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Neurosurgical Emergencies

Dr. Liz Ebbens

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Objectives

  1. Define “neurosurgical emergency”
  2. Describe signs and symptoms of pediatric neurosurgical emergency i.e. increased intracranial pressure (ICP)
  3. Review emergent management of increased ICP
  4. Review common causes of neurosurgical emergency in pediatric patients with corresponding workup and treatment

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Quickly, �A Preview of PEM Boards

  1. Neurotrauma
  2. Hydrocephalus

2. Ventricular shunt complication:

3. Arteriovenous malformation and aneurysm

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Pediatric Neurosurgical Emergencies

In the emergency setting, our job is to recognize that 1. a neurosurgical emergency is happening and 2. (oftentimes) move to treatment BEFORE workup—treatments start before we scan.

When a delay in surgical care may lead to serious permanent neurologic morbidity and death!

When is a neurosurgical problem emergent?

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Recognizing and Treating Increased ICP

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Signs and Symptoms of Increased ICP

Infants:

Irritability/AMS

Poor feeding or emesis

Split sutures (especially lambdoid)

Bulging fontanelle

Altered mental status

Seizures

Parinaud sign (up-gaze paresis)

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Children:

Severe, acute headache

Seizures/AMS

Emesis

Decerebrate or decorticate posture

Focal neurologic deficits

Papilledema

Pupillary abnormalities

Autonomic dysfunction (🡪 Cushing triad)

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Headache

~1/3 of children with brain tumors present with headache

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Altered Mental Status

Use your GCS!

AMS can be difficult to define in infants and young children

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Cerebral Perfusion Pressure

Mean Arterial Pressure – Intracranial Pressure

(MAP-ICP)

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Cushing Triad

ICP increases 🡪

1. MAP increase and HR increase to push more blood to your brain and increase

2. Irregular breathing (due to brainstem compression) and HR decrease (reason for bradycardia is unclear)

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Acute Management of Increased ICP

  1. Maintain Appropriate Level of Analgesia/Sedation
  2. Initiate Mechanical Ventilation (if appropriate).
  3. Maintain Normothermic Core Temperature and Preventing and Treating Fever.
  4. Ensure Appropriate Volume Status.
  5. Maintain Normal Hemoglobin/Correct Coagulopathy
  6. Maintain Neutral Head Positioning With Head-of-Bed Elevation 30 Degrees
  7. Consider Hyperosmolar Therapy
  8. Seizure Control/Prophylaxis
  9. IMAGE

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Analgesia/Sedation

Why?

  • Sedatives and analgesics prevent transient increases of ICP caused by pain and agitation ( and also, increased ICP is painful!)
  • Neuromuscular blockade can reduce metabolic demand, leaving more blood for the brain.

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Drug Choice:

  • Ketamine is a great drug; keeps MAP up and has been shown to help lower ICP, both in boluses and infusions.
  • Etomidate is also a great drug--does not have many hemodynamic effects.
  • Most protocols describe using a benzodiazepine and opiate combination for prolonged sedation with the most common agents being midazolam and fentanyl.

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Ventilation

For initial management, hyperventilation is NOT needed: target PaCO2 between 35 and 40 

Hyperventilation is a “second tier” therapy in many guidelines and is NOT routinely recommended!

  • Short-term use (<2 hours) for patients with active evidence of cerebral herniation is considered acceptable emergency management.
  • Defined as ETCO2 between 25 and 30

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Bed Positioning

Maintaining the head midline and elevated at 30 degrees maximizes cerebral venous return, which lowers ICP without lowering cerebral perfusion pressure.

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Hyperosmolar Therapy

Mannitol: 0.25 to 1 g/kg/dose infused over 20 to 30 minutes; repeat as needed to maintain serum osmolality <320 mOsm/kg

Hypertonic Saline: IV: 2-5 ml/kg up to a maximum dose of 250 mL

“Limited data available; dosing regimens variable”

***There is some evidence that HTS > mannitol in pediatrics for lowering ICP with better morbidity/mortality plus shortened length of stay.

