4.Neurology II Hemorrhagic Stroke 2014A

Apale, Aquino, Aquino, Arceo Chen Page 1 of 12

Outline I. Intracranial Hemorrhage

A. Intracerebral Hemorrhage (ICH) B. Etiology of Spontaneous Hemorrhage

1. Hypertension 2. Cerebral Amyloid Angiopathy 3. Vascular Malformation 4. Cerebral Aneurysm 5. Cerebral Vein Thrombosis 6. Coagulation and Fibrinolysis 7. Blood Dyscrasia 8. Drugs

II. Grading Systems Used to Evaluate Severity of SAH III. Cases IV. Treatment

A. For all ICH B. Specific for AVM C. Specific for Aneurysm

Note: We didnt use Dr. Aquinos photos for this part because the images he used on his slide were of poor quality. Chot. Seriously though, we included the sources of the photos just to be safe. Also, we tried to find photos that were almost similar to the ones Dr. A used. Editor: medyo binago ng group yung arrangement ng topics ayon sa discussion ni sir pero ayos lang dahil nandito naman lahat. Wag matakot sa haba, puro pictures. Recording. Naka-italics din yung ibang recording. Book

Intracranial Hemorrhage

Intracerebral Hemorrhage (ICH)

From: http://www.columbianeuroicu.org/diseases/stroke.html

Intracerebral hemorrhage the hemorrhage is right in the brain parenchyma.

May appear immediately after head injury, but may also be delayed in development by several days (spat apoplexie). Bleeding is in subcortical white matter of one lobe, or in deeper structures such as the basal ganglia or thalamus. [Adams]

Clinical picture: deepening coma with hemiplegia, a dilating pupil, bilateral Babinski, and stertorous and irregular respirations; the additional mass may manifest as an abrupt rise in BP and ICP.

Intraventricular Hemorrhage (IVH)

From: http://jnnp.bmj.com/content/64/5/686.full

Intraventricular hemorrhage if the blood has extended into the ventricles or it could also be a hemorrhagic conversion of an ischemic stroke. In other words, the initial event was ischemia or cerebral infarction but the patient developed hemorrhagic conversion. So this is your hemorrhagic stroke.

Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage where your blood is primarily confined in the subarachnoid space

From: Adams & Victors, Principles of Neurology

Spontaneous subarachnoid hemorrhage (AKA ruptured saccular aneurysms, or berry aneurysms). As a rule, the vessels are located at vessel bifurcations and branchings (90-95% in anterior part of Circle of Willis). [Adams]

Hemorrhagic conversion of Ischemic Stroke

From: http://www.sciencedirect.com/science/article/pii/S000291490000878X

Hemorrhagic conversion of Ischemic stroke- initial event was ischemia or cerebral infarction but the patient developed hemorrhagic conversion

Subdural Hematoma

From: http://emedicine.medscape.com/article/1137207-overview

Subdural hematoma cortical veins or bridging veins [are involved]

Hemorrhagic Stroke: Diagnosis and Management

September 24, 2012

Dr. Abdias V. Aquino


Acute subdural hematomas may be unilateral or bilateral, and may be accompanied by epidural hemorrhage, cerebral contusion, or laceration. A large acute clot causes a midline shift as well as marked compression of one lateral ventricle. Bilateral clots may reveal no midline shift, but the ventricles may appear symmetrically compressed. Rising intracranial pressure usually arrest venous bleeding. Disorders of mentation and consciousness are more prominent than focal signs, such as aphasia or hemiparesis. [Adams]

Epidural Hematoma

From: http://emedicine.medscape.com/article/824029-overview

You will be able to recognize epidural hematoma by its configuration in the imaging.

The epidural hematoma is usually secondary to the rupture of middle meningeal artery, especially in the parietal area or temporoparietal area.

