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XUẤT HUYẾT NÃO: Chẩn đoán,
tiên lương và điều trị
(sau đại học)
PGS.TS Cao Phi Phong
2017
Ca lâm sàng
Bn nam 70 tuổi
Bệnh khởi phát đột ngột đau đầu nhiều, uống aspirin giảm đau.
BN rơi vào bất tỉnh,
Nhiệt độ 38 độ, Mạch 61l/p, Nhịp thở 16l/p, HA 201/96 mmHg
Khám: đồng tử đều 2 bên, còn đáp ứng pxas yếu, mất px nôn,
kích thích đau còn co lại(withdraws), Babinsky (+) phải, GCS: E
0, V=0, M=4. NIHSS: 38
Tiền sử: HA cao uống thuốc không đều, uống rượu và hút
thuốc
Chẩn đoán: ?
(T) (P)
Câu hỏi thảo luận:
1. Dịch tễ học XHN ?
2. Sinh lý bệnh XHN ?
3. Nguyên nhân thường gặp XHN ?
4. Lâm sàng XHN ?
+ thể tích khối máu tụ và GCS trong tiên lượng ?
+ thể tích khối máu tụ tăng theo thời gian?
+ cái gì trông đợi cho kết cục bn XHN?
5. Điều trị XHN ?
• Sinh lý bệnh (Pathophysiology)
• Dịch tễ học(Epidemiology)
• Nguyên nhân/yếu tố nguy cơ
• Lâm sàng(Clinical features)
• Điều trị
MỤC TIÊU
Xuất huyết não
Xuất huyết não tự phát, không chấn thương là nguyên
nhân quan trọng gây bệnh tật và tử vong trên toàn thế giới
Chăm sóc và điều trị tốt về nội khoa có hiệu lực, tác động
trực tiếp đến bệnh tật và tử vong do XHN, ngay cả trước khi
tìm được điều trị chuyên biệt
Chăm sóc tích cực toàn diện XHN liên quan trực tiếp đến
tử vong của bệnh này
Hướng dẫn điều trị này cập nhật hướng dẫn điều trị trước
của AHA-2010
1. Dịch tễ học
10-15% toàn bộ đột quỵ (80% thiếu máu)
Nam nhiều hơn nữ
Thường nhiều hơn sau 55 tuổi
Gia tăng người Mỹ da đen, Nhật, Hispanic
Tử vong 30 ngày: 35-52%
- 50% trong số này trong 48 giờ đầu
10% độc lập( không phụ thuộc) ở 1 tháng
1/5 số sống sót độc lập ở 6 tháng
7000 ca phẫu thuật lấy máu tụ hàng năm ở USA
2. Sinh lý bệnh
• Thrombin và iron, phóng thích khi hồng cầu phân hủy,
là 2 yếu tố quan trong gây tổn thương não sau XHN
• Thrombin nồng độ cao giết neurons và astrocytes in vitro.
• Thoái biến hemoglobin kết quả phóng thích iron. Iron gây
phù não ngay cả nồng độ thấp
Ya Hua, “Intracerebral hemorrhage: introduction brain injury afteriIntracerebral
hemorrhage, ther role of Thrombin and Iron” Stroke.2007; 38: 759-762
Tổn thương nguyên phát -
ảnh hưởng tức thì
Xuất huyết phát triển
Gia tăng áp lực nội sọ
Hematoma lan rộng ≥ 80 ml: tử vong
Ảnh hưởng thứ phát
Ảnh hưởng xuôi dòng
.
Phù não
Thiếu máu
Hematoma khởi đầu phù
Phù do hoạt động thẩm thấu của protein từ cục máu
động(osmotically active proteins)
Vasogenic và cytotoxic edema phá vỡ hàng rào máu não
và chết neuron
Có thể không xác định mediators thứ phát cả tổn thương
neuron và phù (nuclear factor kappa-beta)
3. Nguyên nhân XHN
Nguyên phát
(78-88%)
Hypertensive angiopathy
(fibrohyalinosis)
Amyloid angiopathy
Liên quan Anticoagulant (?)
Thứ phát
AVM
Aneurysm
Cavernoma
Neoplasm
Coagulopathy
Alcoholic liver disease
Hemophilia
Hemorrhagic infarct
Toxic-cocaine
Granulomatous angiitis &
vasculitides
Hyalinosis: hyaline degeneration
XHN nguyên phát
Yếu tố nguy cơ
• Tuổi: tỷ lệ mới mắc tăng gấp đôi cho mỗi thập kỷ
sau 55 tuổi. Trên 80 tuổi nguy cơ tăng gấp 25 lần
• Giới tính: nhiều ở nam hơn
• Chủng tộc: nhiều hơn người da đen, hispanics,
asians, ít gặp da trắng
• Tiền sử đột quỵ
• Uống rượu (Alcohol consumption): >3
lần/ngày gia tăng nguy cơ XHN gấp 7 lần
(>3 drinks per day increases the risk of ICH by 7 folds)
• Thuốc: cocaine, amphetamine
• Hút thuốc lá không gia tăng nguy cơ XHN
• Oral Anticoagulant: warfarin nguy cơ chảy máu
bn rung nhĩ 2.2% /năm
• Antiplatelets: ASA đơn thuần (1.3%/năm) ASA
phối hợp plavix tăng nguy cơ 2.4%/năm.
