Delayed Treatment of Decompression Sickness with Short, No-Air-Break Tables: Review of 140 Cases
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The Use of Heliox in Treating Decompression Illness
The Diving Medical Advisory Committee DMAC, Eighth Floor, 52 Grosvenor Gardens, London SW1W 0AU, UK www.dmac-diving.org Tel: +44 (0) 20 7824 5520 [email protected] The Use of Heliox in Treating Decompression Illness DMAC 23 Rev. 1 – June 2014 Supersedes DMAC 23, which is now withdrawn There are many ways of treating decompression illness (DCI) at increased pressure. In the past 20 years, much has been published on the use of oxygen and helium/oxygen mixtures at different depths. There is, however, a paucity of carefully designed scientific studies. Most information is available from mathematical models, animal experiments and case reports. During a therapeutic compression, the use of a different inert gas from that breathed during the dive may facilitate bubble resolution. Gas diffusivity and solubility in blood and tissue is expected to play a complex role in bubble growth and shrinkage. Mathematical models, supported by some animal studies, suggest that breathing a heliox gas mixture during recompression could be beneficial for nitrogen elimination after air dives. In humans, diving to 50 msw, with air or nitrox, almost all cases of DCI can be adequately treated at 2.8 bar (18 msw), where 100% oxygen is both safe and effective. Serious neurological and vestibular DCI with only partial improvements during initial compression at 18 msw on oxygen may benefit from further recompression to 30 msw with heliox 50:50 (Comex therapeutic table 30 – CX30). There have been cases successfully treated on 50:50 heliox (CX30), on the US Navy recompression tables with 80:20 and 60:40 heliox (USN treatment table 6A) instead of air and in heliox saturation. -
Heat Stroke Heat Exhaustion
Environmental Injuries Co lin G. Ka ide, MD , FACEP, FAAEM, UHM Associate Professor of Emergency Medicine Board-Certified Specialist in Hyperbaric Medicine Specialist in Wound Care The Ohio State University Wexner Medical Center The Most Dangerous Drug Combination… Accidental Testosterone Hypothermia and Alcohol! The most likely victims… Photo: Ralf Roletschek 1 Definition of Blizzard Hypothermia of Subnormal T° when the body is unable to generate sufficient heat to sustain normal functions Core Temperature < 95°F 1979 (35°C) Most Important Temperatures Thermoregulation 95°F (35° C) Hyper/Goofy The body uses a Poikilothermic shell to maintain a Homeothermic core 90°F (32°C) Shivering Stops Maintains core T° w/in 1.8°F(1°C) 80°F (26. 5°C) Vfib, Coma Hypothalamus Skin 65°F (18°C) Asystole Constant T° 96.896.8-- 100.4° F 2 Thermoregulation The 2 most important factors Only 3 Causes! Shivering (10x increase) Decreased Heat Production Initiated by low skin temperature Increased Heat Loss Warming the skin can abolish Impaired Thermoregulation shivering! Peripheral vasoconstriction Sequesters heat Predisposing Predisposing Factors Factors Decreased Production Increased Loss –Endocrine problems Radiation Evaporation • Thyroid Conduction* • Adrenal Axis Convection** –Malnutrition *Depends on conducting material **Depends on wind velocity –Neuromuscular disease 3 Predisposing Systemic Responses CNS Factors T°< 90°F (34°C) Impaired Regulation Hyperactivity, excitability, recklessness CNS injury T°< 80°F (27°C) Hypothalamic injuries Loss of voluntary -
Environmental Injuries
Environmental Injuries Colin G. Kaide, MD, FACEP, FAAEM, UHM Associate Professor of Emergency Medicine Board-Certified Specialist in Hyperbaric Medicine Specialist in Wound Care The Ohio State University Wexner Medical Center 1 The Most Dangerous Drug Combination… Testosterone and Alcohol! The most likely victims… Photo: Ralf Roletschek Accidental Hypothermia 2 Blizzard of 1979 Definition of Hypothermia Subnormal T° when the body is unable to generate sufficient heat to sustain normal functions Core Temperature < 95°F (35°C) 3 Most Important Temperatures 95°F (35° C) Hyper/Goofy 90°F (32°C) Shivering Stops 80°F (26.5°C) Vfib, Coma 65°F(18F (18°C) AtlAsystole Thermoregulation The body uses a Poikilothermic shell to maintain a Homeothermic core Maintains core T° w/in 1.8°F(1°C) Hypothalamus Skin CttTConstant T° 96. 