This kind of blood pressure reduction is easy to cause cerebral infarction, and the correct method is ...

*For medical professionals only

Rapid blood pressure reduction is the predisposing cause of the patient's onset

Cerebral watershed infarction (CWSI) is caused by ischemia at the junction of adjacent vascular blood supply areas, or in watershed areas, and is often caused by hemodynamic reasons
.
Typically occurs when the internal carotid artery is severely narrowed with a decrease in systemic blood pressure
.

Watershed infarction is mostly associated with vascular stenosis, and the annual case fatality rate can reach 9.
9%.

The author has encountered patients with typical watershed cerebral infarction in the clinic, and I share it with you
.

Case analysis

The patient, a 69-year-old male, was admitted to the hospital with the
main complaint of "finding weakness in the right limb for 1 day".
1 day before admission, the patient went to the local hospital for head disease, measured blood pressure 230/130mmHg, gave "nitroglycerin" to reduce blood pressure, and after 3h, the blood pressure dropped to 160/90mmHg, the headache was relieved, but the weakness of the upper and lower limbs on the right side appeared, which gradually worsened, and the immediate head CT scan did not see obvious abnormalities
.

There are 3 episodes of right limb weakness within 1 week before admission, each lasting 5 to 10 minutes, which can be relieved
on its own.
In the past, there were diabetes for 9 years, hypertension for 8 years, and the maximum blood pressure was 230/130mmHg, and the blood pressure and blood sugar control were poor
.
Smoked for more than 40 years, 20 cigarettes a
day.

Physical examination: P: 88 times / min, BP: left 135/80 mmHg, right side 140/78 mmHg
.
There are no abnormalities
on cardiopulmonary auscultation.

Neurologic examination: vascular murmur may be heard in the auscultation area of the left carotid artery, and vascular murmur may be heard in the right carotid artery, bilateral vertebral artery, subclavian artery, and ophthalmic artery auscultation area
.

The right nasolabial fold is slightly shallow, speech is normal, tongue extension is centered, and the gag reflex is present; Right limb muscle strength 5-level, left side 5 grade, normal muscle tone of the extremities, right upper extremity finger-nose test (+), left side normal; mild loss of pain in the right extremities; Increased tendon reflexes of the right upper and lower extremities, right pathological signs (+); Meningeal irritation signs (-); The National Institutes of Health Stroke Scale (NIHSS) scores 3.

After admission, the blood was checked TC 7.
3mmol/L, TG 3.
2mmol/L, LDL-C 3.
8mmol/L, GLU 11.
2mmol/L, hsCRP 3.
71mg/L, and blood homocysteine 24μmol/L
.
The ECG is normal
.

Cardiac color ultrasound: normal left ventricular systolic function, thickening of the ventricular septum, and mild restriction
of left ventricular diastolic function.
Carotid hypersonography: bilateral thickening of the median lining of the carotid artery, stenosis of the initiation of the left internal carotid artery with hypoechoic plaque
.

TCD: moderate increase in blood flow in the left posterior cerebral artery
.
MRI of the skull: multiple cerebral infarction in the left frontotemporomoprotic lobe
.
Cranial CTA: left internal carotid artery begins with narrowing and local plaque formation
.

Admission diagnosis: (1) cerebral infarction; (2) Diabetes; (3) Hypertension
.

Treatment: under ECG monitoring, suspend the use of antihypertensive drugs, give medium molecular weight hydroxyethyl starch expansion, aspirin and clopidogrel antiplatelet aggregation, edaraven scavenging free radicals, insulin control blood sugar, atorvastatin 40mg/day fortified lipid-lowering and vitamin_B1, metcobalammonium, vitamin_B6, folic acid therapy
.

DSA after stable condition: severe stenosis of the starting segment of the left internal carotid artery, the stenosis rate is about 95%; The anterior cerebral artery is left-sided dominant
.
With the consent of the family, the left internal carotid artery stenting is performed, and the DSA is repeated after the stent placement to see the lumen of the left internal carotid artery stenosis enlarged and the stent is pate.

Amlodipine was added to control blood pressure after surgery, and the blood pressure fluctuated at 120-140/70-90mmHg
.
At the time of discharge, the patient's limb muscle strength was basically normal
.

