Neurosurgery Flashcards
What can cause compression of the spinal cord?
Compression of the spinal cord can be due to:
- Trauma
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Non-traumatic causes:
- Tumours - both primary and metastatic tumours
- Infection - staphylococcal abscess, tuberculoma.
- Prolapsed intervertebral disc (central).
- Cyst: arachnoid, syringomyelia.
- Haemorrhage.
- Skeletal deformity: kyphoscoliosis, achondroplasia, spondylolisthesis.
Describe the presentation of cord compression
- Back pain: is usually the first symptom. It often starts weeks before other features and becomes progressively unremitting, keeping the patient awake at night. There may also be thoracic dermatomal pain which is misinterpreted and leads to a long and unrewarding search for the cause of chest or abdominal pain.
- Sensory symptoms: such as paraesthesiae or a sensation of limb heaviness or pulling, may then occur.
- Sensory loss: may be apparent as a sensory level on testing. It is wise to test for pin-prick (spinothalamic function) and joint position sense/vibration sense (dorsal column function)—anterior or posterior portions of the cord may be selectively compressed.
- Weakness: is often first described as clumsiness but soon progresses to clear loss of power.
- Autonomic dysfunction: if the sympathetic pathways are involved, especially in high thoracic or cervical lesions, hypotension, bradycardia, or sometimes cardiac arrest may occur. This may be triggered by noxious stimuli such as pain, UTI, or abdominal distension caused by constipation or bladder outflow obstruction.
- Sphincter dysfunction: commences as hesitancy or urgency of micturition and may progress to painless urinary retention with overflow. Constipation is another consequence of cord compression.
- Respiratory failure: occurs with high cervical cord compression and is one cause of acute neuromuscular respiratory paralysis.
Fever should alert one to the possibility of an infectious cause.
Can also present as conus or cauda equina syndrome
What are the red flags / clinical features of cauda equina syndrome?
Cauda equina lesions present with LMN signs - leading to a flaccid, flexic, and often asymmetric paraparesis. Lumbosacral pain occurs early; bladder and bowel dysfunction appears relatively late. A sensory level is found in a saddle distribution up to L1 (corresponding to roots carried in the cauda equina). The red flags of cauda equina syndrome are:
- Bilateral sciatica (raidculopthy of lumper nerve roots)
- Progressive evolving neurology
- Saddle anaesthesia (numbness over genitals and inner buttocks)
- Urinary symptoms
- Bowel symptoms
Describe the assessment and management of cord compression
A thorough neurological examination is important to localise the pathology (I.e. at what nerve root) and a history is important to determine the cause. A general examination is also very important - remember that a common cause is malignant compression from metastatic disease. Perform a careful examination, including the breasts, testicles, and thyroid if appropriate.
If spinal cord compression is a differential, organise an urgent MRI, CXR (? malignancy).
If the cause appears to be infective (fever, neutrophilia, raised CRP): send blood, sputum, and urine cultures.
Discuss the case with the regional neurosurgical centre, and consult a senior oncologist regarding advice for urgent radiotherapy for neoplastic disease and malignant compression. For non-malignant causes, patients should be treated with corticosteroids (bolus of dexamethasone IV).
- Control pain and act to prevent constipation.
- Urinary catheterization if there is bladder dysfunction.
- Prophylactic SC heparin if immobile.
- Monitor ABG and FVC in cases of high cervical compression or compromise.
- Monitor haemodynamics and watch for autonomic dysfunction.
What is the aetiology of raised intracranial pressure (ICP)?
Causes of raised intracranial pressure:
- Idiopathic intracranial hypertension
- CNS inflammation, infection, and/or abscess
-
Space-occupying lesions
- Intracranial haemorrhage or hematoma
- Aneurysm
- Intracranial tumours
- Elevated venous pressure (e.g., as a result of heart failure)
- Increased CSF (hydrocephalus)
- Metabolic disturbances (e.g., hyponatremia, hepatic encephalopathy)
- Epilepsy and seizures
What is the normal physiological intracranial pressure?
Physiological ICP is ≤ 15 mm Hg in adults (in supine position), children generally have a lower ICP
- ICP varies with the relative position of the head towards the rest of the body and is influenced by certain physiological processes (e.g., cardiac contractions, sneezing, coughing, Valsalva maneuver).
