Neurological emergencies Flashcards
1
Q
What is status epilepticus? What are its causes?
A
- Recurrent seizures without recovery in between, or a single seizure lasting more than 30 mins
- Can cause: Cerebral damage: Failure of compensatory mechanisms /autoregulation
- Excitotoxicity , local hypoxia, metabolite accumulation
- Consider a pre-existing diagnosis of Epilepsy: AED withdrawal, Non-compliance, alcohol use and withdrawal; illicit drugs, infection
- Progression of underlying disease - tumour, encephalitis, vasculitis
- NB: Non-epileptic attacks (NEAD) – prolonged seizures, frequency, normal lactate, psych history
- Causes in those with no history of epilepsy: Cerebral Tumour, Intracranial Infection, Hypoglycaemia, Head Injury, Illicit drugs, Drug withdrawal (alcohol), hypoxia, stroke, electrolyte disturbance (Na, Ca, Mg)
2
Q
What signs are important for an A-E in status epilepticus?
A
- A - Airway – if compromised it needs arrest call and ITU/ anaesthetist
- B – difficult to assess. Sats can be unreliable but Monitor SaO2, give high flow O2
- C – fluids, Bloods: U&E’s, glucose, Ca, Mg, LFT’s, FBC, CRP/ cultures, clotting screen ABG if possible, anticonvulsant levels (if pt was on anti epileptics), toxicology screen, ECG
- ABG - Typical pattern: acidotic, lactate high, glucose OK, 02 can be low
- D – No GCS possible but DEFG: GLUCOSE! BM-10% or 50% glucose if low
3
Q
How is status epilepticus managed?
A
Begin mx after 5 mins of seizure activity
4
Q
What is idiopathic intracranial hypertension? How does it present?
What are its associations?
A
- Most commonly seen in obese females in 3rd decade
- Presentation: narrowed visual fields, blurred vision ± diplopia, vith nerve palsy, and an enlarged blind spot, if papilloedema is present
- Consciousness and cognition are preserved.
- Associations - Endocrine abnormalities (Cushing’s syndrome, hypoparathyroidism, ↑↓tsh), sle, ckd, ida, prv, drugs (tetracycline, steroids, nitrofurantoin, and oral contraceptives).
5
Q
How is IIH managed?
A
- Conservative: Weight loss
- Medical: acetazolamide or topiramate, loop diuretics, and prednisolone (more se than diuretics)
- Surgery: last resort - optic nerve sheath fenestration or lumbar–peritoneal shunt
6
Q
What is normal pressure hydrocephalus and how does it present?
A
- Wobbly: Apraxic gait the way a person walks “on a boat,” with the body bent forward, legs held wide apart and feet moving as if they’re “glued to the deck.”
-
Weird:
- Mild dementia: loss of interest in daily activities, forgetfulness, difficulty completing routine tasks, short-term memory loss.
- Decline in thinking skills that includes overall slowing of thought processes, apathy, impaired planning and decision-making, reduced concentration, and changes in personality and behavior.
- Wet: urinary incontinence (later in disease)
7
Q
How do subdural haemorrhages arise?
A
- Rupture of the bridging veins in the outermost meningeal layer (between the dura and arachnoid)
- Presentation: raised ICP, shifting midline structures away from the side of the clot and, if untreated, eventual tentorial herniation and coning
- Cause: high impact trauma – sometimes minor or long time ago
- Who: elderly (more atrophy – vessels more likely to rupture) or alcoholic patients
8
Q
How does subdural haemorrhage present? Signs and sx?
A
- Sx: Fluctuating level of consciousness ± insidious physical or intellectual slowing, sleepiness, headache, personality change, and unsteadiness.
- Signs: raised ICP, seizures. Localizing neurological symptoms (eg unequal pupils, hemiparesis) occur late, often >1 month after the injury.
9
Q
How are subdural haemorrhages investigated and managed?
A
- Ix: CT/ MRI: banana (crescent shape collection of blood – unilateral) and are not limited by the cranial sutures (they can cross over the sutures).
- Mx: Conservative: address cause
- Medical – urgent reversal of clotting abnormalities
-
Surgery:
- Acute: decompressive craniectomy
- Chronic: conservative (if no deficit); a surgical decompression if clot size: >10mm or midline shift – depressive – craniotomy or burr hole washout
10
Q
What is an extra dural haemorrhage? Who is it most likely to occur in
A
- Associations: fracture of temporal bone - typically after trauma to a temple just lateral to the eye
- Presentation: young patient with a traumatic head injury, ongoing headache
11
Q
What are some of the signs and symptoms of extradural haemorrhages?
A
- Lucid interval: few hours to a few days before a bleed declares itself by ↓GCS from rising ICP
- Increasingly severe headache, vomiting, confusion, and seizures follow, ± hemiparesis with brisk reflexes and an upgoing plantar.
- If bleeding continues, the ipsilateral pupil dilates, coma deepens, bilateral limb weakness develops, and breathing becomes deep and irregular (brainstem compression)
12
Q
What Ix and mx are used for subdural haemorrhages?
A
- Ix: CT: lemon (bi-convex shape and are limited by the cranial sutures)
- Mx: Surgical: stabilize and transfer neurosurgical unit for clot evacuation ± ligation of the bleeding vessel + craniotomy
- Medical: Care of the airway in an unconscious patient
- Reduce ↓ICP: I+V (+ mannitol ivi)
- Medical: Care of the airway in an unconscious patient
13
Q
What are the causes of a SAH?
A
- Pathophysiology: Subarachnoid haemorrhage involves bleeding in to the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured cerebral aneurysm.
- Causes: usually cerebral aneurysm
14
Q
What are the signs + sx of SAH?
A
- Px: sudden onset occipital headache worse from strenuous activity (e.g. sex or exercise), - thunder clap
- Vomiting, collapse, seizures, and coma often follow, Coma/drowsiness may last for days
- Neurological Sx such as speech changes, weakness, seizures and loss of consciousness
- Signs: neck stiffness, kernigs sign (6h to develop), retinal, subhyaloid and vitreous bleeds
- Sentinel headache: pts may earlier have experiences a sentinel headache, perhaps due to small warning leak from offending aneurysm
- Focal neurological deficit: (eg pupil changes indicating a 3rd nerve palsy with a posterior communicating artery aneurysm) or intracerebral haematoma – can help localise
- Signs: neck stiffness, kernigs sign (6h to develop), retinal, subhyaloid and vitreous bleeds
15
Q
What are some of teh causes of spontaneous SAH?
A
- Intracranial aneurysm* (saccular ‘berry’ aneurysms): this accounts for around 85% of cases. Conditions: PCKD, Ehlers-Danlos syndrome and coarctation of the aorta
- Arteriovenous malformation
- Pituitary apoplexy
- Arterial dissection
- Mycotic (infective) aneurysms
- Perimesencephalic (an idiopathic venous bleed)
19
Q
How is a head injury managed?
A