Postoperative follow-up for 4 months without recurrent stroke, re-examination of neck and skull CTA: after left internal carotid artery stenting, the distal end of the left common carotid artery, the beginning of the internal carotid artery are stented, the lumen inside the stent is pate, and the contrast medium is filled
.

Positioning, qualitative diagnosis?

   

▌ Localization diagnosis: (1) Left cortical spinal cord tract:

the patient is paralyzed on the right upper and lower limbs, the tendon reflex of the right upper and lower limbs is increased, and the right side pathological signs (+).

(2) Left cortical brainstem bundle: the patient has mild central facial palsy
on the right side.
(3) Left thalamic cortical tract: the patient's right limb pain is mildly reduced
.
MRI of the skull confirmed to be the left cerebral hemisphere
.

▌ Qualitative diagnosis:
(1) cerebral infarction; (2) hypertension, grade 3, extremely high-risk; (3) Type 2 diabetes; (4) mixed hyperlipidemia; (5) Hyperhomocysteinemia; (6) The beginning of the left internal carotid artery is narrowed
.

Typing and imaging changes in watershed cerebral infarction

Watershed cerebral infarction, also known as marginal band infarction, refers to cerebral infarction that occurs in the marginal band between adjacent artery blood supply areas in the brain
.

According to the characteristics of blood circulation distribution in the brain, CWSI in the cerebral hemisphere is divided into cortical type (lateral type) and subcortical type (medial type); The former is divided into precortical, posterior and upper corticosterotype; The latter is divided into subcortical anterior, superior and lateral types
.

Clinically, the diagnosis and classification of CWSI depends on cranial CT or MRI, and DWI is particularly sensitive to early diagnosis, so CWSI in the cerebral hemisphere can often be divided into the following 6 types
according to brain imaging changes.

(1) The watershed area between the anterior cortical artery (ACA) of the anterior cortex of the cortical type of cortex (ACA) and the middle cerebral artery (MCA) is located in the frontal parietal lobe, in the form of a band or wedge, with the tip facing the lateral ventricle and the bottom facing the cortical plecopeomeninges
.

(2) The watershed between postcortical MCA and the cortical branch of the posterior cerebral artery (PCA) is often located in the temporomopatopal occipital junction, and the lesion is also wedge-shaped, with the tip facing the ventricles, which is the most common
.

(3) The watershed area between the blood supply area of the cortical branch of the upper cortical ACA/MCA/PCA is located in the middle of the frontal gyrus, the upper part of the central anterior and posterior gyrus, the upper lobule of the apex and the upper part of
the occipital lobe.

(4) The watershed area between the subcortical anterior ACA cortical branch and the return branch, the cortical branch of MCA and the bean artery or the anterior choroidal artery, is located laterally laterally on the anterior corner of the lateral ventricle and is cord-like
.

(5) The watershed area between the inferior superior choroidal artery and MCA is located next to the lateral ventricular body, and it travels backwards and forwards in a cord along the outside of the caudal nucleus; Above the lateral ventricles, the center of the semi-ovoid or radial crown, higher than the basal ganglion level, beaded or fused into striped lesions, and there are also linear infarction lesions
that walk anteriorly.

(6) The watershed between the subcortical lateral bean artery and the insula artery is located between
the lateral shell nucleus and the insula.

In addition, cerebellar and brainstem CWSI is less common, cerebellar CWSI is mainly seen in the upper cerebellar artery (SCA) and anterior inferior cerebellar artery (AICA) junction infarction, and some studies have suggested that cerebellar infarction less than 2 cm in diameter is mostly cerebellar CWSI
.

Because the range of blood supply to the ACA, MCA, PCA, SCA, AICA, and the posterior lower cerebellum artery (PICA) varies greatly in different patients, the location of the brain watershed area is not constant, and the location of CWSI lesions may also be "variated"
.

The relationship between watershed cerebral infarction and blood pressure

       

The pathophysiology of subcortical CWSI has traditionally been thought to be associated with carotid artery stenosis and hemodynamic changes (hypotension) leading to hypoperfusion in the brain, and has also been thought to be caused by
microembolism.
The two mechanisms are not considered to be in conflict, with both hypoperfusion and microemboli acting in the subcortical CWSI
.

