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Part I: Not all hemorrhagic strokes are the same
Best of EM:RAP; June 2010 from Logan Plaster on Vimeo.
In this month’s EM:RAP, we discussed several aspects of stroke in the emergency department. Stroke is now the second leading cause of death in the developed world and the leading cause of severe disability. With all of the controversy surrounding tPA in stroke, we often lose sight of all of the other things that are equally, if not more important, in stroke management.
In many ways, stroke is poised to be the new acute coronary syndrome. Although most emergency physicians can provide a robust differential diagnosis of the causes of ST elevation on an ECG, few are facile at identifying all of the various stroke syndromes, and even fewer are familiar with the anatomical correlates of each on neuroimaging.
Up until recently, perhaps it wasn’t that important. The majority of stroke care that has been shown to improve outcomes is conservative – things like keeping patients NPO until they have had a swallowing assessment and elevating the head of their bed to prevent aspiration pneumonia. But the race to find better therapies for acute stroke is intensifying. And as technology and techniques advance and treatments for stroke begin to look a lot more like those for acute coronary syndromes, so must our sophistication with the anatomy and pathology of stroke syndromes.
For most of us, our diagnostic vocabulary gets really thin once we see blood on the CT. But not all blood in the brain is the same. Assuming that we are not dealing with trauma, there are a few basic types of “bloody” strokes. Each has its own characteristic appearance on CT and each has its own specific management priorities. So while we still have to put out a call to the neurosurgeon in most cases, it really helps to know what the next steps will be so that we can anticipate what resources need to be mobilized at 3am.
Subarachnoid hemorrhage (SAH) from a ruptured aneurysm most often is seen in the basal cisterns, at the base of the brain where the vessels of the Circle of Willis live. Hypertensive hemorrhage occurs as the result of chronic vascular disease of the small perforating vessels off the circle of Willis. It is the result of years of uncontrolled hypertension and diabetes – not necessarily an acute BP elevation. The classic sites for this type of hemorrhage are the basal ganglia, the thalamus, the pons, and the cerebellum. In ischemic stroke with secondary hemorrhagic transformation, blood will appear in the vascular territory of one of the major arteries (e.g. a unilateral wedge of the frontal lobe in the case of an anterior cerebral artery).
A patient with SAH is typically treated with aggressive blood pressure reduction, nimodipine (given PO or by NG tube) to prevent vasospasm and a rapid search for the culprit aneurysm or AVM. This can be done with angiography: either conventional, with CT or MR techniques. The greatest risk for re-bleeding of a leaking or ruptured aneurysm is in the first 24 hours after the initial event – thus time is of the essence.
Patients with bleeding in a classic site for hypertensive hemorrhage (such as the basal ganglia) with a clear history of chronic hypertension, need not be worked up for an aneurysm or AVM. In the case of hemorrhagic transformation of an ischemic stroke, the site of bleeding is the injured ischemic tissue itself, and angiography is also not necessary. If the source of bleeding is unclear, however, it is important to proceed to angiography because of the possibility of a leaking aneurysm or AVM.
In all cases of brain bleeding, any coagulopathy should be promptly reversed, regardless of its origin. Even in a patient who is receiving anticoagulation for a mechanical valve, the imminent risk of death from intracranial hemorrhage trumps the chronic risk of thromboembolic disease, at least for the first couple of days.
All types of intracranial hemorrhage may result in hydrocephalus, either by blood getting into the ventricles and plugging them up with clot or by external pressure that pinches off the free flow of CSF. Hydrocephalus is a relatively easy finding to identify on a CT with a bit of practice. It should always be considered because it can result in rapid deterioration and death if not treated and can often be decompressed with a relatively simple procedure (e.g. a bedside ventriculostomy)
Almost all of these patients will be hypertensive. Although the evidence is extremely limited, there is some consensus about how blood pressure should be managed in these various types of intracranial hemorrhage. In SAH, neurosurgeons generally insist upon immediate and dramatic reduction of blood pressure to normal levels to prevent the disruption of a clot in the culprit lesion. Most neurosurgeons and neurologists also recommend emergent blood pressure reduction in patients with hypertensive hemorrhage, although there really is scant data to support this widespread practice. In patients with hemorrhagic transformation of ischemic stroke, the theoretical advantage of lowering blood pressure to prevent worsening bleeding must be balanced against the risk of increasing the size of the ischemic penumbra. This is the area of “at risk” brain tissue that surrounds the infarct that may be dependent upon on chronically elevated blood pressure to stay viable.
The bottom line is that no one really knows what the targets of blood pressure therapy should be, so it is a good idea to document your conversations with consultants as you determine the pace and degree of blood pressure reduction in each individual case. Also, if frequent neurological rechecks (which should be also be documented) reveal an acute deterioration, over vigorous reduction of blood pressure must be considered as a possibility, in addition to re-bleeding, hydrocephalus and progression of the edema that surrounds the injured tissue.
So, not all bloody strokes are the same! In next month’s issue, we will discuss the important differences between lacunar and cortical strokes...
Dr. Swadron is an Associate Professor of Clinical Emergency Medicine at the Keck School of Medicine of the University of Southern California. EM:RAP (Emergency Medicine: Reviews and Perspectives) is a monthly audio program that can be found at EMRAP.org.
Figure 1: Subarachnoid hemorrhage. Blood is seen in the basal cisterns and along both Sylvian fissures. Note also the dilation of the temporal horns of both lateral ventricles – a critical sign of hydrocephalus.
Figure 2: Hypertensive hemorrhage (right thalamic).
Figure 3: Hemorrhagic transformation of a large left middle cerebral artery territory ischemic stroke.