-Small petechia+DAIORx: Small-non operative Large-Sx drainage

Penetrating Head InjuryO Infants and children: fall on sharp objects, NAI,

GSWO CT- Localizes bullet and bone fragments.O MRI-Not advised till magnetic properties of bullet

knownO Treatment: Debridement of entry and exit wounds Remove accessible bullet and bony fragments Control haemorrhage Repair dural lacerations+closure of wounds No attempt to REMOVE BULLET OR BONE beyond

entry and exit wounds.

Diffuse Axonal Injury

OOften from acceleration/deceleration injuries (RTA, falls, shaking)

OWidespread shearing of white matter

OSuspect if patient has subarachnoid bleeding and cerebral edema

OEdema develops over 24-48 hours

• Shearing injury of axons • Deep cerebral cortex, thalamus, basal

ganglia• Punctate hemorrhage and diffuse

cerebral edema

Image from: Neuroscience for Kids www.faculty.washington.edu/chudler/cells/html

Diffuse Axonal Injury

Secondary InjuryO Subsequent factors that secondarily cause

brain tissue damageO Intracranial

O Hemorrhage/IschemiaO EdemaO Increased ICP

O SystemicO Hypoxia/hypercapniaO HypotensionO Hyperglycemia

Assessment of severity

Defining SeverityOMild Brain Injury

OGCS = 13-15OLimited impaired consciousness (<30 min)ONormal CT scanOShows signs of a concussion

OVomitingOLethargyODizzinessOLacks recall about injury

Defining SeverityOModerate Brain Injury

OGCS = 9 - 12O Impaired Consciousness (<24)OCT scan Evidence

OSevere Brain InjuryOGCS = 3 - 8O Impaired Consciousness

(> 24 hours)

CAUTION!!

OGCS of 13 may not be so “mild”

OSC Stein, J Trauma. 2001;50:759-760OReviewed 14 studies (1047 adult patients with GCS of 13) O33.8% had intracranial lesionsO10.8% required surgery

Defining Severity

OGCS, hypoxemia and radiologic evidence of SAH, cerebral edema and DAI are predictive of morbidity.

OGCS alone does not predict morbidity. Ong et al. (1996) Pediatric Neurosurgery, 24(6)

OHypotension is predictive of morbidity.OGCS and Pediatric Trauma Score are

not predictive of outcome. Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)

CT or no CTO A 3months old baby presented with

minor head injury. Fell of the table about 2 feet high. NO LOCGCS 15

O/E well, pupils b/l equal and reacting 6 cm laceration occipital area

CT or no CTO 15 year old boy football injury.

Brief LOC Vomited once at scene

O/EWell, alert, GCS 15

No focal neurology

Admission or no Admission

Admission or no Admission

O 15 year old boy hit by car.O GCS 14/15 E 4 M6 V4O Rest all ok!

CT or no CT?Admission?Neuro obs:

Head injurytriage, assessment, investigation and early management of head injury in infants, children and adults (update)

Implementing NICE guidance

December 2007

NICE clinical guideline 56

Updated guidanceO This guideline replaces ‘Head injury: triage,

assessment, investigation and early management of head injury in infants, children and adults’ (NICE clinical guideline 4, 2003)

O There was sufficient new evidence to prompt an update to be carried out which means changes in clinical practice

O There are new and amended recommendations

Key recommendationsO Initial assessment in the emergency department

O Urgency of imaging

O Admission• Criteria for admission• When to involve the neurosurgeon

O Organisation of transfer of patients between

referring hospital and neuroscience unit

O Advice about long-term problems and support services

Initial assessment in the emergency department (ED)

O All patients presenting to an ED with a head injury should be assessed by a trained member of staff within 15 minutes of arrival at hospital

O This assessment should establish whether they are high risk or low risk for clinically important brain injury and/or cervical spine injury

Urgency of imaging: head CT OCT of the head should be performed and

analysed within 1 hour of imaging request in patients who have any of these risk factors:

OGlasgow Coma Scale (GCS) < 13 on initial assessment in A&E or < 15 at 2 hours after injury

