Figure 13-1
Hypertensive hemorrhage: A 47-year-old male with hypertensive urgency – large, acute hematoma in the right basal ganglia with mild perilesional edema causing mass effect, midline shift, and subfalcine herniation (Images courtesy of Dr. Ajay Malhotra)
Figure 13-2
A 64-year-old hypertensive female with acute headache and sensory symptoms: Left thalamic bleed which increased in size on the 6 h follow-up scan with intraventricular extension and blood layering in the left occipital horn. MRI showing features of acute bleed, isointense on T1 WI, hypointense signal on T2 WI, absence of contrast enhancement, and “blooming” on SWI (Images courtesy of Dr. Ajay Malhotra)
HTN : accounts for 60–70 % of all primary ICH (Fig. 13-1)
Leads to degeneration, fibrinoid necrosis, lipohyalinosis, Charcot–Bouchard aneurysms, and rupture of small penetrating arteries
Most common locations for HTN bleed: basal ganglia (especially putamen), thalamus, pons, cerebellum, deep white matter
Cerebral Amyloid Angiopathy :
15 % of all primary ICH cases
Deposits of beta-amyloid protein in small and medium-sized blood vessels
Typically present as large spontaneous lobar hemorrhages
More common in elderly
Annual risk of recurrence: 11 %
Presence of e2 and e4 allele triples risk of hemorrhagic recurrence
Race: higher incidence in Asian and black ethnicity
Secondary Hemorrhage (Table 13-1)
Table 13-1
Secondary sources of ICH
Secondary sources of ICH |
---|
Intracranial aneurysm |
Cavernous malformation |
Arteriovenous malformation |
Vasculitis |
Dural arteriovenous fistula |
Dural sinus thrombosis |
Anticoagulant use |
Hemorrhagic conversion of ischemic stroke |
Coagulopathies |
Endocarditis |
Drug use |
Tumor |
Vascular malformations: arteriovenous malformations , intracranial aneurysms , cavernomas (discussed in greater detail in the following chapter)
Coagulopathies
Patients treated with OACs account for 12–14 % of ICH cases
Most HTN- related hemorrhages develop over first few hours, whereas coagulopathy-related hemorrhages known to evolve for 24–48 h
Rate of occurrence in the anticoagulated population: 0.2–1.0 % per year
Warfarin- related ICH:
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Reversal of INR: vitamin K, FFP, prothrombin complex concentrates (PCC), recombinant factor VIIa are all options
Vitamin K
Promotes hepatic synthesis of factors II, VII, IX, and X as well as proteins C and S
Takes 12–24 h to reverse coagulopathy due to warfarin
Must give to all patients with warfarin-associated ICH
FFP
Contains all endogenous procoagulants and anticoagulants
Give with vitamin K
Large volume load needs to be given slowly; avoid in patients with CHF
Can take up to 30 h to reverse coagulopathy
Potential for allergic reaction
PCC: plasma-derived concentrates of factors II, VII, IX, X, proteins C and S (faster, lower volume load than FFP)
Alternative to FFP
Can correct INR in less than 30 min in warfarin-associated coagulopathy
Give with vitamin K
Have not shown improved clinical outcomes compared to FFP, but may have fewer complications
Drawbacks include high cost and lack of widespread availability
Recombinant FVIIa: used to treat congenital FVIIa deficiency
Increased risk of thromboembolism
Usefulness of platelet transfusions in patients with ICH is unclear, but may be given to patients on antiplatelet agentsStay updated, free articles. Join our Telegram channel
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