We have registered www.hyperbaricsofsanantonio.com and have pointed it to this site. The former company went out of business in 2011 and the owner passed last February so there is no chance of that corporation reforming. We thought to adopt the name, phone number ((210) 654-6464) and url to give our organization a San Antonio connection and telephone number.
The former company had a good reputation in San Antonio and we hope to capitalize on that and carry out their fine work for the community.
DOI: 10.1186/s13618-015-0030-6
© Harch. 2015
Received: 30 May 2015
Accepted: 4 July 2015
Published: 14 July 2015
Hyperbaric oxygen therapy is a treatment for wounds in any location and of any duration that has been misunderstood for 353 years. Since 2008 it has been applied to the persistent post-concussion syndrome of mild traumatic brain injury by civilian and later military researchers with apparent conflicting results. The civilian studies are positive and the military-funded studies are a mixture of misinterpreted positive data, indeterminate data, and negative data. This has confused the medical, academic, and lay communities. The source of the confusion is a fundamental misunderstanding of the definition, principles, and mechanisms of action of hyperbaric oxygen therapy. This article argues that the traditional definition of hyperbaric oxygen therapy is arbitrary. The article establishes a scientific definition of hyperbaric oxygen therapy as a wound-healing therapy of combined increased atmospheric pressure and pressure of oxygen over ambient atmospheric pressure and pressure of oxygen whose main mechanisms of action are gene-mediated. Hyperbaric oxygen therapy exerts its wound-healing effects by expression and suppression of thousands of genes. The dominant gene actions are upregulation of trophic and anti-inflammatory genes and down-regulation of pro-inflammatory and apoptotic genes. The combination of genes affected depends on the different combinations of total pressure and pressure of oxygen. Understanding that hyperbaric oxygen therapy is a pressure and oxygen dose-dependent gene therapy allows for reconciliation of the conflicting TBI study results as outcomes of different doses of pressure and oxygen.
Hyperbaric Oxygen Traumatic Brain Injury Concussion Pressure Gene Therapy Veteran
Confusion over the conflicting conclusions of recent civilian and United States Department of Defense (DoD) trials of hyperbaric oxygen therapy (HBOT) in the treatment of mild traumatic brain injury (mTBI) persistent post-concussion syndrome (PPCS) [1–6] have focused attention on critical flaws [7, 8] in the historical definition of HBOT [9] that beg the question “What is hyperbaric oxygen therapy?” The answer to this question has led to a re-appraisal of HBOT as a dual-component [7, 8] gene therapy [7] that is poised to not only change, but also expand the field of hyperbaric therapy.
The historical definition of HBOT (“…a treatment in which a patient breathes 100 % oxygen …at… > 1 atmosphere absolute…pressurization should be to 1.4 atm abs or higher.”) [9] focuses solely on the absolute pressure of 100 % oxygen above 1.40 ATA. The 1.4 ATA threshold is both arbitrary and limiting when considering that, by definition, oxygen at 1.399999 ATA would not be hyperbaric oxygen therapy. Yet, there is no published data on a difference in clinical efficacy between 1.40 and 1.399999 ATA oxygen for any diagnosis. Furthermore, any 100 % oxygen exposure greater than ambient atmospheric pressure or between 1.0 and 1.4 ATA, or total pressurization between 1.0 and 1.4 ATA of oxygen-enriched breathing gas > .21 ATA oxygen would not be hyperbaric oxygen therapy. This excludes a substantial body of clinical literature [10], especially Russian hyperbaric literature where pressures between 1.1 and 1.4 ATA were common (See abstracts of 7th International Congress on Hyperbaric Medicine, Moscow, 1981). The definition is also limiting by its exclusion of the acknowledged bioactivity of pressure [7, 11]. While relevant in studies where beneficial effects in pressurized air control groups have been attributed to the increased partial pressure of oxygen [12, 13], it is also relevant to the erroneous claim in DoD studies [3–5] that the 2.0 ATA/normoxic control group is a sham. Both the sham claim and the historical definition of HBOT are further erroneous when considering that every clinical HBOT is a combination of increasing partial pressure of oxygen and total pressure during pressurization and for at least the first 18 min of treatment [14], and decreasing partial pressure of oxygen during decompression.
