DOCSLIB.ORG

Robert Jenkinson, MD

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Robert Jenkinson, MD 8/26/14 LIFE-THREATENING, INTRAOPERATIVE HEMODYNAMIC INSTABILITY IN A QUADRAPLEGIC Robert H. Jenkinson, M.D. Department of Anesthesiology University of Wisconsin Madison, WI Background o 57 year old quadraplegic male, remote C4-C5 spinal injury presenting for cystoscopy. n PMHx: Autonomic dysreflexia, OSA, neurogenic bowel/bladder. n Allergies: Sulfa drugs o Prior history of systolic blood pressure (SBP) near or above 200 mmHg while under GA for cystoscopy on multiple occasions. n Required nitroglycerine infusions. n Stable blood pressure with spinal anesthesia on one prior occasion. Case Description o L4-L5 spinal performed in OR n Intravenous midazolam (2mg) & fentanyl (50 mcg) n Intrathecal hyperbaric bupivacaine (12.5 mg) n Intravenous cefazolin (2g) o On return to supine position: n SBP rapidly decreased from baseline of 140 mmHg to 60 mmHg. n The patient became tachycardic. n Breathing pattern became shallow and bradypneic. n Level of responsiveness quickly decreased. 1 8/26/14 Case Description o Vasopressin and epinephrine boluses given. o Trachea intubated. Intra- arterial BP monitoring & central venous access established. § Vasopressin & epinephrine infusions started. o Diffuse blanching erythema noted. n No mucosal edema or wheezing. Case Description o Procedure cancelled. n Transported to medical ICU. n Weaned off vasopressors & extubated in 3 hours. n Serum tryptase 125 mcg/L (reference range 0.4 – 10.9). o Skin testing to bupivacaine: n No cutaneous, gastrointestinal, cardiovascular or respiratory symptoms. n No evidence of IgE-mediated hypersensitivity to bupivacaine. Discussion o Initial working diagnosis was a high or total spinal. o Tachycardia, skin changes and markedly elevated tryptase most consistent with anaphylactic reaction. n Cephalosporin challenge now pending. 2 8/26/14 Discussion o Elevated tryptase: n An effective marker of recent mast cell degranulation. o Laroche, D. et al. (1991) Anesthesiology 75: 945-949. n Correlation with subsequent positive skin testing. o Fisher, M et al. (1998) Br. J. Anaesthesia 80: 26-29. o Anaphylaxis can be an exceedingly difficult intraoperative diagnosis to make. 3 .
Load more

Recommended publications
  • A Sign It's Time for BOTOX®
    When OAB* due to MS† makes matters worse… A sign it’s time for BOTOX® Ask your patients if they still have leakage or can’t tolerate their current OAB medication *Overactive bladder. †Multiple sclerosis. Indication Detrusor Overactivity Associated With a Neurologic Condition BOTOX® for injection is indicated for the treatment of urinary incontinence due to detrusor overactivity associated with a neurologic condition (eg, SCI, MS) in adults who have an inadequate response to or are intolerant of an anticholinergic medication. IMPORTANT SAFETY INFORMATION, INCLUDING BOXED WARNING WARNING: DISTANT SPREAD OF TOXIN EFFECT Postmarketing reports indicate that the effects of BOTOX® and all botulinum toxin products may spread from the area of injection to produce symptoms consistent with botulinum toxin effects. These may include asthenia, generalized muscle weakness, diplopia, ptosis, dysphagia, dysphonia, dysarthria, urinary incontinence, and breathing difficulties. These symptoms have been reported hours to weeks after injection. Swallowing and breathing difficulties can be life threatening, and there have been reports of death. The risk of symptoms is probably greatest in children treated for spasticity, but symptoms can also occur in adults treated for spasticity and other conditions, particularly in those patients who have an underlying condition that would predispose them to these symptoms. In unapproved uses and in approved indications, cases of spread of effect have been reported at doses comparable to those used to treat Cervical Dystonia