CT scan is definitive and shows a lens-shaped clot with smooth inner margin. As a rule, epidural hematoma arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. Lumbar puncture is contraindicated. Death, which is almost invariable if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory arrest. [Adams] Radiologic features of epidural hematoma - Acute bulging epidural clot

bounded by cranial sutures; lenticular in shape [Adams] o Lenticular shape = biconvex [Oxford dictionary]

Sizes of hematoma (estimate the amount of blood based on neuroimaging) Size of a ping-pong ball = 28mL Size of a golf ball = 43mL

Intracerebral Hemorrhage (ICH)

Epidemiology

Intracerebral hemorrhage is the most devastating form of stroke.

Third most frequent cause of stroke. Most dramatic, and, from ancient times, has been named apoplexy. The prototype is an obese, plethoric, hypertensive male who falls to the ground impervious to shouts, shaking, and pinching breathes stertorously, and dies in a few hours. [Adams]

ICH results in higher mortality (35-52%) and worse functional outcome than any other stroke subtype.

Only 20% of ICH patients are independent at 6 months vs. 60% of ischemic stroke patients.

Remember, it also depends on the size of the hematoma. If the hematoma is small, they are probably better functioning than your ischemic stroke patients. But in general, patients with intracranial hematoma are worse than patients with ischemic stroke.

Location

Deep 50%

Lobar 35%

Cerebellar 10%

Brain Stem 6%

Most common location is deep with 50%. Lobar is either in the temporal lobes or parietal. These locations of hemorrhages are based on hypertensive hemorrhages. In general, the most common cause of hemorrhage is hypertension. If it is located in the deep part of the brain, it is caused by hypertension unless proven otherwise. If it is in the lobar area, think of another etiology besides hypertension, although hypertension could still be the most common cause. [2013B] Deep in the basal ganglia; most common site of spontaneous ICH; most common cause is hypertension Lobar either in frontal, temporal, or parietal lobe *The best patients that will survive large hematoma are those that are found in the surface of the brain as compared to intracerebral or deep portions of the brain

Mortality by Location

Deep 51%

Lobar 57%

Cerebellar 42%

Brain Stem 65%

The worst mortality is associated with the brain stem, (65%). If you have a hematoma there, it can disrupt your ascending reticular activating system, and respiratory center. Next is your Lobar, then deep, and cerebellar parts of the brain. [2013B trans] Worst prognosis in the brain stem Reticular activating system (RAS, and the respiratory center can be found in the brain stem. Best candidate for surgery: Cerebellar stroke If cerebellar hematoma is operated before deterioration of brain stem, patients can recover in as early as right after surgery. Critical size of hematoma is 3cc or 3cm Posterior fossa space is very small. Hematoma as large as a pingpong ball is quite large. Anything below 3cc or 3cm, need not call a neurosurgeon, but watch out because patient may deteriorate Once cerebellum swells, it can compress on the 4th ventricle or the brain stem itself.

Etiology of Spontaneous Cerebral Hemorrhage

Hypertension Hypertension = deep lesion. If you see a deep lesion (i.e. in the basal ganglia, putamen,

caudate, lenticular nucleus) then it must be caused by hypertension unless proven otherwise.

Cerebral Amyloid Angiopathy


If it is in the lobar area, it could be cerebral amyloid angiopathy depending on the age of the patient, this is usually seen in the elderly.

Vascular Malformation Now, it can also be vascular malformation or cerebral

aneurysm, this is seen in all age groups. But if you have a patient who is young and he/she has a intracerebral hemorrhage and is not hypertensive, think of vascular malformation or probably an aneurysm.

Cerebral Aneurysm

Cerebral Vein Thrombosis

Coagulation and Fibrinolysis

Blood Dyscrasia

Drugs

Spontaneous means that it is not related to trauma. Because trauma, it is related to subdural and epidural hematoma. Incidentally, most common cause of subarachnoid hemorrhage is trauma (especially now, with the increasing incidence of motorcycle accidents, which you see around 5-10 of these everyday, nationwide).

Hypertension

Hypertension is directly related to primary and secondary stroke risk

Most important modifiable risk factor for stroke

Hypertensive people are 3-4x more likely to have a stroke than non-hypertensive people

10 to 12 mmHg SBP reduction and a 5 to 6 mmHg DBP reduction confers relative reductions in stroke risk of 38%.

