Case report
Therapeutic hypothermia after prolonged cardiopulmonary resuscitation due to pulmonary thromboembolism. Case report
Hipotermia terapéutica post-reanimación cardiopulmonar prolongada en paro cardiaco debido a tromboembolismo pulmonar. Reporte de caso
Julian Alvarado Ramíreza, Hector Dario Arrovave Paramob, Fabian David Casas Arroyavec,
Corresponding author
fabiandavid68@yahoo.com
Corresponding author at: Hospital Universitario San Vicente Fundación, Calle 64N 51 D-154, Medellín, Colombia.
Corresponding author at: Hospital Universitario San Vicente Fundación, Calle 64N 51 D-154, Medellín, Colombia.
a Physician, Third Year Resident of Anesthesiology and Resuscitation, University of Antioquia, Medellín, Colombia
b Anesthesiologist, Specialist in Medicine and Critical Care. Intensivist. University Hospital San Vicente Fundación, Medellin. Professor of Anesthesiology, University of Antioquia, Medellín, Colombia
c Anesthesiologist, University Hospital San Vicente Fundación, Medellin. Professor of anesthesiology, University of Antioquia, Medellín, Colombia
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Reporte de caso" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Good neurological results following a CA are difficult to achieve. Any intervention during cardiopulmonary resuscitation (CPR) and in the next few hours after recovering spontaneous circulation (SC) is critical to reach this goal. Experimental trials both in humans and in animals show that therapeutic hypothermia (TH) improves the neurological and cardiovascular outcomes in these patients.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2</span></a> There is enough evidence to use moderate TH (32–34<span class="elsevierStyleHsp" style=""></span>°C) in ventricular tachycardia (VT) or ventricular fibrillation (VF), since it improves both, the neurological prognosis and mortality.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,3</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Clinical case</span><p id="par0010" class="elsevierStylePara elsevierViewall">41-year-old patient with distal femoral shaft fracture referred two days later to the University Hospital San Vicente Fundación (HUSVF) in Medellin for osteosynthesis. The patient has a history of untreated diabetes mellitus type II. Paraclinical tests: HbA1c, blood count, glycaemia, ionogram, renal function, PT and PTT normal. Functional class and cardiovascular examination are normal.</p><p id="par0015" class="elsevierStylePara elsevierViewall">The procedure is performed under spinal anesthesia, hyperbaric bupivacaine plus morphine, achieving a T10 level of aesthesia. 30<span class="elsevierStyleHsp" style=""></span>min into surgery, suddenly and unexpectedly, the patient develops cardiorespiratory arrest with PEA. CPR is administered, with capnography monitoring above 15<span class="elsevierStyleHsp" style=""></span>mmHg. The patient had not received thromboprophylactic treatment and the transthoracic ECG showed dilatation of the right ventricle and left-IV septal deviation, leading to a diagnosis of massive pulmonary thromboembolism (PTE). The patient received thrombolysis with tissue plasminogen activator as follows: initial 25<span class="elsevierStyleHsp" style=""></span>mg bolus followed by 25<span class="elsevierStyleHsp" style=""></span>mg in 30<span class="elsevierStyleHsp" style=""></span>min; then 50<span class="elsevierStyleHsp" style=""></span>mg in the next 30<span class="elsevierStyleHsp" style=""></span>min and 100<span class="elsevierStyleHsp" style=""></span>mg during the next hour, for a total of 200<span class="elsevierStyleHsp" style=""></span>mg.</p><p id="par0020" class="elsevierStylePara elsevierViewall">After initiating the resuscitation maneuvers, the patient recovers spontaneous circulation; a femoral arterial catheter is inserted and esophageal temperature monitoring is established after CPR. When the patient was admitted to the ICU, the temperature reported was 33<span class="elsevierStyleHsp" style=""></span>°C (Philips Mx 600 monitor) just with exposure to the OR temperature. The patient is left uncovered, keeping the esophageal temperatures under control between 32.5 and 33.5<span class="elsevierStyleHsp" style=""></span>°C for 18<span class="elsevierStyleHsp" style=""></span>h. No ionotropic support was required and the norepinephrine vasopressors initiated during resuscitation were gradually tapered and well tolerated in the first 24<span class="elsevierStyleHsp" style=""></span>h. The patient received target CVP and diuresis-guided water therapy (approximately 7000<span class="elsevierStyleHsp" style=""></span>ml of crystalloids and transfusion of 2 leukocyte depleted red blood cells). During this time the patient did not develop any new episodes of CA or severe arrhythmia. Volume controlled mechanical ventilation was used – 6<span class="elsevierStyleHsp" style=""></span>ml/kg – and no additional neuromuscular relaxation was needed besides the rapid intubation sequence with 1.2<span class="elsevierStyleHsp" style=""></span>mg/kg rocuronium, sedation analgesia with 100<span class="elsevierStyleHsp" style=""></span>mg/h fentanyl plus midazolam 2<span class="elsevierStyleHsp" style=""></span>mg/h. At the end of 18<span class="elsevierStyleHsp" style=""></span>h, the patient was warmed up to 37<span class="elsevierStyleHsp" style=""></span>°C with blankets at room temperature. 6<span class="elsevierStyleHsp" style=""></span>h later the patient was extubated free of complications. The PTE was confirmed through ventilation/perfusion ultrasound, visualizing multiple apparently residual subsegmental thrombi. The patient experienced no significant bleeding and no neurological deficit.