    [Show full text]
  • Autonomic Dysreflexia – a Medical Emergency a Guide for Patients
    Autonomic Dysreflexia – A Medical Emergency A guide for patients Only applicable to T6 level and above Key Points • Autonomic Dysreflexia (AD) is a medical emergency that occurs due to a rapid rise in blood pressure in response to a harmful or painful stimulus below the level of your Spinal Cord Injury (SCI) • It occurs in people with SCI at T6 and above but has in rare occasions been reported in individuals with SCI as low as T8 • If left untreated your blood pressure can rise to dangerous levels, risking stroke, cardiac problems, seizures, even death • Typically there is a pounding headache as your blood pressure rises. Other symptoms can include redness and sweating above the level of your SCI, slow heart rate, goosebumps, nausea, nasal congestion, blurred vision, shortness of breath and anxiety • Some or all of the symptoms may be present • AD can be triggered by any continuous painful or irritating stimulus below the level of your lesion. The most common causes are related to the bladder or bowel • Relieving the cause of the AD will resolve your AD episode • If the cause cannot be found or treated, medication is required to lower your blood pressure which may require a visit to your nearest emergency department • All people with SCI at T6 and above should carry their Autonomic Dysreflexia Medical Emergency Card at all times • The best treatment for AD is prevention • People at risk of AD often carry an ‘AD Kit’ with them – items useful to resolve AD such as catheters and prescribed medication 1 What is Autonomic Dysreflexia? Autonomic Dysreflexia (AD) is a medical emergency.
    [Show full text]
  • Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal
    Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal Cord Injuries Authors: Dr James Middleton, Director, State Spinal Cord Injury Service, NSW Agency for Clinical Innovation. Dr Kumaran Ramakrishnan, Honorary Fellow, Rehabilitation Studies Unit, Sydney Medical School Northern, The University of Sydney, and Consultant Rehabilitation Physician & Senior Lecturer, Department of Rehabilitation Medicine, University Malaya. Dr Ian Cameron, Head of the Rehabilitation Studies Unit, Sydney Medical School Northern, The University of Sydney. Reviewed and updated in 2013 by the authors. AGENCY FOR CLINICAL INNOVATION Level 4, Sage Building 67 Albert Avenue Chatswood NSW 2067 PO Box 699 Chatswood NSW 2057 T +61 2 9464 4666 | F +61 2 9464 4728 E [email protected] | www.aci.health.nsw.gov.au Produced by the NSW State Spinal Cord Injury Service. SHPN: (ACI) 140038 ISBN: 978-1-74187-972-8 Further copies of this publication can be obtained from the Agency for Clinical Innovation website at: www.aci.health.nsw.gov.au Disclaimer: Content within this publication was accurate at the time of publication. This work is copyright. It may be reproduced in whole or part for study or training purposes subject to the inclusion of an acknowledgment of the source. It may not be reproduced for commercial usage or sale. Reproduction for purposes other than those indicated above, requires written permission from the Agency for Clinical Innovation. © Agency for Clinical Innovation 2014 Published: February 2014 HS13-136 ACKNOWLEDGEMENTS This document was originally published as a fact sheet for the Rural Spinal Cord Injury Project (RSCIP), a pilot healthcare program for people with a spinal cord injury (SCI) conducted within New South Wales involving the collaboration of Prince Henry & Prince of Wales Hospitals, Royal North Shore Hospital, Royal Rehabilitation Centre Sydney, Spinal Cord Injuries Australia and the Paraplegic & Quadriplegic Association of NSW.
