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April 30, 2009

Prevention of Decompression Accidents

Filed under: Article, News, Publication, Uncategorized — admin @ 4:01 pm

Compiled and maintained
by Ernest S Campbell, MD

Self-grading Quiz for Prevention of Decompression Accidents
Some Causes of Decompression Accidents

The best way to categorize the various ways a diver can prevent the occurrence of DCS is by looking for the causes of the accident.

Some predisposing causes for DCS are as follows:

  • Inadequate decompression or violating the no-decompression limits. By surfacing too rapidly and not taking safety stops a diver allows bubbles to form and to get larger as the pressure differential decreases. Nitrogen loads in all the tissues at different pressures and times and violation of the NDL (no-decompression limits) is a major cause of DCS.
  • Inadequate surface intervals (failure to decrease accumulated nitrogen). Surface times are outlined for various diving profiles and failure to adhere to the prescribed length of time does not allow “off-gassing” of onboard nitrogen. The accumulated nitrogen is then added to by the next dive, increasing the risk of DCS.
  • Flying or going to higher altitude soon after diving (12-24 hours), which increases the pressure gradient. This in reality is a continuation of an ascent from a dive. This allows any nitrogen that is in the tissues to come out of solution and form bubbles, leading to DCS.
  • Individual physiological differences that have been traditionally thought of as increasing the risk of DCS are as follows:
    • Dehydration: This is probably the most important of the predisposing factors. Taking in adequate quantities of water (8-10 glasses/day).This is needed to counteract the drying effect of compressed air and the obligatory diuresis that all divers get from immersion. Dehydration, due to any cause (coffee, oral diuretics, alcohol, vomiting and diarrhea states, failure to drink non-alcoholic liquids)
    • Pre-existing illness affecting lung or circulatory efficiency: The lung acts as a filter for the buubles that occur in all divers. Chronic lung disease, heart failure both tend to increase the risk of DCS. Decreased perfusion from any source can increase the possibility of DCS. Intracardiac septal defect (PFO) bypasses the filtering effect of the lungs and increases risk of bubbles. Undeserved DCS (DCS that has no other causative factors) should have investigation for this entity.
    • Scar tissue from previous injury: (scar tissue decreases diffusion). Areas of decreased and increased blood flow have been incriminated in leading to DCS. Whether this is operative in the growth plates of teenagers is unknown. Nitrogen off-gassing is influenced by factors that alter perfusion.
    • Gender; women have been shown to have a slightly higher rate of DCS, particularly during the menses.
    • Obesity (nitrogen is lipid soluble). Several studies have incriminated obesity as a factor in increasing the risk of DCS. Fat is poorly supplied with blood vessels and decreased perfusion (ability to off-gas) can lead to DCS.
    • Fatigue: This clouds the decision making process, often leading to mistakes and DCS. Fatigue is also a subtle symptom of decompression sickness. Exertion during the deep part of the dive is a risk factor.
    • Age: The older diver has long been thought to be have increased tendencies to have DCS. Studies done by the Navy show a definite increase in DCS in older divers (all under 50 years of age). Other studies have not borne this out. Older divers have a higher percentage of body fat. Age and obesity: risk possibly increases in proportion to increase in age. Greater age and higher fat content are traditionally associated with increased incidence of DCS but the evidence is not consistent, recent reports showing no relationship.
    • Poor physical condition: Good physical fitness increases perfusion and ensures good gas exchange.
    • Exercise after diving increases the incidence of DCS from 22% to 46%. Exercise at depth is detrimental, increasing nitrogen uptake. (Requiring three times the decompression). Immersion in cold water with exercise causes increased incidence of DCS. Exercise while decompressing is beneficial.

Environmental factors that are important include the following:

  • Cold water (vasoconstriction decreases nitrogen off-loading). Warm water immersion (vasodilation) and the head down position increases nitrogen elimination.
  • Heavy work (vacuum effect in which tendon use causes gas pockets). Exercise at depth increases nitrogen uptake and is detrimental.
  • Rough sea conditions
  • Heated diving suits (leads to dehydration)
  • Divers who have been chilled on decompression dives (or dives near the no-decompression limit) and take very hot baths or showers may stimulate bubble formation.
Sport divers mainly need to avoid dehydration, dive shallower, ascend slower and spend more time between dives eliminating nitrogen.

