Carbon Monoxide Poisoning

Total Page:16

File Type:pdf, Size:1020Kb

Carbon Monoxide Poisoning J R Army Med Corps: first published as 10.1136/jramc-73-02-02 on 1 August 1939. Downloaded from 79 CARBON MONOXIDE POISONING: A REVIEW. By BREVET LIEUTENANT-COLONEL A. E. RICHMOND, O.B.E., Royal Army Medical Corps. CARBON monoxide, together with the dioxide, occurs in the combustion of organic matter, and the less oxygen there is available the greater the proportion of carbon monoxide produced. It is colourless and odourless, and on these accounts its presence is normally only detectable by the symptoms it causes, which adds much to the risk of poisoning from it. It it also inflammable and in strong concentration may give rise to explosions. It has been recognized as a poison since ancient times, and has assumed special importance within the last half-century owing to the increased amounts of it produced consequent upon the augmented use of gas for by guest. Protected copyright. illuminating, cooking, and heating purposes, and upon the introduction of the internal combustion engine. It is the favourite means of the suicide to encompass his aim, while accidental poisoning with it frequently occurs. From a military point of view carbon monoxide intoxication is a subject which deserves the close attention and study of all military medical officers in these days of intensive mechanization, and unlimited employment of explosives; and the object of the writer is to lay before his readers in as concise and compact a form as possible those details of moment in connexion with the various aspects of this important subject. In endeavouring to attain this object references have been made to certain publications dealing with carbon monoxide poisoning. These references are clearly indicated, so that those desirous of making a more detailed study of the matter may have available the same assistance as has http://militaryhealth.bmj.com/ been at the disposal of the author and which he most gratefully acknowledges. Carbon monoxide enters the body through the lungs and by no other means. Drinker [1], in his recently published and most valuable book on the subject, quotes observations by Sendroy Liu and Van Slyke which appear to have established the affinity of carbon monoxide for hremoglobin compared with that of oxygen as being in the proportion of 210: 1. This is a sig­ nificant fact, and the ease with which the carbon monoxide is taken up by hremoglobin is the essential feature of the toxic syndrome. The oxygen-carrying capacity of the blood is in this way interfered with to a greater or less degree, and in severe cases of poisoning disastrous and on September 27, 2021 enduring states of anoxremia may arise with all their resultant adverse effects. It will be realized also that this amazing affinity of carbon monoxide for hremoglobin is an obvious explanation of the occurrence of cases of poisoning in individuals exposed to comparatively low concentrations of the gas. J R Army Med Corps: first published as 10.1136/jramc-73-02-02 on 1 August 1939. Downloaded from 80 Oarbon Monoxide Poisoning The combination of carbon monoxide with hremoglobin is very slowly reversible, and oxygen will displace it when the individual is removed from the poisonous atmosphere. This is due to the mass action of the oxygen in the air, and the process may be accelerated by the administration of pure oxygen in the usual way. Carbon dioxide exerts a benevolent influence, as this gas affects the combination of both oxygen and carbon monoxide with hremoglobin, which is less able to hold these gases as the carbon dioxide increases. Hence the importance of the administration of carbon dioxide in treatment as it acts not only by aiding the dissociation of carbon monoxide from hremoglobin, but also by stimulating the respiratory centre. When non-fatal concentrations of carbon monoxide are present in the air breathed, the partial pressure in the blood gradually reaches a state of equilibrium with that in the air, and so the blood concentration is prevented from reaching a lethal height. As an example of this, with an­ atmospheric percentage of 0·05 the maximum hremoglobin saturation with by guest. Protected copyright. carbon monoxide produced will be 40 per cent, which will be attained in practically four hours. Perhaps of special importance from a military point of view is the effect of the low barometric pressures, which may be found at great heights, on the absorption of carbon monoxide by the blood. Such influence is clearly adverse owing to the reduction in partial pressure of the oxygen due to the carbon monoxide taken up coupled with that consequent upon the low barometric reading. This will serve to emphasize the danger of subjecting persons to carbon monoxide at high altitudes. It should be noted that mice and small birds die more quickly from carbon monoxide poisoning than men, owing to