revista de medicina si psihologie aeronautica_vol.12_nr.2_2008

Revista de medicin i psihologie aeronautic ___________________________ Volumul 12 Anul 2008 Nr. 2 (43)

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INSTITUTUL NAIONAL DE MEDICIN AERONAUTIC I SPAIAL Gral. Dr. Aviator Victor Anastasiu

Societatea de Medicin Aeronautic din Romnia

Revista

de Medicin i Psihologie

Aeronautic

Preedinte de onoare Dr. CONSTANTIN RDUIC Preedinte Conf. univ. Dr. MARIAN MACRI Vicepreedini Dr. RSVAN HRISTEA

Dr. SIMONA BERBECAR Secretar general Dr. SORIN PERLEA Trezorier Dr. EUGENIA GIGEA

Colegiul de redacie

Acad. prof. univ. dr. VICTOR VOICU Redactor ef Dr. SORIN PERLEA Redactori Dr. MIRELA ANGHEL

Conf. univ. dr. SORIN ARAM Dr. MARIUS BOAR Dr. ILIE CAPANU ef lucrri dr. ADRIANA HRISTEA Dr. ADRIAN MACOVEI Psih. DOINA TRANDAFIR

Prof. univ. dr. MIHAI ZAMFIRESCU Secretar General al Academiei de tiine Medicale din Romnia Prof. univ. dr. NICOLAE IRJI Prof. univ. dr. BENONE CRSTOCEA Prof. univ. dr. MIHAI ANIEI Conf. univ. dr. MARIAN MACRI Membru al Academiei Internaionale de Medicin Aerospaial

Secretar de redacie Dr. DRAGO VLAD Tehnoredactare Op. CRISTINA CIUCHILAN

Revista de Medicin i Psihologie Aeronautic este inclus n nomenclatorul publicaiilor medicale creditate de Colegiul Medicilor din Romnia

Marc nregistrat la OSIM cu nr. 38560/17.07.2000 Revista este cotat CNCSIS n categoria D, cod 819

Apare trimestrial ISSN 1454 - 6205


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Revista de medicin i psihologie aeronautic

Volumul 12 Anul 2008. Nr. 2 (43)

C U P R I N S

Probleme de fiziologie i fiziopatologie

1. Ronhopatia cronic: diagnostic i tratament Dr. Drago tefnescu...................................................................................... 5

Probleme de management medical

2. Sindromul de burn-out al medicului de familie Dr. Mihaela Popescu, Dr. Magdalena Vinescu, Dr. Daniela Cristovescu, Dr. Ctlin Arion, Dr. Rzvan Popescu ......................................................... 19

Probleme de clinic medical

3. Actualiti n tratamentul hipertensiunii arteriale Dr. Mirela Anghel .......................................................................................... 29

4. Febra de origine necunoscut Dr. otcan Mihai, Dr. Popescu Drago, Dr. Copaci Iulian, Dr. Enache Mihaela, Dr. Duescu Victor, Dr. Jurcu Ciprian, Dr. Rusu Cristinel, As.Med.Pr. Vasile Cornelia ............................................................................ 37

5. Posibiliti diagnostice i explorri biochimice ale funciei hepatice modificate Dr. Florica Nftnil, Dr. Mariana Jinga, Dr. Florin Nftnil, Dr. Maria Dumitru, Dr. Magdalena Vinescu............................................................... 46

Probleme de psihologie

6. Intervenia psihologic de suport n stresul traumatic - metode de reducere a reaciilor la stres

Psih. Doina Trandafir .................................................................................... 54

Certificat de acreditare ............................................................................................ 65


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The Revue of Aeronautical Medicine and Psychology

Volume 12 Year 2008 No. 2 (43)

C O N T E N T

Issues of physiology and pathophysiology

1. The chronic roncopathy: diagnostic & treatment Drago tefnescu M.D., PhD ....................................................................... 12

Issues of medical management

2. Burn-out syndrome of the general practitioner Mihaela Popescu M.D., Magdalena Vinescu M.D., Daniela Cristovescu M.D., Ctlin Arion M.D., Rzvan Popescu M.D. ................................................... 24

Issues of medical clinics

3. News in the therapy of arterial hypertension Mirela Anghel M.D., PhD .............................................................................. 33

