netherlands journal of critical care

n eth e rlan ds jou rnal of critical care

Verenigingsnieuws Agenda Oproep regionalisatie Ede, 11 november 2008

Geachte collega,

Naar aanleiding van het congres regionalisatie (u kunt de voordrachten bekijken op nvic.nl/ congressen.php), het onderzoek van de Inspectie voor de Gezondheidszorg (IGZ) naar niveau 1 IC’s, en overleg met de IGZ is ons gebleken dat een aantal IC’s van niveau 1 op dit moment nog niet voldoet aan de minimale voorwaarden die de IGZ stelt. Dit betreft in het bijzonder het beschikbaar zijn van een geregistreerd intensivist binnen de eigen organisatie of via regionale samenwerking, het ontbreken van afspraken met betrekking tot regionale samenwerking inclusief afspraken over interklinisch transport van IC-patiënten, het niet beschikbaar hebben van verschillende protocollen, en/of het afwezig zijn van afspraken binnen het ziekenhuis over het soort patiënten dat op de IC kan worden opgenomen. Alle betrokken IC’s hebben inmiddels bericht gekregen van de IGZ. Het moge duidelijk zijn dat, waar de beroepsgroep een geleidelijker verbetertraject tot 2011 voor ogen had middels de CBO Richtlijn Organisatie en Werkwijze op Intensive Care-afdelingen

voor volwassen (2006), externe factoren een versnelling van deze ontwikkeling opleggen. Ik roep alle intensivisten op om, met ondersteuningen van hun Raden van Bestuur, op korte termijn te komen tot daadwerkelijke samenwerking binnen hun regio. In het bijzonder is deze oproep ook gericht aan intensivisten op IC’s van niveau 2 en 3 om hieraan mee te werken. Op de website (nvic.nl) staan een twee documenten die kunnen dienen als voorbeeld voor een formele basis voor een samenwerkingsovereenkomst tussen IC’s binnen uw regio. Wellicht is het goed er nog eens op te wijzen dat de relevante richtlijnen beschikbaar zijn op nvic.nl/richtlijnen_geaccordeerd.php; deze kunnen uiteraard worden aangepast aan uw eigen situatie. Voor de goede orde meld ik dat IC’s van niveau 2 en 3 de volgende jaren ook onderwerp van onderzoek door de IGZ zullen zijn. Dit betekent met andere woorden dat álle IC’s in Nederland hun zaken goed voor elkaar moeten hebben, niet alleen in de (informele) praktijk maar ook bij formele toetsing. In de hoop u van dienst te zijn geweest, groet ik u vriendelijk, Hans van der Spoel, voorzitter NVIC

Verenigingen die accreditatie verleenden aan NVIC activiteiten in 2008 NIV NVALT NVVN Nederlandse Intensivisten dagen 17 pnt 6 pnt 17 pnt Nemo 11 pnt 5 pnt Neuro 12 pnt 12 pnt Mechanische Beademingsdagen 12 pnt 12 pnt -

NVvH 17 pnt 11 pnt 12 pnt 12 pnt

607 intensivisten en fellows 7 rustende leden 1057 overige leden 40 overige abonnees Totaal 1 augustus 2008: 1681 Totaal 1 oktober 2008: 1711 Totaal lezersbereik: 3934

CPC de Jager Internist-intensivist Jeroen Bosch Ziekenhuis, Den Bosch Bestuurslid E-mail: [email protected]

NVK 17 pnt 10 pnt -

NVMM 2 pnt -

Congressen in 2009 8-9 januari Conferentie: How to organize Intensive Care, Zeist, The Netherlands 22 januari Congres: Een dag om nooit te vergeten; ter gelegenheid van: - opening nieuwe IC Gelre Ziekenhuizen, Apeldoorn - Promotie van José Hofhuis tot doctor - Afscheid van Peter Beelen, technisch verpleegkundige 11,12 en 13 februari NVIC Intensivistendagen, Ede, The Netherlands (in een geheel nieuw format) 28 maart NVIC Cursus Echografie op de Intensive Care, Ziekenhuis Rijnstate, Arnhem, The Netherlands 18-19 juni NVIC Circulatiedagen, Ede, The Netherlands 17-18 september NVIC Traumatologie en Acute Geneeskunde, Ede, The Netherlands 19-20 november NVIC Infectiedagen, Ede, The Netherlands

NVN 16 pnt 11 pnt 12 pnt -

NVZA 15 pnt 11 uren 12 pnt 12 pnt

NVC 8 pnt 11 pnt 12 pnt

NVA 15 pnt 10 uren 12 pnt 12 pnt

NVIC Bestuur JI van der Spoel Internist-intensivist Universitair Medisch Centrum Utrecht, Utrecht Voorzitter E-mail: [email protected] PW de Feiter Chirurg-intensivist St Franciscus Gasthuis, Rotterdam Penningmeester E-mail: [email protected] I van Stijn Internist-intensivist Onze Lieve Vrouwe Gasthuis, Amsterdam Secretaris E-mail: [email protected]

Dr. KH Polderman Internist-intensivist Universitair Medisch Centrum, Utrecht Bestuurslid E-mail: [email protected]

Dr. H Kieft Internist-Intensivist Isala Klinieken, Zwolle Bestuurslid [email protected]

Secretariaat NVIC Stationsweg 73 C, 6711 PL Ede. Telefoon: 0318-693337, Fax: 0318-693338, E-mail: [email protected] Jolien Wiegman

JHJ Meeder Anesthesioloog-intensivist Medisch Centrum Rijnmond-Zuid, Rotterdam Bestuurslid E-mail: [email protected]

Secretariaat NJCC Stationsweg 73C, 6711 PL Ede Telefoon: 0318-693337 Fax: 0318-693338 E-mail: [email protected] Andrea Wijnand

n et h j crit care • volume 12 • no 6 • decembe r 2008

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NVT 16 pnt 11 pnt 12 pnt 6 pnt

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v a c a t u r e

FCCS Commissieleden In de FCCS Commissie zijn vacatures ontstaan voor nieuwe Commissieleden. FCCS organiseert jaarlijks voor meer dan 700 artsen gecertificeerd Intensive Care onderwijs. Voor nadere informatie kunt u via het NVIC- secretariaat contact opnemen met Dr. Arthur van Zanten, intensivist, interim voorzitter FCCS Commissie.

Graag nodigen we u uit om te reageren op deze vacature.

activiteiten nvic • Intensivistendagen (in een geheel nieuw format) 11, 12 en 13 februari 2009

• NVIC Cursus Echografie op de Intensive Care 28 maart 2009

• Circulatiedagen 18-19 juni 2009

• Traumatologie en Acute Geneeskunde 17-18 september 2009

• Infectiedagen

19-20 november 2009

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Verkorte productinformatie ECALTA (januari 2008). Samenstelling: ECALTA bevat 100 mg anidulafungin per injectieflacon, overeenkomend met een 3,33 mg/ml oplossing na reconstitutie en een 0,36 mg/ml oplossing na verdunning. Indicaties: Behandeling van invasieve candidiasis bij volwassen niet-neutropene patiënten. ECALTA is hoofdzakelijk onderzocht bij patiënten met candidemie en slechts bij een beperkt aantal patiënten met diepgelegen Candida infecties of met abcesvorming. Farmacotherapeutische groep: Antimycotica voor systemisch gebruik, andere antimycotica, ATC-code: JO2 AX 06. Contra-indicaties: Overgevoeligheid voor het werkzame bestanddeel of voor één van de hulpstoffen; overgevoeligheid voor andere geneesmiddelen uit de groep van echinocandinen. Waarschuwingen en voorzorgen: De werkzaamheid van ECALTA bij neutropene patiënten met candidemie en bij patiënten met diepgelegen Candida infecties of intra-abdominaal abces en peritonitis is niet vastgesteld. De klinische werkzaamheid is hoofdzakelijk beoordeeld bij niet-neutropene patiënten met C. albicans infecties en bij een kleiner aantal patiënten met niet-albicans infecties, voornamelijk C. glabrata, C. parapsilosis en C. tropicalis. Patiënten met Candida-endocarditis, -osteomyelitis of -meningitis en bekende C. krusei infectie zijn niet onderzocht. Verhoogde waarden van leverenzymen zijn waargenomen bij gezonde personen en patiënten die met anidulafungin werden behandeld. Er zijn geïsoleerde gevallen van significante leverstoornis, hepatitis of verergerend leverfalen gerapporteerd. Bij patiënten met verhoogde leverenzymen tijdens behandeling met anidulafungin dient te worden gecontroleerd op tekenen van verslechterende leverfunctie en dient het risico/voordeel van voortzetting van behandeling met anidulafungin geëvalueerd te worden. In een onderzoek bij ratten is verergering van infusie-gerelateerde reacties door gelijktijdige behandeling met anesthetica waargenomen waarvan de klinische relevantie onbekend is. Men dient voorzichtig te zijn bij het gelijktijdig toedienen van anidulafungin en anesthetica. Dit geneesmiddel bevat 24 vol% ethanol (alcohol). Ethanol kan schadelijk zijn voor personen die alcoholist zijn. Hiermee dient rekening te worden gehouden bij zwangere vrouwen of vrouwen die borstvoeding geven, kinderen en hoogrisicogroepen zoals die met een leveraandoening of epilepsie. De hoeveelheid alcohol in dit geneesmiddel kan de effecten van andere medicatie veranderen. De hoeveelheid alcohol in dit geneesmiddel kan de rijvaardigheid of het vermogen om machines te bedienen, verminderen. Patiënten met een zeldzame erfelijke fructose-intolerantie dienen dit geneesmiddel niet te gebruiken. Bijwerkingen: Bijwerkingen in klinische studies waren meestal licht tot matig en leidden zelden tot stopzetting van de behandeling. De meest gerapporteerde, vaak voorkomende bijwerkingen (≥1/100 tot <1/10) zijn: coagulopathie, convulsies, hoofdpijn, diarree, braken, misselijkheid, verhoogd creatininegehalte in het bloed, uitslag, pruritus, hypokaliëmie, flushing, verhoogde alanine-aminotransferase, verhoogde alkalische fosfatase in het bloed, verhoogde aspartaat-aminotransferase, verhoogd bilirubine in het bloed, verhoogde gamma-glutamyltransferase. Soms (≥1/1000, < 1/100) zijn waargenomen: pijn in de bovenbuik, urticaria, hyperglykemie, hypertensie, opvliegers, pijn op de infusieplaats, cholestase. Afleveringsstatus: UR. Verpakking en Registratienummer: ECALTA, 100 mg poeder en oplosmiddel voor concentraat voor oplossing voor intraveneuze infusie: EU/1/07/416/001 (1 injectieflacon met 100 mg poeder en 1 injectieflacon met 30 ml oplosmiddel). Vergoeding en prijzen: ECALTA is niet opgenomen in het GVS. Voor prijzen wordt verwezen naar de Z-Index taxe. Voor medische informatie over dit product belt u met 0800-MEDINFO (6334636). De volledige productinformatie (SPC van 20 september 2007) is op aanvraag verkrijgbaar. Registratiehouder: Pfizer Limited, Ramsgate Road, Sandwich, Kent CT13 9NJ, Verenigd Koninkrijk. Neem voor correspondentie en inlichtingen contact op met de lokale vertegenwoordiger: Pfizer bv, Postbus 37, 2900 AA Capelle a/d IJssel. Referenties 1. Reboli AC, Rostein C, Pappas PG, Chapman SW, Kett DH, Kumar D, Betts R, Wible M, Goldstein BP, Schranz J, Krause DS and Walsh TJ for the Anidulafungin Study Group. Anidulafungin versus fluconazole for invasive candidiasis. New England Journal of Medicine 2007; 356: 2472-2482. 2. Dowell JA, Stogniew M, Krause D, Henkel T, Weston IE. Assessment of the safety and pharmacokinetics of anidulafungin when administered with cyclosporine. J Clin Pharmacol. 2005;45:227-33. 3. Dowell JA, Schranz J, Baruch A, Foster G.Safety and pharmacokinetics of coadministered voriconazole and anidulafungin. J Clin Pharmacol. 2005;45:1373-82. 4. Dowell JA, Stogniew M, Krause D, Henkel T, Damle B.Lack of pharmacokinetic interaction between anidulafungin and tacrolimus. J Clin Pharmacol. 2007;47:305-14. 5. Dowell, J.S., Stogniew, M., et al., Anidulafungin does not require dosage adjustment in subjects with varying degrees of hepatic or renal impairment. J Clin Pharmacol, 2007. 47:461-70. 6. SPC van 20 september 2007.

* In deze studie werd anidulafungin-IV vergeleken met fluconazol-IV bij 245 patiënten met invasieve candidiasis. Het primaire eindpunt was globale respons (microbiologisch en klinisch) aan het eind van de IV-behandelperiode.


10-12-2008 16:37:18

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a a n k o n d i g i n g

Scholingsdag kwaliteitsindicatoren nationale database De NVIC en de stichting NICE organiseren dat vanaf september 2007 de kwaliteitsindicatoren voor de intensive care kunnen worden geregistreerd in een nationale database. Hiertoe is een scholingsdag opgezet waarin alle items worden toegelicht. Inbegrepen is een scholing in de Minimale Data Set alsmede instructie over aanlevering en softwarematige ondersteuning.

Scholingsdata woensdag 14 januari 2009 donderdag 5 februari 2009 woensdag 11 maart 2009 donderdag 16 april 2009 woensdag 13 mei 2009 aanmelden via de secretaris van de stichting NICE: [email protected] Meer informatie omtrent indicatoren en implementatie traject is te vinden op de volgende websites: http://www.nvic.nl/commissie_kwaliteitsindicatoren.php en www.stichting-NICE.nl


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Complicatieregistratie van de Intensive Care behandeling in Nederland Commissie Complicatieregistratie van de Nederlandse Vereniging voor Intensive Care (CC NVIC)

Bestaande uit 1. mw dr. M.S. Arbous 2. Dr. A. Beishuizen 3. Drs. R.J. Bosman 4. Drs. M.P. Buise 5. mw. drs. L. Dawson 6. Drs. J.H.J. Meeder 7. mw. drs. G.A.M. Salet

Inleiding Intensive Care (IC) geneeskunde heeft in de afgelopen jaren een grote ontwikkeling doorgemaakt die zich nog steeds voortzet. Hierbij nemen kwaliteit van zorg en veiligheid van de patiënt een centrale plaats in, zowel in de klinische zorg, als in de opleiding, het onderwijs, en het wetenschappelijk onderzoek. Door de beroepsgroep van intensivisten wordt al jaren de noodzaak gevoeld de kwaliteit, effectiviteit en doelmatigheid van IC behandeling te evalueren. Daarom zijn er meerdere belangrijke kwaliteitsprojecten geïnitieerd: Zo bestaat er een CBO-richtlijn ‘Organisatie en werkwijze intensive care afdelingen’, die richting geeft aan de uitvoering van IC-geneeskunde voor volwassenen in Nederland. Via visitatie door de NVIC/NVICV vindt onder meer aan de hand van deze richtlijn een kwalitatieve evaluatie plaats van IC-afdelingen door de eigen beroepsgroep intensivisten en IC-verpleegkundigen. Het project interne kwaliteitsindicatoren voor IC-afdelingen (KIIC) heeft geleid tot de structurele registratie van 12 kwaliteitsindicatoren die betrekking hebben op de kwaliteit van structuur, proces en uitkomsten op intensive care afdelingen. Het doel hierbij is om uiteindelijk tot verbetertrajecten op individuele afdelingen te komen. De stichting NICE (Nationale Intensive Care Evaluatie) is opgericht met het doel de gegevens van de IC behandeling in verschillende ziekenhuizen op uniforme wijze te verzamelen voor vergelijk over de tijd en tussen ziekenhuizen onderling (benchmark). De stichting NICE is nu ook in staat om de andere kwaliteitsindicatoren te verwerken, te vergelijken en te rapporteren. Op dit moment nemen 81 ziekenhuizen deel aan de NICE registratie (alleen uitkomsten) en nemen er 21 ziekenhuizen deel aan de KIIC-registratie via NICE. Er is één maal per kwartaal terugkoppeling van de prestaties van individuele IC afdelingen, gespiegeld aan landelijke gemiddelden. Terugrapportage van de kwaliteitsindicatoren zal binnenkort deels gericht worden op daadwerkelijke implementatie van verbetertrajecten in onderzoeksverband (InfoQ).

Complicatieregistratie in Nederland Hoewel complicaties slechts één aspect van kwaliteit weergeven, namelijk de “uitkomst-zijde“ is er vanuit de beroepsgroep behoefte aan betrouwbare informatie over het optreden van complicaties op de IC-afdelingen. Het registreren van complicaties bij medische handelingen is sinds de introductie van de Kwaliteitswet in 1996 wettelijk verplicht. Het ontwikkelen en implementeren van een complicatie-

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registratie is een speerpunt in het kwaliteitsbeleid van medisch specialisten. In de ‘Meerjarenafspraken curatieve somatische zorg’ zijn het Ministerie van Volksgezondheid, Welzijn en Sport (VWS) en de Orde van Medisch Specialisten (OMS) in 1998 overeengekomen dat de OMS het initiatief zou nemen in het project Complicatieregistraties. In 1999 is de OMS begonnen met het ontwikkelen van landelijke systemen voor complicatieregistraties. Dit initiatief, het Programma Complicatieregistratie, is gesubsidieerd door het Ministerie van VWS. Het gaat hierbij om het voor en door medisch specialisten realiseren van complicatieregistraties. Het uiteindelijke doel is om te voldoen aan de behoefte die in Nederland heerst om te beschikken over betrouwbare informatie over complicaties. Sinds 2003 maakt het hebben van een complicatieregistratie door een wetenschappelijke vereniging onderdeel uit van de basisset Prestatie indicatoren van de IGZ. Complicaties zijn ongewenste uitkomsten van zorg die voor de patiënt en voor de zorg belastend zijn. Preventie van complicaties betekent gezondheidswinst voor patiënten, kwaliteitswinst voor professionals en doelmatigheidswinst voor ziekenhuizen. Complicatieregistratie is geen doel op zich maar kan als kwaliteitsinstrument voor en door de medische specialisten worden gebruikt. Met een complicatieregistratie wordt beoogd: (1) betrouwbare informatie te verzamelen over complicaties, (2) factoren te vinden die complicaties kunnen voorkomen, en (3) een kwaliteitscyclus te realiseren gericht op de preventie van complicaties.

Complicatieregistratie op IC-afdelingen In 2005 is er door het bestuur van de NVIC een Commissie Complicatieregistratie ingesteld. De Commissie Complicatieregistratie van de NVIC (CC NVIC) heeft ervoor gekozen zich op hoofdlijnen zich aan te sluiten bij de landelijk ontwikkelde complicatieregistratiesystemen. De belangrijkste reden was dat het een goed ontwikkeld systeem is dat inmiddels door vele wetenschappelijke verenigingen succesvol is geïmplementeerd en waar al veel ervaring mee is opgedaan. Door gebruik van eenzelfde registratiesysteem en uniformiteit in de definitie bestaat er bovendien de mogelijkheid in de toekomst specialisme-overstijgend complicaties over het hele zorgtraject te bestuderen. De OMS heeft landelijke standaarden ontwikkeld voor een complicatieregistratie van een wetenschappelijke vereniging. De drie volgende elementen zijn voor de complicatieregistratie op de IC overgenomen: (1) Een definitie voor het begrip ‘complicatie’. (2) Een minimale dataset die informatie bevat betreffende patiënt, behandelaar, behandeling, context, en de complicatie. Er is voor gekozen dat de minimale dataset de gegevens omvat zoals ze worden verzameld voor de NICE registratie. (3) Functionele specificaties voor software voor lokale en landelijke automatisering van opslag, codering, en rapportage van gegevens.

OMS definitie van complicatie: Complicatie is een onbedoelde en ongewenste gebeurtenis of toestand tijdens of volgend op medisch specialistisch handelen, die voor de gezondheid van de pati-


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ënt zodanig nadelig is dat aanpassing van het medisch (be)handelen noodzakelijk is dan wel dat er sprake is van (onherstelbare) schade. Nader criterium: een complicatie wordt geconstateerd gedurende de behandeling of bij de direct daarop volgende poliklinische controle, dan wel binnen een door de wetenschappelijke vereniging bepaalde periode vanaf het begin van de behandeling. Niet van belang in dit kader is het resultaat van de feitelijke medisch specialistische behandeling, de waarschijnlijkheid van de complicatie en de eventuele aan- of afwezigheid van schuld.

Specifieke aandachtspunten voor complicatieregistratie op de Intensive Care Tijdens de voorbereiding van het opzetten van een complicatieregistratie voor de IC heeft de commissie zich gerealiseerd dat een complicatieregistratie voor de IC unieke aspecten heeft en aan specifieke voorwaarden moet voldoen. Ten eerste zijn op de IC over het algemeen patiënten opgenomen met uitgebreide co-morbiditeit en één of meer falende orgaansystemen, waarbij het niet altijd makkelijk is om het ziektebeloop van een complicatie te onderscheiden. Ten tweede bestaat de IC-populatie gedeeltelijk uit patiënten die een complicatie hebben gekregen tijdens een behandeling door een ander specialisme en voor de behandeling van de complicatie op de IC worden opgenomen. Ten derde is de IC een hoog risico omgeving waarbij door de aard van de aandoening, de kwetsbaarheid van de patiënt en de aard van de zorg, de kans op het optreden van een complicatie aanzienlijk is. De complicaties die zullen worden geregistreerd zullen enerzijds typisch zijn voor de intensive care behandeling en anderzijds gerelateerd zijn aan de opname-indicatie en opname-diagnose. Het zal niet makkelijk zijn onderscheid te maken tussen deze categorieën. Bovendien is het streven op voorhand niet een causaal verband te leggen tussen opname-indicatie, opname-diagnose, en interventie enerzijds en complicatie anderzijds. Dit om bias te verkleinen. De causale verbanden worden later bij analyse van de gegevens over determinanten en uitkomsten gelegd.

Werkwijze van de Commissie Complicatieregistratie Vaststellen Top 9

De Commissie heeft gesteld dat het om behandelingsuitkomsten van een IC patiënt gaat die worden gemeten tijdens opname op een intensive care afdeling. De Commissie benadrukt dat de reden van opname op de IC niet als complicatie wordt beschouwd. Bij een initiële inventarisatie heeft de Commissie vastgesteld dat in de literatuur nog weinig voorbeelden bestaan van een systematische aanpak van complicatieregistratie op de intensive care. Wel zijn er projecten gaande die betrekking hebben op de registratie van incidenten zoals de Australische AIMS-ICU1-3 en het web based ICU Safety Reporting System (ICUSRS).4;5 Vervolgens heeft de commissie door een enquête en het doen van interviews vastgesteld dat het begrip ‘complicatie op de IC’ door intensivisten heel breed geïnterpreteerd wordt. Daarom is de eerste stap geweest dat aan de hand van een vragenlijst alle commissieleden en intensivisten uit een aantal ziekenhuizen in Nederland, voorbeelden van te registreren complicaties aangeleverd hebben. Deze lijst heeft geleid tot het vaststellen van 12 hoofd categorieën van complicaties: (1) Cardiovasculair, (2) Pulmonaal, (3) Neurologie, (4) Infectieus, (5) Urogenitaal, (6) Gastro-intestinaal, (7) Luchtweg, (8) Hemostase en Bloeding, (9) Ingreep gerelateerd, (10) Medicamenteus, (11) Transfusie, en (12) Overig. Vervolgens hebben de leden van

de commissie, volgens een gestructureerd plan (de Werklijst, Bijlage 1), bekeken of de potentiële complicatie voldeed aan de volgende voorwaarden: (1) Van de complicatie bestaat onderbouwing in de literatuur dat er een relatie bestaat met een negatieve uitkomst dan wel schade voor de patiënt op langere termijn. (2) De complicatie moet of zeer ernstig zijn, of regelmatig voorkomen, of beiden. (3) De complicatie moet eenduidig te definiëren en te meten zijn. (4) Van de complicatie bestaat bij voorkeur een mogelijkheid om een interventie ter voorkoming te plegen. Initieel, rekening houdend met de eerste voorwaarde, is uit 68 potentiële complicaties een top 20 vastgesteld. Vervolgens is gekeken welke complicaties daarnaast nog eenduidig te definiëren en te meten zijn, regelmatig voorkomen en/of zeer ernstig zijn, en van welke het optreden te verminderen is door een interventie. Hiermee is uiteindelijk een top 9 van complicaties samengesteld. De Commissie wilde, in navolging van andere wetenschappelijke verenigingen, beginnen met een top 9 van complicaties. De ervaring heeft geleerd dat dan de kans op compliantie en succesvolle implementatie (in een pilot fase en daarna) wordt vergroot.

Software In navolging van andere landelijke complicatieregistratie systemen, en om de haalbaarheid te vergroten, is gekozen voor een geautomatiseerde registratie. In samenwerking met de firma Ité Medical is een software module ontwikkeld waarmee het mogelijk is geautomatiseerd complicaties vast te leggen. Hierbij is het tevens mogelijk de gegevens van de minimale dataset van NICE en de set KIIC vast te leggen. De software wordt in enkele ziekenhuizen al gebruikt en wordt voor de duur van de pilot studie aan de pilot ziekenhuizen ter beschikking gesteld door Ite Medical.

Doelstelling en fasering pilot studie Op 1 januari 2009 zal worden gestart met een pilot studie Complicatieregistratie NVIC. Hierbij zullen gedurende 9 maanden complicaties volgens de top 9 worden bijgehouden op 19 intensive care afdelingen, niveau I, II, en III, verspreid over Nederland. Het doel van de pilot studie is om de hanteerbaarheid van de top 9 en de software te testen en om inzicht te krijgen in problemen en aandachtspunten bij de implementatie van een complicatieregistratiesysteem. Te beantwoorden vragen zijn: Wat is de benodigde tijdsinvestering, zijn de definities bruikbaar, welke belangrijke omissies zijn er in de complicatielijst, hoe functioneert de software en welke problemen zijn er eventueel mee ondervonden? Het gehele project kent drie fasen. Fase 1 bestaat uit het implementeren van de software in de pilot ziekenhuizen, het ontwikkelen van software in ziekenhuizen die geen Mediscore hebben, het verstrekken schriftelijke informatie, en het organiseren van een voorlichtingsavond voor aanvang van de gegevensverzameling. Fase 2 bestaat uit het verzamelen van gegevens. In deze fase zullen voorlichtingsavonden voor de deelnemers worden georganiseerd. Fase 3 bestaat uit het evalueren van de doelstellingen na 9 maanden door middel van een vragenlijst en interviews. Tevens zullen de verzamelde gegevens in samenwerking met de stichting NICE worden verwerkt, geanalyseerd en gerapporteerd. Dit zal leiden tot bijstelling van de gehanteerde definities en van de samenstelling van de complicatielijst, en zo nodig tot aanpassing van de wijze van registreren.