the fact that their volume of breathing per minute compared with the total volume of their blood is greater than in the case of man, and it is stated that the average man ought to be able to remain in an atmosphere with a given concentration of carbon http://militaryhealth.bmj.com/ monoxide twenty times as long as a canary~ It appears to have been definitely established that carbon monoxide inhaled in small amounts over periods of time has the power to increase the red cells and the amount of hremoglobin in the individual [2]. The augmentation of the erythrocytes is thought to be due in the early stages to contraction of the spleen, but it would seem that later true -new red cell formation definitely occurs in the bone-marrow. Finally, the fact must not be lost sight of that on cessation of respiration the excretion of carbon monoxide also ceases, and that evidence of it in the blood may be found for months or even years afterwards. on September 27, 2021 DANGEROUS PERCENTAGES OF CARBON MONOXIDE. In considering this aspect of the subject with which we are dealing, realization of the fact that given concentrations of carbon monoxide in the atmosphere will not affect every individual equally is essential. Not only J R Army Med Corps: first published as 10.1136/jramc-73-02-02 on 1 August 1939. Downloaded from A. E. Richmond 81 do individuals vary in their reactions to this gas, but other modifying influences in the situation are also frequently present. It is also important to realize that dangerous precentages of carbon monoxide will never be reached in open spaces owing to the rapid diffusion of the gas, and that risks from it only arise in enclosed spaces, or in semi­ enclosed in which ventilation is inadequate or stagnation of air exists. Individual susceptibility depends to some extent upon age, and Drinker emphasizes that the very young and very old are at greater risk than others. " The Medical History of the War" [3] states that young men were more susceptible to carbon monoxide than those over 40, due apparently to their greater elasticity of chest wall and deeper inspiration. Although there may be some doubt as to the influence exerted by sex, there appears to be no question that pregnant women are more liable to fall victims to poisoning by carbon monoxide than others. Such abnormal bodily conditions as anffimia, heart disease, asthma, chronic bronchitis, alcoholism and narcotism have a material and detri­ by guest. Protected copyright. mental effect in carbon monoxide intoxication, while of prime importance is the extent of any bodily activity taken in the poisoned atmosphere. In this connexion Drinker quotes certain experiments by Sayers, Meriwether and Yant, [4] which illustrate the effect of rest and strenuous exercise respectively on carbon monoxide absorption. These investigations showed that persons at rest breathing 0·02 per cent of the gas developed 16 to 20 per cent hffimoglobin saturation with mild subjective symptoms at the end of six hours. On the other hand, an individual exercising strenuously in 0·025 per cent of carbon monoxide had 14 to 16 per cent saturation in one hour with moderate subjective symptoms. These experiments serve to emphasize the consideration we must give to the degree of activity of the soldier or anybody else in an atmosphere containing carbon monoxide, if we are to assess correctly the extent of the risk. http://militaryhealth.bmj.com/ As regards atmospheric conditions, low barometric pressure is a factor of considerable moment, and the intake of carbon monoxide at the low pressures of great altitudes will have infinitely more rapid and serious results than would be the case at normal heights. Hence the great necessity for efficient safeguards against the inhalation of exhaust gases of aeroplanes while in flight. High temperatures and humidities also accelerate the rate of combination of the gas with hffimoglobin. Varying susceptibilities of animals and birds as compared with man must also be given passing thought as they are of importance in the selection of test creatures for experimental and other work. In this connexion Drinker on September 27, 2021 quotes Anson, Barcroft, Mirsky and Oinuma [5] as showing that carbon monoxide has an effect on animals, etc., in the following descending order of potency: Dog, horse, cat, man, fowl, mouse, rat, tortoise, sheep, lizard, frog, and rabbit. Similarly, in the case of smaller -animals and birds Burrell, Seibert and Robertson [6] concluded that the following was the order of J R Army Med Corps: first published as 10.1136/jramc-73-02-02 on 1 August 1939. Downloaded from 82 Oarbon Monoxide Poisoning degree of susceptibility: Canary, mouse, chicken, small dog, pigeon, sparrow, guinea-pig, and rabbit. Finally, we must not lose sight of the fact that carbon monoxide varies in its effects according as to whether it is alone or in combination with other gases.