4. Fever of unknown origin otcan Mihai M.D., Popescu Drago M.D., Copaci Iulian M.D., Enache Mihaela M.D., Duescu Victor M.D., Jurcu Ciprian M.D., Rusu Cristinel M.D., Vasile Cornelia, Nurse ................................................................................... 42

5. The possible ways of diagnostic and biochemical exploration of modified hepatic function

Florica Nftnil M.D., Mariana Jinga M.D., Florin Nftnil M.D., Maria Dumitru M.D., Magdalena Vinescu M.D......................................... 50

Issues of psychology

6. Psychological support in case of traumatic stress - methods for stress reactions reducing

Doina Trandafir, Psychologist ...................................................................... 60 Certificate of accreditation ...................................................................................... 65


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RONHOPATIA CRONIC: DIAGNOSTIC I TRATAMENT

Dr. Drago tefnescu1 REZUMAT

Sforitul i sindromul de apnee obstructiv n somn pot avea consecine severe asupra vieii

pacienilor i a familiilor acestora. Articolul de fa i propune analizarea cauzelor pentru care sindromul amintit poate fi considerat uneori ca fiind chiar fatal, precum i a modalitilor de diagnostic/tratament.

Cuvinte cheie: sforit, sindromul de apnee/hipopnee obstructiv n somn, chirurgia sforitului

1 Institutul Naional de Medicin Aeronautic i Spaial

Ronhopatia cronic reunete trei entiti clinice diferite: sforitul simplu, sindromul de rezisten crescut a cilor aeriene superioare i sindromul de apnee/hipopnee obstructiv n somn. Entitile nosologice menionate au cteva trsturi n comun. Dintre acestea, cea mai important se refer la colapsul parial sau total al cii aeriene superioare (CAS) n somn.

Sforie i vei dormi singur! Acest proverb ilustreaz impactul pe care sforitul l poate avea asupra membrilor familiei pacientului, n mod special asupra celui cu care doarme n acelai pat, care poate fi forat s se retrag ntr-o camer separat pentru a dormi bine. Uneori sforitul poate fi att de deranjant nct poate conduce chiar la divor. Problemele de cuplu generate de sforit conduc adesea la cutarea unui remediu pentru problema amintit.

n pofida consecinelor, uneori fatale, sindromul de apnee/hipopnee obstructiv n somn este nc puin cunoscut. Este demonstrat faptul c reprezint cauza cea mai frecvent a tulburrilor respiratorii din timpul somnului. De asemenea, sforitul i sindromul de apnee/hipopnee obstructiv n somn coreleaz pozitiv cu creterea morbiditii i a mortalitii prin:

Tulburri de ritm cardiac; Insuficien cardiac dreapt; Hipertensiune; Angin pectoral;

Migren matinal sever; Modificri ale performanelor intelectu-

ale i ale personalitii; Policitemie; Moarte subit.

Dalmasso (1996) demonstreaz c impotena i reducerea libidoului sunt de asemenea frecvent asociate cu patologia amintit. Alt autor, Prota, n 1996, consider somnolena diurn asociat ca pe un simptom discapacitant major, ce conduce deseori la imposibilitatea continurii activitii, a ofatului sau chiar la terminarea unei conversaii. Implicit pot surveni accidente grave de circulaie, de munc sau casnice. Definirea sindromului de apnee n somn

Sforitul este zgomotul provocat de un flux de aer turbulent, la trecerea prin calea aerian superioar. Limitele sale de severitate variaz de la cel puin deranjant la cel numit eroic sau olimpic. Cel mai puternic sforit nregistrat vreodat, conform Guinness Book of World Records, a avut o intensitate de 87.5 decibeli, echivalentul zgomotului din trafic (o strad aglomerat). Termenul apnee i are originea n limba greac, nsemnnd lipsa/oprirea respiraiei. Se consider episod apneic lipsa trecerii aerului prin CAS o perioad de cel puin 10 secunde. Apneea n somn se caracterizeaz prin perioade de respiraie grea, dificil, un sforit progresiv n intensitate urmat de tcere i apoi un suspin adnc. Aceste pauze respiratorii


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au durate cuprinse ntre 30-100 de secunde, timp n care se por observa contracii compensatorii la nivelul musculaturii toracice sau abdominale. Sindromul de apnee n somn este definit ca o succesiune de cel puin 30 de episoade apneice n timpul celor 7 ore de somn obinuite sau un numr mai mare de 5 episoade apneice pe ora de somn.