• rTPA: tăng nguy cơ XHN 6.4% trong 36 giờ kế
tiếp
Dễ mắc bênh (bẩm chất) di truyền
(Genetic predisposition)
• E2 và E4 alleles(gen tương ứng) của apolipoprotein
E gene giữ vai trò quan trọng xảy ra các thể xuất
huyết như xuất huyết lúc sanh (labor hemorrhages)
O’Donnel et al, 2000
4. Lâm sàng XHN
• Đột ngột đau đầu +/- buồn nôn & nôn
• Khởi phát diễn tiến thầm lặng nhiều phút đến giờ
• Thường trong lúc hoạt động
• Lẩn lộn(confusion)
• Thiếu hụt thần kinh: hemiplegia
• Giảm mực độ ý thức
• Cơn động kinh
Các loại xuất huyết trong não
• Putaminal hemorrhage (35%)
• Caudate Hemorrhage (5%)
• Thalamic Hemorrhage (10-15%)
• Mesencephalic Hemorrhages (rare)
• Pontine Hemorrhage (5%)
• Medullary Hemorrhages (rare)
• Cerebellar Hemorrhage (5-10%)
• Lobar Hemorrhage (25%)
Xuất huyết trong não thất(IVH)
• XHN lan vào trong não thất thường gặp trong
xuất huyết nhân đuôi và đồi thị (caudate and
thalamic) và xuất huyết lớn nhân vỏ hến và thùy
(putaminal and lobar)
Xuất huyết thùy (Lobar Hemorrhages)
• Thường gặp thứ 2 (25%)
• Cơ chế không tăng huyết áp :
- người trẻ (AVM, sympathomimetic agents)
- người già: cerebral amyloid angiopathy
• Thường dưới vỏ thùy trán, đỉnh, thái dương và
chẩm
• Cơn động kinh chiếm 28%
• Tỷ lệ tử vong thấp hơn xuất huyết khác, dự hậu
chức năng lâu dài có thể tốt hơn
N Engl J Med 2001;344(19):1450–1460
Lobar hemorrhage 25%
• - Penetrating cortical
branches of ACA, MCA, &
PCA
• - Peripheral location lower
frequency of coma
• - Lower mortality
• - Better functional outcome
N Engl J Med 2001;344(19):1450–1460
Basal ganglia 35-40%
- Ascending lenticulostriate
branches of MCA
- Wide spectrum of severity
extending to coma and
decerebrate rigidity
- Ventricular extension
carries very poor prognosis
N Engl J Med 2001;344(19):1450–1460
Thalamus 10-15%
- Ascending thalamogeniculate
branches of PCA
- Abrupt hydrocephalus from
aqueductal obstruction from
intraventricular clot
- Responds to ventriculostomy
N Engl J Med 2001;344(19):1450–1460
Pons 5%
- Paramedian branches of
the basilar artery
- Bilateral carries very poor
prognosis (coma,
quadriplegia, decerebrate
posturing, horizontal
ophthalmoplegia, pinpoint
reactive pupils)
N Engl J Med 2001;344(19):1450–1460
Cerebellum 5-10%
- Penetrating branches of the
PICA, AICA, SCA
- Abrupt onset vertigo, h/a, n/v,
inability to walk in absence
of weakness
Ipsilateral ataxia, horizontal
gaze palsy, peripheral facial
palsy
- Unpredictable deterioration to
coma
XHN do tăng huyết áp
• Yếu tố nguy cơ quan trọng nhất (>70% XHN)
• Chia đôi đm xuyên thấu nhỏ (50–700 μm diameter)
• Atherosclerosis – Lipid deposition, layering of platelet and fibrin aggregates,
breakage of elastic lamina, atrophy and fragmentation of smooth muscle, dissections, and granular or vesicular cellular degeneration
• Charcot and Bouchard aneurysm – Fibrinoid necrosis of the subendothelium focal dilatations rupture of microaneurysm
Dị dạng mạch máu (Vascular malformations)
• Aneurysms, AVM, cavernous angiomas
• Người trẻ, bn nữ, tiền sử gia đình
• Hình ảnh có thể biểu hiện đồng thời XHDN
• Chẩn đoán MRI và cerebral angiography
– Usually supratentorial, lobar ICH
– Cavernous angioma: on MRI (T2) central nidus of irregular bright signal mixed with mottled hypointensity, surrounded by peripheral hypointense ring (ổ tín hiệu sáng không đều lẩn giảm đâm độ)
cavernous angiomas (CT)
Vascular malformations (MRI)
U nội sọ (Intracranial tumour)
• Chiếm 10% trường hợp
• GBM hay metastases (melanoma, bronchogenic carcinoma, renal cell carcinoma)
• Hình ảnh gợi ý: – Papilledema
– Atypical location (e.g. corpus callosum)
– Disproportionate amount of surrounding edema
– Multiple sites simultaneously
– Non-contrast CT: ring of high-density hemorrhage with low-density center
– Contrast CT/MRI: presence of enhancing nodules
5. Điều trị XHN
These guidelines provide a framework for goal-directed treatment of the patient with intracerebral
hemorrhage. (Stroke. 2015;46:000-000. DOI: 10.1161/STR.0000000000000069.)