Recommended publications
  • Traveler Information
    Traveler Information QUICK LINKS Marine Hazards—TRAVELER INFORMATION • Introduction • Risk • Hazards of the Beach • Animals that Bite or Wound • Animals that Envenomate • Animals that are Poisonous to Eat • General Prevention Strategies Traveler Information MARINE HAZARDS INTRODUCTION Coastal waters around the world can be dangerous. Swimming, diving, snorkeling, wading, fishing, and beachcombing can pose hazards for the unwary marine visitor. The seas contain animals and plants that can bite, wound, or deliver venom or toxin with fangs, barbs, spines, or stinging cells. Injuries from stony coral and sea urchins and stings from jellyfish, fire coral, and sea anemones are common. Drowning can be caused by tides, strong currents, or rip tides; shark attacks; envenomation (e.g., box jellyfish, cone snails, blue-ringed octopus); or overconsumption of alcohol. Eating some types of potentially toxic fish and seafood may increase risk for seafood poisoning. RISK Risk depends on the type and location of activity, as well as the time of year, winds, currents, water temperature, and the prevalence of dangerous marine animals nearby. In general, tropical seas (especially the western Pacific Ocean) are more dangerous than temperate seas for the risk of injury and envenomation, which are common among seaside vacationers, snorkelers, swimmers, and scuba divers. Jellyfish stings are most common in warm oceans during the warmer months. The reef and the sandy sea bottom conceal many creatures with poisonous spines. The highly dangerous blue-ringed octopus and cone shells are found in rocky pools along the shore. Sea anemones and sea urchins are widely dispersed. Sea snakes are highly venomous but rarely bite.
    [Show full text]
  • Asphyxia Neonatorum
    CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well­ being develop as a result of perinatal asphyxia. Central nervous system ab­ normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas­ sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec­ trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef­ fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in­ molecules brought into the alveoli inadequately com­ Pjury in the newborn. Severe birth asphyxia, evi­ pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte­ and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul­ deprivation has been further enriched by investigators monary capillary blood.
    [Show full text]
  • Failure of Hypothermia As Treatment for Asphyxiated Newborn Rabbits R
    Arch Dis Child: first published as 10.1136/adc.51.7.512 on 1 July 1976. Downloaded from Archives of Disease in Childhood, 1976, 51, 512. Failure of hypothermia as treatment for asphyxiated newborn rabbits R. K. OATES and DAVID HARVEY From the Institute of Obstetrics and Gynaecology, Queen Charlotte's Maternity Hospital, London Oates, R. K., and Harvey, D. (1976). Archives of Disease in Childhood, 51, 512. Failure of hypothermia as treatment for asphyxiated newborn rabbits. Cooling is known to prolong survival in newborn animals when used before the onset of asphyxia. It has therefore been advocated as a treatment for birth asphyxia in humans. Since it is not possible to cool a human baby before the onset of birth asphyxia, experiments were designed to test the effect of cooling after asphyxia had already started. Newborn rabbits were asphyxiated in 100% nitrogen and were cooled either quickly (drop of 1 °C in 45 s) or slowly (drop of 1°C in 2 min) at varying intervals after asphyxia had started. When compared with controls, there was an increase in survival only when fast cooling was used early in asphyxia. This fast rate of cooling is impossible to obtain in a human baby weighing from 30 to 60 times more than a newborn rabbit. Further litters ofrabbits were asphyxiated in utero. After delivery they were placed in environmental temperatures of either 37 °C, 20 °C, or 0 °C and observed for spon- taneous recovery. The animals who were cooled survived less often than those kept at 37 'C. The results of these experiments suggest that hypothermia has little to offer in the treatment of birth asphyxia in humans.