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Top 9 complicaties Er is voor gekozen, teneinde de registratie in deze pilot fase zo eenvoudig mogelijk te maken en om de werklast zo klein mogelijk te houden, om het grootste deel van de complicaties per opname niveau te verzamelen. Hierbij realiseert de commissie zich dat enkele complicaties meerdere malen per opname zouden kunnen optreden. Er is altijd de mogelijkheid om bij te houden of de complicatie zich meerdere malen per opname heeft voorgedaan in de vrije tekst ruimte. Als bij de evaluatie van de pilot studie is gebleken dat er voor enkele complicaties de behoefte is om deze per dag te verzamelen zal dit na de pilot fase worden geïmplementeerd. 1. Myocardinfarct (MI)

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Uit literatuur is gebleken dat het doormaken van een myocardinfarct leidt tot verlenging van ziekenhuisopname (tot 11 dagen) en bijdraagt aan de ziekenhuismortaliteit. Ernst: Een myocardinfarct is een ernstige IC complicatie. Incidentie: De gerapporteerde incidentie van een myocardinfarct tijdens IC opname is hoog (tot 36%), hoewel lastig te herkennen en ondergediagnostiseerd.6 Dit moet gezien worden naast de incidentie van een myocardinfarct die na niet cardiale chirurgie hoog is (1525%). Definitie: Primair zij vermeldt dat het hier niet gaat om het myocardinfarct als reden van IC opname, maar om het myocardinfarct dat zich minimaal 24 uur na IC opname openbaart. Er zijn 5 types MI te onderscheiden.6 Type 1 en 2 zijn secundair aan ischemie: (respectievelijk primair coronair event zoals plaque erosie of ruptuur, fissuur of dissectie danwel disbalans tussen zuurstofvraag en -aanbod). Type 3: plotse dood met symptomen van ischemie, vergezeld door nieuw ST elevaties of LBTB, danwel bewezen coronaire thrombus. Types 4 en 5 treden op na PCI danwel CABG.7-12 De criteria voor type 1-2 omvatten de detectie van een stijging van cardiale biomarkers (bij voorkeur troponine) met tenminste één waarde boven het 99e percentiel van de bovenste referentie limiet in combinatie met tenminste 1 teken van ischemie: klinische symptomen van ischemie, ECG veranderingen (nieuwe ST-T veranderingen of nieuw LBTB), pathologische Q golven, imaging bewijs zoals regionale wandbewegingsstoornissen. Alleen type MI 1-3 zullen worden geregistreerd in het kader van de NVIC IC complicatietegistratie, volgens de criteria zoals hierboven voor type 1-2 beschreven, daar er reeds een registratie bestaat voor type 4-5 door cardiologen en thoraxchirurgen.13 Verbeterplannen c.q interventie: Voor deze complicatie is niet op voorhand duidelijk welke interventies verricht moeten worden om de incidentie op de intensive care te verminderen. Er zijn voor verschillende patiëntengroepen in het het hele zorgtraject verschillende interventies denkbaar. Met registratie in een IC complicatieregistratie wordt een aanvang gemaakt met het in kaart brengen van de epidemiologie van MI op de IC, de vroege herkenning en diagnostiek, waarbij de pittfalls met betrekking tot cardiale biomarkers een rol spelen. Achtergrond: Deze complicatie wordt per opname gescoord. De teller is het aantal patiënten dat gedurende zijn/haar IC opname een myocardinfarct heeft doorgemaakt per tijdseenheid (jaar). De noemer is het aantal patiënten dat per tijdseenheid (jaar) is opgenomen. Hoewel het theoretisch mogelijk is gedurende een IC opname een recidief myocardinfarct te krijgen, is ervoor gekozen deze complicatie niet dagelijks te scoren. Het zal niet eenvoudig zijn een recidief infarct te diagnosticeren: bij welke stijging van enzymmarkers, veranderingen

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in het ECG, en veranderingen in wandbewegingsstoornissen stelt men dat het gaat om het natuurlijk beloop van het initiële infarct en bij welke veranderingen dat het om een nieuw myocardinfarct gaat ? In de zeer zeldzame gevallen dat het evident is dat er een recidief myocardinfarct is opgetreden zal dit in de vrije tekst ruimte bijgehouden kunnen worden. 2. Cardiac Arrest

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Het is evident dat na een cardiac arrest en reanimatie de kans op blijvende neurologische schade of overlijden aanzienlijk is. Ernst: Dodelijk, tenzij reanimatiepoging geslaagd. Incidentie: Het is niet duidelijk wat de incidentie van een cardiac arrest is op de intensive care. Studies die over in-hospital cardiac arrest rapporteren, includeren vooral patiënten van niet IC en niet CCU afdelingen die zijn gereanimeerd. Bovendien zijn er op de intensive care twee categorieën patiënten met een mogelijk cardiac arrest te onderscheiden waarbij de incidentie ook zal verschillen: patiënten die als rede van IC opname een cardiac arrest hadden en patiënten met een andere opname indicatie die op de intensive care een cardiac arrest hebben doorgemaakt. De ziekenhuisoverleving van een in-hospital cardiac arrest wordt gerapporteerd van 0 tot 40%.14-20 Definitie: Cardiale gebeurtenissen zoals ventrikel fibrillatie, ventrikel tachycardie zonder output, asystolie, elektromechanische dissociatie (polsloze electrische activiteit), bradycardie zonder sufficiënte cardiac output, en andere ritmestoornissen, waarvoor hartmassage of defibrillatie nodig is. Het probleem wordt als complicatie geregistreerd als het niet de reden voor IC opname was en zich minimaal 4 uur na opname op de IC openbaarde. De commissie stelt voor het optreden van een cardiac arrest bij de IC populatie te registreren, ongeacht of er een niet reanimeren beleid is afgesproken. Achtergrond: De commissie meent dat deze complicatie te allen tijde geregistreerd dient te worden gezien de ernst. Deze complicatie wordt per opname gescoord hoewel het theoretisch mogelijk is dat een patiënt tijdens zijn/haar IC opname meerdere malen een cardiac arrest doorgemaakt. De teller is het aantal patiënten is dat gedurende zijn/haar IC opname een cardiac arrest heeft doorgemaakt per tijdseenheid (jaar). De noemer is het totaal aantal opgenomen patiënten per tijdseenheid (jaar). In het geval dat een patient meerdere malen een cardiac arrest doormaakt is er ruimte om dit in de vrije tekst ruimte te vermelden. Op deze wijze kan het worden meegenomen bij de evaluatie van de pilot studie. 3. Pneumothorax

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Er is niet veel bewijs dat er een relatie is met de lange termijn uitkomst. Wel leidt het optreden van een pneumothorax op korte termijn tot extra morbiditeit en verminderde kwaliteit van zorg.21-24 Ernst: Indien onbehandeld is een pneumothorax een potentieel ernstige IC complicatie. Incidentie: De gerapporteerde incidentie op de IC varieert van 0.5% tot 3-10% op dag 30 van de IC opname.25 Definitie: Door middel van radiologisch onderzoek vastgesteld lucht in de pleurale holte, die tevoren niet aanwezig was, en/of een interventie ter behandeling van een pneumothorax, zijnde drainage d.m.v. inbrengen van een thoraxdrain. Verbeterplannen c.q interventie: Voor zover het een pneumothorax betreft die gerelateerd is aan het inbrengen van een centrale lijn kan worden gedacht aan scholing en onderwijs van fellows en arts-assistenten, supervisie, en een andere benadering van het centraal veneuze systeem.


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Achtergrond: De commissie beschouwt een pneumothorax als een complicatie die een sterke relatie heeft met de interventies en behandelingen die op een IC plaatsvinden. Deze complicatie wordt per IC behandeldag gescoord omdat het mogelijk is dat bij een patiënt gedurende de IC opname meerdere malen een pneumothorax is opgetreden. De teller is het aantal behandeldagen waarop een pneumothorax voor het eerst is gediagnosticeerd per tijdseenheid (jaar), en de noemer is het totaal aantal behandeldagen per tijdseenheid (jaar). 4. Cerebro-vascular accident (CVA)

Twee categorieën kunnen worden onderscheiden26: 1. Cerebrale ischemie en infarct is in 65-70% van de gevallen het gevolg van atherosclerose en in 30% het gevolg van cardiale emboliebron (atrium fibrilleren, infectieuze endocarditis, niet bacteriële endocarditis, post myocard infarct, cardiomyopathie, post cardiochirurgie). Zeldzamere oorzaken zijn dissectie van A. carotis of A.vertebralis secundair aan hoofd-hals trauma, post carotis endarteriectomie en intracraniële arteriële of veneuze thrombose secundair aan parameningeale infectie en paradoxale embolie. 2. Intracerebrale bloeding t.g.v. een ruptuur van een aneurysma (SAB) of bij een langer bestaande hypertensie, AVM, secundair aan systeemziekte met coagulopathie zoals HUS/TTP, hemofilie, DIC, ernstige trombopenie bijvoorbeeld na beenmerg transplantatie (BMT) en als complicatie van trombolyse of anticoagulantia. Relatie met kwaliteit en lange termijn behandelingsuitkomst: Het optreden van een CVA verlengt de IC opnameduur, verhoogt de morbiditeit (meer infecties) en mortaliteit.27 Ernst: Varieert van een TIA tot een groot herseninfarct /massale bloeding met dood als gevolg. Ten behoeve van de IC complicatieregistratie zal alleen het ernstige cerebrovasculaire incident worden geregistreerd. Incidentie: Na CABG 1.4-1.6%28 tot 2.7%29 ook 4.6%30. Na trombolyse voor myocard infarct 1.4% waarvan vervolgens 41% met dodelijke afloop.31 Na carotis endarteriectomie 1.1 %.32 Na een beenmerg transplantatie 2.9%.33 Definitie: Een nieuwe klinisch manifest CVA aangetoond door blijvende neurologische uitval en bevestigd door radiologisch onderzoek (CT/ MRI) welk niet de reden voor IC opname was en is opgetreden tijdens de IC behandeling. Verbeterplannen c.q. interventie: Procedure gerelateerde events zijn mogelijk te verminderen door aanpassen van de operatie techniek. Bij gebruik van ventricular assist devices: denk aan infectie preventie en adequate antistolling34 Achtergrond: Deze complicatie kan variëren in ernst van restloos herstel tot dodelijk. De commissie is zich ervan bewust dat deze complicatie zeer weinig voorkomt, maar de complicatie is zo ernstig dat zij heeft gemeend deze te moeten includeren in de Top 9. Deze complicatie wordt per opname gescoord. De teller is het aantal patiënten dat gedurende zijn/haar IC opname een cerebrovascular accident heeft doorgemaakt per tijdseenheid (jaar). De noemer is het totaal aantal opgenomen patiënten per tijdseenheid (jaar). 5. Critical Illness Neuro-Myopathie (CIN/CIM)

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Het optreden van CIN/CIM leidt tot verlenging van de duur van het ontwennen van de beademing, en een twee- tot drie maal langere IC- en ziekenhuisopname.35;36 Ernst: CIN/CIM is een ernstige IC complicatie.

Incidentie: Deze is afhankelijk van de specifieke IC subpopulatie, de specifieke risicofactoren voor die populatie, de diagnostische criteria en de timing van de diagnose tijdenshet ziekteproces. Afhankelijk van deze factoren is de gerapporteerde incidentie bij IC patiënten tussen 35 en 80%.37 Definitie: De definitie is zeer moeilijk omdat de literatuur hierover niet eenduidig is. De commissie is van mening dat het vanwege haalbaarheid niet zinvol is om in de pilot fase een EMG onderzoek in de definitie te betrekken. Ten behoeve van deze complicatieregistratie verdient dan een klinische definitie de voorkeur: tijdens IC opname vastgestelde (symmetrische) spierzwakte leidend tot het onvermogen van de patiënt om de armen en benen tegen de zwaartekracht op te tillen, met afwezigheid van reflexen, en meestal een verlies van pijn-, temperatuur-, en vibratiezin, en/of CIN/CIM vastgesteld na neurologisch onderzoek uitgevoerd door een neuroloog.37 Verbeterplannen c.q interventie: Bekende risicofactoren zijn sepsis en het gebruik van steroïden en spierrelaxantia. Achtergrond: CIN/CIM is een ernstige complicatie voor IC patiënten die leidt tot hogere morbiditeit en mortaliteit, verlengde opname duur op IC en in het ziekenhuis, en tot verhoging van de kosten. Helaas is de definitie moeizaam. Wel wordt het probleem door de commissie als een typische IC complicatie gezien en wordt deze opgenomen in de top 9. Deze complicatie wordt per opname gescoord. De teller is het aantal patiënten dat gedurende zijn/haar IC opname een CIN/CIM heeft doorgemaakt per tijdseenheid (jaar). De noemer is het aantal patiënten per tijdseenheid (jaar). 6. Luchtweggerelateerde problemen, problemen tijdens het verkrijgen of behouden van de luchtweg, uitgezonderd tracheostoma gerelateerde problemen

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Een probleem met de luchtweg gaat gepaard met een 2,5 tot 10 maal grotere kans op overlijden. Tevens is er een grotere kans op een pneumonie. De beademingsduur is verlengd en de IC- en ziekenhuisopname zijn verlengd. De kosten kunnen tot 20% zijn toegenomen. Ernst: Een probleem met de luchtweg kan potentieel dodelijk zijn. Incidentie: De gerapporteerde incidentie is 2 tot 25% afhankelijk van de bestudeerde populatie. Definitie:38 Moeilijke Intubatie: Meer dan 3 intubatie pogingen, of intubatiepogingen > 10 minuten. Verlies luchtweg bij plaatsen Endo Tracheale Tube (ETT): Is er tijdens het plaatsen of wisselen van een endo tracheale tube een periode geweest met verlies van de vrije luchtweg, zich uitend in hypercapnie en/of hypoxie. Verlies luchtweg, niet gerelateerd aan plaatsen ETT: Is er een periode geweest met verlies van de vrije luchtweg (verstopte ETT, geknikte ETT), zich uitend in hypercapnie en/of hypoxie. Niet gerelateerd aan het inbrengen of wisselen van een ETT, en niet indien het probleem optrad in relatie met een tracheostoma. Verbeterplannen c.q interventie: Tijdens en na de opleiding tot intensivist zal er aandacht moeten zijn voor het trainen van het luchtwegmanagement. Achtergrond: Dit is een ernstige complicatie die potentieel dodelijk is. Hij heeft ook een zeer nauwe relatie met de dagelijkse werkzaamheden van de intensivist. Daarom is de commissie van mening dat deze niet mag ontbreken bij een Top 9. Deze complicatie wordt per opname gescoord. Er is de mogelijkheid om de verschillende onderdelen van een luchtweg probleem (problemen bij plaatsen ETT



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en luchtwegproblemen niet gerelateerd aan het plaatsen van een ETT) afzonderlijk per opname vast te leggen. De teller is het aantal patiënten waarbij een probleem met de luchtweg is opgetreden per tijdseenheid (jaar). De noemer is het aantal beademde patiënten per tijdseenheid (jaar). De commissie heeft de volgende overweging: patiënten met deze complicatie zullen over het algemeen beademde patiënten zijn. Echter, het is ook mogelijk dat er luchtwegproblemen optreden bij patiënten die nog niet beademd waren en dat ook niet meer geworden zijn na het optreden van het probleem. De rapportage van het aantal luchtwegproblemen zal dan ook in relatie tot het totaal aantal behandelde patiënten geschieden. De teller is dan het aantal patiënten dat een probleem met de luchtweg heeft gekregen per tijdseenheid (jaar). De noemer is het aantal patiënten per tijdseenheid (jaar). 7. Tracheostomie gerelateerde complicaties tijdens inbrengen en tijdens het IC verblijf

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Complicaties van een tracheostomie (percutaan danwel chirurgisch) kunnen vroeg (< 24 uur na het plaatsen van een tracheostoma of het wisselen van een tracheacanule) en laat (≥ 24 uur na het plaatsen van een tracheostoma of het wisselen van een tracheacanule) optreden. De belangrijkste complicaties zijn bloedingen, wondinfecties, subcutaan emfyseem en pneumothorax, malpositie en/of dislocatie van de tracheacanule, verlies van een vrije luchtweg, hypoxie en hypotensie. Al deze complicaties kunnen een nadelig effect hebben op de lange termijn uitkomst. De totale mortaliteit bedraagt overigens slechts < 0.5%. Ernst: Een complicatie van een tracheostomie kan zeer ernstig en potentieel dodelijk zijn. Incidentie: De incidentie van complicaties hang af van het type complicatie. Vroege complicaties (< 24 uur): 1. bloeding (5%) 2. subcutaan emfyseem/ pneumothorax (<1%) 3. tube obstructie 4. fausse route tijdens de procedure 5. verlies van de vrije ademweg tijdens of < 24 uur na de procedure 6. cardiac arrest. Late complicaties (≥ 24 uur): 1. slikstoornissen (tot 10%), 2. trachea stenose (1-2%), 3. trachea-arteriele fistel (< 0.7%), 4. trachea-oesofageale fistel (<1%), 5. bloeding, 6. canule-dislocatie. Definitie: Problemen tijdens en na het electief verkrijgen van een toegang tot de luchtweg via een tracheostoma (chirurgisch danwel percutaan) of tijdens of na het wisselen van een tracheacanule. 1. Vroege tracheostoma gerelateerde bloeding: Is er een significante bloeding opgetreden binnen 24 uur na het plaatsen van een tracheostoma of het wisselen van een tracheacanule waarvoor een een reïnterventie noodzakelijk is geweest. 2. Subcutaan emfyseem of pneumothorax: Is er rond het plaatsen van een tracheostoma of het wisselen van een tracheacanule subcutaan emfyseem of een pneumothorax ontstaan? 3.Verlies van de vrije ademweg bij plaatsing tracheostoma of wissel tracheacanule: Is er gedurende het plaatsen van een tracheostoma of het wisselen van een tracheacanule een periode geweest met verlies van de vrije luchtweg, zich uitend in hypercapnie en/of hypoxie 4. Late tracheostoma gerelateerde bloeding: Is er een significante bloeding opgetreden van het tracheostoma, ≥ 24 uur na het plaatsen van het tracheostoma of het wisselen van een tracheacanule waarvoor een bloedtransfusie > 2 units en/of een reïnterventie noodzakelijk is geweest. 5. Verlies van de vrije luchtweg bij een bestaand tracheostoma: Is er een periode geweest met verlies van de vrije luchtweg (verstopte tracheacanule, geknikte tracheacanule), langer dan 24 uur na het

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inbrengen of het wisselen van een tracheacanule. 6. Anatomische complicaties van een tracheostoma: Zijn er ‘anatomische’ complicaties opgetreden van het tracheostoma (oa. tracheastenose, tracheaoesophageale fistel, n. recurrens letsel). Verbeterplannen c.q interventie: Verbetering en ontwikkeling van percutane tracheotomie technieken, training/opleiding, bronchoscopische controle tijdens en na de procedure. Achtergrond: Dit zijn ernstige complicaties die potentieel dodelijk zijn. Bovendien hebben ze een zeer nauwe relatie met de dagelijkse werkzaamheden van de intensivist. Daarom is de commissie van mening dat deze niet mogen ontbreken in een Top 9. Er wordt per opname bijgehouden of het ging om een patiënt met een tracheostoma en of er een complicatie met het tracheostoma is opgetreden. Er is de mogelijkheid om de verschillende onderdelen van een tracheostomie gerelateerde complicatie (zie boven 1 tot en met 6) afzonderlijk per opname vast te leggen. De teller is het aantal patiënten waarbij een (nieuw) probleem/complicatie met de tracheostomie is opgetreden per tijdseenheid (jaar). De noemer is het aantal patiënten per tijdseenheid (jaar) met een tracheostoma. 8. Problemen gerelateerd aan vaattoegang

Mechanische complicaties (accidentele arteriële punctie, hematoom, aneurysma spurium, hematothorax, en pneumothorax), infecties (catheter gerelateerde bacteriaemie) en catheter gerelateerde thrombose zijn in de literatuur beschreven. Een malpositie en een hematoom worden beschouwd als incidenten behalve wanneer deze een interventie behoeven. Een pneumothorax is al apart genoemd. Bacteriaemie gerelateerd aan catheters wordt buiten beschouwing gelaten i.v.m. problemen rondom de definitie.39-41 Catheter gerelateerde trombose is sterk afhankelijk van de intensiteit van de screening.41-43 Derhalve wordt alleen een ernstige bloeding en een aneurysma spurium ten gevolge van het verkrijgen van een toegang tot een centrale vene of arterie (Vena Femoralis, Vena Jugularis, Vena Subclavia, Arteria Femoralis, arteria radialis, arteria brachialis) opgenomen als complicatie. Relatie met kwaliteit en lange termijn behandelingsuitkomst: Het optreden van met name een bloeding na een interventie die betrekking heeft op het verkrijgen van een vaattoegang leidt tot verlengde IC opname en ziekenhuisopname.41;42;44 Tevens is over het algemeen het inotropie gebruik toegenomen bij de patiënten die hiermee een probleem hebben gehad. Ernst: De ernst van deze complicaties is wisselend, van minimaal tot dodelijk.44-46 Incidentie: In de literatuur wordt een incidentie van 0.5 tot 4 % gerapporteerd.43;47 Dit is de proportie van problemen rondom toegang tot vaten die leidt tot een bloeding. Over de incidentie van een aneurysma spurium na een poging tot het verkrijgen van een vaattoegang bij intensive care patiënten is weinig gerapporteerd.48 Definitie: Een bloeding en/of aneurysma spurium, waarvoor een bloedtransfusie behoefte bestaat en/of die een chirurgische en/of radiologische interventie behoeft. Verbeterplannen c.q interventie: Scholing en onderwijs. Tevens zijn er aanwijzingen dat dat echo geleide procedures minder complicaties hebben.47;49-51 Achtergrond: Deze complicatie kan variëren in ernst van minimaal ernstig tot dodelijk. De commissie vindt deze complicatie zo duidelijk gerelateerd aan de beoefening van intensive care geneeskunde dat zij heeft gemeend deze te moeten includeren in de Top 9. Deze complicatie kan gedurende een IC opname meerdere malen optreden. Indien het verschillende locaties betreft wordt dit als een nieuwe


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complicatie gescoord. De teller is het aantal behandeldagen dat er een (nieuw) probleem met een vaattoegang is opgetreden per tijdseenheid (jaar), de noemer is het totaal aantal behandeldagen per tijdseenheid (jaar). 9. Hoge en Lage Tractus Digestivus Bloeding

Relatie met kwaliteit en lange termijn behandelingsuitkomst: Er is in de literatuur beperkt bewijs dat een hoge en/of lage tractus digestivus bloeding die is opgetreden tijdens een IC opname een duidelijk relatie heeft met langere termijn uitkomst. Veelal is een dergelijke complicatie gerelateerd aan de opname diagnose. Ernst: Dit is een potentieel ernstige complicatie die, indien onbehandeld, tot ernstige morbiditeit en mortaliteit kan leiden. Incidentie: De gerapporteerde incidentie van (vooral hoge) tractus digestivus bloedingen op de IC is 3 tot 25%, indien het gaat om evidente bloedingen dan wel klinisch significante bloedingen.52 Definitie: De meest gehanteerde definitie komt voort uit de landmark trial van Cook et al. uit 1994 waarbij een klinisch belangrijke bloeding werd gedefinieerd als een evidente bloeding (hemeatemesis, meleana) gecompliceerd binnen 24 uur door een bloeddrukdaling, tachycardie, Hb daling gevolgd door een transfusie met een beperkte opbrengst.53 Voor de complicatieregistratie wordt gekozen voor een meer pragmatische definitie: een hoge en/of lage tractus digestivus bloeding met: klinische symptomen, en/of bloedtransfusie, en/of een endoscopische en/of radiologische en/of chirurgische interventie. Ook hier mag de tractus digestivus bloeding niet de reden van opname zijn. Verbeterplannen c.q interventie: De incidentie van bloedingen is sterk afgenomen in het tijdperk na 2000 waarbij mogelijk het veelvuldig gebruik van protonpomp remmers, en vroege enterale voeding, een belangrijke rol spelen. Een andere factor kan de toegenomen aandacht voor de verbetering van de microcirculatie zijn. Stress ulcus profylaxe is op zich zelf controversieel maar moet worden gezien in het licht van de gebruikte antistolling en afgewogen worden tegen het risico op nosocomiale luchtweginfecties.54 Achtergrond: Hoewel bloedverlies via de tractus digestivus bij een IC patient regelmatig voorkomt, heeft de commissie ervoor gekozen de ernstige hoge en/of lage tractus digestivus bloeding, volgens de definitie hierboven, eenmalig per IC opname te scoren. De teller is het aantal patiënten met een ernstige hoge en/of lage tractus digestivus bloeding per tijdseenheid (jaar), de noemer is het totaal aantal patiënten per tijdseenheid (jaar).

Conclusie en beschouwing

Bijlage 1. Werklijst beoordeling potentiële “complicaties” c.q. indicatoren van kwaliteit (met name m.b.t. uitkomst) Epidemiologische feiten Prevalentie Incidentie Relatie met kwaliteit volgens literatuur (single- of multi-center RCT, groot prospectief observatioineel onderzoek) Mortaliteit MODS Beademingsduur LOS IC LOS hospital Interventies Kosten Relatie met kwaliteit volgens expert opinion / empirie

Zegt iets over: Structuur Proces Uitkomst Definti:e Defintie theoretisch Defintie praktisch Risicofactoren (die betrekking hebben op de minimale dataset) Praktijk Teller Noemer Haalbaarheid i/d praktijk Samenvatting

Search Strategy

De huidige set complicaties is zoveel mogelijk samengesteld op basis van literatuurstudie en aangevuld met het oordeel van experts. Uiteraard zijn er veel meer potentiële complicaties voor de intensive care te formuleren: de commissie is begonnen met 68 potentiële complicaties en heeft die op basis van literatuurstudie en het oordeel van experts in eerste instantie teruggebracht tot een top 9. Toch lijkt het de commissie belangrijk om met de registratie van een beperkte set complicaties te beginnen. Het doel van de pilot studie is om de validiteit en de meetbaarheid van de voorgestelde complicaties te testen. Het ligt in de bedoeling dat op basis van commentaar van de intensivisten uit de pilotziekenhuizen de set wordt aangepast. De set van 9 zal worden uitgebreid en definities zullen worden bijgesteld. Vervolgens kan, met een aangepaste en uitgebreidere set, de complicatieregistratie op nog meer Intensive Care afdelingen in Nederland ter hand worden genomen. De commissie stelt dat de samenstelling

Referenties



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en uitbreiding van de complicatie-set een dynamisch proces blijft voor en door de leden van de vereniging. De complicatieregistratie is in eerste instantie bedoeld voor intern gebruik, met als doel om de kwaliteit van zorg te meten en te verbeteren. Tenslotte is om de kwaliteit van zorg te vergroten is het ook noodzakelijk om, naast de registratie van kwaliteitsindicatoren, uitkomsten te meten en vast te leggen, en naar aanleiding hiervan verbeteracties te implementeren. In een latere fase kunnen vastgestelde uitkomsten de start zijn van ziekenhuisoverstijgende projecten ter vergroting van de kwaliteit van zorg en patiënt veiligheid op de intensive care.

Acknowledgement Bij deze danken wij de commissieleden die in het eerste uur zitting in de commissie complicatieregistratie hadden, mw. dr. A Balzereit, mw. dr. S. Dijkstra, prof. dr. J.G. van der Hoeven, en drs. A. Manten hartelijk voor hun enthousiaste inzet en bijdrage.

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22. Fikkers BG, van Veen JA, Kooloos JG, Pickkers P, van den Hoogen FJ, Hillen B, van der Hoeven JG: Emphysema and pneumothorax after percutaneous tracheostomy: case reports and an anatomic study. Chest 2004; 125: 1805-14 23. Keith RL, Pierson DJ: Complications of mechanical ventilation. A bedside approach. Clin.Chest Med. 1996; 17: 439-51 24. Strange C: Pleural complications in the intensive care unit. Clin.Chest Med. 1999; 20: 317-27 25. de Lassence A, Timsit JF, Tafflet M, Azoulay E, Jamali S, Vincent F, Cohen Y, Garrouste-Org, Alberti C, Dreyfuss D: Pneumothorax in the intensive care unit: incidence, risk factors, and outcome. Anesthesiology 2006; 104: 5-13 26. Hall J: Cerebrovascular disease, Prinicples of Critical Care. 2008, 27. Broessner G, Helbok R, Lackner P, Mitterberger M, Beer R, Engelhardt K, Brenneis C, Pfausler B, Schmutzhard E: Survival and long-term functional outcome in 1,155 consecutive neurocritical care patients. Crit Care Med. 2007; 35: 2025-30 28. Filsoufi F, Rahmanian PB, Castillo JG, Bronster D, Adams DH: Incidence, topography, predictors and long-term survival after stroke in patients undergoing coronary artery bypass grafting. Ann. Thorac.Surg. 2008; 85: 862-70 29. Engelman DT, Cohn LH, Rizzo RJ: Incidence and predictors of tias and strokes following coronary artery bypass grafting: report and collective review. Heart Surg.Forum 1999; 2: 242-5 30. Bucerius J, Gummert JF, Borger MA, Walther T, Doll N, Onnasch JF, Metz S, Falk V, Mohr FW: Stroke after cardiac surgery: a risk factor analysis of 16,184 consecutive adult patients. Ann.Thorac. Surg. 2003; 75: 472-8 31. Gore JM, Granger CB, Simoons ML, Sloan MA, Weaver WD, White HD, Barbash GI, Van de WF, Aylward PE, Topol EJ, .: Stroke after thrombolysis. Mortality and functional outcomes in the GUSTO-I trial. Global Use of Strategies to Open Occluded Coronary Arteries. Circulation 1995; 92: 2811-8 32. Ross SD, Tribble CG, Parrino PE, Shockey KS, Kern JA, Kron IL: Intensive care is cost-effective in carotid endarterectomy. Cardiovasc.Surg. 2000; 8: 41-6 33. Coplin WM, Cochran MS, Levine SR, Crawford SW: Stroke after bone marrow transplantation: frequency, aetiology and outcome. Brain 2001; 124: 1043-51 34. Tsukui H, Abla A, Teuteberg JJ, McNamara DM, Mathier MA, Cadaret LM, Kormos RL: Cerebrovascular accidents in patients with a ventricular assist device. J.Thorac.Cardiovasc.Surg. 2007; 134: 114-23 35. Fletcher SN, Kennedy DD, Ghosh IR, Misra VP, Kiff K, Coakley JH, Hinds CJ: Persistent neuromuscular and neurophysiologic abnormalities in longterm survivors of prolonged critical illness. Crit Care Med. 2003; 31: 1012-6


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43. Ruesch S, Walder B, Tramer MR: Complications of central venous catheters: internal jugular versus subclavian access--a systematic review. Crit Care Med. 2002; 30: 454-60 44. Robinson JF, Robinson WA, Cohn A, Garg K, Armstrong JD: Perforation of the great vessels during central venous line placement. Arch.Intern.Med. 1995; 155: 1225-8 45. Haaverstad R, Latto PN, Vitale N: Right subclavian catheter perforation of the aorta due to an incorrect external landmark-guided insertion technique. CJEM. 2007; 9: 43-5 46. Whitteveen AG, Wirds JW, Beek AM, Boon ES, van der Spoel JI: [Heart tamponade: a life-threatening complication of a central venous catheter]. Ned.Tijdschr.Geneeskd. 1997; 141: 2249-51 47. McGee DC, Gould MK: Preventing complications of central venous catheterization. N.Engl.J.Med. 2003; 348: 1123-33 48. Bussieres JS: Iatrogenic pulmonary artery rupture. Curr.Opin.Anaesthesiol. 2007; 20: 48-52 49. Karakitsos D, Labropoulos N, De Groot E, Patrianakos AP, Kouraklis G, Poularas J, Samonis G, Tsoutsos DA, Konstadoulakis MM, Karabinis A: Real-time ultrasound-guided catheterisation of the internal jugular vein: a prospective comparison with the landmark technique in critical care patients. Crit Care 2006; 10: R162

50. Needham DM, Sinopoli DJ, Thompson DA, Holzmueller CG, Dorman T, Lubomski LH, Wu AW, Morlock LL, Makary MA, Pronovost PJ: A system factors analysis of “line, tube, and drain” incidents in the intensive care unit. Crit Care Med. 2005; 33: 1701-7 51. Schummer W, Schummer C, Rose N, Niesen WD, Sakka SG: Mechanical complications and malpositions of central venous cannulations by experienced operators. A prospective study of 1794 catheterizations in critically ill patients. Intensive Care Med. 2007; 33: 1055-9 52. Tryba M: Prophylaxis of stress ulcer bleeding. A meta-analysis. J.Clin.Gastroenterol. 1991; 13 Suppl 2: S44-S55 53. Cook DJ, Fuller HD, Guyatt GH, Marshall JC, Leasa D, Hall R, Winton TL, Rutledge F, Todd TJ, Roy P, .: Risk factors for gastrointestinal bleeding in critically ill patients. Canadian Critical Care Trials Group. N.Engl.J.Med. 1994; 330: 377-81 54. Cook DJ, Reeve BK, Guyatt GH, Heyland DK, Griffith LE, Buckingham L, Tryba M: Stress ulcer prophylaxis in critically ill patients. Resolving discordant meta-analyses. JAMA 1996; 275: 308-14



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n eth e rlan ds jou rnal of critical care Copyright ©2008, Nederlandse Vereniging voor Intensive Care. All Rights Reserved.