The vortex after macrovascular stenosis is the source of microemboli, whereas on the basis of macrovascular stenosis, systemic hypotension or a sharp drop in blood pressure causes hemodynamic abnormalities leading to hypoperfusion, and the two often act
simultaneously.

Cerebral blood flow is the highest in the systemic circulation, brain tissue is most sensitive to ischemia, and the watershed area is the farthest from the heart, is the terminal arterioles, and is most susceptible to the effects of hypotension in
the receptor circulation.

If the patient has stenosis or occlusion of the large arteries inside and outside the skull, it can cause a further decrease in the perfusion pressure of the distal terminal arterioles, and the terminal arteriole blood supply area is prone to ischemic infarction
.
CWSI
is more likely to occur if hypotension or hemodynamic disturbance recurs.

For patients with refractory hypertension who have severe stenosis or occlusion of the aorta, the blood pressure is maintained at a high level, which may be an automatic adjustment mechanism for the body to have severe stenosis or occlusion of the cerebral aortic arteries to ensure adequate blood flow perfusion of
brain tissue.

Rapid antihypertensive can cause abrupt changes in brain hemodynamics in a short period of time, especially in patients with severe stenosis of the cerebral aorta, even if the blood pressure does not drop below normal blood pressure, it may lead to significant hypoperfusion of brain tissue, the occurrence of CWSI
.

In summary, rapid antihypertensive is the predisposing cause
of the onset of the disease in this patient.

Treatment of watershed cerebral infarction

       

In this case, the patient was subcortical CWSI, and the patients with cervical vascular color ultrasound, CTA and DSA found that the initiation segment of the left internal carotid artery was narrowed and had a hypoechoic plaque, and diabetes mellitus was also concomitant, and the pathogenesis was considered to be hypoperfusion/microemboli clearance disorder
.

Therefore, the risk stratification of the antiplatelet drug is extremely high-risk, so the combination of aspirin and clovigrel is selected for intensive antiplatelet aggregation therapy: while the lipid risk stratification is extremely high-risk I, the administration of statin enhancement lipid-lowering should be started immediately, with the goal of reducing LDL-C to less than 2.
1 mmol/L or reducing it by >40%.


In addition, patients with diabetes, poststroke hyperglycemia is not good for prognosis, should be actively controlled, guidelines recommend that blood glucose more than 11.
1 mmol/L should be given insulin therapy
.
Hyperhomocysteinemia is also considered to be one of the independent risk factors for atherosclerosis, and administration of folic acid, vitamin_B12, vitamin_B6, etc.
can effectively reduce homocysteine levels
.

The treatment of CWSI is not the same as
that of general cerebral infarction.
The onset of CWSI in this patient is considered to be related to rapid blood pressure reduction, and antihypertensive drugs should be discontinued first, and the expansion should be given to maintain blood pressure stability
.

Because the patient's blood pressure is higher before the onset of the disease, the blood pressure can be temporarily maintained at the level of 180-200/100-110mmHg, and the blood pressure, heart rate, and cardiac function should be closely monitored
.
Blood dilatomy therapy is not recommended, and dehydration therapy is avoided as much as possible to prevent volume depletion or hypotension and worsening cerebral ischemia
.

Usually 1 week after the onset of the disease, antihypertensive drugs can be added gradually according to the blood pressure situation, and long-acting calcium channel blockers are preferred to slowly reduce
blood pressure.
If the patient has a narrowing of the initiation of the left internal carotid artery without further surgical management temporarily, it is recommended that blood pressure eventually remain slightly higher
than normal.

References:

Yu Jinmei.
Treatment and clinical prognosis of watershed cerebral infarction.
Chinese Journal of Practical Medicine,2020,15(06).

[2] Ahmed AK,Nermeen AE.
Imaging of vascular cognitive impairment.
Clin Imaging,2021.
74：45-54.

Li Yan, Li Guixue, Lei Jie.
A correlation between blood pressure intervention and prognosis in watershed cerebral infarction.
Chinese Medicine Guide.
2020,18(04).

Where to look for more clinical knowledge of neurology?
Come to the "Doctor's Station" and take a look 👇