Apneea n somn poate fi de tip: Central tulburri ale circuitelor

nervoase de reglare a respiraiei; Obstructiv asociat unui obstacol la

nivelul CAS; Mixt o combinaie a celor dou

tipuri anterioare. Scopul urmrit n acest articol este

prezentarea sindromului obstructiv de apnee/ hipopnee n somn. Mecanisme

Pentru nelegerea mecanismelor sforitului i sindromului de apnee obstructiv n somn, este necesar prezentarea modificrilor neurofiziologice ce au loc n timpul somnului. Exist dou faze ale somnului, fiecare cu propriile caracteristici neuroelectrofiziologice. Un somn normal este de fapt o trecere progresiv ciclic (90-120 minute) de la somnul fr micri rapide ale globilor oculari (non-REM) la somnul cu micri rapide ale globilor oculari (REM). Respiraia este i ea diferit n starea de veghe fa de cea de somn, trecerea la veghe fiind prin sine nsi un stimul respirator puternic. Activitatea sistemului de activare n timpul somnului non-REM este extrem de prezent, asfixia determinnd revenirea rapid la starea de veghe. n schimb, n somnul tip REM, activitatea sistemului de activare este mai redus, mecanismele acestuia fiind n mare msur inhibate; implicit este nevoie de un nivel mult mai sczut al saturaiei periferice n oxigen pentru a se produce un stimul de trezire. Aadar, n somnul REM este diminuat capacitatea de rspuns la obstrucia CAS, existnd astfel posibilitatea apariiei eforturilor respiratorii neregulate i uneori a episoadelor apneice.

Feedback-ul respirator. Diminuarea stimulilor efereni, de la centrii respiratori ctre musculatura CAS responsabil de meninerea deschis a orofaringelui/laringelui n timpul inspirului, chiar dac are loc n timpul somnului, este urmat de creterea

rezistenei n CAS. Hipotonia relativ a palatului moale, a muchiului genioglos i a musculaturii posterioare a faringelui pot determina colapsarea pasiv a CAS. Scade saturaia n oxigen iar centrul respirator rspunde prin creterea efortului inspirator. Cnd mecanismul menionat este eficient, CAS este eliberat iar episodul apneic se termin printr-un suspin adnc.

Feedback-ul circulaiei pulmonare. Const n vasoconstricie. Implicit, exist posibilitatea apariiei hipertensiunii pulmonare, tulburrilor de ritm i a infarctului miocardic (rar) ca o consecin a episoadelor hipoxice repetate. Factori predispozani

Bloom (1988) a demonstrat c pacienii care sforie dezvolt un sindrom de apnee/ hipopnee n somn, ca urmare a administrrii de sedative sau a consumului de alcool. De altfel toi cei care sforie sunt predispui la a dezvolta n timp un sindrom de apnee n somn, deoarece organismul lor susine un efort respirator mai mare dect cel normal. Dup mai muli ani, acest fapt conduce la ngustarea ireversibil a CAS i la decompensarea activitii musculaturii dilatatorii faringiene, urmat de colapsarea CAS n somn. Aceasta teorie pare a fi cea mai plauzibil, prevalena sindromului de apnee-hipopnee corelnd pozitiv cu naintarea n vrst, grupul de pacieni int fiind reprezentat de cei de vrst mijlocie. Urmtorii factori sunt considerai deasemenea predispozani:

Fumatul Uvula hipertrofiat naintarea n vrst Laxitatea structurilor oro-faringelui Retrognaia Micrognaia Hipertrofia amigdalelor palatine Diformiti nazale Macroglosia Sindromul Marfan Acromegalia Neoplazii faringiene Mixedemul Anomalii cranio-faciale Sindromul Down Limfomul Sindromul Prader-Willi Sindromul Guillain-Barr


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Diagnostic La prezentarea iniial a pacientului cu

ronhopatie cronic, se pot realiza: Msurarea nlimii i a greutii Examenul aprofundat ORL Monitorizarea nocturn.

Examenul ORL. Examinarea include fibroscopia naso-faringo-laringian, n timpul manevrelor de sforit, sub anestezie local. Se poate efectua i studiul CAS n timpul somnului indus medicamentos, sub control anestezic.

