Hemorrhagic Stroke Flashcards
As we have already discussed, hemorrhagic stroke comprises only 20% of all strokes and these are roughly equally divided between hemorrhage into the brain, i.e., intracerebral or parenchymal hemorrhage and hemorrhage into the subarachnoid space. Once again this slide presents CT scans of patients with hemorrhagic stroke on the left.
The CT scan at the top demonstrates hemorrhage into the basal ganglia and the two scan below present hemorrhage into the subarachnoid space.
Label these cerebral hemorrhages from left to right?
Left to right (top to bottom)
Note the small black arrows pointing to blood filling the sulci overlying the left neocortex (recall you are looking at the brain slice from the bottom up).
The next CT scan presents an example of blood in the basal ganglia, i.e., intracerebral hemorrhage (ICH).
The third scan presents an epidural hemorrhage, i.e. blood between the inner plate of skull bone and the dura. Note the convex or lens shape of the hemorrhage that is characteristic of an epidural bleed.
The last scan presents an example of subdural hemorrhage over the left cerebral hemisphere. This patient has actually suffered at least two subdural hemorrhages separated by several weeks or more in occurrence. Note the layer of bright white blood as the outer most layer and beneath it a second less dense layer that contains two distinct densities. The upper most portion of this inner layer is less dense (darker) than the lower layer.
Recognizing that red blood cells will lyse and release their contents over time can you figure out why this inner layer contains these two distinct density patterns. Also can you determine which of the two layers, the outer or inner layer, represents the most recent hemorrhage.
We have already covered the point that the incidence of cerebral hemorrhage is roughly equally divided between bleeding around the brain, subarachnoid hemorrhage and bleeding into the brain, parenchymal or intracerebral hemorrhage.
What are some common causes of hemorrhagic stroke?
- Berry aneurysm
- Vascular malformation
- Traumatic
- Mycotic aneurysm
- Hypertension
- Tumor
- Bleeding diatheses
- Anticoagulant complication
- Congophilic Angiopathy
- Vasculitis
- Illicit drug use
Subarachnoid hemorrhage is most commonly caused by what?
rupture of a saccular (berry) aneurysm.
Describe berry aneurysms
These aneurysms reflect developmental defects in the blood vessel wall that tend to enlarge with time. Detectable defects in the brain blood vessel walls are common with 20% of the population having an aneurysm measuring 2 mm or less in diameter. Such aneurysms rarely if ever rupture. Approximately 5% of the population has a cerebral aneurysm measuring 2 – 5 mm in diameter and will occasionally bleed. Aneurysms larger than 5 mm in diameter rupture and bleed at a rate of 1-3% per year. Fortunately aneurysms of this diameter are less common and cause approximately 30,000 subarachnoid hemorrhages in the U.S. each year.
This is a Netter slide showing the most common locations for berry aneurysms. They include: 85% anterior circulation (30% ACA, 30% ICA, and 25% MCA), and 15% posterior circulation (2% PCA,, 10% Basilar, 3% Vertebral)
Note that while patients may have multiple (one, two, three, or more) aneurysms, this drawing showing many aneurysms is simply intended to show their most likely locations and not a patient with numerous aneurysms. The lower two figures present an AP (anterior-posterior) view of a cerebral arteriogram with an aneurysm (yellow arrow) of presumably the anterior communicating artery (left figure) and a large posterior communicating aneurysm (right figure)
What are the main risk factors for having a subarachnoid hemorrhage?
- Tobacco use
- Ethanol abuse
- Hypertension
- Oral contraceptives
- Stimulant drugs (cocaine, etc.)
- Low cholesterol
- Genetics (polycystic kidneys, Marfan’s syndrome)
What is the prognsosis of a subarachnoid hemorrhage?
The clinical consequences of subarachnoid hemorrhage from a ruptured berry aneurysm are dire. 10-15% of such patients die before they reach the emergency room. An additional 25% die during the next three months raising the overall mortality to approximately 40%. Those patients that survive the initial bleed have a 40% chance of having neurologic sequelae.
How might a subarachnoid hemorrhage present?
Patients with rupture of a berry aneurysm typically present to the emergency department with complaints of the “worst headache of my life”.
Some but not all patients may rapidly lose consciousness secondary to the large pulse pressure change delivered to the brainstem as a result of arterial blood entering the subarachnoid space.
Neck stiffness and pain, photo- and phonophobia follow the rupture of a berry aneurysm within hours. These later symptoms reflect irritation and inflammation of the meninges secondary to the breakdown products of red blood cell lysis.
Focal neurologic signs are more commonly minor or absent and this helps distinguish this type of stroke from ischemic stroke.
