NEUROEMERGENCY

Syahrul
Consultant Neurologist
June 6, 2011

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NEUROEMERGENCY
Neurocritical Care
Competency-Based Critical Care :
Brain Injury and Dysfunction: The Critical Role of
Primary Management
Monitoring the Injured Brain
The Secondary Management of Traumatic Brain Injury
Central Nervous System Infections
Cervical Spine Injuries
Recent Advances in the Management of Acute
Ischemic Stroke
Seizures on the Adult Intensive Care Unit
Acute Weakness in Intensive Care
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Coma,
Confusion, and Agitation in Intensive Care 2

Brain Injury and Dysfunction:

The Critical Role of Primary Management
1. In traumatic brain injury, maintain mean arterial (MAP)
blood pressure >80 mmHg.
2. Avoid hypoxia at all costs; keep PaO2 >13 kPa, using
PEEP if necessary.
3. Keep PaCO2 4.55.0 kPa; hyperventilate only if there
are signs of impending brainstem herniation.
4. Keep the neck in neutral position; always consider the
possibility of cervical spine injury.
5. Maintain 15 head up position (as long as MAP
adequate).
6. Do not give mannitol if patient is hypotensive. Speak
to a Regional Neurological or Neurosurgical Center
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before
giving additional doses.

Estimated annual brain

injury

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Indications for Patient

Transfer
Group 1: Transfer delayed only for correction of secondary
cerebral insults or for life-saving surgery (e.g., expanding
extradural hematoma with localizing signs).
Group 2: Requires urgent transfer following optimization and
life and limb saving surgery (e.g., subdural hematoma with
no mass effect).
Group 3(a): Patients should only be transferred after absolute
stabilization given that the overall principles of care are to
avoid secondary cerebral insults, rather than to offer neurospecific therapies (e.g., contusional injury with no mass
effect).
Group 3(b): Some non-neurosurgical intensive care units
(ICU) monitor ICP in cases of diffuse axonal injury; transfer
may become necessary if the ICP subsequently becomes
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difficult to control.

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The role of the primary management of

patients with traumatic brain injury
1. Primary resuscitation

2. Neurological assessment
3. Deciding on the need for intubation, sedation and ventilatory
support
4. Management of problems such as convulsions
5. Interpretation of CT scans adequate for prioritization of
treatment options
6. Prioritizing and expediting essential general surgical and
orthopedic interventions
7. Deciding on transfer or retention after such interventions
8. Maintaining neurological observations
9. Avoiding secondary cerebral insults or expansion of any
intracranial pathology
10.
Organizing further CT scans in the event of retaining a patient
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TBI changes in level of

consciousness and cognition.

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Brain Edema Four Mechanisms

1. Hydrostatic edema: occurs when arterial pressure exceeds
the upper limit of autoregulation or when there is venous
congestion (head-down position, pressure on the jugular
veins, high intrathoracic pressure).
2. Osmotic edema: non-ionic crystalloid solutions such as
dextrose become, in effect, free water once the sugar
component ismetabolized.
3. Oncotic edema: due to low plasma proteins; can become
important when the bloodbrain barrier (BBB) is damaged.
4. Inflammatory edema: the inflammatory response to insults
such as trauma or hypoxia can lead to increased capillary
permeability and disruption of the BBB. It is critically
important to avoid preventable insults such as osmotic
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edema
when this has arisen.

Indications for a CT brain scan

after head injury
Depressed conscious level
Focal neurological deficit
Suspected open or basal skull fracture
Age >65, with loss of consciousness or
amnesia
GCS 15 with no fracture, but other concerning
features (severe persistent headache,
vomiting, seizure, altered behavior)
Unable to assess properly (e.g., alcohol, drugs)
Prior to anesthesia for treatment of other
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injuries

Indications for Mannitol

Unilateral pupillary dilatation, or unilateral progressing to bilateral
dilatation (primary bilateral dilatation may represent fitting, drug
intoxication or overdose, or overwhelming brain injury).
Dose: 0.5 g/kg (approximately 200 mL of 20% solution) over 1015 min.
Can be repeated at 12 hourly intervals to maximum serum
osmolarity of 320 mosmol/L or Na+ of 160 mmol/L. Speak to the
Regional Neurological or Neurosurgical Center prior to giving
additional doses.
Alternative: Hypertonic saline (HSL) is being increasingly used for the
same purpose with good effect. We use 30 mL of 20% HSL over 20
min via a CVC, with a similar serum [Na+] cut-off of 160 mmol/L.
Precautions: Mannitol should not be given to patients who are
hypotensive or have evidence of inadequate renal perfusion. All
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patients
require bladder catheterization.