Chẩn đoán và đánh giá cấp cứu
1.Đánh giá “Thang điểm độ nặng” bn XHN : NIHSS, ICH score
(Class I; Level of Evidence B).
(khuyến cáo mới)
2. CT hay MRI phân biệt nhồi máu hay XHN
(Class I; Level of Evidence A).
(Không thay đổi so khuyến cáo trước)
ABC of hematoma size • Bedside ABC/2 method for hemorrhage volume in cm3 1. Identify the CT slice with the largest area of hemorrhage 2. Measure the largest diameter of the hemorrhage on this slice (A) 3. Measure the largest diameter 90° to (A) on the same slice (B) 4. Approximate number of 10-mm slices on which the ICH was seen
was calculated (C) – If area > 75% compared to where the hemorrhage was
largest, the slice was considered 1 hemorrhage slice – If area 25% to 75%, the slice was considered 1/2 a slice – If area < 25%, the slice was not considered a slice
• A, B, and C were then multiplied and the product divided by 2
3. CTA và contrast-enhanced CT có thể giúp xác định nguy
cơ hematoma phát triển (Class IIb; Level of Evidence B),
CTA, CT venography, contrast-enhanced CT, contrast
enhanced MRI, magnetic resonance angiography và
magnetic resonance venography, và catheter angiography
giúp đánh giá sang thương cấu trúc: dị dạng mạch máu, u khi
lâm sàng hay hình ảnh nghi ngờ
(Class IIa; Level of Evidence B). (Unchanged from the previous guideline)
1.Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH
Class I, Level of Evidence A (Unchanged from the previous guideline).
2.CT angiography and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion
Class IIb, Level of Evidence B
3.CT angiography, CT venography, contrast-enhanced CT, contrast-enhanced MRI, MRA and MRV can be useful to evaluate for underlying structural lesions including vascular malformations and tumors when there is clinical or radiologic suspicion
Class IIa, Level of Evidence B (New recommendation).
Khuyến cáo chẩn đoán hình ảnh trong XHN
5.1 Điều trị nội khoa XHN
Chăm sóc trước bệnh viện
“Guidelines for the Early Management of Patients
With Acute Ischemic Stroke.”
Chăm sóc ở cấp cứu
Khí đạo và oxy
. Bảo vệ khí đạo và thông khí đầy đủ khẩn cấp
. Điều trị khí đạo tích cực nếu giảm mức độ ý thức hay
rối loạn chức năng thân não
. Các thuốc dùng trước đặt nội khí quản tránh gây
loạn nhịp và /hay làm xáo trộn huyết động học
ABC
1. Duy trì oxygen bảo hòa ≥92%
2. Nhanh chóng đặt nội khí quản
Endotracheal intubation bn GCS 8 hay thấp hơn hay
không thể điều trị sự bài tiết dịch, nếu cần chuyển từ nơi
theo dõi tích cực, hay thiếu phương tiện, nguy cơ tổn
thương khí đạo bệnh nhân, xem xét bn trạng thái trơ
(obtund)
(ít nhất 20% bn điểm GCS giảm ≥2 điểm từ khởi phát trước bv đến khi
được đánh giá ở cấp cứu)
Endotracheal intubation
. Đặt nội khí quản không đòi hỏi, nhưng bảo vệ
khí đạo và bảo đảm thông khí là cần thiết
. Dựa vào lâm sàng nghi ngờ, không phải GCS
. pCO2 duy trì từ 30-35
- tránh dưới 30
Gây tê trước khi intubation, dùng lidocaine không chứng
minh phòng ngừa tăng áp lực nội sọ và ích lợi còn bàn cải ?
Thuốc tác dụng ngắn, không gia tăng áp lực nội sọ, khuyến
cáo hiện nay: etomidate hay propofol trong XHN cấp (propofol có thể giảm nhanh HA, midazolam nên tránh tác dụng không
mong muốn tăng áp lực nội sọ)
Thuốc tác dụng ngắn không khử cực (nondepolarizing) như
rocuronium thích hợp bn nguy cơ tăng áp lực nội sọ (succinylcholine có thể gây tăng áp lực nội sọ)
Lidocaine : ức chế phản xạ ho, ức chế gia tăng áp lực nội sọ bn đặt nội
khí quản với sang thương chiếm chổ, dùng 3 phút trước laryngoscopy
Sự cầm máu và bệnh lý đông máu, thuốc chống tiểu cầu và phòng ngừa DVT
(Hemostasis and Coagulopathy, Antiplatelet Agents, and
DVT Prophylaxis)
1.BN thiếu hụt các yếu tố đông máu năng hay giảm tiểu cầu
năng (thrombocytopenia) điều trị thay thế các yếu tố thích
hợp hay tiểu cầu tương ứng (Class I; Level of Evidence C). (Unchanged from the previous guideline)
2. BN XHN có INR tăng do dùng VKA, ngưng VKA điều trị
vitamin K–dependent factors, điều chỉnh INR, và intravenous
vitamin K (Class I; Level of Evidence C). (Unchanged from the previous guideline)
3. Phòng ngừa venous thromboembolism Bn XHN bắt đầu
ngày nhập viện bằng intermittent pneumatic compression (Class I; Level of Evidence A). (Revised from the previous guideline)
Kháng đông và XHN
• Anticoagulation gây phát
triển hematoma và tử
vong cao hơn
– Reverse warfarin
promptly and
aggressively
– FFP or prothrombin
complex concentrates
(PCCs)
– IV vitamin K
• Faster than SQ/PO but
a small risk of
anaphylactoid reaction
Khuyến cáo:
Hemostasis and Coagulopathy, Antiplatelet Agents, and
DVT Prophylaxis
1. Patients with a severe coagulation factor deficiency or
severe thrombocytopenia should receive appropriate
factor replacement therapy or platelets, respectively
(Class I; Level of Evidence C).
