Fetal Asphyxia: Pathogenic Mechanisms and Consequences 57

Total Page:16

File Type:pdf, Size:1020Kb

Fetal Asphyxia: Pathogenic Mechanisms and Consequences 57 CHAPTER © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FORFetal SALE OR Asphyxia: DISTRIBUTION PathogenicNOT FOR SALE OR DISTRIBUTION Mechanisms and Consequences © Jones & Bartlett Learning, LLC © Jones5 & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Hypoxia is defined as a reduced or insufficient level of oxygen in the body’s tissues. In clinical and physiologic usage, the term is generally reserved for more substantial degrees of reduced O2 avail- ability, such as occurs at moderately high altitude when a person notices the O2 limitation. When one © Jonestravels &from Bartlett sea level Learning, up to 10,000 feet,LLC mild forms of discomfort© may Jones be noted & suchBartlett as tachypnea, Learning, LLC NOTtachycardia, FOR SALE exercise OR intolerance, DISTRIBUTION and headache, and in general, theNOT higher FOR the altitude,SALE ORthe greater DISTRIBUTION the discomfort. Hypoxia in both adults and fetuses is thus a continuum from normoxia, to easily tolerated reduced O2, to a reduction requiring physiologic adaptation such as tachypnea, to reduced function, to tissue damage, and finally to death. These and other terms are defined in Table 5-1. © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Table 5-1 Definition of Terms Related to Hypoxia Acidemia Increased concentration of hydrogen ions in the blood Acidosis Increased concentration of hydrogen ions in the tissues of the body Aerobic metabolism© Jones Metabolism& Bartlett of glucose Learning, using oxygen; LLC aerobic metabolism generates© 38 Jonesmolecules & of Bartlett Learning, LLC NOT FORadenosine SALE triphosphate OR DISTRIBUTION (ATP) per each glucose molecule for energyNOT use FOR SALE OR DISTRIBUTION Anaerobic metabolism Metabolism of glucose without the use of oxygen; anerobic metabolism generates 2 molecules of ATP per each glucose molecule for energy use Asphyxia Comes from the Greek word for “pulseless”; a decrease in O2 and increase in CO2 due to an interference with gas exchange; asphyxia is a continuum described by degrees of © Jones & Bartlett Learning,acidosis LLC © Jones & Bartlett Learning, LLC NOT BaseFOR SALE OR DISTRIBUTIONA substance that is capable of accepting hydrogenNOT ions FORand thereby SALE decreasing OR DISTRIBUTIONacidity 2 Base excess (BE) The amount of base or HCO 3 that is available for buffering; as metabolic acidosis increases, the base excess decreases 2 2 Bicarbonate (HCO 3 ) HCO 3 (often referred to as bicarb) is the base or hydrogen acceptor that is part of the © Jones & Bartlett Learning, LLC primary buffering system ©within Jones the blood & Bartlett Learning, LLC NOT FOR SALE ORBuffer DISTRIBUTIONA buffer is a chemical substanceNOT that FOR is both SALE a weak ORacid andDISTRIBUTION salt, and can absorb or give up hydrogen ions, thereby maintaining a constant pH value; the primary buffer 2 involved in fetal oxygenation is HCO 3 Hypercarbia Excessive carbon dioxide in blood; sometimes referred to as hypercapnia Hypoxia © Jones Decreased& Bartlett oxygen Learning, in tissue LLC © Jones & Bartlett Learning, LLC Hypoxemia NOT FORDecreased SALE oxygen OR DISTRIBUTIONcontent in blood NOT FOR SALE OR DISTRIBUTION Hypoxemia–ischemia Reduced amount of oxygen and inadequate volume of blood delivered to tissues; can cause brain injury if delivery of oxygen and glucose falls below critical levels Metabolic acidemia Low bicarbonate (negative base excess) Mixed acidosis Low pH that reflects both increased carbon dioxide and decreased base excess © Jones & Bartlett Learning,(i.e., increased LLC lactic acid) © Jones & Bartlett Learning, LLC NOT FORpH SALE OR DISTRIBUTIONpH refers to the concentration of hydrogen ionsNOT in blood FOR and refersSALE to “puissance OR DISTRIBUTION hydrogen,” which is French for strength (or power) of hydrogen; a pH of 7.0 = 0.0000001 (which is 1027) moles per liter of hydrogen ions Respiratory acidemia High PCO2 © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION The authors would like to acknowledge Dr. Austin Ugwumadu for his contributions to this chapter. © Jones & Bartlett Learning, LLC. NOT FOR SALE OR DISTRIBUTION. 