Cerebral edema in childhood diabetic ketoacidosis natural history, radiographic findings, and early identification
Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA. A training sample...
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Veröffentlicht in: | Diabetes care 2004-07, Vol.27 (7), p.1541-1546 |
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description | Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA.
A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed.
The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early- and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs.
CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage. |
doi_str_mv | 10.2337/diacare.27.7.1541 |
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A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed.
The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early- and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs.
CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage.</description><identifier>ISSN: 0149-5992</identifier><identifier>EISSN: 1935-5548</identifier><identifier>DOI: 10.2337/diacare.27.7.1541</identifier><identifier>PMID: 15220225</identifier><identifier>CODEN: DICAD2</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>Adolescent ; Associated diseases and complications ; Biological and medical sciences ; Brain Edema - diagnostic imaging ; Brain Edema - etiology ; Care and treatment ; Cerebral edema ; Child ; Child, Preschool ; Children ; Children & youth ; Diabetes ; Diabetes. Impaired glucose tolerance ; Diabetic acidosis ; Diabetic Ketoacidosis - complications ; Diabetic Neuropathies - classification ; Diabetic Neuropathies - diagnostic imaging ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Health aspects ; Humans ; Infant ; Ketoacidosis ; Medical diagnosis ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neurological disorders ; Neurology ; Radiography ; Retrospective Studies ; Risk factors ; Sensitivity and Specificity</subject><ispartof>Diabetes care, 2004-07, Vol.27 (7), p.1541-1546</ispartof><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 American Diabetes Association</rights><rights>Copyright American Diabetes Association Jul 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15919073$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15220225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MUIR, Andrew B</creatorcontrib><creatorcontrib>QUISLING, Ronald G</creatorcontrib><creatorcontrib>YANG, Mark C. K</creatorcontrib><creatorcontrib>ROSENBLOOM, Arlan L</creatorcontrib><title>Cerebral edema in childhood diabetic ketoacidosis natural history, radiographic findings, and early identification</title><title>Diabetes care</title><addtitle>Diabetes Care</addtitle><description>Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA.
A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed.
The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early- and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs.
CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage.</description><subject>Adolescent</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Brain Edema - diagnostic imaging</subject><subject>Brain Edema - etiology</subject><subject>Care and treatment</subject><subject>Cerebral edema</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Children</subject><subject>Children & youth</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic acidosis</subject><subject>Diabetic Ketoacidosis - complications</subject><subject>Diabetic Neuropathies - classification</subject><subject>Diabetic Neuropathies - diagnostic imaging</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Infant</subject><subject>Ketoacidosis</subject><subject>Medical diagnosis</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurological disorders</subject><subject>Neurology</subject><subject>Radiography</subject><subject>Retrospective Studies</subject><subject>Risk factors</subject><subject>Sensitivity and Specificity</subject><issn>0149-5992</issn><issn>1935-5548</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpt0V9rFDEQAPBFFHutfgBfJAj61F3z97J5LIdWoeCLPi-zyWQvdS85k92H-_ZN6QkiTQID4TfDZNI07xjtuBD6swtgIWPHdac7piR70WyYEapVSvYvmw1l0rTKGH7RXJZyTymVsu9fNxdMcU45V5sm7zDjmGEm6PAAJERi92F2-5QcqfVHXIIlv3FJYINLJRQSYVkfE_ahLCmfrkkGF9KU4biv1IfoQpzKNYHoCEKeTyQ4jEvwwcISUnzTvPIwF3x7jlfNr69ffu6-tXc_br_vbu7aSUi2tFZvceRqlFqCtZahpyB656XA3ng0ztdTDXJlRioR0Ss2OgSn60M9F1fNp6e6x5z-rFiW4RCKxXmGiGktw7YuLnpd4Yf_4H1ac6y9DZwLuqVSP1Zrn9AEMw4h-rRksBNGrLNIEX2o1zeMGS00o6L67hlfdx1zsM8mvD93sY4HdMMxhwPk0_D3ryr4eAZQLMw-Q7Sh_OMMM1QL8QBzGqYe</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>MUIR, Andrew B</creator><creator>QUISLING, Ronald G</creator><creator>YANG, Mark C. K</creator><creator>ROSENBLOOM, Arlan L</creator><general>American Diabetes Association</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7RV</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20040701</creationdate><title>Cerebral edema in childhood diabetic ketoacidosis natural history, radiographic findings, and early identification</title><author>MUIR, Andrew B ; QUISLING, Ronald G ; YANG, Mark C. K ; ROSENBLOOM, Arlan L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g341t-c76eb25b474accc1ef0a38df43e89fe9df9df76ee259b04eeef51bdead7000f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adolescent</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Brain Edema - diagnostic imaging</topic><topic>Brain Edema - etiology</topic><topic>Care and treatment</topic><topic>Cerebral edema</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Children</topic><topic>Children & youth</topic><topic>Diabetes</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic acidosis</topic><topic>Diabetic Ketoacidosis - complications</topic><topic>Diabetic Neuropathies - classification</topic><topic>Diabetic Neuropathies - diagnostic imaging</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Infant</topic><topic>Ketoacidosis</topic><topic>Medical diagnosis</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurological disorders</topic><topic>Neurology</topic><topic>Radiography</topic><topic>Retrospective Studies</topic><topic>Risk factors</topic><topic>Sensitivity and Specificity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MUIR, Andrew B</creatorcontrib><creatorcontrib>QUISLING, Ronald G</creatorcontrib><creatorcontrib>YANG, Mark C. 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K</au><au>ROSENBLOOM, Arlan L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebral edema in childhood diabetic ketoacidosis natural history, radiographic findings, and early identification</atitle><jtitle>Diabetes care</jtitle><addtitle>Diabetes Care</addtitle><date>2004-07-01</date><risdate>2004</risdate><volume>27</volume><issue>7</issue><spage>1541</spage><epage>1546</epage><pages>1541-1546</pages><issn>0149-5992</issn><eissn>1935-5548</eissn><coden>DICAD2</coden><abstract>Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA.
A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed.
The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early- and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs.
CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage.</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>15220225</pmid><doi>10.2337/diacare.27.7.1541</doi><tpages>6</tpages></addata></record> |
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subjects | Adolescent Associated diseases and complications Biological and medical sciences Brain Edema - diagnostic imaging Brain Edema - etiology Care and treatment Cerebral edema Child Child, Preschool Children Children & youth Diabetes Diabetes. Impaired glucose tolerance Diabetic acidosis Diabetic Ketoacidosis - complications Diabetic Neuropathies - classification Diabetic Neuropathies - diagnostic imaging Endocrine pancreas. Apud cells (diseases) Endocrinopathies Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Health aspects Humans Infant Ketoacidosis Medical diagnosis Medical sciences Nervous system (semeiology, syndromes) Neurological disorders Neurology Radiography Retrospective Studies Risk factors Sensitivity and Specificity |
title | Cerebral edema in childhood diabetic ketoacidosis natural history, radiographic findings, and early identification |
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