***Whenever possible, consultation with a neurosurgeon with pediatric expertise should occur before administration of hyperosmolar therapy or therapeutic hyperventilation

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Seizure Control

Both convulsive and nonconvulsive seizures increase cerebral metabolic rate, thereby precipitating increased CBF and increased ICP.

If in status/actively seizing, treat seizures.

You may consider administer a loading dose of long-acting anticonvulsants if delayed definitive care is anticipated- Some recommend a load of 60 mg/kg of levetiracetam with max of 4500 mg.

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Emergent Imaging

CT Head without contrast

Assess for:

1. acute bleed

2. Ventricular enlargement

3. Some mass lesions (supratentorial, not posterior fossa)

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Common Neurosurgical Emergencies

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Neurotraumatic Injury

One of the most common reasons for ER visit in pediatrics

~800,000 visits per year

Mechanisms: Blunt injury (falls, NAT, MVCs, sports-related, assault) and penetrating injury

When is neurotrauma a neurosurgical emergency?

Clinically important traumatic brain injury or ciTBI

- presence of a depressed skull fracture requiring surgery OR any TBI requiring the following: invasive ICP monitoring, ventriculostomy, hematoma evacuation, craniectomy, intubation, admission for monitoring x2 or more nights

ciTBI has an incidence/year of 0.02% to 4.4.%.

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A Note on PECARN

PECARN has been found in multiple studies to be 100% sensitive for identifying ciTBI.

Initial trial of over 40,000 patients; subsequent trials all > 1000 patients

The intent is to “Rule-Out” those with very low risk of ciTBI.

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Increased Risk of ciTBI < 2 Years

AMS

Nonfrontal hematoma

LOC > 5 seconds

Signs of depressed or basilar skull fracture

Bulging fontanelle

Vomiting

Seizure

Suspicion of NAT

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Increased Risk of ciTBI > 2 Years

AMS

Signs of depressed or basilar skull fracture

LOC

Vomiting

Seizure

Focal neurologic deficits

Worsening headache

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Neurotrauma Management

  1. Primary/Secondary Survey and Stabilization
  2. Imaging: CT head without contrast (no role for skull x-ray)
  3. Neurosurgery consult: spectrum of surgical management can vary WIDELY for traumatic injuries and depends on the extent of injury and presence of symptoms increased ICP: Admit for frequent neuro-checks all to the way up to decompressive craniectomy

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Injury Patterns in Blunt Head Injury

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Injury Patterns in Blunt Head Injury

Diffuse Axonal Injury

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Injury Patterns in Blunt Head Injury

Epidural Hematoma (injury to vessels between dura and bone)

Subarachnoid Hemorrhage (injury to vessels suppling pia matter)

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Injury Patterns in Blunt Head Injury

Subdural Hematoma

(injury to bridging veins)

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Injury Patterns in Blunt Head Injury

Cerebral Edema

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Injury Patterns in Blunt Head Injury

Skull Fracture

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A Note on Skull Fractures

Area of the skull most likely to be fractured is the parietal bone, followed by occipital and temporal bones

Signs of basilar skull fractures: Battle sign, periorbital ecchymosis, hemotympanum, CSF otorrhea or rhinorrhea

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A Note on Skull Fractures

Unilateral, non depressed linear skull fractures WITHOUT underlying injury heal spontaneously

--These patients are managed outpatient and data supports this decision: less than 1% of patients DISCHARGED with a skull fracture in this pattern require return for surgical care

In fractures with ANY other pattern (complicated, basilar, open, or with underlying hemorrhage), neurosurgery consult and likely admit for monitoring

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Hydrocephalus

CSF is produced by the choroid plexus and under normal conditions, exits 4th ventricles to circulate in the subarachnoid space to be absorbed BACK into the venous system through arachnoid villi in the superior sagittal sinus.

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Hydrocephalus

OBSTRUCTIVE

Something is keeping the CSF from leaving via the 4th ventricle.