More accurately, the definition of HBOT is a therapy of increased total atmospheric pressure and partial pressure of oxygen over ambient total and oxygen partial pressures [7, 8]. The bioactivity of increased 100 % total atmospheric pressure oxygen is well known [7–9]. The bioactivity of increased atmospheric pressure is unknown to the clinical hyperbaric medicine community, but well-documented in an extensive basic science literature [11]. Dozens of investigators have reported widespread biological effects of increased pressure across the entire phylogenetic spectrum that begin as early as 30 s after compression [11].
HBOT In the United States is primarily applied to acute and chronic wound conditions and certain infections [9]. Infections are wound conditions due to the effects of the inflammatory reaction and scar formation. HBOT has a wide range of effects on wound pathophysiology [9]. The daily input of HBOT produces wound healing. HBOT heals wounds by the trophic processes of blood vessel, connective tissue, bone, and skin growth [15–18]. These trophic effects require mitotic activity, however, the intermediary steps for trophism were a void in hyperbaric science until 1997 [19].
Siddiqui, et al. [19] proposed that HBOT was a deoxyribonucleic acid (DNA) signaling agent based on wound-healing synergy of oxygen and growth factors and an HBOT-induced change in the oxygen capacitance of ischemic animal wounds. Multiple studies on HBOT-generated single gene products followed [20–32]. Recently, gene array analyses have demonstrated widespread gene expression/suppression effects of hyperoxia and/or increased atmospheric pressure: 1) Cells grown in 2 ATA air (~.40 ATA oxygen) versus cells in 40 % oxygen at 1 ATA expressed cell adhesion, stress response, transcription, apoptosis, tumor suppressor-related, and mitogen-activated protein kinase-related genes [33], 2) Independent and overlapping genes are sensitive to increases in pressure, oxygen, or both [34], 3) As many as 8101 genes were either up- or down-regulated over 24 h after a single exposure to HBOT [35] (upregulated genes were primarily growth and repair hormone and the anti-inflammatory genes; downregulated genes were the pro-inflammatory and apoptotic genes), and 4) Differential suppression of inflammatory genes at 1.0, 1.5, and 2.4 ATA oxygen with maximal suppression at 1.5 ATA [36]. While the oxygen studies’ results are partially qualified by in vitro:in vivo oxygen partial pressure differences [34, 37], the pressure results are not. The unqualified conclusion is that a substantial number of human genes are sensitive to increased atmospheric pressure, hyperoxia at increased atmospheric pressure, or both.
The lack of appreciation of the dual-component nature of hyperbaric oxygen therapy and the bioactivity of both pressure and hyperoxia at increased atmospheric pressure is widespread, but most evident in the recent DoD trials of HBOT in mTBI PPCS [1–6]. A review in Medical Gas Research [38] correctly mentions that one of the DoD studies does “…not address any potential therapeutic benefit of higher pressures in the absence of increased oxygen tension,” however, it does not elaborate on the literature describing bioactivity of pressure. An earlier review [39] mentions only the oxygen component of HBOT. A third review [40] noted, “Unfortunately, agreement that HBOT has a positive effect on TBI has not yet been reached due to the difference in external conditions.” Absent in this review was a discussion on the different doses of HBOT used in the various studies and the erroneous assumption in two of the studies that the “sham” groups were not treatment groups that used different doses of hyperbaric therapy. This erroneous assumption is present in all of the DoD mTBI HBOT PPCS studies [7, 8]. When viewed as multi-dose studies the results of the DoD studies become congruent with the results of civilian studies [41–44], suggesting effectiveness of some doses of hyperbaric therapy [1, 6, 41–44], ineffectiveness of others [3–5], and harm of another [2]. This appreciation of dosing differences raises the question of potential effectiveness of many other doses of pressure and hyperoxia in mTBI PPCS. They also spawn a rethinking and re-appraisal of the disputed historical claims of efficacy of HBOT in the treatment of well over one hundred diseases [45] dating to 1662, and the widely differing number of treatable indications in less scientifically restrictive countries, e.g. China [46], versus the United States.