(Unchanged from the previous guideline)
2. Patients with ICH whose INR is elevated because of
VKA should have their VKA withheld, receive therapy
to replace vitamin K–dependent factors and correct the
INR, and receive intravenous vitamin K
(Class I; Level of Evidence C).
PCCs may have fewer complications and correct the INR more
rapidly than FFP and might be considered over FFP (Class IIb; Level of Evidence B).
rFVIIa does not replace all clotting factors, and although the
INR may be lowered, clotting may not be restored in vivo;
therefore, rFVIIa is not recommended for VKA reversal in ICH (Class III; Level of Evidence C).
(Revised from the previous guideline)
Prothrombin complex concentrates
(PCCs)
recombinant activated factor VIIa
(rFVIIa)
Fresh frozen plasma (FFP),
3. For patients with ICH who are taking dabigatran,
rivaroxaban, or apixaban, treatment with FEIBA, other PCCs,
or rFVIIa might be considered on an individual basis.
Activated charcoal might be used if the most recent dose of
dabigatran, apixaban, or rivaroxaban was taken <2 hours
earlier. Hemodialysis might be considered for dabigatran (Class IIb; Level of Evidence C).
(New recommendation)
4. Protamine sulfate may be considered to reverse heparin
in patients with acute ICH (Class IIb; Level of Evidence C).
(New recommendation) FEIBA
(factor VIII inhibitor bypassing activity)
5. The usefulness of platelet transfusions in ICH patients
with a history of antiplatelet use is uncertain (Class IIb; Level of Evidence C).
(Revised from the previous guideline)
6. Although rFVIIa can limit the extent of hematoma
expansion in noncoagulopathic ICH patients, there is an
increase in thromboembolic risk with rFVIIa and no clear
clinical benefit in unselected patients. Thus, rFVIIa is not
recommended (Class III; Level of Evidence A).
(Unchanged from the previous guideline)
7. Patients with ICH should have intermittent pneumatic
compression for prevention of venous thromboembolism
beginning the day of hospital admission
(Class I; Level of Evidence A).
Graduated compression stockings are not beneficial to reduce
DVT or improve outcome (Class III; Level of Evidence A).
(Revised from the previous guideline)
8. After documentation of cessation of bleeding, low dose
subcutaneous low-molecular-weight heparin or
unfractionated heparin may be considered for prevention
of venous thromboembolism in patients with lack of mobility
after 1 to 4 days from onset (Class IIb; Level of Evidence B).
(Unchanged from the previous guideline)
9. Systemic anticoagulation or IVC filter placement is
probably indicated in ICH patients with symptomatic
DVT or PE (Class IIa; Level of Evidence C). The decision
between these 2 options should take into account several
factors, including time from hemorrhage onset, hematoma
stability, cause of hemorrhage, and overall patient condition (Class IIa; Level of Evidence C).
(New recommendation)
inferior vena cava (IVC) filter
Tiềm năng điều trị XHN: vấn đề khối máu tụ lan rộng
Khối máu tụ lan rộng rất thường gặp
Brott, et al., 1997 103 pts., prospective observational study with serial CT scanning (baseline, 1 hr and 20 hrs following ICH) 26% showed >33% enlargement on 1 hr CT 38% showed >33% enlargement on 20 hr CT Neurologic deterioration correlated with hematoma expansion
Brott T et al, Stroke. 1997 Jan;28(1):1-5.
Khối máu tụ lan rộng trong XHN
Tiên lương khối máu tụ lan rộng
Thể tích khối máu tụ và tử vong
Recombinant Activated Factor VII
rFVIIa, NovoSeven©
Used for hemophilia
Induces local hemostasis
when it binds to tissue
factor - The complex can activate
Factors IX and X
- Factor Xa helps convert
prothrombin to thrombin
*Not FDA approved for ICH
“FAST” Trials
A phase II randomized trial showed that treatment with rFVIIa
within four hours after ICH onset limited hematoma growth
improved clinical outcomes relative to placebo
increased frequency of thromboembolic events (7% vs. 2%)
A subsequent phase III study comparing placebo to 20 μg/kg
and 80 μg/kg of rFVIIa:
both doses diminished hematoma enlargement
failed to show differences in clinical outcome
Overall serious thromboembolic adverse event rates were similar, the
higher rFVIIa (80 μg/kg) group had significantly more arterial events
than placebo.