Ontwikkeling van NVIC-richtlijnen Mw. drs. A.M.T.J. Raben, dhr. dr. R. Tepaske namens de NVIC richtlijnencommissie Tabel 1. Waardering van literatuur en niveau van aanbeveling Niveau van Therapie Diagnose Etiologie en prognose bewijs A1 Systematische review van tenminste twee onafhankelijk van elkaar uitgevoerde onderzoeken van A2-niveau A2 Gerandomiseerd dubbelblind vergelijkend Onderzoek ten opzichte van een referentietest (een Prospectief cohort onderzoek van klinisch onderzoek van goede kwaliteit van ‘gouden standaard’) met tevoren gedefinieerde voldoende omvang en follow-up, voldoende omvang afkapwaarden en onafhankelijke beoordeling waarbij adequaat gecontroleerd van de resultaten van test en gouden standaard, is voor ‘confounding’ en selectieve betreffende een voldoende grote serie van opeen- follow-up voldoende is uitgesloten. volgende patiënten die allen de index- en referentietest hebben gehad B Vergelijkend onderzoek, maar niet met alle Onderzoek ten opzichte van een referentietest, Prospectief cohort onderzoek, kenmerken als genoemd onder A2 (hiermaar niet met alle kenmerken die onder A2 zijn maar niet met alle kenmerken als onder valt ook patiënt-controle onderzoek, genoemd genoemd onder A2 of retrospectief cohort-onderzoek) cohort onderzoek of patiënt-controle onderzoek C Niet-vergelijkend onderzoek D Mening van deskundigen Niveau van aanbeveling 1 2 3 4

Conclusie gebaseerd op Onderzoek van niveau A1 of tenminste 2 onafhankelijk van elkaar uitgevoerde onderzoeken van niveau A2 1 onderzoek van niveau A2 of tenminste 2 onafhankelijk van elkaar uitgevoerde onderzoeken van niveau B 1 onderzoek van niveau B of C Mening van deskundigen

Inleiding Zoals bekend, heeft de NVIC commissie Richtlijnenontwikkeling zich tot doel gesteld richtlijnen te ontwikkelen volgens een ‘evidencebased’ methode. De definitie van een richtlijn werd in 1995 door de LSV opgesteld, en is nog steeds actueel: ‘een richtlijn is een advies waarin de verworven wetenschappelijke inzichten en klinische ervaring op adequate wijze tot uitdrukking komen, of waarin, indien geen eensluidend advies kan worden gegeven, wordt vermeld waarover onzekerheid bestaat’ (omschrijving Centraal Begeleidingsorgaan voor de Intercollegiale Toetsing, CBO). Binnen de NVIC is afgesproken dat richtlijnen zoveel mogelijk wetenschappelijk ondersteunde aanbevelingen zijn op medischinhoudelijk of medisch-organisatorisch gebied, die onder meer tot doel hebben de intensivist te ondersteunen in het besluitvormingsproces, de kwaliteit en de doelmatigheid van het medisch handelen te bevorderen, en de uniformiteit in de praktijkuitoefening te bevorderen (Damen J. NVIC-standpunten, NVIC-richtlijnen en de juridische implicaties. NJCC, 04.2002, p. 18-21).

Totstand komen van een NVIC-richtlijn Richtlijnen worden ontwikkeld volgens de methode van ‘evidencebased medicine’. Dit houdt in dat de literatuur, die gebruikt wordt voor de richtlijn, gewaardeerd wordt volgens een uniforme methode, waaraan dan klinische aanbevelingen ontleend kunnen worden. Deze kunnen dan ook weer op een uniforme wijze naar niveau worden gerangschikt. Waardering van methodes en aanbevelingen kan op ver-

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scheidene wijzen gebeuren; de meeste zijn gebaseerd op de methode die reeds in 1989 door Sackett beschreven is: ‘the conscientious and judicious use of current best evidence from clinical care research in the management of the individual patient’. Het CBO heeft ook een ‘Indeling van methodologische kwaliteit van individuele studies’ ontwikkeld, welke gebaseerd is op de methode van Sackett, met daaraan gekoppeld een ‘niveau van conclusie / aanbeveling’. Deze indeling wijkt licht af van die, welke tot voor kort door de NVIC werd gehanteerd, hoewel hij inhoudelijk hetzelfde is. Sinds kort hebben wij onze gradatie van literatuurbeoordeling en niveau van aanbeveling geconformeerd aan die van het CBO (zie tabel I).

Het format van een NVIC-richtlijn Ook hier gaan wij uit van het format dat door het CBO wordt gebruikt; een voorbeeld ziet u in tabel II. Op deze wijze is de vraagstelling van een richtlijn helder en wordt het terrein van het onderwerp ‘afgebakend’. Tevens is inzichtelijk hoe men de benodigde literatuur heeft vergaard en kan deze ook worden geraadpleegd. Sinds april 2003 is het gebruikelijk om de richtlijn in het Engels te publiceren met een abstract in het Nederlands. De achterliggende gedachte is, dat onze richtlijnen zo ook toegankelijk zijn voor artsen die de Nederlandse taal niet beheersen. Aangezien onze richtlijnen met name landelijk gebruikt worden, treedt dit probleem (i.c. het niet machtig zijn van de Nederlandse taal) slechts zeer sporadisch op, terwijl wij wel herhaalde malen het verzoek gekregen hebben om de richtlijn in het Nederlands te publiceren; dit waarschijnlijk ook


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Tabel 2. Format lege richtlijn Uitgangsvraag Inleiding Korte inleiding relevantie uitgangsvraag. Selectiecriteria literatuur: welke criteria zijn ghanteerd bij de selectie van de literatuur (transparantie). Samenvatting van de literatuur Korte samenvatting van onderzoeken -> auteurnaam en jaartal noemen. Conclusies Niveau 1 Niveau 2 Niveau 3 Niveau 4

Het is aangetoond dat: stelling bronnen (mate van bewijs + auteurnaam + jaartal) Het is aannemelijk / waarschijnlijk dat: bronnen (mate van bewijs + auteurnaam + jaartal) Er zijn aanwijzingen / het lijkt waarschijnlijk dat: bronnen (mate van bewijs + auteurnaam + jaartal) De experts / werkgroep zijn / is van mening dat: bronnen (mate van bewijs + auteurnaam + jaartal)

Overige overwegingen Hier kan men informatie kwijt over bijv.: - Veiligheid (bijwerkingen, risico’s, complicaties - Patiëntenperspectief (bijv. behoeften van de patiënt, te verwachten tevredenheid) - Professioneel perspectief (bijv. tijdsbesparing) - Beschikbaarheid van de voorzieningen - Kosten - Zorgorganisatie OFWEL: alle andere aspecten die niet in wetenschappelijke studies zijn onderzocht, maar die wel van belang zijn bij het formuleren van de aanbeveling. Aanbevelingen Deze dienen de uitgangsvraag te beanwoorden Voorkeursformuleringen van aanbevelingen zijn: * Sterk aan te bevelen / dienen / moeten / is de eerste keuze / is geïndiceerd / is vereist / is de standaard / wordt als standaard beschouwe. * Aan te bevelen / adviseren / heeft de voorkeur / streven naar / verdient aanbeveling * Te overwegen / is een optie / kan / eris mogelijk plaats / kan zinvol zijn * Kan geen aanbeveling worden gegeven / niet mogelijk een keuze te maken / er is geen voorkeur uit te spreken * Verdient niet de voorkeur / er is terughoudendheid geboden * Te ontraden / af te raden Literatuurlijst (Vancouverstijl)

ingegeven door het feit dat veel intensive care verpleegkundigen de richtlijnen raadplegen. Daarom is, in goed overleg met het NVIC-bestuur, besloten om hier gehoor aan te geven: de nieuw te ontwikkelen richtlijnen zullen gepubliceerd worden in het Nederlands met een abstract in het Engels. Gedurende de overgangsfase is het ook nog mogelijk richtlijnen in het Engels te publiceren.

gingen en instanties voor wie de richtlijn van belang kan zijn. Deze instanties krijgen dan 2 maanden de tijd om commentaar te leveren, welke door de Richtlijnencommissie in de conceptrichtlijn verwerkt zal worden indien zij het commentaar gefundeerd vinden. Hierna wordt de voltooide conceptrichtlijn geplaatst op de NVIC-website onder het kopje ‘Conceptrichtlijnen’ (alleen toegankelijk voor leden), zodat ook de leden hun kritiek kunnen leveren. Vervolgens zal de conceptrichtlijn in de ALV (Algemene Leden Vergadering) ter discussie komen en, na stemming, al dan niet geaccordeerd worden. Om eenieder voldoende tijd te geven kennis te nemen van en zich te verdiepen in de nieuwe richtlijn(en), dienen conceptrichtlijnen minimaal 2 weken voorafgaand aan een ALV op de NVIC website geplaatst te worden. Bespreking van de conceptrichtlijn wordt aangekondigd in de convocatie voor de ALV, dus minimaal 2 weken voor de vergadering.. Om tot een gefundeerde mening te komen, is het waarschijnlijk zinvol dat de makers van de richtlijn hun ideeën toelichten aan de hand van een presentatie. Aangezien de ALV altijd voorafgegaan wordt door een NVIC-congresdag, zijn wij van zins de mogelijkheden te onderzoeken om op deze dag een sessie ‘conceptrichtlijnen ter discussie’ te houden. Op deze wijze kan dan voorafgaand aan de ALV al een goede discussie gevoerd worden met de experts (i.c. de maker(s) van de richtlijn), zodat tijdens de ALV eenieder een gefundeerde stem kan uitbrengen. Na accordering van de richtlijn in de ALV zal deze gepubliceerd worden in het NJCC, en op de website onder het kopje ‘geaccordeerde richtlijnen’. Er bestaat een groeiende behoefte, zowel bij de leden als bij de Inspectie voor de Gezondheidszorg, aan implementatiestudies, ofwel: hebben de in het verleden geformuleerde richtlijnen daadwerkelijk bijgedragen aan verbetering van de patiëntenzorg? En zo nee, waarom niet? Hopelijk kunnen ook deze vragen in de toekomst (deels) beantwoord worden, als er geld en middelen worden vrijgemaakt om deze implementatiestudies op te zetten.

Conclusie Hoewel intensive care geneeskunde een zeer complex vakgebied is waarin het toepassen van Evidence Based Medicine soms moeilijk is, streven wij er als intensivisten wel naar om goed gefundeerde geneeskunde te bedrijven, zo mogelijk aan de hand van lege artis samengestelde richtlijnen. Aangezien IC-geneeskunde een vak-in-beweging is, waarbij zo zeer vaak nieuwe inzichten worden ontwikkeld, is het belangrijk om bestaande richtlijnen periodiek kritisch te evalueren en waar nodig aan te passen. Dit “updaten” zal dan ook regelmatig gebeuren. De Richtlijncommissie streeft ernaar implementatiestudies uit te (laten) voeren. Referenties 1. Damen J. NVIC-standpunten, NVIC-richtlijnen en de juridische implicaties. NJCC, 04.2002, p. 18-21

Procedure rond het vaststellen van een NVIC-richtlijn Wanneer een conceptrichtlijn is goedgekeurd door de NVIC Richtlijnencommissie, wordt deze aangeboden aan het NVIC-bestuur. Het bestuur zal deze richtlijn dan, nadat deze er ook zijn goedkeuring aan heeft gegeven, aanbieden aan de diverse wetenschappelijke vereni-



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Waterlandziekenhuis Het Waterlandziekenhuis ontwikkelt zich tot hét medisch centrum van de regio Waterland. In onze middelgrote, dynamische ziekenhuisorganisatie realiseert de medische staf een indrukwekkend groeiende productie. We bedienen de patiëntenpopulatie van de regio met ruim 1.200 medewerkers en hebben nagenoeg alle medische specialismen in huis. Het Waterlandziekenhuis wil gekend worden als een goed en ondernemend regionaal ziekenhuis. Het is aanspreekbaar op goede kwaliteit van zorg en realiseert deze zorg in nauwe samenwerking met andere zorgaanbieders in de regio. Voor de Intensive Care Unit zijn wij op zoek naar:

Intensivisten (twee fte) ICU level 2 op bilocatie De afdeling Intensive Care van het Waterlandziekenhuis ontwikkelt samen met het Zaans Medisch Centrum een achttienbeds Intensive Care op bilocatie. Samen, en met een door de verzekeraars geaccordeerd plan, ontstaat zo de IC Zaanstreek-Waterland, een afdeling die voldoet aan alle vereisten voor het verkrijgen van de level 2-status. Medio 2009 moeten de twee IC-afdelingen organisatorisch en bedrijfsmatig tot één unit zijn omgevormd, gebruikmakend van moderne technieken als PDMS en teleconferencing, en geleid door zeven fte intensivisten volgens het closed-format-model. Op de locatie in het Waterlandziekenhuis worden per jaar zo’n 1.500 beademingsdagen gerealiseerd en zijn er mogelijkheden voor nierfunctievervangende therapie en non-invasieve beademing. De intensivisten participeren in het reanimatieteam. Daarnaast leiden zij het Spoed Interventieteam. Voorts wordt de opvang verzorgd van kritisch zieke patiënten op de SEH. De ontwikkeling van de IC is een speerpunt van het ziekenhuisbeleid. De IC neemt deel aan de NICE-registratie. Naast de IC-taken heeft de Intensive Care een consultatieve taak in het ziekenhuis en is de intensivist betrokken bij het interklinisch vervoer van IC-patiënten. Wij vragen Wij willen ons huidige team van drie intensivisten graag uitbreiden met enkele nieuwe intensivisten (twee fte) die bij voorkeur antegraad zijn opgeleid. Van u wordt een actieve bijdrage verwacht aan bovenstaande ontwikkeling en aan het onderwijs aan arts-assistenten en IC-verpleegkundigen. Participatie in ziekenhuis- en stafactiviteiten wordt op prijs gesteld. Ook collega’s in de laatste fase van hun opleiding worden nadrukkelijk uitgenodigd te solliciteren. Wij bieden De mogelijkheid te werken in een mooi ziekenhuis met een goede kwaliteitsreputatie. Salariëring geschiedt volgens de AMS-regeling. Verder bieden wij gunstige secundaire arbeidsvoorwaarden, waaronder een prima pensioenregeling (PGGM)en een meerkeuzesysteem. De regio Waterland is een zeer aantrekkelijke woon- en werkomgeving met de voordelen van een landelijke omgeving vlak bij Amsterdam. Interesse? Neem voor meer informatie over de vacature contact op met de heer E. Boon, longarts-intensivist en medisch hoofd IC, (0299) 45 76 26. Uw sollicitatie richt u aan het Waterlandziekenhuis, ter attentie van mevrouw drs. E. Baars MMO, voorzitter raad van bestuur, Postbus 250, 1440 AG Purmerend. U kunt ook direct online solliciteren. Bij de sollicitatieprocedure zijn ook de heer M. Hoeksema, anesthesioloog-intensivist uit het Zaans Medisch Centrum, en een selectiecommissie van de medische staf betrokken.


10-12-2008 16:37:20


f o r m u l i e r

Aanvraag visitatie Voor medische afdelingen en zeker ook Intensive

Graag nodigen wij uw Intensive Care afdeling uit

goede zorg verleend wordt. Er is vanuit de

Voor het uitvoeren van een visitatie wordt een

Care afdelingen is het essentieel dat kwalitatief

maatschappij - terecht - ook steeds meer een roep

om daarover verantwoording af te leggen. Voor een goede kwaliteit van zorg is het van belang dat de

medewerkers op deze afdeling zich openstellen voor evaluatie door beroepsgenoten.

voor deelname aan de volgende ronde visitaties. vergoeding van € 5.600,00 (per 1 januari 2009

inclusief 19% BTW) in rekening gebracht. De NKIC

ziet een aanvraag voor visitatie met belangstelling tegemoet.

Naam ziekenhuis : Contactpersoon : E-mail adres : Postadres : De volgende data zijn nog beschikbaar om uw IC te visiteren. Wij verzoeken u met de cijfers 1,2 en 3 uw drie voorkeursdata aan te geven! (Waarbij 1 staat voor eerste keuze)

20 januari 2009

03 maart 2009

31 maart 2009

12 februari 2009

17 maart 2009

28 april 2009

24 februari 2009

24 maart 2009

<

Graag contact opnemen om een datum af te stemmen voor 2009

Wilt u dit antwoordformulier sturen aan: NVIC secretariaat visitatie Antwoordnummer 2459 6710 WB Ede Meer informatie kunt u vinden op onze website: www.nvic.nl n et h j crit care • volume 12 • no 6 • decembe r 2008


305

10-12-2008 16:37:20

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Therapeutische indicaties Aanvulling na extracellulair vochtverlies in het geval van isotone dehydratie bij bestaande of dreigende acidose. Contra-indicaties Sterofundin® ISO mag niet worden toegediend indien er sprake is van: – hypervolemie – ernstige decompensatio cordis – nierinsufficiëntie met oligurie of anurie – ernstig gegeneraliseerd oedeem – hyperkaliëmie – hypercalciëmie – metabole alkalose

Bijwerkingen Verschijnselen van overdosering kunnen optreden. Overgevoeligheidsreacties gekenmerkt door urticaria zijn af en toe beschreven na de intraveneuze toediening van magnesiumzouten. Hoewel orale magnesiumzouten de peristaltiek bevorderen is in zeldzame gevallen paralytische ileus waargenomen na intraveneuze infusie van magnesiumsulfaat. Bijwerkingen kunnen ook het gevolg zijn van de techniek bij toediening, bijv. koortsreactie, infectie op de plaats van toediening, lokaal pijn of een plaatselijke reactie, irritatie van de vene, veneuze trombose of flebitis welke zich verspreid vanaf de plaats van injectie en extravasatie. Bijwerkingen kunnen ook het gevolg zijn van medicatie welke

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24 mmol/l 5,0 mmol/l 5,6-6,4 296 mOsmol/l <2,0 mmol/l

Therapeutische indicaties Behandeling van dreigende of manifeste hypovolemie en shock Contra-indicaties – Hyperhydratie inclusief longoedeem. – Nierinsufficiëntie met oligurie of anurie. – Intracraniale bloeding. – Hyperkaliëmie. – Ernstige hypernatriëmie of ernstige hyperchloremie. – Overgevoeligheid voor hydroxyethylzetmeel of

Bijwerkingen Na toediening van hydroxyethylzetmeel kunnen anafylactische reacties in verschillende intensiteiten optreden. Daarom moeten alle patiënten die zetmeelinfusies ontvangen nauwkeurig worden gecontroleerd op anafylactische reacties. In het geval van een anafylactische reactie moet de infusie direct worden gestaakt en moet de gebruikelijke acute behandeling plaatsvinden. Verminderde hematocriet en verminderde concentraties van plasma-eiwitten als gevolg van hemodilutie. Relatief hoge doses hydroxyethylzetmeel resulteren in verdunning van coagulatiefactoren en kunnen daarom de bloed-

Herhaalde infusies met HES gedurende diverse dagen, in het bijzonder wanneer sprake is van hoge cumulatieve doses, resulteren in het algemeen in jeuk die slecht reageert op elke therapie. Deze jeuk kan diverse weken na het einde van de zetmeelinfusies optreden en kan maanden aanhouden. RVG nummer 34094 Op aanvraag is de volledige registratietekst beschikbaar.

* Tetraspan 10% is ingeschreven onder RVG nummer 34095. Op aanvraag is de volledige registratietekst beschikbaar.


10-12-2008 16:37:24

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€ 725,€ 875,€ 800,-

Meer informatie kunt u vinden op www.fccs.nl


10-12-2008 16:37:26

j a a r p r o g r a m m a

n v i c

a c t i v i t e i t e n

2 0 0 9

Nederlandse Intensivistendagen 2009 woensdag 11 februari 2009 donderdag 12 februari 2009 vrijdag 13 februari 2009

Hotel en Congrescentrum de Reehorst, Ede

Nederlandse Vereniging voor Intensive Care (NVIC)


10-12-2008 17:42:43


n v i c


2 0 0 9

ne de rl andse int ens i vi s t en d agen 2 0 0 9 Woensdag 11 februari 2009 Sessie 1 Ochtendprogramma Vz:

ARH van Zanten

09.30

MICU is goed geregeld pro con debat

Hotel en Congrescentrum De Reehorst, Ede

Sessie 2 Ochtendprogramma

ex tr a co r po rel e therap i e Vz:

ABJ Groeneveld & ACJM de Pont

09.40

CPFA bij sepsis

EJ van Lieshout en ARJ Girbes

ABJ Groeneveld

10.05

inf e c ti e e n a n t i b i o t i c a Vz:

JG van der Hoeven & DW de Lange

09.55

25: Epidemiology of fungal infections in critically ill patients: consequences for antimycotic prescriptions MC van Rijk

10.07

Antibiotica voor ‘dummies’? DW de Lange

10.52

Pauze

11.20

1: Outcome of meningococcal septic shock

11.32

MG Vervloet en ACJM de Pont

10.30

10.42

Pauze

vo ed ing Vz:

RJM Strack van Schijndel

11.12

Dosering enterale voeding RJM Strack van Schijndel

in childhood CMP Buysse

11.37

Candida; Van kolonisatie tot infectie

12.02

9: Catheter-related bloodstream infections: a prospective observational study of concurrently sited central venous and arterial catheters M Chalabi

12.09

3: Inducible nitric oxide synthase in septic acute kidney injury S Heemskerk

Krachtvoer ARH van Zanten

A Oude Lashof

11.57

CVVH: Hoe hoger de dosis hoe beter

8: The clinical significance of dimethylarginine MPC Siroen

12.14

Lunch en posterpresentatie

Aspergillus: Wat nu? PE Verweij

12.34

2: Infectious complications in critically ill patients ARH van Zanten

12.46


Abstracts Case reports Educational sessions Pro con debatten Proefschriften State-of-the-art lectures


10-12-2008 17:42:14


n v i c


2 0 0 9

ne de rl andse int ens i vi s t en d agen 2 0 0 9 Woensdag 11 februari 2009


Sessie 1 Middagprogramma


m ijn f a v o r i e t e m e d i a t o r Vz:

ACJM de Pont

hemo d yna mica , mij n fa vori eten Vz:

PHJ van der Voort & SJC Verbrugge

13.45

ADMA

13.15

PAC versus PICCO

PAM van Leeuwen

14.10

RJ Trof

2: Nitric oxide-mediated endothelial dysfunction does not occur during endotoxin tolerance or administration of selective inducible nitric oxidesynthase inhibitor aminoguanidine in humans A Draisma

14.22

15.24

15.49

19: Endotoxemia-induced changes in cytokines, cortisol, EEG, brain specific proteins and cognitive functional tests in humans in vivo MHWA van den Boogaard Thrombine

ScVO2/Lactaat Levosimendan

14.42

23: Cerebral blood flow in hypothermic and normothermic patients after cardiac arrest L Bisschops

14.54

Wat bij wie? ARJ Girbes

MM Levi

15.19

Pauze

ca pita sel ecta

Vz:

AJC Slooter

16.20

Delirium in maat en getal

Pauze

Vz:

I van Stijn & ARH van Zanten

15.50

De intensivist is de hoofdbehandelaar op de MC MS van der Steen en LPH Leenen

AJC Slooter

16.15

24: Post-ICU outpatient clinic (PICOC) initiative foresees unmet needs of post-ICU patients DHT Tjan

16.27

Wat zegt het ECG op de IC? EJ Lust

17.12

22: Severe clozapine-induced cardiomyopathy in a schizophrenic patient related to smoking cessation and ciprofloxacin use R Schellaars

3: On pediatric delirium in critical illness JNM Schieveld

16.57

13.52

PHJ van der Voort

Toll-like receptoren op de ICU

d e lir ium

16.45

of pulmonary artery catheter C Barends

14.17

H Endeman

15.12

1: Recovery from thrombocytopenia after removal

J Bakker

PCT JT van Dissel

14.47

13.40

Prestatie-indicator Delier JM van den Berg en PE Spronk

17.22

Borrel

17.22

Borrel

18.30

Diner

18.30

Diner

20.30 a vondprogramma Fysiologie van het verliefd zijn JH Ravesloot


10-12-2008 17:42:15


n v i c


2 0 0 9

ne de rl andse int ens i vi s t en d agen 2 0 0 9 Donderdag 12 februari 2009 Sessie 1 Ochtendprogramma

o ntbij t s e s si e Vz:

ARH van Zanten


Sessie 2 Ochtendprogramma

multir esistente ba cteri e¨ n o p d e ic

De winst van korter beademen, van theorie naar praktijk

Vz:

ARH van Zanten

08.15

Prof dr J Bakker, Erasmus MC, Rotterdam

09.30

Ze luisteren toch niet

08.45

FW Rozendaal, Jeroen Bosch Ziekenhuis, Den Bosch

A Voss

into x ic a t i e s Vz:

SJA Aerdts & AJHP van Riel

9.30

Over paddo’s en pilletjes A van Riel

10.15

10: Acute intoxication after ingestion of ink remover R Mauritz

10.25

09.55

21: Achromobacter xylosoxidans bacteremia in a critically ill patient caused by ritual washing MAW van Iperen

10.05

Snelle MRSA diagnostiek B Postma

1: An unusual cause of out-hospital-cardac arrest

veil igheid en o rga nisati e Vz:

I van Stijn & DJ Versluis

10.30

18: Pharmacokinetics of continuous intravenous (iv) acetaminophen in patients after cardiac surgery with cardiopulonary bypass (CPB) MBME Doornaar

10.42

Brand- en ontploffingsgevaar

LJ Montenij

10.35

Pauze

DJ Versluis

v o or s p e l l e n i s m o e i l i j k Vz:

JG van der Hoeven & PW de Feiter

11.05

COPD aan de beademing?