9781284090338_CH05.indd 55 17/03/17 2:08 PM 56 PART II Physiology © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE ORIn DISTRIBUTION the fetus, the continuum of hypoxia is mostlyNOT caused FOR by SALE a reduction OR DISTRIBUTIONof either maternal pla- cental (i.e., intervillous) blood flow, or reduced umbilical blood flow. Both of these factors result in reduced exchange of the respiratory gases, so in addition to hypoxia there is also a buildup of carbon dioxide, resulting in what is called a respiratory acidosis. At more severe degrees of reduc- tion of these© two Jones blood &flows, Bartlett and therefore Learning, more severeLLC hypoxia, the cells of the© body Jones will convert& Bartlett Learning, LLC from aerobicNOT to anaerobic FOR SALE metabolism OR DISTRIBUTIONfor energy production, of which the end productNOT FOR is lactic SALE OR DISTRIBUTION acid. This results in reduction of bicarbonate, and therefore a metabolic acidosis (Figure 5-1). Hypoxemia is used to describe a reduced level or concentration of O2 in the blood. The direct measurement of hypoxia in tissues is rarely possible, so measurements of oxygen in the blood are © Jonesused as & surrogates. Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FORHypoxia–ischemia SALE OR describesDISTRIBUTION reduced amount of oxygen and inadequateNOT FOR blood SALE flow OR in tissue. DISTRIBUTION The combination of hypoxia and ischemia can cause brain damage when oxygen and glucose delivery fall below critical levels. Asphyxia has the pathologic meaning of insufficiency or absence of exchange of the respiratory © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC gases, though etymologically it comes from the Greek word meaning pulseless. Although the word NOT FOR SALE ORasphyxia DISTRIBUTION strictly could be applied to any changeNOT in respiratory FOR SALE gas levels OR from DISTRIBUTION normal, by common usage it is generally reserved for the more severe degrees, where compensatory mechanisms are required for tolerance, or tissue damage or death occurs. The severity© Jones of hypoxia & Bartlettor asphyxia Learning, is described LLCin terms of acidemia, hypercarbia,© Jones hypoxemia, & Bartlett Learning, LLC and base excess.NOT In FOR this text, SALE we use OR the DISTRIBUTION terms hypoxia and asphyxia to denote theNOT moderate FOR or SALE OR DISTRIBUTION more severe degrees when the fetus uses physiologic alterations to tolerate the condition. There are basically three common means by which the human fetus can become hypoxic or asphyxiated: (1) insufficiency of uterine blood flow1; (2) insufficiency of umbilical blood flow2; or 3 © Jones(3) a decrease & Bartlett in maternal Learning, arterial LLC oxygen content. Each of these© mechanismsJones & Bartlett converges Learning,into a LLC NOTcommon FOR SALE pathway OR that DISTRIBUTION involves the fetal response to reduction ofNOT available FOR oxygen. SALE In ORaddition, DISTRIBUTION the Insufficient oxygen delivered to fetus Elevated carbon dioxide © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTIONAnaerobic metabolism used to NOT FOR SALE OR DISTRIBUTION generate ATP Increased H2CO3 Lactic acid, an end product of © anaerobicJones metabolism,& Bartlett accumulates Learning, LLC © Jones & Bartlett Learning, LLC NOT FORin the fe SALEtal compartment OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Metabolic acidosis Respiratory acidosis © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION © Jones & Bartlett Learning, LLC Reduced© Jones pH & Bartlett Learning, LLC NOT FOR SALE OR DISTRIBUTION NOT FOR SALE OR DISTRIBUTION Figure 5-1 Consequences of insufficiency of exchange of respiratory gases. © Jones & Bartlett Learning, LLC. NOT FOR SALE OR DISTRIBUTION. 