The authors noted imbalances in treatment groups, particularly
intraventricular hemorrhage in the higher dose rFVIIa group
Mayer SA, et al for the FAST Trial Investigators., N Engl J Med. 2008 May 15;358(20):2127-37.
Mayer SA for the FAST Trial Investigators. N Engl J Med. 2005 Feb 24;352(8):777-85.
Factor VIIa
Factor VIIa can limit hematoma expansion in non-
coagulopathic patients, but also increases
thromboembolic risk.
rFVIIa is not recommended in unselected patients
rFVIIa does NOT replace clotting factors, even
though INR normalizes
rFVIIa is not recommended as the only agent to
reverse INR in ICH patients
Mayer SA, et al for the FAST Trial Investigators., N Engl J Med. 2008 May 15;358(20):2127-37.
Mayer SA for the FAST Trial Investigators. N Engl J Med. 2005 Feb 24;352(8):777-85.
Huyết áp
Is it safe to lower BP in the acute setting?
Safety of Early Intensive BP-Lowering Treatment
Điều trị HA cấp
Cerebral autoregulatory curve
CPP = MAP – ICP
Both the Antihypertensive Treatment of Acute Cerebral
Hemorrhage (ATACH) trial, a 4-tier dose escalation study of
intravenous nicardipine-based BP lowering in 80 patients within
3 hours of ICH,130 and the pilot phase Intensive Blood
Pressure Reduction in Acute Cerebral Hemorrhage
(INTERACT1) trial in 404 mainly Chinese patients within 6
hours of ICH131 found rapid reduction of SBP to <140 mm Hg
to be safe
Most recently, the main phase INTERACT2 trial has shown
no increase in death or serious adverse events from early
intensive BP lowering in eligible patients with elevated SBP.
Nghiên cứu ATACH , INTERACT 1 & 2
A randomized clinical trial using CT perfusion in primarily
small and medium ICH found no clinically significant
reduction in cerebral blood flow within the perihematomal
region related to early intensive BP lowering to an SBP target
of <140 mm Hg within several hours of ICH
In a clinical cohort of 211 patients who received a standard
protocol of nicardipine-based BP lowering to reach an SBP
target of <160 mm Hg at a mean of 30 minutes (range, 15–
45 minutes) within 3 hours of the onset of ICH, the best
outcomes were seen in the group with the lowest achieved
SBP (<135 mm Hg).
BN XHN có HA tâm thu từ 150 đến 220 mmHg và không có
chống chỉ định điều trị HA cấp, hạ huyết áp tâm thu xuống
140 mmHg là an toàn,
(Class I; Level of Evidence A)
và có thể hiệu quả cải thiện dự hậu chức năng
(Class IIa; Level of Evidence B).
(Revised from the previous guideline)
BP: Recommendations
1. For ICH patients presenting with SBP between 150
and 220 mm Hg and without contraindication to acute BP
treatment, acute lowering of SBP to 140 mm Hg is safe (Class
I; Level of Evidence A)
and can be effective for improving functional outcome (Class IIa; Level of Evidence B). (Revised from the previous guideline)
2. For ICH patients presenting with SBP >220 mm Hg,
it may be reasonable to consider aggressive reduction
of BP with a continuous intravenous infusion and frequent BP
monitoring
(Class IIb; Level of Evidence C). (New recommendation)
Blood Pressure Recommendations(2010)
1. Until ongoing clinical trials of BP intervention for ICH are completed, physicians must manage BP on the basis of the present incomplete efficacy evidence.
Class IIb, Level of Evidence C Unchanged from the previous guideline
2. In patients presenting with a systolic BP of 150-220 mmHg, acute lowering of systolic BP to 140 mmHg is probably safe
Class IIa, Level of Evidence B New recommendation
If SBP is >200 mmHg or MAP is >150 mm Hg, then
consider aggressive reduction of blood pressure with
continuous intravenous infusion, with frequent blood
pressure monitoring every 5 minutes.
If SBP is >180 mmHg or MAP is >130 mm Hg and there is
the possibility of elevated ICP, then consider monitoring
ICP and reducing blood pressure using intermittent or
continuous intravenous medications while maintaining a
cerebral perfusion pressure > 60 mmHg
If SBP is >180 mmHg or MAP is >130 mm Hg and
there is not evidence of elevated ICP, then consider a
modest reduction of blood pressure (eg, MAP of 110
mm Hg or target blood pressure of 160/90 mm Hg)
using intermittent or continuous intravenous
medications to control blood pressure, and clinically
reexamine the patient every 15 minutes.
© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited
Theo dõi tổng quát và chăm sóc điều dưỡng
(General Monitoring and Nursing Care)
Theo dõi và chăm sóc ban đầu BN XHN ở ICU ( intensive
care unit hay đơn vị đột quỵ(stroke unit) do BS và Điều
dưỡng chuyên khoa về đột quỵ chăm sóc (Class I; Level of Evidence B).
(Revised from the previous guideline)
Điều trị đường huyết
Theo dõi Glucose, nên tránh cả hyperglycemia và
hypoglycemia. Khuyến cáo mức glucose bình thường
(Class I; Level of Evidence C).