Monitorizarea nocturn. Studiul somnului este absolut necesar pentru un diagnostic de certitudine n sindromul de apnee/hipopnee n somn. Se realizeaz prin polisomnografie, o investigaie modern prin intermediul creia este identificat patern-ul somnului pacientului n cauz, utiliznd:

Electroencefalografia Electromiografia nregistrrile micrilor toraco-

abdominale Fluxul respirator oro-nazal Oximetria Electrocardiografia.

Tratament

Strategia terapeutic depinde n mare msur de localizarea obstruciei:

Nas polipoz, deviaie sept; Faringe hipertrofie amigdalar/

adenoidian, tumori de nazofaringe, macroglosie, micrognaie, acromegalie, disfuncia musculaturii faringiene;

Laringe tumori, edem la acest nivel. Stilul de via.

Iniial, pacienii sunt sftuii s slbeasc (dac este cazul), s evite alcoolul i sedativele, precum si poziia de decubit supin n timpul somnului. Utilizarea redus a cafelei i a ceaiului (stimulani nervoi central) i recomandarea ca partenerul de via al pacientului ronhopat s mearg primul la culcare pot fi alte msuri utile. Dispozitivul de administrare a CPAP (presiune pozitiv continu pe cile aeriene).

Este o intervenie de tip conservator, utilizat de muli specialiti. Const ntr-o masc ce este conectat la un sistem de

pompare care trimite ctre CAS o presiune pozitiv, funcionnd practic ca o protez pneumatic ce mpiedic colapsarea CAS.

Uneori este stnjenitoare, prea scump

sau prost tolerat. Compliana terapeutic pe termen lung este n jurul valorii de 58-69%. Dezavantajele teoretice ale utilizrii CPAP ar fi reprezentate de posibilitatea inducerii


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decompensrii cardiace sau renale. Sunt descrise i alte complicaii, ca de exemplu pneumotoraxul.

O alt opiune este utilizarea unui dispozitiv oral. Scopul urmrit este deplasarea ctre nainte a mandibulei. Realizat dintr-un material plastic, se fixeaz pe dantur n mod similar protezelor utilizate n sport.

Dispozitivele anti-colaps nazal. Aceste clips-uri diminueaz frecvena i severitatea evenimentelor respiratorii la pacienii cu apnee obstructiv n somn. Cu toate acestea, utilizarea lor nu este larg rspndit.

Tratamentul medicamentos lipsit de valoare n terapia sforitului sau a sindromului de apnee n somn.

La anumii pacieni, niciuna dintre opiunile terapeutice nu este adecvat. Pentru ei, opiunea chirurgical este cea mai bun i uneori singura alegere. Pacienii n cauz prezint o obstrucie la nivelul CAS. Implicit chirurgia va ine cont de localizarea obstruciei, cutndu-se eliminarea acesteia. Tratamentul chirurgical

Chirurgia nazal. Rezultatele sale sunt destul de controversate. Este indicat n prezena patologiei de tipul hipertrofiei cornetelor inferioare, a polipozei sau a deviaiei de sept, ulterior pacientul fiind reevaluat n vederea chirurgiei palatului moale.

Uvulopalatofaringoplastia. Include: Amigdalectomia (dac este cazul); Exereza esutului redundant din jurul

muchilor palatofaringian i palatoglos;

Rezecia parial a palatului moale i a uvulei.


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Selecia pacienilor trebuie fcut cu

mult grij, muli dintre acetia prezentnd deja apnee n somn, fiind supraponderali sau avnd patologie asociat respiratorie/ cardio-vascular. Exist riscul edemului local post-operator. Dac n timpul aceleiai intervenii este abordat i patologia nazal, eventualul tamponament pentru controlul epistaxisului ar compromite suplimentar CAS.

S-au descris o serie de complicaii: Durere n post-operator; Insuficien velofaringian (regurgitaii

nazale i modificri ale parametrilor vocali);

Senzaia de uscciune faringian; Hemoragie post-operatorie:

Chirurgia cu radiofrecven. Este denumit i somnoplastie. Undele de radiofrecven sunt utilizate pentru reducerea volumului palatului moale i a bazei de limb, precum i pentru diminuarea hipertrofiei cornetelor sau exereza polipilor.