    [Show full text]
  • Autonomic Hyperreflexia Associated with Recurrent Cardiac Arrest
    Spinal Cord (1997) 35, 256 ± 257 1997 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/97 $12.00 Autonomic hyperre¯exia associated with recurrent cardiac arrest: Case Report SC Colachis, III1 and DM Clinchot2 1Associate Professor and 2Assistant Professor, Department of Physical Medicine and Rehabilitation1, Director, SCI Rehabilitation, The Ohio State University, College of Medicine, Columbus, Ohio, USA Autonomic hyperre¯exia is a condition which may occur in individuals with spinal cord injuries above the splanchnic sympathetic out¯ow. Noxious stimuli can produce profound alterations in sympathetic pilomotor, sudomotor, and vasomotor activity, as well as disturbances in cardiac rhythm. A case of autonomic hyperre¯exia in a patient with C6 tetraplegia with recurrent ventricular ®brillation and cardiac arrest illustrates the profound eects of massive paroxysmal sympathetic activity associated with this condition. Keywords: autonomic hyperre¯exia; spinal cord injury; ventricular ®brillation Introduction Autonomic hyperre¯exia is a condition of paroxysmal by excessive sweating and ¯ushing. Past episodes of re¯ex sympathetic activity which occurs in response to autonomic hyperre¯exia were generally attributed to noxious stimuli in patients with spinal cord injuries re¯ex voiding, position changes and the presence of above the major splanchnic sympathetic out¯ow.1±3 pressure sores. The heightened sympathetic activity during an episode The attendant had completed the patient's morning of autonomic hyperre¯exia accounts for several of the bowel program, hygiene and dressing activities, and clinical features commonly observed including sudo- started to exit the apartment when he heard gasping. motor and pilomotor phenomenon,1,4 ± 6 vasomotor He returned to ®nd him pulseless, apneic, and sequelae,1 ± 4,7 and alterations in cardiac inotropic and cyanotic.
    [Show full text]
  • What Is the Autonomic Nervous System?
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.suppl_3.iii31 on 21 August 2003. Downloaded from AUTONOMIC DISEASES: CLINICAL FEATURES AND LABORATORY EVALUATION *iii31 Christopher J Mathias J Neurol Neurosurg Psychiatry 2003;74(Suppl III):iii31–iii41 he autonomic nervous system has a craniosacral parasympathetic and a thoracolumbar sym- pathetic pathway (fig 1) and supplies every organ in the body. It influences localised organ Tfunction and also integrated processes that control vital functions such as arterial blood pres- sure and body temperature. There are specific neurotransmitters in each system that influence ganglionic and post-ganglionic function (fig 2). The symptoms and signs of autonomic disease cover a wide spectrum (table 1) that vary depending upon the aetiology (tables 2 and 3). In some they are localised (table 4). Autonomic dis- ease can result in underactivity or overactivity. Sympathetic adrenergic failure causes orthostatic (postural) hypotension and in the male ejaculatory failure, while sympathetic cholinergic failure results in anhidrosis; parasympathetic failure causes dilated pupils, a fixed heart rate, a sluggish urinary bladder, an atonic large bowel and, in the male, erectile failure. With autonomic hyperac- tivity, the reverse occurs. In some disorders, particularly in neurally mediated syncope, there may be a combination of effects, with bradycardia caused by parasympathetic activity and hypotension resulting from withdrawal of sympathetic activity. The history is of particular importance in the consideration and recognition of autonomic disease, and in separating dysfunction that may result from non-autonomic disorders. CLINICAL FEATURES c copyright. General aspects Autonomic disease may present at any age group; at birth in familial dysautonomia (Riley-Day syndrome), in teenage years in vasovagal syncope, and between the ages of 30–50 years in familial amyloid polyneuropathy (FAP).