(Revised from the previous guideline)
Điều trị sốt
1. Điều trị sốt sau XHN có thể hợp lý
(Class IIb; Level of Evidence C).
(New recommendation
+ duy trì mức nhiệt độ bình thường
+ acetaminophen 650mg
+ chườm lạnh (cooling blankets)
Cơn động kinh và thuốc chống cơn động kinh (Seizures and Antiseizure Drugs)
Cơn động kinh lâm sàng sẽ được điều trị với thuốc chống cơn
động kinh (Class I; Level of Evidence A).
(Unchanged from the previous guideline)
Bn thay đổi tình trạng tâm thần (mental status) tìm thấy cơn
động kinh trên EEG được điều trị thuốc chống cơn động kinh (Class I; Level of Evidence C).
(Unchanged from the previous guideline)
Seizures and Antiseizure Drugs: Recommendations
1. Clinical seizures should be treated with antiseizure drugs (Class I; Level of Evidence A). (Unchanged from the previous guideline)
2. Patients with a change in mental status who are found to
have electrographic seizures on EEG should be treated with
antiseizure drugs (Class I; Level of Evidence C). (Unchanged from the
previous guideline)
3. Continuous EEG monitoring is probably indicated in ICH
patients with depressed mental status that is out of proportion
to the degree of brain injury (Class IIa; Level of Evidence C).
(Revised from the previous guideline)
4. Prophylactic antiseizure medication is not recommended (Class III; Level of Evidence B).
(Unchanged from the previous guideline)
Điều trị biến chứng nội khoa
Tầm soát nuốt khó cho tất cả bn trước khi cho ăn hay
uống bằng đường miệng để giảm nguy cơ viêm phổi (Class I; Level of Evidence B).
(New recommendation)
Dysphagia and aspiration are major risk
factors for the development of pneumonia
Serious cardiac events and cardiac death after stroke may be caused by
acute myocardial infarction (MI), heart failure, ventricular arrhythmias
including ventricular tachycardia/ fibrillation, and cardiac arrest. Concurrent
stroke and MI are not uncommon
Neurogenic pulmonary edema is an increase in interstitial and alveolar
fluid in the setting of an acute central nervous system injury well
documented in subarachnoid hemorrhage. Radiographically, it is
indistinguishable from cardiogenic pulmonary edema
Other medical complications in ICH patients include
acute kidney injury, hyponatremia, gastrointestinal bleeding,
impaired nutritional status, urinary tract infections, and
poststroke depression
Management of Medical Complications: Recommendations
1. A formal screening procedure for dysphagia should be
performed in all patients before the initiation of oral intake to
reduce the risk of pneumonia (Class I; Level of Evidence B).
(New recommendation)
2. Systematic screening for myocardial ischemia or infarction
with electrocardiogram and cardiac enzyme testing after ICH is
reasonable (Class IIa; Level of Evidence C).
(New recommendation)
Phẫu thuật/thủ thuật (Procedures/Surgery)
Theo dõi và chăm sóc tăng áp lực nội sọ
(ICP Monitoring and Treatment)
ICP Monitoring and Treatment: Recommendations
1. Ventricular drainage as treatment for hydrocephalus
is reasonable, especially in patients with decreased
level of consciousness (Class IIa; Level of Evidence B).
(Revised from the previous guideline)
2. Patients with a GCS score of ≤8, those with clinical
evidence of transtentorial herniation, or those with significant
IVH or hydrocephalus might be considered for ICP monitoring
and treatment. A CPP of 50 to 70 mm Hg may be reasonable
to maintain depending on the status of cerebral autoregulation (Class IIb; Level of Evidence C). (Unchanged from the previous guideline)
3. Corticosteroids should not be administered for treatment
of elevated ICP in ICH (Class III; Level of Evidence B). (New recommendation)
Tiếp cận điều trị TALNS
CSF volume • Mannitol or
hypertonic solution
• External CSF drainage
• Ventricular catheter
• Ventriculo -peritoneal or atrial shunt
• Lumbar drain • Serial lumbar
punctures
Brain volume • Mannitol or
hypertonic saline
• Decompressive craniectomy
• Resection of tumor or other mass lesion
Blood volume
+ Mannitol or
hypertonic saline
+ Hyperventilation
+ Hypothermia
+ Head elevation,
neutral neck
position
+ Deep propofol or
barbiturate
sedation ±
paralysis Seizure Control
Hyperventilation
• Useful in initial resuscitation: effectively and rapidly reduce ICP in acute rises until definitive therapy
• Generalized vasoconstriction: cerebral blood volume, ICP
• Chronic hyperventilation should be avoided because CBF puts the brain at risk of ischemia
– Safety of duration is uncertain
Cắt bỏ khối sang thương (Resection of mass lesion)
• Subdural or epidural hemorrhage
– Hematoma evacuation
• Tumours
– Surgical resection
Dẫn lưu DNT
• Communicating hydrocephalus (e.g. SAH, IVH)
– Temporary external ventricular drain
– Long term VP or VA shunt
• Obstructive hydrocephalus (e.g. tumours)
– Temporary external ventricular drain until definitive tumour resection
Nằm đầu cao
• Head of bed at 20 to 30 is optimizes cerebral venous return
• Ensure neutral neck position
• Caution in hypovolemic patients to avoid reduction in MAP and therefore CPP