Palatoplastia laser. Este un tratament chirurgical mai puin radical ce se utilizeaz n anumite centre. Se pare c eficiena sa n sforit ar fi de 85%. Const din exereza unei bandelete din zona inferioar a palatului moale. Ulterior apar fibroza i rigidizarea palatului moale. Se pare c ar avea mai puine efecte ascunse dect uvulopalatofaringoplastia.

Liposucia cervico-facial. Const n elimi-narea esutului adipos n exces de sub brbie. Are drept efect reducerea presiunii asuprea esuturilor moi ale gtului. Contribuie la dimi-nuarea colapsrii CAS la nivelul bazei de limb.

Chirurgia cervico-facial. Chirurgia de avans mandibular sau bimaxilar este deasemenea folosit. Utilizarea sa este restrns la cazurile de anomalii cranio-faciale de tipul retrognaiei.

Tirohioidoplastia. Se poate realiza n situaiile n care obstrucia este localizat la nivelul bazei de limb.

Traheostomia. A fost utilizat n 1969 pentru tratamentul apneei n somn, la un pacient cu sindrom Pickwick. Wilson (1999) afirma c: la nivelul actual al cunotinelor n domeniu, traheostomia este singurul tratament eficient 100% al sindromului de apnee n somn la adult. n pofida avansului tehnologic, exist anumite cazuri de apnee n somn unde doar acest tip de tratament poate garanta supravieuirea pacientului. Impactul su afectiv asupra pacientului poate fi brutal, acesta putndu-se considerat desfigurat i suplimentar necesit o ngrijire strict.

Determin o voce neobinuit (cu protez) i expune pacientul riscului de stenoz traheal iatrogenic.

Bypass-ul gastric. Acest tip de chirurgie

bariatric este considerat ca un ultim resort n tratamentul obezitii morbide. Const n reducerea dimensiunilor stomacului, pacientul fiind astfel forat s mnnce mai puin.


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Concluzii Rezultatele chirurgicale n aceast

patologie pot s nu fie permanente. La anumii pacieni, apneea n somn poate s reapar dup o perioad de timp. Trebuie realizat urmrirea de lung durat a pacienilor operai de ctre chirurgul ORL.

Costurile ridicate ale studiilor de somn i ale chirurgiei pot face ca muli pacieni s nu beneficieze de un diagnostic de acuratee i de un tratament eficient.

S-a mbuntit nivelul de contientizare al patologiei menionate precum i nivelul documentaiei rezultat din studiile pe aceast tem. Cu toate acestea muli medici nc nu realizeaz c sforitul (apneea n somn) se poate trata. Aceast

infradiagnosticare poate avea consecine majore asupra calitii vieii pacienilor.

Muli pacieni, incluznd ntre acetia i piloii, nu sunt avizai asupra tulburrilor ce pot aprea n timpul somnului i implicit nu-i recunosc cu uurin simptomele afeciunii. De altfel, condiia patologic amintit poate s treac neobservat n timpul expertizei medicale periodice. Cu toate acestea, n prezent poate fi eficient tratat.

Piloii cu sindrom de apnee/hipopnee nu trebuie n mod necesar s-i piard licena medical. Diagnosticul, tratamentul i urmrirea rezultatelor pot fi realizate cu ocazia controalelor periodice.

Bibliografie

1. Coleman SC, Smith T. Midline radiofrequency tissue reduction of the palate for bothersome snoring and sleep-disordered breathing: A clinical trial. Otolaryngol Head Neck Surg 2000; 122: 387-94.

2. Dalmasso F, Prota R. Snoring: analysis, measurement, clinical implications and applications. Eur Respir J 1996; 9: 146-159.

3. Guilleminault C, Eldridge FL, Demert WC. Insomnia with sleep apnea. A new syndrome. Science 1973; 181: 856-858.

4. Lugaresi E, et al. Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 1980; 3: 221-224.

5. Lugaresi E, Grignotta F, Montagna P, et al. Snoring: Pathophysiology and clinical consequences. Semin Respir Med 1988; 9:577-85.

6. Bloom JW, et al. Risk factors in a general population for snoring. Chest 1988; 93: 678-683.

7. Quesada JL, Mohammed A, Lorente J, Quesada P. Epidemiologa de la roncopata crnica. En: Quesada P, Perell E, Lorente J. Roncopata crnica. Sndrome de apnea obstructiva del sueo. Ponencia oficial de la SEORL. Ed. Garsi, Madrid 1998: 44-50.