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0025" class="elsevierStylePara elsevierViewall">Survival and neurological recovery following a CA are the most significant outcomes that vary depending on the underlying pathology, the time elapsed prior to receiving care after the arrest, the initial rhythm and the resuscitation modality.<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a> The survival rate at discharge of the cases that achieve spontaneous circulation has been below 10%.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The stages of the post-cardiac arrest syndrome are: phase one includes the period immediately after returning to spontaneous circulation and up to 20<span class="elsevierStyleHsp" style=""></span>min later. It is characterized by cardiovascular dysfunction, with a corresponding 63% mortality. During the intermediate phase – between 6 and 12<span class="elsevierStyleHsp" style=""></span>h – neurological damage develops accounting for 17% mortality and, to a larger extent, for morbidity at discharge. Finally, the recovery period accounts for 7% mortality from infectious complications and multiple organ failure (MOF). At the end of these three stages, the survival rate is 13%, of which 4% are free from any neurological damage.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,7</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Neurological damage is mediated by several mechanisms.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Early on, the lack of cerebral blood flow depletes the ATP reserves. In the intermediate stage, the release of excitatory amino acids activates the cytotoxic pathways. Then at the late stage, the rupture of the blood–brain barrier worsens the cerebral edema and cell death.</p><p id="par0040" class="elsevierStylePara elsevierViewall">The TH neuroprotective mechanisms are: 6–10% reduction in cerebral metabolism per every degree Celsius of temperature drop; attenuation of the cytotoxic cascade and oxygen reactive species; decreased apoptosis between 48 and 72 after the arrest; reduced inflammatory response; and finally, blood–brain barrier protection.<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9,10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">There are some controversies about which method performs better in achieving the TH goal; however, there is strong literature support in favor of simple physical methods such as cold blankets, ice, or 4<span class="elsevierStyleHsp" style=""></span>°C isotonic solution. Regardless of the method chosen, the key is to have standardized institutional protocols.<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7,9</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">The following are the TH phases:</p><p id="par0055" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Induction</span>: Lower the body temperature to between 32 and 34<span class="elsevierStyleHsp" style=""></span>°C as fast as possible; speed is not associated with adverse events. The recommendation is to start lowering the temperature when initiating the resuscitation maneuvers since this has shown to improve the hemodynamic profile of patients.<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">10–12</span></a> A 2000<span class="elsevierStyleHsp" style=""></span>cc 0.9% saline infusion at 4<span class="elsevierStyleHsp" style=""></span>°C is the first line approach at the University Hospital SVF for achieving the goal.</p><p id="par0060" class="elsevierStylePara elsevierViewall">The TH-associated adverse events are: hypovolemia, diastolic dysfunction, hypokalemia, hypomagnesaemia, hypophosphatemia, hyperglycemia, coagulopathy, arrhythmias and endocraneal hypertension. Most of them are easily controllable.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Since TH causes dynamic changes that favor cardiovascular stability, if instability occurs the underlying cause must be identified.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Maintenance</span>: According to the AHA it should last between 12 and 24<span class="elsevierStyleHsp" style=""></span>h, maintaining a range between 32° and 34° with changes not exceeding 0.5<span class="elsevierStyleHsp" style=""></span>°C. When tremors occur, despite being a good prognostic sign, these should be tempered by improving the sedation or using neuromuscular relaxants.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13,14</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">During this period, the clinical signs of infections will be weakened and so any mild indication of infection shall be studied and treated on a timely basis.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Re-Warming</span>: Inadequate re –warming remove the benefits of TH and is associated with cell injury, water–electrolyte disorders and increases insulin sensitivity. Consequently, active warming should not be faster than 0.5<span class="elsevierStyleHsp" style=""></span>°C/h.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">The good results in this particular case are due to the patient's age and little comorbidity that partially account for a faster and better cardiovascular recovery. Secondly, the arrest was witnessed and hence the response time was immediate and coordinate by expert practitioners. Third, though the arrest rhythm was PEA, this rhythm was not a degeneration of a malignant arrhythmia or a heart attack, which improves the prognosis. And lastly, the implementation of thrombolysis as specific treatment, considerably improved the patient's survival with little associated adverse events, despite the high dose used.