Terri Schiavo R.I.P. Part III: The Brain Speaks

Terri Schiavo R.I.P.

The CodeBlueBlog Papers

Part III

This is a summation in three parts.

Part I is here.

Part II is here.

The Third Revelation

After looking at the medical records of TS late in the game (the feeding tube was to be withdrawn any day), last month, I was emailed a link at the The EmpireJournal that gave a chronology of TS's hospitalization, purportedly written by caregivers on the scene. Three CT scans of the brain were listed thus:

2/25: Normal

2/27: Normal

3/30:  noncommunicating hydrocephalus, changes occurred since 2/27 exam

One must remember that a cornerstone of the "dead cortex/dead brain" rhetoric was that there had occurred, before hospital admission, a massive event of hypoxia-anoxia. What does this mean?

Hypoxia means low oxygen concentration (in this case to the brain) and anoxia means no oxygen. The mechanism finally settled on that was blamed for the hypoxia/anoxia was dysrythmmia/arrhythmia of the heart (ineffective heart pumping due to "electrical" disturbance) secondary to potassium deficiency brought on by diet change.

Translated, this means that TS had severe dietary changes that lead to a decrease in blood potassium that disrupted the normal electrical activity that stimulates the heart to beat (contract and relax). The heart thus contracted abnormally, leading to severe decreased blood flow to the brain and resulting in oxygen deprivation. This lack of blood flow/oxygen severely injured the cerebral cortex.

There are plenty of medical arguments and issues that can be raised regarding the above paragraph and the proposed scenario. None of that is important in my analysis. I am starting from the assumption -- now taken as fact -- that TS suffered severe oxygen deprivation to the brain causing massive anoxic (oxygen deprivation) damage to the cortex before she ever reached the emergency room.

Brain cortex is extremely sensitive to oxygen levels in the blood, and certainly, when there is prolonged oxygen deprivation, widespread cortical injury and  destruction can occur. The experts who repeatedly showed TS's CT brain slice in the media were supporting a direct chain of events from:

irregular heart beat ---> oxygen deprivation ---> cortical injury ---> massive atrophy

In order to manifest that degree of cortical atrophy from the single assumed event of hypoxia/anoxia, before admission, the degree of cortical damage, at the time of oxygen deprivation, must have been great.

So how was the CT scan at 48 hours negative?

Mechanisms of Madness

Severe hypoxia/anoxia leads to rapid injury of the cells in the brain's cortex. When the cells are severely damaged, they leak fluid. This fluid rapidly accumulates in the closed space of the skull.

Damage to the brain, from oxygen loss, has been shown to occur within twenty minutes, and in severe cases, begins to show on CT scans within hours. In a case such as TS, where there is proposed massive damage, one would expect massive reaction to the damage. After 24 hours there usually is substantial brain swelling in a case such as this, evident on the CT scan.

My experience with the handful of cases I've seen is that the CT evidence of massive hypoxia/anoxia (of the extent being proposed by the experts who point to TS's CT) is evident soon after the event. By 24 hours, I'd be surprised not to see some evidence; and, if I did not see swelling and abnormalities by 48 hours after the event, I would be perplexed enough to seek alternative explanations or a reevaluation of the case.

Most research concerning massive hypoxia and anoxia is in newborns, and, obviously, a newborn brain is different from an adult brain. Nonetheless, here's a report from one study:

Hypoxic-ischemic insults to the central nervous system of infants may show a characteristic sequence of imaging findings. CT immediately after the insult may be normal or near normal in appearance. Over 24-48 hours, diffuse cerebral edema causes loss of the distinction between grey and white matter, obliteration of cortical sulci, and diffuse low density

Here's a case, reported in the Japanese literature of a woman who suffered massive cerebral anoxia/hypoxia and had immediate follow-up CT (after resuscitation). According to the authors:

CT revealed massive cerebral edema soon after resuscitation ...