11.07

Pauze

11.30

10: Lorazepam precipitation and line obstruction during continuous infusion at the ICU. How and in what concentration can lorazepam be administered safely? NGM Hunfeld

11.42

Bloedproducten

JG van der Hoeven

11.30

3: Can somatosensory evoked potentials during hypothermia after cardiac arrest be used for prognosis? Results of a pilot study A Bouwes

11.42

11.54

11: Is it worthwhile to offer full treatment and ICU admission to octogenerians with acute abdominal aortic aneurysm? ML Scheer

I van Stijn

12.07

De rol van ICT bij patientveiligheid RJ Bosman

12.32

27: Do Medical Emergency Team activation criteria indeed identify patients at risk? IA Meynaar

12.57


Kanker op de IC D Benoit

12.19

Leverfalen HJ Metselaar

12.44

Zorg tot aan donatie BJM van der Meer

13.09

Abstracts Case reports Educational sessions Pro con debatten


Proefschriften State-of-the-art lectures

De ontbijtsessie wordt mede mogelijk gemaakt door


10-12-2008 17:42:15


n v i c


2 0 0 9

ne de rl andse int ens i vi s t en d agen 2 0 0 9 Donderdag 12 februari 2009 Sessie 1 Middagprogramma



be ad e m i n g Vz:

SJC Verbrugge & D dos Reis Miranda

ca pita sel ecta Vz:

PW de Feiter & JH Zwaveling

14.00

4: Ventilator induced lung injury in children in

14.00

6: Relative adrenal insufficiency in the critically ill,

the intensive care FJJ Halbertsma

14.12

De IC is de enige veilige plaats voor patienten met thuisbeademing pro con debat

the role of ACTH testing MFC de Jong

14.12

and determination of neurological outcome after cardiac arrest: daily practice in ICU’s in the Netherlands A Bouwes

MJ Kampelmacher en ARH van Zanten

14.37

De normale long JG van der Hoeven

15.02

14.49

Nieuwe sedatiestudies

Recruteren is zinloos JMM Verwiel

5: Comfortably calm, soothing sedation of critically ill children without withdrawed symptoms E Ista

Volumina versus drukken D dos Reis Miranda

15.39

14.24

A Beishuizen

9: Lung-protective mechanical ventilation EK Wolthuis

15.14

4: Implementation of therapeutic hypothermia

15.01

Zwaargewichten op de IC JH Zwaveling

15.26

8: ICU admission following bariatric surgery RJC van den Broek

c apita se l e c t a

15.38

Pauze

Vz:

AJC Slooter & ABJ Groeneveld

16.35

26: Three year experience with the surviving sepsis campaign guidelines: Bundle compliance and outcome B Wittekamp

ca pita sel ecta

16.04

16.47

Pauze

16.10

A NICE future

16.35

20: Successful implementation of a delirium assessment tool on the ICU in a Dutch university hospital and the effect on the delirium treatment with haloperidol M van den Boogaard

16.47

22: Cerebrovascular reactivity during hypothermia after cardiac arrest L Bisschops

16.59

28: The selective α7nAChR agonist GTS-21 exerts

4: Health related quality of life in critically ill patients JGM Hofhuis

17.09

E de Jonge & SJA Aerdts

E de Jonge

7: Marburg Hemorrhagic Fever in a returned traveler, a rare but deadly disease J van Paassen

16.57

Vz:

Methodologische problematiek bij IC studies OM Dekkers

17.34

Borrel

19.00

Feestavond met diner

anti-inflammatory effects during experimental human endotoxemia JC Pompe

17.11

J Kesecioglu

17.36


Moeilijke End of life beslissingen

Borrel

10-12-2008 17:42:16


n v i c


2 0 0 9

ne de rl andse int ens i vi s t en d agen 2 0 0 9 Vrijdag 13 februari 2009 Ochtendprogramma


Middagprogramma

o ntbij t s e s si e

Vz:

J Bakker

08.10 – 09.15

14.00

Dopamine and Norepinephrine D de Backer

Met medewerking van Dr M Ranieri

14.35

Stroke treatment on the ICU HB van de Worp

Vz:

JG van der Hoeven

9.00

Echo in the ICU

15.10

Einde programma en borrel

D Lichtenstein

9.35

Citrate hemofiltration HM Oudemans – Van Straaten

10.10

Echinocandine as first choice C Rotstein

10.45

Pauze

Vz:

MB Vroom

11.15

NAVA CA Sinderby

11.50

Extracorporeal CO2 removal: role for lung protection M Ranieri

12.25

Algemene Ledenvergadering

13.10

Lunch

Abstracts Case reports Educational sessions Pro con debatten De ontbijtsessie wordt mede mogelijk gemaakt door


Proefschriften State-of-the-art lectures

10-12-2008 17:42:16


n v i c


2 0 0 9

s pr e kers en voorzi t t er s i nt en s i vi s t en da g e n Dr SJA Aerdts

Prof dr E de Jonge

Internist-intensivist Isala Klinieken, Zwolle

Intensivist Academisch Medisch Centrum, Amsterdam

D de Backer Intensivist Université Libre de Bruxelles, België

Prof dr J Bakker Internist-intensivist Erasmus Medisch Centrum, Rotterdam

MJ Kampelmacher Internist-intensivist Universitair Medisch Centrum, Utrecht

Prof dr J Kesecioglu

Dr A Beishuizen

Anesthesioloog-intensivist Universitair Medisch Centrum, Utrecht

Internist-intensivist VU Medisch Centrum, Amsterdam

DW de Lange

D Benoit, MD, PhD Intensivist Afdeling Intensieve Zorgen Universitair Ziekenhuis Gent, België

JMJ van den Berg Inspecteur Inspectie voor de Gezondheidszorg, Utrecht

Dr RJ Bosman Anesthesioloog-intensivist Onze Lieve Vrouwe Gasthuis, Amsterdam

Dr HM Oudemansvan Straaten Internist-intensivist Onze Lieve Vrouwe Gasthuis, Amsterdam

Dr ACJM de Pont Internist-intensivist Academisch Medisch Centrum, Amsterdam

BH Postma Arts-Microbioloog Ziekenhuis Gelderse Vallei, Ede en Slingeland Ziekenhuis, Doetinchem

Internist-intensivist Universitair Medisch Centrum, Utrecht

M Ranieri, MD

Prof dr LPH Leenen

Prof dr JH Ravesloot

Chirurg-intensivist Universitair Medisch Centrum, Utrecht

Fysioloog Academisch Medisch Centrum, Amsterdam

Prof dr PAM van Leeuwen

Dr D dos Reis Miranda

Chirurg VU Medisch Centrum, Amsterdam

Anesthesioloog-intensivist Erasmus Medisch Centrum, Rotterdam

Prof dr MM Levi

Anesthesioloog-intensivist Università di Torino, Turijn, Italië

Dr RJM Strack van Schijndel Intensivist VU Medisch Centrum, Amsterdam

RJ Trof Internist-intensivist Medisch Spectrum Twente, Enschede

Dr SJC Verbrugge Anesthesioloog-intensivist Sint Franciscus Gasthuis, Rotterdam

Dr DJ Versluis Internist-intensivist Medisch Centrum Haaglanden, Den Haag

MG Vervloet Internist-nefroloog VU Medisch Centrum, Amsterdam

Prof dr PE Verweij Arts-microbioloog Universitair Medisch Centrum St Radboud, Nijmegen

JMM Verwiel Internist-intensivist Universitair Medisch Centrum St Radboud, Nijmegen

AJHP van Riel

Dr OM Dekkers

Internist Academisch Medisch Centrum, Amsterdam

Endocrinoloog Leids Universitair Medisch Centrum

D Lichtenstein

Dr C Rotstein

Internist-infectioloog, Leids Universitair Medisch Centrum

Service de Réanimation Médicale Hôpital Ambroise Paré, Parijs, Frankrijk

Professor of Medicine Division of Infectious Deseases, University of Toronto, Canada

H Endeman

Dr EJ Lust

Internist-intensivist Diakonessenhuis Utrecht

Cardioloog-intensivist VU Medisch Centrum, Amsterdam

PW de Feiter

Dr BJM van der Meer

Intensivist Sint Franciscus Gasthuis, Rotterdam

Intensivist Amphia Ziekenhuis, Breda

Prof dr ARJ Girbes

Prof dr HJ Metselaar

Neuroloog-intensivist Dr HB van der Worp Universitair Medisch Centrum, Utrecht Neuroloog Universitair Medisch Centrum, Utrecht

Internist-intensivist VU Medisch Centrum, Amsterdam

Internist-intensivist Erasmus Medisch Centrum, Rotterdam

Dr PE Spronk Internist-intensivist Gelre Ziekenhuizen, Apeldoorn

Dr A Oude Lashof

MS van der Steen

Internist-infectioloog, Academisch Ziekenhuis Maastricht

Internist-intensivist Ziekenhuis Gelderse Vallei, Ede

Prof dr JT van Dissel

Prof dr ABJ Groeneveld Internist-intensivist VU Medisch Centrum, Amsterdam

Prof dr JG van der Hoeven Internist-intensivist Universitair Medisch Centrum St Radboud, Nijmegen


Toxicoloog RIVM, Bilthoven

CA Sinderby Staff Scientist Department of Critical Care St. Michael's Hospital, Toronto, Canada

Dr PHJ van der Voort Internist-intensivist Onze Lieve Vrouwe Gasthuis, Amsterdam

Prof dr A Voss Arts-microbioloog Ziekenhuis Canisius-Wilhelmina, Nijmegen

Prof dr MB Vroom Anesthesioloog-intensivist Academisch Medisch Centrum, Amsterdam

Dr AJC Slooter

Dr ARH van Zanten Internist-intensivist Ziekenhuis Gelderse Vallei, Ede

Prof dr JH Zwaveling Internist-intensivist Academisch Ziekenhuis Maastricht

I van Stijn Intensivist Onze Lieve Vrouwe Gasthuis, Amsterdam

10-12-2008 17:42:16


Abstracts, Posters & Case reports tijdens Intensivistendagen 2009 De leescommissie van de abstracts en case reports bestaat uit: ABJ Groeneveld, voorzitter, S Aerdts, P de Feiter, JG van der Hoeven, ACJM de Pont, AJC Slooter, I van Stijn, SJC Verbrugge en ARH van Zanten.

1

abstracts

Recovery from thrombocytopenia after removal of pulmonary artery catheter C Barends1 , MWN Nijsten1, ICC van der Horst2, F Ismael1 Departments of 1Intensive Care and 2Cardiology, University Medical Center Groningen, University of Groningen, The Netherlands Introduction. Thrombocytopenia is a common complication in critically ill patients. We frequently noted that platelet counts in thrombocytopenic patients with pulmonary artery catheters (PAC) recover faster after removal of the PAC. Literature on this subject is scarce1,2 and analysis of this phenomenon is compounded by the wide spectrum of causes of thrombocytopenia. Object. The aim of this pilot study was to analyse the quantitative impact of removal of a PAC on platelet counts. Method. From January 2007 up to June 2008 all patients from the Thoracic Intensive Care Unit who were monitored with a PAC for more than 3 days were included. The platelet counts (reference range 150-300 109/L) for these patients were recorded. We studied the period that the PAC was in situ and a period of at least 3 days after removal of the PAC. The day-to-day difference in platelet counts (∆PC; expressed in 109/L/d) was determined.

2

Results. In total 52 patients were identified. 43 had thrombocytopenia on the day of removal of the PAC In 13 patients the nadir of the platelet count occurred 3 or more days before the removal of the PAC. 3 patients did not display thrombocytopenia during their entire stay. As expected, mean ∆PC before PAC removal was significantly lower than mean (±SD) ∆PC after removal -3,9 ± 18,2 vs. 24,5 ± 24,3 109/L/d respectively (p<0.0001). It was also observed that for the 13 patients whose platelet count nadir occurred 3 or more days before removal of PAC the mean ∆PC before removal was positive but significantly lower than mean ∆PC after removal ( 15.0± 10.4 vs. 41,1 ± 24,8 109/L/d respectively; p=0.003). This point to a faster rise in platelet counts after removal of the PAC. After PAC removal there was no significant difference in ∆PC between this subgroup and the main group. Conclusion. In the majority of patients with a PAC, platelet counts tended to decrease until removal of PAC. In those patients who did display a rise in platelet counts before removal of PAC, recovery of the platelet count was lower with a PAC in situ than post removal. These data suggest that in thrombocytopenic patients removal of PAC should be considered as a measure to improve recovery of platelet counts. More research on this subject is warranted. References 1 Laster J, Silver D, Heparin-coated catheters and heparin-induced thrombocytopenia, J Vasc Surg 1988;7:667-72 2 Vicente Rull JR, Loza Aguirre J,Thrombocytopenia induced by pulmonary artery flotation catheters. A prospective study, Intensive Care Med 1984;10:29-31.

Nitric oxide-mediated endothelial dysfunction does not occur during endotoxin tolerance or administration of selective inducible nitric oxide-synthase inhibitor aminoguanidine in humans A Draisma, MJ Dorresteijn, JG van der Hoeven, P Pickkers Department of Intensive Care Medicine, Radboud University Nijmegen Medical Centre, The Netherlands Background. Sepsis is characterized by a blunted vascular response due to endothelial dysfunction. Upregulation of pathological expressed inducible nitric oxide-synthase (iNOS) and downregulation of physiologically essential endothelial NOS (eNOS) due to the inflammation-induced cytokine production are thought to be responsible. The aim of our study was to unravel the role of cytokines in inflammation-induced endothelial dysfunction.

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NJCC_06 v2 06 bwerk.indd 316 NVIC_NJCC abstracts v1.indd 14-15

Methods. 14 healthy volunteers received intravenous injection of 2ng/kg/day LPS on 5 consecutive days (LPS-) to induce LPS tolerance. Another 7 volunteers were given selective iNOS inhibitor aminoguanidine intravenously (loading dose 5 mmol, followed by 1.5 mmol/hr during 5 hrs) starting 1 hour after a single LPS administration (LPS+). Forearm blood flow (FBF) was measured by venous occlusion plethysmography during dose-response curves of endothelial-dependent vasodilator acetylcholine (ACh, 0.5, 2 and 8 µg.min-1.dL-1) and endotheliumindependent vasodilator sodium nitroprusside (SNP, 0.2, 2, 6 µg.min-1.dL-1) before and 4 hrs after LPS administration on day 1 and 5. Main results. No differences in hemodynamic parameters were observed between groups. ACh-induced vasodilation was 187±24%, 333±63% and 775±232% before, compared to 116±8%, 197±27% and 266±36% after LPS administration for the increasing dose of acetylcholine (p=0.006) whereas the vasodilatory response to SNP was not significantly altered (p=0.45). Endotoxemia-induced attenuation to ACh infusion did not occur when tolerance was present after 5 days of LPS administrations (p=0.45) or in the presence of aminoguanidine (p= 0.21). Conclusions. Our study demonstrates that cytokines are responsible for upregulation of iNOS with consequently downregulation of eNOS, which ultimately results in endothelial dysfunction and loss of control on vascular tone.


10-12-2008 16:37:33


3

“Can somatosensory evoked potentials during hypothermia after cardiac arrest be used for prognosis? Results of a pilot study” A Bouwes1,2, DF Zandstra3, JHTM Koelman4, IN van Schaik5, JM Binnekade1, A Hijdra6, J Horn1 1Department of Intensive Care, 4Clinical Neurophysiology and 6Neurology, Academisch Medisch Centrum, Amsterdam; 2Department of Neurology, Sint Lucas Andreas Ziekenhuis, Amsterdam; 3Department of Intensive Care and 5Neurology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands Introduction. In normothermic patients who remain in coma after cardiac arrest, the bilateral absence of the cortical N20 responses of the median nerve somatosensory evoked potentials (SSEP) 24 hours after resuscitation invariably correlates with a poor outcome after 6 months. Nowadays, these patients are treated with mild hypothermia during 12-24 hours, usually together with sedative drugs which hamper neurological assessment. This leads to delayed prediction of prognosis, uncertainty in family members and treating physicians, as well as potentially unnecessary prolongation of intensive care treatment. We investigated whether SSEP performed 4

“Implementation of therapeutic hypothermia and determination of neurological outcome after cardiac arrest: daily practice in Intensive Care Units in the Netherlands” A Bouwes1,2, MA Kuiper3, A Hijdra4, J Horn1 1Department of Intensive Care and 4Neurology, Academisch Medisch Centrum, Amsterdam; 2Department of Neurology, Sint Lucas Andreas Ziekenhuis, Amsterdam; 3Department of Intensive Care, Medisch Centrum Leeuwarden, The Netherlands Introduction. Therapeutic hypothermia is generally accepted to increase survival of out-of-hospital cardiopulmonary resuscitation (CPR), especially in patients with ventricular fibrillation or ventricular tachycardia as initial rhythm. However, lack of initiation of this treatment in daily practice has been frequently reported1. In 2006 an American practice parameter2 was published regarding the determination of the neurological prognosis of these patients. So far, no information is available about the methods for determination of neurological prognosis in the Netherlands. Aim of present study was to evaluate implementation of therapeutic hypothermia after CPR and methods used to predict neurological outcome at Intensive Care Units (ICUs) in the Netherlands. Methods. An email-invitation for an anonymous web-based survey was send to physicians, responsible for critical care medicine at Intensive Care Units in the Netherlands. In each hospital one physician was addressed. Results. Of the 97 physicians surveyed, 76 (78%) responded. The majority was working in a non-academic hospital and admitted more than 20 patients per 5

during hypothermia can predict a poor outcome. Methods. This multicenter prospective cohort study included patients admitted after cardiopulmonary resuscitation and treated with induced mild hypothermia (32–34 °C). Exclusion criteria were age <18 years, confirmed brain death before treatment, impossibility to perform SSEP and no obtained informed consent. Median nerve SSEP was performed during mild hypothermia by the department of clinical neurophysiology. In patients who remained comatose after regaining normal body temperature and wearing off of sedative drugs, a second SSEP was performed. Neurological outcome was assessed 30 days after admission with the Glasgow Outcome Scale (GOS). Poor outcome was defined as death or vegetative state (GOS 1-2). Results. Between July 2006 and April 2008, 78 patients were included in two hospitals. One patient with a subarachnoid hemorrhage was excluded. In 13 patients the cortical N20 response during hypothermia was bilaterally absent. All these patients had a poor neurological outcome, yielding a RR of 7.68 (95% CI 1.45 – 40.55). The cortical response did not return in any of the patients with a negative hypothermic SSEP. Conclusion. The results of this pilot study show that bilaterally absent cortical N20 responses of the median nerve SSEP performed during mild hypothermia after resuscitation can predict a poor neurological outcome. As only 17% of our study population had bilaterally absent N20 responses during hypothermia, we started a larger multicenter prospective cohort study to confirm these results.

year after CPR. Thirty-seven (50%) always treated these patients with therapeutic hypothermia, 42% only treated patients when CPR fulfilled several criteria, such as ventricular fibrillation as presenting rhythm at arrival of ambulance (82%) and duration of time to return of spontaneous circulation (55%). Six (8%) never induced hypothermia. The most important reason for not inducing hypothermia was lack of equipment. Surface cooling (86%) and cold intravenous fluids (71%) were most frequently used to reach the target temperature. Hemodynamic instability was most cited as a reason to discontinue treatment. Neurological outcome was predicted by neurological examination (92%), cortical N20 responses of the median nerve somatosensory evoked potentials (94%), an electroencephalogram (56%) or determination of serum levels of neuron-specific proteins (5%). Conclusion. In the Netherlands, therapeutic hypothermia after CPR is implemented in almost all ICUs, which is compared to previous reports of other countries, exceedingly high. Neurological outcome is predicted by a combination of neurological examination, somatosensory evoked potentials and electroencephalogram. This might change after the publication (spring 2009) of the Dutch guideline for determination of neurological prognosis in patients who remain in coma after CPR. References 1 Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;67(2):203-10 2 Brooks SC, Morrison LJ. Implementation of therapeutic hypothermia guidelines for post-cardiac arrest syndrome at a glacial pace: Seeking guidance from the knowledge translation literature. Resuscitation. 2008;77:286-292

What is the price of one day of Intensive Care? MCH Vijverberg, JJ Zuurbier, F van Tilborg, IA Meynaar ICU, Reinier de Graaf Groep, Delft, The Netherlands Introduction. During the past decades intensive care has been developed in the Netherlands despite the fact that there is no adequate reimbursement: hospitals receive far less money for intensive care than they spend. This has several financial and political reasons, one of which is that the price of intensive care is not known. This study was done to estimate the price of one day of intensive care. Patients and methods. The Reinier de Graaf Groep is a 500-bed teaching hospital with a 10 bed level 2 mixed intensivist-led ICU. We studied the costs as well as the delivered intensive care from January 1st to December 31st in 2007. From the

hospital’s financial records we calculated the costs of medical and nursing staff, drugs, laboratory and radiological investigations, management, overhead, and depreciation. Data on the number of patients and the number of treatment days were derived from the ICU database. Results. In the 1-year study period, 758 patients were treated during 3337 treatment days (occupancy 93%). Patients were ventilated during 1650 days in total (49% of treatment days) and treated with renal replacement therapy during 299 days (9% of treatment days). Total costs are presented in Table 1.



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Table 1. Total costs in euros Nursing staff Medical staff and management Drugs Radiological investigations Laboratory investigations Medical support services like physiotherapy Overhead Depreciation Miscellaneous

2.226.000 562.000 387.000 120.000 400.000 209.000 1.003.000 83.000 104.000 5.094.000 From the total costs of 5,094 million euros and the number of treatment days of 3337, the costs of one day of intensive care is estimated to be 1527 euros.

Conclusion. The average price of one day of intensive care in our unit is 1527 euros. 6

Hospital mortality analysis in a large teaching hospital suggests need for implementation of a rapid response system RKL So1, HH Ponssen1, MCLJ Taks2 1Department of Intensive Care, 2Department of Quality, Albert Schweitzer Hospital Dordrecht, The Netherlands Introduction. The incidence of adverse events experienced by hospital patients in the Netherlands is 5,7 percent. Of these, more than 40 percent are potentially preventable. Our aim was to analyze in our hospital which system-wide interventions should be started in order to avoid (serious) adverse events and possible deaths. Therefore, we participated in a nationwide project Move Your Dot [may 2006-june 2007] in which 9 Dutch hospitals evaluated and analyzed their hospital mortality rates in order to initiate system-wide improvement projects based on the implications of the mortality data. This abstract reports the results and the implications of our hospital mortality analysis. Methods. The Albert Schweitzer Hospital is a large 1000-beds teaching hospital located in Dordrecht, the Netherlands. First, a dedicated team of medical specialists and nurses was trained and then reviewed 50 charts of either internal medicine or general surgery patient deaths using the “IHI Hospital Mortality Review Tool”1; thus we formed a 2x2 matrix [Table: 1a]. Secondly, special attention was paid to charts of patients who on admission were admitted to a general ward for active treatment but who died. Finally, by using the “IHI Global Trigger Tool”2, we performed an incidence analysis both quantitatively [Table: 1b] and qualitatively on the latter charts [Table: 1c]. Results. Table: 1a Comfort Care Only

8

Yes No

ICU Admission

General Ward Admission

20 % (10/50)

68 % (34/50)

0 % (0/50)

12 % (6/50)

Table: 1b

Type of incident

Total

Remaining complications

28

Failure to communicate

44

Decubitus

12

Failure to rescue

12

Delay in diagnosis

12

Adverse events with the use of medication

11

Infection

5

Failure to plan

4

Sepsis

3

Unresponsive to a question Table: 1c

Gradation per type

1

5

Failure to rescue

12

Delay in diagnosis

5

Remaining complications Sepsis

Failure to communicate

Infection

4

-

-

-

5

5

2

-

1

1

3

-

-

-

Total

12

1

11

-

2

1

-

5

2

1

Conclusion. • A total of 132 incidents was found in 34 charts i.e. almost 4 incidents per chart • Miscommunication was the major contributor of all types of incidents • Implementation of a rapid response system could be a system-wide intervention to prevent (severe) adverse events. References 1 Move Your Dot™: Measuring, Evaluating, and Reducing Hospital Mortality Rates (Part 1). IHI Innovation Series white paper. Boston: Institute for Healthcare Improvement; 2003 2 Griffin FA, Resar RK. IHI Global Trigger Tool for Measuring Adverse Events. IHI Innovation Series white paper. Cambridge, MA: Institute for Healthcare Improvement; 2007

ICU admission following bariatric surgery RJC van den Broek1, MP Buise2, F van Dielen3, AJGH Bindels4, A van Zundert5, JF Smulders6 1LUMC, department of Anesthesiology, Leiden, The Netherlands 2MP Buise, Catharina Hospital, department of Anesthesiology, Intensive Care and Pain Therapy, Eindhoven, The Netherlands 3F van Dielen, JF Smulders, Catharina Hospital, department of Surgery, Eindhoven, The Netherlands 4AJGH Bindels, Catharina Hospital, department of Internal Medicine and department of Intensive Care, Eindhoven, The Netherlands 5A van Zundert, Catharina Hospital, department of Anesthesiology, Intensive Care and Pain Therapy, Eindhoven, The Netherlands

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Background. Regarding the complication rate for bariatric surgery and the increasing number of bariatric procedures in an increasing obese prone society, it will interfere with available ICU capacity. (1, 2) In order to assess the need for extra ICU capacity with increasing bariatric surgery in our hospital, we studied ICU admissions after bariatric surgery. Hypothesis. Our goal was to evaluate characteristics and outcome of patients admitted to the ICU following bariatric surgery. Methods. Descriptive study. A review of a prospectively collected database of our bariatric surgery procedures from 2003 until 2006 was performed. The study was performed in a tertiary-level, mixed medical and surgical, adult ICU of a large referral hospital. Results. Of the 265 patients undergoing bariatric surgery (mainly gastroplasties and Roux-en-Y gastric bypasses), 22 (8%) were admitted to the ICU, of which 14 (64%) on an elective basis and 8 (36%) emergently. Hospital length of stay (LOS) for all patients was 4.5 days and ICU LOS was 12 days. Most elective admissions were


10-12-2008 16:37:34


standard procedure because of OSA or super obesity, with a median ICU stay of one day. Emergent admissions were mainly done after emergent surgery due to surgical complications and had a median ICU stay of eight days. Only two patients needed intensive care for more than three days. There were no deaths during ICU stay. Conclusion. The ICU admission rate in our report is 8%. This study showed that 32 ICU days are needed per 100 diverse bariatric procedures. Despite the fact that most patients are admitted to the ICU for only a few days and the majority of the admissions is planned, ICU admission following bariatric surgery is substantial considering its type of surgery; functional and mainly non-emergent. Inadequate 9

References 1 Livingston EH. Procedure incidence and in-hospital complication rates of bariatric surgery in the United States. Am J Surg 2004; 188: 105-10 2 Cendan JC, Obu-aouf D, Gabrielli A, et al. Utilization of intensive care resources in bariatric surgery. Obes Surg 2005; 15: 1247-51

Catheter-related bloodstream infections: a prospective observational study of concurrently sited central venous and arterial catheters M Chalabi1, B Wittekamp1, S van der Geest1, B Winkens2, A Verbon3, DCJJ Bergmans1 Departments of intensive care1, statistics2 and internal medicine3, University Medical Centre Maastricht, The Netherlands Introduction. Intravascular catheters are indispensable in the management of critically ill patients in intensive care units. However, complications including catheter-related bloodstream infections (CRBSIs) may occur and lead to increased rates of morbidity, an increased length of stay in the intensive care unit and a significant increase in attributable costs. Several risk factors for infections related to central venous catheters (CVCs) have been identified. Bloodstream infections due to arterial catheters (ACs), however, have been studied scarcely. The objective of this study was to analyze and compare the incidence of catheter-related bloodstream infection associated with CVCs and ACs and to identify risk factors for CRBSIs. Materials and methods. We performed a prospective observational study in a 16-bed medical/surgical intensive care unit of a 715-bed university hospital. All patients admitted to the intensive care unit for > 24 hours between 1 September 2007 and 30 10

use of admission indications shows the need for stricter indications and possibilities for improvement of patient care.

April 2008 who had or received a CVC or AC were included in the study. A catheter day was defined as one day on which a patient had one or more catheters. CRBSI was defined as a positive blood culture from a peripheral vein, signs of systemic infection and a positive catheter tip culture yielding the same microorganism on the antibiogram as the blood culture with no other apparent source of infection. None of the catheters used in this study had antimicrobial or antiseptic coatings. Catheters were not routinely changed after a fixed insertion time. Results. A total of 219 patients with 258 CVCs and 336 ACs were included in the study and observed for a total of 3172 catheter-days. The number of catheter-days for CVCs and ACs separately were 1679 and 2809 respectively. CRBSI incidence was 1.2 per 1.000 catheter-days for CVCs and 2.1 per 1.000 catheter-days for ACs. The mean length of stay (p= 0.003), the number of days a catheter remained in situ (p= 0.001) and the length of pre-ICU in-hospital stay (p= 0.031) were significantly higher in the CRBSI group. Of the 98 catheters removed due to suspected infection, 90 (92%) turned out negative for CRBSI. When comparing arterial and central venous catheters, we found that 98% of CVCs were inserted under full sterile barrier precautions, whereas only 47% of ACs were inserted using sterile gloves. Conclusion. The incidence of AC- and CVC-related CRBSIs was low and comparable to the incidence reported in the literature. However, the incidence for ACs was higher than for CVCs. From this we can deduct that arterial catheters should be granted the same degree of importance when catheter-related infection is suspected. Measures should be taken to ensure sterile insertion of ACs and prompt removal should be considered whenever a concurrently sited CVC is also suspected of infection.

Lorazepam precipitation and line obstruction during continuous infusion at the ICU. How and in what concentration can lorazepam be administered safely? NGM Hunfeld1, PHGJ Melief3, M Frank3, JWF Uges2 Haga Teaching Hospital, Den Haag, The Netherlands 1Hospital Pharmacist in training, 1,2PharmD, Department of Pharmacy&Toxicology, 3MD, Department of Intensive Care According to the NVIC guidelines [1], lorazepam is the drug of choice when longer duration of sedation is needed. It is administered by continuous infusion in a maintenance dosage of 0.01-0.1 mg/kg/hour. Lorazepam is poorly soluble in aqueous solutions and is a drug that shows precipitation after dilution [2]. This precipitation leads to formation of crystals in infusion lines and may cause obstruction of lines and thrombo-embolic events in patients. Lorazepam solutions are more stable at higher concentrations (>1 mg/ml) or at lower concentrations (<0.08 mg/ml). However, the lower concentrations are less appropriate for the ICU because of the large volume of fluid administration (up to 3L/24h). It shows better solubility at lower pH. Therefore Glucose 5% is preferred for dilution and not NaCl 0.9%. Aims. - To identify the most stable and safest concentration of lorazepam for continuous infusion, with the lowest volume of fluid administration. - To investigate which infusion system (syringe pump or volumetric pump) is most appropriate for continuous lorazepam administration.

syringe (syringe pump, AlarisGH CardinalHealth) and an infusion bag (volumetric pump, AlarisGW CardinalHealth). Visual observation of the total infusion systems occurred once an hour and consisted of checking for particles or crystals. Results. Concentration Syringe pump 2ml/h Syringe 2 mg/ml

No precipitation

0.5 mg/ml

No precipitation

1 mg/ml

0.32 mg/ml

No precipitation

Precipitation after 7 h

Volumetric pump 2ml/h Infusion bag Before pump After pump No precipitation

No precipitation

Precipitation


No precipitation No precipitation



Precipitation occurred as lorazepam crystals (analyzed with Itox® AHZ). The crystals in the infusion line were mainly visible in the part right after the volumetric pump. Visual inspection showed that the influence of the pump itself can cause the precipitation. Higher concentrations of lorazepam (>0.5 mg/ml) did not precipitate during 24 hours infusion by a syringe pump. In contrast, the lower concentration of 0.32 mg/ml did precipitate. Conclusion. Continuous administration of lorazepam by a syringe pump is the optimal system. The concentrations of 2 mg/ml, 1 mg/ml and 0.5 mg/ml are stable during 24 hours. From the perspective of medication safety, the preferred concentration for the ICU setting is 1 mg/ml. A volumetric pump is not suitable for administration of lorazepam. References 1 NVIC Guideline Intravenous analgesia and sedation in adults at the ICU http://www. nvic.nl/richtlijnen_geaccordeerd.php?id=22&titel=Richtlijn-intraveneuze-analgesie-ensedatie-voor-volwassen-patienten-op-de-Intensive-Care. Accessed 12-09-2008 2 Volles DF, et al. More on usability of lorazepam admixtures for continuous infusion, Am J Health-Syst Pharm,1996;53:2753-5

Methods. Different concentrations of lorazepam in glucose 5% (2 mg/ml, 1 mg/ml, 0.5 mg/ml and 0.32 mg/ml) were prepared. In vitro tests were performed during 24 hours in standard clinical ICU setting. Lorazepam solutions were prepared in a



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11

Is it worthwhile to offer full treatment and ICU admission to octogenerians with acute abdominal aortic aneurysm? ML Scheer, JW Haveman, IF Tielliu, EL Verhoeven, JJ van den Dungen, MW Nijsten, CJ Zeebregts Departments of Critical Care and Surgery, University Medical Center Groningen, The Netherlands Introduction. At the regional level we have an integrated system for the rapid transport and subsequent immediate treatment of acute abdominal aortic aneurysm (AAAA). Our strategy is to treat all patients unless they have a very poor performance score. As such, 95% receives full treatment. With the ageing of the population, an increasing proportion of octogenarians reaches the ICU. In view of the demand for health care resources, advanced age may be a factor to refrain from further treatment and ICU admission. The purpose of this study was to investigate whether this holds true for octogenarians suffering AAAA. Methods. All 271 patients with manifest AAAA admitted and treated between January 2000 and February 2008 were included in the study. Six of them died during the operation, the remaining 265 patients form the basis of this report. Acute AAA 12

was defined as either acute non-ruptured (N=82) or ruptured (CT or laparotomyproven, N=183). There were 228 men and 37 women with a mean age of 71.9 ± s.d. 7.8 years (range 54-88). 16% of the patients was 80 years of older (N=42). Open treatment was performed in 191 patients (72%) and endovascular treatment in 74 (28%). When divided in a younger (<80 years) and an older (≥80 years) group, no differences were observed, except for more women in the older group. Results. The mean follow-up was 33.8 ± 30.4 months (including early deaths). Mean hospital length of stay was 17 ± 20 days for patients younger than 80 and 15 ± 17 days for patients older than 80 years of age. Fifty-two patients (20%) died during postoperative ICU and hospital stay. Kaplan Meier survival analysis revealed a significantly better survival for the younger either with a cut off at 75 years (log rank test p<0.001) or 80 years (p<0.05). Stratification based on urgency or type of treatment did not change the difference. Two-year actuarial survival was 72.1% for patients younger than 80 and 59.5% for those older than 80. At 5 years follow-up, these figures were 66.7 and 47.6%, respectively. Mean survival in patients older than 80 was 43.6 ± 7.2 months versus 65.4 ± 3.0 months in those younger than 80. Conclusion. Our liberal strategy of treating patients with AAAA was associated with satisfactory short and long-term outcome, also for octogenarians. Even with a devastating event such as AAAA, a mean survival of more than 3.5 years can be achieved in octogenarians, while hospital- and ICU length of stay is not prolonged compared to the younger, and natural history of disease would give a survival of virtually zero %. Assuming an integrated system for managing AAA is in place, advanced age is not a reason to deny patients surgery or ICU-admission.

