Stroke and TIA

A transient neurologic deficit lasting 24 hours or more, even when imaging studies are unremarkable, is a cerebrovascular accident, not TIA.

Each year, approximately 610,000 Americans have a first stroke or cerebrovascular accident (CVA), while about 185,000 have a recurrent stroke. About 5 million of us have experienced symptoms of transient ischemic attack (TIA), according to a 2015 report from the American Heart Association. While these conditions are very familiar to clinicians, it can be challenging to document them in a way that can be properly coded to accurately reflect severity of illness, resource utilization, and costs of care.

The clinical indicators of CVA should be easily identified: an imaging study (like CT or MRI of the brain) showing an acute infarction or cerebral hemorrhage and/or a persistent focal neurologic deficit of central origin lasting 24 hours or more from the time of onset. Occasionally, a nonhemorrhagic CVA may not be visualized on CT for 24 hours or so. TIA, in contrast to CVA, is defined by the absence of acute imaging findings and a focal neurologic deficit lasting less than 24 hours.

Photo by Thinkstock
Photo by Thinkstock

Sometimes clinicians seem to overlook the fact that a transient neurologic deficit lasting 24 hours or more, even when imaging studies are unremarkable, is a CVA, not TIA. Furthermore, clinicians occasionally use the time of presentation to determine duration of symptoms, when the true starting point is the time of onset. For example, a patient who presents with right upper hemiparesis for 8 hours has had a CVA if the symptoms persist for another 16 hours.

Other important conditions sometimes associated with a CVA that require precise diagnostic documentation include cerebral edema and brain compression. Simply stating that an imaging study shows midline-shift or mass effect is inadequate for accurate code assignment to reflect the potentially life-threatening severity of these conditions.

Coma is another crucial diagnosis sometimes associated with CVA, and a Glasgow Coma Score (GCS) should be determined whenever there is an altered level of consciousness. A GCS of 8 or less is consistent with a diagnosis of coma; obtundation or lethargy is usually used to describe patients with a higher GCS.

When a patient has received a thrombolytic agent, such as tissue plasminogen activator (tPA), at a transferring facility, the record should always indicate whether the treatment was initiated within the 24 hours before arrival at the receiving facility.

For the purposes of correct coding, severity of illness classification, and determination of inpatient medical necessity, CVA is considered a serious medical condition requiring inpatient care. TIA is classified as simply a symptom with an underlying cause that requires further specification. In fact, it is the underlying cause of TIA (either confirmed or suspected) that is treated, not the symptom of TIA itself.

One common cause of TIA is stenosis of a cerebral or precerebral artery (carotid arteries or vertebrobasilar system), typically due to atherosclerotic plaque. There may be thrombosis at the site or, more often, a platelet aggregate embolizing to the brain with transient arterial obstruction. Oddly, “vertebrobasilar syndrome” is classified as a TIA unless specified as vertebrobasilar stenosis or embolism.

Don't be misled by a finding of “noncritical stenosis,” which simply means the degree of stenosis is not severe enough to warrant surgical intervention. Any degree of stenosis may be sufficient for a thrombotic event or the formation of embolic platelet aggregates.

Another frequently encountered situation is embolism to the brain from a more remote site (Table). In this situation, clinicians should document the suspected site. A particularly common situation is transient cerebral embolism from a fibrillating left atrium, especially in cases in which a patient's international normalized ratio (INR) is subtherapeutic.

Terminology that may be used to express the underlying cause of TIA includes the following:

  • “stenosis” of whatever cerebral or precerebral artery is affected,
  • “transient cerebral embolism” from the suspected site (including carotids and distant sites), and
  • “transient thrombosis” of the cerebral or precerebral artery that might be involved.

Remember, too, that terms of uncertainty (like “probable,” “suspected,” “likely,” “consistent or compatible with,” “suggestive or indicative of”) may be used to describe the underlying cause of TIA if that cause is clinically valid but cannot be confirmed with certainty. For example, a clinician could document “transient cerebral embolism probably due to atrial fibrillation.”

In summary, CVA is recognized by acute imaging findings of infarction or hemorrhage and/or focal neurologic deficit of central origin lasting 24 hours or more from onset. TIA is defined by nonacute imaging and focal neurologic deficit lasting less than 24 hours from onset. Identify and document common CVA comorbidities like cerebral edema, brain compression, and coma. Always document the confirmed or suspected underlying cause of TIA symptoms, like cerebral or precerebral artery stenosis, transient cerebral embolism from precerebral arteries or distant sites like a fibrillating atrium, or thrombosis of a cerebral or precerebral artery.