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    Uploaded by

    Carlos Hernández
    772 views191 pages
    This document contains the title and content for a medical graphic about an overlapping fracture. The content includes copyright information and links to print or email the graphic. It also contains the image itself, which is encoded as a base64 string to embed it in the document.

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    This document contains the title and content for a medical graphic about an overlapping fracture. The content includes copyright information and links to print or email the graphic. It also contains the image itself, which is encoded as a base64 string to embed it in the document.

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    © All Rights Reserved
    Download as TXT, PDF, TXT or read online from Scribd
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    772 views191 pages

    15

    Uploaded by

    Carlos Hernández
    This document contains the title and content for a medical graphic about an overlapping fracture. The content includes copyright information and links to print or email the graphic. It also contains the image itself, which is encoded as a base64 string to embed it in the document.

    Copyright:

    © All Rights Reserved
    Download as TXT, PDF, TXT or read online from Scribd
    Flag for inappropriate content
    Download as txt, pdf, or txt
    of 191

    var title_f0_15_240="Overlapping fracture";

    var content_f0_15_240=[" <div id=\"graphicsToolbar\">",


    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=EM
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    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
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    " <a class=\"icontxt textLink\" href=\"?imageKey=EM
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    " Print",
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    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
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    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 540px\">",
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    " Overlapping complete fracture of radius and ulna (100 percent displaced) in a
    7-year-old child.",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Courtesy of Paula Schweich, MD.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
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    " Phenylephrine: Patient drug information",
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    connection in children (The Basics)";
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    " <dl>",
    " <dt class=\"basics\">",
    " The Basics",
    " </dt>",
    " <dd>",
    " <a href=\"UTD.htm?6/31/6642\">",
    " Patient information: Atrial septal defect (The Basics)",
    " </a>",
    " </dd>",
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    " <a href=\"UTD.htm?30/31/31218\">",
    " Patient information: Newborn appearance (The Basics)",
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    " <div id=\"topicTitle\">",
    " Patient information: Total anomalous pulmonary venous connection in children
    (The Basics)",
    " </div>",
    " <span class=\"view\">",
    " View in",
    " <a class=\"lang\" href=\"./es-419/total-anomalous-pulmonary-venous-
    connection-in-children-the-basics?source=topic_page\">",
    " Spanish",
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    " <a class=\"contributor contributor_credentials\" href=\"./authors-and-
    editors/patient-information\">",
    " Written by the doctors and editors at UpToDate",
    " </a>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H257226461\">",
    " <span class=\"h1\">",
    " What is a total anomalous pulmonary venous connection?",
    " </span>",
    " &nbsp;&mdash;&nbsp;A total anomalous pulmonary venous connection is a rare
    condition that involves the veins that carry blood from the lungs to the heart.
    These veins aren&rsquo;t connected to the correct spot in the heart. Doctors call
    this condition &ldquo;TAPVC&rdquo; for short.",
    " </p>",
    " <p>",
    " Normally, blood flows through the heart and lungs in the following way:
    Blood from the body comes into the right atrium. It flows into the right ventricle
    and then to the lungs. In the lungs, the blood picks up oxygen. Then the blood goes
    into the left atrium and into the left ventricle. From there, the heart pumps the
    blood around the body (",
    " <a class=\"graphic graphic_figure graphicRef83996 \" href=\"UTD.htm?
    33/36/34372\">",
    " figure 1",
    " </a>",
    " ).",
    " </p>",
    " <p>",
    " In a TAPVC, blood from the lungs does not return to the left atrium.
    Instead, it returns to the right atrium. Or the blood returns to another vein in
    the body and then to the right atrium. As a result, the blood with the oxygen
    can&rsquo;t easily get to the organs in the body. Plus, sometimes the veins
    carrying the blood from the lungs get blocked. Both of these things can cause
    symptoms.",
    " </p>",
    " <p>",
    " There are different types of TAPVC, depending on where the veins from the
    lungs attach. TAPVC is a condition that children are born with. Doctors don&rsquo;t
    know what causes it.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H257226493\">",
    " <span class=\"h1\">",
    " What are the symptoms of a TAPVC?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Symptoms depend on the type of TAPVC and whether the
    veins carrying blood from the lungs are blocked.",
    " </p>",
    " <p>",
    " Babies whose condition is severe get very sick within the first 12 hours
    after birth. Their skin looks blue and they have a lot of trouble breathing.",
    " </p>",
    " <p>",
    " Babies whose condition is not as severe usually start having symptoms later
    on. These can include:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Breathing faster than usual",
    " </li>",
    " <li>",
    " Not feeding well",
    " </li>",
    " <li>",
    " Not gaining weight or growing well",
    " </li>",
    " <li>",
    " Skin that looks blue",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H257226508\">",
    " <span class=\"h1\">",
    " Will my baby need tests?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Yes. The test most often done to check for a TAPVC is an
    echocardiogram (also called an &ldquo;echo&rdquo;). This test uses sound waves to
    create a picture of the heart as it beats. It shows how blood flows through the
    heart and lungs.",
    " </p>",
    " <p>",
    " Sometimes, doctors do other imaging tests. Imaging tests create pictures of
    the inside of the body.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H257226523\">",
    " <span class=\"h1\">",
    " How is a TAPVC treated?",
    " </span>",
    " &nbsp;&mdash;&nbsp;A TAPVC is treated with surgery. During surgery, the
    doctor will fix or move the veins so that blood from the lungs gets to the correct
    place.",
    " </p>",
    " <p>",
    " But before your child has surgery, his or her breathing and general medical
    condition need to be under control. If your baby&rsquo;s condition is severe, he or
    she might need 1 or more of the following before surgery:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Extra oxygen or other medicines",
    " </li>",
    " <li>",
    " A breathing tube &ndash; This is a tube that goes down the throat and into
    the lungs. The other end is attached to a machine that helps with breathing.",
    " </li>",
    " <li>",
    " A heart procedure that helps the blood with oxygen get to the left
    atrium",
    " </li>",
    " <li>",
    " To be on a heart and lung machine &ndash; This machine, which doctors call
    &ldquo;ECMO,&rdquo; takes over the jobs of the heart and lungs. It pumps blood from
    your baby&rsquo;s body, gives it oxygen, and pumps it back into the body.",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H257226538\">",
    " <span class=\"h1\">",
    " What will my child&rsquo;s life be like after treatment?",
    " </span>",
    " &nbsp;&mdash;&nbsp;It depends on your child&rsquo;s individual situation.
    All children with TAPVC need to see their heart doctor for regular follow-ups.",
    " </p>",
    " <p>",
    " Sometimes after surgery, a problem can happen with 1 of the veins. If this
    happens, a child might need surgery again. Also, children sometimes have heart
    rhythm problems after their surgery.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H257226553\">",
    " <span class=\"h1\">",
    " More on this topic",
    " </span>",
    " </p>",
    " <p>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?30/31/31218?
    source=see_link\">",
    " Patient information: Newborn appearance (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?6/31/6642?
    source=see_link\">",
    " Patient information: Atrial septal defect (The Basics)",
    " </a>",
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    /9k=);\">",
    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Courtesy of Drucilla J Roberts, MD.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_243=[""].join("\n");
    var outline_f0_15_243=null;
    var title_f0_15_244="Septated cystic hygroma";
    var content_f0_15_244=[" <div id=\"graphicsToolbar\">",
    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=OBGYN
    %2F61492&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=OBGYN
    %2F61492&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\"
    title=\"Print this page\">",
    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 470px\">",
    " <div class=\"ttl\">",
    " Sagittal view of the cystic hygroma demonstrating the presence of septations",
    " </div>",
    " <div class=\"cntnt\" style=\"width: 432px; height: 324px; background-image:
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    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Courtesy of Lynn Simpson, MD.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_244=[""].join("\n");
    var outline_f0_15_244=null;
    var title_f0_15_245="Muscle compartments of the foot";
    var content_f0_15_245=[" <div id=\"graphicsToolbar\">",
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    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
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    " <a class=\"icontxt textLink\" href=\"?imageKey=SURG
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    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
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    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
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    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 552px\">",
    " <div class=\"ttl\">",
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    Z);\">",
    " </div>",
    " <div class=\"lgnd\">",
    " Compartments of the foot:",
    " <ul>",
    " <li>",
    " Interosseous (turqoise) &mdash; Interosseus muscles, each in its own
    compartment.",
    " </li>",
    " <li>",
    " Calcaneal (pink) &mdash; Flexor digitorum brevis, quadratus plantae and
    adductor hallucis.",
    " </li>",
    " <li>",
    " Lateral (green) &mdash; Flexor digiti minimi and abductor digiti quinti.",
    " </li>",
    " <li>",
    " Medial (red) &mdash; Abductor hallucis and flexor hallucis brevis muscles.",
    " </li>",
    " <li>",
    " Superficial (blue) &mdash; Flexor digitorum brevis, lumbricals, flexor
    digitorum longus tendons.",
    " </li>",
    " </ul>",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_245=[""].join("\n");
    var outline_f0_15_245=null;
    var title_f0_15_246="Autoimmune lymphoproliferative syndrome (ALPS): Management and
    prognosis";
    var content_f0_15_246=[" <noscript>",
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    " <!-- TC:TOPIC_PAGE -->",
    " <div id=\"topicContent\">",
    " <div id=\"topicTitle\">",
    " Autoimmune lymphoproliferative syndrome (ALPS): Management and prognosis",
    " </div>",
    " <div id=\"topicContributors\">",
    " <div>",
    " <a id=\"authors\">",
    " </a>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/15/246/contributors\">",
    " Author",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/246/contributors\">",
    " Jack JH Bleesing, MD, PhD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/15/246/contributors\">",
    " Section Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/246/contributors\">",
    " E Richard Stiehm, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/15/246/contributors\">",
    " Deputy Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/246/contributors\">",
    " Elizabeth TePas, MD, MS",
    " </a>",
    " <br/>",
    " </div>",
    " </div>",
    " <div id=\"disclosures\">",
    " <a href=\"UTD.htm?0/15/246/contributor-disclosure\" target=\"_blank\">",
    " Disclosures",
    " </a>",
    " </div>",
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    " <span>",
    " All topics are updated as new evidence becomes available and our",
    " </span>",
    " <a href=\"/home/editorial-policy\" target=\"_blank\">",
    " peer review process",
    " </a>",
    " <span>",
    " is complete.",
    " </span>",
    " </div>",
    " <div id=\"literatureReviewDate\">",
    " <span class=\"emphasis\">",
    " Literature review current through:",
    " </span>",
    " Oct 2013.",
    " <span class=\"pipeSpace\">",
    " |",
    " </span>",
    " <span class=\"emphasis\">",
    " This topic last updated:",
    " </span>",
    " Aug 20, 2012.",
    " </div>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H20229218\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;Autoimmune lymphoproliferative syndrome (ALPS) is
    characterized by dysregulation of the immune system, due to an inability to
    regulate lymphocyte homeostasis through the process of lymphocyte apoptosis (a form
    of programmed cell death).",
    " </p>",
    " <p>",
    " This topic reviews management of ALPS. The epidemiology, genetics,
    pathogenesis, clinical manifestations, laboratory findings, diagnosis, and
    differential diagnosis of ALPS are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/58/30629?
    source=see_link\">",
    " \"Autoimmune lymphoproliferative syndrome (ALPS): Epidemiology and
    pathogenesis\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/36/30279?
    source=see_link\">",
    " \"Autoimmune lymphoproliferative syndrome (ALPS): Clinical features and
    diagnosis\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567210\">",
    " <span class=\"h1\">",
    " MANAGEMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;Management of ALPS focuses upon three aspects: treatment of
    disease manifestations,",
    " <span class=\"nowrap\">",
    " treatment/prevention",
    " </span>",
    " of disease and treatment complications, and curative therapy [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/1\">",
    " 1",
    " </a>",
    " ]. Most experience is confined to patients with ALPS-FAS.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567217\">",
    " <span class=\"h2\">",
    " Evaluation and monitoring following initial diagnosis",
    " </span>",
    " &nbsp;&mdash;&nbsp;The presence and extent (disease manifestations and disease
    burden) of lymphoproliferation",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " autoimmunity should be determined before initiating therapy in an individual
    newly diagnosed with ALPS.",
    " </p>",
    " <p>",
    " This can be achieved with a combination of physical examination, imaging
    studies (eg, computed tomography [CT] scan",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " positron emission tomography [PET] scans) of body areas thought to be involved
    (typically neck, chest, abdomen, and pelvis), and laboratory evaluation that
    includes measuring the size of the DNT cell compartment, the level of biomarkers
    (eg, vitamin B12, IL-10, FasL), blood counts, and the presence and nature of
    autoantibodies (eg, directed at blood cells). In patients deemed to need
    immunosuppressive therapy, one should also initiate a basic investigation of the
    integrity of immune system, particularly in young patients. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/58/43945?
    source=see_link\">",
    " \"Laboratory evaluation of the immune system\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " This evaluation should also include an assessment for lymphoma in patients
    with extensive lymphadenopathy, especially those with constitutional symptoms (eg
    fever, weight loss, night sweats). PET imaging may be helpful in this regard, since
    it is often difficult to distinguish between benign (ALPS-specific) lymphadenopathy
    and malignant lymphoma that are typically present concomitantly. PET scans can
    direct the surgeon to the node or nodes most likely to be of diagnostic value.
    Investigation for lymphoma is particularly important if immunosuppressive",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " immunomodulating agents are contemplated, since lymphoma development may be
    altered",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " masked by the use of these agents.",
    " </p>",
    " <p>",
    " There is some evidence to suggest that periodic surveillance using combined
    anatomical (ie, CT scan) and",
    " <span class=\"nowrap\">",
    " functional/metabolic",
    " </span>",
    " (ie, PET scan) imaging may be helpful, although more long-term data collection
    is needed to determine the cost to benefit ratio of expensive imaging [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/2\">",
    " 2",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Many laboratory findings, including the number of DNT cells and amounts of IL-
    10 and other biomarkers, not only serve a diagnostic purpose, but also can be used
    to monitor disease activity and response to therapy.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567224\">",
    " <span class=\"h2\">",
    " Treatment of disease manifestations",
    " </span>",
    " &nbsp;&mdash;&nbsp;The management of disease manifestations is focused on
    the",
    " <span class=\"nowrap\">",
    " control/treatment",
    " </span>",
    " of lymphoproliferation",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " autoimmunity, and the treatment of lymphoma [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/3-8\">",
    " 3-8",
    " </a>",
    " ]. Treatment of lymphoproliferation and autoimmune disease in ALPS is based
    upon observational data and clinical experience, since there are no randomized
    trials. Therapy is individualized and the choice of agent depends upon many
    patient-specific factors and practitioner preference.",
    " </p>",
    " <p>",
    " Once initiated, immunosuppressive",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " immunomodulating therapy may be difficult to stop. The development of
    clinically relevant autoimmune cytopenias often indicates a new phase in the course
    of ALPS in a particular patient. Therapies that affect the immune system cannot be
    used for extended periods of time (years) without complications. For example, long-
    term use of glucocorticoids is associated with obesity, growth retardation,
    hypertension, cataracts,",
    " <span class=\"nowrap\">",
    " osteopenia/osteoporosis",
    " </span>",
    " leading to pathologic bone fractures, and diabetes, among others. Long-term
    use of antiproliferative T cell agents (eg,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?31/39/32368?source=see_link\">",
    " cyclosporine",
    " </a>",
    " ,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/14/32992?source=see_link\">",
    " tacrolimus",
    " </a>",
    " ) may cause significant infections and renal function abnormalities. In
    addition, the immune system may not tolerate suppression for prolonged periods of
    time. Resolution of ALPS manifestations after years of therapy may be due to
    chronic immunosuppression rather than permanent remission of ALPS, and indicates
    the need for an assessment of overall immune competence. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?26/47/27386?
    source=see_link\">",
    " \"Major side effects of systemic glucocorticoids\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/0/29706?
    source=see_link\">",
    " \"Secondary immune deficiency induced by drugs and biologics\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H3894358\">",
    " <span class=\"h3\">",
    " Lymphoproliferation",
    " </span>",
    " &nbsp;&mdash;&nbsp;Manifestations of lymphoproliferation can be suppressed
    with the use of immunosuppressive agents, such as glucocorticoids,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?31/39/32368?source=see_link\">",
    " cyclosporine",
    " </a>",
    " ,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?5/39/5753?source=see_link\">",
    " sirolimus",
    " </a>",
    " ,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/14/32992?source=see_link\">",
    " tacrolimus",
    " </a>",
    " , or",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/29/4569?source=see_link\">",
    " mycophenolate",
    " </a>",
    " mofetil [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/3,9,10\">",
    " 3,9,10",
    " </a>",
    " ]. The benefits of immunosuppression, however, are balanced by the side
    effects. In addition, lymphadenopathy, as well as splenomegaly",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " hepatomegaly, return once immunosuppression is discontinued [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/3\">",
    " 3",
    " </a>",
    " ]. Thus, we suggest use of immunosuppressive therapy only for severe
    complications of lymphoproliferation (eg, airway obstruction)",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " in the presence of concomitant autoimmune manifestations.",
    " </p>",
    " <p>",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/29/4569?source=see_link\">",
    " Mycophenolate",
    " </a>",
    " mofetil is typically well tolerated and requires little monitoring, making it
    our preferred agent with which to start therapy. It appears to induce modest
    improvement in lymphadenopathy and some improvement in splenomegaly (in some
    patients) and laboratory markers, such as lymphocyte counts and IL-10 and vitamin
    B12 levels. Dose and duration of therapy should be individualized to the patient.
    It is reasonable to determine a minimal dose that accomplishes the goals of
    therapy.",
    " </p>",
    " <p>",
    " Early experience with",
    " <a class=\"drug drug_general\" href=\"UTD.htm?5/39/5753?source=see_link\">",
    " sirolimus",
    " </a>",
    " suggests that this agent may affect lymphoproliferation in a more sustained
    manner than other immunosuppressive agents, as demonstrated by more significant
    reduction in adenopathy, splenomegaly, and biomarkers [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/10\">",
    " 10",
    " </a>",
    " ]. This is balanced by the fact that sirolimus requires monitoring of levels,
    side effects, and complications, including infections. On the other hand, it is
    less mutagenic than",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/29/4569?source=see_link\">",
    " mycophenolate",
    " </a>",
    " mofetil,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/14/32992?source=see_link\">",
    " tacrolimus",
    " </a>",
    " , and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?31/39/32368?source=see_link\">",
    " cyclosporine",
    " </a>",
    " [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/11\">",
    " 11",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The author&rsquo;s approach is to determine if therapy is needed, based upon
    considerations discussed above. The author starts with the least immunosuppressive
    agent to accomplish treatment goals. In most patients, this can be achieved with",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/29/4569?source=see_link\">",
    " mycophenolate",
    " </a>",
    " , with or without a short course (approximately two to three weeks) of",
    " <a class=\"drug drug_general\" href=\"UTD.htm?37/43/38585?source=see_link\">",
    " prednisone",
    " </a>",
    " . The author use clinical response, physical examination (eg, degree of
    splenomegaly), and biomarkers to determine response and guide changes in drug dose
    (duration in therapy). In patients with insufficient response to mycophenolate,
    concomitant (or new) autoimmunity, or issues with mycophenolate, the author often
    initiates",
    " <a class=\"drug drug_general\" href=\"UTD.htm?5/39/5753?source=see_link\">",
    " sirolimus",
    " </a>",
    " , starting with a dose to keep drug levels at the lower end of normal.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567231\">",
    " <span class=\"h3\">",
    " Autoimmune manifestations",
    " </span>",
    " &nbsp;&mdash;&nbsp;Autoimmune manifestations typically respond to short
    courses of immunosuppressive agents. Splenectomy is",
    " <strong>",
    " not",
    " </strong>",
    " recommended in patients with ALPS, due to the reported lack of sustained
    therapeutic benefit and increased incidence of postsplenectomy sepsis in both
    children and adults despite presplenectomy vaccinations and postsplenectomy
    antibiotic prophylaxis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/12\">",
    " 12",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/29/4569?source=see_link\">",
    " Mycophenolate",
    " </a>",
    " mofetil",
    " <a class=\"drug drug_general\" href=\"UTD.htm?31/39/32368?
    source=see_link\">",
    " cyclosporine",
    " </a>",
    " ,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/14/32992?
    source=see_link\">",
    " tacrolimus",
    " </a>",
    " , and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?5/39/5753?source=see_link\">",
    " sirolimus",
    " </a>",
    " are effective in chronic recalcitrant autoimmune cytopenias and may spare
    glucocorticoid usage [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/8,10\">",
    " 8,10",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " <a class=\"drug drug_general\" href=\"UTD.htm?40/12/41161?