9781284090338_CH05.indd 56 17/03/17 2:08 PM Chapter 5 Fetal Asphyxia: Pathogenic Mechanisms and Consequences 57 © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOT FOR SALE ORfetus DISTRIBUTION has higher oxygen needs during pyrexia, NOTwhich FORmay play SALE a role OR in the DISTRIBUTION known increased risk for newborn neurologic damage following chorioamnionitis.4,5 Other mechanisms, such as fetal anemia, are relatively rare in clinical practice. The two organ systems that have the most critical roles in the fetal response to hypoxia are the cardiorespiratory© Jones and central & Bartlett nervous Learning, systems. In both, LLC the initial response involves© Jones a series of& Bartlett Learning, LLC physiologic NOTchanges FOR that devolveSALE toOR pathologic DISTRIBUTION responses when asphyxia persists.NOT Similarly, FOR in SALEboth OR DISTRIBUTION systems the response to acute hypoxial stress is different than the response to chronic hypoxia. The sections that follow address physiologic and pathologic responses to acute hypoxia first followed by the effects of chronic hypoxia. © Jones & Bartlett Learning, LLC © Jones & Bartlett Learning, LLC NOTI. FOR FET SALEAL OR C ADISTRIBUTIONRDIORESPIRATORYNOT RES FORPONSES SALE OR DISTRIBUTION TO HYPOXIA In the previously normoxic fetus, a number of compensatory mechanisms occur during acute hy- © Jones & Bartlettpoxia
Recommended publications
  • Risk Factors Associated with the Development
    Biomédica 2017;37(Supl.1):2017;37(Supl.1):51-651-6 Risk factors of perinatal asphyxia doi: http://dx.doi.org/10.7705/biomedica.v37i1.2844 ORIGINAL ARTICLE Risk factors associated with the development of perinatal asphyxia in neonates at the Hospital Universitario del Valle, Cali, Colombia, 2010-2011 Javier Torres-Muñoz, Christian Rojas, Diana Mendoza-Urbano, Darly Marín-Cuero, Sandra Orobio, Carlos Echandía Grupo INSIDE, Departamento de Pediatría, Facultad de Medicina, Universidad del Valle, Cali, Colombia Introduction: Perinatal asphyxia is one of the main causes of perinatal mortality and morbidity worldwide and it generates high costs for health systems; however, it has modifiable risk factors. Objective: To identify the risk factors associated with the development of perinatal asphyxia in newborns at Hospital Universitario del Valle, Cali, Colombia. Materials and methods: Incident cases and concurrent controls were examined. Cases were defined as newborns with moderate to severe perinatal asphyxia who were older than or equal to 36 weeks of gestational age, needed advanced resuscitation and presented one of the following: early neurological disorders, multi-organ commitment or a sentinel event. The controls were newborns without asphyxia who were born one week apart from the case at the most and had a comparable gestational age. Patients with major congenital malformations and syndromes were excluded. Results: Fifty-six cases and 168 controls were examined. Premature placental abruption (OR=41.09; 95%CI: 4.61-366.56), labor with a prolonged expulsive phase (OR=31.76; 95%CI: 8.33-121.19), lack of oxytocin use (OR=2.57; 95% CI: 1.08 - 6.13) and mothers without a partner (OR=2.56; 95% CI: 1.21-5.41) were risk factors for the development of perinatal asphyxia in the study population.