Choice of antihypertensive agents should be individualized. Any hemorrhage seen in the brain, ALWAYS THINK HYPERTENSION FIRST

[2013B trans]

Hypertension = most common cause of ischemic stroke. So you really have to treat hypertension.

In order of frequency, the most common sites of a hypertensive cerebral hemorrhage are (1) the putamen and adjacent internal capsule (50 percent); (2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension); (3) the thalamus; (4) one or the other cerebellar hemisphere; and (5) the pons.

Charcot-Bouchard Aneurysm

Intracerebral hemorrhage related to hypertension; most common cause is the rupture of your lenticulostriate arteries. Thats why the most common site of hypertensive bleed is in the putamen, caudate nucleus and the lenticular nuclei because of your lenticulostriate artery branches, these are end-arteries and they suffer most of the

brunt of hypertension. So if you have a hemorrhage, in this area, thats probably hypertensive bleed. Many years ago, maybe in the 1800s, Charcot and Bouchard described

the Charcot-Bouchard aneurysms. They say this is the pathology or the main reason for ruptured or intracerebral hemorrhage. These are your small aneurysms coming out of the anterior and/or posterior lenticulostriate branches.

Microaneurysms (blood vessels


Feeding vessels (arteries) may be the source of bleeding. Depending on the size of the malformation, you could have a large draining vein, or a large feeding artery. As for the management of this patient, neurosurgeons will just simply occlude the feeding arteries and the malformation will collapse since there will be nothing that will supply blood to the malformation. Clinical Features

Most are clinically silent for a long time

Onset of symptoms most common between ages 10-30 years Age is very important especially if the patient does not

have any other risk factor (e.g. hypertension, bleeding dyscrasias, etc)

Bleeding (usually SAH in 50%) or seizures (30%) are the main modes of presentation

In 20% of patients, headache is the only symptom

Intracerebral steal

Rate of rebleeding: 2-4% per year over decades, may be as high as 6-9% after a first hemorrhage

Age is very important. In seizures, patient may be asymptomatic but then suddenly at the age of 24 or 25 the patient develops seizure, these patients must be evaluated accordingly, since these seizures very rarely or no longer are congenital seizures.

Intracerebral steal- if the malformation is so large you have large arteries there, it can steal blood from the other parts of the brain and this may cause infarction and ischemia. [2013B]

o LOBAR HEMATOMA IN THE YOUNG o Four types of vascular malformations that can cause hemorrhage:

arteriovenous malformation, cavernous angioma, capillary telangiectasia, venous angioma

Spetzler-Martin Grading System for evaluating the risk of surgery aphasias in AV malformations

Characteristic No. of Points Assigned

Size of Lesion

Small (maximal diameter, 6 cm)

1 2 3

Location

Noneloquent site Sensorimotor, language, or visual cortex; hypothalamus or thalamus; internal capsule; brain stem; cerebellar peduncles; or cerebellar

0 1

nuclei

Pattern of Venous Drainage

Superficial only Any deep

0 1

* A score of 4 or 5 is associated with the highest risk of persistent neurologic deficits after surgery. Data are from Spetzler and Martin. Eloquent site usually the dominant hemisphere

Imaging of AV Malformations

Computed Tomography

CT scan calcifications in patients with AV malformation Magnetic Resonance Imaging

On MRI, you can see that there are some blood or hemosiderin

pigments. Angiography that reveals vascular malformation

Cerebral Aneurysm Result from congenital defects, pre-existing conditions such as

high blood pressure and atherosclerosis or head trauma Or even infection like mycotic aneurysms. In fact, in the

very recent study, the most common cause of secondary aneurysm is

Congenital is primary cause. You are born with it like in patients with a family history of a polycystic kidney. These patients may have aneurysms. Thats why in some patients who have relatives with polycystic kidney, we even go to


the extent of doing MRA to see if they have aneurysms as well.

