subarachnoid haemorrhage Flashcards

(45 cards)

1
Q

What does subarachnoid hemorrhage (SAH) refer to?

A

Bleeding into the subarachnoid space

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2
Q

What percentage of subarachnoid hemorrhage cases are nontraumatic or spontaneous?

A

5–10%

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3
Q

What is the most common cause of nontraumatic subarachnoid hemorrhage?

A

Rupture of an aneurysm involving the circle of Willis

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4
Q

What are common symptoms of nontraumatic SAH?

A

Sudden and severe headache, nausea, vomiting, signs of meningism, acute loss of consciousness

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5
Q

What is the best initial diagnostic test for SAH?

A

Head CT without contrast

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6
Q

How does acute subarachnoid bleeding appear on a head CT?

A

As hyperdensities in the subarachnoid space

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7
Q

What additional tests may be necessary if clinical suspicion of SAH remains high after a negative CT?

A

Lumbar puncture or CT angiography

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8
Q

What is always necessary once SAH is confirmed?

A

Angiography to identify the source of bleeding

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9
Q

What are some potential sources of bleeding in SAH?

A

Aneurysms or other vascular abnormalities

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10
Q

What does the management of SAH mostly consist of?

A

Neuroprotective measures, such as control of blood pressure

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11
Q

What is indicated in aneurysmal SAH to prevent potentially fatal rebleeding?

A

Microsurgical clipping or endovascular coiling of the aneurysm

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12
Q

What is a significant complication associated with aneurysmal SAH?

A

Rebleeding and delayed cerebral ischemia
high mortality rate

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13
Q

What is the best initial test for suspected subarachnoid hemorrhage (SAH)?

A

Immediate head CT without contrast

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14
Q

What is the follow-up procedure after confirming SAH?

A

Obtain angiography to confirm source of bleeding and plan treatment

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15
Q

What should be done if the head CT is nondiagnostic but suspicion of SAH persists?

A

Perform second-line diagnostic tests: lumbar puncture or CTA

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16
Q

In a neurologically intact patient, what does a nondiagnostic CT in the first 6 hours indicate?

A

SAH unlikely; consider other differential diagnoses

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17
Q

What are the second-line tests for suspected SAH?

A

Lumbar puncture (LP) or CT angiography (CTA)

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18
Q

What is the implication of a positive CT angiography (CTA)?

A

Consider if additional angiographic imaging is necessary (e.g., DSA, MRA) and plan intervention

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19
Q

What does a negative CT angiography (CTA) suggest?

A

SAH can be ruled out; consider other diagnoses
If suspicion remains high (rare), additional imaging may be needed eg. DSA, MRA

20
Q

Ottawa SAH clinical decision rule

A

use to rule out SAH in selected patients presenting to the ED with acute headache
for alert patients with non traumatic headache reaching maximum intensity within 1 hour

21
Q

What is the defining feature of SAH on a CT scan?

A

Blood in subarachnoid space (hyperdense) with variable extension and location

22
Q

Where is aneurysmal SAH typically located?

A

In the basal cisterns
Most aneurysms are located in the circle of Willis and when they bleed, blood extends along the basal cisterns. Large volumes of blood may extend into the ventricles or parenchyma.

23
Q

What CSF color indicates early findings suggestive of SAH?

A

Pink to red blood-tinged discoloration
This discoloration is an early indicator of possible bleeding.

24
Q

What is xanthochromia in the context of cerebrospinal fluid (CSF)?

A

The presence of bilirubin in the CSF secondary to the breakdown of RBCs, resulting in yellow discoloration
Xanthochromia is a late finding in SAH.

25
What is the RBC:WBC ratio in cerebrospinal fluid (CSF)?
similar to that in peripheral blood, there will be a normal RBC:WCC ratio useful for distinguishing SAH from meningitis
26
What is the expected RBC count in CSF during an SAH evaluation?
Elevated (no specific threshold) WCC may be also be mildly elevated
27
What is the expected glucose level in CSF for SAH?
Normal
28
What is the expected protein level in CSF during an SAH evaluation?
Elevated
29
mainstays of initial management
stabilisation - A-E assessment and secure the airway if needed prevent rebreeding and reverse bleeding diatheses neuroprotection consult neuro and interventional radiology admit to neurocritical care
30
how do you reverse bleeding diatheses
Anticoagulant reversal IV antihypertensive agents if blood pressure is elevated. Target SBP < 160 mm Hg if suspected increased ICP: Consider permissible hypertension (e.g., MAP > 90 mm Hg) to maintain cerebral perfusion pressure and prevent cerebral hypoperfusion. ? art line analgesia and antiemetics as needed. Antifibrinolytic therapy eg. TXA: not routinely recommended; potentially useful for patients with an expected delay in aneurysm repair [18][43]
31
neuroprotective measures to consider
Start ICP management (e.g., elevate head 30°, IV mannitol, short-term controlled hyperventilation). Treatment goals: Euvolemia Euglycemia Normothermia Eunatremia: Patients are at risk for cerebral salt wasting and SIADH. Consider neuroprotective seizure prophylaxis following an intracranial event.
32
endovascular coiling is
insertion of catheter under fluoroscopic guidance and placement of metal coils in the aneurysm lumen to interrupt blood flow and induce thrombotic occlusion minimally invasive, good for patients who are poor surgical candidates
33
microsurgical clipping is
craniotomy and exposure of the aneurysm mechanical occlusion of the neck of the aneurysm using titanium clips more invasive
34
mainstays of further management of aneurysmal SAH
prevention of vasospasm and delayed cerebral ischaemia treatment of hydrocephalus detection of cardiopulmonary complications DVT prophylaxis: mechanical initially, pharmacological 24 hours after repair
35
how to prevent vasospasm after SAH
administer oral nimodipine in all patients frequent neuro examinations CT head 24-48 hours following repair consider transcranial doppler scan, repeated angiography, monitoring of ICP and cerebral perfusion pressure, continuous EEG lower threshold to transfuse packed RBC as anaemia is common
36
What percentage of patients with SAH experience vasospasm?
Approximately 30%
37
What diagnostic tool can help identify vasospasm?
Transcranial doppler ultrasound study vasospasms cause a measurable increase in the velocity of blood flow
38
What is the pathophysiological process leading to nonobstructive hydrocephalus?
Impaired CSF reabsorption from the arachnoid villi causes non obstructive hydrocephalus increases ICP decreases cerebral perfusion pressure causes ischaemia this can lead to ischaemic stroke
39
What substances are released during vasospasm that contribute to ischemia?
Clotting factors and vasoactive substances causing diffuse vasospasm of cerebral vessels oxyhemoglobin is believed to be the substance responsible
40
When does vasospasm typically occur after SAH?
Between 3–10 days after SAH
41
risk of recurrent bleeding in SAH
Occurs in 4–14% of patients with SAH in the first 24 hours Risk of rebleeding is highest in the first 2–12 hours after SAH The cumulative risk of recurrent bleeding within the first six months is about 50%.
42
two types of hydrocephalus following SAH
acute obstructive: occurring minutes to hours after chronic communicating: usually occurs weeks to months after due to impaired CSF resorption from arachnoid villi
43
delayed cerebral ischameia
complication of aneurysmal subarachnoid haemorrhage defined as worsening neurological status that cannot be attributed to other causes 3 days to 2 weeks following SAH
44
why do patients sometimes get seizures following SAH
blood acts as an irritant
45
SIADH following SAH
cerebral salt wasting rare causes hypovolaemic hypotonic hyponatraemia treated with hypertonic saline and fludrocortisone