    [Show full text]
  • Quality of Survival After Severe Birth Asphyxia
    Arch Dis Child: first published as 10.1136/adc.52.8.620 on 1 August 1977. Downloaded from Archives of Disease in Childhood, 1977, 52, 620-626 Quality of survival after severe birth asphyxia ALISON J. THOMSON, MARGARET SEARLE, AND G. RUSSELL From Aberdeen Maternity Hospital and the Royal Aberdeen Children's Hospital SUMMARY Thirty-one children who survived severe birth asphyxia defined by a 1-minute Apgar score of 0, or a 5-minute Apgar score of <4, have been seen at age 5 to 10 years for neurological and psychological assessment. Their progress has been compared with that of controls matched for sex, birthweight, gestational age, and social class. 29 (93 %) of the 31 asphyxiated group and all the controls had no serious neurological or mental handicap. 2 were severely disabled and mentally retarded. Detailed studies of psychological function showed no significant differences between the two groups. 2 apparently stillborn infants have made normal progress. It was not possible to identify any perinatal factor which predicted the occurrence of serious handicap with certainty. We considered that the quality of life enjoyed by the large majority of the survivors was such as to justify a positive approach to the resuscitation of very severely asphyxiated neonates. Perinatal asphyxia is a major cause of morbidity and Patients and methods mortality in the first week of life. The survivors have long been recognized to have an increased risk of Cases. In 1964-68 inclusive there were 14 890 single- handicaps such as cerebral palsy, mental retarda- ton live births to mothers living in the city and copyright.
    [Show full text]
  • Meconium Aspiration Syndrome
    National Neonatal Perinatal Database 2002-2003 Meconium Aspiration Syndrome Subjects and Methods 145,623 neonates born at 18 centers of National Neonatal-Perinatal Database (NNPD) of India over two year duration (2002-2003) Management of Meconium-stained amniotic fluid Contemporary recommendations of American Academy of Pediatrics and American Heart Association through Neonatal Resuscitation Program and Pediatric Working Group of International Liaison Committee on Resuscitation were expected to be followed. Management of a neonate born through MSAF comprised: 1) Suctioning the mouth, pharynx and nose as soon as head was delivered before delivery of shoulders (intrapartum suctioning) regardless of whether the meconium is thick or thin, and 2) if the infant was non-vigorous, intubating and suctioning the trachea before performing other steps of resuscitation. Meconium aspiration syndrome MAS was defined as presence of two of the following: meconium staining of liquor or staining of nails or umbilical cord or skin, respiratory distress within one hour of birth and radiological evidence of aspiration pneumonitis (atelectasis and/or hyperinflation). Findings Figure 1: Management and outcome of neonates born through meconium stained amniotic fluid Meconium-stained amniotic fluid (MSAF) (n=12,156) 8.4% of live births Among neonates with MSAF (n=12,156) Endotracheal suction in 3468 (28.5%) Need of positive pressure ventilation in During 2504 (20.6%) Resuscitation Resuscitation Need of chest compression in 1021 (8.4%) Among neonates with MSAF (n=12,156) MAS in 1896 (15.6%) Morbidities Morbidities HIE in 846 (7%) Among neonates with MAS (n=1,896) Assisted ventilation in 385 (20.3%) Outcome Death in 332 (17.5%) Mean birth weight of babies born through MSAF was significantly lower (2646552 gm vs.
    [Show full text]
  • Approach to Cyanosis in a Neonate.Pdf
    PedsCases Podcast Scripts This podcast can be accessed at www.pedscases.com, Apple Podcasting, Spotify, or your favourite podcasting app. Approach to Cyanosis in a Neonate Developed by Michelle Fric and Dr. Georgeta Apostol for PedsCases.com. June 29, 2020 Introduction Hello, and welcome to this pedscases podcast on an approach to cyanosis in a neonate. My name is Michelle Fric and I am a fourth-year medical student at the University of Alberta. This podcast was made in collaboration with Dr. Georgeta Apostol, a general pediatrician at the Royal Alexandra Hospital Pediatrics Clinic in Edmonton, Alberta. Cyanosis refers to a bluish discoloration of the skin or mucous membranes and is a common finding in newborns. It is a clinical manifestation of the desaturation of arterial or capillary blood and may indicate serious hemodynamic instability. It is important to have an approach to cyanosis, as it can be your only sign of a life-threatening illness. The goal of this podcast is to develop this approach to a cyanotic newborn with a focus on these can’t miss diagnoses. After listening to this podcast, the learner should be able to: 1. Define cyanosis 2. Assess and recognize a cyanotic infant 3. Develop a differential diagnosis 4. Identify immediate investigations and management for a cyanotic infant Background Cyanosis can be further broken down into peripheral and central cyanosis. It is important to distinguish these as it can help you to formulate a differential diagnosis and identify cases that are life-threatening. Peripheral cyanosis affects the distal extremities resulting in blue color of the hands and feet, while the rest of the body remains pinkish and well perfused.