The annual risk of rupture for aneurysms 10 mm in size is 0.51%

Younger patients with aneurysms >10 mm in size may benefit from prophylactic treatment

Most unruptured intracranial aneurysms are completely asymptomatic

Symptoms are usually due to rupture, others maybe due to mass effect

Early aneurysm repair prevents rerupture

Can be clipped or coiled Another risk factor is smoking for (ICH). It is very high risk in cardiovascular diseases. *It is impossible to make a diagnosis of an aneurysm clinically unless it ruptures. Thus if you want to find out, you have to spend for it.

Although there are other clinical signs, like if a patient has a posterior communicating artery aneurysm, they may present clinically with ptosis without necessarily having a headache. Because the PCOM [posterior communicating artery] aneurysm will compress on your third cranial nerve. So its one of the non-headache manifestations of aneurysm. Third nerve compression is an example of a mass effect.

In fusiform aneurysm, wherein there is no neck, the aneurysm

just bulges on the sides of the artery. This is very difficult to treat. Fusiform deformities are also referred to as arteriosclerotic

aneurysms, as they frequently show atheromatous deposition in their walls, but it is likely that they are at least partly developmental in nature.

The giant fusiform aneurysm of the midbasilar artery, with signs of brainstem ischemia and lower cranial nerve palsies, is a relatively common form.

Mycotic aneurysm if you have bacterial endocarditis, you have vegetation in your heart, it can metastasize to the brain and destroy the blood vessels and produce an aneurysm. The source of mycotic aneurysm is usually bacterial endocarditis.

The mycotic aneurysm is caused by a septic embolus that weakens the wall of the vessel in which it lodges, almost always at a site in a distal cerebral vessel, well beyond the circle of Willis.

- an angiographic picture of a cerebral aneurysm.

Cerebral Vein Thrombosis Presence of thrombus within a superficial or deep vein, along

with the accompanying inflammatory response

Predisposing factor includes stasis, vascular damage, and hypercoagulability

Treatment is anticoagulant therapy This may be confusing in that why are you going to treat a

bleed with anticoagulation. Well because you want to prevent further thrombosis. The results are better than those who are not using anticoagulants.

Cerebral Vein Thrombosis = uncommon but it can happen. This happens most commonly in pregnant women due to their hypercoagulable state. And in patients who are severely dehydrated, this can happen or if they have hypercoagulable situations. This is a venous infarct. Because the blood is no longer

absorbed into the venous system and into the subarachnoid and the arachnoid granulation, in your circulation, what happens is that there is a backflow of blood from the venous system. So what happens is, it can rupture and you can have a hemorrhage so thats because of your stasis and vascular damage and hypercoagulability.

[2013B] o Sagital vein thrombosis there is an occlusion o This type of thrombosis can convert into a haemorrhage o If in the area of the sagital sinus and patient had a period of

dehydration, development of thrombosis in the veins occurs. If patient had previous ear infection, it can spread to the sinuses and can cause thrombosis in the sinuses of the brain

Coagulation and Fibrinolysis Hemorrhages can occur at any location

Often lobar or subdural

Usually evolve slowly over 24-48 hours

Should be reversed rapidly Especially if it is related to heparin for AF [atrial

fibrillation] to prevent stroke or any of this new anticoagulants, you should reverse the protime rapidly to avoid further hemorrhage.

If you give thrombolysis nowadays, rTPA, you can cause

hemorrhage in the brain (6%). We usually put 6% bleeding, 30% improvement after about 6 months.

Drugs Cocaine and methamphetamine

Enhances sympathetic activity causing acute sometimes severe hypertension leading to hemorrhage


Blood Dyscrasia Hemophilia, leukemia, dengue

Grading Systems Used to Evaluate Severity of SAH SAH subarachnoid hemorrhage So if a patient comes in with a diagnosis of subarachnoid

hemorrhage, the patient usually presents with neck rigidity. Sudden headache which may not be necessarily the worst headache in the patients life, but they could have a sentinel headache like one day they were ok or while walking and then they develop a very severe sudden headache and may loose consciousness or may feel dizzy. They recover and go back to their normal activity, and then a week later they again develop a sudden severe headache with a loss of consciousness. This is called a sentinel headache. This is always asked in the history.

