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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. John Downs
One doctor consulted with by the State Attorney’s Office during its investigation was John B. Downs, M.D. Again, the 13th district State Attorney’s office chose only the most respected professionals to assist in their efforts. To briefly exemplify that, here is a list of just some of Dr. Downs’ positions:
Medical Director of the Florida Society of Respiratory Care
Professor at the University of South Florida College of Medicine, Department of Anesthesiology.
Professor at the Department of Interdisciplinary Oncology, Anesthesiology Program, H Lee Moffitt Cancer Center and Research Institute
Medical Director of the Respiratory Care Program at Hillsborough Community College, Tampa, FL
These amongst a list of more than 20 previous appointments, and a visiting professor at dozens of medical institutions across this country. Dr. Downs has also written over 75 publications and chapters, and been part in over 100 peer reviews, as well as number of published editorials.
Below is the conclusion of Dr. Downs after reviewing the evidence:
REPORT IN RE: DEATH OF MARTIN LEE ANDERSON
Prepared for the State Attorney’s Office, Thirteenth Judicial Circuit State of Florida Executive Order 06-36 and Amended Executive Order 06-37
October 26, 2006
At the request of the State Attorney’s Office, I have reviewed the medical history records of Martin Anderson, a report of the emergency medical transport personnel on January 5, 2006, Bay Medical Center records, Sacred Heart Hospital records, the Florida Certificate of Death, the Medical Examiners report by Dr. Siebert, the Medical Examiner report by Dr. Adams, a letter from Joseph Davis, M.D. To Dr. Thogmartin, a letter from Dr. Kark to Dr. Siebert and a letter from Dr. Adams to Dr. Kark, the sworn statement of Charles F. Siebert, Jr., M.D. And various versions of the video from the boot camp. In addition, I had a 1 hour discussion with Assistant State Attorney Michael Sinacore and State Attorney Investigator Gloria Porter prior to my review of the records. The morning of October 3, 2006, I had a 1.5 Hour discussion with Michael Sinacore regarding the results of my review and my opinions.
On January 5, 2006, Martin Anderson began the boot camp program in Panama City. While in the exercise yard he complained of difficulty and ammonia inhalant was utilized on several occasions. Video tape analysis confirms that Anderson’s mouth was at least partially occluded during application of the ammonia, on numerous occasions. At various periods of time, Anderson appears to be mobile, to varying degrees. On the “Anderson Tape” Frame A at 3 minutes, Anderson appears lethargic but able to walk with minimal assistance. In segment B, he appears to fall spontaneously at 5:12, is assisted to the wall and taken to the ground at 5:41, where ammonia appears to be applied. At 10:05, he is escorted to a pole. He is walking, possibly with assistance, but falls prior to reaching the pole. Clearly, he requires assistance to stand. At 10:42, an officer summons the nurse, who arrives at 11:02. At 13:05, Anderson appears unable to support his body weight and the officers assist him to a standing position. The nurse appears to be observing Anderson, from the other side of the pole, uses a stethoscope at 13:56, steps back, then says something, whereupon the officers take Anderson to the ground. At 15:37 attempts are made to get him upright, but he appears limp. At 19:10, water is poured on Anderson’s head, he seems to react and at 21:01 he clearly is barely responsive. Water is poured on his head at 20:56, again. The nurse arrives at 21:05 and paces around the scene. With the assistance of at least 3 officers, Anderson is escorted, unable to walk, or support his weight, to another part of the field. At 25:04 a right forearm chop is applied several times, I am told, in response to a clenched fist, as he falls to the ground, once more. At 25:29 vigorous occlusion of his mouth is apparent, with the heaving response from Anderson, as in an apparent attempt to breathe. He appears limp by 25:50. At 26:00 two hands are used to occlude Anderson’s mouth and it is not possible to determine if his nose is similarly occluded. Some movement is detected at 26:44, but not thereafter. A sternal rub is attempted by one of the officers at 27:45. During this period of time the nurse paces and attempts to use her stethoscope at 21:42 At 28:00, Anderson is obviously unresponsive. Paramedics are called and arrive at 34:03.