  • stenosis of cerebral aqueducts (congenital or post hemorrhage/infection)
  • Midbrain/posterior fossa tumors
  • Myelomeningocele
  • Dandy Walker Malformation

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NONOBSTRUCTIVE

Something is keeping the CSF from resorbing appropriately.

  • Scarring of subarachnoid space and villi (prematurity, infection, hemorrhage)
  • Myelomeningocele
  • ***Tumors

True congenital hydrocephalus is RARE; 0.2-0.8/1000

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Hydrocephalus

  • Look for symptoms of increased ICP in addition to ataxia (posterior fossa) and regression in milestones.
  • Symptoms may be more insidious in onset depending on age and cause. Infants are more resistant to changes in ICP due to open fontanelles, so slower processes will take longer to manifest.

Do an eye exam!

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Hydrocephalus

Diagnostic Imaging:

  • CT without contrast

***MRI provides greater detail and is better for posterior fossa masses, but it’s not your first move.

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Hydrocephalus

Management:

  1. ABCs 🡪 to the bay if in extremis
  2. Scan the head

3. Neurosurgery consult:

- Treatment will require surgery for shunt placement +/- tumor resection if present

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Shunt Malfunction

Most Helpful Signs and Symptoms:

  • Nausea and vomiting (PPV 79%)
  • Irritability (PPV 78%)
  • Decreased level of consciousness (PPV 100%)
  • Bulging fontanelle (PPV 92%)

***may also be asymptomatic with changes in exam findings—focal neuro deficits or increased head circumference

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Shunt Malfunction

Diagnostic Imaging:

CT brain OR MRI with shunt series XR

Management:

  1. ABCs
  2. Neurosurgery/Imaging

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Post-Operative Complications

    • meningitis
    • ventriculitis
    • abscess
    • empyema

Infection

Infarction

Hydrocephalus

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Meningitis and Ventriculitis

Most often occur within 1st month of surgery because the insertion surgery exposes the mastoid air cells.

Unfortunately, symptoms of these infections look like the NORMAL post-op period including fever.

If you suspect this, DON’T LP.

-- ABCs, image, call NSGY.

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Abscess/Empyema

- Both are relatively rare complications in the immediate post-operative period.

  • Abscesses: 95% will have NORMAL CSF and will be afebrile. NSGY treats with needle aspiration + IV abx and 85% of the time, this clears the infection.
  • Subdural Empyema: Severe presenting signs and symptoms, happens more often in patients who have had chronic subdural hematomas drained.

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Infarction

Venous infarcts are much more common than arterial because the venous sinuses are often damaged in craniotomy and undergo repair during initial surgery. This places the patient at high risk for cerebral venous thrombosis or dural sinus thrombosis, which then leads to venous infarction.

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Spontaneous (Nontraumatic) Intracerebral Hemorrhage�

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Spontaneous Intracerebral Hemorrhage

Signs and Symptoms

  • Symptoms of increased ICP
  • Neck stiffness

***infants may have very non-specific histories and exam findings

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Spontaneous Intracerebral Hemorrhage

    • Cerebral aneurysm*
    • Cavernous malformation
    • Arteriovenous malformation*

Causes

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Cerebral Aneurysm

Less than 10% of aneurysms present as incidental or unruptured (so any of us might have one…)

Most aneurysms form spontaneously; however, some genetic syndromes are more at risk (Marfan, PCKD, FMD)

Aneurysms are also seen as the result of high energy head trauma leading to artery dissection, hypertension related to aortic coarctation, and Moya Moya Disease

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Cerebral Aneurysm

Imaging:

    • CTA is the best initial screening and diagnostic test (though not as helpful for vessels that run near posterior fossa)
    • MRI/MRA provides higher resolution but is not widely available.
    • Cerebral angiography is the gold standard for diagnosis, however CTA should be performed first to screen due to the invasiveness of the imaging.

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Cerebral Aneurysm

Management:

  1. ABCs
  2. Imaging
  3. Neurosurgery for surgical management including clipping, coiling, or resection

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Cavernous malformation

Cavernomas or cavernous angiomas: vascular channels lined with endothelium only but without the muscular wall structure of arteries or veins.