    [Show full text]
  • The Post-Mortem Appearances in Cases of Asphyxia Caused By
    a U?UST 1902.1 ASPHYXIA CAUSED BY DROWNING 297 Table I. Shows the occurrence of fluid and mud in the 55 fresh bodies. ?ritfinal Jlrttclcs. Fluid. Mud. Air-passage ... .... 20 2 ? ? and stomach ... ig 6 ? ? stomach and intestine ... 7 1 ? ? and intestine X ??? Stomach ... ??? THE POST-MORTEM APPEARANCES IN Intestine ... ... 1 Stomach and intestine ... ... i CASES OF ASPHYXIA CAUSED BY DROWNING. Total 46 9 = 55 By J. B. GIBBONS, From the above table it will be seen that fluid was in the alone in 20 LIEUT.-COL., I.M.S., present air-passage cases, in the air-passage and stomach in sixteen, Lute Police-Surgeon, Calcutta, Civil Surgeon, Ilowrah. in the air-passage, stomach and intestine in seven, in the air-passage and intestine in one. As used in this table the term includes frothy and non- frothy fluid. Frothy fluid is only to be expected In the period from June 1893 to November when the has been quickly recovered from months which I body 1900, excluding three during the water in which drowning took place and cases on leave, 15/ of was privilege asphyxia examined without delay. In some of my cases were examined me in the due to drowning by it was present in a most typical form; there was For the of this Calcutta Morgue. purpose a bunch of fine lathery froth about the nostrils, all cases of death inhibition paper I exclude by and the respiratory tract down to the bronchi due to submersion and all cases of or syncope was filled with it. received after into death from injuries falling The quantity of fluid in the air-passage varies the water.
    [Show full text]
  • Respiratory and Gastrointestinal Involvement in Birth Asphyxia
    Academic Journal of Pediatrics & Neonatology ISSN 2474-7521 Research Article Acad J Ped Neonatol Volume 6 Issue 4 - May 2018 Copyright © All rights are reserved by Dr Rohit Vohra DOI: 10.19080/AJPN.2018.06.555751 Respiratory and Gastrointestinal Involvement in Birth Asphyxia Rohit Vohra1*, Vivek Singh2, Minakshi Bansal3 and Divyank Pathak4 1Senior resident, Sir Ganga Ram Hospital, India 2Junior Resident, Pravara Institute of Medical Sciences, India 3Fellow pediatrichematology, Sir Ganga Ram Hospital, India 4Resident, Pravara Institute of Medical Sciences, India Submission: December 01, 2017; Published: May 14, 2018 *Corresponding author: Dr Rohit Vohra, Senior resident, Sir Ganga Ram Hospital, 22/2A Tilaknagar, New Delhi-110018, India, Tel: 9717995787; Email: Abstract Background: The healthy fetus or newborn is equipped with a range of adaptive, strategies to reduce overall oxygen consumption and protect vital organs such as the heart and brain during asphyxia. Acute injury occurs when the severity of asphyxia exceeds the capacity of the system to maintain cellular metabolism within vulnerable regions. Impairment in oxygen delivery damage all organ system including pulmonary and gastrointestinal tract. The pulmonary effects of asphyxia include increased pulmonary vascular resistance, pulmonary hemorrhage, pulmonary edema secondary to cardiac failure, and possibly failure of surfactant production with secondary hyaline membrane disease (acute respiratory distress syndrome).Gastrointestinal damage might include injury to the bowel wall, which can be mucosal or full thickness and even involve perforation Material and methods: This is a prospective observational hospital based study carried out on 152 asphyxiated neonates admitted in NICU of Rural Medical College of Pravara Institute of Medical Sciences, Loni, Ahmednagar, Maharashtra from September 2013 to August 2015.