    source=see_link\">",
    " Rituximab",
    " </a>",
    " has been used successfully in the treatment of refractory cytopenias in
    ALPS, although it is not yet known how long affected individuals will remain in
    clinical remission [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/8,13\">",
    " 8,13",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " High-dose intravenous immune globulin (IVIG) is sufficient to control
    cytopenias in some patients [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/3\">",
    " 3",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " Severe (recalcitrant) cytopenias or other potentially life-threatening
    autoimmune manifestations may require the use of plasmapheresis in combination with
    other modalities.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The author&rsquo;s approach is to use a combination of immunosuppressive and
    immunomodulating agents. Depending upon severity, this can be high-dose IVIG, a
    course of",
    " <a class=\"drug drug_general\" href=\"UTD.htm?37/43/38585?source=see_link\">",
    " prednisone",
    " </a>",
    " and initiation of a T cell agent (eg,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/29/4569?source=see_link\">",
    " mycophenolate",
    " </a>",
    " ) or switching to a more potent T cell agent (eg, from mycophenolate to",
    " <a class=\"drug drug_general\" href=\"UTD.htm?5/39/5753?source=see_link\">",
    " sirolimus",
    " </a>",
    " or",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/14/32992?source=see_link\">",
    " tacrolimus",
    " </a>",
    " ). If high-dose IVIG does not",
    " <span class=\"nowrap\">",
    " achieve/maintain",
    " </span>",
    " remission (which is commonly the case in ALPS), the author uses",
    " <a class=\"drug drug_general\" href=\"UTD.htm?40/12/41161?source=see_link\">",
    " rituximab",
    " </a>",
    " as the immunomodulating agent, keeping in mind that the patient may require
    immune globulin replacement secondary to development of hypogammaglobulinemia.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567238\">",
    " <span class=\"h3\">",
    " Lymphoma",
    " </span>",
    " &nbsp;&mdash;&nbsp;Lymphoma is treated according to conventional protocols
    (see specific treatment topics for each type of lymphoma). The presence of
    defective Fas-mediated apoptosis does not appear to hinder the response to
    chemotherapeutic agents or radiation.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567245\">",
    " <span class=\"h2\">",
    " Prevention of complications",
    " </span>",
    " &nbsp;&mdash;&nbsp;Most complications are the results of immunosuppressive and
    immunomodulating agents and relate to the increased risk of infections. Intravenous
    or subcutaneous immune globulin therapy is warranted in some cases, as well as
    antimicrobials to prevent opportunistic, fungal, and viral infections. Infections
    caused by immunosuppressive and immunomodulating agents need to be thoroughly
    investigated and aggressively treated. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/0/29706?
    source=see_link\">",
    " \"Secondary immune deficiency induced by drugs and biologics\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " In patients who have had a splenectomy, penicillin prophylaxis is strongly
    recommended and postsplenectomy boost vaccinations are suggested. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?1/9/1177?
    source=see_link\">",
    " \"Prevention of sepsis in the asplenic patient\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567252\">",
    " <span class=\"h2\">",
    " Curative therapy",
    " </span>",
    " &nbsp;&mdash;&nbsp;Hematopoietic cell transplantation (HCT) is the only
    curative treatment for ALPS [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/14,15\">",
    " 14,15",
    " </a>",
    " ]. Reduced-intensity preparative regimens offer lower morbidity and mortality
    than myeloablative preparative regimens and have been used successfully in primary
    immunodeficiencies. Our treatment protocol includes campath,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?9/20/9545?source=see_link\">",
    " fludarabine",
    " </a>",
    " , and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?21/54/22376?source=see_link\">",
    " melphalan",
    " </a>",
    " as the reduced-intensity regimen. This conditioning regimen is well tolerated
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/16\">",
    " 16",
    " </a>",
    " ]. The status of ALPS disease activity needs to be carefully evaluated and the
    potential consequences of long-term treatments, including organ function, need to
    be compared with the risks of transplantation, before HCT is performed.",
    " </p>",
    " <p>",
    " Examples of transplant indications include:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Lymphoma development, because of the potential for relapse after therapy",
    " </li>",
    " <li>",
    " Severe and recalcitrant autoimmune cytopenias, disease manifestations that
    can only be controlled by aggressive and sustained immunosuppression",
    " </li>",
    " <li>",
    " Patients with a severe disease phenotype at the time of diagnosis,
    including, but not limited, to patients with homozygous and compound heterozygous",
    " <em>",
    " FAS",
    " </em>",
    " defects",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567259\">",
    " <span class=\"h2\">",
    " Genetic counseling",
    " </span>",
    " &nbsp;&mdash;&nbsp;Genetic counseling is recommended to provide patients and
    families with information on the nature of the disease, its inheritance, and
    implications for affected relatives and carriers. Patients with ALPS-sFAS did not
    inherit the genetic defect in",
    " <em>",
    " FAS",
    " </em>",
    " from either of the parents and do not appear to carry the mutation in their
    germline DNA. Consequently, their offspring will not inherit the somatic
    mutation.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567266\">",
    " <span class=\"h1\">",
    " PROGNOSIS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Many patients with ALPS have a favorable prognosis, with
    lymphadenopathy decreasing over time and autoimmune features remaining absent or
    manageable with limited need for immunosuppressive therapy. Some patients with
    particular mutations may have a better or poorer prognosis. However, it is
    difficult to determine which path each individual patient will follow, regardless
    of the genotype. Thus, long-term follow-up is indicated for the majority of
    patients to better predict and anticipate the natural history of each
    individual&rsquo;s disease. In addition, patients may need to be monitored for
    subsequent pathogenic events affecting Fas-mediated apoptosis, lymphocyte
    homeostasis in general, or other (still unknown) events [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/246/abstract/17\">",
    " 17",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Patients with mutations in",
    " <em>",
    " FAS",
    " </em>",
    " that affect the extracellular domains, particularly if these mutations cause
    defective apoptosis through haploinsufficiency (rather than dominant-negative
    interference), may have less severe disease",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " be less at-risk for lymphoma development.",
    " </p>",
    " <p>",
    " Patients with homozygous and compound heterozygous",
    " <em>",
    " FAS",
    " </em>",
    " mutations have a worse prognosis and typically require allogeneic bone marrow
    transplantation in order to survive.",
    " </p>",
    " <p>",
    " Longer-term follow-up of patients with ALPS-sFAS is needed to better assess
    the natural history of their clinical disease and their prognosis.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9567273\">",
    " <span class=\"h1\">",
    " SUMMARY",
    " </span>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Autoimmune lymphoproliferative syndrome (ALPS) is a rare disorder
    characterized by defective lymphocyte homeostasis, resulting from defective Fas-
    mediated apoptosis. (See",
    " <a class=\"local\" href=\"#H20229218\">",
    " 'Introduction'",
    " </a>",
    " above and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/58/30629?
    source=see_link\">",
    " \"Autoimmune lymphoproliferative syndrome (ALPS): Epidemiology and
    pathogenesis\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " Management of ALPS focuses upon three aspects: treatment of disease
    manifestations, prevention and treatment of disease",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " treatment complications, and curative therapy (hematopoietic cell
    transplantation). (See",
    " <a class=\"local\" href=\"#H9567210\">",
    " 'Management'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " We suggest use of immunosuppressive therapy only for severe complications of
    lymphoproliferation (eg, airway obstruction)",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " in the presence of concomitant autoimmune manifestations (",
    " <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
    " Grade 2C",
    " </a>",
    " ). Splenectomy is",
    " <strong>",
    " not",
    " </strong>",
    " recommended for autoimmune manifestations in patients with ALPS, due to the
    reported lack of sustained therapeutic benefit and increased incidence of
    postsplenectomy sepsis. (See",
    " <a class=\"local\" href=\"#H9567224\">",
    " 'Treatment of disease manifestations'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Hematopoietic cell transplantation is reserved for selected patients, such
    as those with lymphoma or severe, recalcitrant disease. (See",
    " <a class=\"local\" href=\"#H9567252\">",
    " 'Curative therapy'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Many patients with ALPS have a favorable prognosis, with lymphadenopathy
    decreasing over time and autoimmune features remaining absent or manageable with
    limited need for immunosuppressive therapy. (See",
    " <a class=\"local\" href=\"#H9567266\">",
    " 'Prognosis'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
    " <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
    " REFERENCES",
    " </h1>",
    " <ol id=\"reference\">",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/246/abstract/1\">",
    " Rao VK, Oliveira JB. How I treat autoimmune lymphoproliferative syndrome.
    Blood 2011; 118:5741.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/246/abstract/2\">",
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    " Rieux-Laucat F, Fischer A, Deist FL. Cell-death signaling and human disease.
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    " Van Der Werff Ten Bosch J, Otten J, Thielemans K. Autoimmune
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    " van der Werff Ten Bosch J, Schotte P, Ferster A, et al. Reversion of
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    " Teachey DT, Greiner R, Seif A, et al. Treatment with sirolimus results in
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    " Oliveira VD, Zankl H, Rath T. Mutagenic and cytotoxic effects of
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    " Neven B, Magerus-Chatinet A, Florkin B, et al. A survey of 90 patients with
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    " Wei A, Cowie T. Rituximab responsive immune thrombocytopenic purpura in an
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    " </li>",
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    " Magerus-Chatinet A, Neven B, Stolzenberg MC, et al. Onset of autoimmune
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    " </a>",
    " </li>",
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    " INTRODUCTION",
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    " MANAGEMENT",
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    " Evaluation and monitoring following initial diagnosis",
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    " Treatment of disease manifestations",
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    " - Lymphoproliferation",
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    " - Autoimmune manifestations",
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    " Genetic counseling",
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    " PROGNOSIS",
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    " SUMMARY",
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    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
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    " RELATED TOPICS",
    " </h1>",
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    " <ul>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/36/30279?
    source=related_link\">",
    " Autoimmune lymphoproliferative syndrome (ALPS): Clinical features and
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    var title_f0_15_247="Superficial fibular nerve";
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    BRRRQAUUUUAf/Z);\">",
    " </div>",
    " <div class=\"lgnd\">",
    " The superficial fibular (peroneal) nerve (in yellow) branches from the common
    fibular (peroneal) nerve at or below the proximal fibular head. The nerve descends
    in its 'normal' course (A) in the lateral compartment adjacent the intermuscular
    septum (in blue) of the anterior and lateral compartments. Between 27 and 43
    percent of patients have the superficial fibular (peroneal) in either the anterior
    compartment (B) or both the anterior and the lateral compartments (C) of the leg.
    The superficial fibular (peroneal) nerve has also been found in close proximity to
    the septum that separates the anterior from the lateral compartment (D).",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Redrawn based on information from: Adkison DP, Bosse MJ, Gaccione DR, Gabriel
    KR. Anatomical variations in the course of the superficial peroneal nerve. J Bone
    Joint Surg Am 1991; 73:112.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_247=[""].join("\n");
    var outline_f0_15_247=null;
    var title_f0_15_248="Postpartum thyroiditis";
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    " <div id=\"topicContent\">",
    " <div id=\"topicTitle\">",
    " Postpartum thyroiditis",
    " </div>",
    " <div id=\"topicContributors\">",
    " <div>",
    " <a id=\"authors\">",
    " </a>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/15/248/contributors\">",
    " Author",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/248/contributors\">",
    " Kenneth D Burman, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/15/248/contributors\">",
    " Section Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/248/contributors\">",
    " Douglas S Ross, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/15/248/contributors\">",
    " Deputy Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/248/contributors\">",
    " Jean E Mulder, MD",
    " </a>",
    " <br/>",
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    " Literature review current through:",
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    " Oct 2013.",
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    " Jan 18, 2013.",
    " </div>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H1\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;Postpartum thyroiditis is a destructive thyroiditis induced
    by an autoimmune mechanism within one year after parturition. Postpartum
    thyroiditis can also occur after spontaneous or induced abortion [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/1\">",
    " 1",
    " </a>",
    " ]. It usually presents in one of three ways (",
    " <a class=\"graphic graphic_figure graphicRef75131 \" href=\"UTD.htm?
    28/16/28942\">",
    " figure 1",
    " </a>",
    " ):",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Transient hyperthyroidism alone",
    " </li>",
    " <li>",
    " Transient hypothyroidism alone",
    " </li>",
    " <li>",
    " Transient hyperthyroidism followed by hypothyroidism and then recovery",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The clinical manifestations, diagnosis, and treatment of postpartum
    thyroiditis are reviewed here. Other forms of thyroiditis and the diagnosis and
    management of thyroid dysfunction during pregnancy are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/51/43830?
    source=see_link\">",
    " \"Overview of thyroiditis\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?15/51/16186?
    source=see_link\">",
    " \"Overview of thyroid disease in pregnancy\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?41/48/42760?
    source=see_link\">",
    " \"Hyperthyroidism during pregnancy: Treatment\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?13/47/14073?
    source=see_link\">",
    " \"Hypothyroidism during pregnancy: Clinical manifestations, diagnosis, and
    treatment\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H2\">",
    " <span class=\"h1\">",
    " PREVALENCE AND NATURAL HISTORY",
    " </span>",
    " &nbsp;&mdash;&nbsp;The reported prevalence of postpartum thyroiditis varies
    globally and ranges from 1 to 17 percent [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/2-5\">",
    " 2-5",
    " </a>",
    " ]. In systematic reviews of prospective studies, the mean prevalence in the
    general population of women was approximately 7 to 8 percent [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/2,3\">",
    " 2,3",
    " </a>",
    " ]. Higher rates, up to 25 percent, have been reported in women with type 1
    diabetes mellitus [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/2,3\">",
    " 2,3",
    " </a>",
    " ], and the highest rates occur among women with a prior history of postpartum
    thyroiditis (pooled prevalence 42 percent) and in women with positive antithyroid
    peroxidase antibodies who had normal thyroid function during pregnancy (40 to 60
    percent compared with 0 to 5 percent of women without antibodies) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/2\">",
    " 2",
    " </a>",
    " ]. Postpartum thyroid dysfunction can occur in women already taking thyroid
    hormone replacement for hypothyroidism antedating pregnancy (eg, goitrous
    Hashimoto's thyroiditis), if they have some remaining thyroid tissue capable of
    producing thyroid hormone [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/6\">",
    " 6",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Most women recover and are euthyroid within one year postpartum. However, some
    women never recover from the initial hypothyroid phase and have permanent
    hypothyroidism or goiter [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/7-10\">",
    " 7-10",
    " </a>",
    " ]. In addition, women with reversible hypothyroidism are at increased risk for
    developing permanent hypothyroidism in the future [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/4,11,12\">",
    " 4,11,12",
    " </a>",
    " ]. In a study of 45 patients followed for eight years, 14 (31 percent)
    developed permanent hypothyroidism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/13\">",
    " 13",
    " </a>",
    " ]. Progression to permanent hypothyroidism may be related to higher initial
    TSH concentrations and the antithyroid peroxidase antibody titer [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/4,9,12,13\">",
    " 4,9,12,13",
    " </a>",
    " ], maternal age, and female sex of the infant [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/13\">",
    " 13",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H3\">",
    " <span class=\"h1\">",
    " PATHOGENESIS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Postpartum thyroiditis, like painless thyroiditis, is
    considered a variant form of chronic autoimmune thyroiditis (Hashimoto's
    thyroiditis). The pathologic findings in the two disorders are similar (see",
    " <a class=\"local\" href=\"#H564660\">",
    " 'Pathology'",
    " </a>",
    " below), and both are associated with particular HLA-B and HLA-D haplotypes,
    suggesting that inherited risk factors are important [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/14\">",
    " 14",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Women destined to develop postpartum thyroiditis usually have high serum
    antithyroid peroxidase antibody concentrations early in pregnancy, which decline
    later (as immunologic tolerance increases during pregnancy) and then rise again
    after delivery [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/15\">",
    " 15",
    " </a>",
    " ]. Thus, women destined to develop postpartum thyroiditis have subclinical
    thyroid autoimmune disease early in pregnancy and soon after it.",
    " </p>",
    " <p>",
    " Whatever factors initiate postpartum thyroiditis, the resulting thyroid
    inflammation damages thyroid follicles and activates proteolysis of the
    thyroglobulin stored within the follicles. The result is unregulated release of
    large amounts of thyroxine (T4) and triiodothyronine (T3) into the circulation, and
    subsequent hyperthyroidism. This state lasts only until the stores of thyroglobulin
    are exhausted, because new hormone synthesis ceases, not only because of damage to
    the thyroid follicular cells but also because of inhibition of thyrotropin (TSH)
    secretion by the increased serum T4 and T3 concentrations. As the inflammation
    subsides, the thyroid follicles regenerate and thyroid hormone synthesis and
    secretion resume (",
    " <a class=\"graphic graphic_figure graphicRef75131 \" href=\"UTD.htm?
    28/16/28942\">",
    " figure 1",
    " </a>",
    " ). There may be a transient period of hypothyroidism and increased TSH
    secretion before thyroid secretion becomes normal again.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H17344418\">",
    " <span class=\"h1\">",
    " CLINICAL FEATURES",
    " </span>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H6\">",
    " <span class=\"h2\">",
    " Clinical manifestations",
    " </span>",
    " &nbsp;&mdash;&nbsp;The presentation of postpartum thyroiditis can be identical
    to painless thyroiditis, but the course may be more variable. This apparent
    difference may reflect the greater ease of studying postpartum women prospectively
    than women in the general population. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?24/7/24694?
    source=see_link\">",
    " \"Painless thyroiditis\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Approximately 20 to 30 percent of women with postpartum thyroiditis have the
    characteristic sequence of hyperthyroidism, which usually begins one to four months
    after delivery and lasts two to eight weeks, followed by hypothyroidism, which
    lasts from about two weeks to six months, and then recovery [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/4,16\">",
    " 4,16",
    " </a>",
    " ]. However, 20 to 40 percent have only hyperthyroidism, and the remaining 40
    to 50 percent have only hypothyroidism, which begins two to six months after
    delivery. Some women do not recover from the initial episode of hypothyroidism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/7,8\">",
    " 7,8",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The symptoms and signs of hyperthyroidism, when present, are typically mild
    and consist mainly of fatigue, weight loss, palpitations, heat intolerance,
    anxiety, irritability, tachycardia, and tremor. Similarly, hypothyroidism is also
    usually mild, leading to lack of energy, cold intolerance, constipation,
    sluggishness, and dry skin [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/4\">",
    " 4",
    " </a>",
    " ]. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?13/60/14279?
    source=see_link\">",
    " \"Overview of the clinical manifestations of hyperthyroidism in adults\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?14/10/14503?
    source=see_link\">",
    " \"Clinical manifestations of hypothyroidism\"",
    " </a>",
    " .) The symptoms that occur during the hyperthyroid phase are often only
    apparent retrospectively when the hypothyroid phase is diagnosed. Many of the
    symptoms of postpartum thyroiditis are inadvertently attributed to breastfeeding or
    the stresses of having a newborn child, as many otherwise normal postpartum women
    have fatigue, loss of energy, and anxiety, making the recognition of thyroid
    dysfunction difficult.",
    " </p>",
    " <p>",
    " While it has been suggested that hypothyroidism may be associated with or
    aggravate postpartum depression [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/17,18\">",
    " 17,18",
    " </a>",
    " ], in subsequent prospective studies there was no association despite a high
    prevalence of postpartum thyroid dysfunction (11 to 12 percent) and postpartum
    depression (2 to 9 percent) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/19,20\">",
    " 19,20",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Most women with postpartum thyroiditis have a mildly enlarged, diffuse,
    nontender thyroid gland when their thyroid function is abnormal, which disappears
    with recovery. In some women, however, goiter is the presenting complaint.",
    " </p>",
    " <p>",
    " In addition to the usual clinical consequences of thyroid dysfunction,
    postpartum hypothyroidism may decrease milk volume [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/21\">",
    " 21",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H7\">",
    " <span class=\"h2\">",
    " Laboratory findings",
    " </span>",
    " &nbsp;&mdash;&nbsp;The biochemical findings in patients with postpartum
    thyroiditis are similar to those of painless thyroiditis: high or high-normal serum
    free T4 and T3 concentrations and low serum TSH concentrations during the
    hyperthyroid phase, which may be overt or subclinical. During the hypothyroid
    phase, serum free T4 concentrations are low or low-normal, and serum TSH
    concentrations are high, consistent with either overt or subclinical
    hypothyroidism. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?23/22/23913?
    source=see_link\">",
    " \"Subclinical hyperthyroidism\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?3/48/3850?
    source=see_link\">",
    " \"Subclinical hypothyroidism\"",
    " </a>",
    " .) In those women with hyperthyroidism followed by hypothyroidism, serum T4
    concentrations may be low for several days to weeks before serum TSH concentrations
    rise above the normal range, because of TSH suppression during the hyperthyroid
    phase.",
    " </p>",
    " <p>",
    " Serum antithyroid peroxidase antibody concentrations are high in 60 to 85
    percent of women with postpartum thyroiditis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/10,16,22\">",
    " 10,16,22",
    " </a>",
    " ], and are highest during the hypothyroid phase or soon thereafter. Routine
    laboratory studies are usually normal, but some women have a slightly increased
    erythrocyte sedimentation rate",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " C-reactive protein. No consistent abnormalities in numbers or types of
    peripheral blood (or intrathyroidal) T lymphocytes have been reported.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H564660\">",
    " <span class=\"h2\">",
    " Pathology",
    " </span>",
    " &nbsp;&mdash;&nbsp;Thyroid biopsies in women with postpartum thyroiditis show
    lymphocytic infiltration, with occasional germinal centers, and disruption and
    collapse of thyroid follicles (lymphocytic thyroiditis) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/10,23\">",
    " 10,23",
    " </a>",
    " ]. Fine needle aspiration biopsies reveal lymphocytes, thyroid follicular
    cells, and masses of colloid. During recovery, lymphocytic infiltration is still
    seen, and there may be some fibrosis, but the thyroid follicles are more normal.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H8356863\">",
    " <span class=\"h2\">",
    " Radioiodine uptake",
    " </span>",
    " &nbsp;&mdash;&nbsp;During the hyperthyroid phase of postpartum thyroiditis,
    values for thyroid radioiodine uptake are low, usually less than 1 percent,
    compared with high values in Graves&rsquo; hyperthyroidism. However, breastfeeding
    is a strong relative contraindication to radioiodine (or technetium)
    administration, and must be suspended for at least several days until the breast
    milk is no longer radioactive. Because the hyperthyroid phase of postpartum
    thyroiditis is often only apparent retrospectively when the hypothyroid phase is
    diagnosed, radioiodine scanning is not usually necessary. (See",
    " <a class=\"local\" href=\"#H8\">",
    " 'Differential diagnosis'",
    " </a>",
    " below and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?12/36/12871?
    source=see_link&amp;anchor=H994499#H994499\">",
    " \"Hyperthyroidism during pregnancy: Clinical manifestations, diagnosis, and
    causes\", section on 'Diagnosis'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H17344246\">",
    " <span class=\"h1\">",
    " DIAGNOSIS",
    " </span>",
    " &nbsp;&mdash;&nbsp;The diagnosis of postpartum thyroiditis is based upon
    clinical manifestations and thyroid function tests (TSH, free thyroxine).