    [Show full text]
  • REVIEW Autonomic Assessment of Animals with Spinal Cord
    Spinal Cord (2009) 47, 2–35 & 2009 International Spinal Cord Society All rights reserved 1362-4393/09 $32.00 www.nature.com/sc REVIEW Autonomic assessment of animals with spinal cord injury: tools, techniques and translation JA Inskip1,2,4, LM Ramer1,2,4, MS Ramer1,2 and AV Krassioukov1,3 1International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada; 2Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada and 3Department of Medicine, Division of Physical Medicine and Rehabilitation, University of British Columbia, Vancouver, British Columbia, Canada Study design: Literature review. Objectives: To present a comprehensive overview of autonomic assessment in experimental spinal cord injury (SCI). Methods: A systematic literature review was conducted using PubMed to extract studies that incorporated functional motor, sensory or autonomic assessment after experimental SCI. Results: While the total number of studies assessing functional outcomes of experimental SCI increased dramatically over the past 27 years, studies with motor outcomes dramatically outnumber those with autonomic outcomes. Within the areas of autonomic dysfunction (cardiovascular, respiratory, gastrointestinal, lower urinary tract, sexual function and thermoregulation), not all aspects have been characterized to the same extent. Studies focusing on bladder and cardiovascular function greatly outnumber those on sexual function, gastrointestinal function and thermoregulation. This review addresses the disparity between well-established motor-sensory testing presently used in experimental animals and the lack of standardized autonomic testing following experimental SCI. Throughout the review, we provide information on the correlation between existing experimental and clinically used autonomic tests. Finally, the review contains a comprehensive set of tables and illustrations to guide the reader through the complexity of autonomic assessment and dysfunctions observed following SCI.
    [Show full text]
  • Cardiovascular Complications During the Acute Phase of Spinal Cord Injury
    Cardiovascular Complications during the Acute Phase of Spinal Cord Injury Mirkowski M Faltynek P Benton B McIntyre A Krassioukov A Teasell RW www.scireproject.com Version 7.0 Key Points Pseudoephedrine may be an effective adjuvant for the treatment of neurogenic shock during the acute phase post SCI; however, pseudoephedrine may require up to one month for effectiveness and may result in higher complication rates for older patients. The use of functional electrical stimulation in combination with tilt tables may be effective for the management of orthostatic hypotension during the acute and subacute phase post SCI. Tilt table verticalization may be effective for lowering heart rate in patients post SCI. Midodrine hydrochloride may be effective for the management of orthostatic hypotension during the acute phase post SCI. Methylprednisolone appear to not be effective for the management of heart rate variability post SCI. Hemodynamic support during the acute phase post SCI has been associated with improved neurological outcomes but no cause and effect relationship has been established. Oral albuterol appears to be effective for the management of bradycardia during the acute phase post SCI. Cardiac pacemaker implantation appears to be effective for the management of refractory bradycardia during the acute phase post SCI. Table of Contents 1.0 Executive Summary ................................................................................................................ 1 2.0 Methods ........................................................................................................................................
    [Show full text]
  • Electrical Stimulation-Evoked Contractions Blunt Orthostatic Hypotension in Sub-Acute Spinal Cord-Injured Individuals: Two Clinical Case Studies
    Spinal Cord (2015) 53, 375–379 & 2015 International Spinal Cord Society All rights reserved 1362-4393/15 www.nature.com/sc ORIGINAL ARTICLE Electrical stimulation-evoked contractions blunt orthostatic hypotension in sub-acute spinal cord-injured individuals: two clinical case studies NA Hamzaid1, LT Tean1, GM Davis1,2, A Suhaimi3 and N Hasnan3 Study design: Prospective study of two cases. Objectives: To describe the effects of electrical stimulation (ES) therapy in the 4-week management of two sub-acute spinal cord- injured (SCI) individuals (C7 American Spinal Injury Association Impairment Scale (AIS) B and T9 AIS (B)). Setting: University Malaya Medical Centre, Kuala Lumpur, Malaysia. Methods: A diagnostic tilt-table test was conducted to confirm the presence of orthostatic hypotension (OH) based on the current clinical definitions. Following initial assessment, subjects underwent 4 weeks of ES therapy 4 times weekly for 1 h per day. Post-tests tilt table challenge, both with and without ES on their rectus abdominis, quadriceps, hamstrings and gastrocnemius muscles, was conducted at the end of the study (week 5). Subjects’ blood pressures (BP) and heart rates (HR) were recorded every minute during pre- test and post-tests. Orthostatic symptoms, as well as the maximum tolerance time that the subjects could withstand head up tilt at 60°, were recorded. Results: Subject A improved his orthostatic symptoms, but did not recover from clinically defined OH based on the 20-min duration requirement. With concurrent ES therapy, 60° head up tilt BP was 89/62 mm Hg compared with baseline BP of 115/71 mm Hg. Subject B fully recovered from OH demonstrated by BP of 105/71 mm Hg during the 60° head up tilt compared with baseline BP of 124/77 mm Hg.
