Approach to Cyanosis in a Neonate.Pdf
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Journal of Turgut Ozal Medical Center
OLGU SUNUMU/CASE REPORT J Turgut Ozal Med Cent 2015;22(3):193-6 Journal of Turgut Ozal Medical Center www.jtomc.org The Case of a Patient with Concomitant Popliteal Artery and Ascending Aortic Aneurysm Who Presented with the Blue Toe Syndrome Tevfik Güneş, İhsan Alur, Serkan Girgin, Bilgin Emrecan Pamukkale University, Faculty of Medicine, Department of Cardiovascular Surgery, Denizli, Turkey Abstract Popliteal artery aneurysms (PAAs) are rare though these aneurysms are the most frequently encountered peripheral arterial aneurysms. In this article, we present the treatment of a patient who simultaneously had bilateral popliteal artery and ascending aortic aneurysm but was admitted to the emergency room due to the blue toe syndrome. A 72-old-year female was admitted to the hospital with left lower extremity pain and cyanosis in her toe. Bilateral popliteal artery and ascending aortic aneurysm were observed on computed tomography. Aneurysmectomy and femoropopliteal bypass was performed primarily to the left popliteal artery owing to ischemia. Two months later, we performed valve and ascending aorta replacement followed by right popliteal aneurysmectomy and femoropopliteal bypass 16 months later. In conclusion, since other arterial aneurysms can be simultaneously observed with popliteal artery aneurysm, it is very important to scan whole main arterial system when PAA is evaluated. Key Words: Popliteal Artery; Aorta; Aneurysm; Embolism. Blue Toe Sendromu ile Başvuran Popliteal Arter ve Asendan Aort Anevrizmalı Hasta Özet Popliteal arter anevrizmaları (PAA) nadir görülen patolojilerdir, fakat periferik arter anevrizmaları arasında en sık karşılaşılanıdır. Bu yazıda blue toe sendromu ile başvuran bilateral popliteal arter ve asendan aort anevrizması saptanan hastanın aşamalı tedavisi sunulmaktadır. -
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. -
Review of Systems
code: GF004 REVIEW OF SYSTEMS First Name Middle Name / MI Last Name Check the box if you are currently experiencing any of the following : General Skin Respiratory Arthritis/Rheumatism Abnormal Pigmentation Any Lung Troubles Back Pain (recurrent) Boils Asthma or Wheezing Bone Fracture Brittle Nails Bronchitis Cancer Dry Skin Chronic or Frequent Cough Diabetes Eczema Difficulty Breathing Foot Pain Frequent infections Pleurisy or Pneumonia Gout Hair/Nail changes Spitting up Blood Headaches/Migraines Hives Trouble Breathing Joint Injury Itching URI (Cold) Now Memory Loss Jaundice None Muscle Weakness Psoriasis Numbness/Tingling Rash Obesity Skin Disease Osteoporosis None Rheumatic Fever Weight Gain/Loss None Cardiovascular Gastrointestinal Eyes - Ears - Nose - Throat/Mouth Awakening in the night smothering Abdominal Pain Blurring Chest Pain or Angina Appetite Changes Double Vision Congestive Heart Failure Black Stools Eye Disease or Injury Cyanosis (blue skin) Bleeding with Bowel Movements Eye Pain/Discharge Difficulty walking two blocks Blood in Vomit Glasses Edema/Swelling of Hands, Feet or Ankles Chrohn’s Disease/Colitis Glaucoma Heart Attacks Constipation Itchy Eyes Heart Murmur Cramping or pain in the Abdomen Vision changes Heart Trouble Difficulty Swallowing Ear Disease High Blood Pressure Diverticulosis Ear Infections Irregular Heartbeat Frequent Diarrhea Ears ringing Pain in legs Gallbladder Disease Hearing problems Palpitations Gas/Bloating Impaired Hearing Poor Circulation Heartburn or Indigestion Chronic Sinus Trouble Shortness -
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). -
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. -
Chronic Hypoxemia in the Newborn Lamb: Cardiovascular, Hematopoietic, and Growth Adaptations