8- 100.4° F 4 Thermoregulation The 2 most important factors Shivering (10x increase) Initiated by low skin temperature Warming the skin can abolish shivering! Peripheral vasoconstriction Sequesters heat Only 3 Causes! Decreased Heat Production Increased Heat Loss Impaired Thermoregulation 5 Predisposing Factors Decreased Production –Endocrine problems • Thyroid • Adrenal Axis –Malnutrition –Neuromuscular disease Predisposing Factors Increased Loss RRditiadiation Evaporation Conduction* Convection** *DDdepends on cond dtitilucting material **Depends on wind velocity 6 Predisposing Factors Impaired Regulation CNS injury Hypothalamic injuries Peripheral Injury Atherosclerosis Neuropathy Interfering Agents Systemic Responses CNS -
Dysbarism - Barotrauma
DYSBARISM - BAROTRAUMA Introduction Dysbarism is the term given to medical complications of exposure to gases at higher than normal atmospheric pressure. It includes barotrauma, decompression illness and nitrogen narcosis. Barotrauma occurs as a consequence of excessive expansion or contraction of gas within enclosed body cavities. Barotrauma principally affects the: 1. Lungs (most importantly): Lung barotrauma may result in: ● Gas embolism ● Pneumomediastinum ● Pneumothorax. 2. Eyes 3. Middle / Inner ear 4. Sinuses 5. Teeth / mandible 6. GIT (rarely) Any illness that develops during or post div.ing must be considered to be diving- related until proven otherwise. Any patient with neurological symptoms in particular needs urgent referral to a specialist in hyperbaric medicine. See also separate document on Dysbarism - Decompression Illness (in Environmental folder). Terminology The term dysbarism encompasses: ● Decompression illness And ● Barotrauma And ● Nitrogen narcosis Decompression illness (DCI) includes: 1. Decompression sickness (DCS) (or in lay terms, the “bends”): ● Type I DCS: ♥ Involves the joints or skin only ● Type II DCS: ♥ Involves all other pain, neurological injury, vestibular and pulmonary symptoms. 2. Arterial gas embolism (AGE): ● Due to pulmonary barotrauma releasing air into the circulation. Epidemiology Diving is generally a safe undertaking. Serious decompression incidents occur approximately only in 1 in 10,000 dives. However, because of high participation rates, there are about 200 - 300 cases of significant decompression illness requiring treatment in Australia each year. It is estimated that 10 times this number of divers experience less severe illness after diving. Physics Boyle’s Law: The air pressure at sea level is 1 atmosphere absolute (ATA). Alternative units used for 1 ATA include: ● 101.3 kPa (SI units) ● 1.013 Bar ● 10 meters of sea water (MSW) ● 760 mm of mercury (mm Hg) ● 14.7 pounds per square inch (PSI) For every 10 meters a diver descends in seawater, the pressure increases by 1 ATA. -
Hyperbaric Oxygen Therapy for Decompression Illness/Gas Embolism (All Ages)
Clinical commissioning policy: Hyperbaric oxygen therapy for decompression illness/gas embolism (all ages) For implementation from 1 April 2019 NHS England Reference: 170047P NHS England INFORMATION READER BOX Directorate Medical Operations and Information Specialised Commissioning Nursing Trans. & Corp. Ops. Commissioning Strategy Finance Publications Gateway Reference: 07603 Document Purpose Policy Clinical commissioning policy: Hyperbaric oxygen therapy for Document Name decompression illness/gas embolism (all ages) Author Specialised Commissioning Team Publication Date 20 July 2018 Target Audience CCG Clinical Leaders, Care Trust CEs, Foundation Trust CEs , Medical Directors, Directors of PH, Directors of Nursing, NHS England Regional Directors, NHS England Directors of Commissioning Operations, Directors of Finance, NHS Trust CEs Additional Circulation #VALUE! List Description Routinely Commissioned - NHS England will routinely commission this specialised treatment in accordance with the criteria described in this policy. Cross Reference 0 Superseded Docs 0 (if applicable) Action Required 0 Timing / Deadlines By 00 January 1900 (if applicable) Contact Details for [email protected] further information 0 0 0 0 0 0 Document Status This is a controlled document. Whilst this document may be printed, the electronic version posted on the intranet is the controlled copy. Any printed copies of this document are not controlled. As a controlled document, this document should not be saved onto local or network drives but should always be accessed from the intranet. 