OSuspected open or depressed skull fracture or any sign of basal skull fracture

OTwo or more episodes of vomiting in adults; three or more in children

OPost-traumatic seizure

OCoagulopathy, providing that some loss of consciousness or amnesia has been experienced

OFocal neurological deficit

Urgency of imaging: head CT

O Patients who have any of the risk factors below, and none of the risk factors on the previous slide should have CT imaging of the head performed within 8 hours of the injury:O Amnesia for > 30 minutes of events before impact

(assessment unlikely to be possible in any child aged under 5 years)

O Age 65 years, providing that some loss of consciousness or amnesia has been experienced

O Dangerous mechanism of injury (e.g. a fall from a height of > 1 metre or 5 stairs), providing that some loss of consciousness or amnesia has been experienced.

Admission: Criteria

O Clinically significant abnormalities on imaging

O Patient has not returned to GCS 15 after imaging, regardless of the imaging results

O Criteria for CT scanning fulfilled, but scan not done within appropriate period, either because CT not available or because patient not sufficiently cooperative to allow scanning

O Continuing worrying signs (e.g. persistent vomiting)

O Other sources of concern (e.g. drug intoxication, other injuries, non accidental injury)

Secondary Brain InjuryPotentially Avoidable Or Treatable With Close Monitoring / Treatment of ABC’s

O HypoxiaO HypercarbiaO Hypotension/ischemiaO Intracranial hypertensionO Acidosis O SeizuresO HyperthermiaO HypothermiaO Infections

Evidence based management of severe traumatic brain injury in children

O Guidelines for the Acute Medical Management of severe traumatic Brain Injury in infants, Children, and Adolescents.

Journal of Pediatric Critical Care Medicine. January 2012-Second edition

O Text book of Paediatric critical care Bradley P.Fuhrman, Jerry J.Zimmerman Third edition2006

O NICE Guidelines- Updated December 2007

Level of EvidenceOLevel I Good quality RCT

OLevel II Moderate or poor quality RCT Good quality cohort Good quality case control

OLevel III Moderate or poor quality RCT or cohort Moderate or poor quality case control Case series, databases, registeries

INITIAL MANAGEMENTOAIRWAY with C-Spine control

OBREATHING

OC T SCAN CIRCULATION

ODOEOF & G

EARLY RESUSCITATION OF CHILDREN WITH MODERATE-TO-SEVERE TRAUMATIC BRAIN

INJURY PEDIATRICS 2009;124;56-64 MICHELLE ZEBRACK, CHRISTOPHER DANDOY, KRISTINE HANSEN, ERIC SCAIFE, N. CLAY MANN AND SUSAN L. BRATTON

O CONCLUSIONS: Hypotension and hypoxia are common events in pediatric traumatic brain injury. Approximately one third of children are not properly monitored in the early phases of their management. Attempts to treat hypotension and hypoxia significantly improved out-comes.

Circulatory Support: Maintain Cerebral Perfusion Pressure

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Patient Outcome

Good

Moderate

Severe

Vegetative

Dead

Number of Hypotensive Episodes in the first 24 hours after TBI

Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)

CPP = MAP - ICP

Airway and ventilationCriteria for the intubation of Head injured

childO GCS<10O Decrease in GCS of >3, independent of the

initial GCS.O Anisocoria>1mmO Cervical spine injury compromising

ventilation.O ApnoeaO Hypercarbia(PaCo2>45mmg/6.0Kpa)O Loss of pharyngeal reflexO Spontaneous hyperventilation causing

PaCo2<25mmHg/3.3Kpa

Airway and ventilationO Hypoxia to be avoided. Aim Pao2 of >13kpa Aim PaCo2 of 4.5-5.0kpa

O Avoidance of prophylactic severe hyperventilation to a PaCO2 of <30mmHg(4.0kpa).

O If hyperventilation is used in the management of refractory intracranial hypertension, advanced neuromonitoring like

jugular venous oxygen saturations, brain tissue oxygen tension measurements

for evaluation of cerebral ischemia may be considered.

(LEVEL III)

Head elevation of 30 degrees

OThis improves venous drainage with minimal effect on arterial pressure.