Imaging: CT is more sensitive (for active bleeding) but less specific. MRI is the preferred modality for diagnosis.

Management: Conservative management and close follow up (no surgery unless signs of elevated ICP); bleeding CMs often present sub-acutely and the bleed is self limited.

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Arteriovenous Malformation

Fistulous connection of arteries and veins without the normal capillary bed

Nearly all AVMs are congenital

Most common presentation is acute hemorrhage, followed by seizure

Responsible for 30-50% of hemorrhagic stroke in kids

Smaller size of AVM is at higher risk of hemorrhage

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Arteriovenous Malformation

Imaging:

CT without contrast to screen for active bleed

If not bleeding, MRI/MRA is the best modality to evaluate to the specific vasculature involved

If bleeding, cerebral angiography is the best modality.

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Arteriovenous Malformation

Surgical Treatments:

  1. Microsurgical resection (*GS)
  2. Endovascular Embolization followed by resection
  3. Stereotactic radiosurgery
  4. Embolize🡪 radiosurgery
  5. Embolize only

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Indications for Microsurgical Resection

  1. SM 1-3 🡪 size and location lends itself to success.
  2. Cerebellar/pons AVMs🡪 high rates of bleeding/death if not
  3. Pediatric patients 🡪 lifetime risk of bleed is high

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Extras!

Not on PEM Boards Content Outline

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Spinal Epidural Hematoma

Usually traumatic but sometimes seen with bleeding disorders, hemorrhagic tumors, spinal AVMs, after lumbar puncture

Present with focal neurologic deficits and back pain

MRI spine is definitive diagnostic measure

Manage with spinal cord decompression AS FAST AS POSSIBLE

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Meningitis

Severe cases may present with increased ICP and hydrocephalus due to increased protein in CSF or obstruction to flow 🡪 CT scan patients with symptoms of increased ICP to avoid herniation during LP

Reason for Surgical Consult: hydrocephalus on CT 🡪 may be an indication for extra-ventricular drain placement and surgical tap

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Discitis/Osteomyelitis

Presentation: prodromal illness, back pain, refusal to walk or sit, hip/leg pain

Diagnostic Evaluation: CBC, ESR, CRP, MRI spine with contrast

Management: Broad spectrum antibiotics IV followed by oral antibiotics for 6-8 weeks

Reasons for Surgery Consult: Refractory infection, epidural abscess with neurologic compromise

MIMIC: Chronic recurrent multifocal osteomyelitis🡪 young girls (5:1), episodic, and nonbacterial. No acute surgical intervention.

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Sources

Agbeko RS, Pearson S, Peters MJ, McNames J, Goldstein B. Intracranial pressure and cerebral perfusion pressure responses to head elevation changes in pediatric traumatic brain injury. Pediatr Crit Care Med. 2012;13(1):e39-e47. doi:10.1097/PCC.0b013e31820ac2ad

Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN. Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. J Neurosurg Pediatr. 2009;4(1):40-46. doi:10.3171/2009.1.PEDS08319

Kochanek PM, Tasker RC, Bell MJ, et al. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019;20(3):269-279. doi:10.1097/PCC.0000000000001737

Kochanek PM, Adelson PD, Rosario BL, et al. Comparison of Intracranial Pressure Measurements Before and After Hypertonic Saline or Mannitol Treatment in Children With Severe Traumatic Brain Injury. JAMA Netw Open. 2022;5(3):e220891. Published 2022 Mar 1. doi:10.1001/jamanetworkopen.2022.0891

Pitfield AF, Carroll AB, Kissoon N. Emergency management of increased intracranial pressure. Pediatr Emerg Care. 2012;28(2):200-207. doi:10.1097/PEC.0b013e318243fb72�Shaw KN, Bachur RG, Chamberlain JM. Fleisher & Ludwig’s Textbook of Pediatric Emergency Medicine. Seventh edition /. (Shaw KN, Bachur RG, Chamberlain JM, eds.). Wolters Kluwer Health; 2016.

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