DOCSLIB.ORG

Intervention After Birth Asphyxia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Intervention After Birth Asphyxia Arch Dis Child: first published as 10.1136/adc.64.1.66 on 1 January 1989. Downloaded from Archives of Disease in Childhood, 1989, 64, 66-68 Annotations Intervention after birth asphyxia Despite improvements in fetal monitoring and hour of a 5% solution is given intravenously until neonatal resuscitation, every district general hos- the seizures stop.5 Continued seizures are treated pital has a number of full term infants every year with phenytoin 20 mg/kg and diazepam 0-3 mg/kg who suffer from the effects of severe lack of oxygen intravenously. before or during delivery. Approximately six per Postasphyxial seizures can be very resistant to 1000 full term infants develop hypoxic-ischaemic treatment and intravenous clonazepam, lignocaine, encephalopathy and one per 1000 will die or survive chlormethiazole, and sodium valproate can be with severe neurological disability.1 In Great considered in such cases. Whether one should treat Britain, 300-400 children per year survive birth a comatose, ventilated baby who is having subtle asphyxia with serious brain damage. seizures or purely electrical seizures is arguable. Paediatricians have vigorously tried to improve Neonatal seizures deplete the brain of high energy standards of neonatal resuscitation in the delivery substrates and interfere with brain cell division6 but ward but have found hypoxic-ischaemic encephalo- large doses of anticonvulsants may have adverse pathy a difficult problem to treat. A common effects: particularly respiratory and circulatory attitude is that the damage has been done before depression. It used to be thought that high dose arrival in the neonatal intensive care unit and barbiturate might have a protective effect after treatment is too late to repair neural cell death. The hypoxia by reducing cerebral metabolic require- copyright. prognosis has seemed so hopeless in some cases that ments. A trial of thiopentone in severely asphyxiated withdrawal of intensive care has seemed the kindest infants, however, gave no evidence of benefit. solution.2 Are we being too negative about the Indeed hypotension was a troublesome side effect of encephalopathy? This annotation discusses the thiopentone.7 emerging evidence that management after initial resuscitation may influence neurological outcome. Control of raised intracranial pressure http://adc.bmj.com/ Hypoxic-ischaemic encephalopathy The brain commonly reacts to severe hypoxia by developing oedema over a period of 24-48 hours. After resuscitation a proportion of infants become The skull is able to accommodate some degree of neurologically abnormal during the next 48 hours. brain swelling by squeezing cerebrospinal fluid out This encephalopathy can be clinically classified into: of the cranium. Moreover, neonates can tolerate mild (irritability, poor sucking, and hypotonia), some further brain swelling without the pressure moderate (convulsions, lethargy, and appreciably rising because of the unfused sutures and the open abnormal tone), and severe (comatose with pro- fontanelles. Severe cerebral oedema can exceed the on September 24, 2021 by guest. Protected longed seizures and respiratory failure).3 Out of 24 cranial compliance, however, and cause the pressure infants with moderate encephalopathy, one died and to rise above the normal upper limit of 6 mm Hg five survived with severe handicap. Out of 21 with (0-80 kPa).8 We have used the same subarachnoid severe encephalopathy, 13 died and three survived pressure catheter technique as Levene et a19 to with severe handicap. Of the infants with mild monitor intracranial pressure in asphyxiated encephalopathy, only one became handicapped and neonates and have confirmed their findings that this child had a congenital myopathy. raised pressure in some infants can be temporarily lowered by intravenous mannitol, that sustained Convulsions intracranial hypertension (>15 mm Hg (2-00 kPa)) resistant to treatment has a very bad prognosis, and Generalised tonic-clonic convulsions should be that some infants can have severe encephalopathy treated as they tend to interfere with respiration and and bad outcome without raising intracranial raise intracranial pressure. We start treatment with pressure above 10 mm Hg (1-33 kPa).9 phenobarbitone 20 mg/kg intravenously as a loading We have extensively investigated non-invasive dose.4 If convulsions continue, paraldehyde 3 ml/kg/ measurement of intracranial pressure via the fon- 66 Arch Dis Child: first published as 10.1136/adc.64.1.66 on 1 January 1989. Downloaded from Intervention after birth asphyxia 67 tanelle and have found it too inaccurate for clinical chondria activating phospholipase,14 release of decision making.10 Although we have had no oxygen free radicals,1 and excitatory amino acids complications from subarachnoid catheterisation in such as glutamate.16 Steen et al showed that the 25 cases, the technique is highly invasive and has the calcium channel blocker nimodipine improved potential to cause meningitis. No study has yet survival when given after complete cerebral shown that invasive intracranial pressure monitoring ischaemia in primates.17 Thiringer et al carried out a and