Neurosurgery Flashcards
1
Q
What type of brain bleed is this?
A
Extradural “Epidural” haematoma
2
Q
What is the cause of an extradural haematoma?
A
- Temporal-parietal skull fracture: 85% are due to ruptured middle meningeal artery
- Remainder of cases are due to bleeding from middle meningeal vein, dural sinus, or bone/diploic veins
3
Q
What are the clinical features of a extradural haematoma?
A
- classic sequence (seen in <30%):
- post-traumatic reduced LOC → a lucid interval of several hours → then obtundation, hemiparesis, ipsilateral pupillary dilatation, and coma
- signs and symptoms depend on severity but can include H/A, N/V, amnesia, altered LOC, aphasia, seizures, HTN, and respiratory distress
- deterioration can take hours to days
4
Q
What is seen on CT with a extradural haematoma?
A
- “lenticular-shaped” usually limited by suture lines but not limited by dural attachments
5
Q
What is the Rx for a extradural haematoma?
A
- admission, close neurological observation with serial CT indicated if all of the following are present:
- small volume clot, minimal midline shift (MLS <5 mm), GCS >8, no focal deficit
- otherwise, craniotomy to evacuate clot, follow up CT
- mannitol pre-operative if elevated ICP or signs of brain herniation
6
Q
What is the prognosis of an extradural haematoma?
A
- good with prompt management, as the brain is often not damaged
- worse prognosis if bilateral Babinski or decerebration pre-operative
- death is usually due to respiratory arrest from uncal herniation (injury to the midbrain)
7
Q
What are poor prognostic indicators for an extradural haematoma?
A
- Older age
- Low GCS on admission
- Pupillary abnormalities (especially non-reactive)
- Longer delay in obtaining surgery (if needed)
- Post-operative elevated ICP
8
Q
What type of haematoma is this?
A
Subdural haematoma
9
Q
What is the cause of an acute subdural haematoma?
A
- rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, venous sinus) or cerebral laceration
10
Q
How are subdural haematomas classified?
A
- Acute: 1-2 days after bleeding onset
- Chronic: ≥ 15 days after bleeding onset
11
Q
What are the risk factors for an acute subdural haematoma?
A
- trauma
- acceleration-deceleration injury
- anticoagulants
- alcohol
- cerebral atrophy
- infant head trauma
12
Q
What are the clinical features of an acute subdural haematoma?
A
- no lucid period
- signs and symptoms: can include altered LOC, pupillary irregularity, hemiparesis
13
Q
What is seen on CT in an acute subdural haematoma?
A
hyperdense concave “crescentic” mass, crossing suture lines
14
Q
What is the Rx for an acute subdural haematoma?
A
- craniotomy if clinically symptomatic, if hematoma >1 cm thick, or if MLS >5 mm (optimal if surgery <4 h from onset)
- otherwise observe with serial imaging
15
Q
What is the prognosis of an acute subdural haematoma?
A
- poor overall since the brain parenchyma is often injured (mortality range is 50-90%, due largely to underlying brain injury)
- prognostic factors: initial GCS and neurologic status, post-operative ICP
16
Q
What is the cause of a chronic subdural haematoma?
A
- many start out as acute SDH
- blood within the subdural space evokes an inflammatory response:
- fibroblast invasion of clot and formation of neomembranes within days → growth of
neocapillaries → fibrinolysis and liquefaction of blood clot (forming a hygroma)
- fibroblast invasion of clot and formation of neomembranes within days → growth of
- course is determined by the balance of rebleeding from neomembranes and resorption of fluid
17
Q
What are the risk factors for a chronic subdural haematoma?
A
- older
- alcoholics
- patients with CSF shunts
- anticoagulants
- coagulopathies
18
Q
What are the clinical features of a subdural haematoma?
A
- often due to minor injuries or no history of injury
- may present with minor H/A, confusion, language difficulties, TIA-like symptoms, symptoms of raised ICP ± seizures, progressive dementia, gait problem
- obtundation disproportionate to focal deficit; “the great imitator” of dementia, tumors
19
Q
What is seen on CT in a chronic subdural haematoma?
A
hypodense (liquefied clot), crescentic mass
20
Q
What is the Rx for a chronic subdural haematoma?
A
- seizure prophylaxis only if post-traumatic seizure
- reverse coagulopathies
- burr hole drainage of liquefied clot indicated if symptomatic or thickness >1 cm; craniotomy if recurs more than twice
21
Q
What is the prognosis of a chronic subdural haematoma?
A
good overall as brain usually undamaged, but may require repeat drainage
22
Q
What type of brain bleed is this?
A
Subarachnoid haemorrhage
23
Q
What is the cause of subarachnoid haemorrhages?
A
- trauma (most common)
- spontaneous
- ruptured aneurysms (75-80%)
- idiopathic (14-22%)
- AVMs (4-5%)
- coagulopathies (iatrogenic or primary), vasculitides, tumors, cerebral artery dissections (<5%)
24
Q
What are the risk factors for a subarachnoid haemorrhage?
A
- HTN
- pregnancy/parturition in patients with pre-existing AVMs, eclampsia
- oral contraceptive pill
- substance abuse (cigarette smoking, cocaine, alcohol)
- conditions associated with high incidence of aneurysms
25
Q
What are the clinical features of spontaneous subarachnoid haemorrhage?