003 1-3998/85/19 10-l004$02.00/0 PEDIATRIC RESEARCH Val. 19, No. 10, 1985 Copyright O 1985 International Pediatric Research Foundation, Inc. Printed in U.S. A. Chronic Hypoxemia in the Newborn Lamb: Cardiovascular, Hematopoietic, and Growth Adaptations DAVID TEITEL, DANIEL SIDI,' DANIEL BERNSTEIN, MICHAEL A. HEYMANN, AND ABRAHAM M. RUDOLPH Cardiovascular Research Institute and the Departments of Pediatrics, Physiology, and Obstetrics, Gynecology and Reproductive Sciences, University of California, Sun Francisco, California 94143 ABSTRAm. We have created a model of chronic hypox- developed a model of a common cyanotic heart lesion to assess emia in the newborn lamb by decreasing pulmonary blood some of its cardiovascular and metabolic effects on the newborn flow in the presence of an atrial septal defect. Via a left lamb. lateral thoracotomy, we place an inflatable balloon around Several authors have studied acute hypoxemia in the devel- the pulmonary artery and perform an atrial septostomy oping organism and elucidated its effects on general cardiovas- under direct vision. We also insert several vascular cathe- cular function (1-3), regional blood flow (1, 4, 5), metabolic ters and place an electromagnetic flow transducer around activity (6, 7), and course of decompensation (1). The effects of the ascending aorta. Three days after surgery, we inflated sympathetic blockade (8, 9) and decreasing Hb oxygen affinity the balloon in 11 lambs such that arterial oxygen saturation (10, 11) on the response to acute hypoxemia have also been decreased to 60 to 75%. Studies were performed on these addressed. Few studies have been performed on the chronically lambs twice weekly and weekly on 12 normoxemic lambs. -
Chest Pain and the Hyperventilation Syndrome - Some Aetiological Considerations
Postgrad Med J: first published as 10.1136/pgmj.61.721.957 on 1 November 1985. Downloaded from Postgraduate Medical Journal (1985) 61, 957-961 Mechanism of disease: Update Chest pain and the hyperventilation syndrome - some aetiological considerations Leisa J. Freeman and P.G.F. Nixon Cardiac Department, Charing Cross Hospital (Fulham), Fulham Palace Road, Hammersmith, London W6 8RF, UK. Chest pain is reported in 50-100% ofpatients with the coronary arteriograms. Hyperventilation and hyperventilation syndrome (Lewis, 1953; Yu et al., ischaemic heart disease clearly were not mutually 1959). The association was first recognized by Da exclusive. This is a vital point. It is time for clinicians to Costa (1871) '. .. the affected soldier, got out of accept that dynamic factors associated with hyperven- breath, could not keep up with his comrades, was tilation are commonplace in the clinical syndromes of annoyed by dizzyness and palpitation and with pain in angina pectoris and coronary insufficiency. The his chest ... chest pain was an almost constant production of chest pain in these cases may be better symptom . .. and often it was the first sign of the understood if the direct consequences ofhyperventila- disorder noticed by the patient'. The association of tion on circulatory and myocardial dynamics are hyperventilation and chest pain with extreme effort considered. and disorders of the heart and circulation was ackn- The mechanical work of hyperventilation increases owledged in the names subsequently ascribed to it, the cardiac output by a small amount (up to 1.3 1/min) such as vasomotor ataxia (Colbeck, 1903); soldier's irrespective of the effect of the blood carbon dioxide heart (Mackenzie, 1916 and effort syndrome (Lewis, level and can be accounted for by the increased oxygen copyright. -
Chest Pain in Pediatrics
PEDIATRIC CARDIOLOGY 0031-3955/99 $8.00 + .OO CHEST PAIN IN PEDIATRICS Keith C. Kocis, MD, MS Chest pain is an alarming complaint in children, leading an often frightened and concerned family to a pediatrician or emergency room and commonly to a subsequent referral to a pediatric cardiologist. Because of the well-known associ- ation of chest pain with significant cardiovascular disease and sudden death in adult patients, medical personnel commonly share heightened concerns over pediatric patients presenting with chest pain. Although the differential diagnosis of chest pain is exhaustive, chest pain in children is least likely to be cardiac in origin. Organ systems responsible for causing chest pain in children include*: Idiopathic (12%-85%) Musculoskeletal (15%-31%) Pulmonary (12%-21%) Other (4%-21%) Psychiatric (5%-17%) Gastrointestinal (4'/0-7%) Cardiac (4%4%) Furthermore, chest pain in the pediatric population is rareZy associated with life-threatening disease; however, when present, prompt recognition, diagnostic evaluation, and intervention are necessary to prevent an adverse outcome. This article presents a comprehensive list of differential diagnostic possibilities of chest pain in pediatric patients, discusses the common causes in further detail, and outlines a rational diagnostic evaluation and treatment plan. Chest pain, a common complaint of pediatric patients, is often idiopathic in etiology and commonly chronic in nature. In one study,67 chest pain accounted for 6 in 1000 visits to an urban pediatric emergency room. In addition, chest pain is the second most common reason for referral to pediatric cardiologist^.^, 23, 78 Chest pain is found equally in male and female patients, with an average *References 13, 17, 23, 27, 32, 35, 44, 48, 49, 63-67, 74, and 78. -
Pathophysiology and Treatment of Cheyne-Stokes Respiration Thorax: First Published As 10.1136/Thx.53.6.514 on 1 June 1998
514 Thorax 1998;53:514–518 Pathophysiology and treatment of Cheyne-Stokes respiration Thorax: first published as 10.1136/thx.53.6.514 on 1 June 1998. Downloaded from M T Naughton Cheyne-Stokes respiration is a disorder charac- results from hyperventilation, prolonged circu- terised by recurrent central apnoeas during lation time, and reduced blood gas buVering sleep alternating with a crescendo-decrescendo capacity.21 pattern of tidal volume.12 It is often observed in patients with congestive heart failure, usually HYPERVENTILATION during stages 1 and 2 non-REM sleep when Hyperventilation, the common pathophysi- ventilation is under chemical-metabolic ological feature of all forms of periodic breath- 2 control. Patients with Cheyne-Stokes respira- ing, causes PaCO2 levels to fall below the tion usually present with the symptoms of apnoeic threshold triggering a central apnoea. orthopnoea, paroxysmal nocturnal dyspnoea, Once the peripheral chemoreceptors sense an excessive daytime sleepiness and witnessed apnoea related rise in the PaCO2 level above the apnoeas in the setting of congestive heart apnoea threshold, hyperventilation recurs driv- 13 failure. Excessive weight and snoring may be ing the PaCO2 level below the apnoea threshold absent. Approximately 50% of patients with once again.2 symptomatic congestive heart failure have Increased central hypercapnic ventilatory sleep apnoea, mainly of the Cheyne-Stokes responsiveness has been reported to occur in respiration variety.4-6 As congestive heart failure Cheyne-Stokes respiration with congestive occurs in 1% of the adult population and dou- heart failure22 and in other forms of periodic bles in prevalence for each decade beyond 60 breathing in subjects without congestive heart years,7 Cheyne-Stokes respiration is common failure—namely, idiopathic non-hypercapnic but often left unrecognised. -
Dermatologic Aspects of Fabry Disease ª the Author(S) 2016 DOI: 10.1177/2326409816661353 Iem.Sagepub.Com
Original Article Journal of Inborn Errors of Metabolism & Screening 2016, Volume 4: 1–7 Dermatologic Aspects of Fabry Disease ª The Author(s) 2016 DOI: 10.1177/2326409816661353 iem.sagepub.com Paula C. Luna, MD1,2, Paula Boggio, MD2, and Margarita Larralde, MD, PhD1,2 Abstract Isolated angiokeratomas (AKs) are common cutaneous lesions, generally deemed unworthy of further investigation. In contrast, diffuse AKs should alert the physician to a possible diagnosis of Fabry disease (FD). Angiokeratomas often do not appear until adolescence or young adulthood. The number of lesions and the extension over the body increase progressively with time, so that generalization and mucosal involvement are frequent. Although rare, FD remains an important diagnosis to consider in patients with AKs, with or without familial history. Dermatologists must have a high index of suspicion, especially when skin features are associated with other earlier symptoms such as acroparesthesia, hypohidrosis, or heat intolerance. Once