In conclusion, HBOT is the use of increased total atmospheric pressure and partial pressure of oxygen over ambient total and oxygen partial pressures to treat various disease processes and their diseases. The combination of increased atmospheric pressure and hyperoxia express or suppress upto 8101 genes in human cells [35]. Hyperbaric oxygen therapy appears to be the oldest, most enduring, and most effective gene therapy. Physicians and researchers are playing a symphony with gene expression and suppression, the combination of which is dependent on the different total pressures and partial pressures of oxygen. It is apparent that dosing of hyperbaric therapy is in its infancy, particularly in the pressure ranges from 1–2 ATA and across the spectrum of unexplored fractional inspired oxygen concentrations at pressures ≥ 1 ATA. It is also apparent that multiple doses of hyperbaric therapy are effective in the treatment of PPCS while others are not. With an appreciation of the scientific definition of hyperbaric oxygen therapy the field of Undersea and Hyperbaric Medicine is poised to rapidly expand with investigation of the lower dosing ranges of pressure and hyperoxia for a multitude of diagnoses.
Atmospheres absolute
DeoxyriboNucleic acid
United States department of defense
Hyperbaric oxygen therapy
Mild traumatic brain injury
Persistent post-concussion syndrome
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
TBI AND HBOT STUDY LINK TO ONLINE PDF WITH PICTURES
| Brief Summary | Traumatic brain injuries (TBI) are a major cause of morbidity and mortality worldwide. Due to improvements in emergency medical care, transportation and specialized trauma facilities, the number of people surviving TBI with impairment has significantly increased in recent years. The long term cognitive sequelae, which are often not visible persist far beyond the resolution of the obvious physical disabilities. This combined with the relatively low awareness of the general public has designated TBI as the “silent epidemic” (TBI CDC 2006). Hyperbaric oxygen therapy (HBOT) has been suggested as a possible treatment modality for these cases and preliminary studies are promising.
The purpose of this study is to evaluate the effectiveness of HBOT in the treatment of chronic mild traumatic brain injuries (mTBI). Sequential SPECT scans of the brain and neurocognitive testing will be used to evaluate cerebral blood flow (CBF) response, cognitive and functional improvement following treatment. |
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| Detailed Description | INTRODUCTION Traumatic brain injuries (TBI) are a major cause of morbidity and mortality worldwide. Due to improvements in emergency medical care, transportation and specialized trauma facilities, the number of people surviving TBI with impairment has significantly increased in recent years. The long term cognitive sequelae, which are often not visible persist far beyond the resolution of the obvious physical disabilities. This combined with the relatively low awareness of the general public has designated TBI as the “silent epidemic” (TBI CDC 2006). Hyperbaric oxygen therapy (HBOT) has been suggested as a possible treatment modality for these cases and preliminary studies are promising.
The purpose of this study is to evaluate the effectiveness of HBOT in the treatment of chronic mild traumatic brain injuries (mTBI). Sequential SPECT scans of the brain and neurocognitive testing will be used to evaluate cerebral blood flow (CBF) response, cognitive and functional improvement following treatment. Traumatic brain injuries (TBI) Traumatic brain injuries are a major cause of morbidity and mortality leading to major long term consequences on both a personal and national level with an estimated 5.3 million Americans suffering from permanent TBI related disabilities (24).The prevalence of traumatic brain injury in the United States is estimated to be approximately 1.5 million individuals per year (24,25). This however does not include those individuals who did not receive care in a facility included in national surveillance systems or received no medical care at all and thus probably significantly underestimates the actual number of TBI victims. The 2006 NIH consensus states a prevalence of 2.5 – 6 million people per year suffer form TBI(23). Due to improvements in emergency medical care, transportation and specialized trauma facilities, the number of people surviving TBI with impairment has significantly increased in recent years. The long term consequences of TBI are vast, affecting a large number of people with a substantial effect on the patients themselves, their families and society as a whole. These injuries also impart a significant