Hemorrhagic Stroke Flashcards

1
Q

Causes of intracranial hemorrhage

A
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2
Q

Evaluation of etiology in nontraumatic ICH

A

https://www.uptodate.com/contents/image?imageKey=NEURO%2F132295&topicKey=NEURO%2F129071&search=intracranial%20hemorrhage&source=see_link

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3
Q

Hypertension management in ICH

A

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

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4
Q

Anticoagulant reversal in acute ICH

A

AHA/ ASA 2022

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5
Q

Beriplex mechanism of action

A
  • 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
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6
Q

Andexanet alfa 1) mechanism of action 2) indication

A

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.

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7
Q

Management of anticoagulation and antiplatelet treatment after ICH

A

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.

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8
Q

Management of elevated ICP in ICH

A

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

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9
Q

Surgical management of intraventricular hemorrhage

A

AHA/ ASA 2022

IVH intraventricular hemorrhage

EVD indicates external ventricular drain

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10
Q

Recommendations for Posterior Fossa Hemorrhage

A

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.

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11
Q

Surgical treatment of intracerebral hemorrhage

A
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12
Q

When to suspect hemorrhagic infarction caused by CVT?

A

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

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13
Q

Hyperperfusion syndrome

A

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

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14
Q

How can septic embolism from infective endocarditis lead to ICH

A

infected (mycotic) aneurysm rupture, pyogenic arteritis, or brain abscess formation

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15
Q

Clinical and neuroimaging features of intracerebral hemorrhage associated with underlying causes

A

https://www.uptodate.com/contents/image?imageKey=NEURO%2F132289&topicKey=NEURO%2F129071&search=intracranial%20hemorrhage&source=see_link

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16
Q

Most common causes of spontaneous SAH

A
  • Rupture of an intracranial saccular aneurysm 80%
  • Vascular malformations
  • Infected mycotic aneurysms
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17
Q

Most common sites of aneurysm formation

A

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

18
Q

Condition not to miss before aneurysmal subarachnoid hemorrhage

A

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

19
Q

Aneurysm locations that may involve a third nerve palsy

A
  • Posterior communicating
  • Aneurysms at the junction of SCA and PCA with basilar artery
20
Q

Possible findings in CT scan of a patient with SAH

A

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.

21
Q

Sensitivity of CT scan in subarachnoid hemorrhage

A

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

22
Q

What does convexal SAH suggests

A

reversible cerebral vasoconstriction syndrome (RCVS) in younger patients or cerebral amyloid angiopathy in older patients

23
Q

Lumbar puncture in SAH: indications and findings

A

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.

24
Q

Aneurysmal subarachnoid hemorrhage differential diagnosis

A
  • 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
25
Q

Aneurysmal subarachnoid hemorrhage: identifying the source of bleeding

A

Of the available tests, digital subtraction angiography (DSA) has the highest resolution to detect intracranial aneurysms and define their anatomic features and remains the gold standard test for this, but CT angiography is being increasingly used as a first-line vascular test.

Repeat angiography is necessary if the initial study is negative, unless the pattern of hemorrhage is perimesencephalic, in which a repeat angiography may be considered optional.

26
Q

Common causes of non-aneurysmal subarachnoid hemorrhage

A

Common causes include

  • Perimesencephalic NASAH
  • Cerebral vascular malformations
  • Intracranial arterial dissection
  • Reversible cerebral vasoconstriction syndrome
  • Cerebral venous thrombosis
  • Cerebral amyloid angiopathy
  • Minor or unsuspected trauma
  • Spinal causes, such as vascular malformation, aneurysm, or tumor
27
Q

Characteristic features and initial diagnostic imaging for common underlying causes of spontaneous isolated convexity subarachnoid hemorrhage

A
28
Q

Acute care of aneurysmal subarachnoid hemorrhage

A

Patients with aneurysmal subarachnoid hemorrhage (SAH) should be admitted to an intensive care setting for constant hemodynamic, cardiac, and neurologic monitoring.

*Blood pressure management – Elevated blood pressure should be treated while avoiding hypotension. For most patients, we use a target systolic blood pressure (SBP) <160 mmHg or mean arterial pressure (MAP) <110 mmHg.
*Stopping antithrombotic agents – All antithrombotic agents should be discontinued, and anticoagulation reversed, until the aneurysm is repaired by surgery or coiling.
*Selective antiseizure prophylaxis – The use of antiseizure medications for seizure prophylaxis after SAH is controversial. Antiseizure prophylaxis prior to aneurysm repair may be reasonable for some patients with poor neurologic grade, unsecured aneurysm, and associated intracerebral hemorrhage
*Maintaining euvolemia – Euvolemia should be maintained and monitored by documentation of fluid input and output to decrease the risk of ischemic complications.
*Nimodipine – Nimodipine 60 mg every four hours is administered for 21 days to improve outcomes for patients aneurysmal SAH
*Other supportive measures – Other general measures for all patients with acute aneurysmal SAH include bedrest, analgesia for pain control, and venous thromboembolism prophylaxis. Hypoxemia, hyperglycemia, and fever should be prevented and promptly treated

Aneurysm repair with surgical clipping or endovascular coiling is the only effective treatment to prevent rebleeding and should be performed as early as feasible, preferably within 24 hours, and immediately if rebleeding does occur.