the diagnosis is established, prompt screening of family members should be performed. In all cases, a multidisciplinary team is necessary for the long-term follow-up and treatment. Keywords Fabry disease, angiokeratomas, lysosomal storage disorders Introduction Diffuse AKs are characterized by the presence of multiple lesions that affect more than 1 area of the skin. Although any Fabry disease (FD, also known as Anderson-Fabry disease or region of the skin can be affected, lesions usually localize to the angiokeratoma corporis diffusum [ACD]) is a rare X-linked bathing suit area (from the umbilicus to the upper thighs); this disease caused by the partial or complete deficiency of a lyso- phenotype is known as ACD. -
A Case of Extreme Hypercapnia
119 Emerg Med J: first published as 10.1136/emj.2003.005009 on 20 January 2004. Downloaded from CASE REPORTS A case of extreme hypercapnia: implications for the prehospital and accident and emergency department management of acutely dyspnoeic patients L Urwin, R Murphy, C Robertson, A Pollok ............................................................................................................................... Emerg Med J 2004;21:119–120 64 year old woman was brought by ambulance to the useful non-invasive technique to aid the assessment of accident and emergency department. She had been peripheral oxygen saturation. In situations of poor perfusion, Areferred by her GP because of increasing dyspnoea, movement and abnormal haemoglobin, however, this tech- cyanosis, and lethargy over the previous four days. On arrival nique may not reliably reflect PaO2 values. More importantly, of the ambulance crew at her home she was noted to be and as shown in our case, there is no definite relation tachycardic and tachypnoeic (respiratory rate 36/min) with a between SaO2 values measured by pulse oximetry and PaCO2 GCS of 5 (E 3, M 1, V 1). She was given oxygen at 6 l/min via values although it has been shown that the more oxygenated a Duo mask, and transferred to hospital. The patient arrived at the accident and emergency department 18 minutes later. In transit, there had been a clinical deterioration. The GCS was now 3 and the respiratory rate 4/min. Oxygen saturation, as measured by a pulse oximeter was 99%. The patient was intubated and positive pressure ventilation started. Arterial blood gas measurements taken at the time of intubation were consistent with acute on chronic respiratory failure (fig 1). -
Cocats 4 (Pdf)
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. 65, NO. 17, 2015 ª 2015 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 0735-1097/$36.00 PUBLISHED BY ELSEVIER INC. http://dx.doi.org/10.1016/j.jacc.2015.03.017 TRAINING STATEMENT ACC 2015 Core Cardiovascular Training Statement (COCATS 4) (Revision of COCATS 3) A Report of the ACC Competency Management Committee Task Force Introduction/Steering Committee Task Force 3: Training in Electrocardiography, Members Jonathan L. Halperin, MD, FACC Ambulatory Electrocardiography, and Exercise Testing (and Society Eric S. Williams, MD, MACC Gary J. Balady, MD, FACC, Chair Representation) Valentin Fuster, MD, PHD, MACC Vincent J. Bufalino, MD, FACC Martha Gulati, MD, MS, FACC Task Force 1: Training in Ambulatory, Jeffrey T. Kuvin, MD, FACC Consultative, and Longitudinal Cardiovascular Care Lisa A. Mendes, MD, FACC Valentin Fuster, MD, PHD, MACC, Co-Chair Joseph L. Schuller, MD Jonathan L. Halperin, MD, FACC, Co-Chair Eric S. Williams, MD, MACC, Co-Chair Task Force 4: Training in Multimodality Imaging Nancy R. Cho, MD, FACC Jagat Narula, MD, PHD, MACC, Chair William F. Iobst, MD* Y.S. Chandrashekhar, MD, FACC Debabrata Mukherjee, MD, FACC Vasken Dilsizian, MD, FACC Prashant Vaishnava, MD Mario J. Garcia, MD, FACC Christopher M. Kramer, MD, FACC Task Force 2: Training in Preventive Shaista Malik, MD, PHD, FACC Cardiovascular Medicine Thomas Ryan, MD, FACC Sidney C. Smith, JR, MD, FACC, Chair Soma Sen, MBBS, FACC Vera Bittner, MD, FACC Joseph C. Wu, MD, PHD, FACC J. Michael Gaziano, MD, FACC John C. Giacomini, MD, FACC Quinn R. Pack, MD Donna M.