economic burden on those involved, both personally and as a society. Approximately 80,000 – 90,000 individuals suffer from long term disabilities annually, and the estimated costs including both direct medical care and indirect expenses such as lost earning potential were over 60 million dollars in 2001 in the US (28). The long term sequelae of TBI may include impairment of the individuals physical, cognitive and psychosocial functioning. The neurological consequences are numerous and complex affecting various sites and functions. Sensory, motor and autonomic systems may all be affected and symptoms may include headaches, seizures, visual defects, movement disorders and sleep disorders. The cognitive consequences likewise are broad and varied. Amongst the symptoms most commonly noted are memory deficits and problems with attention and concentration. There may be impaired executive function, problem solving abilities and language difficulties as well as problems with planning, information processing, judgment and insight. While some of these symptoms may be apparent immediately after the injury, others may present days, weeks or months after the initial trauma(Kushner,24). Moreover, there can be vast fluctuations and changes in the severity and presentation over time. Another realm of difficulties resulting from TBI includes behavioral, emotional and psychological impairments. There can be vast personality changes including loss or decreased ability to initiate responses and activities, disinhibition, impulsivity, aggressive behaviors – both verbal and physical, and changes in sexual behavior. Personality and mood disorders may appear and depression, anxiety and changes in emotional control are often noted after TBI.(23) The social consequences may also be widespread and often devastating. There is an increased incidence of divorce, chronic unemployment, suicide and substance abuse following TBI. Even in the more chronic stages as the patient is in the recovery stage, the increased demands placed on him in the workplace or upon undertaking new tasks may uncover problems with executive functions and planning abilities that had as of yet been unnoticed. These problems and the burden of caring for these individuals on a long term basis place cumulative strains on the family and their support network. Family members and care givers report an increased occurrence of depression, anger and social isolation. These combine to result in disrupted family functioning and relationships and these problems may persist or worsen with time.(24) HBO for TBI Hyperbaric Oxygen Therapy (HBOT) has been in use since the 1930’s when it was initially used for decompression sickness. Shortly thereafter physicians started usingHBOT for a variety of other conditions. The use of HBOT for neurological indications started in the early 1960s with the work by Smith et al showing its protective effect in cerebral ischemia and that of Saltzman showing effectiveness in stroke patients.(Jain) HBOT is the inhalation of 100% oxygen at pressures exceeding 1 atmospheres absolute (ATA) in order to enhance the amount of oxygen dissolved in the blood and body fluids, thereby allowing for increased oxygen delivery to the tissues. The mechanism by which HBOT is thought to improve the outcome of brain injury is multifaceted. The Neubauer and Walker(2000) theory postulates that HBOT improves cerebral metabolism by improving functioning of the dormant neurons and stimulating axonal growth (10). Zhang et al suggest that potential targets of oxygen therapy include prevention of apoptosis, inhibition of neuroinflammation and BBB damage (Zhang pathophysiology 2005,Rossignol). There is stimulation of angiogenesis and neovascularization, as well as direct effects on blood vessels in the brain, and maintenance of BBB integrity. (1((5-12)),20) . Similarly, SPECT scans have demonstrated a positive effect on the cerebral blood flow (CBF) in the damaged brain following HBOT (2,8,10,16,19,17,neubauer HBOT of closed head,20,). HBOT also brings about improved neurocognitive functioning in patients suffering from chronic brain injury. (14,9,6,13,20,21). Under normobaric conditions, the amount of oxygen dissolved in the blood is only 0.3 ml/dl. At 1.5 ATA this amount increases 10 fold to 3.2 ml/dl. Using an animal model of brain injured mice Daughrty et al (rockswall 9) found a 250% increase in the local brain tissue oxygen levels between 100% oxygen administered at 1 ATA (103 mmHg) as opposed to that given at 1.5 ATA (247 mmHg). This seems to suggest that the this dissolved O2 is more readily available to the brain tissue than hemoglobin bound oxygen (20). Additionally, work by several investigators seems to indicate that HBOT allows for more efficient use of baseline oxygen levels by injured brain tissue following treatments, which in turn leads to a positive persistent affect on this tissue (20). It has been theorized that following brain injury from any cause, there is an area of “idling neurons” in the ischemic penumbra zone which are still viable and potentially salvageable if given the right treatment. This area consists of dormant neurons between the areas of dead tissue and the unaffected healthy tissue surrounding it. .