Here are some of the factors found to increase the risk of decompression accidents:

      • Repetitive diving
      • Exceeded No-decompression limits
      • Running out of air, rapid ascent
      • Diving on the edge of No-decompression limits
      • Deep or repetitive dives using computer outside the limits of the tables or no-decompression limits
      • Flying after diving
      • Diving at altitude
There are other factors that are thought to increase the chances of getting DCS but have little data in support; some of these are:
  • Alcohol and hangover state (related to dehydration)
  • Medical problems increasing the viscosity of the blood (Sickle cell anemia and trait)
  • Injury to muscle, bone or joint (due to increased blood flow to inflamed area)
  • Rate of ascent
  • Repetitive, multiday dives after a long lay-off; deep prolonged air diving
  • Failure to do safety stops
  • Patent foramen ovale
  • Smoking habits
  • Adaptation or recent diving history
  • Underestimated depth
  • Table “fudging”
  • Neurological DCS symptoms are most common after short, deep dives. less common after altitude exposure, slow saturation decompression and low-pressure caisson exposure.
  • Slow ascent near the surface more effective in reducing neurologic DCS than was slow ascent from depth.
  • Fewer VGE with short safety stops. (venous gas emboli)
  • Off-gassing greatest in subjects tilted head down, immersed in warm water and exercising. Increasing venous return to the thorax increases off-gassing.(Head down tilt)
  • Exercise in warm water immersion decreases DCS (decrease by about 30%)
  • Some believe that the use of aspirin might help prevent the adherence of platelets to bubbles, thereby reducing the chance of bubble damage.
References:
Gorman, Pearce and Webb, Dysbaric illness treated at the Royal Adelaide Hospital, 1987: A factorial analysis. SPUMS Journal 18:95-101, 1988

Wilmshurst PT, Byrne JC, Webb-Peploe MM: Relation between inter-atrial shunts and decompression sickness in divers. Lancet, 2:1302-1306, 1989.

Moon RE, Camporesi EM, Kisslo JA: Patent foramen ovale and decompression sickness in divers. Lancet 1: 513-514, 1989.

Approved Indications for HBO Therapy

Filed under: Uncategorized — admin @ 3:51 pm

Approved Indications for HBO Therapy

Indications (UHMS)

UHMS HBO, Therapy Committee Report - 1996

Indication Recommended
Protocol [pressure, ATA]		 Lower
threshold
levels		 Upper
threshold
levels
Air or gas embolism 2.8 - 6.0 10 - 14
Carbon monoxide poisoning
and smoke inhalation		 2.5 - 3.0 QD or BID 5
Clostridial myonecrosis (gas
gangrene)		 3.0 TID x 1d,
then BID x 4-5 d. 		5 10
Crush Injury, Compartment Syndrome, Other acute traumatic Ischemia TID x 2 d, BID x 2 d, QD x 2 d 3 12
Decompression Sickness 2.8 - 6.0 Until improvement plateaus or 14 days
Enhancement of Healing in Selected Problem Wounds 2.0-2.5 QD or BID 10 60
Exceptional Blood loss
(anemia)		 Until Hct 22.9%
Necrotizing Soft
Tissue Infections		 2.0-2.5 BID initially, then QD 5 30
Osteomyelitis (refractory) 2.0-2.5 QD 20 60
Radiation Tissue Damage
(Osteoradionecrosis)		 2.0-2.4 QD 20 60
Skin Grafts and Flaps (Compromised) 2.0-2.5 BID initially, then QD 6 40
Thermal Burns 2.0-2.5 TID x 1d, then BID 5 45
Adjunctive Hyperbaric Oxygen
in Intracranial Abscess		 QD or BID

QD=1 time in 24 h; BID= 2 times in 24 h; TID= three times in 24h

April 29, 2009

Recent Abstracts of Articles Sent by Sunny Sonnenrein

Filed under: Publication — admin @ 2:45 pm

Beliefs of Croatian surgeons and internists on hyperbaric oxygenation-a preliminary report
MED   09-26   200819382629 NDN- 230-0960-8209-7

AUTHORS- BiociA., Matea; Petri, Nadan M; Kardum, Goran

JOURNAL NAME- Acta Med Croatica
VOLUME 62
NUMBER 5
PUBLICATION DATE- 2008 Dec
PP 469-73
DOCUMENT TYPE- English Abstract; Journal Article
JOURNAL CODE- 9208249
JOURNAL SUBSET- MEDJSIM
ISSN- 1330-0164
CORPORATE AUTHOR- GospiA. General Hospital, GospiA., Croatia.
PUBLICATION COUNTRY- Croatia
LANGUAGE- Serbo-Croatian (Roman)

BACKGROUND/INTRODUCTION: Hyperbaric oxygenation (HBO) has been accepted in many countries as a method of treatment in selected indications, but in Croatia it is still perceived with skepticism.

OBJECTIVE: To determine beliefs, knowledge, and possible experience of Croatian surgeons and internists with HBO.

SUBJECTS AND METHODS: An anonymous questionnaire was applied to test surgeons (N=56; 45%) and internists (N=68; 55%), employed in general hospitals in Zadar, Sibenik, Split, and Dubrovnik, Republic of Croatia. We believed that the subjects had been previously exposed to information campaigns about HBO and its clinical applications, and should have been informed about the method at a level enabling correct establishment of indications and routine usage of HBO in clinical practice.