What is the optimal time for aPTT measurement after heart surgery: clinical evidence K Filoda, F Ismael, MWN Nijsten, D Douma, AJ de Vries Department of Intensive Care, University Medical Center Groningen, The Netherlands Introduction. High dose heparin is used during cardiac surgery for anticoagulation during extracorporeal circulation, but is despite adequate initial reversal with protamine associated with a rebound effect [1]. This heparin rebound effect is attributed to differences in elimination half-life between heparin and protamine and means that after the surgery again anticoagulation occurs which increases chest tube losses [2]. Postoperative bleeding increases morbidity and mortality. The activated prothrombin time (aPTT) is commonly used to measure residual heparin effects after cardiac surgery. We hypothesised that due to the heparin rebound effect, the aPTT one hour after admission to the ICU (aPTT 2) would be more predictive for the risk of postoperative bleeding than aPTT values directly at arrival (aPTT 1) at the ICU. Material and methods. 54 consecutive patients undergoing coronary artery bypass grafting or simple valve replacement were included in this observational study. Heparin was given in an initial dose of 3 mg/kg before the start of the extracorporeal circulation with incremental doses of 1 mg/kg to maintain an activated clotting time >400s. Protamine was given in a 1:1 ratio to neutralise the heparin. The following parameters were registered: aPTT 1, aPTT 2, blood loss during the first 12 hours after admission on the ICU, the amount of retransfused residual heart-lung machine blood. We consider a maximal aPTT of 33 seconds as a normal value. Student’s t-test was used for differences in the various groups. A P-value 14

<0.05 was considered significant. Results. The mean aPTT 1 was 33,3 ± 5,0 seconds (mean±SD) and aPTT 2 was 34,0 ± 12,7 seconds. The average blood loss in the study group in the first 12 hours was 623 ± 447 ml. 19 patients with abnormal aPTT 1 or both aPTT 1 and aPTT 2 had an average blood loss of 876 ± 627 ml / 12 h compared to 35 patients with a normal aPTT 1 with an average loss of 487 ± 219 ml / 12 h (p=0,0016). 14 patients had an abnormal aPTT 2. These patients received an average of 869 ± 383 ml of residual heart lung machine blood, whereas the patients with normal aPTT 2 received 581 ± 426 ml (p=0,013). Table 1. aPTT [s], n= number of patients n

aPTT 1

aPTT 1

aPTT 2 d” 33

n = 32

n = 8

aPTT 2 >33

d” 33

n = 3

> 33

n = 11

Conclusion. Our data show that those patients with abnormal aPTT 1 and/or aPTT 2 on ICU admission had a higher blood loss than patients with a normal aPTT. Our data suggest that the retransfusion of residual heart-lung machine blood is more important than the heparin rebound with respect to postoperative blood loss. However, as most patients with a prolonged aPTT 1 also had a prolonged aPTT 2 it is appropriate to measure aPTT immediately after arrival in the ICU in patients that had cardiac surgery. References 1 J Thorac cardiovasc surg 2004; 128:211 2 anest analg 2002; 94:514

Procalcitonin kinetics in Legionella pneumophila pneumonia CPC de Jager1, NCJ de Wit2, G Weers-Pothoff3, T van der Poll4, PC Wever3 1 Department of Intensive Care and Emergency Medicine, Jeroen Bosch Ziekenhuis, ’s-Hertogenbosch, The Netherlands 2 Department of Clinical Chemistry & Hematology, Jeroen Bosch Ziekenhuis, ’s-Hertogenbosch, The Netherlands 3 Department of Medical Microbiology and Infection Control, Jeroen Bosch Ziekenhuis, ’s-Hertogenbosch, The Netherlands 4 Center of Infection and Immunity Amsterdam and Center of Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, The Netherlands Study objective. Little is known about procalcitonin (PCT) levels in patients with

320

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community-acquired pneumonia (CAP) due to Legionella pneumophila. The aim of the present study was to investigate this infection marker in patients admitted with L. pneumophila pneumonia in relation to conventional inflammatory parameters, pneumonia severity upon admission and clinical outcome. Methods. Eighteen patients admitted with CAP caused by L. pneumophila serogroup 1 were retrospectively examined. PCT measurements were carried out during the first week of admission in addition to measurements of C-reactive protein (CRP), white blood cell (WBC) count and registration of pneumonia severity upon admission (CURB-65 score). Results. The mean PCT level upon admission in patients with L. pneumophila pneumonia was 13.5 ng/ml (range: 0.3-55.7). Mean CRP level was 397 mg/l (range 167-595) and mean WBC count 11,7 x 10e9/l (range 4.5-20.4). Initial high PCT levels were indicative of more severe disease as reflected by prolonged Intensive Care Unit (ICU) stay and/or inhospital death. Patients admitted to the ICU showed significantly higher PCT levels compared to the remaining patients (26.7 ng/ml (range 4.6-55.7) versus 6.9 ng/ml (range 0.3-29.3); p-value 0.019). There was a significant correlation


10-12-2008 16:37:36


100 d4 d25

procalcitonin (ng/ml)

between APACHE-II scores upon ICU admission and initial PCT levels upon hospital admission (r = 0.86; p-value 0.027). PCT and CRP kinetics in 15 patients during the first week of admission are shown in figure 1 and 2, respectively. In three patients, only an admission day serum sample was available so kinetics could not be studied. Persistently increased PCT levels during treatment were indicative of unfavourable clinical outcome. Conventional inflammatory parameters (CRP and WBC) and the CURB-65 score lacked this discriminatory capacity in our study population. Conclusion. PCT may be a valuable tool in the initial clinical assessment and followup of patients with L. pneumophila pneumonia.

10

1

100

procalcitonin (ng/ml)

d4 d25

0,1

adm

1

2

3

4

5

6

7

time (days)

10

Figure 2. C-reactive protein kinetics with Legionella pneumophila pneumonia during the first week after admission (n=15). Solid lines correspond to C-reactive protein kinetics in patients admitted to the Intensive Care Unit and interrupted lines to C-reactive protein kinetics in patients admitted to the regular ward. Adm = time of admission.

1

600 d4 0,1

adm

1

2

3

4

5

6

500

7

Figure 1. Procalcitonin kinetics in patients with Legionella pneumophila pneumonia during the first week after admission (n=15). Solid lines correspond to procalcitonin kinetics in patients admitted to the Intensive Care Unit and interrupted lines to procalcitonin kinetics in patients admitted to the regular ward. Adm = time of admission.

15 600 Sepsis and inflammation

C-reactive protein (mg/l)

500

300

400

300

d25

200

100

d4

400

C-reactive protein (mg/l)

time (days)

Prevalence and causes of pneumocystis carinii pneumonia at an intensive care unit d25

A Hartgring, JE Tulleken, JJM Ligtenberg, OM Peters-Polman, JHJM Meertens, JG Zijlstra Department of Critical Care, University Medical Center Groningen, The Netherlands 100 200

Introduction. The incidence of ICU admissions for pneumocystis carinii pneumonia 0 adm 1 Clinical2 parameters 3 5 7 different (PCP) is increasing. and4 mortality differs6 between time (days) underlying immunosuppressive conditions. We conducted a retrospective study of all consecutive patients with PCP admitted to the ICU in order to asses the clinical parameters and mortality in our ICU. Methods. We collected the medical charts of all consecutive PCP patients admitted to our ICU from January 1st 2002 through August 1st 2008. Results. We identified 12 PCP patients admitted to our ICU. The median age was 52.5 years (range, 24-71 years). The median APACHE II score at admission was 27 (range, 9-37). Seven patients (58.3%) had undergone a renal transplantation; only 2 patients (16.6%) were HIV positive. For both patients PCP was the first manifestation of HIV infection. Seven patients were on steroids, with a median duration of 106.5 days (range, 99 days - 7 years) before admission. Six of these patients also received a calcineurin-inhibitor. Five of these six patients also received mycophenlate mofetil. One other patient, who did not use prednison at time of admission, received a calcineurin-inhibitor and mycophenlate mofetil. One patient received chemotherapy until five weeks before admission. Only two patients did not receive any type of immunosuppressive medication. No patient received prophylaxis for PCP prior to onset of pneumonia. The yearly incidence of ICU admissions for PCP is increasing. Ten patients (83.3%) needed intubation and mechanical ventilation, all within 24 hours of admission. During the ICU stay, circulatory failure occurred in five patients (45%). The treatment for all patients consisted of trimethoprim-sulfamethoxazole 3 dd 1920 mg intravenously and adjunctive corticosteroids (prednison 60 mg/day).

The median length of stay in the ICU was 12.5 days (range, 2-31 days). Seven patients 0 1 stay, yielding 2 3 ICU mortality 4 5 58.3%. 6 Predictors 7 died duringadmtheir ICU an of of ICU time (days) mortality at bivariate analysis are presented in table 1. Table 1. Predictors of Intensive care mortality

Number of patients

5

Non-survivors 7

P value

Female gender n (%)

3 (60)

5 (70)

0.70

APACHE II score, median (range)

26 (12-29)

28 (9-37)

0.27

Age (years), median (range)

Circulatory failure at admission n (%)

Hemoglobin (mmol/l), median (range)

39 (24-68) 0

6.2 (5.7-6.4)

Lactate dehydrogenase (mmol/l), median (range) 409 (404-848) Occurrence of renal failure n (%)

0

Ciclosporin/tacrolimus n (%)

3 (60)

Mycophenlate mofetil n (%)

2 (40)

Occurrence of ventilation in prone position n (%) 0 Occurrence of pneumothorax n (%)

Duration of mechanical ventilation median (range) ICU length of stay median (range)

0

3 (3-13) 5 (2-14)

58 (23-71) 5 (70%)

5.6 (5.3-6.6)

555 (268-794) 2 (28) 3 (43)

5 (70) 2 (28)

2 (28)

13 (8-25) 13 (8-31)

0.27

0.006 0.34 1.0

0.19

0.68 0.19

0.47 0.19 0.15

0.03

Conclusion. Acute respiratory failure due to PCP still is a serious illness with a high mortality. There seems to be an increase in ICU admissions for PCP in the last two years, this is yet to be explained. All patients in our cohort failed to receive PCP prophylaxis, which should strongly be considered for all patients receiving prolonged systemic corticosteroid therapy, and/or cytotoxic chemotherapy. PCP in our ICU is mostly related to solid organ transplantation and HIV related PCP has almost vanished. Solid organ transplantation related PCP is a disease with its own characteristics.



Survivors

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05-12-2008 10-12-2008 15:26:16 16:37:36


16

Microvascular perfusion in oral mucosa, pleura and diaphragm during cardiopulmonary bypass in 3 children EAB Buijs1, PC Top1, AJJC Bogers2, D Tibboel1 1 Erasmus MC-Sophia Children’s Hospital Department of Intensive Care, Rotterdam, The Netherlands 2 Erasmus MC Department of Cardio-Thoracic Surgery, Rotterdam, The Netherlands

Aim of study. To describe potential changes in microvascular perfusion in children undergoing cardiopulmonary bypass (CPB). To assess feasibility of intra-operative measurements of microvascular perfusion in pleura and diaphragm. Study design. Observational prospective case report. Methods. Microvascular perfusion was measured using Orthogonal Polarization Spectral imaging in 3 patients with congenital heart defects. Perfusion was assessed in oral mucosa, pleura and diaphragm after anaesthetic induction (T1), during CPB (T2), during surgery after CPB (T3) and, for oral mucosa only, directly after arrival on the ICU (T4) and 1 day after surgery (T5). For analysis of perfusion we used a validated semi-quantitative Microvascular Flow Index (MFI-score) in small (Ø < 25µm), medium (Ø = 25-50µm) and large vessels (Ø = 50-100µm). Data were compared to data of 3 healthy age-matched children. MFIscores are shown in median (range). Results. T1 oral MFI-scores did not differ compared to controls: MFI-small= 3,0 (0,50) vs. 3,0 (0,12), MFI-medium= 3,00 (0,50) vs. 3,00 (0,12), MFI-large= 3,00 (0,25) vs. 3,00 (0,12). During CPB MFI-scores decreased in all vessel types. T5 oral MFI-scores persisted to be significantly lower than controls in small and medium vessels: MFI-small= 2,83 (0,08) vs. 3,0 (0,12) (P=,043) and MFI-medium= 2,83 (0,21) vs. 3,0 (0,12) (P=,046). Microvascular perfusion could be observed in pleura and diaphragm. However 17

Introduction. Cardiac surgery with the use of cardiopulmonary bypass (CPB) is associated with post-operative organ failure. Severe inflammatory response syndrome (SIRS) is believed to be causative, possibly by way of altered microvascular perfusion. We found two publications on adult patients suggesting changes of microvascular perfusion during CPB.1,2 To our knowledge there are no reports about altered microvascular perfusion in pediatric patients receiving CPB. Moreover no reports about microcirculatory measurements in pleura and diaphragm have been published.

feasibility was low due to influences of the beating heart and ventilated lung which caused unstable images with pressure artefacts. At T1, T2 and T3 a trend was seen toward lowered pleura and diaphragm MFI-scores for all vessels compared to oral MFI-scores. T2 pleura MFI-scores for small and medium vessels were lower when compared to T1: 2,38 (1,24) vs. 2,75 (0,28) (P=,109) and 2,50 (1,40) vs. 2,75 (0,33) (P=,109). No direct correlation with macrovascular perfusion parameters could be found. Conclusion. We observed deteriorations of oral microcirculation during surgery with the use of CPB, which did not restore in post-operative measurements. Feasibility to observe microcirculatory alterations in pleura and diaphragm was low. References 1 Bauer A, Kofler S, Thiel M, Eifert S, Christ F. Monitoring of the sublingual microcirculation in cardiac surgery using orthogonal polarization spectral imaging: preliminary results. Anesthesiology. 2007 Dec;107(6):939-45. 2 den Uil CA, Lagrand WK, Spronk PE, et al. Impaired sublingual microvascular perfusion during surgery with cardiopulmonary bypass: a pilot study. The Journal of thoracic and cardiovascular surgery. 2008 Jul;136(1):129-34.

The effects of continuous intravenous infusion of acetaminophen in cardiac surgery patients on liver enzymes

T van den Ende1, RBP de Wilde1, FHM Engbers2, MS Arbous1, J den Hartigh3, LG Krikken-Hogenberk2, J Burggraaf 4 Department of Intensive Care1, Cardiothoracic Anaesthesiology2, Clinical Pharmacy and Toxicology3, Leiden University Medical Center and Centre for Human Drug Research3, The Netherlands Objective. Intravenous (i.v.) acetaminophen (Perfalgan®) is used as adjunctive treatment for post-operative pain. There is evidence that single or repeated doses of i.v. acetaminophen (AAP) only temporarily result in an adequate (therapeutic) concentration (10-20 µg/ml). This problem may be circumvented by using continuous i.v. administration of AAP. Cardio Pulmonary Bypass (CPB) and AAP are possibly associated with liver dysfunction. For AAP this is possibly due to a toxic alkylating metabolite, N-acetyl-p-benzoquinone-imine. It is unknown whether i.v. AAP administered as a continuous infusion aimed at presumed therapeutic concentrations (10-20 µg/ml) has untoward hepatic effects in patients after CPB. Aim of study: to investigate the effects of a continuous i.v. AAP on the liver by measurements of serum markers of liver function. Methods. We studied 15 patients undergoing cardiac surgery with CPB. All patients received identical standard treatment for anaesthesia and analgesia. In addition, 8 patients received continuous i.v. AAP (total dose: 2 gram) for 8 hours, initiated at wound closure. Blood samples of liver enzymes were taken at time points that are routine practice; prior to surgery and at 5 time points there after (direct, 1, 2, 3 and 5 days post-operatively). Samples were analysed for ALAT, ASAT, Alkaline Phosphatase (AlkPh), total bilirubin and LDH (routine assays). Analysis was done by comparison of medians and time-corrected AUC of the markers between the groups using one-way ANOVA; p < 0.05 was considered statistical significant. Results. Characteristics for both groups were similar (table 1). Treatment with i.v. AAP did not change the routine care for the patients. Initial AAP concentrations

322


ranged between 13 and 21 µg/ml, and were 7-17 µg/ml during the plateau. The median values for the biochemical markers are in table 2. For all, p-value for differences exceeded 0.15. Conclusion. Continuous infusion of AAP resulting in therapeutic concentrations in cardiac surgery patients did not result in differences in serum markers of liver function and damage compared to control patients. Although data are based on a small population, further studies into safety and efficacy of i.v. AAP in these patients seem warranted. Table 1

Perfalgan

Controls

Age year (sd) BSA m2 (sd)

62 (5.8)

70 (3.1)

Anesthesia Min (sd)

330 (16)

349 (50)

323 (12)

350 (24)

Gender male/female 7/1

2.05 (0.05)

Operation Min (sd)

LDH pre-op u/l (sd)

0.45 0.54

1.91 (0.08)

255 (21)

Clamp time Min (sd)

p-value

5/2

87 (10)

0.23

334 (40)

0.19

77 (11)

0.40

0.77

0.26

Table 2 Time course of median values for hepatic markers for intervention (A) and control (C) patient group Bilirubin AlkPh (U/L) ASAT (U/L) ALAT (U/L) LDH (μmol/L) (U/L) A C A C A C A C A C Pre-OK

7

8

-

-

38

31

19

26

344

344

Dag1

7

15

46

45

79

53

24

19

686

542

direct post ok Dag2 Dag3

Dag5

10 8

9

9

9

12 9

11

38 -

46 52

37

55

65

69

52

44

48 45

41

43 32

29

18

20 30

30

17

17

16 21

628

569 579 481

399 477

458 522


10-12-2008 16:37:37


Pharmacokinetics of continuous intravenous (iv) acetaminophen in patients after cardiac surgery with cardiopulmonary bypass (CPB) MBME Doornaar1, RBP de Wilde1, FHM Engbers2, LG Krikken-Hogenberk2, J den Hartigh3, MS Arbous1, J Burggraaf 1,4 1 Department of Intensive Care, 2 Department of Cardiothoracic Anesthesiology, 3 Department of Clinical Pharmacy and Toxicology of Leiden University Medical Center, 4Centre of Human Drug Research, The Netherlands Objective. Enteral acetaminophen (AA) is used in the treatment of post-operative pain. Evidence suggests that the absorption of AA is variable and that therapeutic concentrations (10-20 µg/ml) are not always reached. This can be circumvented by iv administration which is of particular interest for patients after cardiac surgery for which analgesia with (selective) COX-inhibitors is associated with excess mortality. Previous studies show that single iv doses of AA (1gr) resulted in concentrations above the therapeutic threshold for only 2-3 hrs. This suggests that continuous iv infusion should be used for adequate analgesia. The aim of this study is to investigate a dosing regime in patients after cardiac surgery with CPB to maintain AA concentrations within the therapeutic range. Methods. The study was performed in 8 patients after cardiac surgery and CPB. The iv AA dosing regimen was started at wound closure, and consisted of a two-step loading infusion and a maintenance infusion (300mg in 10 min, 500mg in 50min and 180mg/hr for 7 hrs). Samples for AA concentrations were taken regularly during and after the infusion. AAP was measured with fluorescence polarisation immunoassay (AxSYM system, Abbott Laboratories, Il, USA). The assay has a lower limit of detection of 1.0 µg/ml, the total CV in the measurement range is <10%. The AA concentration-time profiles were inspected for the maximal concentration and whether steady-state concentrations were achieved by calculating the slope of the concentration-time profile over the 60-480 min timespan. 19

Results. The average concentration-time profile (figure 1) shows that the peak plasma AA concentration was reached after 10 min with an average concentration of 18.3 (range 15-24) µg/ml. During the second loading infusion, the concentrations declined slightly and remained stable during maintenance infusion at an average of 12.3 (range 8-17) µg/ml. The average slope value of the time-concentrations during the 60-480 min timespan was not different from zero except one patient in whom an increase in AA concentrations from 9 to 17 µg/ml was observed. In 2 patients AA concentrations below 10 µg/ml were observed (8 and 9 µg/ml respectively) during the maintenance phase. AA concentrations greater than 20 µg/ml were not observed. Conclusion. The current data suggest that the described dosing regimen for continuous iv infusion of AA can be used to achieve therapeutic AA concentrations. However, the regimen should be refined if it is to be used for a longer duration as in its present form the total dose will be 5 gr/24hrs. 25 Acetaminophen (µg/ml)

18

20 15 10 5 0

0

2

4

6

Time (hrs)

8

10

12

Figure 1. Average (SD; n=8) concentration-time profile of Acetaminophen over continuous iv infusion.

Endotoxemia-induced changes in cytokines, cortisol, EEG, brain specific proteins, and cognitive functional tests in humans in vivo MHWA van den Boogaard1, BP Ramakers1, N van Alfen2, SP van der Werf 3, I Fick1, CH Hoedemakers1, MM Verbeek4, L Schoonhoven5, JG van der Hoeven1, P Pickkers1 1 Department of Intensive Care Medicine, 2 Department of Clinical Neurophysiology, 3 Department of Psychology, 4 Department of Laboratory of Pediatrics and Neurology, 5 Department for IQ healthcare, Radboud University Nijmegen Medical Centre, The Netherlands Introduction. The effects of systemic inflammation on cerebral function are not clear, as both inflammation-induced encephalopathy as well as stress-hormone mediated alertness have been described. We determined endotoxemia-induced effects on cytokines, cortisol, EEG changes, brain specific proteins (BSP), and cognitive functions (CF) and their correlations in humans in vivo. Methods. Healthy male volunteers (n=15) received intravenous 2 ng/kg E. coli LPS. Cytokines, temperature, heart rate, cortisol and BSP were determined at 0-0.5-1-1.52-4-8 hrs after LPS infusion. CF-tests were performed at 0-2-8 hrs, and EEG changes were monitored continuously.

Results. Volunteers experienced the expected flu-like symptoms, illustrated by an increase in temperature (mean±SEM) of 1.4±0.1oC and an increase in heart rate of 27±2 bpm. Circulating cytokines increased to 814±133 (TNF-α), 1111±142 (IL-6), 108±28 pg/ml (IL-10) and 22915±1856 pg/ml (IL-1Ra). Cortisol increased significant from 0.31±0.07 to 0.60±0.07 µmol/L. Although endotoxemia induced a transient mild encephalopathic episode on EEG in one subject, this was without objective cognitive dysfunction and this subject had a very low inflammatory response (TNF-α 169 pg/ml). No clinically relevant EEG changes by both visual and quantitative analysis could be detected in any of the other volunteers. All measured brain specific proteins remained within the normal range. NSE decreased from 11.5±2.0 to 7.7±1.4 µg/l (P<0.0001), S100-β showed a significant cubic change (P=0.038), whereas GFAP did not change. During endotoxemia the cognitive functions: attention under time pressure (P<0.0001), reading speed (P<0.0001) and psychomotor speed capacity (P<0.0001) improved. The working memory and fine motor control also improved but not significantly. The increase cortisol was significantly correlated with improvement a reading speed test (r= 0.714, P=0.003). No other correlations between cytokines or cortisol levels and changes in EEG parameters, BSP and CF were found. Conclusion. Experimental human endotoxemia results in high levels of circulating cytokines and increased cortisol concentrations. In healthy volunteers this can sporadically lead to a transient mild deterioration of brain function without clinical correlate. Overall, cognitive function improved after LPS infusion. Short-term systemic inflammation does not provoke or explain the occurrence of a septic encephalopathy, and primarily results in more alertness. A short duration of high cytokine concentrations in humans is not neurotoxic.



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20

Successful implementation of a delirium assessment tool on the ICU in a Dutch university hospital and the effect on the delirium treatment with haloperidol M van den Boogaard1, P Pickkers1, JG van der Hoeven1, G Roodbol2, Th van Achterberg3, L Schoonhoven3 Department of Intensive care1, Department of Psychiatry2, Institute for Quality Health Care 3 Radboud University Medical Centre Nijmegen, The Netherlands Introduction. In critically ill patients delirium is a serious and frequent disorder. As early recognition of the delirium is important for adequate treatment, routine screening of the patients is necessary. To be meaningful for practice this screening should be performed frequently and interrater reliability (IRR) should be high. The study aim was to evaluate the implementation of the confusion assessment methodICU (CAM-ICU) in our ICU (scoring rate of >80%, an IRR score of >0.80 and a higher level of knowledge concerning delirium). Another aim was determine what the effect is on the frequency of haloperidol use as a proxy of the delirium incidence, the total haloperidol doses and the haloperidol treatment duration. Methods. The implementation strategy was focused on potential barriers for screening with the CAM-ICU, i.e. lack of knowledge and availability of the assessment 21

tool. The CAM-ICU was integrated in our patient data management system (PDMS) and necessary testing tools became available at every bed. ‘Delirium key-nurses’ take for further instruction and introduction in the ICU. Instruction and feedback were regularly supplied. Scoring rate was calculated by the percentage scored patients per day. Cohen’s Kappa (IRR) was calculated between the score on the CAM-ICU scored by the ICU nurse and by an expert psychiatric nurse. Knowledge level of the ICU-nurses was determined with a pre- and post test. To determine what the effect was of the regularly use of a delirium assessment tool on the delirium treatment we compared the haloperidol use (total doses per patient and per day) before and after the implementation of the CAM-ICU. Results. During 4 months, 78 patients were screened for IRR. After intensive training on the job and feedback twice a week, the IRR increased relevantly from 0.78 to 0.89 (95%CI: 0,75-1,0). The scoring rate of the CAM-ICU increased significantly from 77% to 92% (p<0.001). The delirium knowledge level of the nurses increased from 6.2±1.7 to 7.4±1.2 (p=0.0001). With the use of the CAM-ICU more patients per month are treated with haloperidol. The median treatment duration and the median haloperidol doses decreased respectively from 5 to 3 days and 18 mg to 6 mg per patient. Conclusion. Tailoring our implementation strategy to our ICU was successful. The main goals were achieved in a relatively short time. Early recognition of delirium with the CAM-ICU has become a standard component of the daily care of our ICU nurses and contributes to the quality of care. Early detection of delirium can possibly lead to shortening the delirious period and treatment.

Triage based on the ‘crossed limb sign’ in accident & emergency patients MMJ van Eijk, AJC Slooter Department of Intensive Care, University Medical Centre, Utrecht, The Netherlands Introduction. As a medical student, one of the authors was told, in joke, that the most efficient tool for triage in the accident & emergency (A&E) department was the ‘crossed limb sign’. A patient presenting with either limbs crossed was supposed to be in no immediate distress, and consultation could wait. Objective. The objective of this study was to study the predictive value of the ‘crossed limb sign’ to be send home from the A&E department. Methods. 146 patients presenting at two large A&E departments (Academic Medical Center Amsterdam and University Medical Center Utrecht) were included in this prospective, observational study. No patients were excluded. Age, gender, position (sitting or lying) and posture of arms and legs were registered by A&E nurses. After diagnosis and (if necessary) treatment, the nurse registered whether or not the patient was admitted to the ward. The sensitivity, specificity, positive predictive

value (PPV) and negative predictive value (NPV) to be send home were calculated with simple two-by-two tables. Results. There was no difference between admitted (n=74) and non-admitted (n=72) patients with regard to age, gender or posture. Based on the table, a ‘crossed limb sign’ showed a sensitivity of 51% (95% CI 39-63), a specificity of 43% (95% CI 3255), a PPV of 47% (95% CI 36-58) and a NPV of 48% (95% CI 35-60) to be send home. No association was found with the crossed legs- or crossed arms sign either (data not shown). Conclusion. The nurse who classified the determinant (posture), had no influence on the outcome (non-admission or admission). Bias, is therefore unlikely. As predictive values approximated 50%, posture seems not be predictive for hospital admission in A&E patients. Table. Presence of the crossed limb sign and hospital admission in accident & emergency patients Send home Admission Total Crossed limb sign +

37

42

79

Total

72

74

146

Crossed limb sign -

35

32

67

22

Cerebrovascular reactivity during hypothermia after cardiac arrest L Bisschops, CWE Hoedemaekers, K Simons, JG van der Hoeven Department of Intensive Care, Radboud University Nijmegen Medical Centre, The Netherlands Introduction. Cerebral blood flow after cardiac arrest is reduced during the delayed hypoperfusion phase. Hypocapnia can induce cerebral vasoconstriction with subsequent cerebral ischemia. Comatose patients after cardiac arrest have a preserved cerebrovascular reactivity to changes in PaCO2 under normothermic conditions. Aim of this study was to determine if cerebrovascular reactivity to changes in PaCO2 is preserved during mild therapeutic hypothermia. Methods. We performed an observational study in 10 adult comatose patients after out-of-hospital cardiac arrest. All patients were cooled to 32-34ºC for 24 hours, followed by passive rewarming. Blood flow velocity in the middle cerebral artery (MCA) was measured by transcranial Doppler (TCD). Oxygen saturation in the

324


jugular bulb (SjbO2) was measured by repeated bloodsampling. Hypocapnia and hypercapnia were induced by a 20% increase and decrease in minute ventilation during 20 minutes. Data are expressed as mean±SEM. Changes over time between hypothermia and normothermia were analysed by ANOVA. The relation between changes in PaCO2, SjbO2, MFV and PI were determined by linear regression. Results. We studied 10 comatose patients successfully resuscitated from an outof-hospital cardiac arrest. Ventricular fibrillation was the cause of cardiac arrest in all patients. The estimated time between collapse and ROSC was 25±15 minutes. Five patients survived until hospital discharge. At the start of the experiment MFV in the MCA was low (32.2±9.6 cm/sec), increasing significantly to 67.5±11.0 cm/ sec at 48hours (P<0.001). The SjbO2 increased from 66.2±2.6% at the start of the experiment to 82.9±1.5% at 48hours (P<0.001).We found a significant correlation between the delta PaCO2 and delta MFV (P<0.001) (Figure 1A). A 1kPa decrease in PaCO2 resulted in a 7.2cm/sec decrease in MFV. A significant correlation also existed between the delta PaCO2 and delta SjbO2 (P<0.001) (Figure 1B). A 1kPa decrease in PaCO2 resulted in a 7.4% decrease in SjbO2. Conclusion. During mild hypothermia after cardiac arrest cerebrovascular reactivity to changes in PaCO2 is preserved. Arterial blood gas analysis should be performed regularly to avoid unintentional changes in PaCO2 with risk of cerebral ischemia.