A
- sudden onset (seconds) of severe “thunderclap” H/A usually following exertion and described as the “worst headache of my life” (up to 97% sensitive, 12-25% specific)
- N/V, photophobia
- meningismus (neck pain/stiffness, positive Kernig’s and Brudzinski’s sign)
- decreased LOC (due to either raised ICP, ischemia, seizure)
- focal deficits: cranial nerve palsies (CN III, IV), hemiparesis
- ocular hemorrhage in 20-40% (due to sudden raised ICP compressing central retinal vein)
- reactive HTN
- sentinel bleeds
- represents undiagnosed SAH
- SAH-like symptoms lasting <1 d (“thunderclap H/A”)
- may have blood on CT or LP
- ~30-60% of patients with full blown SAH give history suggestive of sentinel bleed within past 3 wk
- differential diagnosis: sentinel bleed, dissection/thrombosis of aneurysm, venous sinus thrombosis, benign cerebral vasculitis, benign exertional H/A
26
Q
What Ix need to be order for a suspected subarachnoid haemorrhage?
A
- non-contrast CT – for diagnosis of SAH
- 98% sensitive within 12 h, 93% within 24 h; 100% specificity
- may be negative if small bleed or presentation delayed several days
- acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible
- lumbar puncture (highly sensitive) – for diagnosis of SAH if CT negative but high suspicion:
- elevated opening pressure (>18 cmH 2 O)
- bloody initially, xanthochromic supernatant with centrifugation (“yellow”) by ~12 h, lasts 2 wk
- RBC count usually >100,000/mm 3 without significant drop from first to last tube (in contrast to traumatic tap)
- elevated protein due to blood breakdown products
- four vessel cerebral angiography (“gold standard” for aneurysms)
- demonstrates source of SAH in 80-85% of cases
- angiogram negative SAH: repeat angiogram in 7-14 d, if negative → “perimesencephalic SAH”
- MRA and CTA: sensitivity up to 95% for aneurysms, CTA>MRA for smaller aneurysms and delineating adjacent bony anatomy
27
Q
What is the Rx for a subarachnoid haemorrhage?
A
- admit to ICU or NICU
- oxygen/ventilation prn
- NPO, bed rest, elevate head of bed 30º, minimal external stimulation, neurological vitals q1h
- aim to maintain sBP = 120-150 (balance of vasospasm prophylaxis, risk of re-bleed, risk of hypotension since CBF autoregulation impaired by SAH)
- cardiac rhythm monitor, Foley prn, strict monitoring of ins and outs
- medications
- IV NS with 20 mEq KCl/L at 125-150 cc/h
- nimodipine 60 mg PO/NG q4h x 21 d for delayed cerebral ischemia neuroprotection; may discontinue earlier if patient is clinically well
- seizure prophylaxis: levetiracetam (Keppra®) 500 mg PO/IV q12h x 1 wk
- mild sedation prn
28
Q
What are the complications of subarachnoid haemorrhage?
A
- vasospasm: vasoconstriction and permanent pathological vascular changes in response to vessel irritation by blood – can lead to delayed cerebral ischemia and death
- onset: 4-14 d post-SAH, peak at 6-8 d; most commonly due to SAH, rarely due to ICH/IVH
- clinical features (new onset ischemic deficit): confusion, decreased LOC, focal deficit (speech or motor e.g. pronator drift)
- risk factors: large amount of blood on CT (high Fisher grade), smoking, increased age, HTN
- “symptomatic” vasospasm in 20-30% of SAH patients
- “radiographic” vasospasm in 30-70% of arteriograms performed 7 d following SAH
- diagnosed clinically, and/or with transcranial Doppler (increased velocity of blood flow)
- risk of cerebral infarct and death
- treatment
- hyperdynamic (“triple H”) therapy using fluids and pressors, usually after ruptured aneurysm has been clipped/coiled
- direct vasodilation via angioplasty or intra-arterial verapamil for refractory cases
- hydrocephalus (15-20%): due to blood obstructing arachnoid granules
- can be acute or chronic, requires extraventricular drain (EVD) or shunt, respectively
- neurogenic pulmonary oedema
- hyponatremia: due to cerebral salt wasting (increased renal sodium loss and ECFV loss), not SIADH
- diabetes insipidus
- cardiac: arrhythmia (>50% have ECG changes), MI, CHF
29
Q
What is the ‘triple H’ therapy for vasospasm in subarachnoid haemorrhage?
A
- HTN
- Hypervolaemia
- Haemodilution
30
Q
What is the prognosis of a subarachnoid haemorrhage?
A
- 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 wk)
- 30% of survivors have moderate to severe disability
- a major cause of mortality is rebleeding, for untreated aneurysms:
- risk of rebleed: 4% on first day, 15-20% within 2 wk, 50% by 6 mo
- if no rebleed by 6 mo, risk decreases to same incidence as unruptured aneurysm (2%)
- only prevention is early clipping or coiling of “cold” aneurysm
- rebleed risk for “perimesencephalic SAH” is approximately same as for general population
31
Q
A