(2,16,17,18,19,jain,22). There appears to be sufficient oxygen available to these cells to maintain cell life and ion pump mechanisms, but not enough to generate action potentials and allow them to act as functioning neurons (17,19). The hyperoxia from HBOT causes vasoconstriction of the cerebral blood vessels which has been shown to cause a decrease in brain edema and ICP (11,13,6,7,12 fr rockswald ). This vasoconstriction does not appear to have any harmful affect on the brain tissue due to the greatly increased oxygen availability to the tissue. There is also a beneficial effect effect on the BBB, evidence by reduce post ischemic BBB permeability defect (jaine,veltkamp, rockswald 52,55,63). There are well documented animal models of TBI and a growing body of literature using HBOT on these animal models verifying the above stated hypotheses and findings. Sun et al demonstrated improved penumbral oxygenation following HBO treatment in focal ischemia using an animal model by measuring both extrinsic and intrinsic markers of hypoxia (SUN). Harch et al used a rat model of TBI to evaluate HBO effects on spatial learning and memory, as well as it’s affect on blood vessel density. After receiving a unilateral cortical contusion, Long-Evans rats were tested in the Morris Water Task (MWT) 31-33 days post injury. The rats were divided into an untreated control group, a sham-treated normobaric air group and an HBO group which received 80 bid treatments of HBO at 1.5 ATA/90 mins. The rats were subsequently retested in the MWT and then euthanized. Blood vessel density was measured bilaterally in the hippocampus and correlated with the MWT performance. The HBOT caused a significant increase in the hippocampal vascular density (p< 0.001) and an associated significant improvement in spatial learning (p< 0.001) compared to the control groups. Similarly, the increased vascular density and the improved MWT in the HBOT group were highly correlated (p<0.001). (11) SPECT for investigation and follow up Single photon emission CT (SPECT) scans have been found to be effective in evaluating post traumatic lesions in mTBI patients and are useful as a means of follow up of recovery. In a prospective study to evaluate the usefulness of SPECT scans in the diagnosis of patients with mTBI and it’s correlation with common clinical symptoms such as post concussion syndrome (PCS), post traumatic amnesia (PTA) and loss of consciousness (LOC), Gawda et al found perfusion abnormalities in 63% of the patients. This as opposed to positive CT findings in only 34% of these patients. In adults, the frontal lobe was most commonly affected whereas the temporal lobes were more likely to be involved in children. The SPECT scan was found to be more sensitive than CT in patients presenting with LOC, PTA and PCS (14). Jacobs et al evaluated the predictive value of SPECT scans for clinical outcome of 136 mTBI patients in a prospective study. None of the patients had abnormal findings on CT. All patients underwent initial SPECT scans and CT scans within 4 wks of the trauma. Follow up evaluations were performed 3, 6, and 12 months post injury. All patients with abnormal SPECT studies or deteriorating clinical findings had follow up SPECT scans performed at the subsequent time of evaluation. The initial SPECT was positive in 54% of the patients with a gradual decrease in the number of positive scans over time. The clinical normalization occurred more rapidly than did the normalization of the imaging studies. The SPECT was shown to have high sensitivity and negative predictive value from 3 months post injury onward so that a negative early SPECT is a reliable criteria in the exclusion of clinical sequelae. A positive initial SPECT scan did not exclude a positive clinical outcome, however, a positive SPECT scan at 12 months post injury was a reliable predictor for clinical outcome (13). Golden et al showed improved blood flow as measured by sequential SPECT studies in 50 patients with chronic neurological disorders (10). SHI Xiao -yan presented a large study of 310 patients in which the effect of HBOT on CBF as well as the usefulness of SPECT in the diagnosis and assessment of neurocognitive disorders following TBI was examined. Pre and