2 For implementation from 1 April 2019 Standard Operating Procedure: Clinical Commissioning Policy: Hyperbaric oxygen therapy for decompression illness/gas embolism (all ages) First published: July 2018 Prepared by NHS England Specialised Services Clinical Reference Group for Hyperbaric oxygen therapy Published by NHS England, in electronic format only. -
Short Update on Dysbaric Osteonecrosis: Concepts and Decompression Management
Dysbaric Osteonecrosis Review Short Update on Dysbaric Osteonecrosis: Concepts and Decompression Management Niladri Kumar Mahato1 Abstract Dysbaric osteonecrosis (DON) is caused by inadequate decompression after exposure to very high ambient air pressures. Different pathological events have been shown to occur in conjunction to result in DON. New observations from clinical and experimental data in this field have led investigators to reformat the etiology, pathogenesis and modify existing modalities of treatment of DON. This short review revisits concepts related to pathophysiology of DON occurring as a part of generalized decompression sickness and discusses newer therapeutic insights stemming from recent advancements in DON research. Keywords: Decompression; Dysbarism; Embolism; Hyperbaric Juxta-articular; Metaphysis; Rhizomelic J Bangladesh Soc Physiol. 2015, December; 10(2): 76-81 For Authors Affiliation, see end of text. http://www.banglajol.info/index.php/JBSP Introduction ysbarism or musculoskeletal pointed towards several etiologies of DON8-13. decompression sickness (DCS) is Given the typical anatomy of vasculature around Dusually observed in people who undergo the end of long bones, it seems plausible that deep-sea diving or are exposed to environments DON is linked to occurrence of micro-embolisms of high air pressures1-5. Dysbarism or Caisson with gas or lipid bubbles following a rapid Disease (CD) is characterized by an array of decrease in surrounding air pressure at those systemic complications involving soft tissues, the sites3,10,14-17. Other investigators have proposed cardio-pulmonary, nervous, renal and external compression of blood flow in such musculoskeletal systems when individuals or vessels due to similar bubbles arising in structures experimental animals are brought back to normal around an artery or a vein to induce external pressure. -
Decompression Illness
Decompression Illness DCI • Decompression illness (DCI) includes DCS and • Diagnosis – generally hx, estimation of AGE likelihood • ~1-10/10,000 dives • Sx depend on location of insult • Higher in cold water, deep; lower in recreational • <24 hrs possible, >24 hrs unlikely, >36 hrs warm water diving (1-4/10k) very unlikely, >48 hrs almost impossible • Traditional/Golding Classification unless altitude change • Type I (MSK, skin, lymph, fatigue) • There is no pathognomonic test for DCI • Type II (neuro, cardio-resp, ENT, shock) • AGE • Tx 100% Surface O2 • Descriptive/Francis Smith Class • • Evolution (spontaneous recovery, static, relapsing) • IVF • Progressive (increasing #, severity of s/sx) • Evacuation considerations • Organ System • Airway, foley, pressurized cabin or as low as • Neuro, cardio-pulm, MSK, skin, lymph, ENT possible • Time of onset (before or after surfacing) • HBOT • Gas burden • Low (conservative within NoD), Med (D Dive), High (violation dive table) • Evidence of barotrauma DCS Pathophysiology • Henry’s Law – amount of inert gas • Inflammatory & thrombogenic absorbed by blood/tissue increased at processes depth • Association with oxidative stress, microparticles • Boyle’s Law P1V1= P2V2 • Bubbles biologically active – form • Bubble effects plasma-protein coat activating WBC, plts, • Intravascular - embolism, vasospasm, fibrin web ischemia, transbolism, venous stasis, • “Thick skin” stabilizes bubble, decreases hemorrhage, blood-bubble interactions, diffusion of inert gas out of bubble mechanical stripping of endothelial -