An entity known as "sentinel headache" has been used in an imprecise way to refer to both a headache that precedes subarachnoid hemorrhage and to a small leakage prior to a major rupture. [Adams]

There are several ways of assessing patients who come in with a so-called subarachnoid hemorrhage and once you have made the diagnosis, headaches, severe headaches, worst or may not be the worst headache, something like a thunderclap headache, and the patient may lose consciousness and when you examine them, they don't have neurologic deficits, but they have neck rigidity only, they can be fully conscious, you have to watch out and admit that patient for work-up.

A distinctive type of headache is produced by subarachnoid hemorrhage; it is very intense and very sudden in onset and is associated with vomiting and neck stiffness. It is not uncommon for the rupture of an aneurysm that gives rise to subarachnoid hemorrhage to be precipitated by exertion, even of minor degree.

"Thunderclap headache" may be a variant of migraine, or less often, cerebral venous thrombosis, diffuse vasospasm (the Call-Fleming syndrome), or even less often, pituitary apoplexy, hypertensive encephalopathy, intracranial hypotension, and intracranial or extracranial arterial dissection The details of the CSF examination assume great importance in the diagnosis of subarachnoid hemorrhage and the exclusion of the disorders mentioned above.

You grade them according to your Hunt and Hess scale [seen below]

The Glasgow Coma Scale - measures the motor response, verbal response, and eye-opening response with these values

Response Score

Eye Opening Response

Spontaneous--open with blinking at baseline To verbal stimuli, command, speech To pain only (not applied to face) No response

4 3 2 1

Verbal Response

Oriented 5 points Confused conversation, but able to answer questions Inappropriate words Incomprehensible speech No response

5 4 3 2 1

Motor Response

Obeys commands for movement Purposeful movement to painful stimulus Withdraws in response to pain Flexion in response to pain (decorticate posturing) Extension response in response to pain (decerebrate posturing) No response

6 5 4 3 2

1

Fishers CT Grading of SAH classifies the appearance of subarachnoid hemorrhage on CT scan

Normal scan 1

1 mm thickness of blood 3

Any amount of blood with ventricular bleeding

4

Hunt and Hess Scale

Grade Signs and Symptoms Survival

1 A symptomatic or minimal headache and slight nuchal rigidity

70%

2 Moderate to severe headache nuchal rigidity, no neurologic deficit except cranial nerve palsy

60%

3 Drowsy, confusion, or mild focal deficit 50%

4 Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances

20%

5 Deep coma; decerebrate rigidity; moribund appearance

10%

There is a caveat here. Sometimes, if you say that this patient has a minimal headache, symptomatic only with a slight nuchal rigidity, they don't necessarily have 70% survival especially if they rerupture. Because a second rupture can make them 60% mortality.

This is at initial evaluation and is also based on management. In UERM, if you are exposed to the neurosurgeons here, if a

patient is a Hunt and Hess 3 or 4, they will wait for 2 weeks before they operate on the patient. There are some neurosurgeons who would go in right away. So if varies, it depends on how you assess your patient.

Other management is coiling. Regardless of the grade, you can coil a patient.

World Federation of Neurological Surgeons Scale

Grade Glasgow Coma Scale Major Focal Deficit

0 Unruptured

1 15 Absent

2 13-14 Absent

3 13-14 Present

4 7-12 Present/Absent

5 3-6 Present/Absent

Interpretation: Maximum score of 15 has the best prognosis Minimum score of 3 has the worst prognosis Scores of 8 or above have a good chance for recovery Scores of 3-5 are potentially fatal, especially if accompanied by fixed pupils or absent oculovestibular responses Young children may be nonverbal, requiring a modification of the coma scale for evaluation