OHead in midline to ensure no pressure or kinking of neck veins.

O If head raised more then 30 degrees possible adverse effect on cerebral arterial pressure.

Carter BG, Butt W, Taylor A: ICP and CPP: Excellent predictors of long term outcome in severely brain injured children. Childs Nerv Syst 2008; 24:245–251

Keep neck mid-line and elevate head of bed …. To what degree?Feldman et al. (1992) Journal of Neurosurgery, 76

March et al. (1990) Journal of Neuroscience Nursing, 22(6)

Parsons & Wilson (1984) Nursing Research, 33(2)

Normal Cerebral MetabolismOBrain tissue relies on aerobic

metabolism.

ONormal cerebral metabolism requires a blood flow of approximately 50 mL/100g/min.

OSerious neurological deficits begin to occur at 20 mL/100g/min.

OProlonged Cerebral Blood Flow < 12 mL/100g/min. results in cerebral infarction.

CBF AutoregulationO CBF maintained within CPP range of 50 – 150 mmHg.O CPP =MAP – ICPO <50 CPP= Maximal dilation CBF fallsO >150 CPP=Maximal constric CBF raisesAutoregulation 1)Completely lost-linear relation CBF & CPP2)Incompletely lost-Plateau after CPP of 80 mmHg

Copied from: Rogers (1996) Textbook of Pediatric Intensive Care p. 646

ICP Monitoring-Level III

O A frequently reported high incidence of intracranial hypertension in children with severe TBI.

O A widely reported association of intracranial hypertension and poor neurologic outcome

O The concordance of protocol-based intracranial hypertension therapy and best-reported clinical outcomes

O Improved outcomes associated with successful ICP-lowering therapies

Monitoring of Intracranial pressure

O Indications: GCS <8 Abnormal head CT Rapid neurological deteriorationNormal CT head in adultsO Age>40O Unilateral or bilateral motor posturingO Systolic BP <90

Treatment of raised ICPOTreatment of intracranial pressure (ICP)

may be considered at a threshold of 20 mm Hg (LEVELIII).

Grinkeviciute DE, Kevalas R, Matukevicius A, et al.: Significance of intracranial pressure and cerebral perfusion pressure in severe pediatric traumatic brain injury. Medicina (Kaunas, Lithuania) 2008; 44:119–125

Cerebral perfusion pressure

OA minimum CPP OF 40mmHg (Level III) may be considered in children with TBI.

OA CPP threshold of 40-50mmHg may be considered; infants at lower end and adolescents at the upper end of this range.

(Level III).

ICP Measurement-InvasiveO Intraventricular catheter coupled to ICP

transducer is Gold standard. Adv: CSF can be drained Dis adv: Infection, Ventricular compression leads to inaccuracyO Fiberoptic cath: Adv: Improved Longevity, can be placed intraparenchymal/intraventricular/subdural Dis adv: Not able to drain CSFO Subdural/subarachnoid Bolts: Occulusion of ports can lead to inaccuracy

Advanced Neuromonitoring

OIf brain oxygenation monitoring is used, maintenance of partial pressure of brain tissue oxygen (PbtO2) >10 mm Hg may be considered.(LEVEL III)

O Figaji AA, Zwane E, Thompson C, et al.: Brain tissue oxygen tension monitoring in pediatric severe traumatic brain injury. Part 1: Relationship with outcome. Childs Nerv Syst 2009; 25:1325–1333

O Narotam PK, Burjonrappa SC, Raynor SC, et al.: Cerebral oxygenation in major pediatric trauma: its relevance to trauma severity and outcome. J Pediatr Surg 2006; 41:505–513

Neuroimaging

O In the absence of neurologic deterioration or increasing intracranial pressure (ICP), obtaining a routine repeat computed tomography (CT) scan >24hrs after the admission and initial follow-up study may not be indicated for decisions about neurosurgical intervention. (LEVEL III)

Hyperosmolar therapy

O Hypertonic saline should be considered for the treatment of severe paediatric traumatic brain injury associated with intracranial hypertension. Effective doses for acute use range between 6.5 and 10 mL/kg (of 3%) (LEVEL II).