    [Show full text]
  • 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]
  • Hyperventilation Syndrome
    Hyperventilation Syndrome INTRODUCTION ● hyperventilation in the presence of the following should immediately confirm an alternative Hyperventilation syndrome is defined as “a rate of diagnosis: ventilation exceeding metabolic needs and higher than that required to maintain a normal level of plasma CO2”. – cyanosis Physiological hyperventilation can occur in a number of – reduced level of consciousness situations, including life-threatening conditions such as: – reduction in SpO2. ● pulmonary embolism ● diabetic ketoacidosis MANAGEMENT 1,2 ● asthma If ABCD need correction then treat as per medical ● hypovolaemia. guidelines as it is unlikely to be due to hyperventilation syndrome but is more likely to be physiological As a rule, hyperventilation due to emotional stress is hyperventilation secondary to an underlying rare in children, and physical causes are much more pathological process. likely to be responsible for hyperventilation. Maintain a calm approach at all times. Specific presenting features can include: Reassure the patient and try to remove the source of ● acute anxiety the patient’s anxiety, this is particularly important in ● tetany due to calcium imbalance children. ● numbness and tingling of the mouth and lips Coach the patient’s respirations whilst maintaining a calm environment. ● carpopedal spasm ● aching of the muscles of the chest ADDITIONAL INFORMATION ● feeling of light headedness or dizziness. The cause of hyperventilation cannot always be determined with sufficient accuracy (especially in the HISTORY early stages) in the pre hospital environment. Refer to dyspnoea guide Always presume hyperventilation is secondary to hypoxia or other underlying respiratory disorder until proven otherwise. 1,2 ASSESSMENT The resulting hypocapnia will result in respiratory Assess ABCD’s: alkalosis bringing about a decreased level of serum ionised calcium.
    [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]
  • Prolonged Post-Hyperventilation Apnea in Two Young Adults With
    Munemoto et al. BioPsychoSocial Medicine 2013, 7:9 http://www.bpsmedicine.com/content/7/1/9 CASE REPORT Open Access Prolonged post-hyperventilation apnea in two young adults with hyperventilation syndrome Takao Munemoto1,4*, Akinori Masuda2, Nobuatsu Nagai3, Muneki Tanaka4 and Soejima Yuji5 Abstract Background: The prognosis of hyperventilation syndrome (HVS) is generally good. However, it is important to proceed with care when treating HVS because cases of death following hyperventilation have been reported. This paper was done to demonstrate the clinical risk of post-hyperventilation apnea (PHA) in patients with HVS. Case presentation: We treated two patients with HVS who suffered from PHA. The first, a 21-year-old woman, had a maximum duration of PHA of about 3.5 minutes and an oxygen saturation (SpO2) level of 60%. The second patient, a 22-year-old woman, had a maximum duration of PHA of about 3 minutes and an SpO2 level of 66%. Both patients had loss of consciousness and cyanosis. Because there is no widely accepted regimen for treating patients with prolonged PHA related to HVS, we administered artificial ventilation to both patients using a bag mask and both recovered without any after effects. Conclusion: These cases show that some patients with HVS develop prolonged PHA or severe hypoxia, which has been shown to lead to death in some cases. Proper treatment must be given to patients with HVS who develop PHA to protect against this possibility. If prolonged PHA or severe hypoxemia arises, respiratory assistance using a bag mask must be done immediately. Keywords: Post-hyperventilation apnea, PHA, Hyperventilation syndrome, HVS, Hypocapnia, Hypoxemia Background incidence of death, severe hypoxia, or myocardial infarc- Hyperventilation syndrome (HVS) is characterized by tion in association with the paper-bag method [2].