RESULTS: The majority of study subjects (N=66; 53%) had very little or no information at all about HBO and half of them (N=50; 40%) had no experience in its application. Almost all (N=123; 99%) subjects considered the method valuable in the treatment of decompression sickness, 56 subjects (45%) considered the method efficient in carbon monoxide poisoning, 31 (25%) in cerebral arterial gas embolism, 87 (70%) in problem wounds, and 70 (56%) in gas gangrene. The only statistically significant difference between the two groups of subjects was recorded in case of cerebral arterial gas embolism (chi2 = 7.26, P = 0.007), which was recognized as an indication for HBO by more internists (N=23) than surgeons (N=8). DISCUSSION: Insufficient understanding of HBO amongst Croatian surgeons and internists is probably the consequence of several factors, of which most important probably are insufficient curricula of undergraduate studies and residencies, as well as administrative obstacles. A small number of responders and polled hospitals necessarily resulted in a significant bias, so additional studies are necessary to shed more light on the issue.

Combined treatment of intrapancreatic autologous bone marrow stem cells and hyperbaric oxygen in type 2 diabetes mellitus.
MED   09-25   200819364067 NDN- 230-0958-0132-3

AUTHORS- Estrada, Esteban J; Valacchi, Fabian; Nicora, Eduardo; Brieva, Sergio; Esteve, Claudio; Echevarria, Laura; Froud, Tatiana; Bernetti, Karina; Cayetano, Shari Messinger; Velazquez, Omaida; Alejandro, Rodolfo; Ricordi, Camillo

JOURNAL NAME- Cell Transplant
VOLUME 17
NUMBER 12
PUBLICATION DATE- 2008
PP 1295-304
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 9208854
JOURNAL SUBSET- MEDJSIM
ISSN- 0963-6897
CORPORATE AUTHOR- Stem Cell Argentina, Buenos Aires, Argentina. info@stemcellargentina.com
PUBLICATION COUNTRY- United States
LANGUAGE- English

The objective of this study was to determine whether the combination therapy of intrapancreatic autologous stem cell infusion (ASC) and hyperbaric oxygen treatment (HBO) before and after ASC can improve islet function and metabolic control in patients with type 2 diabetes mellitus (T2DM). This prospective phase 1 study enrolled 25 patients with T2DM who received a combination therapy of intrapancreatic ASC and peri-infusion HBO between March 2004 and October 2006 at Stem Cells Argentina Medical Center Buenos Aires, Argentina. Clinical variables (body mass index, oral hypoglycemic drugs, insulin requirement) and metabolic variables (fasting plasma glucose, C-peptide, HbA1c, and calculation of C-peptide/glucose ratio) were assessed over quartile periods starting at baseline and up to 1 year follow-up after intervention. Means were calculated in each quartile period and compared to baseline. Seventeen male and eight female patients were enrolled. Baseline variables expressed as means +/- SEs were: age 55 +/- 2.14 years, diabetes duration 13.2 +/- 1.62 years, insulin dose 34.8 +/- 2.96 U/day, and BMI 27.11 +/- 0.51. All metabolic variables showed significant improvement when comparing baseline to 12 months follow-up, respectively: fasting glucose 205.6 +/- 5.9 versus 105.2 +/- 14.2 mg/dl, HbAlc 8.8 +/- 0.2 versus 6.0 +/- 0.4%, fasting C-peptide 1.5 +/- 0.2 versus 3.3 +/- 0.3 ng/ml, C-peptide/glucose ratio 0.7 +/- 0.2 versus 3.5 +/- 0.3, and insulin requirements 34.8 +/- 2.9 versus 2.5 +/- 6.7 U/day. BMI remained constant over the 1-year follow-up. Combined therapy of intrapancreatic ASC infusion and HBO can improve metabolic control and reduce insulin requirements in patients with T2DM. Further randomized controlled clinical trials will be required to confirm these findings.

.

Hyperbaric oxygen therapy and cerebral ischemia: neuroprotective mechanisms.
MED   09-25   200919298750 NDN- 230-0957-4113-1

AUTHORS- Matchett, Gerald A; Martin, Robert D; Zhang, John H

JOURNAL NAME- Neurol Res
VOLUME 31
NUMBER 2
PUBLICATION DATE- 2009 Mar
PP 114-21
DOCUMENT TYPE- Journal Article; Research Support, N.I.H., Extramural
JOURNAL CODE- 7905298
JOURNAL SUBSET- MEDJSIM
ISSN- 0161-6412
CORPORATE AUTHOR- Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
CONTRACT OR GRANT NUMBER- HD43120.HD.NICHD NIH HHS; NS43338.NS.NINDS NIH HHS
PUBLICATION COUNTRY- United States; United States; England
LANGUAGE- English

INTRODUCTION: Numerous studies have demonstrated a protective effect of hyperbaric oxygen therapy in experimental ischemic brain injury, and many physiological and molecular mechanisms of hyperbaric oxygen therapy-related neuroprotection have been identified.

METHODS: Review of articles pertaining to hyperbaric oxygen therapy and cerebral ischemia in the National Library of Medicine and National Institutes of Health database, emphasizing mechanisms of hyperbaric oxygen therapy-related neuroprotection.