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Monitoring the Injured Brain

1. Repeated clinical assessment through the
Glasgow Coma Scale (GCS) is the cornerstone of
neurological evaluation.
2. Ventilated head-injured patients with intracranial
pathology on CT require ICP monitoring.
3. Invasive or noninvasive neuro-specific
monitoring requires careful interpretation when
assisting goal-directed therapies.
4. Multimodal monitoring using a combination of
techniques can overcome some of the limitations
of individual methods.
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Neuro-Specific Monitoring
1. The Glasgow Coma Scale
2. Pupillary Response
Sudden unilateral fixed pupil: Compression of the
third nerve, e.g., ipsilateral uncal herniation or
posterior communicating artery aneurysm
Unilateral miosis: Horners syndrome (consider
vascular injury)
Bilateral miosis: Narcotics, pontine hemorrhage
Bilateral fixed, dilated pupils: Brainstem death,
massive overdose (e.g. tricyclic antidepressants).
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Invasive Monitoring
Intracranial Pressure Monitoring
ICP values

Normal ICP <15 mmHg.

Focal ischemia occurs at ICP >20 mmHg
Global ischemia occurs at ICP >50 mmHg
Usual treatment threshold is 20 mmHg

Measuring ICP
Intraventricular
Extraventricular
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Indications for ICP

monitoring

Head injury + ventilator + abnormal CT brain scan =

ICP monitor
Traumatic brain injury, in particular:
Severe head injury (GCS <8)
Focal pathology on CT brain scan
Head injury and age >40
Normal CT brain scan but systolic blood pressure
persistently <90 mmHg
Where other injuries and their treatment necessitate the
use of sedation or anesthesia

Subarachnoid hemorrhage with associated

hydrocephalus.
Hydrocephalus
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The Secondary Management of

Traumatic Brain Injury
1. The management of traumatic brain injury (TBI) has increasingly
become more tailored to the individual patient; measuring adequacy
of cerebral oxygenation may allow lower cerebral perfusion
pressures to be targeted and more rational adjustments of PaCO2
levels.
2. Patients with TBI who are hypothermic at presentation should not
be rapidly rewarmed.
3. Hypertonic saline can be a useful alternative to mannitol in the
management of intracranial hypertension.
4. Steroids are not currently recommended in the management of TBI.
5. Recombinant Factor VIIa may be useful in cases where correction of
acidosis and hypothermia and administration of appropriate blood
products has failed to control continued nonsurgical bleeding.
6. Decompressive craniectomy is a useful therapeutic maneuver in
selected cases of refractory intracranial hypertension.
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Central Nervous System Infections

1. Do not delay antibiotic or antiviral therapy if there is
any suspicion of CNS infection
2. Get a senior review and seek help from the criticalcare team
3. Seek urgent neurosurgical opinion if suspected
cerebral abscess, subdural empyema, epidural
abscess or ventriculitis
4. Immunocompromised patients may be infected with
unusual organisms
5. UK guidelines for treatment of meningitis in adults
and children are readily available [[Link]]
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Meningitis
Definition: Inflammation of the meninges, often
infective.
Causes: Many cases are aseptic meningitis,
usually viral (5570% enteroviruses); Neisseria
meningitidis (meningococcal) is the commonest
form of bacterial meningitis (75%); Streptococcus
pneumoniae (pneumococcus) Second commonest
cause of bacterial meningitis (10%); Haemophilus
influenzae (2%); Listeria monocytogenes;
Mycobacterium tuberculosis; Fungal meningitis
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Clinical features of bacterial meningitis

Meningism-headache, stiff neck, fever,
reduced conscious level.
Sepsis
Rash with meningococcal disease.
Raised intracranial pressure
(bradycardia, hypertension,
papilledema, focal neurology, reduced or
fluctuating GCS)
Seizures
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Early purpuric rash

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Empirical Treatment for Bacterial Meningitis

in Adults
Cefotaxime 2 g IV 46-hourly, or
Ceftriaxone 2 g IV 12-hourly.

