[From 2014, slightly modified]
NOTE: This answer is long [TL:DR warning]
This is an important issue, reminding me of the Terry Schiavo case of some years ago in Florida, on which I also opined along with my colleague Roger Blackburn.
To answer this question, we need to understand the definition of brain death, and then we need to understand the progression of physiology – the natural history of death, as it were – in the human body. Finally, with these two pieces of information, we can ask the question as to whether a 14 week old fetus CAN be kept alive in a dead host until it is viable.
Further, from what was reported in the press, Ms. Muñoz was unresponsive – pulse-less – for an hour prior to return of spontaneous circulation. This means that the fetus was without blood flow for that period as well. One is forced to ponder the state of the fetus’ central nervous system after a prolonged period of hypoxia / hypo-perfusion. It will not be a good outcome for the fetus / child even if the mother is forced to play host until term. Translated, this means that the fetus is very likely to have severe brain damage, if it is kept “alive in a dead-mother’s uterus”
The other question: Does / should the state have the right to force a family to keep a dead person on “life support” to serve as a host for the fetus ?
I use herein some material I have written in the recent past, with references.
Definition of Clinical Brain Death
In a landmark manuscript, Harvey Cushing described the “Experimental and Clinical Observations Concerning States of Increased Intracranial Tension” (1). Utilizing an animal model and differentiating local compression from a general compression of the brain, Cushing examined the physiology of intracranial hypertension and its effect upon systemic hemodynamics, now known as Cushing’s triad (irregular respirations, decreased heart rate and increased blood pressure).
In contrast to animal models used by Cushing and others, where the experimentation is undertaken in a controlled setting, the physiology of human brain death remains challenging for multiple reasons: the time of actual brain death may be significantly different from the certification time with significant physiologic changes occurring in the interval, treatment of the patient in the period antecedent to brain death and in the immediate post brain death period may result in abnormalities independent of brain death and, lastly, there will never be a human model of brain death (2). As a consequence, an understanding of brain death physiology is derived from animal models and data inferred from human case series.
Somatic death (death of the body) after clinical brain death will inevitably occur in the absence of aggressive support. In an era when brain death was not accepted, prolonged survivorship, with a mean the duration of 23 days, was noted in a study that aggressively maintained brain dead patients (3). Autopsy studies of patients that were declared brain dead revealed histopathologic evidence of necrosis and liquefaction of the brain (4) (meaning the brain died and turned to a thick liquid).
In 1956, Lofstedt and von Reis described 6 mechanically ventilated patients with absent reflexes, apnea, hypotension, hypothermia, and polyuria associated with absent angiographic cerebral blood flow (5). Death was declared when cardiac arrest occurred, between 2 and 26 days after the clinical examination.
However, it was only after the description of “Le Coma Depasse” by Mollarat and Goulon, in 1959, that the description and understanding of coma and death changed forever (6). These authors presented 23 cases from their Paris hospital in which they described irreversible or “irretrievable coma”. This was coma that was associated with a lack of cognitive and vegetative functions, and went beyond any description of coma that had been previously discussed. This description initiated the discussion of, and formed the basis for, what is contemporarily recognized as brain death. The authors defined the necessity of considering the circumstances of the injury, the role of the neurologic examination, the results of electroencephalography (EEG), and the consequence of brain death on other organs. They found that the majority of injuries to the brain were confined to trauma, subarachnoid hemorrhage, meningitis, cerebral venous thrombosis, massive stroke, and brain death after craniotomy for posterior fossa tumor. In this series, they detailed problems including deterioration of pulmonary function, polyuria, hyperglycemia, and tachycardia. It is intriguing that this paper, even though published in a relatively well known European journal, took more than 15 years before it became known in the United States and Great Britain.
In 1963, Schwab and associates reported utilizing EEG as an adjunct for determining death when cardiac activity was present (7). These authors proposed that the patient was dead when: 1. spontaneous respirations were absent for 30 minutes; 2. tendon reflexes of any type were absent; 3. pupillary reflexes were absent; 4. the occulocardiac reflex was absent; and 5. the EEG was iso-electric for 30 minutes.
In 1968, Doctor Henry Beecher chaired a committee at Harvard Medical School which attempted to define irreversible coma as new criteria for death. The committee defined death as the irreversible loss of all brain function and proposed the criteria necessary to make that determination (8). These included non-receptivity and unresponsiveness, no movements or breathing, no reflexes, and a flat EEG. The committee suggested that the tests should be repeated at 24 hours and, in the absence of hypothermia and central nervous system depressants and with no change in examination, the patient would fulfill criteria for the diagnosis of brain death; that is the patient who met these criteria was dead.