RESULTS: Hyperbaric oxygen therapy has been shown to ameliorate brain injury in a variety of animal models including focal cerebral ischemia, global cerebral ischemia, neonatal hypoxia-ischemia and subarachnoid hemorrhage. Small human trials of hyperbaric oxygen therapy in focal ischemia have not shown benefit, although one trial of hyperbaric oxygen therapy before cardiopulmonary bypass demonstrated improved neuropsychological and inflammatory outcomes with hyperbaric oxygen therapy. Hyperbaric oxygen therapy is associated with improved cerebral oxygenation, reduced blood-brain barrier breakdown, decreased inflammation, reduced cerebral edema, decreased intracranial pressure, reduced oxidative burden, reduced metabolic derangement, decreased apoptotic cell death and increased neural regeneration.

CONCLUSION: On a molecular level, hyperbaric oxygen therapy leads to activation of ion channels, inhibition of hypoxia inducible factor-1alpha, up-regulation of Bcl-2, inhibition of MMP-9, decreased cyclooxygenase-2 activity, decreased myeloperoxidase activity, up-regulation of superoxide dismutase and inhibition of Nogo-A (an endogenous growth-inhibitory factor). Ongoing research will continue to describe the mechanisms of hyperbaric oxygen therapy-related neuroprotection, and possibly expand hyperbaric oxygen therapy use clinically.

Heparin and hyperbaric oxygenation in enteric autonomic neuron preservation for transplant.
MED   09-26   200919376362 NDN- 230-0960-0263-2

AUTHORS- Guimaroaes, F A G; Taha, M O; Fagundes, D J; Simo.es, R S; Simo.es, M J; Caricati-Neto, A

JOURNAL NAME- Transplant Proc
VOLUME 41
NUMBER 3
PUBLICATION DATE- 2009 Apr
PP 824-6
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 0243532
JOURNAL SUBSET- MEDJSIM
ISSN- 0041-1345
CORPORATE AUTHOR- Departments of Science and Tecnology, Universidade Santa Ceco.lia (UNISANTA), Santos, Brazil.
PUBLICATION COUNTRY- United States
LANGUAGE- English

BACKGROUND: Previous studies have suggested that the addition of heparin to a preservation solution attenuated the autonomic dysfunction observed in rat jejunum and in addition that hypothermic hyperbaric oxygenation may play a role as a preservation technique. However, these studies did not address the lesion indices of the autonomic enteric neurons. We sought to investigate whether the autonomic enteric neurons are injured during cold ischemic preservation and whether administration of heparin or hyperbaric oxygenation prevents this lesion.

METHODS: Jejunal segments (2 cm; n = 20) of Wistar rats (12-16 weeks old) were maintained in lactated Ringer’s solution without or with heparin (H- and H+, respectively) at 4 degrees C under normobaric conditions. Other jejunal segments (n = 10) were maintained at 4 degrees C in H- under hyperbaric oxygenation conditions (HBO). After preservation for 12 hours, H-, H+, and HBO preparations fixed in 10% formaldehyde were stained with hematoxylin and eosin. The lesion indices were expressed as the mean number of affected neurons (karyorhexis, nuclear dislocation, cytoplasmic vacuolisation) per 100 neurons present in intramural ganglia. Statistical analysis was performed using the Mann-Whitney test (P < .05).

RESULTS: The histologic studies showed that enteric autonomic neurons were damaged in H- jejunal segments. The lesion indices observed were: karyorhexis 90/100, nuclear dislocation 85/100, and cytoplasmic vacuolization 82/100. The autonomic neurons in H+ and HBO segments seemed to be normal and significantly well-preserved (P < .001).

CONCLUSION: Hypothermic hyperbaric oxygenation and heparin prevented lesions in cold ischemic preservation of enteric autonomic neurons.

Hyperbaric oxygen causes both antiinflammation and antipyresis in rabbits.
MED   09-26   200919374861 NDN- 230-0960-7463-1

AUTHORS- Niu, Ko-Chi; Huang, Wu-Tein; Lin, Mao-Tsun; Huang, Kuo-Fong

JOURNAL NAME- Eur J Pharmacol
VOLUME 606
NUMBER 1-3
PUBLICATION DATE- 2009 Mar 15
PP 240-5
DOCUMENT TYPE- Journal Article; Research Support, Non-U.S. Gov’t
JOURNAL CODE- 1254354
JOURNAL SUBSET- MEDJSIM
ISSN- 1879-0712
CORPORATE AUTHOR- Department of Biotechnology, Southern Taiwan University, Tainan, Taiwan.
PUBLICATION COUNTRY- Netherlands
LANGUAGE- English