What are the physiological consequences of raised intracranial pressure (ICP)?
- Decreased cerebral perfusion pressure (CPP). CPP is the effective pressure that delivers blood to the cerebral tissue. CPP = mean arterial pressure - ICP. Therefore, if the ICP rises, the CPP diminishes (as long as the arterial pressure remains constant).
-
Herniation. As a bony structure, the skull is rigid and can not expand to compensate elevated internal pressure.
- This may result in direct physical damage or in blocking of cerebral vessels and subsequent ischemia.
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Cushing triad.
- ↑ Intracranial pressure → decreased perfusion pressure within the brain → compensatory activation of the sympathetic nervous system to maintain cerebral perfusion → increase systolic blood pressure
- This leads to stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia
- ↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing (Cheyne Stokes style respiration).
What are the clinical features of raised intracranial pressure (ICP)?
- Cushing’s triad: irregular breathing, widening pulse pressure and bradycardia
- Reduced levels of consciousness
- Headache
- Vomiting
- Papilloedema
- Psychiatric changes
In infants: macrocephaly, bulging fontanel, sunset sign.
What are the investigations for raised intracranial pressure (ICP)?
CT/MRI: may indicate mass lesions, midline shift, or effacement of the basilar cisterns
Invasive ICP monitoring may be useful in patients who are at high risk of developing raised ICP, such as those with trauma or intracranial haemorrhage. Intraventricular monitors are the gold standard.
- > 20 mmHg indicates elevated intracranial pressure that requires treatment
Describe the acute management of raised intracranial pressure (ICP)
To acutely reduce ICP:
- Head elevation
- Controlled hyperventilation. Cerebral blood flow is largely dependent on PaCO2. Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP.
- IV mannitol
Patients also need:
- Cardiopulmonary support
- Sedation, analgesia, antipyretic therapy, antiseizure medication
Describe the post-acute management of raised intracranial pressure (ICP)
Goal of ICP management is generally to keep ICP < 20 mm Hg.
- Positioning : e.g., head elevation (about 30 degrees), avoiding neck flexion/rotation or circumstances that may provoke Valsalva responses.
- Fluid management: patients should be euvolemic, blood hypoosmolarity should be avoided
- Hyperventilation: up to a pCO2 of 26–30 mm Hg
- Hypothermia
Causal treatment (e.g., removal of brain tumor) if possible
Medical therapy - osmotic diuretics draw water out of the brain and into the blood from which it can be excreted in the urine:
- IV mannitol: can generally be administered every 6–8 hours, effects last for up to 24 hours
- IV hypertonic saline: particularly for short-term treatment
Removal of CSF via an intraventricular monitor with drainage system (e.g., external ventricular drain or lumbar drain) or a cerebral shunt (e.g., in hydrocephalus patients).
What is the definition and epidemiology of idiopathic intracranial hypertension?
Idiopathic intracranial hypertension (also known as pseudotumour cerebri and formerly benign intracranial hypertension) is a condition classically seen in young, overweight females characterised by chronically elevated intracranial pressure (ICP).
What are the clinical features of raised idiopathic intracranial hypertension?
Patients present with:
- Diffuse headaches
- Visual symptoms including blurred vision (due to papilloedema), photopsia (seeing flashes of light), diplopia and retrobulbar pain.
- Pulsatile tinnitus
Also may present with sixth nerve palsy (abducens nerve) due to it being tethered as its exits the pons and inside Dorello’s canal.
What are the investigations for raised intracranial pressure (ICP)?
The following tests should always be performed:
- Ophthalmologic examination which may show bilateral papilledema. Visual field test may show peripheral loss of vision
- MRI to rule out other causes of increased ICP
- Lumbar puncture: elevated opening pressure >20-25 cm H2O (with patient lying on the side, legs extended). Normal CSF analysis with no signs of inflammation or bleeding.
Describe the management of raised idiopathic intracranial hypertension
- Weight loss
-
Medical (first-line):
- Diuretics e.g. acetazolamide (carbonic anhydrase inhibitor)
- Topiramate is also used, and has the added benefit of causing weight loss in most patients
-
Surgery:
- Optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
- A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