Cardiovascular Responses to Diving in the Turtle, Pseudemys Scripta Stuart Keith Ware Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1980 Cardiovascular responses to diving in the turtle, Pseudemys scripta Stuart Keith Ware Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Animal Sciences Commons, Physiology Commons, and the Veterinary Physiology Commons Recommended Citation Ware, Stuart Keith, "Cardiovascular responses to diving in the turtle, Pseudemys scripta " (1980). Retrospective Theses and Dissertations. 6813. https://lib.dr.iastate.edu/rtd/6813 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. INFORMATION TO USERS This was produced from a copy of a document sent to us for microfilming. While the most advanced technological means to photograph and reproduce this document have been used, the quality is heavily dependent upon the quality of the material submitted. The following explanation of techniques is provided to help you understand markings or notations which may appear on this reproduction. 1. The sign or "target" for pages apparently lacking from the document photographed is "Missing Page(s)". If it was possible to obtain the missing page(s) or section, they are spliced into the film along with adjacent pages. This may have necessitated cutting through an image and duplicating adjacent pages to assure you of complete continuity. 2. When an image on the film is obliterated with a round black mark it is an indication that the film inspector noticed either blurred copy because of movement during exposure, or duplicate copy. -
Power Equation for Predicting the Risk of Central Nervous System Oxygen Toxicity at Rest
fphys-11-01007 August 17, 2020 Time: 14:44 # 1 ORIGINAL RESEARCH published: 17 August 2020 doi: 10.3389/fphys.2020.01007 Power Equation for Predicting the Risk of Central Nervous System Oxygen Toxicity at Rest Ben Aviner1, Ran Arieli1,2* and Alexandra Yalov3 1 The Israel Naval Medical Institute, Israel Defense Forces Medical Corps, Haifa, Israel, 2 Eliachar Research Laboratory, Western Galilee Medical Center, Nahariya, Israel, 3 HP – Indigo Division, Nes Ziona, Israel Patients undergoing hyperbaric oxygen therapy and divers engaged in underwater activity are at risk of central nervous system oxygen toxicity. An algorithm for predicting CNS oxygen toxicity in active underwater diving has been published previously, but not for humans at rest. Using a procedure similar to that employed for the derivation of our active diving algorithm, we collected data for exposures at rest, in which subjects breathed hyperbaric oxygen while immersed in thermoneutral water at 33◦C(n = 219) Edited by: or in dry conditions (n = 507). The maximal likelihood method was employed to solve for Costantino Balestra, Haute École Bruxelles-Brabant the parameters of the power equation. For immersion, the CNS oxygen toxicity index 2 10:93 (HE2B), Belgium is KI = t × PO2 , where the calculated risk from the Standard Normal distribution 0:5 2 12:99 Reviewed by: is ZI = [ln(KI ) – 8.99)]/0.81. For dry exposures this is KD = t × PO2 , with risk Enrico M. Camporesi, 0:5 ZD = [ln(KD ) – 11.34)]/0.65. We propose a method for interpolating the parameters at USF Health, United States Thijs Wingelaar, metabolic rates between 1 and 4.4 MET. -
Comments on Unresponsive Decompression Illness Case Bengusu Mirasoglu* and Samil Aktas
Mirasoglu and Aktas Journal of Intensive Care (2018) 6:77 https://doi.org/10.1186/s40560-018-0347-z LETTERTOTHEEDITOR Open Access Comments on unresponsive decompression illness case Bengusu Mirasoglu* and Samil Aktas Abstract We have read the case report about a decompression sickness that was unresponsive to hyperbaric oxygen treatment in your journal. Presented case is intriguing; however, we think there are some contradictive issues in the discussion of the case. In this letter, we aim to comment on these issues that may raise further question. Bubble formation plays a very important role for decompression sickness, but proposed mechanism is incorrect as nitrogen does not change state during decompression. Use of terminology for diving-related diseases and comments on properties of helium may cause misunderstandings. Also importance of