What are the signs of a SAH?
Blood pressure may be elevated and the patient may manifest cardiac arrhythmias. The latter cardiac symptoms are related to red blood cell breakdown products that irritate brainstem centers regulating heart rate.
Retinal hemorrhages may be present
While focal neurologic signs are infrequent, some when present help to localize the arterial site of the aneurysm. For example, third CN paresis resulting in a dilated pupil and ophthalmoparesis is consistent with an aneurysm at the junction of the internal carotid and PCOM arteries; paraparesis (bilateral leg weakness) suggests an aneurysm of the anterior cerebral artery; hemiparesis is consistent with a middle cerebral artery aneurysm.
Irritation of the meninges with the signs described earlier is usually delayed for several hours after rupture of the aneurysm and the onset of headache.
What is the most helpful noninvasive diagnostic test to identify a subarachnoid hemorrhage?
non-contrast CT scan
The amount of blood and its location help determine the site of the berry aneurysm and also the likelihood of a delayed complication called “vasospasm”. Recognize that the CT scan may be negative in a patient with a ruptured berry aneurysm, especially if the bleeding is slight or if the scan is delayed for a day or more after the rupture.
Importantly, if you suspect a subarachnoid hemorrhage you must perform a lumbar puncture to look for subarachnoid blood. A lumbar puncture is the only method to 100% rule out a subarachnoid bleed.
Rules for an LP with a SAH
It is important to delay the lumbar puncture for 3 to 4 hours after onset of a headache that you believe to be caused by a subarachnoid hemorrhage.
The reason for this is to allow time for some of the red blood cells in the subarachnoid space to lyse and release hemoglobin into the spinal fluid. The presence of hemoglobin or its breakdown products in spinal fluid will help significantly in your being able to distinguish between the appearance of blood in the spinal fluid that occurred from nicking a vein while performing the spinal tap and blood that resulted from the rupture of a berry aneurysm hours earlier.
To distinguish the two conditions you must have the blood tinged spinal fluid centrifuged IMMEDIATELY. Red blood cells derived from a nicked vein during the tap will remain intact and be ‘spun down’ during centrifugation leaving the supernatant crystal clear. In contrast, a red tinge or discoloration of the supernatant after centrifugation indicates that hemoglobin is dissolved in the spinal fluid from red blood cells that have been in the spinal fluid for several hours, i.e. from a ruptured aneurysm.
This is a Netter slide summarizing some of the points we have just reviewed in regards to SAH.
The man presents with a severe headache, he may lose consciousness, and he may demonstrate a positive Kerning’s or Brudzinski sign (both signs of meningeal irritation).
The lower figures demonstrate bloody spinal fluid that does not clear after collecting several tubes indicating a ruptured berry aneurysm and spinal fluid that tends to clear after collecting three tubes suggesting the blood came from a traumatic spinal tap, i.e. a nicked vein.
The three yellow tubes reflect discoloration of the spinal fluid, called xanthochromia, that results from the break down of hemoglobin. Such yellow discoloration takes a day or more after rupture of the an aneurysm to develop.
Once the diagnosis of a SAH is confirmed with either a CT scan or lumber puncture, the next task is to to what?
identify the site of the ruptured blood vessel. The MRI is an excellent noninvasive method to identify aneurysm that are larger than 5 mm but the gold standard diagnostic procedure is the 4-vessel digital subtraction arteriogram
This is a Netter slide showing the surgical approach prior to clipping a basilar artery aneurysm.
This slide shows a variety of clips that have been developed to seal of berry aneurysms.
This slide presents a DSA of a basilar tip aneurysm (yellow arrow) before placement of coils in the lumen of the aneurysm (left) and after placement of the coils (right). Note after coil placement the aneurysm has clotted off and the arteriographic dye cannot enter the aneurysm.
In addition to coiling aneurysms, interventionalists can divert arterial blood flow away from an aneurysm using flexible stents. This reduce pressure and movement of blood into the aneurysm, and blood that is not continuously moving tends to clot. Clotting off the aneurysm prevents it from rupturing, essentially obliterating it. This is shown in the upper panel. In the lower panel is shown how a top of the basilar artery aneurysm can be managed with stents and coiling, thereby avoiding what once was considered the Mount Everest of all neurosurgical procedures, the clipping of a basilar tip aneurysm.
This is a Netter slide depicting the formation and rupture of Charcot Bouchard aneurysms.
The series of figures on the right present the typical location for these hemorrhages and a CT example of hemorrhage in these locations.
One additional slide to emphasize the locations of parenchymal hemorrhages and their etiology.