Current study was attempted to assess whether hyperbaric oxygen pretreatment or treatment exerts its antipyresis by reducing circulating interleukin-6 and hypothalamic glutamate, hydroxyl radicals and prostaglandin-E(2) in rabbits. It was found that systemic administration of lipopolysaccharide induced increased levels of both core temperature and hypothalamic levels of glutamate, hydroxyl radicals, and prostaglandin E(2) accompanied by increased plasma levels of interleukin-6. The rise in both the core temperature and hypothalamic glutamate, hydroxyl radicals and prostaglandin-E(2) could also be induced by intracerebroventricular injection of interleukin-6. Pretreatment or treatment with hyperbaric oxygen significantly reduced the lipopolysaccharide-induced overproduction of circulating interleukin-6, and hypothalamic glutamate, prostaglandin E(2), and hydroxyl radicals. The febrile response caused by central administration of interleukin-6 could also be suppressed by hyperbaric oxygen pretreatment or treatment. Simultaneous administration of an anti-oxidant (e.g., N-acetyl-L-cysteine) significantly enhanced the antipyretic effects exerted by hyperbaric oxygen treatment. These results indicate that hyperbaric oxygen pretreatment or treatment may exert its antipyresis by inhibiting the glutamate-hydroxyl radicals-prostaglandin-E(2) pathways in the hypothalamus and circulating interleukin-6 accumulation during lipopolysaccharide-fever.

Hyperbaric oxygen preconditioning activates ribosomal protein S6 kinases and reduces brain swelling after intracerebral hemorrhage.
MED   09-26   200819388337  NDN- 230-0961-6545-4

AUTHORS- Qin, Z; Hua, Y; Liu, W; Silbergleit, R; He, Y; Keep, R F; Hoff, J T; Xi, G

JOURNAL NAME- Acta Neurochir Suppl
VOLUME 102
PUBLICATION DATE- 2008
PP 317-20
DOCUMENT TYPE- Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov’t
JOURNAL CODE- 100962752
JOURNAL SUBSET- MEDJSIM
ISSN- 0065-1419
CORPORATE AUTHOR- Department of Neurosurgery, Room 5018, BSRB, University of Michigan, Ann Arbor, MI 48109-2200, USA.
CONTRACT OR GRANT NUMBER- NS-017760.NS.NINDS NIH HHS; NS-039866.NS.NINDS NIH HHS; NS-047245.NS.NINDS NIH HHS
PUBLICATION COUNTRY- United States; United States; United States; Austria
LANGUAGE- English

BACKGROUND: New protein synthesis is key to ischemic tolerance induced by preconditioning and ribosomal protein S6 kinases (p70 S6 K) are important enzymes in protein synthesis. Hyperbaric oxygen preconditioning (HBOP) reduces ischemic brain damage. This study investigated if HBOP can activate p70 S6 K and increase new protein synthesis and if HBOP induces brain tolerance against brain swelling after intracerebral hemorrhage (ICH).

METHODS: There were two parts of the studies. 1) Rats received five consecutive sessions of HBOP. Twenty-four hours after HBOP, the rats had an ICH and were sacrificed one or three days later for brain edema measurement. 2) Rats received five sessions of HBOP or control pretreatment and were sacrificed for Western blot analysis and immunohistochemistry of activated p70 S6 K and heme oxygenase-1 (HO-1).

FINDINGS: Five sessions of HBOP significantly reduced brain edema in the ipsilateral basal ganglia after ICH. Western blot analysis showed that HBOP activated p70 S6 K and increased HO-1 levels in the basal ganglia. Strong activated p70 S6 K immunoreactivity was also found in the basal ganglia.

CONCLUSIONS: Our results suggest activation of p70 S6 K may have a role in heat shock protein synthesis after HBOP and may contribute to HBOP-induced brain protection.
Hyperbaric oxygen therapy for consciousness disturbance following head injury in subacute phase.
MED   09-26   200819388281  NDN- 230-0961-6489-5

AUTHORS- Nakamura, Takehiro; Kuroda, Yasuhiro; Yamashita, Susumu; Kawakita, Kenya; Kawai, Nobuyuki; Tamiya, Takashi; Itano, Toshifumi; Nagao, Seigo

JOURNAL NAME- Acta Neurochir Suppl
VOLUME 102
PUBLICATION DATE- 2008
PP 21-4
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 100962752
JOURNAL SUBSET- MEDJSIM
ISSN- 0065-1419
CORPORATE AUTHOR- Department of Neurobiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki, Kita, Kagawa 761-0173, Japan. tanakamu@kms.ac.jp
PUBLICATION COUNTRY- Austria
LANGUAGE- English

BACKGROUND: Hyperbaric oxygen (HBO) therapy has been shown to improve outcome after brain injury, however its mechanisms are not understood. The purpose of the present study was to investigate the effect of hyperbaric oxygen (HBO) therapy on the cerebral circulation and metabolism of patients with disturbances in consciousness after head injury in the subacute phase.

METHODS: Seven head injury patients underwent HBO treatment after leaving the intensive care unit. Oxygen (100% O2, 2.7 atm absolute) was delivered to patients in a hyperbaric chamber for 60 min every 24 h (total five treatments/patient). Cerebral circulation monitoring (mean flow velocity: mFV, and pulsatility index: PI at horizontal portion of middle cerebral artery by transcranial Doppler) and cerebral metabolism monitoring (arterio-jugular venous difference of oxygen: AJDO2 and jugular venous lactate: lac-JV) before and after the series of treatments were evaluated.