post treatment scans were compared and the percent of positive initial SPECT scans was substantially higher than those found with CT alone (81.3% vs. 15.2%). Following HBOT 63.5% of the SPECT scans had normalized concomitant with marked improvement of the clinical symptoms of headache, dizziness, poor concentration and poor memory. An additional 36.5% of the initial positive SPECT scans showed between 33-66% improvement in CBF along with clinical improvement as well. Proposed Study Design Sixty consenting TBI patients at any age who are at least one year post injury with stable cognitive deficits will be recruited. Any patient with previous neurological deficits, head trauma or substance abuse will be excluded as well as anyone with any contraindications for HBOT. All patients or their trustees will sign written informed consent before their inclusion and the study protocol will be approved by the local Helsinki committee. Patients will be excluded if they will have one of the following criteria:
The patients will be randomly assigned to two groups. Group I will initially receive 40 consecutive HBOT treatments and Group II no HBOT treatment. At the end of this first phase of approximately two months, both groups will be revaluated with a second SPECT scan and neurocognitive testing. There will then be a cross over of the two groups and Group II (previously none treated) will receive HBOT treatment while Group I (previously treated) will not receive any further treatments. Again at the end of this second phase there will be follow up SPECT scans and neurocognitive testing for both groups. Additionally at the end of each phase there will be a detailed questioner assessing adverse effects and evaluating any changes in ADL. There will be an evaluation of the results after the first phase comparing the differences between the treated and non treated groups as well as allowing for evaluation of any spontaneous changes occurring in the non treated group due to the passage of time or a learning curve for the cognitive evaluation. Following completion of the second phase there will be another evaluation of the results comparing the effect of HBOT on Group II as compared to their baseline as well as evaluating whether the effects seen in Group I are maintained after two months with no treatment. The HBOT treatment will consist of 40 consecutive one hour treatments at 1.5 ATA with 100% O2 in either a multiplace or monoplace unit per patient preference. The treatments will be given once daily five times a week. Cognitive evaluation Statistical analysis This is a pilot randomized crossover study. The sample size of 30 patients in each subgroup (total 60 patients) in the post ischemic stroke as well as in the post hemorrhagic stroke was determined in order to achieve 90% power based on the following assumption related to the expected change in neurologic evaluation: mean difference between the groups of at least 25% with drop rate of 16% and alpha 5% before the cross match period. Statistical analysis will be performed using the statistical software SPSS-version 13. Parametric data will be expressed as means ± standard deviations and compared by one way ANOVA. Non-parametric data will be compared using Kolmogorov-Smirnov test. Differences between the results yielding p values less than 0.05 (p<0.05) will be considered statistically significant. |
I have had the good fortune to meet Dr. Dunn at the Foundation Hospital Hyperbaric and Wound clinic where he is seeing me for my self-inflicted foot wound.
I learned that he is qualified in emergency medicine as well as hyperbaric medicine and has practiced for 40 years now. He and I were both born at West Suburban Hospital in Oak Park IL , I in 1948 and he a bit later, nice to meet someone about my own age.
He has recently practiced at the Nix hospital and was the head of the hyperbaric department as well as being an instructor with International ATMO where I recently attended the hyperbaric safety director course..
He is interested in this project and what role he will play in the future will a matter of future conversations. I know I will have an opportunity to talk to him since it will be some time before i heal up completely.
Speaking of Foundation Hospital’s hyperbarics department, I was advised by Ms. Audrey Duffin who is in charge of that department that she has openings for HBO treatment as well as wound care patients. Call her at 210-478-5390 for an appointment.
CMS officials believe they can reduce HBOT spending while maintaining or improving quality of care by ensuring services are provided in compliance with Medicare coverage and payment rules before the claims are paid. This article provides an update on these reporting procedures.