    [Show full text]
  • Perinatal Asphyxia Neonatal Therapeutic Hypothermia
    PERINATAL ASPHYXIA NEONATAL THERAPEUTIC HYPOTHERMIA Sergio G. Golombek, MD, MPH, FAAP Professor of Pediatrics & Clinical Public Health – NYMC Attending Neonatologist Maria Fareri Children’s Hospital - WMC Valhalla, New York President - SIBEN ASPHYXIA From Greek [ἀσφυξία]: “A stopping of the pulse” “Loss of consciousness as a result of too little oxygen and too much CO2 in the blood: suffocation causes asphyxia” (Webster’s New World Dictionary) On the influence of abnormal parturition, difficult labours, premature birth, and asphyxia neonatorum, on the mental and physical condition of the child, especially in relation to deformities. By W. J. Little, MD (Transactions of the Obstetrical Society of London 1861;3:243-344) General spastic contraction of the lower Contracture of adductors and flexors of lower extremities. Premature birth. Asphyxia extremities. Left hand weak. Both hands awkward. neonatorum of 36 hr duration. Hands More paralytic than spastic. Born with navel-string unaffected. (Case XLVII) around neck. Asphyxia neonatorum 1 hour. (Case XLIII) Perinatal hypoxic-ischemic encephalopathy (HIE) Associated with high neonatal mortality and severe long-term neurologic morbidity Hypothermia is rapidly becoming standard therapy for full-term neonates with moderate-to-severe HIE Occurs at a rate of about 3/1000 live-born infants in developed countries, but the rate is estimated to be higher in the developing world Intrapartum-related neonatal deaths (previously called ‘‘birth asphyxia’’) are the fifth most common cause of deaths among children under 5 years of age, accounting for an estimated 814,000 deaths each year, and also associated with significant morbidity, resulting in a burden of 42 million disability adjusted life years (DALYs).
    [Show full text]
  • Perinatal Asphyxia in the Term Newborn
    www.jpnim.com Open Access eISSN: 2281-0692 Journal of Pediatric and Neonatal Individualized Medicine 2014;3(2):e030269 doi: 10.7363/030269 Received: 2014 Oct 01; accepted: 2014 Oct 14; published online: 2014 Oct 21 Review Perinatal asphyxia in the term newborn Roberto Antonucci1, Annalisa Porcella1, Maria Dolores Pilloni2 1Division of Neonatology and Pediatrics, “Nostra Signora di Bonaria” Hospital, San Gavino Monreale, Italy 2Family Planning Clinic, San Gavino Monreale, ASL 6 Sanluri (VS), Italy Proceedings Proceedings of the International Course on Perinatal Pathology (part of the 10th International Workshop on Neonatology · October 22nd-25th, 2014) Cagliari (Italy) · October 25th, 2014 The role of the clinical pathological dialogue in problem solving Guest Editors: Gavino Faa, Vassilios Fanos, Peter Van Eyken Abstract Despite the important advances in perinatal care in the past decades, asphyxia remains a severe condition leading to significant mortality and morbidity. Perinatal asphyxia has an incidence of 1 to 6 per 1,000 live full-term births, and represents the third most common cause of neonatal death (23%) after preterm birth (28%) and severe infections (26%). Many preconceptional, antepartum and intrapartum risk factors have been shown to be associated with perinatal asphyxia. The standard for defining an intrapartum hypoxic-ischemic event as sufficient to produce moderate to severe neonatal encephalopathy which subsequently leads to cerebral palsy has been established in 3 Consensus statements. The cornerstone of all three statements is the presence of severe metabolic acidosis (pH < 7 and base deficit ≥ 12 mmol/L) at birth in a newborn exhibiting early signs of moderate or severe encephalopathy. Perinatal asphyxia may affect virtually any organ, but hypoxic-ischemic encephalopathy (HIE) is the most studied clinical condition and that is burdened with the most severe sequelae.
    [Show full text]
  • Carbon Monoxide Poisoning in the Home Cyril John Polson
    Journal of Criminal Law and Criminology Volume 44 | Issue 4 Article 15 1954 Carbon Monoxide Poisoning in the Home Cyril John Polson Follow this and additional works at: https://scholarlycommons.law.northwestern.edu/jclc Part of the Criminal Law Commons, Criminology Commons, and the Criminology and Criminal Justice Commons Recommended Citation Cyril John Polson, Carbon Monoxide Poisoning in the Home, 44 J. Crim. L. Criminology & Police Sci. 531 (1953-1954) This Criminology is brought to you for free and open access by Northwestern University School of Law Scholarly Commons. It has been accepted for inclusion in Journal of Criminal Law and Criminology by an authorized editor of Northwestern University School of Law Scholarly Commons. CARBON MONOXIDE POISONING IN THE HOME* Cyril John Poison Cyril John Polson, M.D., F.R.C.P., is a Barrister-at-Law and Professor of Legal Medicine, University of Leeds, England. This article, the second of his to be published in this Journal, is based upon a public lecture delivered in the Uni- versity of Leeds, October 24, 1952.-EDIToR. Carbon monoxide poisoning in the home has for long been a common- place. It is clear, however, that so long as accidental poisoning con- tinues to occur there is room for recurrent reminders of the dangers of carbon monoxide. The present account is based on a detailed examination of the records of over 700 fatalities which have occurred during the past twenty five years in the City of Leeds. THE DANGERS PECULIAR TO CARBON MONOXIDE It requires no reflection to appreciate that any poison which is gaseous, and at the same time colourless, non-irritant and, may be, odourless, has grave potential dangers.