FINDINGS: Both PI and lac-JV were significantly decreased after HBO theatment, while there were no significant changes in mFV and AJDO2. The decreased PI and lac-JV after HBO therapy might indicate that this treatment couples cerebral circulation and metabolism.

CONCLUSIONS: The measurement of cerebral circulation and metabolism parameters, especially PI and lac-JV, is useful for estimation of effect of HBO therapy in patients with distubances in consciousness after head injury in the subacute phase.
Loss of protein kinase Cgamma in knockout mice and increased retinal sensitivity to hyperbaric oxygen
MED   09-25   200919365031  NDN- 230-0958-0343-6

AUTHORS- Yevseyenkov, Vladimir V; Das, Satyabrata; Lin, Dingbo; Willard, Lloyd; Davidson, Harriet; Sitaramayya, Ari; Giblin, Frank J; Dang, L; Takemoto, Dolores J

JOURNAL NAME- Arch Ophthalmol
VOLUME 127
NUMBER 4
PUBLICATION DATE- 2009 Apr
PP 500-6
DOCUMENT TYPE- Journal Article; Research Support, N.I.H., Extramural
JOURNAL CODE- 7706534
JOURNAL SUBSET- MEDJSAIM; MEDJSIM
ISSN- 1538-3601
CORPORATE AUTHOR- Department of Biochemistry, 141 Chalmers Hall, Kansas State University, Manhattan, Kansas 66506, USA.
CONTRACT OR GRANT NUMBER- EY07158.EY.NEI NIH HHS; R01-13421.PHS HHS; R24 EY02027.EY.NEI NIH HHS; R24 EY04803.EY.NEI NIH HHS
PUBLICATION COUNTRY- United States; United States; United States; United States; United States
LANGUAGE- English

OBJECTIVE: To determine if loss of protein kinase Cgamma (PKCgamma) results in increased structural damage to the retina by hyperbaric oxygen (HBO), a treatment used for several ocular disorders.

METHODS: Six-week-old mice were exposed in vivo to 100% HBO 3 times a week for 8 weeks. Eyes were dissected, fixed, embedded in Epon, sectioned, stained with toluidine blue O, and examined by light microscopy.

RESULTS: The thicknesses of the inner nuclear and ganglion cell layers were increased. Destruction of the outer plexiform layer was observed in the retinas of the PKCgamma-knockout mice relative to control mice. Exposure to HBO caused significant degradation of the retina in knockout mice compared with control mice. Damage to the outer segments of the photoreceptor layer and ganglion cell layer was apparent in central retinas of HBO-treated knockout mice.

CONCLUSIONS: Protein kinase Cgamma-knockout mice had increased retinal sensitivity to HBO. Results demonstrate that PKCgamma protects retinas from HBO damage. CLINICAL RELEVANCE: Care should be taken in treating patients with HBO, particularly if they have a genetic disease, such as spinocerebellar ataxia type 14, a condition in which the PKCgamma is mutated and nonfunctional.

Mortality in necrotizing fasciitis.
MED   09-26   200819385468  NDN- 230-0961-2764-5

AUTHORS- Rajput, Akram; Waseem; Samad, Abdul; Khanzada, Tariq Wahab; Shaikh, Gul Muhammad; Channa, Ghulam Asghar

JOURNAL NAME- J Ayub Med Coll Abbottabad
VOLUME 20
NUMBER 2
PUBLICATION DATE- 2008 Apr-Jun
PP 96-8
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 8910750
JOURNAL SUBSET- MEDJSIM
ISSN- 1025-9589
CORPORATE AUTHOR- Department of Surgery, Isra University, Hyderabad. akramrajput2006@yahoo.com
PUBLICATION COUNTRY- Pakistan
LANGUAGE- English

OBJECTIVE: The objective of this study was to determine the mortality rate in patients presenting with Necrotizing Fasciitis. This prospective study was conducted at ward 26, JPMC Karachi over a period of two years from March 2001 to Feb 2003.
METHODS: All patients above the age of 12 years diagnosed to be having Necrotizing Fasciitis and admitted through the Accident and emergency department were included in this study. After resuscitation, the patients underwent the emergency exploration and aggressive surgical debridement. Post-operatively, the patients were managed in isolated section of the ward. The patients requiring grafting were referred to plastic surgery unit. The patients were followed up in outpatients department for about two years.
RESULTS: Over all, 25 male and 5 female patients fulfilled the inclusion criteria and were included in this study. The common clinical manifestations include redness, swelling, discharging abscess, pain, fever, skin necrosis and foul smelling discharge etc. The most common predisposing factor was Diabetes mellitus whereas the most commonly involved site was perineum. All patients underwent aggressive and extensive surgical debridements. The common additional procedures included Skin grafting, Secondary suturing, Cystostomy and Orchidectomy. Bacteroides and E. coli were the main micro-organisms isolated in this study. Bacteroides was the most common microorganism isolated among the eight patients who died.
CONCLUSION: Necrotizing Fasciitis is a potentially life threatening emergency condition and carries the mortality rate of about 26.6%. The major contributing factors to increase the mortality missed initially diagnosed, old age, diabetes mellitus truncal involvement and late presentation. Anorectal involvement of disease carry worse prognosis. Hyperbaric oxygen therapy and proper use of unprocessed honey reduced the mortality rate.