The Centers for Medicare & Medicaid Services (CMS) has implemented a prior authorization model for nonemergent hyperbaric oxygen therapy (HBOT) in the states of Illinois, Michigan, and New Jersey. CMS officials have also openly stated that the goal of this project is to determine whether or not prior authorization reduces Medicare expenditures. It is the position of CMS that it can reduce spending on HBOT services while maintaining or improving quality of care by ensuring services are provided in compliance with Medicare coverage and payment rules before the claims are paid. CMS officials argue that prior authorization does not create new clinical documentation requirements because the information required should be no different than would be required if the record went to post-payment review. In the view of CMS, prior authorization allows providers to address issues with claims prior to rendering services, thus avoiding an appeal process. The information required to support Medicare payment must be sent to the Medicare Administrative Contractors (MACs) in each of the affected states:
• Illinois facilities serviced by A/B MAC Jurisdiction 6 NGS (National Government Services),
• Michigan facilities serviced by A/B MAC Jurisdiction 8 WPS (Wisconsin Physician Services), and
• New Jersey facilities serviced by A/B MAC Jurisdiction L Novitas Solutions Inc.
Prior authorization was not implemented on the same date in all three jurisdictions because the details of the review process took some time to establish. However, all three are now active. (Details are available at: www.cms.gov.) The Undersea and Hyperbaric Medical Society and the Association for the Advancement of Wound Care have been collecting information regarding the reasons for denial of HBOT under the prior authorization process. Today’s Wound Clinic is also accepting feedback from wound care clinicians who are interested in submitting information pertaining to the reasons given for denied treatments. Some wound care clinics and hospitals have experienced challenges in getting their treatments authorized. The list below is not an exhaustive list of reasons for HBOT denials. (Charting deficiencies can be corrected and resubmitted).
Reasons for HBOT Denials During Prior Authorization
A) For a patient with a failing flap: HBOT was denied because the tissue at risk was not a skin graft. (“Flap” is not in the language of the national coverage determination.)
B) For patients living with a diabetic foot ulcer:
1) HBOT was denied because there was no documentation of 30 days of standard wound care.
2) HBOT was denied because there was no documentation of vascular screening (physical exam is insufficient) or documented action to correct peripheral artery disease (PAD) if present.
3) HBOT was denied because, if action was taken to correct PAD (as a result of an abnormal vascular screen), a subsequent vascular screening was needed to determine response to vascular intervention.
4) HBOT was denied because hemoglobin A1C was not recorded at the time of initial visit and then after 30 days.
C) HBOT was denied on a general patient assessment/visit due to incorrect charting, inconsistent location of wound (eg, left leg improperly documented as “right leg.”)
D) HBOT was denied because there was no HBOT physician order within a patient’s chart (for each daily treatment).
NOTE: HBOT prior authorization must be requested in segments (meaning, the 30-minute segments that comprise the typical HBOT protocol for one’s facility).
Caroline E. Fife is chief medical officer at Intellicure Inc.; executive director of USWR; medical director of St. Luke’s Wound Clinic, The Woodlands, TX; and co-chair of the Alliance of Wound Care Stakeholders. Helen Gelly is emeritus medical director of Hyperbaric Physicians of Georgia and chief executive officer of HyperbaRXs.
Posted Wednesday, December 2nd 2015 @ 12pm
Researchers at the U.T. Health Science Center told the Association of Military Surgeons of the United States at their annual meeting underway in San Antonio that the Post Traumatic Stress Disorder and other emotional problems facing veterans of the Iraq and Afghan Wars will require care and treatment for decades, News Radio 1200 WOAI reports.
That’s because, according to Dr. Alan Peterson, chief of the Division of Behavioral Medicine and a former Air Force lieutenant colonel who did three tours of duty in Iraq as a combat psychologist, of the nation of blast wounds and their impact on victims and survivors alike.
“Individuals who have been exposed to a blast are a group of individuals we need to monitor carefully over the next several decades,” he said. “It is the underlying cause of many type sof medical injuries, and also brain injuries and psychological health injuries.”
Dr. Peterson says blast injuries were far more widespread than in previous wars. He says Improvised Explosive Devices were a main weapon of insurgents, and he says Joint Base Balad, where he was stationed, was referred to by troops as ‘Mortar-ita-ville’ due to the prevalance of blasts caused by mortat rounds lobbed into the base.
“80% of individuals who have been injured and killed in Iraq and Afghanistan have been wounded due to the effects of a blast.”
He says that is far higher than in previous warns, where gunshots were the primary cause of death and injury.
Dr. Peterson says the nature of blast wounds causes emotional and psychological problems not only for the person who is wounded, but for those who only witness the attack and those who are charged with helping the victims.
