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Charles Helms Jr |
Henry Dickens |
Charles Enfinger |
Patrick Garrett |
Raymond Hauck |
Henry Mcfadden
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Joseph Walsh II
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Kristin Schmidt |
Dr. Martin Steinberg
The doctor is a Sickle Cell Trait expert, highly regarded in the field. I will add his CV as soon as one of us has time to transcribe it.
Re Death of Martin
The following are my opinions in the case of the death of Martin Lee Anderson. These opinions are based on results of autopsies by Dr. Siebert and Dr. Adams, the records of the Boot Camp, Bay Medical Center, Sacred Heart Hospital, the testimony of Drs. Charles Siebert, Samir Abied, Jennifer Jenkins, Jason Foland, William Clark, Jeffery Appel, and Monica Belisle, testimony of Felicia Reed, Cassie Elliott, Chuck Jeter, Dennis Arnold, Lisa Ward, Diane Houser, Young Hall, Chelsea Pollock, Anita Segers, Ruth Bacher, Michael Dobbs, Jill Barry, Sharon Holler, Laura Morette, Shelly Vogt, Carla Alvarez, reports of Dr. John Downs and Thomas Andrews, a letter from Dr. John Kark, a letter by Dr. Siebert to Dr. John Kark, a review of the medical literature, viewing the video tapes, my knowledge and experience.
I will begin with some background information about sickle cell trait (HbAS). Less than half the hemoglobin in the HbAS erthrocyte is sickle hemoglobin (HbS), the remainder, mainly being normal HbA. HbS is evenly distributed in all cells of carriers of HbAS. As HbS polymer concentrations sufficient to injure the red blood cell is a prerequisite for the expression of the phenotype of sickle cell disease, in HbAS, high concentrations of HbA preclude clinically significant HbS polymer formation at the oxygen saturation and physiological conditions normally present in most tissues. HbS polymer appears in HbAS cells only when oxygen saturation falls below 60 percent and under physiological conditions this does not occur to the extent that symptoms occur. Despite the multitudinous reports of innumerable complications of HbAS, with rare exceptions, this is a benign carrier state.
Medical history, clinical examination or routine laboratory testing cannot diagnose HbAS. Neither hematologic indices nor peripheral blood film reviews are useful fro diagnosis since bath are normal in HbAS. Detecting HbAS requires the quantification HbS and HbA in hemolysate. HbAS carriers with four a-globin genes usually have 40+-4 percent HbS as did Mr. Anderson. I believe that Mr. Anderson, before his terminal event had typical and uncomplicated HbAS.
Abundant data suggest that HbAS is not a risk factor for excess mortality in African Americans. Reports of sudden death or life-threatening episodes during exercise in HbAS abound and have been extensively reviewed. Most deaths were attributed to exertional heat illness. Case reports and small clusters of unexpected sudden death in people with HbAS in special situations like military recruits undergoing basic training and athletes engaging in physically stressful sports, raised the possibility that under extremely rigorous conditions, HbAS could be associated with higher risk of sudden death. Over a span of five years during with 2.1 million recruits underwent basic training in the US Armed Forces, the risk of sudden unexplained death in black recruits with HbAS, compared with those without the trait, was 27.6. Compared with all recruits -- blacks without HbAS and whites -- the relative risk was 40. The risk increased progressively with increasing age from a death rate of 12 per 100,000 at ages 12-18 years to 136 per 100,000 at ages 31-34 years. It was not possible to tell if the fractional percent of HbS was associated with sudden death. Individuals with HbAS and coincident a thalassemia have a lower amount of HbS and better preserved urine-concentrating ability than those with the trait alone. Using percent HbS used as a reasonable surrogate for a thalassemia, studies suggested that a thalassemia was under-represented in individuals with sudden death. Based on the red cell indices and fractional percent of HbS, Mr Anderson did not appear to be a carrier of a thalassemia. HbAS is not a risk factor for excess mortality in the general population.
Physiological responses to exercise in HbAS appear normal and HbAS does not seem to impair exercise tolerance and performance. Black athletes with HbAS are well represented in elite competitive sports. The percentage of African marathon runners and other competitive athletes with HbAS competing and among the top performers is similar to , or more than, that of the general population. Based upon the total body of work on exercise ability and capacity, there is no reason to restrict exercise of any type in persons with HbAS if access to fluids is unrestricted.
2. Mr. Anderson, during physical fitness assessment at a boot camp for juvenile offenders in Panama City on 01/05/06, at about 0909 hours, became non-responsive after a period of exercise. The exercise consisted of 18 pushups followed by a rest period of unknown duration and 48 sit-ups followed by an unknown rest period. He then started a 1 to 1.5 Mile run, said to be at his own pace, and completed about half of this before the events occurred that preceded his death. At the time of his collapse, the dry bulb temperature was 64 degrees F, wet bulb temperature 59 degrees F and relative humidity 73%. He was not wearing restrictive clothing while exercising.
The records available to me and the video tape show that he initially voluntarily stopped his run, was suspected to be malingering, was ‘taken down’ and counseled and then resumed running. After an additional 2 min of running he collapsed, became poorly responsive or unresponsive and received ammonia for about 1-minute followed be about 5 to 10 minutes without ammonia. Following this, they gave ammonia for a period of about 5 minutes. During ammonia administration his mouth was covered by the hand of the officer administering the ammonia. Between the episodes of ammonia administration he apparently breathed spontaneously however the effectiveness of his respiratory effort and his respiratory rate is unknown. During this time he also received blows to his forearm to prevent him from forming a fist and strikes to his knees to help bring him to the ground. Whether or not he had total occlusion of his airway anytime during his restraint is unclear.
