Surgery: NeuroSurgery Flashcards

1
Q

Criteria for Brain Stem Death

A
  • Deep Coma: Patient in a deep coma with a known cause.
  • Reversible Causes Excluded: Rule out reversible causes.
  • No Sedation: Patient should not be under sedation.
  • Normal Electrolytes: Confirm normal electrolyte levels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Testing for Brain Death

A

Fixed Pupils: Pupils don’t respond to light changes.
No Corneal Reflex: Absence of corneal reflex.
Absent Oculo-Vestibular Reflexes: No eye movements after injecting ice-cold water into each ear.
No Response to Supraorbital Pressure: Lack of response to pressure.
No Cough Reflex: No cough reflex to bronchial stimulation.
Absence of Gagging Response: No gagging response to pharyngeal stimulation.
No Observed Respiratory Effort: No respiratory effort upon ventilator disconnection for at least 5 minutes.
Conditions: Arterial partial pressure of carbon dioxide elevated to at least 6.0 kPa (6.5 kPa in chronic CO2 retention).
Precautions: Adequate oxygenation to avoid anoxic drive stimulus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Testing procedure for brain death

A

Conducted by two experienced doctors on separate occasions.
Both doctors must have at least 5 years of post-graduate experience.
One doctor must be a consultant.
Neither doctor can be a member of the transplant team if organ donation is considered.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is brain herniation

A

Definition: Herniation results from elevated intracranial pressure, forcefully displacing normal brain structures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Consequences and urgency of brain herniation

A

Consequences:
Decompensation of normal brain anatomy.
Compression of vital structures, especially the brain stem.
Urgency:
Neurosurgical emergency requiring immediate intervention.
Interventions may include osmotherapy (hypertonic saline or mannitol) or surgical decompression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Types of Herniation

A

Subfalcine: Cingulate gyrus under the falx cerebri.
Central: Downward brain displacement.
**Transtentorial/Uncal: **Uncus displacement under the tentorium cerebelli.

Consequences: Ipsilateral fixed, dilated pupil; contralateral paralysis.
Tonsillar (Coning): Cerebellar tonsils through the foramen magnum.
ICP Impact: Compression of cardiorespiratory center.
Chiari 1 Malformation: Tonsillar herniation without raised ICP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Transcalvarial Herniation

A

Definition: Brain displacement through a skull defect (e.g., fracture or craniotomy site).
Clinical Significance: Represents a distinct type of herniation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Coning

A

Flashcard: Coning
- ICP Accommodation:
- Cranial vault is confined.
- Initial ICP rises accommodated by CSF shifts.

  • Brisk ICP Rise:
    • Once CSF capacity exhausted, ICP rises rapidly.
  • Autoregulation and Circulation Changes:
    • Brain autoregulates blood supply.
    • Rising ICP prompts systemic circulation changes, often hypertension.
  • Severe Consequences:
    • Brain compression, nerve palsies, and brain stem compression.
    • Cardiac center involvement leads to bradycardia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

General approach to head injury management

A

General Approach:
Manage according to ATLS principles.
Address extracranial injuries alongside cranial trauma.
Inadequate cardiac output compromises CNS perfusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Types of traumatic brain injury

A

Extradural Hematoma:
Bleeding between dura mater and skull.
Features: Raised ICP, possible lucid interval.
Subdural Hematoma:
Bleeding into outermost meningeal layer.
Risk factors: Old age, alcoholism.
Subarachnoid Hemorrhage:
Often spontaneous or associated with traumatic brain injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pathophysiology of Brain Injury

A

Primary Injury:
Focal (contusion/haematoma) or diffuse (axonal injury).
Secondary Injury:
Cerebral edema, ischemia, herniation.
Cushing’s Reflex (Late):
Hypertension and bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management of brain injury

A

Extradural Hematoma:
IV mannitol/frusemide for life-threatening rising ICP.
Diffuse Cerebral Edema:
Decompressive craniotomy.
Skull Fractures:
Surgical reduction for open fractures; nonoperative for closed with minimal displacement.
ICP Monitoring:
GCS 3-8 with abnormal CT.
Cerebral Perfusion Pressure (CPP):
Maintain minimum: 70mmHg in adults, 40-70 mmHg in children.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pupillary findings on brain injury

A

Unilaterally Dilated:
Tentorial herniation.
Bilaterally Dilated:
Poor CNS perfusion or 3rd nerve palsy.
Unilaterally Dilated or Equal:
Cross-reactive (Marcus-Gunn): Optic nerve injury.
Bilaterally Constricted:
Opiates, pontine lesions, metabolic encephalopathy.
Unilaterally Constricted:
Sympathetic pathway disruption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CT Head Within 1 Hour - Indications

A

GCS < 13 on initial assessment.
GCS < 15 at 2 hours post-injury.
Suspected open or depressed skull fracture.
Signs of basal skull fracture (e.g., haemotympanum, ‘panda’ eyes, CSF leakage, Battle’s sign).
Post-traumatic seizure.
Focal neurological deficit.
More than 1 episode of vomiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

CT Head Within 8 Hours - Risk Factors

A

Age 65 years or older.
History of bleeding or clotting disorders, including anticoagulants.
Dangerous mechanism of injury (e.g., pedestrian/cyclist struck by a vehicle, occupant ejected from a vehicle, fall from a height >1 meter or 5 stairs).
More than 30 minutes’ retrograde amnesia after the head injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Special Consideration for Warfarin Patients

A

Perform CT head scan within 8 hours for head injury, even with no other indications.