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Sepsis: Recognition and

Treatment
Warning signs:
Rapidly progressive non-blanching petechial or
purpuric rash
Poor peripheral perfusion, capillary refill time >4
s, oliguria, systolic BP <90 mmHg
Respiratory failure: Rate <8 or >30, SpO2 <95%
Circulatory failure: HR <40 or >140 bpm
pH <7.3 or base deficit worse than 5
WCC <4
Confusion, agitation, or reduced GCS (GCS <12)
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Treatment: ([Link]).
Remember airway, breathing, circulation
1. High-flow oxygen, early decision to intubate and ventilate
if oxygenation poor or comatose.
2. Large-bore IV access, colloid bolus (children 20 mL/kg HAS
4.5%); fluid boluses may need to be repeated, depending
on the response, but should not exceed 60 mL/kg in
children without intubation and ventilation (risk of
pulmonary edema).
3. Routine bloods including blood cultures, blood sugar, and
markers of disseminated intravascular coagulopathy (DIC)
e.g., D-dimers, FDPs.
4. Monitoring: ECG, Sa02, BP (preferably invasive), hourly
urine output and central venous pressure.
5. Antibiotics: Cefotaxime 2 g IV 46-hourly, do not delay
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administration.

6. Inotropes may be required. Dobutamine can be given

peripherally until central access has been gained.
Calcium may be required.
7. Repeat arterial blood gases regularly to monitor
oxygenation, ventilation, acid base balance, glucose,
and calcium.
8. ICU referral, senior review, and repeated review.
9. Activated Protein C if severe sepsis and >2 organ
failure.
10. Consider steroids if evidence of adrenal insufficiency
(e.g., vasopressor resistant shock or hypoglycemia)
11. CT scan and lumbar puncture when stable.
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Right frontal cerebral

abcesses

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Clinical Features
Focal neurological deficits
Raised intracranial pressure
Signs of infection not as common as
expected. Fever in <50%
Seizures in 40%

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Treatment
Urgent neurosurgical opinion. Referral to ICU if
obtunded or having seizures.
Empirical antibiotics, cefotaxime 2 g IV 6-hourly
and metronidizole 500 mg 8-hourly; add
flucloxacillin 2 g 6-hourly or vancomycin 1 g 12hourly if trauma or recent surgery. Antibiotic
therapy can be amended according to culture and
susceptibility results following discussion with a
microbiologist. Duration is likely to be 36 weeks in
total.

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Cervical Spine Injuries

1. Cervical spine injuries account for about 50% of spinal
injuries
2. 1030% of spinal trauma results in spinal cord injury
(SCI)
3. Cervical spine injuries are often associated with other
injuries, including head injury in up to 25%
4. 510% of patients with a cervical SCI will be unconscious
at presentation
5. Mortality for combined head and cervical spine injuries
exceeds 10%
6. SCI should be assumed in any patient who present with
a depressed conscious level
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Initial Stabilization
Trauma victims are now routinely
immobilized
on a spine board with their neck in the
neutral
position in a rigid cervical collar

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This X-ray shows what looks like an

acute slip at C4/5

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Posterior occipito-cervical fixation with bone

graft to treat an unstable fracture in the upper
cervical spine

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Hangmans fracture (hyperextension

injury)

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Recent Advances in the Management

of Acute Ischemic Stroke
1. Acute ischemic stroke is amenable to early
intervention, either by influencing the events
involved in initial ischemia and propagation of brain
injury, or by secondary prevention.
2. To date, there has been inertia on the part of the
medical profession and public in recognizing that
acute stroke is a potentially treatable emergency.
3. Improved education, together with better
organization of stroke services is likely to improve
the recovery from this potentially devastating
condition.
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MCA infarction.