history of the dive in evaluating an accident should be emphasized. Letter venous bubbles is possible in the presence of PFO (or We read the case report entitled “A case of decompres- right to left shunt); however, this does not change the sion illness not responding to hyperbaric oxygen” with name of the disease [3]. Either by bubble formation in great interest [1]. We totally agree with authors about the arterial system or arterialization from a right to left multidisciplinary approach to decompression sickness. shunt, this condition is not named AGE, it is DCS. On In our opinion, presence of a diving physician, an expert the other hand, AGE is considered a form of barotrauma of diving diseases, in this team is crucial. Otherwise, un- in diving medicine. Barotrauma is totally a different en- fortunate mistakes can be encountered. -
Research Article a New Measure of Decompression Sickness in the Rat
Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 123581, 6 pages http://dx.doi.org/10.1155/2014/123581 Research Article A New Measure of Decompression Sickness in the Rat Peter Buzzacott, Aleksandra Mazur, Qiong Wang, Kate Lambrechts, Michael Theron, Jacques Mansourati, and François Guerrero Laboratoire Optimisation des Regulations´ Physiologiques (ORPhy), UFR Sciences et Techniques, UniversitedeBretagneOccidentale,´ 6avenueLeGorgeu,CS93837,29200BrestCedex3,France Correspondence should be addressed to Peter Buzzacott; [email protected] Received 28 February 2014; Revised 1 May 2014; Accepted 2 May 2014; Published 25 May 2014 Academic Editor: Stephen C. Land Copyright © 2014 Peter Buzzacott et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In this study we assessed the reliability of a tilting-board grip score as a measure of decompression sickness in rats. In experiments using a hyperbaric compression/decompression protocol, rats were observed for signs of decompression sickness and their grip strength measured on a tilting particle board hinged to a metal frame. Angles at which rats lost grip were converted to gravitational vectors. Decreased mean grip scores following decompression were fitted to a logistic regression model with strain, age, and weight. Decrease in grip score was significantly associated with observed decompression sickness ( = 0.0036). The log odds ratio for decompression sickness = 1.40 (decrease in grip score). In rats with no decrease in mean grip score there was a 50% probability of decompression sickness (pDCS). This increased steadily with decreases in mean grip score. -
Decompression Sickness in Inside Attendants
SECTION VI 643 CHAPTER 2 DECOMPRESSION SICKNESS IN INSIDE ATTENDANTS PAUL J. SHEFFIELD AND CHRISTY J. PIRONE WHAT IS DECOMPRESSION SICKNESS? Decompression Sickness (DCS) Defined: DCS is an illness that occurs when environmental pressure is reduced sufficiently to cause gases that are dissolved in body tissues to evolve as bubbles. Primarily consisting of nitrogen, the bubbles evolve from solution when the inside attendant surfaces too fast for the body to compensate. Patients do not have the problem because the oxygen they breathe during hyperbaric oxygen treatment elimi- nates the nitrogen from their bodies. Signs and Symptoms of DCS: Bubbles that cause DCS can form in all parts of the body and the anatomic location accounts for the variety of signs and symptoms. (1) DCS can manifest itself from minor to life-threatening symptoms. Minor skin itching or tingling usually passes within 20 to 30 min- utes, and no treatment is necessary, all other forms of DCS are treated in the hyperbaric chamber with immediate compression and hyperbaric oxygen. “Bends pain” seen in about 90% of cases, may appear anywhere in the body, but is more frequent in legs or arms that were exercised during the exposure. Neurologic symptoms involving the brain or spinal cord occur in about 25% of cases, and are manifested by a wide variety of symptoms but mainly by headache, numbness, paralysis of an arm or leg, loss of sensation, vertigo, visu- al distortions or blindness, and extreme fatigue. Chokes is a rare but life-threat- ening respiratory disorder caused by gas emboli in the lungs, and manifested by wheezing, chest pain, or troublesome cough.