A 45 year old man presented with mild left hemiparesis. He had significant neuorologic deterioration in the Emergency Department. CT scan at presentation (left) and one hour later (right) shows dramatic hematoma enlargement. Shows hematoma, probably hypertensive since the location of the hematoma is in the basal ganglia, and there is compression of the anterior horns already. One hour later, the patient deteriorated and the CT scan showed that the hematoma enlarged. *Blood clot will not stop the bleeding. If initially the size of the hematoma is as big as a pingpong ball and then progressed into the size of a golf ball, this indicates that the hematoma will become life threatening. You have to be very watchful in this case, thats why when my patient comes in with cerebral hemorrhage, I usually monitor them closely in the first 24 hours and repeat a scan after 6 hours because usually at the first 3 hours, thats when the hematoma enlarges, but it can also enlarge anytime in the 24 hour period. However, if your patient does not deteriorate after 24-48 you are almost certain that the hematoma will not enlarge anymore. Nobody knows about the mechanism, it may be due to [uncontrolled] hypertension and hemodynamic changes. Early Hemorrhage Growth in Patients with ICH (n=103) Criteria: in hematoma size by 33%

26 % between baseline & 1 hr CT 12 % between baseline & 20th hr CT 38%

very elevated BP seems a plausible contributory factor

Cases

Case 1

L.C., 50/M, right-handed, known hypertensive, was admitted with an 18 hour history of dizziness, right-sided weakness, slurring of speech and facial asymmetry. So you know right away that there is a localization here, a

lateralizing sign.

He was brought to a local hospital where CT scan showed a pontine hemorrhage and was transferred for further management.

Blood pressure at the emergency room was 180/100 mmHg.

On examination, the patient was drowsy but arousable, had paralysis of lateral and upward gaze with primary gaze at the midline.

Sensation was impaired on the right V1-V3 distribution.

Peripheral facial paralysis, a weak gag were noted on the left, and the tongue was deviated to the left.

Motor strength was 3/5 on the right upper and 4/5 on the right lower extremity.

DTRs were hyperactive with bilateral Babinski signs.

There was no nystagmus, dysmetria or dysdiadokinesia.

No meningeal irritation was noted.

Patient had paralysis of lateral and upward gaze with primary gaze at the midline. this means that there is involvement of the cranial nerves. Peripheral facial paralysis- since the lesion is nuclear, it is in the pons where your 7

th cranial nerve nucleus is.

With bilateral Babinski signs- caused by the compression of pyramidal tracts bilaterally. Based on the clinical profile, CT scan is no longer needed, since you already know that the lesion in the brainstem. You have a pontine hemorrhage.

Hemorrhage into the pons is almost invariably associated with deep coma within a few minutes; the remainder of the clinical picture is dominated by total paralysis with bilateral Babinski signs, decerebrate rigidity, and small (1-mm) pupils that react to light. Lateral eye movements, evoked by head turning or caloric testing, are impaired or absent. Death usually occurs within a few hours, but there are exceptions in which consciousness is retained and the clinical manifestations indicate a smaller lesion in the tegmentum of the pons (disturbances of lateral ocular movements, crossed sensory or motor disturbances, small pupils, and cranial nerve palsies) in addition to signs of bilateral corticospinal tract involvement.

[2013B] o This is probably a brain stem hemorrhage o Picture showed that patient had a pontine bleed o Pontine bleeds management and clinical presentation will

depend on size and location o Best management: PRAY


Case 2 G.C., a 59/M right-handed, known hypertensive was admitted

due to headache, dizziness, left-sided weakness and vomiting episodes of 6 1/2 hours duration.

He was initially brought to a nearby hospital where CT scan showed an intracerebral hemorrhage in the right thalamus. He was transferred per request.

Initial blood pressure at the ER was 180/100 mmHg.

Upon examination, the patient was stuporous with purposeful movement of the right upper and lower extremities.

Pupils were 3mm sluggishly reactive to light with downward deviation of primary gaze and presence of limited extraocular movement.

There was weakness of the corneal reflex on the left, with left central facial palsy and left-sided hemiplegia with motor strength of 1/5 on both upper and lower extremities. Left central facial palsy why central? Because it is

supratentorial.

The patient was normoreflexive but bilateral babinski was present.

There was no nystagmus and no signs of meningeal irritation were noted.