Subsequently, concern regarding the relevance of EEG unfolded, with the Conference of the Royal Colleges and Faculties of the United Kingdom publishing the Diagnosis of Brain Death, first in 1976 and then again in 1995. This publication altered the definition from brain death to brain stem death (9): if the brain stem was dead, the brain was dead, and if the brain was dead, the patient was dead. The conference required that the etiology of the condition that led to coma be established, and a search for reversible factors – such as central nervous system depressant drugs, neuromuscular blocking agents, respiratory depressants, and metabolic or endocrine disturbances – be under-taken. A period of observation was recommended and the technique for apnea testing was described (9, 10).
The only prospective attempt to develop guidelines for determination of brain death based on neurologic criteria was the 1977 NIH-sponsored study (11). Enrollment required demonstration of cerebral unresponsiveness and apnea, and at least one isoelectric EEG. The investigators recommended examinations at least 6 hours after the onset of coma and apnea, with the examination demonstrating cerebral unresponsiveness, dilated pupils, absent brain stem reflexes, apnea, and an isoelectric EEG. As defined in this study, the apnea examination only required that the patient not make any effort to breathe over the ventilator.
The Quality Standards Subcommittee of the American Academy of Neurology formally redefined brain death in 1993, utilizing an evidence-based approach from the literature. They defined criteria for evaluating brain death as the presence of coma, evidence for the cause of the coma, including the absence of confounding factors, such as hypothermia, drugs, and electrolyte or endocrine disturbances. Fulfilling the preceding criteria, brain-stem and motor reflexes needed to be absent. An apnea test was finally established as a criteria and part of the exam to define brain death. The Sub-Committee recommended a repeat evaluation 6 hours after the initial evaluation, but recognized that the time was arbitrary and suggested that confirmatory studies should only be required when specific components of clinical testing could not be reliably evaluated (12).
Ishii and colleagues evaluated the use of Magnetic Resonance Imaging (MRI) and MR Angiography (MRA) in patients diagnosed as brain dead by, at the time, standard methods (13). In the four cases they studied, SPECT – using 99mTc HMPAO – scanning before or immediately after the MRI studies showed no uptake of radioactivity, the “hollow skull” sign. MRI findings were diffuse brain swelling, central and tonsillar herniation, and loss of the flow void in the intracranial portions of both internal carotid arteries. These investigators suggest that MRA provides a noninvasive and reliable method for the diagnosis of brain death.
Falini and associates (14) followed the structural and biochemical changes in a single patient after severe hypoxic ischemic brain injury, using serial MR and proton MR spectroscopy. While this case report did not touch on the issue of brain death, the biochemical metric of the severe neuronal insult – a sharp decrease in cortical N-acetylaspartate and subsequent increase in choline – are of interest.
In another single-case study, Lövblad and Bassetti utilized diffusion-weighted MRI (DWI) to evaluate for brain death (15). They again reported – in a 79 year old woman with sudden onset of coma and Glasgow Coma Score of 4 – transtentorial herniation with compression of the brain stem, the absence of flow voids on T2 weighted images, and the absence of intracranial vessels on MRA. The DWI images with severe diffusion coefficient decrements suggested profound ischemia secondary to absent cerebral blood flow. Although only a single case, the authors point out that the DWI may demonstrate severe ischemic changes that are simply not consistent with survival, thus potentially providing a non-invasive method to diagnose brain death.
Young and colleagues (16), in a brief review of ancillary studies useful for the determination of brain death, point out that the diagnosis remains essentially clinical and only studies that evaluate for brain perfusion are of merit; the authors note that CT angiogram and MRA may be of use.
Although not done in conjunction with an MRI study, Zuckier and Kolano (17), and Sinha and Conrad (18) note the utility of using the accepted 99mTc – HMPAO radio-nuclear study as a confirmatory test for brain death. An obvious potential downside to this technique is the need to move a potentially unstable patient to the Nuclear Medicine suite.
Most US institutional policies are modeled after the Quality Standards Sub-Committee of the American Academy of Neurology (19).