And a repeat CT the next day showed:

on the following day (after anoxia/hypoxia) the CT demonstrated low attenuation area of white matter and gray matter in the cerebrum and brainstem

By 48 hours it is hard to imagine that the CT scan would not show some evidence of swelling and/or changes in the relative appearance of different parts of the brain.

The cases of massive hypoxia/anoxia I have seen, have been in adults, and have been grossly, markedly abnormal by 24-48 hours. The swelling can be so bad that a neurosurgeon has to remove a part of the skull so that the brain has an outlet to bulge.

Some have written me to explain that the CT used may have been an old model and not been as sensitive as newer models; however, as early as 1983 The American Journal of Radiology (AJR Am J Roentgenol. 1983 Dec;141(6):1227-32), reporting on a study of adults said:

Even with no clinical information, neuroradiologists can assess CT signs of cerebral infarction within the first 6 hours of symptom onset with moderate to substantial interobserver agreement.

I was incredulous to read that TS's CT was interpreted as "normal" 48 hours after the proposed event of hypoxia/anoxia. Surely, given the amount of damage being proposed in the media -- with that famous CT slice -- there would be some sign of the brain's distress at 48 hours. But the CT report produced on The Empire Journal said that the 48 hour CT was "normal." And a CT report from a scan done one month later (3/30) reported "noncommunicating hydrocephalus, changes occurred since 2/27 exam." This report was given by a different radiologist than the report of 2/27, indicating that this different radiologist re-evaluated the CT of 2/27 to compare it with 3/30, so the CT of 2/27 was seen twice, by two experts.

Pictures at an Exhibition

Here are some CT images of brains -- taken at 24 hours -- that suffered massive hypoxia/anoxia:

                     

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These brains show diffuse swelling, with loss of the normal spaces between cortical folds, and abnormally different shades of "grayness" that are immediately evident to an interpreter. According to a prominent University's teaching file, here are the CT findings of massive cerebral hypoxia/anoxia after 24 hours:

CT immediately after the insult may be normal or near normal in appearance. Over 24-48 hours, diffuse cerebral edema causes loss of the distinction between grey and white matter, obliteration of cortical sulci, and diffuse low density. Frequently there is relative sparing of the cerebellum and or basal ganglia which appear hyperdense compared to the abnormally low density cerebral hemispheres.

Mirrored Spectacles

How could this be?

Here are the possibilities:

• I think that the least likely explanation is that the CT actually was negative.
• The CT may have been misinterpreted. Sometimes when there is uniform, massive abnormality -- and all things in the brain are equally abnormal -- there can be the phenomenon when the interpreter sees everything in a uniform state and calls it negative. This happens, and it is not necessarily malpractice or incompetence. Interpreting CT's is just that: interpreting. I look at a Rorschach image and call it a butterfly, you call it a wildebeest. However, given the history of a massive event of anoxia/ hypoxia, one is usually on the alert for the appropriate changes.

• The CT scanner may have been an old model that was less sensitive than newer models available at that time. Not everyone upgrades their equipment every time a new generation of equipment is available, same way you don't upgrade your computer every time there is a new memory chip. Older CT's in 1990, could produce pretty poor images, at times, and if you throw in a little motion artifact (patient moving her head, etc), the combination of these two factors might lead to misinterpretation.

• The CT was actually negative, or normal. If the CT was actually normal, it is hard to postulate massive hypoxic injury two days prior. So if the brain was really negative, then the inciting event (massive hypoxia/anoxia) did not occur before TS was admitted to the hospital, it occurred after she arrived at the ER on 2/25/90 occurred after that time.

My impression that this discrepancy needed -- at the very least -- to be reevaluated by a second look at those CT scans before the removal of TS's feeding tube, lead to my attempts to draw attention to my observations.

Once again, my only contention when I reported this finding was that it needs to be explained. That's all. Like the bone scan, it is difficult for me to understand how results like these could be left alone and not commented upon. This was the crux of my issue. If one does not explain why the bone scan was abnormal or why the CT scans did not fit the clinical history, then by everything I know and have learned, one is obligated to investigate and pursue.

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