Hemorrhagic Stroke Flashcards
(40 cards)
Causes of intracranial hemorrhage
Evaluation of etiology in nontraumatic ICH
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Hypertension management in ICH
For patients with acute ICH who present with systolic blood pressure (SBP) between 150 and 220 mmHg, we suggest rapid lowering of SBP to a target of 140 mmHg, provided the patient remains clinically stable
For patients with acute ICH who present with SBP >220 mmHg, we suggest rapid lowering of SBP to <220 mmHg. Thereafter, the blood pressure is gradually reduced (over a period of hours) to a target range of 140 to 160 mmHg, provided the patient remains clinically stable
**
Immediate treatment to reduce SBP below 220 mmHg: nicardipine starting at 5 mg/hour IV; alternate: labetalol 20 mg IV bolus, may repeat every 10 minutes
Anticoagulant reversal in acute ICH
AHA/ ASA 2022
Beriplex mechanism of action
- Το Beriplex παρασκευάζεται από ανθρώπινο πλάσμα και περιέχει τους ανθρώπινους παράγοντες πήξης ΙΙ, VII, IX και X.
- Πυκνά διαλύματα που περιέχουν αυτούς τους παράγοντες πήξης ονομάζονται προϊόντα συμπλέγματος προθρομβίνης.
- Οι παράγοντες πήξης ΙΙ, VII, IX και X εξαρτώνται από τη βιταμίνη Κ και είναι σημαντικοί για την πήξη του αίματος.
- Η έλλειψη οποιουδήποτε από αυτούς τους παράγοντες συνεπάγεται ότι το αίμα δεν πήζει όσο γρήγορα θα έπρεπε και γι’ αυτό υπάρχει αυξημένη τάση για αιμορραγίες.
- Η αντικατάσταση των παραγόντων πήξης ΙΙ, VII, IX και X με το Beriplex θα αποκαταστήσει τους μηχανισμούς πήξης
Andexanet alfa 1) mechanism of action 2) indication
1) Το andexanet alfa αποτελεί ανασυνδυασμένη μορφή της πρωτεΐνης του ανθρώπινου FXa.
Aποτελεί ειδικό παράγοντα αναστροφής για τους αναστολείς του FXa
2) Για ενήλικες ασθενείς που υποβάλλονται σε θεραπεία με άμεσο αναστολέα του παράγοντα Xa (απιξαμπάνη ή ριβαροξαμπάνη) όταν απαιτείται αναστροφή της αντιπηκτικής δράσης λόγω απειλητικής για τη ζωή ή ανεξέλεγκτης αιμορραγίας.
Management of anticoagulation and antiplatelet treatment after ICH
Management of antiplatelet therapy –
We suggest resuming antiplatelet therapy for most patients with ICH who have a specific indication for such therapy.
For patients with ICH in whom antiplatelet therapy is being resumed, we typically start aspirin within a few days after the ICH has stabilized.
Management of anticoagulation –
We balance the risks of recurrent ICH and thromboembolism to help make decisions about resuming anticoagulation for each patient
** Early resumption of anticoagulation may be indicated for select patients with a compelling indication (eg, mechanical prosthetic heart valve). For most other patients who resume anticoagulation, we generally suggest waiting for at least four weeks after onset of the ICH to restart the anticoagulant
** For patients with atrial fibrillation, prediction models such as the HAS-BLED score may be used to help assess bleeding risk and CHADS2 or CHA2DS2-VASc scores used to help assess thromboembolic risks
For many patients with atrial fibrillation, the risk-benefit analysis favors resuming anticoagulation after ICH.
** For most patients with atrial fibrillation who develop ICH while on warfarin and in whom oral anticoagulation is resumed, we suggest a DOAC over warfarin.
DOACs generally have a lower risk of bleeding, including ICH, than warfarin.
Warfarin may be selected for patients with valvular atrial fibrillation, a mechanical heart valve, or an inability to take a DOAC.
Management of elevated ICP in ICH
General preventive measures:
Elevate head of bed >30 degrees
Give mild sedation as needed for comfort for intubated patients (eg, midazolam)
Give antipyretics for temperature >38°C (eg, acetaminophen [paracetamol] 325 to 650 mg orally or PR every 4 to 6 hours or 650 mg IV every 4 hours)
Maintain neutral head positioning; avoid rotating the neck or placing IV lines or devices in or at the neck that may impede venous outflow
Use isotonic solutions for volume resuscitation and maintenance fluids; maintain serum sodium >135 mEq/L
Repeat imaging (eg, head CT) for neurologic deterioration or signs of elevated ICP
Obtain immediate neurosurgical consultation for surgical indications
Give osmotic therapy via central venous catheter for clinical signs or imaging findings of elevated ICP:
Hypertonic saline 23.4%: 15 to 30 mL IV bolus every 6 hours, or
Mannitol: 0.25 to 1 g/kg IV bolus every 6 hours
Surgical management of intraventricular hemorrhage
AHA/ ASA 2022
IVH intraventricular hemorrhage
EVD indicates external ventricular drain
Recommendations for Posterior Fossa Hemorrhage
For patients with cerebellar ICH who are deteriorating neurologically, have brainstem compression and/or hydrocephalus from ventricular obstruction, or have cerebellar ICH volume ≥15 mL, immediate surgical removal of the hemorrhage with or without external ventricular drain is recommended in preference to medical management alone to reduce mortality.