    [Show full text]
  • Lost Floodplain Wetland Environments and Efforts to Restore Connectivity, Habitat, and Water Quality Settings on the Great Barrier Reef
    fmars-06-00071 February 25, 2019 Time: 15:47 # 1 POLICY AND PRACTICE REVIEWS published: 26 February 2019 doi: 10.3389/fmars.2019.00071 Lost Floodplain Wetland Environments and Efforts to Restore Connectivity, Habitat, and Water Quality Settings on the Great Barrier Reef Nathan J. Waltham1,2*, Damien Burrows1, Carla Wegscheidl3, Christina Buelow1,2, Mike Ronan4, Niall Connolly3, Paul Groves5, Donna Marie-Audas5, Colin Creighton1 and Marcus Sheaves1,2 1 Centre for Tropical Water and Aquatic Ecosystem Research, College of Science and Engineering, James Cook University, Townsville, QLD, Australia, 2 Science for Integrated Coastal Ecosystem Management, School of Marine Biology and Aquaculture, College of Science and Engineering, James Cook University, Townsville, QLD, Australia, 3 Rural Economic Development, Department of Agriculture and Fisheries, Queensland Government, Townsville, QLD, Australia, 4 Department of Environment and Science, Queensland Government, Brisbane, QLD, Australia, 5 Great Barrier Reef Marine Park Authority, Australian Government, Townsville, QLD, Australia Edited by: Mario Barletta, Departamento de Oceanografia da Managers are moving toward implementing large-scale coastal ecosystem restoration Universidade Federal de Pernambuco projects, however, many fail to achieve desired outcomes. Among the key reasons for (UFPE), Brazil this is the lack of integration with a whole-of-catchment approach, the scale of the Reviewed by: A. Rita Carrasco, project (temporal, spatial), the requirement for on-going costs for maintenance, the Universidade do Algarve, Portugal lack of clear objectives, a focus on threats rather than services/values, funding cycles, Jacob L. Johansen, New York University Abu Dhabi, engagement or change in stakeholders, and prioritization of project sites. Here we United Arab Emirates critically assess the outcomes of activities in three coastal wetland complexes positioned *Correspondence: along the catchments of the Great Barrier Reef (GBR) lagoon, Australia, that have Nathan J.
    [Show full text]
  • A Review of SCUBA Diving Impacts and Implication for Coral Reefs Conservation and Tourism Management
    SHS Web of Conferences 12, 01093 (2014) DOI: 10.1051/shsconf/20141201093 C Owned by the authors, published by EDP Sciences, 2014 A Review of SCUBA Diving Impacts and Implication for Coral Reefs Conservation and Tourism Management Siti Zulaiha Zainal Abidin1 , Badaruddin Mohamed2 1Sustainable Tourism Research Cluster, Universiti Sains Malaysia, 11800, Penang, Malaysia 1,2School of Housing, Building and Planning, Universiti Sains Malaysia, 11800, Penang, Malaysia Abstract. Dive tourism has become important in term of magnitude and significantly contributes to regional economies. Nevertheless, in the absence of proper controls and enforcement, unplanned tourism growth has caused environmental degradation which undermines the long-term sustainability of the tourism industry. The purpose of this paper is to explore factors that contribute to the SCUBA diving impacts on coral and fish communities. This paper explains the causes of a certain event, validating the problem of impacts, defining the core issues and identifies possible causes leading to an effect. The phenomenon of diving impacts on coral reefs is a result of intensive use of dive site over the long-term. The divers can reduce their impacts towards coral reefs through responsible diving behaviors. The causes of cumulative diver’s contacts are more complicated than it seems. In response, this paper proposes the best mitigation strategies that need to be considered for future dive tourism management. 1 Introduction Marine tourism or tourism based on ocean and coral reefs is an important component of the global tourism industry and is rapidly growing than any other tourism sector particularly in many tropical countries [1]. The increasing interest in marine tourism can be considered at two levels.