17
Q

Types of Traumatic Brain Injury - Basics

A

Primary Brain Injury:

Focal (contusion/haematoma) or diffuse (diffuse axonal injury).
Diffuse axonal injury results from mechanical shearing, causing axonal disruption and tearing.
Intracranial Hematomas and Contusions:

Extradural, subdural, or intracerebral hematomas.
Contusions may be adjacent (coup) or contralateral (contre-coup) to the impact side.
Secondary Brain Injury:

Occurs due to cerebral edema, ischemia, infection, herniation.
Disrupted cerebral auto-regulatory processes increase susceptibility to blood flow changes and hypoxia.
Cushing’s Reflex:

Late occurrence, usually pre-terminal event.
Manifests as hypertension and bradycardia.

18
Q

Types of Traumatic Brain Injury - Specific Injuries

A

Extradural (Epidural) Hematoma:

Bleeding between dura mater and skull.
Often from acceleration-deceleration trauma or side head blow.
Features: Raised intracranial pressure, possible lucid interval.
Subdural Hematoma:

Bleeding into outermost meningeal layer.
Risk factors: Old age, alcoholism, anticoagulation.
Slower onset than epidural hematoma; fluctuating confusion/consciousness.
Subarachnoid Hemorrhage:

Sudden occipital headache.
Spontaneous or associated with traumatic brain injury.

19
Q

Types of Traumatic Brain Injury - Intracerebral Hematoma

A

Intracerebral Hematoma:
Collection of blood within brain substance.
Causes/risk factors: Hypertension, vascular lesions, trauma, tumors, infarcts.
Presentation similar to ischemic stroke or decreased consciousness.
CT imaging shows hyperdensity.
Treatment: Conservative under stroke physicians; surgical evacuation for large clots in impaired consciousness.

20
Q

Hydrocephalus Overview

A

Definition:

Excessive cerebrospinal fluid (CSF) volume in the brain ventricular system.
Caused by an imbalance between CSF production and absorption.
Presentation:

Symptoms due to raised intracranial pressure.
Headache (worse in the morning, lying down, during Valsalva).
Nausea, vomiting, papilloedema, coma (severe cases).

21
Q

Hydrocephalus in Infants

A

Infant Presentation:

Skull sutures not fused; rise in pressure increases head circumference.
Bulging, tense anterior fontanelle.
Failure of upward gaze (‘sunsetting’ eyes) in severe cases.
Categories:

Obstructive (non-communicating) hydrocephalus.
Non-obstructive (communicating) hydrocephalus.

22
Q

Obstructive vs. Non-Obstructive Hydrocephalus

A

Obstructive Hydrocephalus:

Structural pathology blocks CSF flow.
Ventricular dilatation seen superior to the obstruction.
Causes: Tumors, acute hemorrhage, developmental abnormalities.
Non-Obstructive Hydrocephalus:

Imbalance in CSF production/absorption.
Causes: Increased CSF production or reabsorption failure.
Includes normal pressure hydrocephalus with dementia, incontinence, disturbed gait.

23
Q

Investigation and Treatment of hydroc

A

Investigation:

CT head as first-line imaging.
MRI for detailed investigation, especially for suspected underlying lesions.
Lumbar puncture for diagnosis and therapeutic drainage in some cases.
Treatment:

External ventricular drain (EVD) for acute, severe hydrocephalus.
Ventriculoperitoneal shunt (VPS) for long-term CSF diversion.
Surgical treatment for obstructive hydrocephalus.
Note:

Caution with Lumbar Puncture:
Must not be used in obstructive hydrocephalus.
Induced pressure difference may cause brain herniation.

24
Q

Subarachnoid Hemorrhage (SAH) Overview

A

Definition:

Intracranial hemorrhage in the subarachnoid space, deep to the meninges.
Distinguished into traumatic SAH (head injury) and spontaneous SAH (non-traumatic).
Spontaneous SAH Causes:

Intracranial aneurysm (85% of cases).
Conditions associated with aneurysms: Hypertension, polycystic kidney disease, Ehlers-Danlos syndrome, coarctation of the aorta.
Arteriovenous malformation, pituitary apoplexy, mycotic aneurysms.

25
Q

Clinical Presentation and Investigation

SAh

A

Presenting Features:

Sudden-onset severe headache (‘thunderclap’).
Occipital pain peaking within 1 to 5 minutes.
Nausea, vomiting, meningism, coma, seizures, ECG changes.
Investigation:

Non-contrast CT head is the first-line.
CT shows blood in basal cisterns, sulci, and ventricular system.
Lumbar puncture if CT done >6 hours after onset, showing normal results.

26
Q

Management of Aneurysmal SAH

A

Supportive Measures:

Bed rest, analgesia, thromboembolism prophylaxis.
Discontinue antithrombotics, if present.
Oral nimodipine to prevent vasospasm.
Prompt Intervention for Aneurysms:

Most aneurysms treated with coil by interventional neuroradiologists.
Some require craniotomy and clipping by a neurosurgeon.

27
Q

Complications and Predictive Factors SAh

A

Complications:

Re-bleeding (10% cases, high mortality).
Hydrocephalus (temporary external ventricular drain or long-term shunt).
Vasospasm (delayed cerebral ischemia, 7-14 days post-onset).
Hyponatremia (e.g., SIADH), seizures.
Predictive Factors:

Conscious level on admission.
Age.
Amount of visible blood on CT head.