Surgical treatment of intracerebral hemorrhage
When to suspect hemorrhagic infarction caused by CVT?
This diagnosis should be considered in patients with
high-convexity parietal lobar hemorrhage who are at high risk for thrombotic events with conditions including
* pregnancy and puerperium
* disseminated cancer
* collagen-vascular or other diseases predisposing to hypercoagulability
Hyperperfusion syndrome
Cerebral hyperperfusion syndrome is an uncommon sequela of carotid endarterectomy (CEA) occurring in only a small percentage of patients after carotid revascularization (from less than 1 to as high as 3 percent in various reports)
Hyperperfusion syndrome is characterized by the following clinical features:
●Headache ipsilateral to the revascularized internal carotid, typically improved in upright posture, may herald the syndrome in the first week after endarterectomy.
●Focal motor seizures are common, sometimes with postictal Todd’s paralysis mimicking post-endarterectomy stroke from carotid thrombosis.
●Intracerebral hemorrhage is the most feared complication, occurring in approximately 0.6 percent of patients after CEA, usually within two weeks of surgery
How can septic embolism from infective endocarditis lead to ICH
infected (mycotic) aneurysm rupture, pyogenic arteritis, or brain abscess formation
Clinical and neuroimaging features of intracerebral hemorrhage associated with underlying causes
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Most common causes of spontaneous SAH
- Rupture of an intracranial saccular aneurysm 80%
- Vascular malformations
- Infected mycotic aneurysms
Most common sites of aneurysm formation
Eighty-five percent of saccular aneurysms occur in the anterior circulation.
The most common sites for aneurysm formation are:
* the anterior communicating artery/anterior cerebral artery junction
* the junction of the posterior communicating and internal carotid arteries
* the middle cerebral artery bifurcation
* the basilar artery apex
Condition not to miss before aneurysmal subarachnoid hemorrhage
Sentinel hemorrhage
10-50% of the patients
Days or weeks before SAH Headache:
* so severe that the patient cannot carry out normal activities
* comes on much more rapidly and lasts longer than migraines
Aneurysm locations that may involve a third nerve palsy
- Posterior communicating
- Aneurysms at the junction of SCA and PCA with basilar artery
Possible findings in CT scan of a patient with SAH
CT scans may show blood surrounding the circle of Willis at the base of the brain, over the convexity, or in the interhemispheric or sylvian fissures
May also reveal:
coexisting hydrocephalus or intraventricular hemorrhage, uncal transtentorial herniation, or mass effect from a large intra- or extra-axial hematoma.
Sensitivity of CT scan in subarachnoid hemorrhage
The sensitivity of modern head CT for detecting SAH is highest within the first six hours after SAH (nearly 100 percent when interpreted by expert reviewers), and then progressively declines over time to approximately 58 percent at day 5
What does convexal SAH suggests
reversible cerebral vasoconstriction syndrome (RCVS) in younger patients or cerebral amyloid angiopathy in older patients
Lumbar puncture in SAH: indications and findings
Lumbar puncture is typically required to exclude a SAH for most patients with a normal head CT, with the exception of selected patients with isolated headache, a normal examination, and a negative CT scan of optimal quality performed within six hours from onset of headache and interpreted by an expert reviewer.
Findings in SAH —The classic lumbar puncture findings of SAH are an elevated opening pressure, an elevated RBC count that does not diminish from CSF tube 1 to tube 4, and xanthochromia.
Aneurysmal subarachnoid hemorrhage differential diagnosis
- head trauma with traumatic SAH (usually over the brain convexity and not in the basal cisterns)
- spontaneous SAH due to bleeding diathesis
- rupture of an infected (mycotic) aneurysm
- cerebral sinus, or cortical vein thrombosis
- ruptured cranial dural arteriovenous fistula
- intracranial arterial dissection
- cervical vertebral artery dissection with leakage of blood into the cervical subarachnoid space
- rupture of a cortical AVM
- vasculitis or vasculopathy involving intracranial arteries
- Call-Fleming syndrome of reversible cerebral vasoconstriction
- rupture of a spinal arteriovenous malformation or spinal dural fistula