10-12-2008 16:37:38


Figure 1A

23

Figure 1B

Cerebral blood flow in hypothermic and normothermic patients after cardiac arrest L Bisschops1, CWE Hoedemaekers1, K Simons1, G Buunk2, JG van der Hoeven1 1Department of Intensive Care, Radboud University Nijmegen Medical Centre, The Netherlands 2Department of Internal Medicine, Franciscus Hospital, Roosendaal, The Netherlands Introduction. Anoxic neurological injury is a major cause of morbidity and mortality in cardiac arrest patients. After restoration of spontaneous circulation (ROSC), cerebral blood flow is decreased for a period of 6 – 24 hours. The effects of mild therapeutic hypothermia on cerebral blood flow (CBF) are unknown. Aim of this study was to assess cerebral blood flow in patients after cardiac arrest treated with mild hypothermia. Methods. We performed a prospective observational study in 10 adult comatose patients after out-of-hospital cardiac arrest. All patients were cooled to 32-34ºC for 24 hours, followed by passive rewarming. Blood flow velocity in the middle cerebral artery (MCA) was measured by transcranial Doppler (TCD). Oxygen saturation in the jugular bulb (SjbO2) was measured by repeated blood sampling. Data from this prospective trial were compared to data from a similar observational study in 10 patients under normothermic conditions(1). Data are expressed as mean±SEM. Changes over time between hypothermia and normothermia were analysed by ANOVA. Figure 1A

Results. We studied 10 comatose patients successfully resuscitated from an out-ofhospital cardiac arrest. Ventricular fibrillation was the cause of cardiac arrest in all patients. The estimated time between collapse and ROSC was 25±15 minutes. Five patients survived until hospital discharge. At the start of the experiment, MFV was comparable between hypothermia and normothermia patients (30.3±3.2 cm/s vs 28.7±3.6 cm/s, respectively, P=0.76) (Figure 1A). In the first 18 hours, MFV remained significantly lower in hypothermia patients compared to normothermia patients. Concomitant with the increase in body temperature, MFV increased to 53.4±8.5 cm/s in hypothermia patients and 57.8±8.5 cm/s in normothermia patients after 24 hours. In the hypothermia group, a further increase in MFV to 67.5±11.0 cm/s at 48 hours was measured. Jugular bulb oxygen saturation was comparable at the start of the experiment in both groups (66.2±2.6% in the hypothermia and 59.8±3.5% in the normothermia group, P=0.18) and gradually increased to 80.1 ± 2.4 in hypothermia patients and 73.9±3.4 in normothermia patients at 24 hours, P=0.15) (Figure 1B). Conclusion. The cerebral blood flow during mild hypothermia is lower in hypothermic compared to normothermic patients, while cerebral oxygen extraction remained similar, suggesting decreased cerebral metabolic activity during hypothermia. This reduction in cerebral metabolic activity may contribute to the protective effect of mild hypothermia in these patients. References 1 Buunk, G., van der Hoeven, J. G., Frolich, M., and Meinders, A. E. (1996) Cerebral vasoconstriction in comatose patients resuscitated from a cardiac arrest? Intensive Care Med. 22:1191-1196 Figure 1B



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24

Post-ICU outpatient clinic (PICOC) initiative foresees unmet needs of post-ICU patients DHT Tjan, N van der Kam, A van Dieren, M Schouwmans, A van der Ploeg, ARH van Zanten Department of Intensive Care, Gelderse Vallei Hospital, Ede, The Netherlands Introduction. Intensive Care focuses on survival by preventing death from life threatening conditions. However, survivors of critical illnesses may experience a spectrum of morbidities that may influence recovery, quality of life and daily health. Limited data are available regarding the extent of these problems. In order to gain insight and provide better aftercare for our post-ICU surviving patients we started a post ICU outpatient clinic (PICOC) in November 2007. We aimed to evaluate the physical and psychosocial problems encountered during the first year after ICU discharge. Methods. We prospectively gathered data from patients visiting our PICOC. We analysed data from 35 patients that visited our PICOC from November 2007 until June 2008 with respect to medical problems and ICU related morbidity. Patients with prolonged mechanical ventilation (> 10 days) were invited to voluntarily visit the PICOC at one, three, and six months after hospital discharge. Most patients were diagnosed with severe sepsis or septic shock. Pre-visit health questionnaires were send addressing general health status and daily activity. Each patient was seen by both an intensivist and an ICU nurse for half an hour consecutively. The intensivist mainly focused on physical aspects and general health, while the nurse discussed psychosocial and emotional aspects and daily activities. The PICOC operated two afternoon sessions per month. Results. Of 40 invited patients 12,5% declined. Two patients because of readmission to the hospital and three patients didn’t feel any need because they didn’t experience any medical problems. Of 35 patients that visited our PICOC 32 patients had a diagnosis of severe sepsis. Three patients were seen after cardiac arrest treated with mild therapeutic hypothermia. Sixty percent were males. The majority of complaints were reported within the first three months after hospital 25

discharge and summarised in table 1. The duration of complaints varied from two weeks to one year after hospital discharge. Most patients did not have received any form of treatment or guidance with respect to ongoing complaints. Table 1

Physical and psychosocial problems during PICOC visit 1-3: n=35

- vivid dreams and nightmares 89 % - weight loss >10%

- muscle weakness

86 %

80%

- memories of disorientation 51% and delirium during ICU stay - sleep disturbances 40% - concentration difficulties

- signs of posttraumatic stress 20% disorder - skin problems 17% - loss of appetite - loss of libido

34%

14% 11%

- hoarseness and itchy cough 14% - dry mouth - other

9%

14%

Conclusion. Many survivors of critical illness and intensive care experience significant physical and psychosocial problems that may influence daily life and recovery after hospital discharge. Potential benefits could be expected from psychological treatment and feeding interventions. The attention for complaints and feed back on ICU care, as well as the opportunity to revisit the ICU were much appreciated by patients. Post-ICU morbidity should be taken seriously and warrants more research. In defining post-ICU quality-of-life these factors should be taken into account. We feel a PICOC is an excellent organisational solution to improve long-term outcome in ICU patients and monitor QOL aspects after hospital discharge.

Epidemiology of fungal infections in critically ill patients: consequences for antimycotic prescriptions MC van Rijk1, E de Jong1, DHT Tjan1, L Nohlmans2, MA Schouten2, ARH van Zanten1 1Department of Intensive Care, 2Department of Microbiology, Gelderse Vallei Hospital, Ede, The Netherlands Introduction. Invasive fungal infections (IFI) are associated with significant morbidity and mortality. Surveillance data suggest that in the Netherlands candidemia is caused by Candida non-albicans species (e.g. C. glabrata and C. parapsilosis) in 50% of cases. Fluconazol resistance is reported in 1-30% of C. glabrata species. Recently new guidelines have been proposed for treatment of invasive candidiasis [1]. In severely ill patients first line therapy with echinocandins (anidulafungin or caspofungin) or voriconazol is advised until resistance patterns are determined. These latter named medications are more expensive than commonly used fluconazol. Methods. We retrospectively analysed all positive culture data from mechanically ventilated patients admitted to our mixed surgical-medical ICU patients in 2007 to address the potential impact of these guidelines on antimycotic medication use. No SDD is used. We analysed candidemia and positive fungal cultures from both relevant (abdomen, central line, etc.) and irrelevant sites (urine, trachea aspirate, etc.). Per patient only one positive culture was used. Then we simulated calculated treatment days for echinocandins or voriconazol assuming an IV treatment duration of 14 days in case of fluconazol resistance [2]. Furthermore, in case of an unknown Candida species in blood cultures 3 days were used to calculate non-fluconazol days. We then calculated non-fluconazol treatment days for C. non-albicans species for all IV days (model A). Or in case of susceptibility

326


testing we assumed a 20% continuation of echinocandins or voriconazol in case of fluconazol resistance after 5 days needed for susceptibility testing (model B). Additional daily costs of € 400 for non-fluconazol treatment per day was assumed. Costs for susceptibility testing were not included in model B. No outcome benefits were compared. No reimbursement for expensive medications was calculated. Results. In 560 ventilated patients 65 positive blood cultures were found. Of these two (3.1%) were caused by C. albicans and C. glabrata. From all positive cultures from irrelevant sites (972) 10,7% were positive for Candida species. Of those 28% were C. non-albicans species. Of 328 positive cultures from relevant sites 7.0% (23) was positive for Candida species. Of these only 3 (13%) were C. non-albicans species. IFIs were diagnosed in 4.5% of our patients. Based on model B and A respectively, candidemia would cause 8-19 and IFI would cause 86-111 non-fluconazol days per year. Annual additional costs are estimated at € 37,600 – 52,000. Conclusion. Candidemia is rare in our ICU (0.35%). However, 4.5% of patients have invasive fungal infections. The incidence of C. non-albicans species is lower in IFI (13%) than in surveillance cultures from irrelevant sites (28%). Candida epidemiology based on all cultures could overestimate the role of C. non-albicans species in IFI. Implementation of the Dutch SWAB IFI guidelines incurs marked additional medication costs. Not taken into account the costs of susceptibility testing, we estimated that performing susceptibility testing in C. non-albicans species costs could be reduced by 28% as step-down therapy to fluconazol would be possible in many patients. References 1 Stichting Werkgroep Antibioticabeleid (SWAB). SWAB-guidelines for the treatment of invasive fungal infections, 2008. http://www.swab.nl. 2 Reboli AC, Rotstein C, Pappas PG, et al. Anidulafungin versus fluconazole for invasive candidiasis. N Engl J Med 2007;356:2472-82.


10-12-2008 16:37:40


26

Figure 1: Bundle Compliance

Three year experience with the surviving sepsis campaign guidelines: Bundle compliance and outcome B Wittekamp, DHT Tjan, ARH van Zanten Department of Intensive Care, Gelderse Vallei Hospital, Ede, The Netherlands

100%

100%

92%

90%

85%

80%

65%

70%

63%

60%

30% 20%

29%

30%

10% 0% <3 IPP

eC

l

ibi

nt

eA or

ce an pli

tro

0 H2

on

m 0c

os uc Gl

m

so Va

Co

s Hr

s C oid i aP er St se Do s w Hr Lo <6 % 70 2> vO Sc AP s M Hr rs <6 so 8 es P> pr CV

s& id

ic

iot t ib

ef eb ur

ult

nly

<6

ics

ot

Heart rate

3

Systolic blood pres- <70 sure Respiratory rate Temperature

Consciousness

2

1

0

70-80

81-100

101-200

<40

<9

<35.1

40-50

51-100

1

101-110

2

111-130 >200

3

>130

9-14

15-20

21-30

>30

A

V

P

U

35.1-36.5 36.6-37.5 >37.5

A=alert, V=verbal response, P=response to pain, U=unresponsive. Add 3 points if oxygen saturation< 90% despite supplemental oxygen. Add 1 point if you are concerned about the patient. Add 1 point if urinary output is less than 75 ml in the last 4 hours.

Table 2. Results of MET activation in 570 patients Transfer to ICU

294 (52%)

Treatment continues on ward with change of resuscitation code

50 (9%)

Transfer to coronary care unit

Treatment continues on ward with treatment advice from MET

Miscellaneous interventions (CPR, transfer to OR, transfer to other hospital) No treatment changes or transfer after MET call

19 (3%)

150 (26%) 18 (3%)

40 (7%)

The 294 patients admitted to the ICU had a mean age of 65.1 years (SD 18.3), mean APACHE II score at admission was 18.0 (SD 7.6), APACHE II expected mortality was 32.5%, 153 were mechanically ventilated, 39 received renal replacement therapy. Conclusion. The patients identified in the wards by the MET procedure are indeed at risk. Transfer to the ICU is necessary for more than half of the patients, advice on treatment while the patient stays in the ward is necessary for most of the remaining patients.



Flu

dC

te ta lac

nly

tO

nO

en

Introduction. It is widely recognized that hospitalized patients are at risk for unexpected and unrecognized deterioration of vital functions resulting in increased and unnecessary morbidity and mortality. When locally available, medical emergency teams (MET) are activated by hospital staff triggered by changes in vital parameters. In our hospital a MET was implemented in 2004. We studied our data to see if patients for whom the MET was activated were indeed at risk. Patients and methods. The Reinier de Graaf Groep is a 500-bed teaching hospital with a 10 bed mixed intensivist-led ICU. A MET was implemented starting in 2004. In the MET procedure, hospital staff, nurses and doctors, are instructed to score any patient on the ward with suspected deterioration using the scoring card (Table 1). If a patient has 3 points or more, the patient’s doctor has to see him within 30 minutes and come up with a treatment plan. The MET, consisting of intensivist and ICU nurse, is activated if the patient’s own doctor judges this to be necessary or when initial treatment does not reduce the score within 30 minutes. The MET will then visit the patient at the bedside and either give treatment advice or transfer the patient, for instance to the ICU. Each MET activation is recorded in a database for evaluation purposes. We studied all MET calls between 2005 and 2007. Results. Between 2005 and 2007, the MET was activated 570 times. The mean age of the patients was 66 years (SD 18), 314 (55%) were male. The mean MET score was 5.8 (SD 2.2). Patients were mostly seen in surgical wards (205, 36%), medical wards (196, 35%) or emergency department (156, 27%). Results of the MET activation are presented in Table 2.

An

m ru

m

Points

IA Meynaar, H van Dijk, M van Spreuwel , L Dawson, S Sleeswijk Visser, PL Tangkau Reinier de Graaf Groep, Delft, The Netherlands

o Blo

Se

e ag an M

s dle

tio ita cc

su

Individual bundle element compliance varied from 45-100%. Mean total bundle compliance was 68±19%. Mean resuscitation bundle compliance was 66±20% and mean management bundle compliance was 71±22%. A complete resuscitation bundle was scored only in 29% of patients and a complete management bundle in 30% of cases. In only 15% of patients all 10 bundle elements were met. Compliance with bundle elements improved over time (data not shown). Conclusion. Severe sepsis and septic shock mortality are significant. Large variations in bundle elements compliance are noted. Only three bundle elements reached the target compliance of 80%. Resuscitation elements such as the CVP and ScVO2 targets are more difficult to achieve within 6 hours. With respect to the management bundle tight glucose control is achieved in only half of the patients. Considering an average bundle element compliance is achieved in only 68%, and performance improved over time a target of 80% for the average of all individual bundle elements seems rational. In contrast, an aggregated resuscitation bundle or management bundle compliance or both bundle compliance of at least 80% will probably unrealistic.

Table 1. MET scoring card

Do Medical Emergency Team activation criteria indeed identify patients at risk?

49%

45%

15%

un hB

40%

Re

27

45%

50%

t Bo

Introduction. Severe sepsis may lead to global tissue hypoxia, organ failure and shock, and ultimately death. International Surviving Sepsis Campaign guidelines (SSC) have been developed and transformed into a 6 hour resuscitation bundle and a 24 hour management bundle to apply in patients with severe sepsis and septic shock. Implementation of these guidelines may improve sepsis mortality. A national safety programme for optimal therapy in severe sepsis will aim for individual bundle element compliance of at least 80% at the end of 2010. We hypothesize that a mean compliance of all elements of 80% would be an achievable target. A large single center sample is presented. Methods. We analyzed 332 patients enrolled and admitted to our ICU between January 2006 and August 2008 with severe sepsis or septic shock, who were intended to be treated according to the SSC guidelines. The compliance with various interventions in the 6 hour resuscitation bundle (arterial lactate, cultures taken, antibiotic started, MAP>65 mmHg, CVP>8 mmHg, ScvO2 > 70%) were measured. Also the 24 hour management bundle (steroids, glucose 4,4 - 8,3 mmol/L and inspiratory plateau pressure < 30 cm H20 and aPC) was analysed. SSC-points were given for every SSC-goal reached after 6 and 24 hours. aPC is not available, therefore compliance of 100% is stated. Results. Main sepsis categories were pneumosepsis (37.2%), abdominal sepsis (39.9%), and urosepsis (6.6%). Total in-hospital mortality for severe sepsis and septic shock was 36.7%. Severe sepsis mortality was 28.1% and septic shock mortality 41.7%. Bundle compliance of both the resuscitation and management bundle are depicted in figure 1.

72%

61%

327

10-12-2008 15:26:18 16:37:40 05-12-2008


28

The selective α7nAChR agonist GTS-21 exerts anti-inflammatory effects during experimental human endotoxemia JC Pompe, M Kox, MC Gordinou de Gouberville, CWE Hoedemaekers, AB van Vugt, JG van der Hoeven, P Pickkers Radboud University Nijmegen Medical Centre, The Netherlands Introduction. Efferent vagus nerve activity exerts anti-inflammatory effects in animal experiments. This ‘vagal anti-inflammatory pathway’ is mediated by the αlpha7 nicotinergic acetylcholine receptor (α7nAChR). Vagus nerve stimulation and α7nAChR agonists ameliorate inflammation and improve outcome in in vitro experiments and animal models of endotoxemia, sepsis and experimental arthritis. GTS-21 is a selective α7nAChR agonist. Up to now, the anti-inflammatory effects of oral administration of GTS-21 in humans in vivo have not been investigated. Aim of this study was to investigate the anti-inflammatory effects of oral administration of GTS-21 on the inflammatory response in the human endotoxemia model. Methods. We performed a double-blind placebo-controlled randomized cross-over intervention study in 10 healthy human volunteers during experimental endotoxemia. Subjects were randomly assigned to one of two groups: GTS-21 followed by Placebo or Placebo followed by GTS-21. Subjects received 150mg GTS-21 or placebo orally tid 3 days before LPS injection and on the day of the experiment, the last dose 1 hour before LPS administration (t=0). One hour after the last dose of GTS-21 or placebo, E coli LPS was injected (2 ng/kg iv in 1 minute). A washout period of at least 10 days (10-18 days) was instituted after which the second experiment was performed. Main study parameters/endpoints. To determine the effect of GTS21 on inflammation we compared the concentrations of circulating pro- and anti-inflammatory cytokines after the administration of LPS in the absence and presence of GTS-21 Results. The anti-inflammatory effect of GTS-21 is shown below. GTS-21 significantly reduced the concentration of the pro-inflammatory cytokines TNF-α, IL-6 and MCP-1 compared to placebo (p<0,05, two-way ANOVA repeated measures). The anti-inflammatory cytokine IL-10 was mildly elevated after GTS-21 treatment. Conclusion. Stimulation of the vagal anti-inflammatory pathway by GTS-21 has anti-inflammatory effects during experimental endotoxemia in healthy human volunteers reflected by a decrease in pro-inflammatory cytokine production and an increase in anti-inflammatory cytokine production. Pharmacological modulation of the ‘vagal anti-inflammatory pathway’ represents a novel mechanism to influence the innate immune response.

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10-12-2008 16:37:41


case reports

Case Report

An unusual cause of out-of-hospital cardiac arrest LJ Montenij 1, EJF van Reij1, JPW Vogelaar1, M Frank1, DJ Touw2 Departments of Intensive Care 1 and Pharmacy2, HAGA Hospital, The Hague, The Netherlands Introduction. Outcome after out-of-hospital cardiac arrest is generally poor. Research has identified somatosensory evoked potential (SEP) studies as one of the most reliable methods to predict poor outcome in comatose survivors. Yet, decisions to withdraw treatment should be made cautiously, and all factors influencing SEP studies and neurological examination should be identified. Case report. A 51-year-old general practitioner, was brought to the Emergency Department after an out-of-hospital cardiac arrest. He had a history of depression and dilated cardiomyopathy with insertion of a biventricular pacemaker and an Implantable Cardioverter Defibrillator (ICD). In the ER, the patient was hypotensive but stable, with good peripheral circulation. In contrast, neurologic examination showed a Glasgow Coma Score of 3, absence of brain stem reflexes, and no spontaneous breathing. This discrepancy in the cardiac and neurologic condition, triggered us to do further investigations. A CT-cerebrum showed no abnormalities. Serum toxicology screening showed a pentobarbital level of 37 mg/l. The patient remained clinically brain dead for 3 days, but gradually woke up from day 5. He recovered completely. Discussion. Pentobarbital is a short-acting barbiturate with strong brain-protective effects. It is used in the treatment of status epilepticus, refractory intracranial hypertension, and during surgery of the ascending aorta under cardiac arrest. Pentobarbital is also the primary drug in euthanasia (1). A serum level of 37 mg/l matches the ingestion of ca. 9 grams of pentobarbital, which is exactly the amount present in oral euthanasia kits. Our patient participated in a team of general practitioners who performed euthanasia, and he ordered a kit one week earlier. Therefore, we suspect an attempted suicide or “auto-euthanasia”. The extremely high serum levels of pentobarbital in the first 3 days (figure 1) explain why our patient was still clinically brain dead on day 3, and would probably 2

influence SEP studies, since pentobarbital effects SEPs in a dose-related manner (2). Therefore, without the results of the serum toxicology screening, treatment would possibly have been withdrawn on day 3. We are the first to report a case of “auto-euthanasia”, in which the patient survived. The brain-protective effects of pentobarbital, combined with the presence of a pacemaker and ICD, have undoubtedly contributed to the full recovery of our patient. 40 35

pentobarbital level (mg/l)

1

30 25 20 15 10 5 0

0

24

48

72

96

120

144

time (hours)

Figure 1. Serum pentobarbital levels during the first six days in the ICU

Conclusion. After out-of-hospital cardiac arrest, other causes than a primary cardiac problem should be carefully evaluated. References 1 Admiraal, P. Ned Tijdschr Geneesk (1995) 2 Sloan, T.B. J Clin Neurophysiol (1998)

Case Report

Fatal cerebral aspergillosis after orthotopic liver transplantation C Engel1, MGG Rodgers1, JWC Alffenaar2, H Delwig1, M van Meurs1, LM Dijkema1, MWN Nijsten1 1Department of Intensive Care, 2Hospital Pharmacy, University Medical Center Groningen, The Netherlands Introduction. Invasive aspergillosis is a well-known and feared complication after orthotopic liver transplantation especially in high-risk patients. Aim of this report is to present a case of invasive cerebral aspergillosis in a high-risk patient despite prophylaxis. Case report. A 58-year-old male was admitted to the ICU after orthotopic liver transplantation. He had recently been accepted for high-urgency transplantation in conjunction with auto-immune hepatitis followed by progressive icterus, ascites and hepatic precoma. Pre-operatively he was treated with high dose corticosteroids for the hepatitis. He received a liver from a heart-beating donor. The procedure was complicated by 9 litres blood loss. Post-operatively the patient received continuous amphotericin B (0,3 mg/kg/24hrs) as antifungal prophylaxis according to our institutional protocol. A few days after admission repeated sputum cultures were positive for Aspergillus fumigatus. Treatment was started with voriconazole orally in a dose of 400 mg twice daily. Intravenous administration of voriconazole was contraindicated as sulfobutylether β-cyclodextrine, an excipient of the intravenous solution, accumulates in case of renal failure. Immunosuppression was reduced to optimize

antifungal treatment. Serum levels showed adequate absorption of voriconazole. Because the patient remained in a comatose state despite good liver function and after stopping the sedation, a CT scan of the brain and lungs was performed. This showed pulmonary aspergillosis and indications for cerebral aspergillosis which was confirmed on MRI (Fig. 1). Despite voriconazole treatment with therapeutic levels for 12 days, the patient did not improve. It was decided to switch treatment to combination therapy consisting of liposomal amphotericin B and caspofungin for 18 days. A repeated MRI after this period showed progressive lesions and signs of a probable focus of the aspergillus from the sphenoid sinus (Fig. 2), which on retrospect was visible on the first CT scan more than three weeks earlier. Considering the latest scan and the clinical picture of the patient who remained comatose, it was decided to withdraw ventilatory support. Conclusion. This case illustrates the fatal consequences of invasive cerebral aspergillosis despite prophylaxis and early, long and aggressive treatment. The nidus of infection was most likely the sphenoid sinus, which probably should have been evacuated after the first CT scan. Clearly, this patient with acute liver failure and pre-operative corticosteroid use still developed invasive aspergillosis despite prophylaxis with “low-dose” continuous amphotericin B. In critically ill patients with organ failure, standard prophylaxis seems not always effective and antifungal prophylaxis in a therapeutic dose can be advocated. This policy has now been adopted in our protocol. References 1 ISDA Guidelines for Aspergillosis, Clinical Infectious Diseases 2008; 46: 327-60 2 Bruggemann RJ, Donnelly JP, Aarnoutse RE et al. Therapeutic Drug Monitoring of Voriconazole. Ther Drug Monit 2008.



329

05-12-2008 10-12-2008 15:26:18 16:37:41


Figure 1

3

Figure 2

Case Report

Epstein-Barr virus pneumonia: treatment with rituximab complicated by invasive aspergillosis WJ van den Wildenberg1, IHM van Loo2, M Christiaans3, S van der Geest1, DCJJ Bergmans1 Departments of intensive care1, microbiology2 and nephrology3 Maastricht University Medical Center+, The Netherlands. Introduction. A renal transplant patient is presented with respiratory insufficiency related to primary Epstein-Barr virus (EBV) infection, who developed pulmonary invasive aspergillosis during treatment with rituximab. Case report. Seven weeks after a dual kidney transplantation (donor 4-year-old child), a 60-year-old man was admitted with rapidly progressive respiratory failure, requiring mechanical ventilation. He had a fever of 40 ºC and pulmonary infiltrates. Immunosuppressive treatment: tacrolimus and low-dose (1mg) Sirolimus. Empirically ciprofloxacine and amoxicillin/clavunalate were started, co-trimoxazole and prednisone were added one day later for suspected pneumocystis pneumonia. Immunosuppressive treatment was discontinued. Cultures from blood, sputum, bronchoalveolar lavage (BAL) fluid were negative, as were tests for legionella and pneumococcal urinary antigen and an aspergillus galactomannan antigen test. Qualitative PCR on BAL fluids were negative for common respiratory viruses and pneumocystis jirovecii, but proved positive for EBV. Serum EBV viral load showed rapid increase from 139,743 to 772,930 copies/mL in eight days time. Since the patient was EBV IgM and IgG negative, whereas the renal transplant donor was EBV IgG positive, the diagnosis of respiratory insufficiency caused by pneumonia due to primary EBV infection was made.

330


Despite this therapy the patient’s condition deteriorated. Although no evidence of post-transplantation lymphoproliferative disease (PTLD) was present, rituximab (single dose of 375mg/m2 body surface area) was started as last resort therapy. Despite a fast drop in EBV viral load the patient’s respiratory condition did not improve. At this point there was evidence for probable invasive pulmonary aspergillosis (positive sputum culture and aspergillus galactomannan antigen test, positive halo and crescent signs on high-resolution CT of thorax). Amphotericin B was started, but didn’t lead to clinical improvement. The patient developed fulminant septic shock, from which he died twenty-five days after admission. Autopsy results showed bilateral pneumonia with abscesses, caused by Aspergillus. Qualitative PCR on tissue samples of lungs, pleural fluid, abdominal fluid, and spleen were positive for EBV with highest viral loads in the lungs. Discussion. EBV pneumonia is a rare entity. In our patient, the diagnosis was made by the combination of clinical features of pneumonia and the exclusion of other infectious causes of pneumonia. The optimal treatment for EBV pneumonia is unclear. Acyclovir has been used in acute infections with varying results. In this case, rituximab was chosen because of the high EBV viral load, and the possibilty of PTLD. Rituximab effectively decreased viral load in the blood, but gave no improvement in the clinical condition. Invasive aspergillosis is normally not seen in our renal transplant recipients, unless immunosuppression is intensified (e.g. after rejection). In this case this might be due to the rituximab therapy. Conclusion. Although a steep drop in EBV viral load was established after rituximab therapy, patient’s condition deteriorated and was complicated by invasive pulmonary aspergillosis infection, possibly associated with rituximab therapy.