    Clinicians caring for women after pregnancy should be alert to the possibility of
    postpartum thyroid dysfunction as a cause of many symptoms during this period.
    Routine measurement of thyroid function tests is not usually required, unless the
    woman has type 1 diabetes mellitus, had postpartum thyroiditis after a previous
    pregnancy, or was known to have high serum antithyroid peroxidase antibody
    concentrations prior to pregnancy. (See",
    " <a class=\"local\" href=\"#H522339\">",
    " 'Screening'",
    " </a>",
    " below.) In addition, women with clinical manifestations of postpartum
    thyroiditis should have laboratory assessment of thyroid function. Because of the
    potential association between postpartum depression and postpartum hypothyroidism,
    and because hypothyroidism is a reversible cause of depression, women with
    postpartum depression should also be assessed for hypothyroidism.",
    " </p>",
    " <p>",
    " We typically measure TSH and free thyroxine (T4), rather than TSH alone,
    because thyroid function tests may fluctuate during the course of postpartum
    thyroiditis, and changes in TSH concentrations lag behind changes in serum free T4.
    If the TSH is low, T3 should also be measured.",
    " </p>",
    " <p>",
    " For women presenting with postpartum hypothyroidism, we do not routinely
    measure antithyroid peroxidase antibodies. If hypothyroidism resolves within
    several weeks without thyroid hormone replacement, the diagnosis of postpartum
    thyroiditis is confirmed.",
    " </p>",
    " <p>",
    " For women presenting with hyperthyroidism, radioiodine uptake (if not
    contraindicated, eg, active or recent breast feeding) or measurement of thyroid
    stimulating immunoglobulins (TSI) may help to differentiate postpartum thyroiditis
    from other causes of hyperthyroidism (ie, Graves&rsquo; disease). In addition,
    thyroid ultrasound may be useful to differentiate Graves&rsquo; disease from the
    hyperthyroid phase of postpartum thyroiditis. (See",
    " <a class=\"local\" href=\"#H8\">",
    " 'Differential diagnosis'",
    " </a>",
    " below.) We obtain radioiodine uptake (if not contraindicated)",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " serum TSI levels in women with clinical manifestations of Graves&rsquo;
    disease (ophthalmopathy), women with persistent hyperthyroidism (&gt;1 month), or
    severe hyperthyroidism (markedly elevated T3 &gt; T4). In women without these
    findings, we repeat thyroid function tests (TSH, free T4, T3) in three to four
    weeks. By that time, most women with postpartum thyroiditis will have improved,
    whereas those with Graves' hyperthyroidism will usually be unchanged or worse.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H8\">",
    " <span class=\"h1\">",
    " DIFFERENTIAL DIAGNOSIS",
    " </span>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H2060224\">",
    " <span class=\"h2\">",
    " Hyperthyroid phase",
    " </span>",
    " &nbsp;&mdash;&nbsp;For women who present with clinical",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " laboratory (high or high-normal serum free T4 and T3 and low serum TSH)
    manifestations of hyperthyroidism, it may be difficult to distinguish the
    hyperthyroid phase of postpartum thyroiditis from Graves' hyperthyroidism, which
    can also begin during the postpartum period, either as recurrent or new-onset
    hyperthyroidism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/3\">",
    " 3",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The primary clinical differences between women with postpartum thyroiditis and
    those with Graves' hyperthyroidism are that hyperthyroidism in women with
    postpartum thyroiditis is usually mild (both clinically and biochemically), thyroid
    enlargement is minimal, and Graves' ophthalmopathy is absent. In contrast, women
    with Graves' hyperthyroidism are usually more symptomatic, have higher serum
    thyroid hormone concentrations, more thyroid enlargement, and may have
    ophthalmopathy or pretibial myxedema. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?25/57/26520?
    source=see_link&amp;anchor=H19#H19\">",
    " \"Diagnosis of hyperthyroidism\", section on 'Determining the etiology'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " In women without new-onset ophthalmopathy, the distinction may be difficult.
    In Graves&rsquo; disease, the serum T3 is typically elevated (in comparison with
    the upper limits of normal) to a greater degree than is the free T4, whereas the
    opposite is true in postpartum thyroiditis. Thus, a high T3 to T4 ratio (the value
    of which is assay and unit dependent) suggests Graves&rsquo; disease, while a ratio
    close to that of euthyroid patients suggests a destructive thyroiditis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/24\">",
    " 24",
    " </a>",
    " ]. The two disorders can often be distinguished by reevaluation in three to
    four weeks. By that time, most women with postpartum thyroiditis will have
    improved, whereas those with Graves' hyperthyroidism will be unchanged or worse.",
    " </p>",
    " <p>",
    " The two disorders can also be distinguished by measurements of serum thyroid
    stimulating immunoglobulins (TSI) or thyroid radioiodine uptake. Serum TSI levels
    are typically elevated in Graves&rsquo; hyperthyroidism but not in postpartum
    thyroiditis. Radioiodine uptake values are low in postpartum thyroiditis and high
    in Graves' hyperthyroidism. However, radioactive iodine testing should be avoided
    in women who are breast-feeding or have breast-fed recently. In addition, care must
    be taken to ensure topical iodine preparations were not used during delivery as the
    absorbed iodine may falsely lower the radioiodine uptake. When radioiodine uptake
    is contraindicated, thyroid ultrasound with Doppler flow may be helpful in
    differentiating these two conditions. Hypervascularity typically occurs with
    Graves' hyperthyroidism and there is decreased vascularity in hyperthyroidism
    associated with postpartum thyroiditis. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?20/62/21482?
    source=see_link&amp;anchor=H29#H29\">",
    " \"Overview of the clinical utility of ultrasonography in thyroid disease\",
    section on 'Autoimmune thyroid disease'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H2060231\">",
    " <span class=\"h2\">",
    " Hypothyroid phase",
    " </span>",
    " &nbsp;&mdash;&nbsp;For women who present with clinical manifestations of
    hypothyroidism, the hypothyroid phase of postpartum thyroiditis (low or low-normal
    serum free T4 and high TSH) must be differentiated from lymphocytic hypophysitis,
    which also may occur during late pregnancy or the postpartum period. Lymphocytic
    hypophysitis may cause deficiency of TSH as well as one or more additional
    pituitary hormones including ACTH [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/25,26\">",
    " 25,26",
    " </a>",
    " ]. Spontaneous recovery of pituitary gland function or, alternatively,
    persistent and chronic hypopituitarism may occur [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/27\">",
    " 27",
    " </a>",
    " ]. In lymphocytic hypophysitis, the serum TSH is expected to be normal or low
    in the context of a low free T4, whereas in hypothyroidism with postpartum
    thyroiditis, the TSH should be elevated in conjunction with a decreased FT4. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?9/38/9833?
    source=see_link&amp;anchor=H9#H9\">",
    " \"Causes of hypopituitarism\", section on 'Hypophysitis'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Postpartum thyroiditis is considered a variant form of chronic autoimmune
    thyroiditis (Hashimoto's thyroiditis). (See",
    " <a class=\"local\" href=\"#H3\">",
    " 'Pathogenesis'",
    " </a>",
    " above.) It is not necessary to measure antithyroid peroxidase antibodies in
    women with postpartum hypothyroidism. Women who do not recover from the initial
    hypothyroid phase within one year postpartum likely have chronic autoimmune
    thyroiditis and permanent hypothyroidism.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H522339\">",
    " <span class=\"h1\">",
    " SCREENING",
    " </span>",
    " &nbsp;&mdash;&nbsp;The frequency of postpartum thyroiditis raises the question
    of whether screening is indicated [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/28\">",
    " 28",
    " </a>",
    " ]. This could be done by periodic clinical evaluation or serum TSH assay after
    delivery. Alternatively, serum antithyroid peroxidase antibodies could be measured,
    either early in pregnancy or soon after delivery. High antibody concentrations at
    these times predict (but not with certainty) the later development of postpartum
    thyroiditis, and low concentrations make it very unlikely [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/11,15,16,29\">",
    " 11,15,16,29",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " We agree with the Endocrine Society clinical guidelines that there is
    insufficient evidence to support a recommendation for screening all pregnant women
    for postpartum thyroiditis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/3\">",
    " 3",
    " </a>",
    " ]. However, women at highest risk for developing postpartum thyroiditis (eg,
    antithyroid peroxidase antibody positive, type 1 diabetes, previous episode of
    postpartum thyroiditis) should have a serum TSH measurement at three and six months
    postpartum [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/3\">",
    " 3",
    " </a>",
    " ]. If the TSH level is abnormal, it should be repeated along with a free
    thyroxine level and T3 (if TSH is low), within one to two weeks.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9\">",
    " <span class=\"h1\">",
    " PREVENTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;There are no established therapies to prevent the
    occurrence of postpartum thyroiditis in patients with antithyroid peroxidase
    antibodies. Administration of T4 or iodine to pregnant women with high serum
    antithyroid antibody concentrations did not prevent postpartum thyroiditis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/30,31\">",
    " 30,31",
    " </a>",
    " ]. In contrast,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?13/37/13907?source=see_link\">",
    " selenium",
    " </a>",
    " supplementation may decrease inflammatory activity in pregnant women with
    autoimmune hypothyroidism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/32\">",
    " 32",
    " </a>",
    " ], and may reduce the risk of postpartum thyroiditis in women who are positive
    for thyroid peroxidase (TPO) antibodies. This was illustrated in a trial of 151
    TPO-positive women randomly assigned to receive selenium (200 mcg daily) or placebo
    (beginning at about the 12",
    " <sup>",
    " th",
    " </sup>",
    " week of gestation). The prevalence of postpartum thyroiditis was significantly
    lower in the selenium group (22 of 77 women [29 percent] versus 36 of 74 [49
    percent]) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/33\">",
    " 33",
    " </a>",
    " ]. The routine clinical application of this supplementation requires further
    study, especially since selenium deficiency may have existed in this cohort from
    Italy.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H11\">",
    " <span class=\"h1\">",
    " TREATMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;In the absence of randomized trials comparing different
    treatment strategies, treatment recommendations are based upon observational
    studies and clinical experience [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/3,7-9,13\">",
    " 3,7-9,13",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Our approach, which is similar to that of the Endocrine Society [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/3\">",
    " 3",
    " </a>",
    " ] and the American Thyroid Association [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/5\">",
    " 5",
    " </a>",
    " ], is outlined below:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " The majority of women with postpartum thyroiditis need no treatment during
    either the hyperthyroid or the hypothyroid phases of their illness. However,
    thyroid function tests (TSH, free T4, and if hyperthyroid, T3) should be monitored
    every four to eight weeks to confirm resolution of biochemical abnormalities or to
    detect the development of more severe hypothyroidism, indicating possible permanent
    hypothyroidism.",
    " </li>",
    " <li>",
    " Women who have bothersome symptoms of hyperthyroidism can be treated with 40
    to 120 mg",
    " <a class=\"drug drug_general\" href=\"UTD.htm?8/49/8986?source=see_link\">",
    " propranolol",
    " </a>",
    " or 25 to 50 mg",
    " <a class=\"drug drug_general\" href=\"UTD.htm?29/46/30440?
    source=see_link\">",
    " atenolol",
    " </a>",
    " daily until their serum T3 and serum free T4 concentrations are normal. For
    women who are breastfeeding, propranolol is preferred because, due to high plasma
    protein binding, it is not concentrated in breast milk as much as other beta
    blockers [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/34\">",
    " 34",
    " </a>",
    " ]. In the hyperthyroid phase, radioiodine treatment and antithyroid drugs
    (ie,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?18/39/19062?
    source=see_link\">",
    " methimazole",
    " </a>",
    " ) are of no value because the synthesis of T4 and T3 is decreased, not
    increased as in most other disorders causing hyperthyroidism.",
    " </li>",
    " <li>",
    " Women with symptomatic hypothyroidism should be treated with",
    " <a class=\"drug drug_general\" href=\"UTD.htm?40/43/41656?
    source=see_link\">",
    " levothyroxine",
    " </a>",
    " (T4) (typically about 50 to 100",
    " <span class=\"nowrap\">",
    " mcg/day",
    " </span>",
    " although requirements may vary), irrespective of the degree of TSH
    elevation. In asymptomatic women, we prefer to treat when the TSH exceeds 10",
    " <span class=\"nowrap\">",
    " mU/L.",
    " </span>",
    " Asymptomatic women who have a mildly elevated serum TSH (between the upper
    limit of the normal range and 10",
    " <span class=\"nowrap\">",
    " mU/L),",
    " </span>",
    " and who are not planning another pregnancy, do not necessarily require
    intervention.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The duration of thyroid hormone therapy once initiated is uncertain. Since
    postpartum thyroid dysfunction is often transient, many experts favor weaning T4
    after 6 to 12 months, unless the woman is pregnant, attempting pregnancy, or
    breastfeeding [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/4\">",
    " 4",
    " </a>",
    " ]. The dose can be halved and thyroid tests (TSH, free T4) reevaluated in six
    to eight weeks. Up to 30 percent of women never recover from the initial
    hypothyroid phase, and a rising TSH level is indicative of persistent
    hypothyroidism, requiring long-term T4. In some reports, high titers of antithyroid
    peroxidase antibodies and the severity of the initial hypothyroid phase predicted
    the development of permanent hypothyroidism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/7,12,13,35\">",
    " 7,12,13,35",
    " </a>",
    " ]. Thus, in women with very elevated initial TSH values (&gt;50 or 100",
    " <span class=\"nowrap\">",
    " mU/L),",
    " </span>",
    " an alternative approach is to continue thyroid hormone indefinitely.",
    " </p>",
    " <p>",
    " Because there are no prospective, controlled data confirming the best
    approach, the decision to withdraw thyroid hormone therapy should be based upon
    individual patient characteristics and preferences. We favor withdrawing thyroid
    hormone therapy in most women after 12 months of therapy. Monitoring for persistent
    hypothyroidism is required after thyroid hormone withdrawal, initially after six to
    eight weeks, three months, six months, and then annually if thyroid tests remain
    normal.",
    " </p>",
    " <p>",
    " Any woman who has had postpartum thyroiditis should be told that recurrence is
    likely after future pregnancies and that she is at substantial risk for the later
    development of hypothyroidism or goiter, and she should be educated regarding the
    possible development of symptoms. For women who have fully recovered from
    postpartum thyroiditis, we measure serum TSH levels annually, particularly within 5
    to 10 years after the initial diagnosis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/248/abstract/3\">",
    " 3",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"PATIENT_INFORMATION\">",
    " <span class=\"h1\">",
    " INFORMATION FOR PATIENTS",
    " </span>",
    " &nbsp;&mdash;&nbsp;UpToDate offers two types of patient education materials,
    &ldquo;The Basics&rdquo; and &ldquo;Beyond the Basics.&rdquo; The Basics patient
    education pieces are written in plain language, at the 5",
    " <sup>",
    " th",
    " </sup>",
    " to 6",
    " <sup>",
    " th",
    " </sup>",
    " grade reading level, and they answer the four or five key questions a patient
    might have about a given condition. These articles are best for patients who want a
    general overview and who prefer short, easy-to-read materials. Beyond the Basics
    patient education pieces are longer, more sophisticated, and more detailed. These
    articles are written at the 10",
    " <sup>",
    " th",
    " </sup>",
    " to 12",
    " <sup>",
    " th",
    " </sup>",
    " grade reading level and are best for patients who want in-depth information
    and are comfortable with some medical jargon.",
    " </p>",
    " <p>",
    " Here are the patient education articles that are relevant to this topic. We
    encourage you to print or e-mail these topics to your patients. (You can also
    locate patient education articles on a variety of subjects by searching on
    &ldquo;patient info&rdquo; and the keyword(s) of interest.)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Basics topics (see",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?5/50/5922?
    source=see_link\">",
    " \"Patient information: Thyroiditis after pregnancy (The Basics)\"",
    " </a>",
    " )",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H521341\">",
    " <span class=\"h1\">",
    " SUMMARY AND RECOMMENDATIONS",
    " </span>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Postpartum thyroiditis is a destructive thyroiditis induced by an autoimmune
    mechanism within one year after parturition. It occurs more often in women with a
    previous history of postpartum thyroiditis, positive antithyroid peroxidase
    antibody titers, and type 1 diabetes. (See",
    " <a class=\"local\" href=\"#H2\">",
    " 'Prevalence and natural history'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Approximately 20 to 30 percent of women with postpartum thyroiditis have the
    characteristic sequence of hyperthyroidism, which usually begins one to four months
    after delivery and lasts two to eight weeks, followed by hypothyroidism, which also
    lasts from about two weeks to six months, and then recovery (",
    " <a class=\"graphic graphic_figure graphicRef75131 \" href=\"UTD.htm?
    28/16/28942\">",
    " figure 1",
    " </a>",
    " ). However, other women have only hyperthyroidism or only hypothyroidism.