Anderson was transported to Bay Medical Center where his blood pressure was noted to be 80/63 and his pulse rate 141 bpm, breathing spontaneously 10 times a minute with an oxygen saturation of 87%. It was felt that he need ventilatory assistance and he was nasaotracheally intubated with a 7.0 tracheal tube, following administration of succinylcholine. His hematocrit was 47.1%, likely secondary to mild dehydration. Similarly, sodium concentration was mildly elevated. CO2 was less than 25% of normal, indicating an extremely low bicarbonate. Arterial blood analysis revealed PHa of 6.784, PaCO2 20.9 and PaO2 240.7, likely shortly after tracheal intubation and during ventilation with a bag, valve, mask. It is noteworthy that the nurse at the boot camp noted his pupils to be sluggish reactive and the paramedic noted pupils to be equal, round , and reactive to light. However, the emergency room triage nurse noted the pupils to be nonresponsive to light, indicating a significant degree of neurologic damage upon admission to the emergency room. Due to absence of a pediatric intensive care unit at Bay Medical Center, Anderson was transferred to Sacred Heart hospital where his medical course continued severely downward. Upon admission, his hematocrit was 41.3%, likely secondary to intravenous hydration that occurred at Bay Medical Center and during transport. However, his hemoglobin decreased steadily and within four and a half hours was 15.8 %. Following blood transfusion, his hematocrit rose to 22.7 %, at 22:15 hours. Coagulation tests upon admission to Sacred Heart revealed the early onset of diffuse intravascular coagulation (DIC), which progressed steadily throughout his hospital course and resulted in severe bleeding. Requiring multiple blood transfusions. Total CPK on admission was 8,722 IU/L, indicating massive muscle injury. Arterial blood analysis repeatedly showed normal pulmonary gas exchange, throughout his hospital stay. Ultimately, Anderson died of massive hemorrhage from DIC. In addition, he had obvious severe hypoxic encephalopathy with, in my opinion, no chance of recovery.
Assuming he weighed 90Kg and had 60 ml/Kg body volume, his total blood volume normally would have been 5.5 liters. With a 45 % hematocrit, he would have had 2310 ml of red blood cells. Of that, 947 mls (41%) would have been hemoglobin S. Had he bled to a hematocrit of 15 %, he would have had 825 mls of RBC’s, of which 338 would have been hemoglobin S. He was transfused with blood bank cells to a hematocrit of 22 %. Therefore , at the time of his death, it is likely that he had circulating hemoglobin S less than 25 %. In view of his high oxygen tension at the time of his death, it is unlikely that significant sickling would have occurred at, or about, the time of his death.
In my review of the sworn statement of Charles F. Siebert, Jr., M.D., I noted several inaccuracies. First, Dr. Siebert clearly believes that asphyxia is associated with an increase in carbon dioxide tension in arterial blood that will remain elevated for a prolonged period of time. This in incorrect. Although acute asphyxia will result in an elevation of arterial carbon dioxide tension, that value will return to normal within minutes of resuming of spontaneous breathing. Further, mechanical ventilation likely will result in a marked lowering of arterial carbon dioxide tension to less then normal values. Both Dr. Siebert and I conclude that airway obstruction likely would occur if an ammonia capsule was inserted into the nose, during occlusion of the mouth by an officer’s hand.
Analysis of the rate of decline in oxygen in the blood can be relatively accurately determined. Assuming a functional residual capacity (FRC) of 1500ml, Anderson would have had 300 ml of oxygen in his lungs at the time of airway occlusion. If one assumes oxygen consumption two to three times normal, due to exercise, excitement, etc, the oxygen reserve in his FRC would have been 30 seconds, or less. In the event of total airway obstruction rapid desaturation of arterial blood would have occurred, causing sickling of the red blood cells with hemoglobin S. Thus, severe arterial hypoxemia would have occurred with airway occlusion less than two minutes in duration. Further, it is likely that such a degree of arterial hypoxemia would cause severe brain damage. Partial obstruction of the airway by manual means, or by laryngospasm, would decrease ventilation of the lungs. Such a degree would lead to fall in PaO2 and O2 saturation, but with less rapidity that would occur with total airway occlusion. Levels of arterial oxygen saturation of 70 % are noted to be associated with changes in mental status, which is likely were observed on the video tape. Such levels of saturation would be caused by partial occlusion of the airway, either manually, or by ammonia induced laryngo spasm.
It is my opinion that the nurse who appears in the video at 11:06 should have observed the clinical signs of decreased mentation exhibited by Anderson. Further, his critical medical condition could have and should have been recognized by 17:00, when he became limp. It should have been obvious prior to 25:40, when he appears to make gasping efforts to breathe, that he was in severe straits. However, it isn’t until around 27:00 that the nurse appears attentive to Anderson’s medical condition. Obviously, at 27:45 when a sternal rub is observed, Anderson is unresponsive. There appears to be a flurry of activity around 31:06, perhaps when paramedics are called. Paramedics arrive at 34:03. It is my opinion that the nurse was in attendance for more than 20 minutes during this entire episode and should have recognized the critical medical condition that was developing in Anderson. It is my opinion that airway occlusion led to severe arterial hypoxemia, sickling, and irreversible brain damage.
In review of two medical examiner reports, it is noteworthy that lacerations of the lower lip may have resulted from attempts at mouth occlusion at the boot camp. it is unlikely that attempts at tracheal intubation would cause such and injury, although it is possible.
The degree of sickling, noted in various organs throughout the body, likely occurred hours before death. It is my opinion that capillary occlusion by sickled cells was present at the time of admission to Sacred Heart, and such occlusion led to DIC and hemorrhage. Although i do not believe the sickling of red blood cells caused the brain injury, I believe that the multiple organ failure that was noted in the laboratory results was secondary to sickling of red blood cells. I believe that the majority of the brain injury was secondary to asphyxiation that occurred at the boot camp.
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