mannitol treatment improves later outcome. randomised trial of oxygen free radical scavengers Dexamethasone has been used for certain types of (methionine, mannitol, and magnesium sulphate) cerebral oedema associated with tumour or abscess. and the calcium channel blocker lidoflazine in lambs There is no evidence, however, that it gives benefit subjected to acute umbilical cord occlusion.'8 She after birth asphyxia." found that the lambs treated within 5 minutes of Hyperventilation to produce hypocapnoea has resuscitation retained cerebral blood flow better been used to reduce raised intracranial pressure in than controls. The treated lambs also had better adults. However, this effect is achieved by reducing somatosensory evoked potentials and cerebral cerebral blood flow which seems undesirable. cortical function. There are no published studies on glutamate antagonists, free radical scavengers, or Circulatory support calcium channel blockers in human neonates. Neonates are generally not good at raising arterial Prognosis pressure in response to raised intracranial pressure (Cushing response) and the combination of low Nelson and Ellenberg found that an Apgar score of arterial pressure and raised intracranial pressure is <4 at 20 minutes gave a 57% chance of cerebral particularly devastating. We have not found any palsy in survivors. 19 Steiner and Nelligan found that normal survivors from a cerebral perfusion pressure all full term infants who failed to establish respira- (mean arterial pressure-intracranial pressure) tion by 30 minutes subsequently had spastic quadri- below 20 mm Hg (2.67 kPa). plegia and mental retardation.20 It has been a copyright. Hypovolaemia may be associated with asphyxia common practice to discontinue further resuscita- because of shunting of blood from the vasocon- tion if there is no respiratory effort after 30 minutes. stricted fetus to the placenta, from blood loss, or Infants with severe encephalopathy who have persis- from hypoxic capillaries leaking plasma into the tently raised intracranial pressure (>15 mm Hg interstitial space. Peripheral vasoconstriction, mean (2-00 kPa)) resistant to mannitol also have an arterial pressure below 40 mm Hg (5-33 kPa), and extremely poor outlook. In the future, electro- metabolic acidosis are suggestive of hypovolaemia. encephalography, cerebral blood velocity by http://adc.bmj.com/ Colloid at 10 to 20 ml/kg should be given intra- Doppler, and phosphorus magnetic resonance venously and larger volumes may be necessary. spectroscopy may help to give us an accurate Myocardial ischaemia may also occur with reduced prognosis at an early stage. Asphyxiated infants who cardiac output. This diagnosis would be suggested are assessed very early to have a bad prognosis are by finding cardiomegaly on chest radiography and the ones who should be considered for therapeutic ischaemic ST changes on electrocardiography. If trials of cerebral protection. arterial pressure remains low despite volume re- placement, a dopamine infusion should be started References on September 24, 2021 by guest. Protected after any remaining metabolic acidosis has been Levene MI, Sands C, Grindulis H, Moore JR. Comparison of corrected with sodium bicarbonate. The dopamine two methods of predicting outcome in perinatal asphyxia. infusion can start at 5 rig/kg/minute but should be Lancet 1986;i:67-8. increased to 10, 15, or 20 Rg/kg/minute if mean 2 Whitelaw A. Death as an option in neonatal intensive care. arterial pressure does Lancet 1986;ii:328-31. not reach 40 mm Hg (5-33 3 Levene MI, Kornberg J, Williams THC. The incidence and kPa).'2 severity of post-asphyxial encephalopathy in full term infants. Early Hum Dev 1985;11:21-6. Cerebral protection 4 Painter MJ, Pippenger C, Macdonald H, Pitlick P. Phenobar- bital and diphenylhydantoin levels in neonates with seizures. J Pediatr 1978;92:315-9. Studies of hypoxia in experimental animals have 5 Giacoia GP, Gessner PK, Zaleska MM, Boutwell WC. Pharma- indicated that processes continuing for some hours cokinetics of paraldehyde disposition in the neonate. J Pediatr after a hypoxic insult has ceased can bring about 1984;104:291-5. further cerebral These 6 Wasterlain C, Plum F. Vulnerability of developing rat brain to damage. mechanisms include electroconvulsive seizures. Arch Neurol 1973;29:38-45. a prolonged fall in cerebral blood flow (the no 7 Eyre JA, Wilkinson AR. Thiopentone induced coma after reflow phenomenon),'3 calcium loading of mito- severe birth asphyxia. Arch Dis Child 1986;61:1084-9. Arch Dis Child: first published as 10.1136/adc.64.1.66 on 1 January 1989. Downloaded from 68 Whitelaw 8 Kaiser A, Whitelaw A. Normal cerebrospinal fluid pressure in damage: the role of excitatory activity and of calcium entry. Br J the newborn. Neuropediatrics 1986;17:100-2. Anaesth 1985;57:44-6. 9 Levene MI, Evans DH, Forde A, Archer LNJ. Value of 17 Steen PA, Gisvold SE, Milde JH, et al. Nimodipine improves intracranial pressure monitoring of asphyxiated newborn in- outcome when given after complete cerebral ischemia in fants. Dev Med Child Neurol 1987;29:311-9.
Load more

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]
  • 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.
    [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]