    The symptoms and signs of hyperthyroidism, when present, are typically mild and
    consist mainly of fatigue, weight loss, palpitations, heat intolerance, anxiety,
    irritability, tachycardia, and tremor. Similarly, hypothyroidism is also usually
    mild, leading to lack of energy, cold intolerance, constipation, sluggishness, and
    dry skin. The biochemical findings depend upon the phase of postpartum thyroiditis:
    high or high-normal serum free T4 and T3 and low serum TSH during the hyperthyroid
    phase, and low or low-normal serum free T4 concentrations and high serum TSH during
    the hypothyroid phase. (See",
    " <a class=\"local\" href=\"#H6\">",
    " 'Clinical manifestations'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " The diagnosis of postpartum thyroiditis is based upon clinical
    manifestations and thyroid function tests. In women with symptoms or signs of
    hyperthyroidism or hypothyroidism in the postpartum period, we measure TSH and free
    thyroxine, rather than TSH alone. Thyroid function tests may fluctuate during the
    course of postpartum thyroiditis, and changes in TSH concentrations lag behind
    changes in serum free T4. If the TSH is low, T3 should also be measured. (See",
    " <a class=\"local\" href=\"#H17344246\">",
    " 'Diagnosis'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " For women presenting with postpartum hypothyroidism, we do not routinely
    measure antithyroid peroxidase antibodies. If hypothyroidism resolves within
    several weeks without thyroid hormone replacement, the diagnosis of postpartum
    thyroiditis is confirmed. For women presenting with postpartum hyperthyroidism, we
    obtain radioiodine uptake (if not contraindicated) or serum TSI levels in women
    with clinical manifestations of Graves&rsquo; disease (ophthalmopathy), women with
    persistent hyperthyroidism (&gt;1 month), or severe hyperthyroidism (markedly
    elevated T3 &gt; T4). In women without these findings, we repeat thyroid function
    tests (TSH, free T4, T3) in three to four weeks. By that time, most women with
    postpartum thyroiditis will have improved, whereas those with Graves'
    hyperthyroidism will be unchanged or worse. (See",
    " <a class=\"local\" href=\"#H17344246\">",
    " 'Diagnosis'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " For women at high risk for developing postpartum thyroiditis (eg, previously
    known to be thyroid peroxidase antibody positive, type 1 diabetes, prior history of
    postpartum thyroiditis), we suggest routine screening for postpartum thyroiditis
    (",
    " <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
    " Grade 2C",
    " </a>",
    " ). We typically measure a TSH level three and six months postpartum. If the
    TSH level is abnormal, it should be repeated along with a free thyroxine level and
    T3 (if TSH is low), within one to two weeks. (See",
    " <a class=\"local\" href=\"#H522339\">",
    " 'Screening'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Most women with postpartum thyroiditis have only mild symptoms during the
    hyperthyroid phase and do not require any treatment. Such women should have repeat
    thyroid tests in four to eight weeks to confirm resolution of hyperthyroidism. Beta
    blockers may be useful to relieve bothersome palpitations or tremulousness in
    symptomatic women. In breastfeeding women, we prefer",
    " <a class=\"drug drug_general\" href=\"UTD.htm?8/49/8986?source=see_link\">",
    " propranolol",
    " </a>",
    " because it has the lowest transfer into milk. There is no role for
    antithyroid drugs (ie,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?18/39/19062?
    source=see_link\">",
    " methimazole",
    " </a>",
    " ) or radioiodine in the treatment of the hyperthyroid phase of postpartum
    thyroiditis. (See",
    " <a class=\"local\" href=\"#H11\">",
    " 'Treatment'",
    " </a>",
    " above and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?41/48/42760?
    source=see_link&amp;anchor=H4#H4\">",
    " \"Hyperthyroidism during pregnancy: Treatment\", section on 'Beta
    blockers'",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " During the hypothyroid phase of postpartum thyroiditis, symptomatic women
    require treatment with thyroxine (T4). For asymptomatic women with a TSH level
    &ge;10",
    " <span class=\"nowrap\">",
    " mU/L,",
    " </span>",
    " we also suggest T4 replacement (",
    " <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
    " Grade 2C",
    " </a>",
    " ). We do not routinely treat asymptomatic women with TSH levels below 10",
    " <span class=\"nowrap\">",
    " mU/L.",
    " </span>",
    " (See",
    " <a class=\"local\" href=\"#H11\">",
    " 'Treatment'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Most women recover and are euthyroid within one year postpartum. Thus, we
    typically continue thyroid hormone for one year before attempting withdrawal.
    However, up to 30 percent of women never recover from the initial hypothyroid phase
    and have permanent hypothyroidism. Women with reversible hypothyroidism are also at
    increased risk for developing permanent hypothyroidism in the future and,
    therefore, require yearly monitoring of TSH. (See",
    " <a class=\"local\" href=\"#H11\">",
    " 'Treatment'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
    " <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
    " REFERENCES",
    " </h1>",
    " <ol id=\"reference\">",
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    " Lucas A, Pizarro E, Granada ML, et al. Postpartum thyroid dysfunction and
    postpartum depression: are they two linked disorders? Clin Endocrinol (Oxf) 2001;
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    " Miyake A, Tahara M, Koike K, Tanizawa O. Decrease in neonatal suckled milk
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    " Gerstein HC. How common is postpartum thyroiditis? A methodologic overview
    of the literature. Arch Intern Med 1990; 150:1397.",
    " </a>",
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    " Mizukami Y, Michigishi T, Nonomura A, et al. Postpartum thyroiditis. A
    clinical, histologic, and immunopathologic study of 15 cases. Am J Clin Pathol
    1993; 100:200.",
    " </a>",
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    " Izumi Y, Hidaka Y, Tada H, et al. Simple and practical parameters for
    differentiation between destruction-induced thyrotoxicosis and Graves'
    thyrotoxicosis. Clin Endocrinol (Oxf) 2002; 57:51.",
    " </a>",
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    " Patel MC, Guneratne N, Haq N, et al. Peripartum hypopituitarism and
    lymphocytic hypophysitis. QJM 1995; 88:571.",
    " </a>",
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    " Landek-Salgado MA, Gutenberg A, Lupi I, et al. Pregnancy, postpartum
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    " Unl&uuml;hizarci K, Bayram F, Colak R, et al. Distinct radiological and
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    86:1861.",
    " </a>",
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    " Amino N, Tada H, Hidaka Y, et al. Therapeutic controversy: Screening for
    postpartum thyroiditis. J Clin Endocrinol Metab 1999; 84:1813.",
    " </a>",
    " </li>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/29\">",
    " Premawardhana LD, Parkes AB, John R, et al. Thyroid peroxidase antibodies in
    early pregnancy: utility for prediction of postpartum thyroid dysfunction and
    implications for screening. Thyroid 2004; 14:610.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/30\">",
    " K&auml;mpe O, Jansson R, Karlsson FA. Effects of L-thyroxine and iodide on
    the development of autoimmune postpartum thyroiditis. J Clin Endocrinol Metab 1990;
    70:1014.",
    " </a>",
    " </li>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/31\">",
    " N&oslash;hr SB, J&oslash;rgensen A, Pedersen KM, Laurberg P. Postpartum
    thyroid dysfunction in pregnant thyroid peroxidase antibody-positive women living
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    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/32\">",
    " Mazokopakis EE, Papadakis JA, Papadomanolaki MG, et al. Effects of 12 months
    treatment with L-selenomethionine on serum anti-TPO Levels in Patients with
    Hashimoto's thyroiditis. Thyroid 2007; 17:609.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/33\">",
    " Negro R, Greco G, Mangieri T, et al. The influence of selenium
    supplementation on postpartum thyroid status in pregnant women with thyroid
    peroxidase autoantibodies. J Clin Endocrinol Metab 2007; 92:1263.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/34\">",
    " Beardmore KS, Morris JM, Gallery ED. Excretion of antihypertensive
    medication into human breast milk: a systematic review. Hypertens Pregnancy 2002;
    21:85.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/15/248/abstract/35\">",
    " Premawardhana LD, Parkes AB, Ammari F, et al. Postpartum thyroiditis and
    long-term thyroid status: prognostic influence of thyroid peroxidase antibodies and
    ultrasound echogenicity. J Clin Endocrinol Metab 2000; 85:71.",
    " </a>",
    " </li>",
    " </ol>",
    " </div>",
    " <div id=\"topicVersionRevision\">",
    " Topic 7831 Version 7.0",
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    " <a href=\"#\" title=\"Collapse Topic Outline\">",
    " <img alt=\"\" src=\"./../images/orange_arrow_left.myextg\"/>",
    " </a>",
    " </div>",
    " <div id=\"innerOutline\">",
    " <h1>",
    " TOPIC OUTLINE",
    " </h1>",
    " <div id=\"outline\">",
    " <ul>",
    " <li>",
    " <a class=\"sr_button\" href=\"#H521341\" id=\"summRecButton\">",
    " <span>",
    " SUMMARY &amp; RECOMMENDATIONS",
    " </span>",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H1\">",
    " INTRODUCTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H2\">",
    " PREVALENCE AND NATURAL HISTORY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H3\">",
    " PATHOGENESIS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H17344418\">",
    " CLINICAL FEATURES",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H6\">",
    " Clinical manifestations",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H7\">",
    " Laboratory findings",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H564660\">",
    " Pathology",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H8356863\">",
    " Radioiodine uptake",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H17344246\">",
    " DIAGNOSIS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H8\">",
    " DIFFERENTIAL DIAGNOSIS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H2060224\">",
    " Hyperthyroid phase",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H2060231\">",
    " Hypothyroid phase",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H522339\">",
    " SCREENING",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H9\">",
    " PREVENTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H11\">",
    " TREATMENT",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#PATIENT_INFORMATION\">",
    " INFORMATION FOR PATIENTS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H521341\">",
    " SUMMARY AND RECOMMENDATIONS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a href=\"#references\">",
    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " <div class=\"openRelatedGraphics\" id=\"ENDO/7831\" rel=\"outline_link\">",
    " GRAPHICS",
    " <a class=\"graphics_icon\" href=\"#\" title=\"View All Related Graphics\">",
    " View All",
    " </a>",
    " </div>",
    " </h1>",
    " <div id=\"relatedGraphics\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <div class=\"openRelatedGraphics\" id=\"ENDO/7831|FIG\">",
    " <a href=\"#\" title=\"FIGURES\">",
    " FIGURES",
    " </a>",
    " </div>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?28/16/28942\"
    title=\"figure 1\">",
    " Course of thyroiditis",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " RELATED TOPICS",
    " </h1>",
    " <div id=\"relatedTopics\">",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?9/38/9833?
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    source=related_link\">",
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    var title_f0_15_249="Pathophysiology of ischemic stroke";
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    " <div id=\"topicContent\">",
    " <div id=\"topicTitle\">",
    " Pathophysiology of ischemic stroke",
    " </div>",
    " <div id=\"topicContributors\">",
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    " </a>",
    " <a class=\"contributor contributor_credentials contributorType\"
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    " Authors",
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    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/249/contributors\">",
    " Arshad Majid, MB, ChB, FRCP",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/249/contributors\">",
    " Daniel B Zemke, PhD",
    " </a>",
    " <br/>",
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    0/15/249/contributors\">",
    " Mounzer Kassab, MD",
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    " <p class=\"headingAnchor\" id=\"H21816440\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;The term ischemic stroke is used to describe a variety of
    conditions in which blood flow to part or all of the brain is reduced, resulting in
    tissue damage. Although in some cases this may be a chronic condition, most strokes
    occur acutely. Research over the last four decades has resulted in a significant
    expansion of our knowledge and understanding of the molecular and cellular
    processes that underlie ischemia-induced cellular injury.",
    " </p>",
    " <p>",
    " The goal of this review is to provide an overview of the underlying factors,
    such as the hemodynamic changes and molecular and cellular pathways, which are
    involved in stroke-related brain injury. A better understanding of these processes
    may help in the development of new therapies that are needed to treat this
    devastating disease.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21816470\">",
    " <span class=\"h1\">",
    " STROKE SUBTYPES",
    " </span>",
    " &nbsp;&mdash;&nbsp;The etiology and clinical classification of ischemic stroke
    subtypes is reviewed here briefly and discussed in greater detail separately.
    (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/63/9208?
    source=see_link&amp;anchor=H3#H3\">",
    " \"Etiology and classification of stroke\", section on 'Brain ischemia'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?39/17/40216?
    source=see_link\">",
    " \"Clinical diagnosis of stroke subtypes\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Acute ischemic stroke subtypes are often classified in clinical studies using
    a system developed by investigators of the TOAST trial, based upon the underlying
    cause (",
    " <a class=\"graphic graphic_table graphicRef62571 \" href=\"UTD.htm?
    3/28/3531\">",
    " table 1",
    " </a>",
    " ) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/1\">",
    " 1",
    " </a>",
    " ]. Under this system, strokes are classified into the following categories:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Large artery atherosclerosis",
    " </li>",
    " <li>",
    " Cardioembolism",
    " </li>",
    " <li>",
    " Small vessel occlusion",
    " </li>",
    " <li>",
    " Stroke of other, unusual, determined etiology",
    " </li>",
    " <li>",
    " Stroke of undetermined etiology",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Ischemic strokes are due to a reduction or complete blockage of blood flow [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ]. This reduction can be due to decreased systemic perfusion, severe stenosis
    or occlusion of a blood vessel. Decreased systemic perfusion can be the result of
    low blood pressure, heart failure, or loss of blood. Determination of the type of
    stroke can influence treatment to be used. The main causes of ischemia are
    thrombosis, embolization, and lacunar infarction from small vessel disease.
    Ischemic strokes represent about 80 percent of all strokes. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?39/17/40216?
    source=see_link&amp;anchor=H6#H6\">",
    " \"Clinical diagnosis of stroke subtypes\", section on 'Incidence and
    prevalence'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Thrombosis refers to obstruction of a blood vessel due to a localized
    occlusive process within a blood vessel [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ]. The obstruction may occur acutely or gradually. In many cases, underlying
    pathology such as atherosclerosis may cause narrowing of the diseased vessel. This
    may lead to restriction of blood flow gradually, or in some cases, platelets may
    adhere to the atherosclerotic plaque forming a clot leading to acute occlusion of
    the vessel. Atherosclerosis usually affects larger extracranial and intracranial
    vessels. In some cases, acute occlusion of a vessel unaffected by atherosclerosis
    may occur because of a hypercoagulable state. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/63/9208?
    source=see_link&amp;anchor=H4#H4\">",
    " \"Etiology and classification of stroke\", section on 'Thrombosis'",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " Embolism refers to clot or other material formed elsewhere within the
    vascular system that travels from the site of formation and lodges in distal
    vessels causing blockage of those vessel and ischemia [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ]. The heart is a common source of this material, although other arteries
    may also be sources of this embolic material (artery to artery embolism). In the
    heart, clots may form on valves or chambers. Tumors, venous clots, septic emboli,
    air and fat can also embolize and cause stroke. Embolic strokes tend to be cortical
    and are more likely to undergo hemorrhagic transformation, probably due to vessel
    damage caused by the embolus. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/63/9208?
    source=see_link&amp;anchor=H7#H7\">",
    " \"Etiology and classification of stroke\", section on 'Embolism'",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " Lacunar infarction occurs as a result of small vessel disease. Smaller
    penetrating vessels are more commonly affected by chronic hypertension leading to
    hyperplasia of the tunica media of these vessels and deposition of fibrinoid
    material leading to lumen narrowing and occlusion [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ]. Lacunar strokes can occur anywhere in the brain but are typically seen in
    sub-cortical areas. Atheroma can also encroach on the orifices of smaller vessels
    leading to occlusion and stroke. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?3/59/4026?
    source=see_link\">",
    " \"Lacunar infarcts\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " Nonatherosclerotic abnormalities of the cerebral vasculature, whether
    inherited or acquired, predispose to ischemic stroke at all ages, but particularly
    in younger adults and children. These can be divided into noninflammatory and
    inflammatory etiologies. The following list, though not exhaustive, highlights the
    major nonatherosclerotic vasculopathies associated with ischemic stroke:",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " <ul class=\"hyphen-block\">",
    " <li>",
    " Arterial dissection (",
    " <a class=\"graphic graphic_figure graphicRef57866 \" href=\"UTD.htm?
    17/18/17698\">",
    " figure 1",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Fibromuscular dysplasia (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?33/42/34471?
    source=see_link\">",
    " \"Clinical manifestations and diagnosis of fibromuscular dysplasia\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Vasculitis (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?36/23/37241?
    source=see_link\">",
    " \"Classification of and approach to the vasculitides in adults\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?39/42/40616?
    source=see_link\">",
    " \"Classification and incidence of childhood vasculitis\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Moyamoya disease (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?3/44/3786?
    source=see_link\">",
    " \"Moyamoya disease: Etiology, clinical features, and diagnosis\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Sickle cell disease arteriopathy (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?31/11/31930?
    source=see_link\">",
    " \"Cerebrovascular complications of sickle cell disease\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Focal cerebral arteriopathy of childhood (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?22/61/23513?
    source=see_link&amp;anchor=H9#H9\">",
    " \"Ischemic stroke in children and young adults: Etiology and clinical
    features\", section on 'Focal cerebral arteriopathy'",
    " </a>",
    " )",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Decreased systemic perfusion due to systemic hypotension may produce
    generalized ischemia to the brain [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ]. This is most critical in the borderzone (or watershed) areas, which are
    territories that occupy the boundary region of two adjacent arterial supply zones.
    The ischemia caused by hypotension may be asymmetric due to preexisting vascular
    lesions. Areas of the brain commonly affected include the hippocampal pyramidal
    cells, cerebellar Purkinje cells, and cortical laminar cells discussed below.
    (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/63/9208?
    source=see_link&amp;anchor=H11#H11\">",
    " \"Etiology and classification of stroke\", section on 'Systemic
    hypoperfusion'",
    " </a>",
    " .)",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H1222833\">",
    " <span class=\"h1\">",
    " CEREBRAL AUTOREGULATION",
    " </span>",
    " &nbsp;&mdash;&nbsp;Under normal conditions, the rate of cerebral blood flow is
    primarily determined by the amount of resistance within cerebral blood vessels,
    which is directly related to their diameter [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/3\">",
    " 3",
    " </a>",
    " ]. Dilation of vessels leads to an increased volume of blood in the brain and
    increased cerebral blood flow, whereas constriction of vessels has the opposite
    effect. Cerebral blood flow is also determined by variation in the cerebral
    perfusion pressure.",
    " </p>",
    " <p>",
    " Cerebral autoregulation is the phenomenon by which cerebral blood flow is
    maintained at a relatively constant level despite moderate variations in perfusion
    pressure. The mechanism by which autoregulation occurs is not well understood, and
    may involve multiple pathways. Evidence suggests that the smooth muscle in cerebral
    vessels can respond directly to changes in perfusion pressure, contracting when
    pressure increases and relaxing when pressure drops. Reductions in cerebral blood
    flow may also lead to dilation of blood vessels through the release of vasoactive
    substances, although the molecules responsible for this have not been identified.
    The endothelial release of nitric oxide also appears to play a role in
    autoregulation.",
    " </p>",
    " <p>",
    " Maintenance of cerebral blood flow by autoregulation typically occurs within a
    mean arterial pressure range of 60 to 150 mmHg. The upper and lower limits vary
    between individuals, however. Outside of this range, the brain is unable to
    compensate for changes in perfusion pressure, and the cerebral blood flow increases
    or decreases passively with corresponding changes in pressure, resulting in the
    risk of ischemia at low pressures and edema at high pressures (",
    " <a class=\"graphic graphic_figure graphicRef66923 \" href=\"UTD.htm?
    23/22/23918\">",
    " figure 2",
    " </a>",
    " ).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H1222840\">",
    " <span class=\"h2\">",
    " Cerebral autoregulation during stroke",
    " </span>",
    " &nbsp;&mdash;&nbsp;Cerebral autoregulation is impaired during some disease
    conditions, including ischemic stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/3-5\">",
    " 3-5",
    " </a>",
    " ]. As cerebral perfusion pressure falls, cerebral blood vessels dilate to
    increase cerebral blood flow. A decrease in perfusion pressure beyond the ability
    of the brain to compensate results in a reduction in cerebral blood flow.
    Initially, the oxygen extraction fraction is increased in order to maintain levels
    of oxygen delivery to the brain. As the cerebral blood flow continues to fall,
    other mechanisms come into play (",
    " <a class=\"graphic graphic_figure graphicRef77705 \" href=\"UTD.htm?
    10/46/10990\">",
    " figure 3",
    " </a>",
    " ).",
    " </p>",
    " <p>",
    " Inhibition of protein synthesis occurs at flow rates below 50",
    " <span class=\"nowrap\">",
    " mL/100",
    " </span>",
    " g per minute. At 35",
    " <span class=\"nowrap\">",
    " mL/100",
    " </span>",
    " g per minute, protein synthesis ceases completely and glucose utilization is
    transiently increased. At 25",
    " <span class=\"nowrap\">",
    " mL/100",
    " </span>",
    " g per minute, glucose utilization drops dramatically with the onset of
    anaerobic glycolysis, resulting in tissue acidosis from the accumulation of lactic
    acid. Neuronal electrical failure occurs at 16 to 18",
    " <span class=\"nowrap\">",
    " mL/100",
    " </span>",
    " g per minute, and failure of membrane ion homeostasis occurs at 10 to 12",
    " <span class=\"nowrap\">",
    " mL/100",
    " </span>",
    " g per minute. This level typically marks the threshold for the development of
    infarct (",
    " <a class=\"graphic graphic_figure graphicRef77705 \" href=\"UTD.htm?
    10/46/10990\">",
    " figure 3",
    " </a>",
    " ).",
    " </p>",
    " <p>",
    " In hypertensive individuals, autoregulation has adapted to occur at higher
    arterial pressures. Reduction of blood pressure to normal levels could actually
    exacerbate the derangement to autoregulation that occurs during stroke and lead to
    a further decrease in cerebral blood flow (",
    " <a class=\"graphic graphic_figure graphicRef66923 \" href=\"UTD.htm?