Necrotizing fasciitis following transobturator tape treated by extensive surgery and hyperbaric oxygen
MED   09-26   200918509584  NDN- 230-0960-0530-4

AUTHORS- Flam, Folke; Boijsen, Magnus; Lind, Folke

JOURNAL NAME- Int Urogynecol J Pelvic Floor Dysfunct
VOLUME 20
NUMBER 1
PUBLICATION DATE- 2009 Jan
PP 113-5
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 9514583
JOURNAL SUBSET- MEDJSIM
ISSN- 1433-3023
CORPORATE AUTHOR- Department of Gynecology, Capio S:t Goeran Hospital, S-112 81 Stockholm, Sweden. folke.flam@gynekologkliniken.se
PUBLICATION COUNTRY- England
LANGUAGE- English

The transobturator sling procedure (TVT-O) was developed to minimize surgical risks involved in treating genuine stress incontinence. All data suggest that most risks associated with the retropubic route such as injuries to the bladder, intestines or vessels are practically obsolete with the obturator route. However, severe soft-tissue infections have been reported with this new technique. In this case report, necrotizing fasciitis (NF) developed shortly after a TVT-O procedure. This life-threatening complication required extensive debridements, a diverting colostomy, antibiotics, and eight sessions of hyperbaric oxygen (HBO) therapy. We emphasize the importance of a unified interdisciplinary clinical approach in severe NF with rapid progression and systemic toxemia. Primary, aggressive but tissue-saving debridements together with antibiotics are the cornerstones of therapy. HBO therapy can oxygenate infected hypoxic tissues to help marginally viable tissues survive, reduce the inflammatory response, improve leukocyte bacterial oxidative killing capacity, and achieve infection control and healing.
Protective effect of hyperbaric oxygen therapy on experimental brain contusions.
MED   09-26   200819388363  NDN- 230-0961-6571-0

AUTHORS- Voigt, Cornelia; Foerschler, Annette; Jaeger, Matthias; Meixensberger, Jourgen; Kouppers-Tiedt, Lea; Schuhmann, Martin U

JOURNAL NAME- Acta Neurochir Suppl
VOLUME 102
PUBLICATION DATE- 2008
PP 441-5
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 100962752
JOURNAL SUBSET- MEDJSIM
ISSN- 0065-1419
CORPORATE AUTHOR- Department of Neurosurgery, University of Leipzig, 04103 Leipzig, Germany. dat, conny@web.de
PUBLICATION COUNTRY- Austria
LANGUAGE- English

BACKGROUND: We evaluated the effect of hyperbaric oxygen therapy (HBO) on experimental brain contusions in rats using magnetic resonance imaging (MRI).

MATERIALS AND METHODS: Ten Sprague-Dawley rats were investigated at 24 h and 72 h after controlled cortical impact injury. One hour after trauma, 5 rats were treated for 60 min with 100% oxygen at 2.5 absolute atmosphere (ATA), 5 were kept at normobaric room air. MRI was performed longitudinally at 24 h and 72 h after injury. Lesion volume was determined in T2 weighted MRI scans. Relative apparent diffusion coefficient (ADC) changes were calculated in comparison to the contralateral side.

RESULTS: Following HBO, T2 lesion volume was smaller at 24 h versus controls (63.1 +/- 16.5 mm3 vs. 87.4 +/- 13.8 mm3, p < 0.05), and decreased further at 72 h (46.8 +/- 17.8 mm3 vs. 92.5 +/- 13.1 mm3, p < 0.01). At 24 h, the mean relative ADC change in the lesion area decreased from + 26.8 +/- 2.3% in controls to + 2.3 +/- 12.2% in HBO animals (p < 0.01). At 72 h, the HBO effect on relative ADC values was less when compared to 24 h.

DISCUSSION: A 60-minute exposure to hyperbaric oxygen starting 1 h after impact injury significantly attenuated lesion growth and relative increase of ADC values within the contused area for up to 72 h. Thus, a “single-shot” HBO treatment seems to have long-lasting neuroprotective effects on the contused brain and its penumbra.
Pulmonary Barotrauma in Divers During Emergency Free Ascent Training: Review of 124 Cases
BIO   12-20   PREV200900270187  NDN- 244-0594-8340-8

AUTHORS- Lafere, Pierre; Germonpre, Peter; Balestra, Costantino

JOURNAL NAME- Aviation Space and Environmental Medicine
VOLUME 80
NUMBER 4
PUBLICATION DATE- APR 2009
PP 371-375
RELEASE YEAR OR PUBLICATION YEAR- 2009
DOCUMENT TYPE- Article
ISSN- 0095-6562
ADDRESS- Mil Hosp Queen Astrid, Ctr Hyperbar Oxygen Therapy, Bruynst 1, B-1020 Brussels, Belgium
EMAIL- doc.lafere@skynet.be
DOCUMENT URL OR DOI- 10.3357/ASEM.2402.2009
LANGUAGE- English