– CPP = MAP – ICP
Paralysis, Sedation, Hypothermia
• To prevent excess motor activity (posturing, coughing, straining against ventilator)
• To cerebral metabolic rate and CBF (must maintain MAP to improve CPP, caution in HD unstable patients)
• Role of EEG
– Rule out ongoing seizure activity
– Titration of sedation with goal of achieving burst suppression
• Hypothermia, controversial
– Attenuates deleterious biochemical cascade
– cerebral metabolic rate
– risk pneumonia, wound infection, abnormal
lytes/coags
Mannitol and Hypertonic saline (HS)
• Mannitol 20% or 25% solution (0.25 – 1gm/kg IV) – Intravascular fluid shift from osmotic effect
– Decreased blood viscosity and improved flow (? reflex vasocontriction)
– Decreases production of CSF
• Follow serum osmolarity (<320 mOsm) – Avoid systemic dehydration & renal injury
• Can consider adding Furosemide
• Hypertonic saline, if refractory to mannitol – BBB is impermeable to Na+ ions Osmotic
gradient
– Less severe electrolyte disturbances, less brisk diuresis
– Lack of standard guideline (3-7.5% solution at 20-40cc/h)
– Slow taper to avoid rebound hyponatremia
Decompressive craniectomy
• Surgical removal of cranial bone flap to relieve
intracranial pressure
• Useful in large ischemic CVA with profound edema
• Role in traumatic brain injury still needs to be
established
Intraventricular Hemorrhage (IVH)
Hydrocephalus
Hydrocephalus có thể kết hợp
với XHN, đặc biệt vỡ trong não
thất (IVH)
Tăng ALNS
Kết quả dấu thần kinh xấu đi
sớm hay trễ
CLEAR-IVH Trial
52 pts with IVH
Open-label intra-ventricular rt-PA to accelerate blood
clearance and lysis
Adverse events
Symptomatic bleeding 4%
Bacterial ventriculitis 2%
30 day mortality 17%
Efficacy requires confirmation before use of
intraventricular fibrinolysis can be recommended,
Phase III trial in progress.
IVH: Recommendations
1. Although intraventricular administration of rtPA in
IVH appears to have a fairly low complication rate,
the efficacy and safety of this treatment are uncertain (Class IIb; Level of Evidence B). (Revised from
the previous recommendation)
2. The efficacy of endoscopic treatment of IVH is uncertain (Class IIb; Level of Evidence B).
(New recommendation)
Patients with a GCS score of 8 or less, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus might be considered for ICP monitoring and treatment. A CPP of 50-70 mmHg may be reasonable to maintain depending on the status of cerebral autoregulation
Class IIb, Level of Evidence C New recommendation
Ventricular drainage as treatment for hydrocephalus is reasonable in patients with decreased level of consciousness
Class IIa, Level of Evidence B New Recommendation
Although intraventricular administration of rt-PA in IVH appears to have a fairly low complication rate, efficacy and safety of this treatment is uncertain and is considered investigational
Class IIb, Level of Evidence B New Recommendation
ICP Monitoring and Ventriculostomy
©2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited
Surgical Treatment of ICH (Clot Removal)
STICH Trial
902 ICH pts randomized trial of early hematoma
evacuation (<96 hrs) vs medical
Excluded cerebellar ICH
If ICH >1 cm from cortical surface, OR
GCS < 8
Surgical patients tended to do worse than medical
If ICH < 1cm from surface
Trended toward better outcomes with surgery, but
not significant (OR 0.69, 95% CI 0.47-1.01)
Mendelow AD, et al for the STICH Investigators. Lancet
2005;365(9457):387-397
Surgical ICH Trials
Timing of surgery: What is “early”? - Trials have been done using <24, 48, 72, and 96 hours
- Regardless of definition, no clear benefit for surgery
Minimally invasive techniques are being studied
Minimally Invasive Surgical Evacuation of ICH
Several recent randomized studies have compared minimally
invasive aspiration to standard craniotomies and suggested
better outcomes with less invasive approaches
Timing of Surgery
Timing of surgery for ICH remains controversial
Patients with cerebellar hemorrhage who are deteriorating
neurologically or who have brainstem compression and/or
hydrocephalus from ventricular obstruction should undergo
surgical removal of the hemorrhage as soon as possible
(Class I; Level of Evidence B).
(Unchanged from the previous guideline)
Khuyến cáo Surgical Treatment of ICH
1. Patients with cerebellar hemorrhage who are deteriorating
neurologically or who have brainstem compression and/or
hydrocephalus from ventricular obstruction should undergo
surgical removal of the hemorrhage as soon as possible (Class I; Level of Evidence B).
Initial treatment of these patients with ventricular drainage
rather than surgical evacuation is not recommended (Class III; Level of Evidence C).
(Unchanged from the previous guideline)
Evacuation: sự thụt rửa)
2. For most patients with supratentorial ICH, the usefulness of
surgery is not well established (Class IIb; Level of Evidence A). (Revised from the previous
guideline). Specific exceptions and potential subgroup
considerations are outlined below in recommendations
3 through 6.