    23/22/23918\">",
    " figure 2",
    " </a>",
    " ).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21816535\">",
    " <span class=\"h1\">",
    " CONSEQUENCES OF REDUCTION IN BLOOD FLOW DURING STROKE",
    " </span>",
    " &nbsp;&mdash;&nbsp;The human brain is exquisitely sensitive and susceptible to
    even short durations of ischemia. The brain is responsible for a large part of the
    body's metabolism and receives about 20 percent of the cardiac output although it
    is only 2 percent of total body weight [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/3\">",
    " 3",
    " </a>",
    " ]. The brain contains little or no energy stores of its own, and therefore
    relies on the blood for their delivery. Even brief deprivation can lead to death of
    the affected brain tissue. During stroke, reduction of blood flow to a portion or
    all of the brain results in a deprivation of glucose and oxygen [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Most strokes are caused by focal ischemia, affecting only a portion of the
    brain, typically involving a single blood vessel and its downstream branches. The
    region directly surrounding the vessel is the most affected. Within this region,
    cells in a central core of tissue will be irreversibly damaged and die by necrosis
    if the duration of ischemia is long enough. At distances farther from the affected
    vessel, some cells may receive a small amount of oxygen and glucose by diffusion
    from collateral vessels. These cells do not die immediately, and can recover if
    blood flow is restored in a timely manner. The central core of tissue destined to
    die, or containing tissue that is already dead, is called the infarct. The region
    of potentially salvageable tissue is known as the penumbra.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21816542\">",
    " <span class=\"h2\">",
    " Mechanisms of ischemic cell injury and death",
    " </span>",
    " &nbsp;&mdash;&nbsp;Brain ischemia initiates a cascade of events that
    eventually lead to cell death, including depletion of ATP, changes in ionic
    concentrations of sodium, potassium, and calcium, increased lactate, acidosis,
    accumulation of oxygen free radicals, intracellular accumulation of water, and
    activation of proteolytic processes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2,6,7\">",
    " 2,6,7",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " As a consequence of the electrical failure that occurs during ischemia, the
    release of the excitatory amino acid glutamate at neuronal synapses is increased
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2\">",
    " 2",
    " </a>",
    " ]. This leads to the activation of glutamate receptors and the opening of ion
    channels that allow potassium ions to exit the cell and sodium and calcium ions to
    enter, which has a number of physiologic effects. The primary glutamate receptor
    subtype involved in ischemic damage is the N-methyl-D-aspartate (NMDA) receptor. In
    addition, the alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) and
    metabotropic glutamate receptors are thought to play a role. Activation of these
    receptors leads to membrane depolarization and increased calcium influx.",
    " </p>",
    " <p>",
    " Numerous cellular signaling pathways respond to calcium levels, and the influx
    of calcium resulting from glutamate receptor stimulation leads to their activation.
    These pathways have both beneficial and detrimental effects. The influx of sodium
    ions is balanced by the influx of water into the cell, leading to edema. Sodium
    influx also causes reversal of the normal process of glutamate uptake by astrocyte
    glutamate transporters, resulting in increased glutamate release [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/8-11\">",
    " 8-11",
    " </a>",
    " ]. As a result of its increased release and decreased uptake, glutamate
    accumulates to excessive levels and leads to continuous stimulation. This condition
    is often referred to as excitotoxicity.",
    " </p>",
    " <p>",
    " Another effect of NMDA receptor activation is the production of nitric oxide
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/12\">",
    " 12",
    " </a>",
    " ]. The activity of nitric oxide synthase (NOS) and the total amount of nitric
    oxide present in the brain are increased following exposure to hypoxia [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/13\">",
    " 13",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Nitric oxide is an important signaling molecule within the body and can be
    beneficial at normal physiologic levels. As an example, endothelial nitric oxide
    synthase (eNOS) leads to the production of low levels of nitric oxide that cause
    vasodilation and increase blood flow [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/14\">",
    " 14",
    " </a>",
    " ]. However, neuronal nitric oxide synthase (nNOS) and inducible nitric oxide
    synthase (iNOS) result in larger amounts of nitric oxide that may lead to brain
    injury. Nitric oxide is a free radical and reacts directly with cellular components
    to damage them. Nitric oxide can also react with another free radical, superoxide,
    to produce the highly reactive peroxynitrite. Peroxynitrite causes single strand
    breaks in DNA [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/15\">",
    " 15",
    " </a>",
    " ]. This results in the activation of DNA repair enzymes, which consume vital
    energy needed for other processes. DNA damage also may activate the process of
    apoptosis, leading to cell death.",
    " </p>",
    " <p>",
    " The production of reactive oxygen species, a normal byproduct of oxidative
    metabolism, is also increased during ischemia. Like nitric oxide, they can react
    with and damage cellular components. Injury to the plasma membrane of a cell can
    lead to the inability to control ion flux, resulting in mitochondrial failure.
    Reactive oxygen species, as well as calcium influx and other factors, can also
    permeabilize the mitochondrial membrane [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/16\">",
    " 16",
    " </a>",
    " ]. This leads to metabolic failure as well as the release of initiators of
    apoptosis and DNA damage. Metabolic failure results in the depletion of cellular
    ATP levels. ATP is required for nuclear condensation and DNA degradation in the
    final stages of apoptosis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/17\">",
    " 17",
    " </a>",
    " ]. In the absence of ATP, cell death occurs by necrosis rather than apoptosis
    (see below).",
    " </p>",
    " <p>",
    " The release of byproducts from cellular damage and death by necrosis activates
    components of the inflammatory pathway [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/18\">",
    " 18",
    " </a>",
    " ]. The role that inflammation plays during ischemia is mixed, having both
    positive and negative effects [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/19\">",
    " 19",
    " </a>",
    " ]. On the one hand, inflammation results in an increase in blood flow to the
    ischemic region, which may deliver vital glucose and oxygen to cells. On the other
    hand, increased blood flow may also deliver more calcium to the area, resulting in
    increased tissue damage.",
    " </p>",
    " <p>",
    " Inflammation also results in the migration of activated leukocytes to damaged
    tissue [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/20\">",
    " 20",
    " </a>",
    " ]. Although these leukocytes may remove damaged and necrotic tissue, they also
    release cytokines to attract additional inflammatory cells. Under severe
    inflammatory conditions, these cytokines can accumulate to toxic levels.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21816549\">",
    " <span class=\"h3\">",
    " Necrosis and apoptosis",
    " </span>",
    " &nbsp;&mdash;&nbsp;Cell death following cerebral ischemia or stroke can occur
    by either necrosis or by apoptosis. The process of necrosis is not well understood.
    In early stages, cellular chromatin becomes uniformly compacted, the endoplasmic
    reticulum is dilated, and ribosomes are dispersed [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/21\">",
    " 21",
    " </a>",
    " ]. In later stages, swelling of the cell and mitochondria is followed by
    rupture of the nuclear, organelle, and plasma membranes, leading to the release of
    cellular material into the surrounding environment. This release of material
    results in the stimulation of inflammatory processes within the brain.",
    " </p>",
    " <p>",
    " Apoptosis is highly regulated and has been studied in more detail than
    necrosis. As in necrosis, the chromatin begins to condense during early stages of
    apoptosis. Instead of cellular swelling, however, the contents of the cytoplasm
    also condense, and the mitochondria and other organelles remain intact. In later
    stages, the nucleus is broken into discrete fragments and the entire contents of
    the cell are divided into membrane bound bodies that are subsequently phagocytosed
    by macrophages.",
    " </p>",
    " <p>",
    " There are three known pathways by which apoptosis can be initiated [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/22\">",
    " 22",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Mitochondrial permeabilization",
    " </li>",
    " <li>",
    " Death receptor (Fas) pathway",
    " </li>",
    " <li>",
    " Endoplasmic reticulum stress",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The most well-known pathway involves permeabilization of the mitochondria and
    release of cytochrome c into the cytoplasm. Activation of membrane-bound Fas, the
    so called \"death receptor,\" and the accumulation of misfolded proteins at the
    endoplasmic reticulum during stress, can also lead to apoptosis. These initiators
    all lead to the activation of caspases that cleave cellular proteins and eventually
    cause cell death. Caspase-independent mechanisms of apoptosis have also been
    proposed.",
    " </p>",
    " <p>",
    " The pattern of cell death after cerebral ischemia, as seen in animal models,
    depends on the nature of the insult to cerebral tissue [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/23\">",
    " 23",
    " </a>",
    " ]. In global cerebral ischemia, such as occurs after cardiac arrest and
    resuscitation or transient severe systemic hypotension, the entire brain is exposed
    to ischemia. Formation of infarct is not immediate, but rather occurs after a delay
    of 12 hours to several days. Cell death is limited to those regions of the brain
    that are particularly susceptible to ischemic damage, such as the CA1 and CA4
    regions of the hippocampus, the striatum, and cortical layers two and five. Cell
    death in these regions occurs primarily by apoptosis.",
    " </p>",
    " <p>",
    " Focal cerebral ischemia is a more common pattern than global ischemia in human
    stroke. In animal models of focal ischemia, changes in cell morphology are visible
    microscopically as early as two to three hours after the insult, and the infarct
    develops rapidly over a period of 6 to 24 hours. Cell death occurs by necrosis in
    the core, with apoptotic cells located on the periphery [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/6\">",
    " 6",
    " </a>",
    " ]. In addition to the type of insult, the duration of ischemia also affects
    the pattern by which cell death occurs. Longer ischemic insults produce greater
    damage to cerebral tissue, resulting in an increased proportion of necrosis and
    decreased proportion of apoptosis.",
    " </p>",
    " <p>",
    " There have been few studies of apoptosis in the brain following stroke in
    human patients. However, accumulating evidence suggests that apoptosis is involved
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/24-27\">",
    " 24-27",
    " </a>",
    " ], as illustrated by the following observations:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " In a neuropathology study that compared specimens from 27 patients who had
    cerebral infarction with specimens from rat brains subjected to experimental
    transient forebrain ischemia, the patterns of cell death were similar in human and
    animal brain tissue and included both morphologic and histochemical findings
    typical of apoptosis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/24\">",
    " 24",
    " </a>",
    " ]. In the human stroke specimens, apoptosis was apparent during the subacute
    stage, but was not seen in acute or chronic stages.",
    " </li>",
    " <li>",
    " In another neuropathology report that compared 13 cases of fatal ischemic
    stroke with three patients who died of non-neurologic causes, histochemical and
    morphologic changes indicative of apoptosis were seen in cells throughout the brain
    of both patients and controls [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/27\">",
    " 27",
    " </a>",
    " ]. The morphologic changes were more advanced in the peri-infarct region and
    infarct core of the patients with stroke. Apoptotic cells were located primarily
    within the peri-infarct region, consisting of up to 26 percent of all cells.
    Increased ischemic damage and neuronal necrosis was associated with a decrease in
    the percentage of apoptotic cells.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The deciding factor in determining whether cells undergo necrosis or apoptosis
    seems to be the level of energy available in the form of ATP, which is required for
    formation of the apoptosome. Apoptosis is unable to proceed in its absence. When
    energy levels are limiting, cell death therefore occurs by necrosis rather than
    apoptosis. The role of ATP in the mechanism of cell death has been investigated
    primarily using cell culture models. Cultured neurons depend on the presence of
    serum in the culture medium for survival [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/22\">",
    " 22",
    " </a>",
    " ]. If the serum is removed, the cells die by necrosis. In serum-free media
    with added glucose, however, the cells die by apoptosis.",
    " </p>",
    " <p>",
    " Levels of ATP in the brain are decreased during stroke due to the lack of
    glucose and oxygen required for normal cellular metabolism. Glucose metabolism is
    decreased by about 50 percent in both global and focal ischemia models of stroke.
    As a consequence, ATP levels may fall to 10 percent of normal in global models or
    25 percent in the infarct core in focal ischemia models. ATP levels in the
    penumbra, however, only drop to 50 percent to 70 percent of normal [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/28\">",
    " 28",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " ATP levels in the brain may also be decreased by mitochondrial damage or
    failure, activity of DNA repair enzymes, such as PARP, and neuronal depolarization
    related to glutamate excitotoxicity. In stroke, therefore, low levels of ATP within
    the core infarct are insufficient to support apoptosis, and cell death occurs by
    necrosis. In the penumbra, ATP levels are sufficient enough that cell death by
    apoptosis can occur. As the duration of ischemia increases, however, ATP levels are
    eventually depleted and the proportion of cells that undergo necrosis is increased,
    with a decrease in the number of apoptotic cells.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H1223338\">",
    " <span class=\"h2\">",
    " Loss of brain structural integrity",
    " </span>",
    " &nbsp;&mdash;&nbsp;Cerebral ischemia and infarction leads to loss of the
    structural integrity of the affected brain tissue and blood vessels [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/6\">",
    " 6",
    " </a>",
    " ]. This process of tissue destruction and neurovascular disruption is mediated
    in part by the release of various proteases, particularly the matrix
    metalloproteases (MMP) that degrade collagens and laminins in the basal lamina [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/7,29\">",
    " 7,29",
    " </a>",
    " ]. The loss of vascular integrity leads to a breakdown of the blood-brain-
    barrier and development of cerebral edema. Catastrophic failure of vascular
    integrity is postulated to cause hemorrhagic conversion of ischemic infarction by
    allowing extravasation of blood constituents into the brain parenchyma [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/30\">",
    " 30",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H1223360\">",
    " <span class=\"h3\">",
    " Cerebral edema",
    " </span>",
    " &nbsp;&mdash;&nbsp;Cerebral edema complicating stroke can cause secondary
    damage by several mechanisms, including increased intracranial pressure, which may
    decrease cerebral blood flow, and mass effect causing displacement of brain tissue
    from one compartment to another (ie, herniation), a process that can be life-
    threatening.",
    " </p>",
    " <p>",
    " Two types of cerebral edema can occur as a consequence of ischemic stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/2,6,30,31\">",
    " 2,6,30,31",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Cytotoxic edema is caused by the failure of ATP-dependent transport of
    sodium and calcium ions across the cell membrane. The result is accumulation of
    water and swelling of the cellular elements of the brain, including neurons, glia,
    and endothelial cells.",
    " </li>",
    " <li>",
    " Vasogenic edema is caused by increased permeability or breakdown of the
    brain vascular endothelial cells that constitute the blood-brain barrier [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/32\">",
    " 32",
    " </a>",
    " ]. This allows proteins and other macromolecules to enter the extracellular
    space, resulting in increased extracellular fluid volume.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Roughly 10 percent of ischemic strokes are classified as malignant or massive
    because of the presence of space-occupying cerebral edema that is severe enough to
    produce elevated intracranial pressure and brain herniation. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?0/35/569?
    source=see_link&amp;anchor=H2#H2\">",
    " \"Decompressive hemicraniectomy for malignant middle cerebral artery
    territory infarction\", section on 'Clinical features of malignant hemispheric
    infarction'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21816556\">",
    " <span class=\"h1\">",
    " GENETICS OF STROKE",
    " </span>",
    " &nbsp;&mdash;&nbsp;Many of the known risk factors for stroke are variable
    traits influenced by multiple genes, making it difficult to sort out the genetics
    behind them. The study of stroke genetics is also impaired by interactions between
    different risk factors that modulate their effects. It is widely accepted, however,
    that there is a genetic component to stroke that can lead to increased or decreased
    risk. Outside of the monogenic disorders discussed below, it is probable that many
    alleles with small effect sizes contribute to the risk of ischemic stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/33\">",
    " 33",
    " </a>",
    " ]. Much of the evidence for this comes from studies of twins and from families
    with a history of stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/34\">",
    " 34",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Earlier studies of twins have been troubled by low sample numbers and poor
    classification of stroke type [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/34\">",
    " 34",
    " </a>",
    " ]. However, these studies indicate that stroke-related death in one sibling
    is associated with a higher risk of stroke-related death in the other sibling among
    monozygotic (identical) twins versus dizygotic (fraternal) twins. This observation
    suggests that genetic factors shared by the monozygotic twins played a role in
    their strokes. As an example, in one of the larger twin studies that evaluated 990
    same-sex twin pairs, stroke death affecting both siblings was twice as likely among
    monozygotic twin pairs compared with dizygotic twin pairs (10 versus 5 percent),
    and the difference was statistically significant [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/35\">",
    " 35",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " A family history of stroke is associated with an increased risk of stroke
    among the offspring [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/36\">",
    " 36",
    " </a>",
    " ]. This has been observed for offspring with maternal and paternal histories
    of stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/34\">",
    " 34",
    " </a>",
    " ], and among individuals having a sibling with a prior stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/37\">",
    " 37",
    " </a>",
    " ].",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Familial inheritance is often studied in isolated populations, such as those
    of Iceland, where it is easier to detect an increased risk of stroke caused by a
    mutation within a single gene. However, the data from these studies has often been
    inconsistent.",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " In a study of 296 Icelandic families, a four-marker haplotype spanning the
    ALOX5AP gene was associated with a twofold greater risk of stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/38\">",
    " 38",
    " </a>",
    " ]. However, a meta-analysis with 5194 stroke cases and 4566 controls found a
    nonsignificant association with two different haplotypes of ALOX5AP and stroke risk
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/39\">",
    " 39",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " Another susceptibility locus for stroke in Icelandic populations is the gene
    encoding phosphodiesterase 4D (PDE4D). However, a meta-analysis of 16 studies with
    over 5200 cases and 6000 controls found no association between PDE4D and ischemic
    stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/40\">",
    " 40",
    " </a>",
    " ], and a Bayesian meta-analysis with greater statistical power also found no
    association [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/41\">",
    " 41",
    " </a>",
    " ].",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " A 2012 meta-analysis of genome-wide association studies (GWAS) that analyzed
    data from over 12,000 subjects of European ancestry with ischemic stroke and 60,000
    controls identified three loci (PITX2, ZFHX3, and HDAC9) with genome-wide
    significance for ischemic stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/42\">",
    " 42",
    " </a>",
    " ]. Importantly, each locus was associated with a specific stroke subtype:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " PITX2 and ZFHX3, previously identified as risk factors for atrial
    fibrillation [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/43-45\">",
    " 43-45",
    " </a>",
    " ], were associated with cardioembolic stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/42\">",
    " 42",
    " </a>",
    " ]",
    " </li>",
    " <li>",
    " HDAC9 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/45\">",
    " 45",
    " </a>",
    " ] was associated with large vessel ischemic stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/42\">",
    " 42",
    " </a>",
    " ]",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The 9P21 locus [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/46\">",
    " 46",
    " </a>",
    " ] was also associated with large vessel ischemic stroke in the 2012 meta-
    analysis but did not reach statistical significance at the genome-wide level [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/42\">",
    " 42",
    " </a>",
    " ]. The association of PRKCH as a risk factor for small vessel stroke,
    previously demonstrated in a Japanese population [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/47\">",
    " 47",
    " </a>",
    " ], could not be confirmed in the meta-analysis because the locus is
    monomorphic in those of European ancestry [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/42\">",
    " 42",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Ethnic differences may also contribute to stroke risk. Although differences in
    lifestyle may be partly responsible for increased or decreased likelihood of
    stroke, genetic factors also play a role. As an example, individuals of African
    descent have a significantly higher rate of stroke than Caucasians, even after
    adjusting for differences in nongenetic risk factors [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/34,48\">",
    " 34,48",
    " </a>",
    " ]. This may or may not be related to the increased frequency among African
    populations of the sickle cell trait, which is a known cause of stroke due to the
    obstruction of small blood vessels by abnormal red blood cells. Even in monogenic
    disorders such as sickle cell disease, multiple genes may interact to modify risk.
    In a study of 1398 individuals with sickle cell anemia, 12 genes were found to
    interact with the mutated hemoglobin and modulate the risk of stroke [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/49\">",
    " 49",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H86785844\">",
    " <span class=\"h2\">",
    " Monogenic disorders",
    " </span>",
    " &nbsp;&mdash;&nbsp;A number of monogenic syndromes are associated with an
    increased risk of ischemic stroke, including the following [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/50\">",
    " 50",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Marfan syndrome and Ehlers-Danlos syndrome, which predispose to cervical
    artery dissection (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?10/30/10730?
    source=see_link&amp;anchor=H163601524#H163601524\">",
    " \"Spontaneous cerebral and cervical artery dissection: Clinical features
    and diagnosis\", section on 'Predisposing conditions'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?20/3/20538?
    source=see_link\">",
    " \"Genetics, clinical features, and diagnosis of Marfan syndrome and related
    disorders\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Familial moyamoya disease (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?3/44/3786?
    source=see_link&amp;anchor=H2#H2\">",
    " \"Moyamoya disease: Etiology, clinical features, and diagnosis\", section
    on 'Etiology'",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Fabry disease (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?26/49/27414?
    source=see_link\">",
    " \"Neurologic manifestations of Fabry disease\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Pseudoxanthoma elasticum (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/7/7285?
    source=see_link&amp;anchor=H12#H12\">",
    " \"Metabolic and inherited diseases affecting the skin\", section on
    'Pseudoxanthoma elasticum'",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Homocystinuria (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?22/61/23513?
    source=see_link&amp;anchor=H14#H14\">",
    " \"Ischemic stroke in children and young adults: Etiology and clinical
    features\", section on 'Metabolic disorders'",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Menkes disease (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?22/61/23513?
    source=see_link&amp;anchor=H14#H14\">",
    " \"Ischemic stroke in children and young adults: Etiology and clinical
    features\", section on 'Metabolic disorders'",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Cerebral autosomal dominant arteriopathy with subcortical infarctions and
    leukoencephalopathy (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?11/16/11530?
    source=see_link\">",
    " \"Cerebral autosomal dominant arteriopathy with subcortical infarcts and
    leukoencephalopathy (CADASIL)\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Cerebral autosomal recessive arteriopathy with subcortical infarctions and
    leukoencephalopathy (CARASIL) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/51\">",
    " 51",
    " </a>",
    " ]",
    " </li>",
    " <li>",
    " Hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS)
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/52,53\">",
    " 52,53",
    " </a>",
    " ]",
    " </li>",
    " <li>",
    " Sickle cell disease (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?31/11/31930?
    source=see_link\">",
    " \"Cerebrovascular complications of sickle cell disease\"",
    " </a>",
    " )",
    " </li>",
    " <li>",
    " Mitochondrial encephalopathy with lactic acidosis and stroke-like episodes
    (MELAS) (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?22/61/23513?
    source=see_link&amp;anchor=H15#H15\">",
    " \"Ischemic stroke in children and young adults: Etiology and clinical
    features\", section on 'MELAS and disorders causing metabolic stroke'",
    " </a>",
    " )",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " It is important to note that all of these conditions together account for only
    a small percentage of ischemic strokes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/249/abstract/54\">",
    " 54",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21816563\">",
    " <span class=\"h1\">",
    " SUMMARY",
    " </span>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Under normal conditions, the rate of cerebral blood flow is primarily
    determined by the amount of resistance within cerebral blood vessels. Dilation of
    vessels leads to an increased volume of blood in the brain and increased cerebral
    blood flow, whereas constriction of vessels has the opposite effect. Cerebral blood
    flow is also determined by variation in the cerebral perfusion pressure. (See",
    " <a class=\"local\" href=\"#H1222833\">",
    " 'Cerebral autoregulation'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " The brain is exquisitely sensitive to even short durations of ischemia.