Note that figures B, C, D, and E reflect hemorrhage of microaneurysms secondary to chronic hypertension. However, figure A is not one of the areas that harbors the small penetrating arterioles that are the site of Charcot Bouchard aneurysms and thus the etiology of these cortical, polar (poles of the brains) hemorrhages is not usually related to hypertension.
This slide presents another cause for intracranial hemorrhage, the arteriovenous malformation (AVM). AVMs occur in several varieties with greater or lesser tendencies to rupture and bleed.
The upper figure presents a typical AVM with its appearance on DSA and CT scans.
How is hypertensive hemorrhage tx?
The treatment of hypertensive hemorrhages is to reduce the blood pressure and treat elevated intracranial pressure appropriately. If signs of herniations develop then hyperventilation, osmotic agents, and neurosurgical intervention are required.
Before we end this lecture, recall the 80 year old man with stupor, global aphasia and left hemiplegia. Stupor means that he opens his eyes briefly to stimulation but otherwise is unresponsive and seems asleep. You should have figured out the location of the lesion. The deficits involved the language areas, presumably in the left hemisphere, but he is left handed and stands a roughly one in 3 chance of being right hemisphere dominant. The right brain is clearly affected with respect to the motor pathways. We are not given a full exam.
We are not given key information about pupillary light reactivity, eye movements, response to visual threat, and latency of grimacing to nailbed pinch, all bedside tests that would aid our quest in localizing the lesion. Thus, with a large right hemispheric lesion, we would expect the eyes to be deviated to the right due to loss of the right frontal eye fields, and based on the next slide, they probably were in this patient. Flicking your fingers in front of the patient’s eyes would not have produced an asymmetric eye blink with less blinking in the left visual field versus the right, indicating a left hemianopia, again based on the next slide. This patient was probably too drowsy to get a reliable response this way but what you can do, is test with nailbed pinching which momentarily arouses the patient, who opens his eyes and then flick your fingers at his eyes to see how quickly he blinks. If the visual pathways were affected by the lesion, eye blink would be absent or decreased in frequency when the visual threat came from the left visual hemifield, again as compared to the right hemifield. If the large right hemispheric stroke extended to disrupt the parietal cortex and/or its sensory input from the thalamus, a sudden pinch of the finger nailbed on the left would probably have caused a slight but consistent delay in grimacing when compared to the right nailbed pinch.
There is a huge right cerebral bleed and that explains the motor deficit. Furthermore this man is very likely right hemispheric dominant! Now everything falls into place anatomically. The parietal lobe and visual pathways were probably spared even though the lesion is quite large.
So what caused the large right frontal lobe bleed?
There were multiple risk factors for cerebral hemorrhage including hypertension, diabetes and age. With age, cerebral amyloid angiopathy becomes increasingly more prevalent, especially after the age of 80. The deposition of amyloid into the arterial walls makes the arteries more brittle and more likely to rupture.
Unlike hypertensive bleeds that usually involve deep grey structures, cerebral amyloid angiopathy affects the cortical lobes, which is the case here. The patient’s stupor suggests there is early transtentorial herniation with compression of the arousal centers in the midbrain reticular formation, again a key concept introduced to you earlier and that will be emphasized again in a future lecture on coma. Transtentorial herniation should have produced an enlarged and poorly reactive pupil on the right side, and it is part of your education to recognize that critical information was missing in this case.
This figures shows a microscopic view of a section of a brain with cerebral amyloid angiopathy. The round structures are blood vessels cut in cross section. The walls of the vessels contain amyloid, which stains pink with H&E, upper left, and brown with Congo red stain for amyloid, upper right, and with greenish streaks when illuminated by the technique used in the bottom figure (apple-green birefringence under polarized light of a Congo red section).
One last item. Remember the CT of the subdural hematoma shown on slide 5? The denser (whiter) outer component is the more recent bleed as shown by the arrow. Why? Because, as blood lyses and releases its hemoglobin and iron, its density decreases. Hence a fresh intracranial bleed appears much denser than older bleeds. The effect of gravity separates the denser red cells from the less dense serum as the clot matures and contracts to produce a hematocrit-like effect which you can see with the cell layering.
By the way, where is the left ventricle? It is pushed over past the midline to the opposite side with other left hemispheric structures. The midline is shown by the falx cerebri (blue arrows). This is a case of transfalcian herniation (brain shoved across the falx cerebri) and you can bet there is transtentorial herniation present as well. Brain herniation is a very important concept that is being introduced now and that you will hear more about in the coma lecture. You should expect coma and the left pupil to be dilated and fixed to light, and death if the subdurals are not immediately decompressed.