29
Q

Subarachnoid hemorrhage early complications

A
  • Rebleeding
  • Vasospasm and delayed cerebral ischemia
  • elevated intracranial pressure - hydrocephalus
  • hyponatremia (either the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or from cerebral salt wasting)
  • seizures
  • anemia
  • cardiopulmonary: Pulmonary edema, ECG abnormalities, Left ventricular dysfunction, Troponin release
  • Hypothalamic-pituitary dysfunction
  • hyperglycemia
  • fever
30
Q

Syndromes that predispose in aneurysm formation

A

Polycystic kidney syndrome
Marfan Syndrome
Ehlers-Danlos syndrome

31
Q

Indications for unruptured aneurysm surgery

A

Small (<7 mm) anterior circulation aneurysms in patients with no history of SAH have a 5-year rupture risk of 0%, and therefore likely require no treatment.

At the other extreme, large posterior circulation aneurysms have a 5-year risk between 15% and 50%, and treatment may be justified.

32
Q

Mycotic aneurysm: pathogenesis clincal findings

A

● An infected aneurysm is a localized dilation of an artery due to destruction of the vessel wall by infection. An infected aneurysm can develop when infection of the arterial wall causes development of a new aneurysm or when a pre-existing aneurysm becomes secondarily infected.

● The organisms with the greatest affinity for the arterial wall and more likely to cause infected aneurysm are Staphylococcus spp and Salmonella spp. Other organisms include Streptococcus pneumoniae, Treponema pallidum, and Mycobacterium tuberculosis, as well as other bacterial, fungal, or anaerobic pathogens.

Infected aneurysm of the intracerebral vessels may present as stroke or subarachnoid hemorrhage, particularly in the setting of endocarditis.

33
Q

Mycotic aneurysm management

A

●Prior to the availability of culture results, we favor treatment with a combination of vancomycin and an agent with activity against gram-negative organisms, especially Salmonella and enteric gram-negatives; reasonable choices include ceftriaxone, a fluoroquinolone, and piperacillin-tazobactam. Antibiotics should be tailored to culture and susceptibility results when they become available. The duration of therapy is individualized.

unruptured aneurysms may be managed with antibiotics alone, but, whenever possible, ruptured aneurysms should be managed with a combination of antibiotics and surgery

34
Q

arteriovenus malformations clinical findings

A

intracranial hemorrhage, seizure, focal neurologic deficit, or headache

annual hemorrhage rates from brain AVMs are between 2 and 3 percent (very high!!)

35
Q

arteriovenus malformations management

A

*For most patients with a ruptured AVM, we suggest intervention. In some cases, intervention may not be technically feasible or safe or desired by the patient.

*For patients with an unruptured AVM who are not at high risk of rupture, we suggest conservative management. However, interventional treatment of unruptured AVMs may be performed in select patients at low treatment-related risks, with symptoms (eg, seizures) refractory to medical treatment, or with AVM features posing high risk for rupture.

*For patients selected for intervention, microsurgical excision is often preferred for patients with brain AVMs associated with a low risk of poor treatment outcomes, with radiosurgery as an alternative.
Conservative medical management is usually preferred for patients with brain AVMs associated with a high risk of poor treatment outcomes, although some may benefit from partial obliteration with endovascular treatment.

36
Q

Genetic testing for cavernous malformations

A

Genetic testing — Genetic testing for pathogenic variants in CCM1 (KRIT1), CCM2, and CCM3 (PDCD10) is indicated for patients with multiple CMs on imaging, a history of brain radiation therapy, or a positive family history of CMs
Testing should include direct sequencing and deletion/duplication analysis.

For new cases of CMs, clinicians should obtain a three-generation family history at the time of diagnosis, with particular attention to family members with a history of hemorrhagic stroke, abnormal MRI scan, epilepsy, or other neurologic complications.
However, family history may be confounded by the incomplete penetrance and variable presentation, even within families, of familial CMs.

37
Q

Best imaging modality for cavernous malformation

A

MRI

Often not visible in angiography!

38
Q

Most common neoplasm that cause intracranial hemorrhage

A

Glioblastoma multiforme

Among cerebral metastatic tumors, melanoma, bronchogenic carcinoma, renal cell carcinoma, and choriocarcinoma most commonly bleed

39
Q

Signs suggesting underlying neoplasm in ICH

A
  • A history of subacute neurologic decline before the acute presentation
  • ring-enhancement on gadolinium MRI within the first 48 hours
  • unusual location such as the corpus callosum
40
Q

Appearance of Intracerebral Hemorrhage on Noncontrast CT and MRI by Stages

A