    [Show full text]
  • Pathophysiology of Autonomic Dysreflexia
    Spinal Cord (1998) 36, 761 ± 770 ã 1998 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/98 $12.00 http://www.stockton-press.co.uk/sc Pathophysiology of autonomic dysre¯exia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysre¯exic episodes S Vaidyanathan, BM Soni, P Sett, JWH Watt, T Oo and J Bingley Regional Spinal Injuries Centre, District General Hospital, Southport Merseyside PR8 6PN, UK Introduction: Spinal cord injury (SCI) results in disruption of synaptic in¯uences on the sympathetic preganglionic neurones. Remodelling of spinal cord circuits takes place in spinal neurones caudal to cord injury. There is an increased vascular alpha-adrenoceptor responsiveness, and peripheral aerent (bladder) stimulation in SCI subjects induces a marked noradrenaline spillover below the level of spinal lesion. These neurophysiological changes possibly contribute to the development of autonomic dysre¯exia, a condition of sympathetic hyper-excitability that develops after cervical, or upper dorsal cord injury with resultant paroxysmal rise in arterial pressure, and provide the scienti®c basis for the use of terazosin, a once-a-day, selective alpha-one adrenergic blocking drug. Objectives: The use of terazosin, a long-acting, alpha 1-selective blocking agent was investigated in SCI patients who developed recurrent symptoms of autonomic dysre¯exia, eg headache, sweating ¯ushing of the face together with an increase in the arterial pressure. Design: An open, prospective study of the ecacy of terazosin in controlling recurrent autonomic dysre¯exia in traumatic tetraplegic/paraplegic patients manifesting clinical features of dysre¯exia in the absence of an acute precipitating cause such as a blocked catheter.
    [Show full text]
  • Differential Diagnosis of Dizziness in SCI Jordan Cabrera, PT, DPT, NCS Jorge Neira, PT, DPT, NCS Learning Objectives
    Differential Diagnosis of Dizziness in SCI Jordan Cabrera, PT, DPT, NCS Jorge Neira, PT, DPT, NCS Learning Objectives • Participant will be able to identify the need to perform a basic oculomotor and vestibular screen to assist in the differential diagnosis of dizziness. • Participant will be able to identify ways to adapt their plan of care to address vestibular impairment with the SCI population. Introduction • When an SCI patient complains of dizziness, what do you assess first? • Dizziness can have various meanings based on – Symptoms – Culture/language of patient – Several causes • Important to address the cause of dizziness to optimize outcomes and participation What is Dizziness? • Types of Dizziness – Vertigo: False sense of movement, complaints of a sensation that the environment is spinning – Lightheadedness: feeling faint or pre-syncope symptoms – Disequilibrium: feeling “off-balance” or inability to walk • Many cultures may confuse dizziness with headache • Some patients may also complain of floating sensations, rocking, or swaying Sources of Dizziness in SCI • Autonomic Dysreflexia – Hypertension – Common Symptoms • Pounding headache • Profuse sweating and flushing above level of injury • Blurry vision • Nausea • Nasal Stuffiness • Goosebumps or clammy skin below level of injury Sources of Dizziness in SCI • Orthostatic Hypotension – Feeling faint – Pre-Syncope/Lightheadedness – Can include • Nausea • Fatigue • Pallor • Perioral and facial numbness Consider other reasons for dizziness • Why? • Individuals may have other sources
    [Show full text]