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusions</span><p id="par0085" class="elsevierStylePara elsevierViewall">TH is becoming increasing popular in situations beyond the non-shockable rhythms, mainly due to a better understanding of its protective mechanisms, particularly neuronal, and to the increasing evidence of the last few years. The indications for TH are not just growing, but the contraindications are decreasing because the side effects are easily manageable. Nevertheless, the huge impact of this therapy is that it has been adopted as part of the institutional protocols, regardless of the method used. It should be kept in mind that the conventional cooling methods are probably the most cost-effective and easy to use in every scenario. Although the perioperative environment offers the least evidence, it is well known that the faster the TH is established, the short and long term outcomes are potentially improved. However, further trials with an improved epidemiological profile are needed to support this approach.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Funding</span><p id="par0090" class="elsevierStylePara elsevierViewall">None.</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflicts of interest</span><p id="par0095" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:2 [ "identificador" => "xres371179" "titulo" => "Abstract" ] 1 => array:2 [ "identificador" => "xpalclavsec350346" "titulo" => "Keywords" ] 2 => array:2 [ "identificador" => "xres371178" "titulo" => "Resumen" ] 3 => array:2 [ "identificador" => "xpalclavsec350345" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Clinical case" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Conclusions" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Funding" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Conflicts of interest" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2014-03-18" "fechaAceptado" => "2014-05-28" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec350346" "palabras" => array:5 [ 0 => "Hypothermia" 1 => "Pulmonary Embolism" 2 => "Heart Arrest" 3 => "Cardiopulmonary Resuscitation" 4 => "Anesthesia" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec350345" "palabras" => array:5 [ 0 => "Hipotermia" 1 => "Embolia pulmonar" 2 => "Paro Cardíaco" 3 => "Resucitación cardiopulmonar" 4 => "Anestesia" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">This is a report of a 41-year-old patient undergoing femur osteosynthesis (OS) who develops intraoperative cardiac arrest (CA) with pulseless electrical activity (PEA). Massive pulmonary thromboembolism (PTE) was diagnosed as the cause for the CA and a thrombolysis performed 30<span class="elsevierStyleHsp" style=""></span>min later reestablished spontaneous circulation with no new CA events. Therapeutic hypothermia (TH) was then established with local measures for 18<span class="elsevierStyleHsp" style=""></span>h for brain protection. The patient was extubated 24<span class="elsevierStyleHsp" style=""></span>h later with no neurological deficit. There is an increasing evidence of TH and its protective mechanisms in patients with non-shockable arrest rhythms leading to a widespread use of the technique in various institutions around the world, with particular emphasis on neurological outcomes. This article discusses a review of the current literature on TH, in addition to describing each of the stages in TH and how to approach these stages.</p>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Se reporta un caso de un paciente de 41 años quien es llevado a osteosíntesis (OS) de fémur y que presenta paro cardiaco (PC) intraoperatorio con ritmo de actividad eléctrica sin pulso. Se diagnostica tromboembolismo pulmonar masivo como causa del PC y 30 min después se hace trombólisis, obteniéndose circulación espontánea sin nuevos episodios de PC. Posteriormente se instaura hipotermia terapéutica (HT) con medidas locales durante 18 h para protección cerebral. El paciente es extubado 24 h después sin ningún déficit neurológico. Es importante entender que la evidencia actual de la HT en pacientes con ritmos de paro no desfibrilables y sus mecanismos de protección es creciente, y que cada vez más se está imple-mentando esta técnica en los diferentes centros del mundo, sobre todo haciendo énfasis en desenlaces neurológicos. En este artículo se hace una revisión de la literatura actual sobre HT, además de describir cada una de las etapas de la HT y la forma en que se deben abordar.</p>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Ramirez JA, Paramo HDA, Arroyave FDC. Hipotermia terapéutia pos reanimación cardio pulmonar prolongado en paro cardiaco debido a tromboembolismo pulmonar. Reporte de caso. Rev Colomb Anestesiol. 2014;42:317–320.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:14 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest" "autores" => array:1 [ 0 => array:2 [ "colaboracion" => "The Hypothermia After Cardiac Arrest Study Group" "etal" => false ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1056/NEJMoa012689" "Revista" => array:6 [ "tituloSerie" => "N Engl J Med" "fecha" => "2002" "volumen" => "346" "paginaInicial" => "549" "paginaFinal" => "556" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/11856793" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Therapeutic hypothermia following resuscitation" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "K. 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