    [Show full text]
  • Postnatal Complications of Intrauterine Growth Restriction
    Neonat f al l o B Sharma et al., J Neonatal Biol 2016, 5:4 a io n l r o u g y DOI: 10.4172/2167-0897.1000232 o J Journal of Neonatal Biology ISSN: 2167-0897 Mini Review Open Access Postnatal Complications of Intrauterine Growth Restriction Deepak Sharma1*, Pradeep Sharma2 and Sweta Shastri3 1Neoclinic, Opposite Krishna Heart Hospital, Nirman Nagar, Jaipur, Rajasthan, India 2Department of Medicine, Mahatma Gandhi Medical College, Jaipur, Rajasthan, India 3Department of Pathology, N.K.P Salve Medical College, Nagpur, Maharashtra, India Abstract Intrauterine growth restriction (IUGR) is defined as a velocity of fetal growth less than the normal fetus growth potential because of maternal, placental, fetal or genetic cause. This is an important cause of fetal and neonatal morbidity and mortality. Small for gestational age (SGA) is defined when birth weight is less than two standard deviations below the mean or less than 10th percentile for a specific population and gestational age. Usually IUGR and SGA are used interchangeably, but there exists subtle difference between the two terms. IUGR infants have both acute and long term complications and need regular follow up. This review will cover various postnatal aspects of IUGR. Keywords: Intrauterine growth restriction; Small for gestational age; Postnatal Diagnosis of IUGR Placental genes; Maternal genes; Fetal genes; Developmental origin of health and disease; Barker hypothesis The diagnosis of IUGR infant postnatally can be done by clinical examination (Figure 2), anthropometry [13-15], Ponderal Index Introduction (PI=[weight (in gram) × 100] ÷ [length (in cm) 3]) [2,16], Clinical assessment of nutrition (CAN) score [17], Cephalization index [18], Intrauterine growth restriction (IUGR) is defined as a velocity of mid-arm circumference and mid-arm/head circumference ratios fetal growth less than the normal fetus growth potential for a specific (Kanawati and McLaren’s Index) [19].
    [Show full text]
  • 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).
    [Show full text]
  • The Effects of Inhaled Albuterol in Transient Tachypnea of the Newborn Myo-Jing Kim,1 Jae-Ho Yoo,1 Jin-A Jung,1 Shin-Yun Byun2*
    Original Article Allergy Asthma Immunol Res. 2014 March;6(2):126-130. http://dx.doi.org/10.4168/aair.2014.6.2.126 pISSN 2092-7355 • eISSN 2092-7363 The Effects of Inhaled Albuterol in Transient Tachypnea of the Newborn Myo-Jing Kim,1 Jae-Ho Yoo,1 Jin-A Jung,1 Shin-Yun Byun2* 1Department of Pediatrics, Dong-A University, College of Medicine, Busan, Korea 2Department of Pediatrics, Pusan National University School of Medicine, Yangsan, Korea This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Purpose: Transient tachypnea of the newborn (TTN) is a disorder caused by the delayed clearance of fetal alveolar fluid.ß -adrenergic agonists such as albuterol (salbutamol) are known to catalyze lung fluid absorption. This study examined whether inhalational salbutamol therapy could improve clinical symptoms in TTN. Additional endpoints included the diagnostic and therapeutic efficacy of salbutamol as well as its overall safety. Methods: From January 2010 through December 2010, we conducted a prospective study of 40 newborns hospitalized with TTN in the neonatal intensive care unit. Patients were given either inhalational salbutamol (28 patients) or placebo (12 patients), and clinical indices were compared. Results: The dura- tion of tachypnea was shorter in patients receiving inhalational salbutamol therapy, although this difference was not statistically significant. The dura- tion of supplemental oxygen therapy and the duration of empiric antibiotic treatment were significantly shorter in the salbutamol-treated group.
    [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]