  • Clinical Practice Guidelines
    Clinical practice guidelines Version 2.3 June 2013 Page 1 05 – Obstetric 59 08 – Toxicology 131 10 – Other 213 CLINICAL PRACTICE GUIDELINES 01 -Breech delivery 60 01 -Alcohol toxidrome 132 01 -Abuse and assault 214 01 - Cardiac 3 02 -Cord prolapse 64 02 -Anticholinergic toxidrome 134 02 -Agitated patient 218 03 -Ectopic pregnancy 66 03 –Benzodiazepines 136 04 -Non SJANT transportation 222 01 -Acute coronary syndrome (ACS) 4 04 -Miscarriage 68 04 -Beta blocker toxidrome 138 05 -Patient refusal of treatment or 02 -Brady arrhythmia 8 05 -Normal cephalic delivery 70 05 -Calcium channel blocker toxicity 140 transport 226 03 -Broad complex tachycardia (BCT) 10 06 -Placental abruption 74 06 -Carbon monoxide 142 06 -Recognition of life extinct (ROLE) 232 04 -Cardiogenic shock 12 07 -Placenta previa 76 07 -Corrosives 144 and management of a deceased 05 -Narrow complex tachycardia (NCT) 14 08 -Pre-eclampsia 78 08 -Cyanide 146 person 06 -Pulmonary embolus (PE) 16 09 -Primary postpartum haemorrhage 80 09 -Gamma-hydroxybutyrate 148 07 -Standard cares 238 10 -Secondary postpartum haemorrhage82 10 -Marine envenomation 150 08 -Suicidal patient 240 02 - Environmental 19 11 -Shoulder dystocia 84 11 -Opioid toxicity 152 09 -Palliative care patients 242 01 -CBRIE 20 12 -Uterine inversion 88 12 -Organophosphate/cholinergic 154 02 -Dysbarism 22 13 -Uterine rupture 90 13 -Paraquat 156 03 -Hyperthermia 24 14 -Psychostimulant emergencies 158 04 -Hypothermia 26 06 – Respiratory 93 15 -Serotonin toxidrome 160 01 -Acute pulmonary oedema (APO) 94 16 -Snake bite 162
    [Show full text]
  • Spinal Injury Patients with Autonomic Dysreflexia
    Title: AUTONOMIC DYSREFLEXIA, PREVENTION OR Ref: 0901 Version 3 MANAGEMENT OF SPINAL INJURY PATIENTS WITH Classification: Guideline Spinal injury at T6 and above Directorate: Organisation Wide Due for Review: 20/04/21 Responsible Clinical Skills Facilitator Torbay and South Devon NHS Document Control for review: Foundation Trust (TSDFT) Community Nurse Manager, Community Nursing Team Clinical Lead Bladder & Bowel Care, Northern Devon Healthcare NHS Trust. Head of Midwifery Ratified by: Care and Clinical Policies Group Clinical Director of Pharmacy Chief Nurse Medical Director Applicability: Related to persons who have sustained a spinal cord injury at or above the 6th thoracic vertebrae These guidelines have been developed to assist the healthcare professionals involved with a clear and structured approach and one that hopes to minimise the likelihood of Autonomic Dysreflexia occurring. Introduction These guidelines have been written to assist the health care professionals with a clear plan of action to be followed to prevent an event of Autonomic Dysreflexia in those patients who are at risk of its occurrence. If it is not recognised early or if it is left untreated it can be fatal. By being aware of the signs and symptoms of this condition and treatment options available, the event can be managed in a safe and effective manner. Further episodes of Autonomic Dysreflexia can be avoided by educating patients on how they can implement prevention strategies. When assessing spinal injury patients on admission; a healthcare professional should ask the patient if they are aware of or have previously suffered from Autonomic Dysreflexia. It is important to record information from the patient if they had any previous episodes of Autonomic Dysreflexia in their medical notes under the Alert system.
    [Show full text]