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Year 4 > Neurosurgery > Flashcards

Neurosurgery Flashcards

1
Q

What type of brain bleed is this?

A

Extradural “Epidural” haematoma

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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
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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
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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
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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
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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)
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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
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8
Q

What type of haematoma is this?

A

Subdural haematoma

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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
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10
Q

How are subdural haematomas classified?

A
  • Acute: 1-2 days after bleeding onset
  • Chronic: ≥ 15 days after bleeding onset
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11
Q

What are the risk factors for an acute subdural haematoma?

A
  • trauma
  • acceleration-deceleration injury
  • anticoagulants
  • alcohol
  • cerebral atrophy
  • infant head trauma
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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
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13
Q

What is seen on CT in an acute subdural haematoma?

A

hyperdense concave “crescentic” mass, crossing suture lines

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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
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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
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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)
  • 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

Year 4 (25 decks)

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