“Many people are killed, there are mutilating injuries, there is gore that occurs after a blast exposure which is far beyond anything that you could possibly prepare for,” he said.
The military surgeons are discussing the impact of the wars in Iraq and Afghanistan and the ongoing medical treatment which the veterans of the wars will require in the years and decades ahead.
Read more: http://www.woai.com/articles/woai-local-news-sponsored-by-five-119078/ptsd-emotional-scars-from-iraq-afghanistan-14167579/#ixzz3tNIhxkS7
Nov. 11, 2013: A Vietnam veteran holds an American flag as he marches during the annual Veterans Day Parade in San Diego, Calif. (Reuters)
Higher than average death rates among Vietnam War veterans with post-traumatic stress disorder (PTSD) suggest that combat trauma may still be affecting veterans’ health even decades after the war, according to a new study.
U.S. veterans of the Vietnam War followed from the 1980s to 2011 were almost twice as likely to die during that period if they had PTSD compared to those without the disorder.
The findings can inform healthcare for Vietnam veterans, now mostly in their 60s and older, and prevention efforts for the next generation of soldiers, the study team writes in the American Journal of Epidemiology.
“The study offers really valuable empirical information that can help us better understand how to care for our Vietnam veterans . . . and also more recent veterans,” said study author Nida Corry, of Abt Associates in Durham, North Carolina.
PTSD can develop after a person has been through a traumatic event like combat, child abuse or sexual abuse, terrorism attacks and other disasters, according to the Department of Veterans Affairs. Symptoms can include flashbacks, avoiding reminders of the traumatic events, changes in beliefs and activities and being overly alert, according to the VA.
A study published earlier this year estimated that more than 1 in 10 Vietnam war zone veterans still have PTSD or some symptoms of the disorder (see Reuters Health story of July 22, 2015, here: http://reut.rs/1NsyrVe).
Previous studies have also suggested that Vietnam vets – especially those who served in the war zone – are at increased risk of death, and that the added risk may be related to PTSD. However, those studies were often limited, according to the authors of the current study.
For the current study, the researchers from Abt Associates, New York University in New York City and other organizations analyzed information collected from 1987 to 2011 on nearly 2,400 Vietnam veterans, including 1,632 who served in the combat theater, which included Vietnam, Laos and Cambodia.
Overall, about 9 percent of theater vets had PTSD at the time of the initial interviews in the 1980s, which was significantly higher than the 1 percent rate in vets who served outside the war zone.
About 16 percent of all Vietnam veterans who were alive in the 1980s are now dead, with most deaths due to cancer and heart disease, the authors estimate.
Male Vietnam War theater veterans who had PTSD were about 87 percent more likely to die between 1987 and 2011 than those without the condition – even after adjusting for demographic, social and economic factors.
“What we found is that having PTSD was associated with a greater risk of death from cancer and external causes,” Corry said, such as traffic accidents, suicide, murder and other accidental injuries.
Male and female veterans who were exposed to high levels of stress in the war zone – but not necessarily diagnosed with PTSD – were also at increased risk of death during the study period, the researchers found.
The combination was even deadlier. Veterans with high levels of war zone stress exposure who developed PTSD were at the greatest risk of death, Corry said.
The study can’t explain why PTSD and war zone stress raise the risk of death, but the explanation is likely complex, said Alan Peterson, a PTSD researcher from The University of Texas Health Science Center at San Antonio.
For example, he said, PTSD may create a consistent level of stress in the body – like a false alarm for impending danger – that eventually affects different organ systems throughout the body.
“There is this physiological arousal that in theory affects all organ systems and that’s going to wear over time,” said Peterson, who was not involved in the new study.
The study authors point out that Vietnam vets still make up the majority of living veterans, so it’s important to keep studying the long-term mental and physical health effects of their wartime experiences and to understand how they might interact with the aging process.
Corry said findings like these – and other analyses of the same data – may provide an opportunity to provide better care for veterans through earlier screenings and treatments.
“This is sort of the best data we have to foreshadow those long term needs,” she said.