    Multiple mechanisms are involved in tissue damage that results from brain ischemia.
    (See",
    " <a class=\"local\" href=\"#H21816535\">",
    " 'Consequences of reduction in blood flow during stroke'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Brain ischemia initiates a cascade of events that eventually lead to cell
    death, including depletion of ATP, changes in ionic concentrations of sodium,
    potassium, and calcium, increased lactate, acidosis, accumulation of oxygen free
    radicals, intracellular accumulation of water, and activation of proteolytic
    processes. (See",
    " <a class=\"local\" href=\"#H21816542\">",
    " 'Mechanisms of ischemic cell injury and death'",
    " </a>",
    " above.).",
    " </li>",
    " <li>",
    " Cell death following cerebral ischemia or stroke can occur by either
    necrosis or by apoptosis. Low levels of ATP within the core infarct are
    insufficient to support apoptosis, and cell death occurs by necrosis. In the
    ischemic penumbra, ATP levels are sufficiently high that cell death by apoptosis
    can occur. As the duration of ischemia increases, however, ATP levels are
    eventually depleted and the proportion of cells that undergo necrosis is increased.
    (See",
    " <a class=\"local\" href=\"#H21816549\">",
    " 'Necrosis and apoptosis'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
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    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
    " REFERENCES",
    " </h1>",
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    " </li>",
    " </ol>",
    " </div>",
    " <div id=\"topicVersionRevision\">",
    " Topic 14085 Version 8.0",
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    " <a href=\"#\" title=\"Collapse Topic Outline\">",
    " <img alt=\"\" src=\"./../images/orange_arrow_left.myextg\"/>",
    " </a>",
    " </div>",
    " <div id=\"innerOutline\">",
    " <h1>",
    " TOPIC OUTLINE",
    " </h1>",
    " <div id=\"outline\">",
    " <ul>",
    " <li>",
    " <a class=\"sr_button\" href=\"#H21816563\" id=\"summRecButton\">",
    " <span>",
    " SUMMARY",
    " </span>",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21816440\">",
    " INTRODUCTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21816470\">",
    " STROKE SUBTYPES",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H1222833\">",
    " CEREBRAL AUTOREGULATION",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H1222840\">",
    " Cerebral autoregulation during stroke",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21816535\">",
    " CONSEQUENCES OF REDUCTION IN BLOOD FLOW DURING STROKE",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H21816542\">",
    " Mechanisms of ischemic cell injury and death",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H21816549\">",
    " - Necrosis and apoptosis",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H1223338\">",
    " Loss of brain structural integrity",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H1223360\">",
    " - Cerebral edema",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21816556\">",
    " GENETICS OF STROKE",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H86785844\">",
    " Monogenic disorders",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21816563\">",
    " SUMMARY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a href=\"#references\">",
    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " <div class=\"openRelatedGraphics\" id=\"NEURO/14085\" rel=\"outline_link\">",
    " GRAPHICS",
    " <a class=\"graphics_icon\" href=\"#\" title=\"View All Related Graphics\">",
    " View All",
    " </a>",
    " </div>",
    " </h1>",
    " <div id=\"relatedGraphics\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <div class=\"openRelatedGraphics\" id=\"NEURO/14085|FIG\">",
    " <a href=\"#\" title=\"FIGURES\">",
    " FIGURES",
    " </a>",
    " </div>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?17/18/17698\"
    title=\"figure 1\">",
    " Arterial dissection",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?23/22/23918\"
    title=\"figure 2\">",
    " Cerebral autoregulation",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?10/46/10990\"
    title=\"figure 3\">",
    " Effects of decreased cerebral blood flow",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <div class=\"openRelatedGraphics\" id=\"NEURO/14085|TAB\">",
    " <a href=\"#\" title=\"TABLES\">",
    " TABLES",
    " </a>",
    " </div>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?3/28/3531\" title=\"table
    1\">",
    " TOAST classification",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " RELATED TOPICS",
    " </h1>",
    " <div id=\"relatedTopics\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?11/16/11530?
    source=related_link\">",
    " Cerebral autosomal dominant arteriopathy with subcortical infarcts and
    leukoencephalopathy (CADASIL)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?31/11/31930?
    source=related_link\">",
    " Cerebrovascular complications of sickle cell disease",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
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    " </ul>",
    " </div>",
    " </div>"].join("\n");
    var title_f0_15_250="Syndromes with craniofacial abnormalities";
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    " <div id=\"topicContent\">",
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    " Syndromes with craniofacial abnormalities",
    " </div>",
    " <div id=\"topicContributors\">",
    " <div>",
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    " </a>",
    " <a class=\"contributor contributor_credentials contributorType\"
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    " Authors",
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    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/250/contributors\">",
    " Edward P Buchanan, MD",
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    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/15/250/contributors\">",
    " Patrick Cole, MD",
    " </a>",
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    0/15/250/contributors\">",
    " Larry H Hollier, Jr, MD",
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    href=\"UTD.htm?0/15/250/contributors\">",
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    " Leonard E Weisman, MD",
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    " Helen V Firth, DM, FRCP, DCH",
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    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H1\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;Interruption of normal embryologic growth and
    differentiation of the face and skull results in a wide variety of craniofacial
    abnormalities. Craniofacial surgery, which consists of reconstruction of the
    cranial vault",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " facial skeleton, with or without simultaneous soft-tissue reconstruction, can
    be performed when these deformities interfere with physical",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " mental well-being.",
    " </p>",
    " <p>",
    " Specific syndromes in which craniofacial abnormalities are the primary feature
    will be reviewed here. The pathogenesis, diagnosis, and surgical management of
    craniosynostosis, a subset of craniofacial anomalies, and syndromes in which
    craniosynostosis is a primary abnormality, are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?10/37/10841?
    source=see_link\">",
    " \"Overview of craniosynostosis\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/18/8487?
    source=see_link\">",
    " \"Craniosynostosis syndromes\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H2\">",
    " <span class=\"h1\">",
    " CRANIOFACIAL MICROSOMIA (CFM)",
    " </span>",
    " &nbsp;&mdash;&nbsp;Craniofacial microsomia (CFM), also referred to as
    hemifacial microsomia, oculo-auriculo-vertebral spectrum, or first and second
    branchial arch syndrome, is a sporadically acquired association of anomalies that
    results from a defect in development of the first and second branchial arches (",
    " <a class=\"graphic graphic_figure graphicRef76109 \" href=\"UTD.htm?
    36/40/37504\">",
    " figure 1",
    " </a>",
    " and",
    " <a class=\"graphic graphic_figure graphicRef69339 \" href=\"UTD.htm?
    7/16/7428\">",
    " figure 2",
    " </a>",
    " ) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/1-3\">",
    " 1-3",
    " </a>",
    " ]. It is sometimes associated with vertebral",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " ocular anomalies. Goldenhar syndrome appears to be part of this spectrum (MIM
    #164210) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/4,5\">",
    " 4,5",
    " </a>",
    " ]. The disorder occurs in approximately 1 in 5500 live births [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/6\">",
    " 6",
    " </a>",
    " ]. It is typically sporadic, but [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/7\">",
    " 7",
    " </a>",
    " ] autosomal dominant inheritance have been reported [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/8,9\">",
    " 8,9",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The mechanism underlying craniofacial microsomia is uncertain. A vascular
    insult to the developing branchial arches is the most widely accepted explanation.
    In an animal model, hemorrhage induced in the region of the first and second
    branchial arches produced the characteristic facial features; the degree of
    abnormality was proportional to the size of the hematoma [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/10\">",
    " 10",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H3\">",
    " <span class=\"h2\">",
    " Clinical features of CFM",
    " </span>",
    " &nbsp;&mdash;&nbsp;The stigmata of this disorder are indicated by the acronym
    OMENS, for",
    " <strong>",
    " o",
    " </strong>",
    " rbit,",
    " <strong>",
    " m",
    " </strong>",
    " andible,",
    " <strong>",
    " e",
    " </strong>",
    " ar, facial",
    " <strong>",
    " n",
    " </strong>",
    " erve,",
    " <strong>",
    " s",
    " </strong>",
    " oft tissue [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/11,12\">",
    " 11,12",
    " </a>",
    " ]. Orbital distortion is typically present, as is mandibular hypoplasia. Ear
    anomalies include microtia, accessory preauricular tags",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " pits, and middle ear defects with hearing impairment (",
    " <a class=\"graphic graphic_picture graphicRef57724 \" href=\"UTD.htm?
    43/2/44067\">",
    " picture 1",
    " </a>",
    " ) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/2\">",
    " 2",
    " </a>",
    " ]. Facial nerve involvement leads to hypoplasia of the facial muscles. Soft
    tissue deficiency, such as profound hypoplasia or absence of the parotid gland and
    masticatory muscles (temporalis, masseter) may be present.",
    " </p>",
    " <p>",
    " The defects are unilateral in 85 to 90 percent of cases. In these cases, the
    right side predominates [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/2\">",
    " 2",
    " </a>",
    " ]. The abnormalities occur in variable combinations and range in extent from
    imperceptible to severe.",
    " </p>",
    " <p>",
    " The mandibular abnormalities are described using the Pruzansky classification
    (",
    " <a class=\"graphic graphic_figure graphicRef81249 \" href=\"UTD.htm?
    11/35/11839\">",
    " figure 3",
    " </a>",
    " and",
    " <a class=\"graphic graphic_figure graphicRef71316 \" href=\"UTD.htm?
    7/8/7299\">",
    " figure 4",
    " </a>",
    " ) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/13\">",
    " 13",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Type 1 is characterized by mild hypoplasia of the ramus with little
    abnormality of the mandibular body.",
    " </li>",
    " <li>",
    " In type 2, the mandible has a small condylar head and ramus. The condyle is
    flat, the glenoid fossa is poorly developed or absent, and the infratemporal
    surface assumes a flat contour.",
    " </li>",
    " <li>",
    " In type 3, the temporomandibular joint fails to form and the ramus may exist
    as a thin bony lamina or may be completely absent. The increasing degree of
    mandibular hypoplasia is associated with increased difficulty with endotracheal
    intubation for anesthesia and surgery [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/14\">",
    " 14",
    " </a>",
    " ].",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Bony abnormalities include a decreased maxillary height on the affected side
    and an occlusal cant, which is defined as rotation of the occlusal plane (a plane
    passing through the biting surface of the teeth) in the sagittal view [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/15\">",
    " 15",
    " </a>",
    " ]. As a general guide, each degree of rotation of the occlusal plane results
    in a 0.5 mm change in the dental occlusal relationship. This rotation occurs in all
    types of HFM, with increasing severity from type 1 to type 3. Occlusal cant can be
    demonstrated clinically by having the child bite down on a tongue depressor to
    identify any angulation (",
    " <a class=\"graphic graphic_figure graphicRef80119 \" href=\"UTD.htm?
    36/36/37454\">",
    " figure 5",
    " </a>",
    " ).",
    " </p>",
    " <p>",
    " The zygomatic arch is frequently hypoplastic and the distance between the
    lateral orbit and the tragus of the ear is decreased. Cleft palate occurs in 25
    percent of cases [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/16\">",
    " 16",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Auricular abnormalities are described using the OMENS+ classification [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/17\">",
    " 17",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Grade 1 describes an external ear that is small but contains all of its
    components; the auditory canal is not affected.",
    " </li>",
    " <li>",
    " A grade 2 abnormality is characterized by a vertical auricular remnant and
    complete atresia of the external auditory canal.",
    " </li>",
    " <li>",
    " The most severe deformity is grade 3, in which there is a limited remnant of
    the ear lobe. Hearing does not correlate with the extent of external ear
    abnormality.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " One study reviewed the clinical features of 121 patients with HFM [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/16\">",
    " 16",
    " </a>",
    " ]. Extracraniofacial anomalies occurred in 55 percent and ranged from one
    anomaly (13 percent) to multiple affected organ systems (42 percent). No gender or
    side predominance was detected. Central nervous system, cardiac, and skeletal
    anomalies each occurred in more than 10 percent of cases; pulmonary,
    gastrointestinal, and renal deformities were less common. The majority of the heart
    defects involved the outflow tract or septum. The increased frequency of cardiac
    anomalies in this condition suggests that abnormal development of neural crest may
    result in both HFM and conotruncal defects.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H4\">",
    " <span class=\"h2\">",
    " Surgery for CFM",
    " </span>",
    " &nbsp;&mdash;&nbsp;The majority of patients with HFM do not require surgical
    correction; this is usually reserved for severe cases. Surgical correction of
    craniofacial microsomia is usually performed in stages [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/18\">",
    " 18",
    " </a>",
    " ]. Preauricular skin tags are typically excised before the child is two years
    old. This is often comforting to the parents, who see steps being taken to remedy
    their child's problem. Cranial remodeling may be required at approximately 8 to 12
    months of age if the craniofacial abnormality is severe and orbital dystopia
    (malalignment of the orbits) is present. Surgical reconstruction of the oral
    commissure is performed before two years of age in patients with HFM.",
    " </p>",
    " <p>",
    " Distraction osteogenesis of the mandible can be used to correct severe
    mandibular hypoplasia with airway compromise [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/19,20\">",
    " 19,20",
    " </a>",
    " ]. Children with a Pruzansky type 1 mandibular deformity are followed
    clinically from two to six years of age. Type 2 abnormalities respond favorably to
    distraction osteogenesis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/21\">",
    " 21",
    " </a>",
    " ]. The more severe type 3 deformities require reconstruction with a
    costochondral rib graft. There is still significant debate regarding the optimal
    timing to perform distraction osteogenesis. It has been postulated that by
    normalizing dimensions at a younger age, the maxilla and overlying soft tissue may
    have longer time to develop with a balanced &ldquo;functional matrix&rdquo;,
    thereby improving long-term facial symmetry [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/20\">",
    " 20",
    " </a>",
    " ]. However, this hypothesis has yet to be confirmed by prospective outcome
    studies.",
    " </p>",
    " <p>",
    " The data on recurrence of the facial deformity after surgery over time are
    inconsistent as well. One study, for example, found that facial asymmetry improved
    significantly after distraction, and despite mild relapse observed during the first
    year, surgical correction was stable in the later years of follow-up [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/22\">",
    " 22",
    " </a>",
    " ]. However, another study found that the facial proportions gradually returned
    to their original asymmetry after the growth of the patient in those treated with
    mandibular distraction osteogenesis in early childhood, and this growth was similar
    to the outcomes in an untreated group of patients [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/23\">",
    " 23",
    " </a>",
    " ]. While early surgery may have aesthetic and psychologic advantages, some of
    these patients may require a second procedure once their growth has completed.",
    " </p>",
    " <p>",
    " Orthodontic treatment is started at anywhere from 6 to 14 years of age [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/24\">",
    " 24",
    " </a>",
    " ], and ear reconstruction is performed at approximately eight years. Ears can
    be fashioned from rib cartilage and placed under the mastoid skin. Alternatively,
    an osseointegrated post can be surgically implanted in the mastoid area, allowing a
    prosthetic ear to be firmly attached. The ear is displaced in a downward and
    anterior direction to accommodate future growth, and calvarial bone grafts may be
    needed to reconstruct the appropriate topography [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/25\">",
    " 25",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Craniofacial growth is completed at approximately 14 to 15 years of age [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/26\">",
    " 26",
    " </a>",
    " ]. Further surgical intervention is initiated at that time. Maxillary
    repositioning (Le Fort 1), mandibular advancement [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/27\">",
    " 27",
    " </a>",
    " ], and soft tissue augmentation in the form of microsurgical flap transfers
    and fat grafting are used to improve both form and function [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/28\">",
    " 28",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H5\">",
    " <span class=\"h1\">",
    " TREACHER COLLINS SYNDROME",
    " </span>",
    " &nbsp;&mdash;&nbsp;Treacher Collins syndrome (TCS), also called
    mandibulofacial dysostosis, is an autosomal dominant disorder of craniofacial
    development with a variable degree of penetrance. It occurs with a frequency of 1
    in 25,000 to 50,000 live births [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/29\">",
    " 29",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H6\">",
    " <span class=\"h2\">",
    " Genetics and pathogenesis",
    " </span>",
    " &nbsp;&mdash;&nbsp;In the majority of cases, abnormal bilateral first and
    second branchial arch development is due to mutations in the gene TCOF1 (Treacher
    Collins syndrome 1, MIM #154500) located on chromosome 5 (5q31.3-q33.3) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/30-34\">",
    " 30-34",
    " </a>",
    " ]. This gene encodes the protein treacle that plays an essential role in rRNA
    transcription [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/35\">",
    " 35",
    " </a>",
    " ] and ribosome biogenesis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/36\">",
    " 36",
    " </a>",
    " ] and shows peak expression in the neural crest cells of the branchial arches
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/32,37\">",
    " 32,37",
    " </a>",
    " ]. Missense mutations in the POLR1D gene located at 13q12.2 (Treacher Collins
    syndrome 2, MIM #613717). Treacher Collins type I and II are autosomal dominant. A
    third type, Treacher Collins syndrome 3 is autosomal recessive and caused by
    compound heterozygous mutations in the POLR1C gene located at 6p22.3 (MIM #248390)
    that encode subunits of RNA polymerases I and III have been detected in individuals
    with Treacher Collins syndrome who are negative for TCOF1 mutations [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/38\">",
    " 38",
    " </a>",
    " ]. The underlying genetic defect is still unknown in about 10 percent of
    patients with TCS.",
    " </p>",
    " <p>",
    " Macroscopically, craniofacial tissues such as cartilage, bone, and connective
    tissues fail to develop correctly as a direct result of neural crest cell
    dysfunction [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/39\">",
    " 39",
    " </a>",
    " ]. One hypothesis posits that significant craniofacial malformations largely
    arise through defects in the formation, migration, or differentiation of this
    particular cell population [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/40\">",
    " 40",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " According to Tessier's classification of clefts, this syndrome consists of a
    cleft between the 6 through 8 positions [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/41\">",
    " 41",
    " </a>",
    " ]. TCS may result from insufficient mesodermal penetration affecting soft
    tissue thickness and leading to aplasia or hypoplasia of maxilla and zygoma. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?43/34/44581?
    source=see_link&amp;anchor=H5#H5\">",
    " \"Facial clefts and holoprosencephaly\", section on 'Classification of
    clefts'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H7\">",
    " <span class=\"h2\">",
    " Clinical features of TCS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Affected patients have malar hypoplasia and a cleft in the
    zygoma [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/29,42\">",
    " 29,42",
    " </a>",
    " ]. The eyes have an antimongoloid slant with colobomas (eyelid notch) along
    the lateral one-third of the lower lid. Lashes are absent from the medial two-
    thirds of the lower eyelid. The face has a convex profile with a retrusive chin and
    jaw, which is associated with a class 2 malocclusion (overbite).",
    " </p>",
    " <p>",
    " External ear abnormalities are common. Profound sensorineural hearing loss is
    common in severe cases, and children must be fitted early with bone-conducting
    hearing aids to facilitate development of normal speech. Cleft lip and palate and
    choanal atresia may occur. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/14/29927?
    source=see_link&amp;anchor=H13#H13\">",
    " \"Treatment of hearing impairment in children\", section on 'Bone conduction
    hearing devices'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?19/44/20169?
    source=see_link\">",
    " \"Etiology, prenatal diagnosis, obstetrical management, and recurrence of
    orofacial clefts\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?34/47/35575?
    source=see_link&amp;anchor=H10#H10\">",
    " \"Congenital anomalies of the nose\", section on 'Choanal atresia'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " The craniofacial abnormalities can result in airway narrowing and respiratory
    compromise. As a result, affected patients may require prone positioning or surgery
    to maintain a patent airway. Weak, uncoordinated swallowing may necessitate gavage
    feedings or placement of a gastrostomy tube. (See",
    " <a class=\"local\" href=\"#H8\">",
    " 'Surgery for TCS'",
    " </a>",
    " below.)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H8\">",
    " <span class=\"h2\">",
    " Surgery for TCS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Patients with airway and feeding difficulties may require
    surgery during the first couple years of life [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/43-45\">",
    " 43-45",
    " </a>",
    " ]. These procedures may include tongue-lip adhesion (glossopexy), distraction
    osteogenesis of the mandible, tracheostomy, correction of cleft lip",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " palate and choanal atresia, and gastrostomy tube placement.",
    " </p>",
    " <p>",
    " Surgical correction of the facial abnormalities in patients with severe
    Treacher Collins syndrome is initiated at approximately seven years of age when a
    significant degree of facial growth has occurred. The zygomatic contour is improved
    using split calvarial bone grafts or iliac crest grafts [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/44,46-48\">",
    " 44,46-48",
    " </a>",
    " ]. Lower eyelid colobomas are treated with a layered approach to
    reconstruction, using mucosal grafts to replace missing lining in conjunction with
    a lateral canthopexy.",
    " </p>",
    " <p>",
    " Surgical correction of the mandible is undertaken at 13 to 16 years of age as
    the jaw reaches dental and skeletal maturity. In the presence of a functioning
    temporomandibular joint (TMJ), the preferred treatment is ramus osteotomies and
    orthodontic manipulation. If the TMJ is absent, a costochondral graft is placed at
    6 to 10 years of age and followed up with orthognathic surgery in adolescence.