3. A policy of early hematoma evacuation is not clearly
beneficial compared with hematoma evacuation when patients
deteriorate (Class IIb; Level of Evidence A). (New recommendation)
4. Supratentorial hematoma evacuation in deteriorating
patients might be considered as a life-saving measure (Class IIb; Level of Evidence C). (New recommendation)
5. DC with or without hematoma evacuation might
reduce mortality for patients with supratentorial ICH who are
in a coma, have large hematomas with significant midline
shift, or have elevated ICP refractory to medical management (Class IIb; Level of Evidence C). (New recommendation)
6. The effectiveness of minimally invasive clot evacuation
with stereotactic or endoscopic aspiration with or without
thrombolytic usage is uncertain (Class IIb; Level of Evidence B).
(Revised from the previous guideline)
Outcome Prediction and Withdrawal of
Technological Support
Outcome Prediction and Withdrawal of Technological
Support: Recommendation
1. Aggressive care early after ICH onset and postponement
of new DNAR orders until at least the second full day of
hospitalization is probably recommended
(Class IIa; Level of Evidence B). Patients with preexisting
DNAR orders are not included in this recommendation.
Current prognostic models for individual patients early after
ICH are biased by failure to account for the influence of
withdrawal of support and early DNAR orders. DNAR status
should not limit appropriate medical and surgical interventions
unless otherwise explicitly indicated (Class III; Level of Evidence C). (Revised from the previous guideline)
Prevention of Recurrent ICH
BP should be controlled in all ICH patients
(Class I; Level of Evidence A). (Revised from the previous guideline)
Measures to control BP should begin immediately after ICH
onset
(Class I; Level of Evidence A). (New recommendation)
1. When stratifying a patient’s risk for recurrent ICH
may affect management decisions, it is reasonable
to consider the following risk factors for ICH recurrence:
(1) lobar location of the initial ICH;
(2) older age;
(3) presence and number of microbleeds on gradient
echo MRI;
(4) ongoing anticoagulation; and
(5) presence of apolipoprotein E ε2 or ε4 alleles
(Class IIa; Level of Evidence B).
(Revised from the previous guideline)
2. BP should be controlled in all ICH patients (Class I; Level of Evidence A). (Revised from the previous guideline)
Measures to control BP should begin immediately after
ICH onset (Class I; Level of Evidence A). (New recommendation)
A long-term goal of BP <130 mm Hg systolic and 80 mm
Hg diastolic is reasonable (Class IIa; Level of Evidence B). (New recommendation)
3. Lifestyle modifications, including avoidance of alcohol
use greater than 2 drinks per day, tobacco use,
and illicit drug use, as well as treatment of obstructive
sleep apnea, are probably beneficial
(Class IIa; Level of Evidence B).
(Revised from previous guideline)
4. Avoidance of long-term anticoagulation with warfarin
as a treatment for nonvalvular atrial fibrillation is probably
recommended after warfarin-associated spontaneous lobar
ICH because of the relatively high risk of recurrence (Class IIa; Level of Evidence B).
(Unchanged from the previous guideline)
5. Anticoagulation after nonlobar ICH and antiplatelet
monotherapy after any ICH might be considered, particularly
when there are strong indications for these agents (Class IIb; Level of Evidence B).
(Revised from the previous guideline)
6. The optimal timing to resume oral anticoagulation
after anticoagulant-related ICH is uncertain. Avoidance of
oral anticoagulation for at least 4 weeks, in patients without
mechanical heart valves, might decrease the risk of ICH
recurrence
(Class IIb; Level of Evidence B). (New recommendation), if indicated,
aspirin monotherapy can probably be restarted in the days
after ICH, although the optimal timing is uncertain (Class IIa; Level of Evidence B).
(New recommendation)
7. The usefulness of dabigatran, rivaroxaban, or apixaban
in patients with atrial fibrillation and past ICH to decrease
the risk of recurrence is uncertain (Class IIb; Level of Evidence C).
(New recommendation)
8. There are insufficient data to recommend restrictions
on the use of statins in ICH patients
(Class IIb; Level of Evidence C).
(Unchanged from the previous guideline)
Phục hồi chức năng và hồi phục (Rehabilitation and Recovery)
Given the potentially serious nature and complex pattern of
evolving disability and the increasing evidence for efficacy,
it is recommended that all patients with ICH have access to
multidisciplinary rehabilitation (Class I; Level of Evidence A).
(Revised from the previous guideline)
Rehabilitation and Recovery: Recommendations
1. Given the potentially serious nature and complex
pattern of evolving disability and the increasing evidence
for efficacy, it is recommended that all patients
with ICH have access to multidisciplinary rehabilitation (Class I; Level of Evidence A).
(Revised from the previous guideline)
2. Where possible, rehabilitation can be beneficial
when begun as early as possible and continued in the
community as part of a well-coordinated (“seamless”)
program of accelerated hospital discharge and home-
based resettlement to promote ongoing recovery
(Class IIa; Level of Evidence B).
(Unchanged from the previous guideline)
Thank you!