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Physiological Stabilization
Arterial Reperfusion: Systemic
Thrombolysis
Neuroprotection

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Seizures on the Adult Intensive Care

Unit
1. Seizures are commonly encountered
in the ICU. They can be provoked by
acute illness, medicines, or alcohol
2. The causes of seizures tend to differ in
different age groups
3. Tonic-clonic status epilepticus carries
a significant mortality

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4. Early and effective treatment is

essential
5. EEG can distinguish between tonicclonic status and non-epileptic attack
disorder (NEAD) and diagnose
nonconvulsive status
6. Long-term treatment of epilepsy
depends on the type of seizures and
the characteristics of the patient
involve an expert
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Recommendations for ICU

Admission
Status epilepticus
Seizures occurring as part of an
acute illness or following
neurosurgery
Incidental seizures in a patient with
epilepsy
Non-epileptic attack disorder (NEAD)
(pseudostatus)
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Seizures on the Adult Intensive Care

Unit
Airway, Breathing, Circulation,
Disability
Check blood glucose
Give thiamine or pyridoxine if
appropriate

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Established status: 30-60

minutes
Phenytoin 15-20mg / kg IV @
50mg / min, or
Fosphenytoin 15-20mg / kg IV / IM
@ 150mg / min

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Acute Weakness in Intensive Care

1. Acute weakness may directly lead to a
requirement for critical care or may occur
during an episode of critical illness (critical
care neuropathy).
2. Treatment requires a multidisciplinary
approach. Pain control, nutrition, pressure
area care, thrombo-prophylaxis,
physiotherapy, and psychological care must
all be addressed for the best outcome to be
achieved.
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3. GuillainBarr syndrome is one of the

commonest causes of acute weakness seen
on the ICU.
4. Serial assessments of the respiratory
system, including spirometry help to evaluate
the progress of the disease, and the need for
critical care support.
5. Bulbar palsy and swallowing difficulties must
be recognized early, otherwise aspiration and
subsequent pneumonia may occur.
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Specific Acute Weaknesses

GuillainBarr Syndrome (GBS)
1. Acute inflammatory demyelinating polyradiculopathy
(AIDP) accounts for 8590% of cases.
2. Acute motor axonal neuropathy (AMAN) less severe
axonal form, most often described in children and
young adults in Northern China.
3. Acute motor sensory axonal neuropathy (AMSAN)
more severe form of GBS presenting with severe
paralysis after a prodromal illness.
4. MillerFisher syndrome characterized by ataxia,
areflexia, and ophthalmoplegia and associated with the
presence of antibodies to GQ1b ganglioside.
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Recommendations for ICU

Admission
1. Rapid progression of motor weakness
including respiratory muscles
2. Presence of bulbar dysfunction and
bilateral facial palsy
3. Autonomic dysfunction
4. Medical complications (e.g., myocardial
infarction sepsis, pulmonary embolism)

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Treatment
Plasma exchange (plasmapheresis)
involves substituting 250 mL/kg of
plasma with 4.5% human albumin,
typically five times at a specialist center.
Treatment must commence within 2
weeks of the onset of the disease
Immunoglobulin therapy (IVIG) has the
advantage of being easily administered
in a dose of 400 mg/kg for 5 days
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Coma, Confusion, and Agitation

in Intensive Care
1. Coma and delirium are very common in critically ill patients,
and represent an independent risk factor for poor outcome.
2. Management of the comatose patient involves rapid initial
assessment and correction of easily reversible causes,
protecting the brain from further injury, diagnosing and
specifically treating the underlying cause, plus good generic
multidisciplinary care.
3. Management of delirium includes rapid assessment,
treatment of easily reversible causes (pain, urinary retention,
hypoxia, hypotension etc.) and investigation of other causes.
Nonpharmacological measures are as important as drug
therapy.

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4. Guidelines (and adherence to them) are

useful for both the assessment of delirium
and monitoring of sedation scores.
5. The ideal sedative agent does not exist.
Choice of agent(s) should be patient-specific,
monitored closely to achieve the desired endpoint with the minimum of side effects and
given for the shortest time necessary.
6. Inappropriate use of sedatives may actually
worsen or prolong delirium.
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Management of the Comatose

Patient
Rapid initial assessment and
correction of easily reversible causes
Protecting the brain from further
injury
Diagnosing the underlying cause
Management of the specific cause
General care of the comatose
patient
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