    Bilateral distraction osteogenesis of the mandible is also used in an attempt to
    correct the mandibular hypoplasia [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/43\">",
    " 43",
    " </a>",
    " ]. Finally, the contour of the facial soft tissues generally requires
    correction at a later stage when the patient has achieved facial skeletal maturity.
    The use of microsurgical free flap transfer has improved correction of facial soft
    tissue contours [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/49\">",
    " 49",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Improvement in facial appearance has positive psychosocial and social
    influences. In one report, 20 patients with Treacher Collins syndrome (mean age
    12.2 years) were studied before and at intervals up to four years after
    craniofacial reconstruction [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/50\">",
    " 50",
    " </a>",
    " ]. Although intellectual ability was unchanged, appearance, self-esteem, and
    adaptive function improved. The improvement peaked at the one year postoperative
    assessment and subsequently leveled off.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9\">",
    " <span class=\"h1\">",
    " ROBIN SEQUENCE",
    " </span>",
    " &nbsp;&mdash;&nbsp;Robin sequence, also known as Pierre Robin sequence and
    Pierre Robin syndrome, is a condition with multiple causes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/51,52\">",
    " 51,52",
    " </a>",
    " ]. Most cases are thought to result from hypoplasia of the mandible that
    occurs before the ninth week of development. Prior to the eighth week, the tongue
    is interposed between the developing palatal shelves. In the normal course of
    development, the tongue is drawn down during the tenth and eleventh weeks, allowing
    fusion of the palatal shelves. In the Robin sequence, hypoplasia of the mandible
    results in posterior displacement of the tongue, preventing palatal closure and
    producing a cleft palate. The etiology of Robin sequence is uncertain; possible
    mechanisms include genetic disorders, oligohydramnios (which may limit chin
    growth), myotonia, or connective tissue disease. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?1/59/1977?
    source=see_link&amp;anchor=H5#H5\">",
    " \"Congenital anomalies of the jaw, mouth, oral cavity, and pharynx\", section
    on 'Robin sequence'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Robin sequence often is an isolated abnormality. However, some cases (37
    percent in one series of 74 patients) occur as part of a syndrome with multiple
    malformations [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/53\">",
    " 53",
    " </a>",
    " ]. One-third of the patients with associated malformations had Stickler or
    velocardiofacial syndromes. Some cases of Robin sequence may thus result from
    developmental misexpression of SOX9 due to disruption of very-long-range-cis
    regulatory elements [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/54\">",
    " 54",
    " </a>",
    " ]. Ophthalmologic examination and fluorescent in situ hybridization study for
    chromosome 22 deletion should be performed on patients with Robin sequence because
    of the association with Stickler syndrome and velocardiofacial syndromes. (See",
    " <a class=\"local\" href=\"#H18\">",
    " 'Stickler and Marshall syndromes'",
    " </a>",
    " below and",
    " <a class=\"local\" href=\"#H15\">",
    " 'Velocardiofacial (Shprintzen) syndrome'",
    " </a>",
    " below.)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H10\">",
    " <span class=\"h2\">",
    " Clinical features of Robin sequence",
    " </span>",
    " &nbsp;&mdash;&nbsp;The clinical features of Robin sequence are micrognathia,
    glossoptosis, and cleft palate (",
    " <a class=\"graphic graphic_picture graphicRef68928 \" href=\"UTD.htm?
    30/48/31491\">",
    " picture 2",
    " </a>",
    " ). The tongue tends to prolapse backward, leading to airway obstruction that
    can be life-threatening. Respiratory compromise can lead to hypoxia,
    cardiopulmonary arrest, pulmonary hypertension, and failure to thrive. Feeding
    problems are common [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/53\">",
    " 53",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The rapid facial growth that occurs from 3 to 12 months of age leads to
    resolution of airway problems in a majority of cases. The mortality associated with
    Robin sequence is generally related to airway compromise, and is higher when
    associated with prematurity. Mortality rates in term infants with Robin sequences
    range from 1.7 to 11.3 percent [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/52,55\">",
    " 52,55",
    " </a>",
    " ]. However, the reported mortality rate increases to 26 percent when other
    anomalies are present [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/52\">",
    " 52",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H11\">",
    " <span class=\"h2\">",
    " Management of Robin sequence",
    " </span>",
    " &nbsp;&mdash;&nbsp;The two primary issues in patients with Robin sequence are
    upper airway obstruction and feeding difficulties [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/52,56\">",
    " 52,56",
    " </a>",
    " ]. Affected patients should be monitored to detect apnea and airway
    obstruction. Prone positioning is indicated, especially during feeding, to minimize
    airway obstruction. A rubber tube placed through the nose (nasopharyngeal trumpet)
    may protect the airway while awaiting compensatory growth. More invasive
    temporizing procedures are needed if respiratory obstruction is unresponsive to
    conservative measures.",
    " </p>",
    " <p>",
    " Nonsurgical options for treatment of upper airway obstruction include
    noninvasive respiratory support (NRS) and a nasopharyngeal airway (NPA). Surgical
    options include mandibular distraction osteogenesis and glossopexy. Cases of airway
    obstruction that are refractory to these measures may require a tracheostomy [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/53\">",
    " 53",
    " </a>",
    " ]. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?11/42/11945?
    source=see_link\">",
    " \"Overview of tracheostomy\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Noninvasive respiratory support (NRS) uses continuous positive airway
    pressure or noninvasive positive pressure ventilation to correct the airway
    obstruction. In a series of 81 patients over 10 years, 63 percent were treated with
    positioning and medical treatment, 12 percent required temporary intubation and
    positioning, 16 percent required tracheotomy, and 9 percent were treated with NRS
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/57\">",
    " 57",
    " </a>",
    " ]. NRS was shown to improve breathing patterns, respiratory efforts, and
    transcutaneous carbon dioxide pressures in infants with severe upper airway
    obstruction due to Robin sequence. None of the seven infants treated with NRS
    required tracheostomy and six out of seven were able to discontinue nutritional
    support.",
    " </li>",
    " <li>",
    " A second nonsurgical option to relieve airway obstruction is placement of a
    nasopharyngeal airway (NPA) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/58-60\">",
    " 58-60",
    " </a>",
    " ]. Improved oxygen saturation and weight gain has been documented with this
    method.",
    " </li>",
    " <li>",
    " Distraction of the mandible, in which osteotomy or fracture of the mandible
    is performed and an external fixator is used to open the oral passage, is the most
    commonly used surgical procedure [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/61-63\">",
    " 61-63",
    " </a>",
    " ]. Distraction has the benefit of affecting permanent change in mandibular
    size creating adequate space for the tongue. It has allowed many patients to avoid
    tracheostomy.",
    " </li>",
    " <li>",
    " Historically, glossopexy or tongue-lip adhesion, where the tongue is sutured
    to the lip to prevent retrusion, was the surgical method of choice. The use of
    glossopexy has decreased in popularity; however, it is associated with decreased
    morbidity and normalized weight gain and remains a valid alternative [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/64,65\">",
    " 64,65",
    " </a>",
    " ].",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12\">",
    " <span class=\"h1\">",
    " NAGER SYNDROME",
    " </span>",
    " &nbsp;&mdash;&nbsp;Nager syndrome, also known as Nager acrofacial dysostosis
    syndrome, is a rare disorder [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/66,67\">",
    " 66,67",
    " </a>",
    " ]. Most cases are sporadic, although both autosomal recessive and autosomal
    dominant inheritance have been reported [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/68\">",
    " 68",
    " </a>",
    " ]. Mutations in",
    " <em>",
    " SF3B4",
    " </em>",
    " (splicing factor 3B, subunit 4) leading to haploinsufficiency were identified
    in 61 percent of affected individuals in one cohort [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/69\">",
    " 69",
    " </a>",
    " ].",
    " <em>",
    " SF3B4",
    " </em>",
    " encodes spliceosome-associated protein 49 kD (SAP49), a subunit of the pre-
    mRNA spliceosome complex.",
    " </p>",
    " <p>",
    " The craniofacial features of Nager syndrome are similar to those of Treacher
    Collins. Nager syndrome is distinguished from Treacher Collins by the absence of
    eyelid colobomas. Severe cleft palate is always present. The palatal defect is
    unique in that the cleft is wide, but the hard and soft palates are shortened in
    the anterior-posterior dimension. Characteristic limb anomalies include preaxial
    deformities such as hypoplasia or agenesis of the radius and thumb [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/70\">",
    " 70",
    " </a>",
    " ]. Affected children have short stature. Intelligence is normal, although
    delays in speech and language development may occur secondary to hearing impairment
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/66,71\">",
    " 66,71",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Infants with Nager syndrome frequently have respiratory and feeding problems
    that may require gavage feeding or gastrostomy tube placement. The high perinatal
    mortality rate (approximately 11 percent) is related to respiratory compromise [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/72\">",
    " 72",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Management is similar to that for the Robin sequence as described above [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/73\">",
    " 73",
    " </a>",
    " ]. (See",
    " <a class=\"local\" href=\"#H9\">",
    " 'Robin sequence'",
    " </a>",
    " above.)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H14\">",
    " <span class=\"h1\">",
    " BINDER SYNDROME",
    " </span>",
    " &nbsp;&mdash;&nbsp;Binder syndrome, also known as maxillonasal dysplasia, is a
    very rare disorder of unknown etiology [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/74\">",
    " 74",
    " </a>",
    " ]. It is hypothesized that Binder syndrome is the mildest form of
    chondrodysplasia punctata [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/75\">",
    " 75",
    " </a>",
    " ]. Binder syndrome is characterized by a shortened nose with an acute
    nasolabial angle and a convex upper lip (",
    " <a class=\"graphic graphic_picture graphicRef53807 \" href=\"UTD.htm?
    16/50/17191\">",
    " picture 3",
    " </a>",
    " ). Class III malocclusion may be present. An underdeveloped frontal sinus and
    cervicospinal abnormalities occur in 40 to 50 percent of cases [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/76\">",
    " 76",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The treatment consists of nasal and maxillary correction, followed by
    orthodontic rehabilitation [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/77,78\">",
    " 77,78",
    " </a>",
    " ]. Depending on the involvement of the malformation, surgical treatment can be
    limited to reconstruction of the nasal dorsum and apex only, or extend to include
    maxillary advancement. Grafting to the nasal osteochondral scaffold can be
    performed in early adolescence; however, osteotomy with maxillary advancement
    should be reserved until the late teenage years [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/79\">",
    " 79",
    " </a>",
    " ]. Surgeons have reported the use of bone and cartilage grafts, and a
    comparison between the two demonstrated that either option is adequate for creating
    a normal nasolabial angle and tip projection [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/80,81\">",
    " 80,81",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H15\">",
    " <span class=\"h1\">",
    " VELOCARDIOFACIAL (SHPRINTZEN) SYNDROME",
    " </span>",
    " &nbsp;&mdash;&nbsp;Velocardiofacial syndrome (VCFS), also known as Shprintzen
    syndrome, is an autosomal dominant disorder caused by a deletion in chromosome
    22q11 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/82,83\">",
    " 82,83",
    " </a>",
    " ]. This deletion has also been identified in the majority of patients with
    DiGeorge sequence and conotruncal anomaly face syndrome, suggesting that these are
    phenotypic variants of the same disorder [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/83\">",
    " 83",
    " </a>",
    " ]. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?31/37/32343?
    source=see_link\">",
    " \"DiGeorge syndrome: Epidemiology and pathogenesis\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " The deletion occurs in approximately 1 in 4000 live births [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/83\">",
    " 83",
    " </a>",
    " ] and can be detected by fluorescent in situ hybridization (FISH), multiple
    ligation-dependent probe amplification (MLPA), and array comparative genomic
    hybridization (array CGH). The deletion occurs 'de novo' in the majority of cases,
    but approximately 15 percent are inherited from an affected parent. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/55/28536?
    source=see_link&amp;anchor=H15538597#H15538597\">",
    " \"Cytogenetic and molecular genetic diagnostic tools\", section on 'Detecting
    cytogenetic abnormalities'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/27/28087?
    source=see_link&amp;anchor=H16722234#H16722234\">",
    " \"Genomic disorders: An overview\", section on 'Detection of genomic
    disorders'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H16\">",
    " <span class=\"h2\">",
    " Clinical features of VCFS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Affected patients have retrognathia, a long face with a
    prominent nose [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/84\">",
    " 84",
    " </a>",
    " ]. Velopharyngeal incompetence (weak pharyngeal musculature) producing speech
    abnormalities, such as hypernasal speech is very common. Submucous or overt clefts
    of the secondary palate can occur. Chronic otitis media is present in 75 percent of
    cases. Transient neonatal hypocalcemia occurs in 20 percent. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?26/23/26999?
    source=see_link\">",
    " \"Neonatal hypocalcemia\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Congenital heart defects occur in 85 percent of cases [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/84\">",
    " 84",
    " </a>",
    " ]. The most common are ventricular septal defect (62 percent), right-sided
    aortic arch (52 percent), and tetralogy of Fallot (21 percent). The carotid
    arteries frequently follow an anomalous course that may complicate the performance
    of pharyngeal surgical procedures (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/19/8506?
    source=see_link\">",
    " \"Pathophysiology and clinical features of isolated ventricular septal
    defects in infants and children\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/5/27735?
    source=see_link\">",
    " \"Vascular rings\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?13/27/13752?
    source=see_link\">",
    " \"Pathophysiology, clinical features, and diagnosis of tetralogy of
    Fallot\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/2/43048?
    source=see_link\">",
    " \"Diagnosis and initial management of cyanotic heart disease in the
    newborn\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Learning disabilities are frequent and mild intellectual impairment occurs in
    approximately 40 percent of patients. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?31/57/32665?
    source=see_link&amp;anchor=H6#H6\">",
    " \"Specific learning disabilities in children: Clinical features\", section on
    'Risk factors'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Psychiatric disorders, primarily schizophrenia and paranoid delusions, develop
    in 10 to 30 percent of cases [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/85,86\">",
    " 85,86",
    " </a>",
    " ]. Magnetic resonance imaging studies comparing patients with VCFS and
    controls have demonstrated structural changes in the temporal lobe, left
    hippocampal, frontal, and caudate areas that are similar to the alterations of
    these regions that are seen in patients with schizophrenia [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/87,88\">",
    " 87,88",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H17\">",
    " <span class=\"h2\">",
    " Management of VCFS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Pharyngeal surgery (pharyngoplasty) is frequently required
    to treat the nasal air escape that causes abnormal speech [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/89,90\">",
    " 89,90",
    " </a>",
    " ]. High inset of the pharyngeal flap is indicated because of severe,
    refractory velopharyngeal incompetence. This is technically difficult because of
    visualization issues; some authors report success with through-and-through
    dissection of the soft palate to allow direct visualization of flap placement [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/91\">",
    " 91",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Removal of the tonsils and adenoids is contraindicated, because they aid in
    velopharyngeal closure [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/92\">",
    " 92",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H18\">",
    " <span class=\"h1\">",
    " STICKLER AND MARSHALL SYNDROMES",
    " </span>",
    " &nbsp;&mdash;&nbsp;Stickler (also known as hereditary arthroophthalmopathy)
    and Marshall syndromes are related disorders of connective tissue with overlapping
    characteristics [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/93-95\">",
    " 93-95",
    " </a>",
    " ]. It is unclear whether they are distinct entities or different clinical
    manifestations of a single syndrome. Most patients have autosomal dominant
    inheritance, although autosomal recessive forms of Stickler syndrome occur.",
    " </p>",
    " <p>",
    " Mutations of the gene for the alpha-1 chain of type II collagen (COL2A1)
    located on chromosome 12q13.11-q13.2 cause Stickler syndrome type I (MIM #108300)
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/96\">",
    " 96",
    " </a>",
    " ]. These mutations result in the abnormal production and assembly of type II
    collagen, which is a major component of cartilage, vitreous, and nucleus pulposus.
    Mutations in the COL11A1 gene located at 1p21 that encodes the alpha-1 chain of
    type XI collagen have been found in patients with Stickler syndrome type II (MIM
    #604841) or Marshall syndrome (MIM #154780), or with overlapping phenotypes of both
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/97\">",
    " 97",
    " </a>",
    " ]. Stickler syndrome type III (MIM #184840) is caused by mutation in the
    COL11A2 gene located at 6p21.3 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/98\">",
    " 98",
    " </a>",
    " ]. Rare autosomal recessive forms of Stickler syndrome are caused by biallelic
    mutations in any of the three genes encoding collagen IX (ie, COL9A1, COL9A2, and
    COL9A3) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/99,100\">",
    " 99,100",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H19\">",
    " <span class=\"h2\">",
    " Clinical features",
    " </span>",
    " &nbsp;&mdash;&nbsp;The clinical features of Stickler syndrome include
    characteristic orofacial and ophthalmologic abnormalities, deafness, and arthritis
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/94,95,97\">",
    " 94,95,97",
    " </a>",
    " ]. Affected patients typically have a flat midface with a depressed nasal
    bridge, short nose, anteverted nares, and micrognathia. Midline cleft palate can
    occur, and ranges in severity from a cleft in the soft palate to the Pierre Robin
    sequence (see",
    " <a class=\"local\" href=\"#H9\">",
    " 'Robin sequence'",
    " </a>",
    " above). Abnormal architecture of the vitreous gel is pathognomonic of this
    disorder, and is usually associated with high myopia. Retinal detachment occurs
    frequently. Joint hypermobility is present in infancy and decreases with age.
    Patients typically develop osteoarthritis in the third or fourth decade. Some
    patients have sensorineural deafness. Mitral valve prolapse may occur.",
    " </p>",
    " <p>",
    " Marshall syndrome has clinical features similar to Stickler syndrome. These
    include a craniofacial appearance characterized by a flat midface, depressed nasal
    bridge, short nose, and anteverted nares. Patients have ocular abnormalities (eg,
    cataracts, myopia), sensorineural hearing loss, and spondyloepiphyseal
    abnormalities [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/101\">",
    " 101",
    " </a>",
    " ]. Anhidrotic ectodermal dysplasia may occur [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/102\">",
    " 102",
    " </a>",
    " ]. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?24/0/24586?
    source=see_link&amp;anchor=H36#H36\">",
    " \"The genodermatoses\", section on 'Anhidrotic ectodermal dysplasia'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?22/14/22761?
    source=see_link&amp;anchor=H11#H11\">",
    " \"Cataract in children\", section on 'Clinical features'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Eye findings are usually nonprogressive and are found in neonates. Early
    ophthalmologic examination is indicated. Treatment of Robin sequence is discussed
    above. (See",
    " <a class=\"local\" href=\"#H11\">",
    " 'Management of Robin sequence'",
    " </a>",
    " above.) Cleft palate, if present, should be repaired prior to speech
    production. Surgery is performed earlier in infancy if the airway is unstable.