Thus, several things are evident from this review:
1. The definition of brain death is a clinical one.
2. In the presence of clinical brain death, the body will shut down, on average, 23 days after brain death has occurred. This means that even if we try to keep the body functioning, it will, ultimately, stop working. If this 14 week old fetus needs to be at least 24 to 30 weeks old to survive in the neonatal ICU, then nearly 3 months, not 23 days are needed. It is unliklely that the body of Ms. Muñoz can be kept functioning for that long.
3. This has obvious implications. Even if the State of Texas orders Ms. Muñoz act as a host, this will likely not be possible for a long enough period that the fetus becomes viable outside of the uterus.
And finally, even if it were possible to use Ms. Muñoz’ body as an incubator, the fact that she was in circulatory arrest for an hour before being found means that the fetus / child was without blood flow, oxygen, and nutrients for a prolonged period and will be, most likely, severely neurologically damaged.
Is the great State of Texas going to provide financial support to the child and his / her family in perpetuity? Or will these so-called Right to Lifers behave the way they often do: Very concerned about life while it is in utero, but unresponsive and dismissive after the child is born.
Medically, this is a disaster.
Morally and ethically, the State of Texas has no right to do what they are doing.
It is abuse – of Ms. Muñoz and her family – plain and simple. Texans should be ashamed that their state government abuses the dead and manipulates the emotions of the living.
I hope they find forgiveness.
1. Cushing H. Some experimental and clinical observations concerning states of increased intracranial tension. The American Journal of the Medical Sciences. 1901;124:375.
2. Power BM, Van Heerden PV. The physiological changes associated with brain death–current concepts and implications for treatment of the brain dead organ donor. Anaesth Intensive Care. 1995;23:26 – 36.
3. Yoshioka T, Sugimoto H, Uenishi M, et al. Prolonged hemodynamic maintenance by the combined administration of vasopressin and epinephrine in brain death: a clinical study. Neurosurgery. 1986;18:565 – 567.
4. Black PM. Brain death (first of two parts). N Engl J Med. 1978;299:338-344.
5. Lofstedt S. Intracranial lesions with abolished passage of x-ray contrast throughout the internal carotid arteries. Pacing and Clin Electrophysiology. 1956;8:99.
6. Mollaret P, Goulon M. [The depassed coma (preliminary memoir)]. Rev Neurol (Paris). 1959;101:3 – 15.
7. Schwab R. EEG as an aid in determining death in the presence of cardiac acuity. Electroencephalography Clin Neurophys. 1963;15:147.
8. A definition of irreversible coma. Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. JAMA. 1968;205:337 – 340.
9. Diagnosis of brain death. Statement issued by the honorary secretary of the Conference of Medical Royal Colleges and their Faculties in the United Kingdom on 11 October 1976. Br Med J. 1976;2:1187 – 1188.
10. Criteria for the diagnosis of brain stem death. Review by a working group convened by the Royal College of Physicians and endorsed by the Conference of Medical Royal Colleges and their Faculties in the United Kingdom. J R Coll Physicians Lond. 1995;29:381 – 382.
11. An appraisal of the criteria of cerebral death. A summary statement. A collaborative study. JAMA. 1977;237:982 – 986.
12. Practice parameters for determining brain death in adults (summary statement). The Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 1995;45:1012 – 1014.
13. Ishii K, Onuma T, Kinoshita T, Shiina G, Kameyama M, Shimosegawa Y: Brain Death – MR and MR Angiography. Am J Neuroradiol, 1996;17: 731 – 735.
14. Falini A, Barkovich AJ, Calabrese G, Origgi D, Triulzi F, Scotto G: Progressive brain failure after diffuse hypoxic ischemic brain injury – A serial MR and proton MR spectroscopic study. Am J Neuroradiol, 1998;19:648 – 652.
15. Lövblad K-O, Bassetti C: Diffusion-weighted magnetic resonance imaging in brain death. Stroke, 2000;31:539 – 542.
16. Young GB, Shemie SD, Doig CJ, Teitelbaum J: Brief Review – The role of ancillary tests in the neurological determination of death. Can J Anesth, 2006;53:620 – 627.
17. Zuckier LS, Kolano J: Radionuclide studies in the determination of brain death – Criteria, concepts, and controversies. Semin Nuc Med 2008;38:262 – 273.
18. Sinha P, Conrad GR: Scintigraphic confirmation of brain death. Semin Nuc Med, 20123;42:27 – 32.
19. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM, American Academy of N. Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2010;74:1911 – 1918.