Breathing Pattern Abnormalities in Full Term Asphyxiated Newborn Infants
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Hypothermia Brochure
Visit these websites for more water safety and hypothermia prevention in- formation. What is East Pierce Fire & Rescue Hypothermia? www.eastpiercefire.org Hypothermia means “low temperature”. Washington State Drowning When your body is exposed to cold tem- Prevention Coalition Hypothermia www.drowning-prevention.org perature, it tries to protect itself by keeping a normal body temperature of 98.6°F. It Children’s Hospital & tries to reduce heat loss by shivering and Regional Medical Center In Our Lakes moving blood from your arms and legs to www.seattlechildrens.org the core of your body—head, chest and and Rivers abdomen. Hypothermia Prevention, Recognition and Treatment www.hypothermia.org Stages of Hypothermia Boat Washington Mild Hypothermia www.boatwashington.org (Core body temperature of 98.6°— 93.2°F) Symptoms: Shivering; altered judg- ment; numbness; clumsiness; loss of Boat U.S. Foundation dexterity; pain from cold; and fast www.boatus.com breathing. Boat Safe Moderate Hypothermia www.boatsafe.com (Core body temperature of 93.2°—86°F) Symptoms: Semiconscious to uncon- scious; shivering reduced or absent; lips are blue; slurred speech; rigid n in muscles; appears drunk; slow Eve breathing; and feeling of warmth can occur. mer! Headquarters Station Sum Severe Hypothermia 18421 Old Buckley Hwy (Core body temperature below 86°F) Bonney Lake, WA 98391 Symptoms: Coma; heart stops; and clinical death. Phone: 253-863-1800 Fax: 253-863-1848 Email: [email protected] Know the water. Know your limits. Wear a life vest. By choosing to swim in colder water you Waters in Western Common Misconceptions Washington reduce your survival time. -
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. -
Apnea and Control of Breathing Christa Matrone, M.D., M.Ed
APNEA AND CONTROL OF BREATHING CHRISTA MATRONE, M.D., M.ED. DIOMEL DE LA CRUZ, M.D. OBJECTIVES ¢ Define Apnea ¢ Review Causes and Appropriate Evaluation of Apnea in Neonates ¢ Review the Pathophysiology of Breathing Control and Apnea of Prematurity ¢ Review Management Options for Apnea of Prematurity ¢ The Clinical Evidence for Caffeine ¢ The Role of Gastroesophageal Reflux DEFINITION OF APNEA ¢ Cessation of breathing for greater than 15 (or 20) seconds ¢ Or if accompanied by desaturations or bradycardia ¢ Differentiate from periodic breathing ¢ Regular cycles of respirations with intermittent pauses of >3 S ¢ Not associated with other physiologic derangements ¢ Benign and self-limiting TYPES OF APNEA CENTRAL ¢ Total cessation of inspiratory effort ¢ Absence of central respiratory drive OBSTRUCTIVE ¢ Breathing against an obstructed airway ¢ Chest wall motion without nasal airflow MIXED ¢ Obstructed respiratory effort after a central pause ¢ Accounts for majority of apnea in premature infants APNEA IS A SYMPTOM, NOT A DIAGNOSIS Martin RJ et al. Pathogenesis of apnea in preterm infants. J Pediatr. 1986; 109:733. APNEA IN THE NEONATE: DIFFERENTIAL Central Nervous System Respiratory • Intraventricular Hemorrhage • Airway Obstruction • Seizure • Inadequate Ventilation / Fatigue • Cerebral Infarct • Hypoxia Infection Gastrointestinal • Sepsis • Necrotizing Enterocolitis • Meningitis • Gastroesophageal Reflux Hematologic Drug Exposure • Anemia • Perinatal (Ex: Magnesium, Opioids) • Polycythemia • Postnatal (Ex: Sedatives, PGE) Cardiovascular Other • Patent Ductus Arteriosus • Temperature instability • Metabolic derangements APNEA IN THE NEONATE: EVALUATION ¢ Detailed History and Physical Examination ¢ Gestational age, post-natal age, and birth history ¢ Other new signs or symptoms ¢ Careful attention to neurologic, cardiorespiratory, and abdominal exam APNEA IN THE NEONATE: EVALUATION ¢ Laboratory Studies ¢ CBC/diff and CRP ¢ Cultures, consideration of LP ¢ Electrolytes including magnesium ¢ Blood gas and lactate ¢ Radiologic Studies ¢ Head ultrasound vs. -
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. -
Sleep Apnea Sleep Apnea