    Further surgery for speech competence is often indicated, because of the increased
    incidence of velopharyngeal insufficiency in these patients. Otolaryngologists
    should be consulted for auditory concerns. Orthopedic surgery and physical therapy
    are often involved in patient care for early onset of arthritis, which is most
    commonly treated with over-the-counter antiinflammatories.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H20\">",
    " <span class=\"h1\">",
    " VAN DER WOUDE SYNDROME",
    " </span>",
    " &nbsp;&mdash;&nbsp;Van der Woude syndrome is an autosomal dominant disorder
    with a high degree of penetration. It is characterized by pits",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " sinuses in the lower lip and cleft lip",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " cleft palate [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/103\">",
    " 103",
    " </a>",
    " ]. This condition represents 1 percent of cleft lip and palate cases and
    should be suspected when lower lip pits are present (",
    " <a class=\"graphic graphic_picture graphicRef50289 \" href=\"UTD.htm?
    13/41/13983\">",
    " picture 4",
    " </a>",
    " ). Identification of this syndrome is important for genetic counseling because
    of the 50 percent risk of occurrence in the offspring of an affected individual.
    The syndrome is usually caused by mutations in the IRF6 gene located on chromosome
    1q32-41, but another locus has been identified at 1p34 where the candidate gene
    WDR65 resides [",
    " <a class=\"abstract\" href=\"UTD.htm?0/15/250/abstract/103-106\">",
    " 103-106",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H14783287\">",
    " <span class=\"h1\">",
    " SUMMARY",
    " </span>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Interruption of normal embryologic growth and differentiation of the face
    and skull results in a wide variety of craniofacial abnormalities (",
    " <a class=\"graphic graphic_figure graphicRef76109 \" href=\"UTD.htm?
    36/40/37504\">",
    " figure 1",
    " </a>",
    " and",
    " <a class=\"graphic graphic_figure graphicRef69339 \" href=\"UTD.htm?
    7/16/7428\">",
    " figure 2",
    " </a>",
    " ). Specific syndromes in which craniofacial abnormalities are the primary
    feature include hemifacial microsomia, Treacher Collins syndrome, Robin sequence,
    Nager syndrome, Binder syndrome, Velocardiofacial syndrome, Stickler and Marshall
    syndromes, and Van der Woude syndrome. (See",
    " <a class=\"local\" href=\"#H1\">",
    " 'Introduction'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " The defects in hemifacial microsomia involve the orbit, mandible, ear,
    facial nerve, soft tissue, and are typically unilateral (",
    " <a class=\"graphic graphic_picture graphicRef57724 \" href=\"UTD.htm?
    43/2/44067\">",
    " picture 1",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H2\">",
    " 'Craniofacial microsomia (CFM)'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Patients with Treacher Collins syndrome have jaw defects, a notch in the
    lower eyelid at the junction of the inner two-thirds and outer one-third (eyelid
    colobomas), partially absent lashes on the lower eyelids, and sensorineural hearing
    loss. Cleft lip and palate and choanal atresia may occur. The craniofacial
    abnormalities can result in respiratory compromise and feeding difficulties. (See",
    " <a class=\"local\" href=\"#H5\">",
    " 'Treacher Collins syndrome'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Robin sequence, also known as Pierre Robin sequence and Pierre Robin
    syndrome, is a condition with multiple causes. Most cases are thought to result
    from hypoplasia of the mandible that occurs before the ninth week of development
    (",
    " <a class=\"graphic graphic_picture graphicRef68928 \" href=\"UTD.htm?
    30/48/31491\">",
    " picture 2",
    " </a>",
    " ). Some cases occur as part of a syndrome with multiple malformations (eg,
    Stickler or velocardiofacial syndrome). (See",
    " <a class=\"local\" href=\"#H9\">",
    " 'Robin sequence'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " The craniofacial features of Nager syndrome are similar to those of Treacher
    Collins. Nager syndrome is distinguished from Treacher Collins by the absence of
    eyelid colobomas. Severe cleft palate is always present. (See",
    " <a class=\"local\" href=\"#H12\">",
    " 'Nager syndrome'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Binder syndrome is characterized by a shortened nose with an acute
    nasolabial angle and a convex upper lip. (See",
    " <a class=\"local\" href=\"#H14\">",
    " 'Binder syndrome'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Velocardiofacial syndrome (VCFS), also known as Shprintzen syndrome, is an
    autosomal dominant disorder caused by a deletion in chromosome 22q11. This deletion
    has also been identified in the majority of patients with DiGeorge sequence and
    conotruncal anomaly face syndrome. Common clinical features include cleft palate,
    velopharyngeal incompetence (weak pharyngeal musculature) producing speech
    abnormalities, chronic otitis media, hypotonia, and congenital heart defects.
    (See",
    " <a class=\"local\" href=\"#H15\">",
    " 'Velocardiofacial (Shprintzen) syndrome'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Stickler and Marshall syndromes have similar clinical features, including a
    craniofacial appearance characterized by a flat midface, depressed nasal bridge,
    short nose, and anteverted nares. Stickler syndrome is also characterized by
    abnormal architecture of the vitreous gel and osteoarthritis. However, there is
    limited information to distinguish the two syndromes aside from clinical
    manifestations. (See",
    " <a class=\"local\" href=\"#H18\">",
    " 'Stickler and Marshall syndromes'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Van der Woude syndrome is characterized by pits",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " sinuses in the lower lip and cleft lip",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " cleft palate (",
    " <a class=\"graphic graphic_picture graphicRef50289 \" href=\"UTD.htm?
    13/41/13983\">",
    " picture 4",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H20\">",
    " 'Van der Woude syndrome'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Patients with airway and feeding difficulties may require surgery during the
    first couple years of life. The most common surgical procedure used to correct
    mandibular hypoplasia is that distraction osteogenesis of the mandible. Other
    surgeries may be performed during early and later childhood for functional reasons,
    as well as for aesthetic and psychologic reasons. (See",
    " <a class=\"local\" href=\"#H4\">",
    " 'Surgery for CFM'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H8\">",
    " 'Surgery for TCS'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H11\">",
    " 'Management of Robin sequence'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H17\">",
    " 'Management of VCFS'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H89678066\">",
    " <span class=\"h1\">",
    " ACKNOWLEDGMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;We are saddened by the untimely death of Samuel Stal, MD.
    UpToDate wishes to acknowledge his dedicated work on this review and his
    contributions to its Genetic diseases in children section.",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
    " <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
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    " </ol>",
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    " <div id=\"innerOutline\">",
    " <h1>",
    " TOPIC OUTLINE",
    " </h1>",
    " <div id=\"outline\">",
    " <ul>",
    " <li>",
    " <a class=\"sr_button\" href=\"#H14783287\" id=\"summRecButton\">",
    " <span>",
    " SUMMARY",
    " </span>",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H1\">",
    " INTRODUCTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H2\">",
    " CRANIOFACIAL MICROSOMIA (CFM)",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H3\">",
    " Clinical features of CFM",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H4\">",
    " Surgery for CFM",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H5\">",
    " TREACHER COLLINS SYNDROME",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H6\">",
    " Genetics and pathogenesis",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H7\">",
    " Clinical features of TCS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H8\">",
    " Surgery for TCS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H9\">",
    " ROBIN SEQUENCE",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H10\">",
    " Clinical features of Robin sequence",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H11\">",
    " Management of Robin sequence",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H12\">",
    " NAGER SYNDROME",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H14\">",
    " BINDER SYNDROME",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H15\">",
    " VELOCARDIOFACIAL (SHPRINTZEN) SYNDROME",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H16\">",
    " Clinical features of VCFS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H17\">",
    " Management of VCFS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H18\">",
    " STICKLER AND MARSHALL SYNDROMES",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H19\">",
    " Clinical features",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H20\">",
    " VAN DER WOUDE SYNDROME",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H14783287\">",
    " SUMMARY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H89678066\">",
    " ACKNOWLEDGMENT",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a href=\"#references\">",
    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " <div class=\"openRelatedGraphics\" id=\"ALLRG/2926\" rel=\"outline_link\">",
    " GRAPHICS",
    " <a class=\"graphics_icon\" href=\"#\" title=\"View All Related Graphics\">",
    " View All",
    " </a>",
    " </div>",
    " </h1>",
    " <div id=\"relatedGraphics\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <div class=\"openRelatedGraphics\" id=\"ALLRG/2926|FIG\">",
    " <a href=\"#\" title=\"FIGURES\">",
    " FIGURES",
    " </a>",
    " </div>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?36/40/37504\"
    title=\"figure 1\">",
    " First branchial arch",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?7/16/7428\" title=\"figure
    2\">",
    " Branchial arch derivatives",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?11/35/11839\"
    title=\"figure 3\">",
    " Pruzansky classification of mandibular abnormalities",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?7/8/7299\" title=\"figure
    4\">",
    " Normal anatomy of the mandible",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?36/36/37454\"
    title=\"figure 5\">",
    " Occlusal cant",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <div class=\"openRelatedGraphics\" id=\"ALLRG/2926|PIC\">",
    " <a href=\"#\" title=\"PICTURES\">",
    " PICTURES",
    " </a>",
    " </div>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_picture\" href=\"UTD.htm?43/2/44067\"
    title=\"picture 1\">",
    " Hemifacial microsomia",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_picture\" href=\"UTD.htm?30/48/31491\"
    title=\"picture 2\">",
    " Pierre Robin sequence",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_picture\" href=\"UTD.htm?16/50/17191\"
    title=\"picture 3\">",
    " Binder syndrome",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_picture\" href=\"UTD.htm?13/41/13983\"
    title=\"picture 4\">",
    " Congenital lip pits",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " RELATED TOPICS",
    " </h1>",
    " <div id=\"relatedTopics\">",
    " <ul>",
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    " Cataract in children",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?1/59/1977?
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    " Congenital anomalies of the jaw, mouth, oral cavity, and pharynx",
    " </a>",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?34/47/35575?
    source=related_link\">",
    " Congenital anomalies of the nose",
    " </a>",
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    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/18/8487?
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    " Craniosynostosis syndromes",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?27/55/28536?
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    " Cytogenetic and molecular genetic diagnostic tools",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?31/37/32343?
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    " <a class=\"medical medical_review\" href=\"UTD.htm?42/2/43048?
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    " <a class=\"medical medical_review\" href=\"UTD.htm?19/44/20169?
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    " Etiology, prenatal diagnosis, obstetrical management, and recurrence of
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    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?43/34/44581?
    source=related_link\">",
    " Facial clefts and holoprosencephaly",
    " </a>",
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    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/27/28087?
    source=related_link\">",
    " Genomic disorders: An overview",
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    " </li>",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?26/23/26999?
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    " Neonatal hypocalcemia",
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    in infants and children",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?13/27/13752?
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    source=related_link\">",
    " Vascular rings",
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    " </div>",
    " </div>"].join("\n");
    var title_f0_15_251="Impairment and lung function";
    var content_f0_15_251=[" <div id=\"graphicsToolbar\">",
    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=PULM
    %2F73018&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=4\" onclick=\"\">",
    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=PULM
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    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\">",
    " <div class=\"ttl\">",
    " Conditions with impairment not directly related to lung function",
    " </div>",
    " <div class=\"cntnt\">",
    " <table cellspacing=\"0\">",
    " <tbody>",
    " <tr>",
    " <td>",
    " Asthma",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Hypersensitivity pneumonitis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Pneumoconiosis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Sleep disorders",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Lung cancer",
    " </td>",
    " </tr>",
    " </tbody>",
    " </table>",
    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_251=[""].join("\n");
    var outline_f0_15_251=null;
    var title_f0_15_252="Clinical findings by stage of hypothermia";
    var content_f0_15_252=[" <div id=\"graphicsToolbar\">",
    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=EM
    %2F62978&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=EM
    %2F62978&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\"
    title=\"Print this page\">",
    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\">",
    " <div class=\"ttl\">",
    " Clinical findings by stage of hypothermia*",
    " </div>",
    " <div class=\"cntnt\">",
    " <table cellspacing=\"0\">",
    " <colgroup width=\"20%\">",
    " </colgroup>",
    " <colgroup span=\"2\" width=\"40%\">",
    " </colgroup>",
    " <tbody>",
    " <tr>",
    " <td class=\"subtitle1\">",
    " Stage",
    " </td>",
    " <td class=\"subtitle1\">",
    " Core temperature",
    " </td>",
    " <td class=\"subtitle1\">",
    " Possible findings",
    " </td>",
    " </tr>",
    " <tr>",
    " <td rowspan=\"3\">",
    " Mild",
    " </td>",
    " <td rowspan=\"3\">",
    " <p>",
    " 32-35&deg;C",
    " </p>",
    " (90-95&deg;F)",
    " </td>",
    " <td>",
    " Shivering but conscious",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Cyanosis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Prolonged capillary refill",
    " </td>",
    " </tr>",
    " <tr class=\"divider_top\">",
    " <td rowspan=\"5\">",
    " Moderate",
    " </td>",
    " <td rowspan=\"5\">",
    " <p>",
    " 28-32&deg;C",
    " </p>",
    " (82-90&deg;F)",
    " </td>",
    " <td>",
    " Shivering stops, impaired consciousness",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Clumsiness",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Confusion or delirium",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Slurred speech",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Decreasing BP",
    " </td>",
    " </tr>",
    " <tr class=\"divider_top\">",
    " <td rowspan=\"8\">",
    " Severe",
    " </td>",
    " <td rowspan=\"8\">",
    " <p>",
    " &lt;28&deg;C",
    " </p>",
    " (&lt;82&deg;F)",
    " </td>",
    " <td>",
    " No shivering, unconscious, vital signs may or may not be present",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Muscle rigidity",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Erythema and edema",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Stupor or coma",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Absent pulses",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Fixed, dilated pupils",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Ventricular fibrillation",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Asystole",
    " </td>",
    " </tr>",
    " </tbody>",
    " </table>",
    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " * When present, findings are typical of the stage shown, but may vary in
    their presence and their temperature of onset.",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_252=[""].join("\n");
    var outline_f0_15_252=null;
    var title_f0_15_253="Radiologic Ddx IIP";
    var content_f0_15_253=[" <div id=\"graphicsToolbar\">",
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    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=PULM
    %2F60070&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=5\" onclick=\"\">",
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    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=PULM
    %2F60070&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=5\" onclick=\"\"
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    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\">",
    " <div class=\"ttl\">",
    " Radiologic features and differential diagnosis of idiopathic interstitial
    pneumonias",
    " </div>",
    " <div class=\"cntnt\">",
    " <table cellspacing=\"0\">",
    " <tbody>",
    " <tr>",
    " <td class=\"subtitle1\">",
    " Clinical diagnosis",
    " </td>",
    " <td class=\"subtitle1\">",
    " Histologic pattern",
    " </td>",
    " <td class=\"subtitle1\">",
    " Radiographic features",
    " </td>",
    " <td class=\"subtitle1\">",
    " Typical distribution",
    " </td>",
    " <td class=\"subtitle1\">",
    " Typical CT findings",
    " </td>",
    " <td class=\"subtitle1\">",
    " Differential diagnosis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " IPF/CFA",
    " </td>",
    " <td>",
    " UIP",
    " </td>",
    " <td>",
    " Basal-predominant reticular abnormality with volume loss",
    " </td>",
    " <td>",
    " Peripheral, subpleural, basal",
    " </td>",
    " <td>",
    " Reticular, honeycombing, traction bronchiectasis/bronchiolectasis;
    architectural distortion. Focal ground glass",
    " </td>",
    " <td>",
    " Asbestosis, collagen vascular disease, hypersensitivity pneumonitis,
    sarcoidosis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " NSIP",
    " </td>",
    " <td>",
    " NSIP",
    " </td>",
    " <td>",
    " Ground glass and reticular opacity",
    " </td>",
    " <td>",
    " Peripheral, subpleural, basal, symmetric",
    " </td>",
    " <td>",
    " Ground glass attenuation, irregular lines, consolidation",
    " </td>",
    " <td>",
    " UIP, DIP, COP, hypersensitivity pneumonitis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " COP",
    " </td>",
    " <td>",
    " OP",
    " </td>",
    " <td>",
    " Patchy bilateral consolidation",
    " </td>",
    " <td>",
    " Subpleural/peribronchial",
    " </td>",
    " <td>",
    " Patchy consolidation and/or nodules",
    " </td>",
    " <td>",
    " Infection, vasculitis, sarcoidosis, alveolar carcinoma, lymphoma,
    eosinophilic pneumonia, NSIP",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " AIP",
    " </td>",
    " <td>",
    " DAD",
    " </td>",
    " <td>",
    " Progressive diffuse ground glass density/consolidation",
    " </td>",
    " <td>",
    " Diffuse",
    " </td>",
    " <td>",
    " Consolidation and ground glass opacity, often with lobular sparing.
    Traction bronchiectasis later",
    " </td>",
    " <td>",
    " Hydrostatic edema, pneumonia, acute eosinophilic pneumonia",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " DIP",
    " </td>",
    " <td>",
    " DIP",
    " </td>",
    " <td>",
    " Ground glass opacity",
    " </td>",
    " <td>",
    " Lower zone, peripheral predominance in most",
    " </td>",
    " <td>",
    " Ground glass attenuation, reticular lines",
    " </td>",
    " <td>",
    " RB-ILD, hypersensitivity pneumonitis, sarcoidosis, PCP",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " RB-ILD",
    " </td>",
    " <td>",
    " RB",
    " </td>",
    " <td>",
    " Bronchial wall thickening; ground glass opacity",
    " </td>",
    " <td>",
    " Diffuse",
    " </td>",
    " <td>",
    " Bronchial wall thickening, cenrilobular nodules, patchy ground glass
    opacity",
    " </td>",
    " <td>",
    " DIP, NSIP, Hypersensitivity pneumonitis",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " LIP",
    " </td>",
    " <td>",
    " LIP",
    " </td>",
    " <td>",
    " Reticular opacities, nodules",
    " </td>",
    " <td>",
    " Diffuse",
    " </td>",
    " <td>",
    " Centrilobular nodules, ground glass attenuation, septal and
    bronchovascular thickening, thin-walled cysts",
    " </td>",
    " <td>",
    " Sarcoidosis, lymphangitic carcinoma, Langerhans' cell histiocytosis",
    " </td>",
    " </tr>",
    " </tbody>",
    " </table>",
    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " AIP: acute interstitial pneumonia; CFA: cryptogenic fibrosing alveolitis;
    COP: cryptogenic OP (also called idiopathic bronchiolitis obliterans organizing
    pneumonia [BOOP]); DAD: diffuse alveolar damage; DIP: desquamative interstitial
    pneumonia; IPF: idiopathic pulmonary fibrosis; LIP: lymphoid interstitial
    pneumonia; NSIP: nonspecific interstitial pneumonia; OP: organizing pneumonia; PCP:
    Pneumocystis jirovecii (carinii) pneumonia; RB-ILD: respiratory bronchiolitis-
    associated intersitial lung disease: UIP: usual interstitial pneumonia.",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
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    var title_f0_15_254="Algorithm for cell free fetal DNA testing for fetal Rh
    status";
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    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=OBGYN
    %2F86944&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
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    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=OBGYN
    %2F86944&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\"
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    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 516px\">",
    " <div class=\"ttl\">",
    " Algorithm for determining the results of cell-free fetal DNA testing to
    determine the fetal RHD status",
    " </div>",
    " <div class=\"cntnt\" style=\"width: 496px; height: 371px; background-image:
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    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " SNP: single-nucleotide polymorphism;",
    " <em>",
    " RHD",
    " </em>",
    " : Rhesus D gene.",
    " </div>",
    " <div class=\"reference\">",
    " Reproduced with permission from: Moise KJ Jr, Argoti PS. Management and
    prevention of red cell alloimmunization in pregnancy: A systematic review. Obstet
    Gynecol 2012; 120:1132. Copyright &copy; 2012 Lippincott Williams &amp; Wilkins.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
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    var outline_f0_15_254=null;
    var title_f0_15_255="Map of the MHC";
    var content_f0_15_255=[" <div id=\"graphicsToolbar\">",
    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=RHEUM
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    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
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    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=RHEUM
    %2F51352&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=0\" onclick=\"\"
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    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
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    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 470px\">",
    " <div class=\"ttl\">",
    " Map of the major histocompatibility complex",
    " </div>",
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    ">",
    " </div>",
    " <div class=\"lgnd\">",
    " The left portion represents the entire MHC region on chromosome 6, with the
    Class I, II, and III regions designated. The right portion is an enlargement of the
    Class II region and includes pseudogenes, other genes involved in immune function,
    and genes of unrelated or unknown function, as well as the \"classical\" Class II
    genes. The expressed \"classical\" Class II dimers are noted on the far right in
    bold letters (DR, DQ, and DP), and the genes encoding them are connected with
    dotted lines. Two different DR dimers are expressed, each sharing the same DR alpha
    chain (DRA), but using different DR beta chains (DRB1 and DRB3).",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_15_255=[""].join("\n");
    var outline_f0_15_255=null;

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