Thalamic hemorrhage The central feature here is severe multimodal

sensory loss on the entire contralateral body. If large or moderate in size, thalamic hemorrhage also produces a hemiplegia or hemiparesis by compression or destruction of the adjacent internal capsule. The sensory deficit involves all of the opposite side including the trunk and may exceed the motor weakness. A fluent aphasia or anemia may be present with lesions of the dominant side and amorphosynthesis and contralateral neglect, with lesions of the nondominant side. A homonymous field defect, if present, usually clears in a few days.

[2013B] o Presumably hypertensive ICH o Very large hematoma in the thalamus; it is compressing on the

midbrain; hematoma extending to the midbrain is a poor sign o Very deep hematoma, if operated, may hit a lot of brain tissue,

damage may create more problems

downward deviation of primary gaze and presence of limited extraocular movement. Why is there a downward deviation? The lesion is in the thalamus, the hematoma is compressing in the midbrain. The midbrain contains the 3

rd nerve nuclei, which is

responsible for upward and downward ocular movement, and medial rectus movement.. Etc..

If you have a thalamic bleed, which is right on top of your midbrain, it will compress your midbrain, and therefore your eyes will be looking down. In fact, that is one of the clinical signs of a thalamic bleed. If you see a patient in the ER and you look at the eyes, check the pupils, where is the eyes directed to? If the eyes are downward, unless proven otherwise, thats thalamic or it could also be brainstem but anyway, it simply means that there is involvement of your midbrain.

Thalamic hemorrhage, by virtue of its extension into the subthalamus and high midbrain, may also cause a series of ocular disturbancespseudoabducens palsies with one or both eyes turned asymmetrically inward and slightly downward, palsies of vertical and lateral gaze, forced deviation of the eyes downward, inequality of pupils with absence of light reaction, skew deviation with the eye ipsilateral to the hemorrhage assuming a higher position than the contralateral eye, ipsilateral ptosis and miosis (Horner syndrome), absence of convergence, retraction nystagmus, and tucking in (retraction) of the upper eyelids. Extension of the neck may be observed.

Case 3

60/F, right-handed, known hypertensive and diabetic was brought to the ER for a 2-hour history of left sided weakness, dysarthria, and episodes of vomiting. On examination, BP was 240/120 mmHg, HR 52, with Cheyne-Stokes respiration. Neurologic examination showed a stuporous patient with unsustained eye opening to painful stimulation. Pupils were 4mm EBRTL and preferential gaze to the right. There was left central facial palsy, motor weakness on the left with strength of 2/5 and babinski on the left.

o [2013B] Lobar hematoma dont usually evacuate the hematoma, patient deteriorates

Where is the lesion? Where is the patient looking at? The preferential gaze is to the right, if this is supratentorial the eyes should be looking at the side of the lesion, if this infratentorial the eyes should be looking at the opposite side. Based on the findings, this is a supratentorial lesion because the paralysis is on the other side, this is a destructive lesion in frontal lobe area. There is a large hematoma in the right side.

Case 4 68 year old right handed male retired salesman from Sta Mesa,

Manila who complained of severe headache and decreased sensorium of few hours

Approximately 2 hours PTA, patient suddenly experienced severe temporoparietal headache, PS 10/10, non throbbing with associated vomiting episodes

Relatives noted patient to be less responsive and drowsy. Patient was rushed to UERM ER and subsequently admitted.

Physical Examination

BP 250/110 HR 110 RR 28 Temp 37

No eye opening/posturing to painful stimulus, shallow apneic breathing

Absent nuchal rigidity


Pupils midline 2-3mm sluggish reaction to light, weak bilateral corneals, intact Dolls eye

Flaccid paralysis, hyporeflexive, abnormal flexion on all extremities on painful stimulus, absent babinski bilateral

Where is the lesion? Dolls eye is intact, therefore the brainstem is intact. The blood is in the ventricles, everywhere except the brainstem. This is a patient with severe aneurysmal rupture. There is blood in the 4 ventricles, the patient had a sentinel headache earlier. The patient is now dead.