Health and Safety Guidelines 1 Sleep Apnea Sleep Apnea Normally while sleeping, air is moved at a regular rhythm through the throat and in and out the lungs. When someone has sleep apnea, air movement becomes decreased or stops altogether. Sleep apnea can affect long term health. Types of sleep apnea: 1. Obstructive sleep apnea (narrowing or closure of the throat during sleep) which is seen most commonly, and, 2. Central sleep apnea (the brain is causing a change in breathing control and rhythm) Obstructive sleep apnea (OSA) About 25% of all adults are at risk for sleep apnea of some degree. Men are more commonly affected than women. Other risk factors include: 1. Middle and older age 2. Being overweight 3. Having a small mouth and throat Down syndrome Because of soft tissue and skeletal alterations that lead to upper airway obstruction, people with Down syndrome have an increased risk of obstructive sleep apnea. Statistics show that obstructive sleep apnea occurs in at least 30 to 75% of people with Down syndrome, including those who are not obese. In over half of person’s with Down syndrome whose parents reported no sleep problems, sleep studies showed abnormal results. Sleep apnea causing lowered oxygen levels often contributes to mental impairment. How does obstructive sleep apnea occur? The throat is surrounded by muscles that are active controlling the airway during talking, swallowing and breathing. During sleep, these muscles are much less active. They can fall back into the throat, causing narrowing. In most people this doesn’t affect breathing. However in some the narrowing can cause snoring. -
The Hazards of Nitrogen Asphyxiation US Chemical Safety and Hazard Investigation Board
The Hazards of Nitrogen Asphyxiation US Chemical Safety and Hazard Investigation Board Introduction • Nitrogen makes up 78% of the air we breath; because of this it is often assumed that nitrogen is not hazardous. • However, nitrogen is safe to breath only if it is mixed with an appropriate amount of oxygen. • Additional nitrogen (lower oxygen) cannot be detected by the sense of smell. Introduction • Nitrogen is used commercially as an inerting agent to keep material free of contaminants (including oxygen) that may corrode equipment, present a fire hazard, or be toxic. • A lower oxygen concentration (e.g., caused by an increased amount of nitrogen) can have a range of effects on the human body and can be fatal if if falls below 10% Effects of Oxygen Deficiency on the Human Body Atmospheric Oxygen Concentration (%) Possible Results 20.9 Normal 19.0 Some unnoticeable adverse physiological effects 16.0 Increased pulse and breathing rate, impaired thinking and attention, reduced coordination 14.0 Abnormal fatigue upon exertion, emotional upset, faulty coordination, poor judgment 12.5 Very poor judgment and coordination, impaired respiration that may cause permanent heart damage, nausea, and vomiting <10 Inability to move, loss of consciousness, convulsions, death Source: Compressed Gas Association, 2001 Statistics on Incidents CSB reviewed cases of nitrogen asphyxiation that occurred in the US between 1992 and 2002 and determined the following: • 85 incidents of nitrogen asphyxiation resulted in 80 deaths and 50 injuries. • The majority of -
Potential Protective Mechanism of Arousal in Obstructive Sleep Apnea
Editorial Potential protective mechanism of arousal in obstructive sleep apnea Naomi Deacon, Atul Malhotra Department of Medicine, Pulmonary, Critical Care and Sleep Medicine, University of California San Diego, La Jolla, California, USA Correspondence to: Naomi Deacon, PhD. 9300 Campus Point Drive #7381, La Jolla, CA 92037-7381, USA. Email: [email protected]. Submitted Jul 01, 2016. Accepted for publication Jul 02, 2016. doi: 10.21037/jtd.2016.07.43 View this article at: http://dx.doi.org/10.21037/jtd.2016.07.43 Obstructive sleep apnea (OSA) pathophysiology is thought increase the magnitude of post-occlusion hyperventilation to be due to the interaction of traits including airway (and consequently hypocapnia) due both to arousal associated anatomy and neuromuscular control which vary between sympathetic activation and the state dependent differences individuals. These traits include a low arousal threshold in eupneic CO2 and sensitivity. This theory is based on (wake easily from sleep), upper airway gain (how effectively the founding work by Iber and colleagues in 1986 (7) activation of upper airway dilator muscles improves who studied tracheostomized OSA patients following ventilation), loop gain (stability of the negative feedback experimental tracheal occlusion during stable NREM sleep. chemoreflex control system) and upper airway collapsibility They found that tracheal occlusion yielded arousal and (anatomical predisposition to passive airway collapse) (1). pharyngeal opening which resulted in hyperventilation and While deficits in these traits and how they interact varies hypocapnia, followed by a reduction in minute ventilation between individuals, generally mechanisms that increase and prolongation of expiratory time. The magnitude of activation of upper airway dilator muscles are considered to hypocapnia correlated with expiratory prolongation and help protect the airway from collapse. -