10-12-2008 16:37:42


4

Case Report

Interhospital transport resulting in resuscitation limitations of capnography in severe lung disease CPM Donkers, RM Schnabel, DCJJ Bergmans, NM van Dijk, U Strauch Department of Intensive Care, Maastricht University Medical Centre+, The Netherlands Introduction. Capnography is a reliable tool in monitoring ventilated patients during interhospital transport, giving continuous information about airway patency, breathing and circulation. The limitations of capnography in patients with abnormal lung physiology is illustrated here. Case. A 40-year-old man presented to the emergency department with progressive respiratory insufficiency interpreted as infectious exacerbation of COPD. He had a history of pneumonectomy due to aspergillosis under chemotherapy for myelodysplastic syndrome. Allogenic stem cell transplantation was complicated by Graft-versus-host disease resulting in severe fibrosis of the remaining lung. He required nocturnal non-invasive ventilation and continuous oxygen therapy and was awaiting lung transplant since 4 years. After intubation and ventilation he was transferred to our university hospital. The patient (1,70m/56 kg) was ventilated with the Pneupac®ParaPAC respirator (Smith medical, UK) volume controlled, respiratory frequency 20/min, tidal volume 300 ml and PEEP 5 cmH2O. The upper pressure limit was set at 80 cmH2O. The SaO2 couldn’t reliably be measured due to peripheral vasoconstriction. During transport etCO2 was approximately 6 kPa. On arrival the patient was connected to the Evita-4® respirator (Dräger, Germany) pressure controlled, frequency 30/min with increasing inspiratory pressure. Even after muscle relaxation it was impossible to achieve sufficient tidal volumes resulting in bradycardia and circulatory arrest. The patient was disconnected from the respirator for manual ventilation, and CPR and epinephrine were applied successfully.The first ABG revealed serious hypercapnia (16 kPa) and respiratory acidosis (pH 7,07). After stabilization we tried to establish a mode of ventilation to achieve sufficient minute volume. The flow-curve showed a steep inspiratory rise and expiratory decline with peakflow above 100 L/min. At breathing frequencies of 20-30/min the next inspiration cycle started before the patient exhaled completely. Flow registration did not reach baseline. The CO2-curve was cut off before reaching a plateau corresponding to end-tidal state (figure 1). There was a large gap between 5

expiratory CO2-registration and measurement. The combination of unnoticed respiratory acidosis and quickly developing exuberant intrinsic PEEP probably caused circulatory arrest. Discussion. End-tidal CO2 generated by the capnograph does not necessarily reflect the true value. If the expiratory curve does not reach a stable plateau no endexpiratory value can be generated. In this case the restrictive pulmonary component resulted in a very steep increase of the end-expiratory CO2-curve, that suddenly evolves into a further slowly inclining curve due to the obstructive pulmonary component, without ever reaching a stable plateau before the following inspiration (figure 1). This resulted in a large difference between capnograph value and arterial CO2 measurement.

Figure 1

Case Report

Hyperthermia due to impaired thermoregulation in a critically ill obese patient M Verstegen1, B Langenhorst2, R Strack van Schijndel3, AC Toornvliet1, MLH Honing1 Departments of Intensive Care1 and Surgery2, Medical Center Alkmaar, The Netherlands Department of Intensive Care3, VU Medical Center, Amsterdam, The Netherlands Body fat, with its low thermal conduction, is an important insulator in protecting the body from cooling in cold environments. However, subcutaneous fat can also interfere with thermoregulation through diminished heat dissipation1,2. We present an obese patient who developed hyperthermia after a high energetic trauma. A 30-year-old man with a BMI of 39.3 kg/m2 was admitted to our ICU after a high energetic trauma. His medical history was uneventful and the family history did not mention malignant hyperthermia. Before admission to our hospital he gave way to a car and crashed with his truck against a tree. Thereafter, he was trapped inside his truck for almost 2 hours. His left lower leg was crushed with severe deglovement injury of his upper leg. He was operated on directly, his left lower leg was amputated and debridement of his upper leg was performed. Patient was given tetanus profylaxis and treatment with amoxicillin and clavulanate potassium was started. He remained intubated and mechanically ventilated. The next day the patient developed a temperature of 40 oC. Because wound infection was suspected a total of 3 re-explorations of the upper left leg were performed the following days. Every time necrotic tissue was removed and no abcesses were found. No succinylcholine or halotane was given during anesthesia. Total body CT scanning revealed no other sites of infection. All cultures remained negative and antibiotics were switched pragmatically to clindamycin, gentamicin and cefuroxim. Despite necrotectomy, antibiotics, and the application of

different cooling techniques the temperature gradually rose to 41,6 oC over the next 5 days. Severe rhabdomyolysis developed (maximal creatinin kinase of 111.008 U/L, figure 1) together with acute renal insufficiency, pulmonary edema, and elevated liver enzymes. A short trial of dantrolene had no effect. Only after high-volume CVVH was started with 2 machines for internal cooling together with infusion of cold saline, an air cooling device, and ice packs the temperature dropped. His clinical condition gradually improved and after 38 days the patient was dismissed from the ICU. In this case hyperthermia developed in the absence of evidence of a microbial infection. We presume that a systemic inflammatory response syndrome (SIRS) developed in response to the severe deglovement injury of the left leg. SIRS persisted and body temperature increased further. The presence of severe obesity interfered with thermoregulation and the rate of heat production exceeded the rate of heat dissipation. Only when aggressive internal cooling techniques were applied the temperature could be controlled. References 1 Keatinge WR. The effects of subcutaneous fat and of previous exposure to cold on the body temperature, peripheral blood flow and metabolic rate of men in cold water. J. Physiol 1960;153:166-178 2 Simon HB. Hyperthermia. New Engl J Med 1993;329:483-487

Legend Figure 1. The increase in creatinin kinase in relation to body temperature.



331

10-12-2008 15:26:19 16:37:43 05-12-2008


6

Case Report

Deadly vasospasm DPH Eijking1, CLA Reichert2, AM Wagenvoort3, MG Charbon4, AC Toornvliet1, MLH Honing1 Departments of Intensive Care1, Cardiology2, Radiology3, Neurology4, Medical Center Alkmaar, The Netherlands Prinzmetal’s variant angina (PVA) is characterized by spontaneous episodes of chest pain which are associated with ST-segment elevation caused by coronary vasospasm. Reports have been published on the association of PVA with other vasospastic disorders such as Raynaud’s phenomenon and migraine headaches, suggesting the presence of a generalized vasospastic disorder1. We present a case of PVA associated with lethal cerebral vasospasm. A 45-year-old man was admitted to the ICU after an out-of-hospital cardiac arrest caused by ventricular fibrillation. One year before admission he developed a myocardial infarction. Coronary angiography performed at that time showed normal coronary arteries without any sign of early coronary atherosclerosis. PVA was diagnosed and treatment with a calcium channel blocker was started. His medical history further revealed the use of valproic acid for epilepsy of unknown origin. Before collapsing the patient had experienced severe chest pain. After a short delay basic life support was started and after arrival of the ambulance circulation was restored by defibrillation. In the emergency department the ECG showed ST segment elevations in leads I, AvL, V2 to V5. Coronary angiography again showed 7

normal coronary arteries. The creatine kinase level increased to 928 U/L with a maximal MB fraction of 117 U/L. After admission to the ICU the patient was sedated and therapeutic hypothermia was induced for 24 hours. After passive rewarming, and after discontinuation of sedation, the patient remained comatose. Testing of electrical responses in the central nervous system to somatosensory stimulation (SSEP) was positive. Gradually, the neurologic condition improved to a Glascow coma scale of E4M5Vt. However, on day 7 his EMV-score suddenly deteriorated to E1M2Vt. CT scanning of the brain showed diffuse hypodense changes throughout the brain consistent with ‘a white cerebrum sign’. An additional perfusion CT of the brain was performed demonstrating irregular shaped cerebral arteries caused by diffuse cerebral vasospasm. The clinical condition of the patient deteriorated rapidly, diabetes insipidus developed and eventually all cerebral and brainstem functions disappeared. Brain death was diagnosed. Autopsy showed no coronary atherosclerosis. Unfortunately, no permission was given to perform autopsy of the brain. To our knowledge, the association of PVA with severe cerebral vasospasm has never been described. The combination of severe PVA resulting in ventricular fibrillation, and brain death due to severe cerebral vasospasm suggest that this patient had a generalized vasospastic disorder. To what extent the prior epileptic insults in this patient were the result of cerebral vasospasm remains speculative. Also, to what extent the presence of anoxic brain injury provoked the cerebral vasospasm is not known. References 1 Buchanan Keller K and Lemberg L. Prinzmetal’s Angina. Am J of Crit Care 2004;13:350354

Case Report

Marburg Hemorrhagic Fever in a returned traveler, a rare but deadly disease J van Paassen, MP Bauer, JT van Dissel, MS Arbous Department of Intensive Care, Leiden University Medical Center, The Netherlands Introduction. The filo-viruses, Marburg and Ebola, are amongst the most virulent pathogens of humans. The first epidemic of Marburg hemorrhagic fever (MHF) occurred in a vaccine factory in Marburg, Germany.1 As a result of contact with from Uganda imported, infected, green monkeys, thirty-two workers became infected and seven died. Further cases and outbreaks of MHF have only occurred in Africa.2 We describe an exceedingly rare case of a fatal Marburg hemorrhagic fever infection in a returned traveller. Case. A 41 year old woman presented to a Dutch hospital with a three days history of fever, rigours, myalgia and headache. Symptoms developed four days after returning from a three week journey through Uganda, where, amongst others, she visited a cave that was inhabited by bats. Physical examination was unremarkable. Blood examination showed leukopenia, thrombocytopenia and mildly elevated transaminases. Malaria was excluded. Shortly after admission nausea, vomiting and frequent watery diarrhoea developed. On the third day blood tests were suggestive of acute liver failure and patient was transferred to an intensive care unit of a liver-transplantation centre. Concomitant symptoms existed of dyspnoea with a non-productive cough, a vague central abdominal pain, gradually progressive hearing loss, bilateral conjunctivitis, palatal petechiae and a papular rash of the face and trunk. Under suspicion of viral

332


hemorrhagic fever isolation according to protocol was initiated. Abdominal ultrasonography didn’t show any abnormalities. Several causes of liver failure were ruled out by serologic testing and plasma polymerase chain reaction (PCR) assays. It was only after two days that a plasma real time PCR for Marburg virus was positive. In the meanwhile mechanical ventilation and hemodynamic support for profuse bleeding and capillary leakage were necessary. Continuous venovenous hemofiltration in combination with a Molecular Absorbent Recirculation System was initiated. Massive cell death occurred (creatine phosphokinase [CK]: over 23000 U/l), resulting in almost incorrectable hyperphosphataemia and hyperkalaemia. Furthermore, due to acute liver failure cerebral oedema developed and mannitol and hypertonic saline were added to the therapy. On day seven, after a short period of slight improvement, dilated, non-responsive pupils developed. A transcranial Doppler test showed no signs of cerebral blood flow, indicating cerebral herniation. In view of the unfavourable prognosis treatment was discontinued, leading to death. Conclusion. Marburg hemorrhagic fever is a rare, but potential fatal disease, without any efficacious antiviral therapy or vaccine. This case-report illustrates that Marburg hemorrhagic fever should be considered in returning travellers. Although later features such as rash, conjunctivitis and liver necrosis may point to the diagnosis, the initial clinical picture is non-specific. A history of visiting African caves inhabited by bats may provide an additional clue to the diagnosis. References 1. Marburg Agent Desease: in Man. G.A. Martini. Trans R Soc Trop Med Hyg 1969;63;2:295302 2. Treatment of Marburg and Ebola hemorrhagic fevers: A strategy for testing new drugs and vaccines under outbreak conditions. D.G. Bausch et al. Antiviral Research 2008;78:150-161


10-12-2008 16:37:44


8

Case Report

CMV pneumonia after complicated cardiothoracic surgery BD Westerhof1, M Jager2,C Meijers3, RJM Strack van Schijndel1 1Department of Intensive Care Medicine, VU University Medical Center, Amsterdam, The Netherlands 2Department of Medical Microbiology, VU University Medical Center, Amsterdam, The Netherlands 3Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands A case of cytomegalovirus pneumonia in a post cardiothoracic surgery patient is presented. A 69 year old female patient was admitted to the intensive care unit after urgent mitral valve repair. After initial recovery and extubation eleven days after admission, the patient had to be reintubated and ventilated because of pleural effusions. Thereafter it was impossible to achieve negative fluid balances. Pleural effusions and peripheral oedema persisted. Reasonable cardiac function on echocardiography and negative rethoracotomy didn’t explain the clinical course. We suspected a low grade sepsis, and broad spectrum antibiotics were started without any effect. Blood, pleural and sputum cultures remained negative. After 38 days the patient died. The diagnosis CMV pneumonia was made by post-mortum 9

References 1 Papazian L, Fraisse A, Garbe L et all. CMV. An unexpected cause of VAP. Anesthesiology 1996;84: 280-287 2 Rizos M, Falagas ME et all. Usual interstitial pneumonia associated cytomegalovirus infection after percutaneous transluminal coronary angioplasty. Eur J Clin Microbiol Infect Dis 2004;23:848-850 3 von Muller, Klemm et all. Active Cytomegalovirus infection in patients with septic shock. Emerging Infectious diseases 2006;1517-1522 4 Heininger A, Jahn et all. Human cytomegalovirus infections in nonimmunosuppressed critically ill patients Crit Care Med 2001; 29: 541-547 5 Jaber S, Chanques G, Borry J et all.Cytomegalovirus infection in critically ill patients: associated factors and consequences. Chest 2005;127:233-241 6 von Muller Lutz, Mertens T. Human cytomegalovirus infection and antiviral immunity in septic patients without canonical immunosuppression. Med Microbiol Immunol 2008;197:75-82 7 Gandhi MK, Khanna R. Human cytomegalovirus:clinical spects, immune regulation, and emerging treatments. Lancet Infect Dis 2004; 4:725-3

Case Report

An 83-year-old woman with Candida pneumonia due to a rare cause N Guion, W van Mook, C Linssen, JH Zwaveling, DCJJ Bergmans Department of Intensive Care, Maastricht University Medical Center+, The Netherlands Introduction. Pneumonia is frequently diagnosed in the ICU and mostly caused by well known bacteria or viruses. In a few instances, rare causal pathogens are discovered, as in the next case. Case report. An 83-year-old woman was brought to the emergency room with dyspnoea and coughing. Since one week she had diarrhoea and flu-like symptoms. Since months her intake was diminished due to difficulties with swallowing. She did not visit restaurants anymore because she was ashamed of frequent choking. Medical history revealed uterus extirpation and cholecystectomy. She smoked 6 to 8 cigarettes daily and used no regular medication. At time of presentation she used moxifloxacine and paracetamol as recently prescribed by her family physician under suspicion of pulmonary infection. Chest X-ray showed bilateral micronodular abnormalities and a possible infiltrate in the right upper lobe. Legionella and pneumococcal urine antigen testing was negative. The patient was admitted under the diagnosis of community acquired pneumonia and transferred to the ICU the next day because of progressive respiratory 10

examination, confirmed by immunohistochemical staining and PCR. The possibility of CMV reactivation in ICU patients is discussed. In ongoing capillary leak after cardiothoracic surgery, clinicians should be aware of CMV associated pneumonia if bacterial and cardiac causes are excluded.

insufficiency due to massive vomiting and aspiration of gastric contents. She was subsequently intubated and bronchoalveolar lavage (BAL) performed. Initial BAL fluid analysis revealed 360.000 cells per ml, >1% polymorphonuclear cells, no squamous epithelium, many leukocytes but no bacteria on Gram-staining. With this negative BAL and suspicion of interstitial pneumonitis on X-ray, prednisolon was started. Final analysis of the BAL fluid showed 6.2% intracellular yeasts, thereby revealing Candida pneumonia and no intracellular bacteria. Differentiation showed 97.4% polymorphonuclear cells, 2.2% lymphocytes and 0.2% macrophages. Treatment with fluconazol was initiated and prednisolon discontinued. Further analysis excluded any underlying immunodeficiencies. However, thoracic CTscanning revealed bullae, interstitial abnormalities with fibrosis and nodules as well as a cystic mediastinal abnormality, probably a Zenkers diverticulum. On gastroscopy a large Zenkers diverticulum filled with food remains was visualised. Culture of the aspirate also revealed Candida. After five days of supportive and causal therapy the patient was successfully extubated. The Candida pneumonia was treated with fluconazol for two weeks in total and the patient made a full clinical recovery. Thereafter an uncomplicated stapler diverticulostomy of the Zenkers diverticulum was performed, after which she could resume her normal diet without any problems. Conclusion. Yeasts are an uncommon cause of community acquired pneumonia in an ICU, especially in the absence of immunodeficiencies. In these cases other predispositions for the diagnosis have to be considered. In the case herein presented yeast pneumonia with Candida albicans proved to be due to recurrent aspiration of yeasts originating from the contents of a large Zenkers diverticulum.

Case Report

Acute intoxication after ingestion of ink remover R Mauritz, LPHJ Aarts Department of Intensive Care, Leiden University Medical Center, The Netherlands Case. A 48-year-old man was admitted to our Intensive Care Unit with a decreased level of consciousness after a fall down a flight of stairs at his son’s home. At presentation to the emergency department he was unresponsive with a Glascow Coma Score of 4. His pupils were small with intact reflexes. Further physical examination was unremarkable. He was intubated because of his decreased level of consciousness. A CT scan of his brain showed no abnormalities, in particular no signs of intracranial haemorrhage. Other traumatic injuries were excluded by additional radiologic examinations. The patient was known with alcohol abuse but apparently this day he had been sober as the serum ethanol level was below 0,1 g/L. Since the cause of the fall and of the coma was unclear a toxicological screening was requested. In the mean time the patient suddenly opened his eyes and appeared fully awake. He denied the use of any recreational drug. However, his son told us that he thought his farther had ingested gamma-butyrolactone (GBL) because he had

found an empty vial of ink remover containing this compound in his father’s home. This was confirmed by the detection of gamma-hydroxybutyrate (GHB) in the serum and urine of our patient. The son uses GBL as an ink cartridge cleaner in his printer cartridge recycling company. Discussion. GBL is a colourless oily liquid with a weak characteristic odour. It is a common solvent and reagent in chemistry and is used as an aroma compound and as an ink, paint and glue remover. Biochemically, GBL is a precursor of GHB. Once ingested, GBL is rapidly metabolised into GHB by lactamase enzymes in the blood. The pharmacological and toxic effects of GBL resemble those of GHB; the primary effect is central nervous system depression. GBL has approximately 85% oral bioavailability (higher than GHB) and a slightly different biodistribution. These factors are believed to account for its extended duration of action. The management of acute toxic effects of GBL is the same as that of GHB and is primarily supportive with emphasis on aspiration precautions. While GHB is an illegal drug, the sale and possession of GBL is unrestricted in many countries including the Netherlands and it can be easily purchased via the internet. Conclusion. This case illustrates that misuse of unsuspected products can result in coma due to GHB intoxication. History taking is an essential piece to solve the diagnostic puzzle.



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11

Case Report

As old as Methusalem, yet still the ongoing interaction issue of Erythromycin and Midazolam I Blum Department of Intensive Care, University Medical Center Utrecht, The Netherlands Introduction. It is well known that Erythromycine inhibits the hepatic Cytochrome P 450 3A(CCYP3A) related monooxygenase Among others the metabolism of Midazolam is slowed down and the blood concentration levels rise above therapeutic ranges. Case. A male patient aged 75 is hospitalised in our ICU with respiratory failure due to pneumonia. He required breathing assistance from the respirator and was sedated with Midazolam. Simultaneously he was treated with the antibiotics Erythromycine and Ceftazidim (community acquired pneumonia). The patient suffers from esophageal cancer which was unable to be removed by surgery, as well as from alcohol abuses. Results. 12

Case Report

Amphetamine fatality in a 31-year old male: a case report JN Brinkman, LJ Monteny, NGM Hunfeld, PHGJ Melief Haga Teaching Hospital, The Hague, The Netherlands Amphetamine abuse in the general population in the Netherlands is relatively limited and stable. Approximately 0.2% of the Dutch population used amphetamine in 2005.1 Fatal cases of amphetamine-associated cardiotoxicity (myocardial infarction or necrosis, acute cardiac failure or cardiac arrhythmia) are rarely reported in medical literature. A 31-year-old male was standing before his bedroom window, swinging an axe and 13

• Midazolam (dosage 15 mg/hr) is stopped after 19 hrs. • Remarkably the patient does not wake up and so the staff decided to wait and observe. • On the 3rd day after end of IV therapy the blood level of Metamizol is 0,44 mg/l and Hydroxymidazolamlevel is 0,12mg/l • Blood concentration on the 4th day 0.27 mg/l for Metamizol and<0,05mg for Hydroxymidazolam. Erythromycin treatment was stopped on the 4th day. • Normal range voor Midazolam is 0,08mg/l -0,25mg/l • 7 days after intubations the suspicion of relationship between Erythromycin and Midazolam is documented in the patient charts. • 8 days after intubations the patient awakes and was ex-tubated successfully. Conclusion. Pharmacology is an important aspect of the daily work of an intensive care physician. This case report shows how elementary factors are over looked. On one hand well known, on the other hand not appearing frequently enough or so remarkable that they are not forgotten. There is always a challenge for intensive care physicians – and this is not only in spectacular situations.

threatening to jump. During a struggle with the police in which pepperspray was used, the patient suddenly collapsed and lost consciousness. Police officers immediately started with basic life support. After twenty-one minutes of resuscitation there was a sinus tachycardia and output. The evening prior to his struggle with the police, the patient smoked 1.5 gram of speed. Toxicological analysis in serum demonstrated a concentration of 26mg/l of amphetamine (toxicological level >0.2mg/l) and 18 ųgr/l of methamphetamine (toxicological level >0.2mg/l). No traces of pepperspray were found. Initial electrocardiogram revealed diffuse ischemia. On our ICU, refractory cardiogenic shock developed eventually followed by death, approximately 30 hours after admission. References 1 National Drug Monitor, Trimbos Institute, The Netherlands. 111-130. 2008.

Case Report

Fulminant T-cell post-transplantation lymphoproliferative disorder after renal transplantation AMF Rutten, HW van Hamersvelt, BG Fikkers Radboud University Nijmegen Medical Centre, The Netherlands Introduction. A post-transplantation lymphoproliferative disorder (PTLD) is seen in 1-10% of all solid organ transplantations. Main risk factors include degree of overall immunosuppression and Epstein-Barr virus (EBV) primo infection or reactivation. The clinical presentation differs, but most patients present with either fever or lymphadenopathy. Rarely a fulminant PTLD develops after solid organ transplantation, presenting as a rapid progression of disease with multi-organ failure. Reported cases are EBV-associated and of B-cell lineage. We now present a fulminant EBV-negative PTLD of T-cell lineage. Case report. A 54-year old woman presented with a fever of unknown origin. Two years earlier she underwent renal transplantation due to a mesangiocapillary glomerulonephritis. The transplant kidney was removed 3 weeks earlier as a rejection was suspected. Histology however only revealed recurrence of mesangiocapillary glomerulonephritis. The hospitalization for the transplant kidney removal was prolonged due to pancytopenia and fever. Various cultures, PCR of EBV and cytomegalovirus, bone marrow aspiration, chest and abdominal CT did not reveal a other explanation therefore the pancytopenia was attributed to azathioprine and possibly drug fever. Temperature normalized over time. She was now readmitted with complaints of fever, chills and general discomfort. Physical examination

334


showed a moderately sick woman with a temperature of 38,7°C, a pulse rate of 119/ min without localizing features such as lymphadenopathy. Laboratory examination showed lactate dehydrogenase: 1379 U/l, C-reactive protein 11 mg/l and persistent pancytopenia. Various cultures, PCR of EBV and cytomegalovirus were still negative, and a new bone marrow aspiration was performed. Chest x-ray revealed no infiltrates. Antibiotic therapy was not effective and therefore discontinued. Six days later she was increasingly drowsy and was admitted to our ICU with a temperature of 40,1°C, pulse rate of 123/min, breathing 30 times/min with a saturation of 96% with 5 liter of oxygen through a nasal tube. Abdominal palpation induced pain at the right lower quadrant. Lactate was 4,5 mmol/l and lactate dehydrogenase had increased to 6005 U/l. Her blood pressure dropped for which fluid resuscitation was initiated. Abdominal ultrasound revealed no further information. Bowel ischemia was suspected but considered unlikely by the consulted surgeon. Broad spectrum antibiotics and hydrocortisone were initiated under the suspicion of sepsis. Our patient continued to deteriorate and 18 hours after admission to the ICU the lactate dehydrogenase had increased to 14106 U/l and lactate levels to 11,2 mmol/l. An abdominal CT showed no additive clues. Chest x-ray revealed bilateral pulmonary infiltrates suggesting acute respiratory distress syndrome (ARDS). Patient was intubated and norepinephrine was administered. Despite maximal support, adequate oxygenation and circulation could not be maintained. Therefore, active treatment was withdrawn and our patient died. Autopsy and bone marrow aspiration revealed massive PTLD of T-cell origin with localization predominantly in the bone marrow but also diffuse localization in spleen and liver. CD-20 and EBV-encoded RNA were negative. The lungs showed possible ARDS. Conclusion. PTLD should be considered in post-transplantation patients presenting with multiple organ failure.


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14

Case Report

Muscle rigidity and respiratory compromise in a term neonate during morphine infusion; serious adverse event determined by using the naranjo algorithm R van der Lee1, I Ceelie1, IT de Leeuw2, SN de Wildt1 1Pediatric Intensive Care, 2 Pediatric Anesthesia, Erasmus MC Sophia Children’s Hospital, Rotterdam, The Netherlands Introduction. Sudden onset of muscle rigidity with subsequent respiratory compromise is described in the literature as a rare serious adverse event after infusion of fentanyl in predominantly young infants1. Recently, a term infant experienced generalized muscle rigidity resulting in acute respiratory failure at two occasions after morphine administration. Hypothesis. Life-threatening generalized muscle rigidity can result from morphine use in newborn infants. Methods. To determine the probability of life-threatening muscle rigidity as an adverse event to morphine in our patient, we used the The Adverse Drug Reaction Probability Scale by Naranjo et al2. We searched the literature for previous reports of opioid related muscle rigidity in Pubmed and Embase. Results. The Naranjo algorithm used for the second occasion is presented below: A score of 10 or higher suggests that the muscle rigidity is a highly probable adverse event of morphine. The infant reacted favourably after administration of naloxone which confirmed the diagnosis. 15

Table: Naranjo Algorithm Questions

1)

2)

Are there previous conclusive reports on this reaction?

3)

Did the ADR appear after the suspected drug was administered? Did the ADR improve when the drug was discontinued?

5)

Are there alternative causes for the ADR?

4) 6) 7)

8) 9) 10)

Did the ADR appear with re-challenge?

Did the reaction appear when placebo was given? Was the drug detected in blood at toxic levels?

Yes No Don’t know +1

0

0

+1

0

0

-1

+2 0

+2

+2 -1

+1

Was the reaction more severe when the dose was +1 increased, or less severe when the dose was decreased? Did the patient have a similar reaction to the same or simi- +1 lar drug in any previous exposure? Was the ADR confirmed by any objective evidence? +1

-1

-1

0

0

+1 0 0

0

0

0

0

0

0

0

Conclusion. To our knowledge this is the first case in human newborns of lifethreatening muscle rigidity after morphine administration. References 1 J Clin Anesth. 2002 Nov;14(7):494-9, 2 Clin Pharmacol Ther. 1981 ;30:239-245

Case Report

Aberrant course of a pulmonary artery catheter M Koeman, WK Lagrand, LPHJ Aarts Department of Intensive Care, University Medical Center Leiden, The Netherlands Case report. A 43-year-old woman was admitted with dyspnoe, coughing and peripheral edema, rapidly progressing into respiratory insufficiency necessitating mechanical ventilation. Bilateral pulmonary embolism and chronic thromboembolic pulmonary hypertension were diagnosed by CT-scanning. Patient was referred to our ICU because of difficult weaning from mechanical ventilation despite adequate anticoagulant therapy. Repeated chest X-rays revealed pulmonary congestion, insufficiently responding to pharmacological treatment. Echocardiographic evaluation showed, besides mild tricuspid valve regurgitation with mildly elevated pulmonary artery pressures, no abnormalities. To judge volume status and to measure cardiac performance, it was decided to perform pulmonary artery catheterization (PAC). To this, we insert a PAC via the right internal jugular vein. Guided by intraluminal pressures, the PAC was advanced to the right atrium, right ventricle and pulmonary artery, respectively. Advancing the PAC in the right position was difficult and took several attempts in order to obtain a right ventricular and, finally, adequate pulmonary artery pressure curves. Apart from mild pulmonary hypertension, the obtained data were within normal limits (Pulmonary artery pressure 35/15 mmHg, pulmonary artery wedge pressure 12 mmHg, cardiac index 3.0 L.min-1.m-2). Intracardiac shunts were excluded by repeated echocardiography and estimation of oxygen saturations of vena cava, right ventricle and pulmonary artery. After the procedure a chest X-ray was performed which showed an aberrant course of the PAC, suggestive for persistent left superior vena cava (PLSVC). In retrospect, a wide coronary sinus was seen by echocardiography, endorsing the presumed diagnosis of PLSVC. Additional CT-scanning with intra venous contrast confirmed PLSVC with absence of a right superior vena cava (RSVC). The PLSVC drains into the right atrium via a wide coronary sinus. No other cardiac anomalies were found. Etiology and pathofysiology. PLSVC is the most common venous anomaly in humans, occurring in 0.5% of the normal population and in 0.47% of patients undergoing pacemaker or implantable cardioverter defibrillator implantation (1). A frequency of 5 to 10% has been reported among patients with congenital heart defects. The

right superior vena cava is absent in only 1% of patients with PLSVC, as is the case in our patient. In a small percentage of cases the left superior vena cava drains into the left atrium, which is usually associated with an atrial septal defect. Otherwise, when draining into the right atrium a wide coronary sinus is present, like in our patient. Associated cardiac anomalies are diverse, including atrial septal defect, ventricular septal defect, tetralogy of Fallot, situs inversus and coarctatio aorta. Extra-cardiac anomalies included VACTERL*-association and CHARGE^-association. Conclusion. PLSVC. Once among ICU patients pulmonary artery catheterisation, pacemaker and defibrillator implantation is performed frequently, the clinician should consider and recognize this venous system anomaly, its possible additional anomalies and its clinical consequences in critical care patients. *VACTERL = vertebral defects, anal atresia, cardiac malformations, tracheo-esophageal fistula with esophageal atresia, radial and renal dysplasia and limb abnormalities.; ^CHARGE = coloboma, heart defects, atresia of choanae, retardation, genital and ear abnormalities.