The initial finding on blood gas measurement, taken most likely after intubation (how long after intubation is not known), suggests to me that his primary acid-base disturbance was a severe metabolic acidosis. Paramedics who arrived within four minutes of being summoned at 0935 found him to have tachycardia, be hypotensive and unresponsive but with spontaneous respirations. While they provided oxygen at 0937, they did not provide any assisted respiration as he was breathing spontaneously. For unknown reasons, the paramedics were unable to measure O2 saturation.
3. Subsequently, the medical records suggest that he died with rhabdomyolysis, metabolic acidosis, acute oliguric renal failure, disseminated intravascular coagulation and shock. The questions are was the death a result of exercise-induced rhabdomyolysis in a man with HbAS, was rhabdomyolysis a result of asphyxiation during his restraint or was spontaneous exercise-induced rhabdomyolysis contributed to by his restraint? It is unclear to me how one can distinguish among these possibilities based on autopsy findings alone, as in either case, as in either case, in an individual with HbAS, post mortuum hypoxia would lead to the polymerization of HbS and the deformation of the HbAS erythrocytes. Absent findings at autopsy of damage to the airway that would be a clear cause of asphyxia, i am left with the opinion that the nonstandard use of ammonia capsules with at least partial occlusion of his airway was likely to have produced hypoxia.
4. The autopsy showed similar results but were interpreted differently. One found that death was a result of hbAS, the other concluded that death was by suffocation. Neither autopsy suggested a primary cardiac cause of death, which is the most common cause of sudden death in previously healthy young people. Initial blood counts at Bay Medical Center were normal. Hemoglobin electrophoresis showed 55% HbA and 41% HbS and this result was said to be confirmed by citrate agar electrophoresis. Taken with blood counts, these results indicate that Mr. Anderson had HbAS.
5. Initial blood gases, obtained by the respiratory therapist who noted ‘agonal’ respirations, most likely were obtained just after intubation and showed a severe anion gap metabolic acidosis with some component of respiratory acidosis. It is likely that the metabolic acidosis was related to lactic acid production secondary to hypoperfusion. With pure metabolic acidosis, his pCO2 should have been lower. While they reported him to be breathing normally, it was likely that his respiratory effort was insufficient to compensate for the metabolic acidosis, especially in view of the description of his respirations on admission to Bay Medical Center.
Initial laboratory results also suggest acute renal failure with a creatinine of 2.4, rhabdomyolysis, a BUN creatinine ratio of 10 2.4. His Na was increased at 147 and hemoglobin, possibly measured on a blood specimen obtained by the paramedics, was 17.3 G/dL suggesting dehydration. The K was normal and CO2 <5.
While formally possible, it seems that, if he were asphyxiated between 0909 and 0920, was said to have normal respirations at 0920, was still breathing on his own at the time he was first seen be the paramedics team at 0935 and had a reduced respiratory effort on his arrival at Bay Medical Center about 1001, it would be unlikely for the hypercapnea expected with the respiratory acidosis of asphyxiation to be totally resolved. Undoubtedly, this and all subsequent blood gases were consistent with severe metabolic acidosis. The very low HCO3 in the initial blood gas is inconsistent with isolated respiratory acidosis.
6. Moderate temperature and humidity during the morning of 01/05/06, his youth, the apparently mild nature of his exercise and the absence of fever, suggest that this is not a typical instance of exertional heat illness leading to rhabdomyolysis. Nevertheless, in some individuals, rhabdomyolysis occurs with minor degrees of exertion and with normal body temperature. Why one individual with HbAS and not all people with HbAS, under identical circumstances, develops rhabdomyolysis is unknown. This observation is likely to be explained by many different factors including the level of physical conditioning, state of hydration, prior use of prescription medication, drugs or performance enhancing agents, and differences in genes that regulate energy metabolism, body temperature, the integrity of cell membranes, heterogeneity in muscle metabolism. The same is true of individuals who develops sudden death during exercise and do not have HbAS.
7) Death in this case was, to a reasonable degree of medical certainty, due to the unfortunate confluence of multiple factors. I believe that he likely had exercise-induced rhabdomyolysis that occurred spontaneously. Initial laboratory studies suggest he might have been dehydrated during exercise. Rhabdomyolysis is more likely to be fatal in individuals with HbAS. The officers responsible for his training did not make a distinction between malingering and a potentially fatal pathophysiological process and the attendant medical personnel did little to help this differentiation. This lead to physical restraint and the repetitive administration of ammonia that appeared to be associated with occlusion of the upper airway. This was likely to cause additional hypoxia that contributed to rhabdomyolysis and the irreversible events culminating in his death.
Quick Links
What Happened - 10/17/07
Autopsies - 11/01/07
Court of Public Opinion - not available
Matter of Law - 10/03/07
Ammonia Facts - 10/03/07
Sickle Cell Trait and EHI - 10/10/07
Dr. Siebert 10/13/07
Dr. Adams
Dr. Andrews 11/26/07
Dr. Gravenstein 11/29/07
Dr. Downs 10/29/07
Dr. Steinberg 11/27/07
Dr. Eichner
Science for Suffocation - Must read 10/10/07