Clinical Management of Severe Acute Respiratory Infections When Novel Coronavirus Is Suspected: What to Do and What Not to Do
INTERIM GUIDANCE DOCUMENT Clinical management of severe acute respiratory infections when novel coronavirus is suspected: What to do and what not to do Introduction 2 Section 1. Early recognition and management 3 Section 2. Management of severe respiratory distress, hypoxemia and ARDS 6 Section 3. Management of septic shock 8 Section 4. Prevention of complications 9 References 10 Acknowledgements 12 Introduction The emergence of novel coronavirus in 2012 (see http://www.who.int/csr/disease/coronavirus_infections/en/index. html for the latest updates) has presented challenges for clinical management. Pneumonia has been the most common clinical presentation; five patients developed Acute Respira- tory Distress Syndrome (ARDS). Renal failure, pericarditis and disseminated intravascular coagulation (DIC) have also occurred. Our knowledge of the clinical features of coronavirus infection is limited and no virus-specific preven- tion or treatment (e.g. vaccine or antiviral drugs) is available. Thus, this interim guidance document aims to help clinicians with supportive management of patients who have acute respiratory failure and septic shock as a consequence of severe infection. Because other complications have been seen (renal failure, pericarditis, DIC, as above) clinicians should monitor for the development of these and other complications of severe infection and treat them according to local management guidelines. As all confirmed cases reported to date have occurred in adults, this document focuses on the care of adolescents and adults. Paediatric considerations will be added later. This document will be updated as more information becomes available and after the revised Surviving Sepsis Campaign Guidelines are published later this year (1). This document is for clinicians taking care of critically ill patients with severe acute respiratory infec- tion (SARI). -
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. -
Acute Respiratory Failure As the First Sign of Arnold-Chiari Malformation Associated with Syringomyelia
Eur Respir J, 1995, 8, 661–663 Copyright ERS Journals Ltd 1995 DOI: 10.1183/09031936.95.08040661 European Respiratory Journal Printed in UK - all rights reserved ISSN 0903 - 1936 CASE REPORT Acute respiratory failure as the first sign of Arnold-Chiari malformation associated with syringomyelia D. Alvarez*, I. Requena**, M. Arias**, L. Valdés*, I. Pereiro+, R. De la Torre++ Acute respiratory failure as the first sign of Arnold-Chiari malformation associated with Services of *Pneumology, **Neurology, syringomyelia. D. Alvarez, I. Requena, M. Arias, L. Valdés, I. Pereiro, R. De la Torre. +Neuroimaging and ++Intensive Care, Hos- ERS Journals Ltd 1995. pital Provincial and Dept of Medicine of ABSTRACT: We report a rare case of acute respiratory failure in a previously the University of Santiago de Compostela, Santiago de Compostela, Spain. asymptomatic patient showing clinical signs of inferior cranial nerve palsy together with weakness and muscular atrophy of the upper limbs. Correspondence: D. Alvarez García, c) Magnetic resonance imaging revealed Arnold-Chiari malformation associated with Rosalía de Castro 57, 4º I., 15706 Santiago platybasia, basilar impression, syringomyelia and Klippel-Feil syndrome. Episodes de Compostela, Spain of apnoea required tracheostomy and recurred upon tentative closure of the tracheostome, but remitted upon decompression of the posterior fossa. Keywords: Adult respiratory distress, This case involved both obstructive mechanisms and dysfunction of the respiratory Arnold-Chiari malformation, sleep apnoea, centre. Patients with respiratory failure not explained by pulmonary pathology syringomyelia should be checked for underlying neurological disease. Received: October 29 1993 Eur Respir J., 1995, 8, 661–663. Accepted after revision September 13 1994 Arnold-Chiari malformation is a dysraphic congenital attempts at extubation were each followed by respiratory disorder, frequently associated with other malformations failure. -
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. -
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.