Temperature controlO Moderate hypothermia (32–33°C) beginning

early after severe traumatic brain injury (TBI) for only 24hr’s duration should be avoided

O Moderate hypothermia (32–33°C) beginning within 8 hrs after severe TBI for up to 48 hrs’ duration should be considered to reduce intracranial hypertension.

O If hypothermia is induced for any indication, rewarming at a rate of >0.5°C/hr should be avoided (LEVEL II).

O Moderate hypothermia (32–33°C) beginning early after severe TBI for 48 hrs, duration may be considered (LEVEL III).

Cerebrospinal fluid drainageO Cerebrospinal fluid (CSF) drainage through an

external ventricular drain may be considered in the management of increased intracranial pressure (ICP) in children with severe traumatic brain injury (TBI).

O The addition of a lumbar drain may be considered in the case of refractory intracranial hypertension with a functioning external ventricular drain, open basal cisterns, and no evidence of a mass lesion or shift on imaging studies (LEVEL III).

BarbituratesO High-dose barbiturate therapy may be

considered in haemodynamically stable patients with refractory intracranial hypertension despite maximal medical and surgical management.

O When high-dose barbiturate therapy is used to treat refractory intracranial hypertension, continuous arterial blood pressure monitoring and cardiovascular support to maintain adequate cerebral perfusion pressure are required (LEVEL III).

Decompressive craniectomy

O Decompressive craniectomy (DC) with duraplasty, leaving the bone flap out, may be considered for paediatric patients with TBI who are showing early signs of neurologic deterioration or herniation or are developing intracranial hypertension refractory to medical management during the early stages of their treatment.

(LEVEL III).

CorticosteroidsO The use of corticosteroids is not

recommended to improve outcome or reduce intracranial pressure (ICP) for children with severe traumatic brain injury.(LEVEL III)

Analgesics, sedatives, and neuromuscular blockade

OThiopental may be considered to control intracranial hypertension.

OPropofol Not recommended.(LEVEL III)OEtomidate can be used as a one off bolus but look for adrenal suppression.

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Before During After

TurningSuctioningBathing

Nursing Activities and ICP

Rising (1993) Journal of Neuroscience Nursing, 25(5)

ICP

Glucose and nutrition

O The evidence does not support the use of an immune-modulating diet for the treatment of severe traumatic brain injury (TBI) to improve outcome (LEVEL II).

O In the absence of outcome data, the specific approach to glycemic control in the management of infants and children with severe TBI should be left to the treating physician (LEVEL III)

Antiseizure prophylaxis

O Prophylactic treatment with phenytoin may be considered to reduce the incidence of early posttraumatic seizures (PTS) in paediatric patients with severe TBI (LEVEL III).

O The incidence of early PTS in paediatric patients with TBI is approximately 10% given the limitations of the available data. Based on a single class III study, prophylactic anticonvulsant therapy with phenytoin may be considered to reduce the incidence of early posttraumatic seizures.

Questions?

SummaryOSerial neurologic assessments and

physical examinationOContinuous cardio-respiratory, ICP,

and CPP monitoring, +/- cerebral metabolism monitoring adjuncts

OMaximize Oxygenation and Ventilation Maximize oxygenation Normo-ventilate Support circulation / maximize cerebral perfusion

pressure Maintain mean arterial blood pressure and maintain CPP.

SummaryODecrease intracranial pressure

O Evacuate mass occupying hemorrhages/lesions.

O Consider draining CSF when possibleO Hyperosmolar therapy, cautious use to

avoid hypovolemia and decreased BPO Mid-line neck, elevated head to 30

degree.O Treat pain and agitation - consider pre-

medication for nursing activities, +/- neuromuscular blockade.

O Careful monitoring of ICP during nursing care, cluster nursing activities and limit handling when possible

Summary

ODecrease Cerebral Metabolic RateO Prevent seizures O Reserve thiopentone for refractory

conditionsO Avoid hyperthermia, +/- hypothermiaO Avoid hyperglycemia (early)