Introduction: Experience from treating diving accidents indicates that a large proportion of divers suffering from pulmonary barotraumas (PBT) or arterial gas embolism (AGE) were engaged in training dives, specifically emergency free ascent (EFA). We tried to verify this relationship and to calculate, if possible, the risk associated with normal recreational dives, training dives, and EFA training dives.
Methods: All diving accidents treated at the Centre for Hyperbaric Oxygen Therapy (Brussels, Belgium) from January 1995 until October 2005 were reviewed, Data on the average lumber of dives performed and the proportion of in-water skills training dives were obtained from the major Belgian dive associations.
Results: A total of 124 divers were treated, of whom 34 (27.4%) were diagnosed with PBT. Of those, 20 divers (58.8%) had symptoms of AGE. In 16 of those, EFA training exercise was deemed responsible for the injury. The association between EFA training and PBT proved to be very significant, with an odds ratio of 11.33 (95%, confidence interval: 2.186 to 58.758). it was possible to calculate that a training dive (0.456 to 1.36/10,000) carries a 100 to 400 times higher risk, and an ascent training dive (1.82 to 5.46/10,000 dives) a 500 to 1500 times higher risk for PBT than a non-training dive (0.0041 to 0.0043/10,000 dives).
Discussion: This Study confirms a significant association between El-A training dives and the occurrence of PBT.
Tension pneumocephalus: a rare complication after hyperbaric oxygen therapy.
MED   09-25   200919371560  NDN- 230-0959-3709-3

AUTHORS- Lee, Ching-Hsing; Chen, Wei-Chun; Wu, Chao-I; Hsia, Te-Chun

JOURNAL NAME- Am J Emerg Med
VOLUME 27
NUMBER 2
PUBLICATION DATE- 2009 Feb
PP 257.e1-3
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 8309942
JOURNAL SUBSET- MEDJSIM
ISSN- 1532-8171
CORPORATE AUTHOR- Department of Emergency Medicine, Chang Gung Memorial Hospital, Taipei, Chang Gung University College of Medicine, Taoyuan, Taiwan, ROC.
PUBLICATION COUNTRY- United States
LANGUAGE- English

The study aimed to describe a patient with multiple skull bone fractures and a cerebrospinal fluid (CSF) leak who received hyperbaric oxygen therapy (HBOT). A 40-year-old man presented with subdural hemorrhage, skull bone fractures, facial bone fractures, sinus fractures, and CSF leakage after a one-story fall. He received HBOT as an adjunctive treatment to reduce brain edema and increase oxygen availability in brain tissue. Tension pneumocephalus developed after HBOT. Bur hole drainage was performed emergently to relieve the tension pneumocephalus. Cranioplasty and repair of skull base fracture were subsequently performed. The patient was discharged in a vegetative state. We proposed a possible mechanism by which tension pneumocephalus developed after HBOT sessions in this patient. Pneumocephalus, untreated skull base fracture, and CSF leakage should be considered contraindications to HBOT.
Utility of hyperbaric oxygen in treatment of bisphosphonate-related osteonecrosis of the jaws.
MED   09-26   200919371820  NDN- 230-0961-1774-5

AUTHORS- Freiberger, John J

JOURNAL NAME- J Oral Maxillofac Surg
VOLUME 67
NUMBER 5 Suppl
PUBLICATION DATE- 2009 May
PP 96-106
DOCUMENT TYPE- Journal Article; Research Support, Non-U.S. Gov’t
JOURNAL CODE- 8206428
JOURNAL SUBSET- MEDJSAIM; MEDJSD; MEDJSIM
ISSN- 1531-5053
CORPORATE AUTHOR- Center for Hyperbaric Medicine and Environmental Physiology, Duke University Medical Center, Durham, NC 27710, USA. freib002@mc.duke.edu
PUBLICATION COUNTRY- United States
LANGUAGE- English

Bisphosphonates suppress bone turnover by disrupting osteoclast signal transduction, maturation, and longevity. In some patients, it has been hypothesized that suppressed turnover can impair oral wound healing, leading to a distressing, osteopetrosis-like jaw necrosis called bisphosphonate-related osteonecrosis of the jaws (BRONJ). Hyperbaric oxygen (HBO), as an adjunct to surgery and antibiotics, might have utility in the treatment of BRONJ because it produces reactive oxygen and nitrogen species that positively modulate the redox-sensitive intracellular signaling molecules involved in bone turnover. The efficacy of HBO in the treatment of BRONJ is currently under investigation in randomized controlled trials at Duke University and the University of Minnesota, and the early results have been encouraging. This report discusses osteoclast biology, how HBO has the potential to augment bone turnover by way of the signaling effects on osteoclasts, the available clinical data on HBO in the treatment of BRONJ, the ongoing randomized controlled trials of HBO, and the study-associated efforts to find biomarkers to characterize an individual’s risk of developing this disease.


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