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16

Case Report

Cave Canem Hemolytic Uremic Syndrome after a dog bite due to Capnocytophaga Canimorsus NA Dijkman, EJ Lust, YJ Debets, ARJ Girbes Department of Intensive Care Medicine, VU University Medical Centre, Amsterdam, The Netherlands Department of Medical Microbiology, VU University Medical Centre, Amsterdam, The Netherlands Capnocytophaga Canimorsus (“eater of carbondioxide, transmitted by dog bite”), formerly described as Dysgonic Fermenter (DF-2), is commonly found in the canine oropharyngeal flora, and can be transmitted to humans by an animals bite, scratch or lick. Immunodeficiency, splenectomy and alcoholic liver disease are risk factors for infection. Clinical features of the infection ranges from wound infection, blepharitis, cellulitis, peritonitis, meningitis, endocarditis to full blown sepsis. We present a 40 year old male patient with known alcohol- and drug abuse suffering a C.canimorsus infection due to a dog bite, who developed haemolytic uremic syndrome (HUS). The haemolytic uremic syndrome (HUS) is known to have several causes including drugs, pregnancy, malignant diseases and infectious diseases. The patient presented with purpura fulminans, acute anuric renal failure and extremely painful extremities with gangrene. He was initially surprisingly hemodynamically and respiratory stable. On admission, laboratorial tests showed a hematocrit of 0.27, haemoglobine 5.6 mmol/l, white blood count 15.4 10*9/l and a plateletcount of 15 10*9/l. Bloodsmear showed fragmentocytes, and increased 17

Case Report

Aortic Dissection in Pregnancy HW Willemsen, A Schoe, MS Arbous, LPHJ Aarts Department of Intensive Care, Leiden University Medical Centre, The Netherlands Introduction. Aortic dissection during pregnancy is a life threatening condition for both mother and child. On the ICU of the LUMC we recently treated a young woman with this severe condition. Case presentation. A 34 year old woman, with a history of 3 miscarriages, was treated for hypertension during her 4th pregnancy and was admitted for labour induction during the 38th week of pregnancy. During intravenous stimulation with oxytocin she developed dizziness, chest pain and pain from the shoulders to her lower back. Because of ongoing maternal discomfort a caesarean section under spinal anaesthesia was performed. A healthy child was born. Medical examination, EKG and chest X-ray did not deliver a diagnosis at that time and the patient was discharged home after her complaints had subsided. A few days later she became again dyspnoeic and was readmitted with a working diagnosis of pulmonary embolism. CT scan showed a type A aortic dissection from the aortic root to the iliac arteries with the left renal artery originating form the false lumen. The patient was transferred to a tertiary referral centre. Immediate surgical repair was performed with aortic valve plasty, replacement of the supracoronary ascending aorta and repair of the arch using bioglue. Opening of the pericardium showed 500 cc of 18

lactate dehydrogenase (LDH) 2250 IU/l, increased bilirubin 35µmol/l and lowered haptoglobin 0.08 g/l suggested microangiopathic hemolysis. Serum creatinine was 507 µmol/l, urea 26 mmol/l. The prothrombin time and activated partial thromboplastin time was respectively 1,55 INR and 41 seconds; fibrinogen 4,3 g/l. Bloodcultures revealed - later - growth of a slow growing, fusiform gram negative rod: C.canimorsus. Shortly after admission in the ICU he was diagnosed as haemolytic uremic syndrome (HUS) because of the clinical manifestation of microangiopathic hemolysis, thrombopenia, renal failure and relatively normal clotting times. On second examination, sign of a dog bite were found. Although in septic patients the distinction between HUS and diffuse intravascular coagulation (DIC) may be difficult, it can be made mainly by laboratorial testing, related to difference in pathogenesis. DIC results from activation of the coagulation system, triggering intravascular coagulation and systemic bleeding diathesis; HUS results from primary platelet activation without activation of the coagulation cascade. Because of different therapeutic consequences, it is important to distinguish both entities. The gold standard in treating HUS is plasmapheresis. Our patient was treated in the intensive care and developed later respiratory failure, requiring mechanical ventilation. He remained hemodynamically relatively stable. Antibiotic treatment with clindamycin and ceftriaxone was promptly started. Because of the diagnosed HUS plasmapheresis were started early. After ten sessions of plasmapheresis all laboratory features of HUS returned to normal and renal function recovered almost completely. In the literature, only few cases of renal failure following C.canimorsus septicaemia have been published. This was however, mostly following hypotension or diffuse intravascular coagulation, which was not the case in our patient. HUS should be considered as a cause of thrombopenia, microangiopathic hemolysis and acute renal failure and the possibility of a dog bite, resulting in C.canimorsus bacteraemia should be strongly considered.

sanguinolent fluid in a thickened pericardium, indicating that the initial dissection may have occurred days before. Because there was adequate perfusion to all organs no immediate surgical intervention was performed on the distal aorta. Recovery was uneventful and the patient was discharged after 14 days. Twenty days after sternotomy the patient experienced decreased motor function of the legs due to thrombosis of the distal false lumen which obliterated the flow in the true lumen of the dissection. Emergency laparotomy was performed and an infrarenal aortic bifemoral prosthesis was placed with fenestration of the false lumen. Without neurologic deficit the patient was discharged after 20 days. Discussion. Most aortic dissections in pregnancy occur in the third trimester.. Changes in the aorta during pregnancy and inherited defects in the arterial wall can be aetiological factors in aortic dissection. In 50% of cases no systemic disease can be identified. Possibly oxytocin infusion led to additional hemodynamic stress resulting in aortic dissection. No randomized trials have been reported to guide management in type A or B aortic dissections. Type A dissections are considered an indication for acute surgical intervention, because of the risk of myocardial infarction, acute aortic insufficiency and pericardial tamponade. Furthermore, in the management of type A dissections the extent of the distal resection to be done is controversial. In this case the distal aorta was initially not repaired and the patient experienced a serious complication without permanent sequalae. Conclusion. Aortic dissection in pregnancy requires a multidisciplinary approach with medical treatment of the mother, delivery of the child by caesarean section and surgical treatment of the dissection a soon as possible.

Case Report

Fulminant EBV-reactivation in an immunocompromised septic patient ThA Ruys1, S van Thiel1, EHR van Essen1, AJM Schuerwegh2, WAF Marijt3, MS Arbous1 Departments of Intensive Care1, Rheumatology2, Haematology3, Leiden University Medical Center, The Netherlands Case. A 56 year old male was admitted to our ICU with abdominal pain, fever, rigors, hypotension and respiratory distress. Four days before admission symptoms started with diarrhea, dry cough, dyspnea, myalgia, fever and oliguria. Medical history showed systemic sclerosis with pulmonary involvement. Because of disease progression autologous hematopoetic stemcell transplantation (HSCT) with cyclophosphamide and antithymocyte

336


globuline (ATG) preconditioning was performed 44 days before presentation. Two weeks after HSCT herpes labialis was diagnosed and treated with valaciclovir. Despite prolonged treatment, herpetic infection persisted. On presentation he was orientated, hypotensive and tachypnoeic. Rectal temperature was 37.9° C. Examination showed eruptive herpes labialis. There was no lymphadenopathy or tonsilar or splenic enlargement.. There was tenderness of the right upper abdominal quadrant and active guarding on palpation..Laboratory investigation showed anemia, thrombocytopenia, leucocytosis and lymfocytosis and severe liver and renal dysfunction. Resuscitation and empiric antibiotic treatment was started in this immunocompromised patient for a sepsis with a presumed intra-abdominal infection. CTscan investigation showed an abnormal gallbladder with a thickened wall without signs of hydrops or rupture. No other infectious focus was evident. Multi-organ failure developed and laparotomy was performed the second day of admission. No acute cholecystitis or other abdominal source of infection was identified. Further laboratory analysis showed an increase of the leukocytosis (> 40.10e9/L)


10-12-2008 16:37:46


with a striking increase of monoclonal B-lymfocytes. Quantitative PCR for EBVDNA showed a high titer (log 5.4 or 238.10e3 copies/mL) which was undectable 5 weaks earlier. The fulminant EBV-reactivation with monoclonal B-lymfocytes post HSCT suggested an EBV-associated post-transplantation lymphoproliferative disorder (EBV-PTLD). Treatment with CD-20-antibodies (Rituximab®) was not given because of rapid clinical deterioration. As a result of rapidly progressive multi-organ failure the patient died on the third day of admission, 47 days after bone marrow transplantation. Post-mortem examination revealed massive organinfiltration with a diffuse large-cell B-cell-lymphoma. Discussion. HSCT is a complex and expensive procedure. It is considered the treatment of choice for several defined disease categories and it is likely that the need for HSCT will increase. We report a fatal case of EBV-PTLD 7 weeks after 19

Case Report

Fatal Varicella-zoster infection presenting as fulminant hepatitis in a patient with Wegener’s granulomatosis A Hartgring, H Delwig, CA Stegeman, MWN Nijsten Department of Critial Care, University Medical Center Groningen, The Netherlands Introduction. Varicella-zoster virus (VZV) causes chickenpox in cases of primary infection, and herpes zoster in cases of reactivation of endogenous latent VZV infection. VZV hepatitis is a rare complication in immunocompromised hosts but once it occurs, the outcome is frequently fatal.1 Case report. A fifty-five year old male patient presented with generalised myalgia. He had a history of Wegener’s granulomatosis since 2003 as well as a childhood history of chickenpox. Three weeks earlier he was diagnosed with pulmonary embolism and started with anticoagulant therapy. The Wegener’s granulomatosis was treated with prednison 10 mg and mycophenolate mofetil 2 x 1000 mg. The following laboratory results were obtained: haemoglobin 8.0 mmol/l, platelet count 298 109/L, leukocyte count 7.5 109/L, lactate dehydrogenase 615 IU/l, aspartate aminotransferase 98 IU/l, alanine aminotransferase 208 IU/l. The patient was admitted at the department of internal medicine. Laboratory tests revealed rising of aminotransferases. Serological studies were negative for hepatitis A, B, C, E, cytomegalovirus and Epstein-Barr virus. Ultrasound of the upper abdomen showed no abnormalities, complementary Doppler revealed revealed no thrombosis. Transthoracic echocardiography showed no signs of right sided heart failure.

20

autologous HSCT. PTLD is an uncommon complication after autologous HSCT and seen more frequently after allogenic HSCT. PTLD can present with a diverse spectrum of clinical symptoms and signs, most notably a sepsis-like syndrome with rapidly progressive lymphoma, as in our patient, or a mononucleosis-like illness. EBV-PTLD results from profound T-cell suppression, leading to uncontrolled growth of EBV-infected B cells. Recently, 2 other fatal cases of EBV-PTLD were reported after autologous HSCT, both associated with an increased degree of T-cell suppression after preconditioning with rabbit ATG, as in our case. We did not strongly consider EBV-PTLD at presentation. However, in patients after autologous HSCT with increased T-cell suppression presenting with a sepsis-like syndrome, EBV-PTLD should be considered and treated.

Six days after admission the patient was admitted to the ICU. His blood pressure was 75/40 mm Hg, pulse rate 130 and body temperature was 38.7 °C. He had a generalised rash with a few vesicles on his face. The lactate dehydrogenase had risen to 3104 IU/l, aspartate aminotransferase 2395 IU/l, alanine aminotransferase 3756 IU/l. The platelet count had decreased to 55 109/L. An abdominal CT revealed generalised infarctions of both the liver and spleen. Awaiting the cultures broad spectrum antibiotics were started. A polymerase-chain reaction -assay for VZV then showed very high levels of VZV DNA. VZV IgG antibodies were positive, and VZV IgM antibodies were negative. Treatment was started with acyclovir 10 mg/ kg/8h intravenously. The patient’s condition declined with need for vasopressors, intubation and mechanical ventilation and renal replacement therapy. Five days later we observed a decline in the levels of aminotransferases but a further deterioration of the patient’s condition with signs of adult respiratory distress syndrome, due to VZV pneumonia and/or a secondary pulmonary infection with proteus mirabilis. Thirteen days after admission the patient died. Conclusion. VZV is a rare cause of fulminant hepatitis that should be systematically searched for in immunocompromised patients developing unexplained liver failure. Prompt initiation of acyclovir is warranted and should be started as soon as VZV is considered as cause for the hepatitis, as delay in therapy leads to a fatal outcome.2 References 1 Patti ME, Selvaggi KJ, Kroboth FJ. Varicella hepatitis in the immunocompromised adult: a case report and review of the literature. Am J Med. 1990; 88: 77-80 2 Pishvaian AC, Bahrein M, Lewis JH. Fatal varicella-zoster hepatitis presenting with severe abdominal pain: a case report and review of literature. Dig Dis Sci 2006; 51: 1221-1225

Case Report

Necrotizing pneumonia in a previously healthy young adult ME Langemeijer, NX de Rijk, JW Fijen Department of Intensive Care, Diakonessenhuis, Utrecht, The Netherlands A previously healthy 25-year-old man presented with thoracic pain, haemoptysis, fever of 39°C and dyspnoea after flu-like symptoms. He was in severe distress and septic. The oxygen saturation was 82% despite maximum oxygen administration. Initial chest X-ray showed no abnormalities. C-reactive-protein: 49 mg/l and leukocytes: 1.4x103/l, 40% bands. CT-angiography revealed bilateral consolidations with a blotchy pattern (figure 1). Invasive mechanical ventilation and initial treatment with penicillin and ciprofloxacin i.v. were started. The second day a bronchoscopy was performed (figure 2) with bronchoalveolar lavage that confirmed S. aureus- and influenza type B-infection. The antibiotic regimen was subsequently changed to flucloxacillin and oseltamivir. The clinical situation deteriorated and he was intermittedly turned to prone position. Furthermore rifampin was added to the medication. Panton-Valentine-Leukocidin-(PVL) gene was identified in the initial S. aureus strain explaining the findings on chest-CT at day 11 (figure 3). After a total hospital stay of 151 days he was discharged to a rehabilitation facility remaining a mutistic disorder and severe muscle weakness. S. aureus is responsible for 2% of community acquired pneumonias. PVL is a potent cytotoxin produced by less than 5% of all S. aureus strains and is associated with primary skin infections and necrotizing pneumonia.1, 2 It generally affects young, immunocompetent patients and has a typical presentation characterized by high fever, haemoptysis, severe sepsis, multilobular infiltrates and respiratory failure following flu-like symptoms.3 Mortality is 75% compared to 47% when PVL is absent.3

PVL-toxin induces pores in the membranes of leukocytes causing the release of chemotactic factors and other pro-inflammatory mediators leading to severe inflammation, tissue necrosis and abscess formation.4 Although PVL-positive S. aureus strains tend to be more methicillin-resistant (6-47%), in the Netherlands flucloxacillin-succeptibility is still widespread, but addition of rifampin can be considered. Clindamycine or linezolid might suppress PVL-toxin-production and intravenous immunoglobulin may neutralise PVL-toxin, but evidence is lacking.2,3 In conclusion, PVL-positive S. aureus causes devastating pneumonia affecting previously healthy young people and is associated with a very high mortality rate. Early clinical diagnosis followed by proper empirical treatment is essential for survival. References 1 Gillet Y, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet. 2002 Mar 2;359(9308):753-9. 2 Morgan MS. Diagnosis and treatment of Panton-Valentine leukocidin (PVL)-associated staphylococcal pneumonia. Int J Antimicrob Agents. 2007 Oct;30(4):289-96. Epub 2007 Jul 12. Review. 3 Van Nieuwkoop C, et al. Community-acquired Staphylococcus aureus pneumonia following influenza and the choice of empirical antibiotic treatment. Ned Tijdschr Geneeskd. 2008 Apr:5;152(14):822-6. 4 Francis JS, et al. Severe community-onset pneumonia in healthy adults caused by methicillin-resistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes. Clin Infect Dis. 2005 Jan1;40(1):100-7.



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Figure 1: Tree-in-bud configuration caused by endobronchial spreading .

Figure 3: severe necrotizing pneumonia with multiple cavitations.

Figure 2: endobronchial pus collections with hemorrhagic lesions, typical for S. aureus infection.

21

Case Report

Achromobacter xylosoxidans bacteremia in a critically ill patient caused by ritual washing MAW van Iperen 1, MA Schouten2, ARH van Zanten3 1Department of Intensive Care, Rivierenland Hospital Tiel, The Netherlands 2Department of Microbiology, Gelderse Vallei Hospital, Ede, The Netherlands 3Department of Intensive Care, Gelderse Vallei Hospital, Ede, The Netherlands Achromobacter xylosoxidans (Alcaligenes xylosoxidans subsp. xylosoxidans) is an aerobic gram-negative organism first described by Yabuuchi en Ohyama in 1971. Achromobacter is often found in aqueous environments and has been isolated in duck pond water, well-water, swimming pools, distilled water and chlorhexidin solutions [1-2]. It is resistant to most antimicrobial agents and causes infections in immunocompromised patients with underlying diseases like diabetes and malignancy [3]. The most frequently encountered infections are catheter-associated bacteremia and pneumonia, however surgical wound infections, meningitis, biliary tract infections, urinary tract infections and osteomyelitis have also been described [4].

338


We present a patient with Achromobacter xylosoxidans bacteremia and recurrent sepsis due to ritual washing with well-water. Case Report. A 67-year old Indonesian man with a medical history of colitis ulcerosa, treated with azathioprine, was admitted to the ICU of an university hospital for respiratory insufficiency. Sepsis and tuberculous meningitis was diagnosed. He was intubated, mechanically ventilated and treated with isoniazide, rifampicine, pyrazinamide en dexamethasone. During the weaning-process Candida albicans and Pseudomonas aeruginosa strains were isolated from sputum and treatment with voriconazol en ceftazidime was commenced. In cultures from bronchoalveolar lavage and perineum Achromobacter species was isolated. Subsequently contact isolation was instituted. After two months the patient was transferred to the ICU of our hospital. Neurological impairment and profound muscle weakness was noted. No antibiotics were given except for the anti tuberculosis medication and there were no signs or symptoms of infection. Surveillance cultures were taken and from the nasal swab Achromobacter species was isolated, sensitive only to trimethoprim-sulfamethoxazol. As it was considered to be colonization no antibiotic treatment was started and the patient was discharged to the general ward. Few days later he was readmitted to the ICU for septic shock and respiratory insufficiency. Mechanical ventilation and treatment with fluids and vasopressor was necessary. Imipenem was started empirically. Candida glabrata was isolated from


10-12-2008 16:37:48


bronchoalveolar lavage and voriconazol was added to the antibiotics. The patient responded well to the treatment and recovered. Some weeks later the patient developed high fever and blood cultures were taken which yielded Achromobacter xylosoxidans subsp. xylosoxidans. Trimethoprimsulfamethoxazol therapy was started based on susceptibility results of surveillance cultures. All intravascular lines were removed. Cultures were taken from the intravascular lines, sputum, urine and a decubital ulcer at the sacral region. Achromobacter was isolated from the decubital ulcer and from the tip of a peripheral intravascular line. We noted that during visiting hours the family was ritual washing the patient with well-water from the patients hometown in Indonesia. In retrospect these washings had already started at the university hospital. Consent was obtained from the family to culture the water they used for these ritual washings. From this water Achromobacter xylosoxidans subsp. xylosoxidans was isolated. 16S rRNA sequention analysis was performed of both the Achromobacter xylosoxidans strain isolated from the blood and the strain isolated from the well-water and it showed 100% homology. Our hypothesis that the patient was colonized with Achromobacter xylosoxidans due to ritual washings by relatives with contaminated water leading to bacteremia and recurrent sepsis seems hereby proven. Both hospitals did not reveal cultures positive for Achromobacter in other patients in the ICU. The family was confronted with these findings but their faith in healing power of the water was too intense to stop the ritual washings. 22

The patients clinical condition improved and he was discharged to the general ward. One week later the patient became septic again and died. Autopsy was not performed. Conclusion. This case report shows that ritual washing with well-water may lead to Achromobacter xylosoxidans bacteremia and sepsis. In religion-driven rituals by patients or relatives involving liquid solutions we suggest to culture or heat sterilize these solutions before application as it may lead to colonization and exogenous infection. References 1 Spear JB, Fuhrer J, Kirby BD. Achromobacter xylosoxidans (Alcaligenes xylosoxidans subsp. xylosoxidans) bacteremia associated with a well-water source: case report and review of the literature. J Clin Microbiol 1988;26:598-599. 2 van Hal S, Stark D, Marriott D et al. Achromobacter xylosoxidans subsp. xylosoxidans prosthetic aortic valve infective endocarditis and aortic root abscesses. J Med Microbiol. 2008 Apr;57(Pt 4):525-7. 3 Ren-Wen Tsay, Li-Chen Lin, Chien-Shun Chiou et al. Alcaligenes xylosoxidans bacteremia: clinical features and microbiological characteristics of isolates. J Microbiol Immunol Infect 2005;38:194-199. 4 Duggan JM, Goldstein SJ, Chenoweth CE et al. Achromobacter xylosoxidans bacteremia: report of four cases and review of the literature. Clin Infect Dis 1996;23:569-576.

Case Report

Severe clozapine-induced cardiomyopathy in a schizophrenic patient related to smoking cessation and ciprofloxacin use R Schellaars1, CJPW Keijsers 2, DHT Tjan1, YG van der Meer3, ARH van Zanten1 1 Department of Intensive Care, Gelderse Vallei Hospital, Ede, The Netherlands 2 Department of Internal Medicine, Gelderse Vallei Hospital, Ede, The Netherlands 3 Department of Pharmacy, Gelderse Vallei Hospital, Ede, The Netherlands Introduction. Clozapine is frequently prescribed for therapy resistant psychoses in schizophrenia and low incidence of tardive dyskinesia and extrapyramidal side effects [1]. Clozapine depends mainly on cytochrome P450 1A2 (CYP1A2) for its metabolic clearance. CYP1A2 is inducible by smoking, and lower plasma concentrations of clozapine are measured in smokers than in nonsmokers [2-3]. Smoking cessation may increase clozapine drug levels. After ciprofloxacin use also increased drug levels up to 31% have been described due to inhibition of CYP1A2 [4]. We report a case of reversible cardiomyopathy due to clozapine in a schizophrenic patient. Case. A forty-year-old schizophrenic patient presented with fever, fatigue and dry cough for prolonged time. No prior cardiac history was known. Due to discomfort he quit heavy smoking two days earlier. He was on several psychiatric medications. Two months before admission clozapine 100mg bid was added. Seven days before admission clozapine drug levels were normal i.e. 225 µg/L (200-600 µg/L). Physical examination revealed: temperature 38.6 oC, heart rate: 126 bpm, and blood pressure 100/65mmHg. Cardiac and pulmonary auscultations were normal, Oxygen saturation was 95%. Chest X-ray revealed no abnormalities. Laboratory findings showed: Hb 7.3 mmol/L, MCV 76 fl, CRP 179 mg/L, CK 454 IU/L, Urea 10.6 mmol/L and creatinine 122 mcmol/L. ECG showed supraventricular tachycardia. Sputum, blood and urine cultures were taken. Empirically, cefotaxim and ciprofloxacin were prescribed for suspected CAP. Over 24 hours patient’s condition deteriorated. Heart rate increased to 160 bpm and blood pressure dropped to 90/60 mmHg. New findings were tachypnoea (30/ min) and a decrease in oxygen saturation (92%).Repeated chest X-ray showed no pulmonary infiltrations, however heart size had slightly increased. Patient was admitted to the ICU, intubated and treated according the surviving sepsis guidelines for assumed pneumosepsis. One hour after ICU admission bradycardia

and pulseless electrical activity was noted. Cardiopulmonary resuscitation was initiated and successful. A transthoracic echocardiography was performed and showed a low ejection fraction (<10%). Severe mitral valve regurgitation due to dilated cardiomyopathy was diagnosed. No pericardial effusion was noted. Cultures never became positive. Viral causes such as HIV, EBV, CMV, HSV, VZV, Q-fever, enterovirus and respiratory viruses were tested negative. ANA and ANCA assays were negative and the thyroid functions appeared to be normal. Drug related causes were considered. Five hours after the cardiac event, clozapine levels appeared to be 480 µg/L more than double his normal level, eight hours later it had dropped to 374 µg/L. Therefore the peak level was considered even higher. Clozapine was discontinued and the patient fully recovered. After 3 days echocardiography showed an ejection fraction of 35% and a grade III mitral valve insufficiency. Sixteen days after the event the ejection fraction was 45%. Coronary angiography did not show coronary artery disease. Patient was discharged after twenty-three days but still on metoprolol 25 mg bid, Tritace 5 mg bid, amiodarone 200 mg tid, hydrochloorthiazide 25 mg once daily, Ascal 100 mg once daily, acenocoumarol vv, haloperidol 5mg once daily, oxazepam 10mg tid, temazepam 20mg once daily, Adalat 30 mg once daily. Conclusion. We presented a rare case of severe cardiomyopathy or myocarditis induced by clozapine leading to respiratory insufficiency, ICU admission, mechanical ventilation and cardiopulmonary resuscitation. Although initially sepsis was suspected drug-induced cardiac side-effects of clozapine proved to be causative and fully reversible. Drug levels were probably elevated due to smoking cessation and ciprofloxacin use. Although SIRS criteria may be present and infection suspected leading a presumptuous diagnosis of sepsis, clozapine-induced cardiomyopathy may fully mimic severe sepsis. Discontinuation of clozapine may reverse this serious condition. Rechallenge is not advised as cardiomyopathy may reoccur with drug levels in the therapeutic range. References 1. Baldessarini RJ, Frankenburg FR. Clozapine: a novel antipsychotic agent. N Engl J Med 1991;324:746-754 2. Bondolfi G, Morel F, Crettol S, Rachid F, Baumann P, Eap CB. Increased clozapine plasma concentrations and side effects induced by smoking cessation in 2 CYP1A2 genotyped patients. Ther Drug Monit. 2005;27(4):539-43. 3. Brownlowe K, Sola C. Clozapine toxicity in smoking cessation and with ciprofloxacin. Psychosomatics. 2008 Mar-Apr;49(2):176. 4. Raaska K, Neuvonen PJ. Ciprofloxacin increases serum clozapine and N-desmethylclozapine: a study in patients with schizophrenia. Eur J Clin Pharmacol. 2000 Nov;56(8):585-9



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23

Case Report

Prolongation of the QT segment and ventricular fibrillation due to Adisson’s disease and subclinical hypothyroidism HW Hom1, SLE Lambooij2, A Schoe1, WK Lagrand1, LPHJ Aarts University Medical Center Leiden Department of Intensive Care1 and Department of Internal Medicine2, The Netherlands Introduction. The QT interval on an electrocardiogram represents the ventricular depolarization and repolarization, mediated through specific sodium, calcium and potassium channels in the myocardial cell. Functional defects in those ion channels may result in specific electrocardiographic changes including prolongation of the QT interval. This elongation may predispose to torsade de pointes, ventricular fibrillation and cardiac arrest. Several genetic and acquired factors are known to induce prolongation of the QT interval. An extensive list of pharmacological agents is involved, as well as several metabolic derangements, cardiac ischemia, myocarditis and cardiomyopathy. Also, several endocrine abnormalities have been associated with lengthening of the QT interval. Here, we present a case of a patient with undiagnosed Addison’s disease, prolonged QT interval and subclinical hypothyroidism who was successfully resuscitated after cardiac arrest.

24

Case report. A 45-year-old woman was admitted to the emergency department because of an out of hospital cardiac arrest due to ventricular fibrillation. At home adequate rescucitation was immediately started. Paramedics arrived 8 minutes later and documented ventricular fibrillation. After a single defibrillation with 360 Joules sinusrithm was achieved with restoration of circulation. The electrocardiogram showed an incomplete right bundle branch block and a prolonged QTc of > 600 ms. Echocardiography and coronary angiography revealed no abnormalities. Other (extra)cardial causes like electrolye disorders or dehydration, of the documented, life threatening, ventricular arrhythmia were unlikely or excluded. Instead, Addison’s syndrome with a measured cortisol of 0.005 µmol/l and a adrenocorticotrope hormone concentration of > 1250 ngram/l, together with a subclinical hypothyroidism was diagnosed. After supplementation with hydrocortisone and fludrocortisone the QT interval decreased gradually to normal without re-occurence of (ventricular) arrhythmias in the course of several weeks. Conclusion. The list of potential causes for lengthening of the QT segment (especially pharmacologic agents) is extensive. Individual susceptibility for prolonged QT may play a pivotal role. Therefore, hormonal derangements, in our case Addison’s disease, must be considered as a cause of QT segment prolongation resulting in lifethreatening ventricular arrhythmias, especially when other causes excluded. References 8 Joseph J. Krug: Cardiac arrest secondary to Addison’s disease. 9 Ann Emerg Med june 1986;15:735-737 10 Birger Wolff, Klaus Machill e.a: Acute reversible cardiomyopthy with cardiogenic shock in a patient with addisonian crisis: A case report. Int J. Cardiol 116(2007):e71-e73

Case Report

A not lethal tramadol-intoxication MM Eysink Smeets1, NGM Hunfeld2, M Frank1 1 Intensive Care Unit, Haga Teaching Hospital, Leyenburg, The Hague, The Netherlands, 2 Central Hospital Pharmacy, The Hague, The Netherlands Introduction. Tramadol is an opioid-agonist commonly used in the treatment of acute and chronic moderate to severe pain. Its use is largely considered save. Several cases, but not much, have been reported about tramadol overdosage. The ones being reported are almost all lethal. We discuss a case of intoxication with a tramadol level

340

NJCC_06 v2 06 bwerk.indd 340 NVIC_NJCC abstracts v1.indd 38

of 8 mg/L, far above the therapeutic level of 0,1-0,75 mg/L. Case report. A 30-year old woman was admitted to our Intensive Care Unit with a severe intoxication according to the Poisoning Severity Score. Besides the toxic level of tramadol, high levels of diazepam, midazolam and venlafaxine were also detected. The intoxication resulted in respiratory insufficiency, hypothermia, short term hypotension and a Glasgow Coma Score of 3. The patient survived the intoxication and could leave the ICU the day after with a mild intoxication according to the Poisoning Severity Score. Conclusion. This case report is exceptional, because other cases report fatal intoxications at equal or much lower blood levels of tramadol. From our case and other cases reported in literature, it can be concluded that on the basis of the tramadol blood level it is not possible to give a judgement about the outcome.


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