    [Show full text]
  • A Retrospective Study of 51 Pediatric Cases of Traumatic Asphyxia
    A Retrospective Study of 51 Pediatric Cases of Traumatic Asphyxia luo huirong Chongqing Medical University Pediatric College: Chongqing Medical University Aliated Children's Hospital https://orcid.org/0000-0002-2741-2238 xin jin ( [email protected] ) Chongqing Medical University Pediatric College: Chongqing Medical University Aliated Children's Hospital https://orcid.org/0000-0001-9549-6704 Research Article Keywords: Traumatic asphyxia, pediatric, thoracic trauma Posted Date: April 5th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-357514/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/14 Abstract Background traumatic asphyxia (TA) is a rarely reported disease characterized as thoraco-cervico-facial petechiae, facial edema and cyanosis, subconjunctival hemorrhage and neurological symptoms. This study aimed to report 51 children of TA at the pediatric medical center of west China. Methods scanned medical reports were reviewed and specic variables as age, sex, cause of injury, clinical manifestations and associated injuries were analyzed using SPSS 25.0. Results aged as 5.3±2.9 (1.3-13.2), 30 (58.8%) were boys and 21 (41.2%) were girls. Most TAs occurred during vehicle accident, object compression and stampede. All patients showed facial petechiae (100.0%, CI 93.0%-100.0%), 25 (49.0%, CI 34.8%-63.2%) out of 51 presented with facial edema, 29 (56.9%, CI 42.8%-70.9%) presented with subconjunctival hemorrhage, including bilateral 27 and unilateral 2. 6 patients had facial cyanosis (11.8%, CI 2.6%-20.9%). Other symptoms were also presented as epileptic seizure, vomiting, incontinence, paraplegia, etc.
    [Show full text]
  • Diving Physiology 3
    Diving Physiology 3 SECTION PAGE SECTION PAGE 3.0 GENERAL ...................................................3- 1 3.3.3.3 Oxygen Toxicity ........................3-21 3.1 SYSTEMS OF THE BODY ...............................3- 1 3.3.3.3.1 CNS: Central 3.1.1 Musculoskeletal System ............................3- 1 Nervous System .........................3-21 3.1.2 Nervous System ......................................3- 1 3.3.3.3.2 Lung and 3.1.3 Digestive System.....................................3- 2 “Whole Body” ..........................3-21 3.2 RESPIRATION AND CIRCULATION ...............3- 2 3.2.1 Process of Respiration ..............................3- 2 3.3.3.3.3 Variations In 3.2.2 Mechanics of Respiration ..........................3- 3 Tolerance .................................3-22 3.2.3 Control of Respiration..............................3- 4 3.3.3.3.4 Benefits of 3.2.4 Circulation ............................................3- 4 Intermittent Exposure..................3-22 3.2.4.1 Blood Transport of Oxygen 3.3.3.3.5 Concepts of and Carbon Dioxide ......................3- 5 Oxygen Exposure 3.2.4.2 Tissue Gas Exchange.....................3- 6 Management .............................3-22 3.2.4.3 Tissue Use of Oxygen ....................3- 6 3.3.3.3.6 Prevention of 3.2.5 Summary of Respiration CNS Poisoning ..........................3-22 and Circulation Processes .........................3- 8 3.2.6 Respiratory Problems ...............................3- 8 3.3.3.3.7 The “Oxygen Clock” 3.2.6.1 Hypoxia .....................................3-
    [Show full text]