Expand Diagnostic Testing

Limit Diagnostic Testing

Age Young 45 yrs

Pre-existing Hypertension

Absent Present

ICH Location Lobar Deep or Cerebellar

If the ICH is located in the lobar area, do additional tests to rule out vascular malformation. If the patient is more than 45 years old with pre-existing hypertension and the ICH is located at the deep or cerebellar area this may probably hypertensive and further testing is unnecessary.

SUMMARY OF EYE SIGNS OF INTRACEREBRAL HEMORRHAGE [ADAMS]

In the localization of an intracerebral hemorrhage, ocular signs may be particularly useful.

In putaminal hemorrhage, the eyes are deviated to the side opposite the paralysis;

In thalamic hemorrhage, the most common ocular abnormality is downward deviation of the eyes and the pupils may be unreactive;

In pontine hemorrhage, the eyeballs are fixed and the pupils are tiny but reactive; and

In large cerebellar hemorrhage, the eyes may be deviated laterally to the side opposite the lesion and ocular bobbing may occur (as often in cerebellar hemorrhage in awake patients there are no eye signs).

Treatment

Medical Treatment for All ICH

The goals are to prevent complications and carefully manage BP

Maintain MAP < 130, but not lower than 110 mmHg Now lately, there are several studies that have shown that

it is safe to bring down the blood pressure to as low as 140 [systolic BP} without necessarily compromising cerebral blood flow/cerebral perfusion.

Based on hypertensive emergencies, since this is a hypertensive emergency, you should lower your blood pressure to 20-25%.

Manage increased ICP accordingly

Start anticonvulsants only if with seizures o The incidence of seizures is higher in ICH, especially in lobar

hematomas o The role of prophylactic anticonvulsants in deep hemorrhages

is unclear. It is justified to withhold anticonvulsants until clinically indicated.

Prevent and treat respiratory complications. Endotracheal intubation is performed in patients to provide airway protection and in those in coma or with respiratory failure. Sometimes, it is better to put tracheostomy right away

especially with a large hematoma.

Prevent and treat infections.

Maintain adequate nutrition.

Ensure proper fluid and electrolyte balance; maintain normothermia and normoglycemia

Rehabilitate once stable

Practice bedsore precautions

Deep-vein thrombosis and pulmonary embolism prophylaxis should be instituted (Use anti-embolic stockings or intermittent pneumatic compression devices) Usually, we start DVT [deep vein thrombosis] prophylaxis

even in hemorrhages after 2-4 days but you have to be sure that the patient is not bleeding.

Specific Treatment: AVM

Conservative Management

Surgical Excision

Stereotactic Radiosurgery o For AVMs less than 3cm o Obliteration of occurs in a delayed manner, usually with a

latency of at least 18 to 24 months after treatment, during which the patient is unprotected from re-bleeding


o The likelihood of successful radiotherapy treatment and the nature of the risks depend on the location and size of the AVM and the radiation dose delivered

o After 2 years, 75 to 80 % of AVMs smaller than 2.5 cm in diameter have been obliterated If it is larger than 3 cm, forget about radiation because it is

not going to work, remember that.

Endovascular Treatment o 25% or more of AVMs, mostly of small and medium size, have

been completely obliterated o mortality rate below 3% and morbidity of 5-7%, both of which

compare favorably with surgical outcomes o Suited to lesions of a combined AVM and an aneurysm on the

feeding vessel What they usually do, they either clip the mother artery or they

inject a glue that will occlude the feeding vessel then find out afterwards, if the patients AV malformation is completely obliterated. If you occlude the feeding vessel, the malformation gets smaller but it may still remain. So you have to decide whether youre going to radiate the patient or surgically intervene.

Combination Therapy

Specific Treatment: Aneurysm

Treatment for aneurysm: 1. Coiling catheter is inserted to obliterated the aneurysm. 2. Clipping

END

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4.Neurology II Hemorrhagic Stroke 2014A

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Transcript of 4.Neurology II Hemorrhagic Stroke 2014A