As I write this, my home state of California has reported over 2.3 million cases of COVID-19, and recorded over 26,000 deaths. The United States has already seen over 20 million recorded COVID cases, and the death toll stands at over 350,000. These are only “so far” numbers, and the slow vaccine roll out to date ensures we are nowhere near the final count on these statistics. And these numbers are only the cases we know about, not the equally massive number of cases where there was a recovery without a laboratory diagnosis or deaths where COVID may have been a major unreported factor—particularly in the elderly.
Thankfully, the number of COVID affected individuals has resulted in a large amount of recovered cases. Or what we assume are recovered cases. Many have gone back to their lives and situations with residual symptoms, even if mild. A small but significant amount who have “recovered” from the acute phase of the illness still have a degree of disability which affects their day-to-day living. These are the “long haulers”—those in whom COVID has spared in the short term but in whom we have truly no idea of what the long term prognosis will be, either morbidity or mortality wise.
Disease-impacted underwriting depends on estimating life expectancy (for life insurance), degree and duration of disability, and long term costs of care for health, disability and long term care. Much of this is based on experience of watching the course of illnesses in multitudes of people and understanding both the process and course of the disease. COVID however is a horse of a different color—we have no experience in how this has played out at other times and only guesstimates of how it will work in the future. Cases followed in the United States have barely reached the one-year point. It has become obvious, even in that short time, that recovery is not always complete, and that remaining objective signs and symptoms have potential to cause continued decompensation in the long run.
Cases of regular exposure where a COVID test is positive and there are minimal symptoms and a return to work without problems are still standard to preferred cases as they were before the infection. Those who were admitted to the hospital but required no ICU care or intubation and had a recovered course likewise don’t appear to date to have recurrent symptoms or compromise. Where it gets more difficult are three categories where more intensive treatment was necessary. Those include admission to the hospital with symptoms and the need for more than routine treatment (remdesivir, oxygen support, etc.), those who were hospitalized for a significant amount of days and whose course required an ICU admission (even not intubated), and those with an ICU admission where other medical problems surfaced with a prolonged hospital stay and where rehabilitation was needed.
Underwriting these cases requires much more care toward these latter classes. Besides perhaps a postpone period to see how symptoms persist or progress, additive testing may be required. Repeat chest X-rays and even chest CTs may be required. Laboratories in follow-up visits must be reported. Face-to-face follow-up care may be required above and beyond tele-visits. Exercise echocardiograms may be particularly helpful in assessing any long lasting cardiac compromise or continued decompensation. And even psychometric testing to screen for PTSD, continued severe anxiety and depression and failure to cope post infection may also be important to assess.
Maybe most perplexing are the long haulers still affected after what seem to be mild or moderate symptoms from the initial infection. Many patients haven’t fully recovered their normal activity level, and remain incapacitated or house bound. Coronavirus may leave patients with a condition called POTS (postural orthostatic tachycardia syndrome), where heart rates can double or triple on standing, blood pressure can drop precipitously, and just about all conditions that are dependent on normal regulation of blood pressure and pulse go out of whack. Dizziness, headaches, shortness of breath, chest pain and “brain fog” (where periods of time without clear thinking occur) cause short term problems and may worsen other body functions. The long effects of this on the heart, the autonomic nervous system, and pulmonary and brain functions are truly unknown. What is the course of COVID induced POTS? We truly don’t know with this limited time experience.
Underwriting is going to be a lot tougher and with a lot more caution in COVID cases and certainly in long haulers where the infection continues to cause symptoms and impairments well into months after infection. Careful examination of medical records and longer periods waiting for in-person visits may be necessary. Testing, whether as routine as for blood, or with scanning and testing cardiac and lung function, may be required. Return to work for a defined period of time without decompensation may need to be demonstrated. And in long haulers, an indefinite period of postponement may be required until we are best able to evaluate the long term effects of this pandemic virus which has caused so much disruption and harm in our lives as a people.
Carotid Artery Stenosis
Carotid artery stenosis is a narrowing or constriction of any part of the carotid arteries, generally caused by atherosclerosis. One of the body’s largest arteries, the common carotid artery is the one you can generally feel pulsations of on each side of your neck. It comes off of the aorta and divides into the internal carotid artery (which supplies blood to the brain) and the external carotid, which supplies the face. The area where it divides is a common site for atherosclerosis, which is a buildup of plaque that narrows the vessel or provides the tendency to rupture and shoot through the bloodstream.
In most cases the cause of carotid artery stenosis is a degeneration of the wall of the artery, usually from fatty or cholesterol deposits. Sometimes the plaque is stable, and causes a narrowing of the blood flow through the brain and face. Other times, a part of the plaque may break off and travel through the circulation to the brain or other body organs. When the emboli shut off blood flow to a given cerebral area, a TIA (if it is temporary) or a full blown stroke can ensue.
The characteristic signs of carotid stenosis are a bruit (rumbling sound) over the carotid artery or the end result—a TIA or stroke. In those with risk factors (high cholesterol, HTN, obesity, diabetes) carotid artery screening may be done in the absence of a precipitating event. This has become quite controversial as we will discuss shortly. A Doppler ultrasound can determine the extent and the degree of the stenosis. Cerebral angiograms were a diagnostic tool but are used less frequently now with the advent of very sensitive MRI and MRA (angiogram) testing.
Treatment is generally aimed at the prevention of problems, including strokes and other complications of atherosclerosis. Anticoagulants (blood thinners like Coumadin or Eliquis) may be given as well as antiplatelet drugs to retard clotting. Surgery (usually a carotid endarterectomy), an open removal of carotid plaque, has been less used because of the risks of preoperative angiography and surgery, however angioplasty and stenting are still the main procedure used for significant symptomatic carotid stenosis.
Recently the USPSTF (US Preventative Services Task Force) reviewed evidence for screening for carotid artery stenosis in asymptomatic individuals and gave it a “D” or unnecessary recommendation. They focused on cost of testing relative to positive findings, false positive testing requiring further work-up which proved to be negative, and potential harm from the angiography, surgery and other interventions. Their position is very controversial, especially in those who have been spared potential life threatening stroke or sudden death.
Prognosis of carotid artery stenosis depends on the degree of stenosis and the contributing co-morbid conditions that may cause progression not only in the carotid arteries but in other major blood vessels in the body. With stenosis less than 50 percent there is a small risk of stroke. At 70 percent or higher the risk becomes quite significant and intervention becomes a consideration (surgical or medical). Risk factor modification such as lowering blood pressure, using cholesterol lowering drugs, smoking cessation and weight loss are important preventative steps.
Most applicants will be rated with stenosis over 50 percent or if significant stenosis has occurred at younger ages (less than 50 for example). Aggressive medical therapy and intervention may be credited in these circumstances. When TIA, stroke or carotid intervention has occurred, the ratings increase. As mentioned active risk modification and close doctor follow-up is necessary, as carotid artery dissection (tearing) and major stroke are distinct causes of mortality.