8. Kauffmann F, Annesi I, Neukirch F, et al. The relation between snoring and smoking, body mass index, age, alcohol consumption and respiratory symptoms. Eur Respir J 1989; 2:599-603.

9. Wilson K, Stoohs RA, Mulrooney TF, Johonson LJ, Guilleminault C, Huang Z. The snoring spectrum. Chest 1999; 115:762-770.


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10. Gislason T, Almqvist M, Eriksson G, Boman G, Taube A. Prevalence of sleep apnea syndrome among Swedish men-an epidemiological study. J Clin Epidemiol 1988; 41(6):571-6.

11. Dickens Ch. The pothumous papers of the Pickwick club. Chapman and Hall, London 1837 (Cit. Fairbanks NF. Snoring and obstructive sleep apnea. Raven Press, New York 1987; 1-18).

12. Findley LJ; Unverzagt ME; Suratt PM. Automobile accidents involving patients with sleep apnea. Am Rev Respir Dis 1988; 138:337-40.

13. Coleman RM; Dement WC. Falling asleep at work: a problem for continuing operations. Sleep Res 1986; 15:265.

14. Ulfberg J, Carter N, Edling C. Sleep-disordered breathing and occupational accidents. Scand J Work Environ Health 2000; 26(3):237-42.

15. Hoffstein, V. Snoring. Chest 1996; 109: 201-222.

16. Hoffstein V. Blood pressure, snoring, obesity and nocturnal hypoxemia. Lancet 1994; 344:643-45.

17. Ohayon MM, Guilleminault C, Priest RG, Zulley J, Smirne S. Is sleepdisordered breathing an independent risk factor for hypertension in the general population (13.057 subjects)?. J Psychosom Res 2000; 48(6):593-601.

18. Silverberg DS, Oksenberg A. Are sleep-related breathing disorders important contributing factors to the production of essential hipertension?. Curr Hypertens Rep 2001;3(3):209-15.

19. DAlessandro R; Magelli C; Gamberini G; et al. Snoring every night as a risk factor for myocardial infarction: a case-control study. BMJ 1990; 300:1557-58.

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The Revue of Aeronautical Medicine and Psychology________________________Volume 12 - Year 2008 Nr. 2 (43)

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THE CHRONIC RONCOPATHY: DIAGNOSTIC & TREATMENT

Drago tefnescu M.D., Ph.D.1 SUMMARY

Snoring and the associated syndrome of obstructive sleep apnoea can have severe effects on the lives of sufferers and their families. This article discusses why obstructive sleep apnoea is potentially fatal, and how it may be identified and managed.

Key words: snoring, obstructive sleep apnoea/hypopnea syndrome, sleep surgery

1 National Institute of Aeronautical and Space Medicine

Chronic roncopathy comprises three different clinical entities: simple snoring, over-resisting upper airways syndrome and obstructive sleep apnoea/hypopnea. All three conditions have some common features. The most important being the partial or total collapse of the upper airways during sleep.

Snore and you sleep alone! This adage illustrates the impact that snoring can have on family members, particularly the bed partner, who may be forced to retreat to a separate room for a good nights sleep. Occasionally, snoring may be so pronounced that it is cited as a reason for divorce. Marital disharmony can often drive the patient to seek a resolution to the problem of snoring.

The associated syndrome of sleep apnoea is less well known, but it is potentially fatal. Obstructive sleep apnoea/hypopnea syndrome (OSAHS) has been shown to be the most common cause of respiratory failure during sleep. A relationship between snoring and sleep apnoea and increased morbidity and mortality has now been recognized in:

Cardiac arrhythmias; Right-sided heart failure; Hypertension; Angina pectoris; Severe morning headaches; Intellectual and personality changes; Polycythaemia; Sudden unexpected death.

Dalmasso (1996) suggested that impotence and reduced libido are frequently

present. Prota (1996) cited daytime somnolence as a major disabling symptom, often making it impossible for people to work, drive or even complete a conversation. This can lead to potentially fatal road, occupational or domestic accidents.

Defining Sleep Apnoea Snoring is the noise caused by the

turbulent flow of air in the upper airway. It ranges in severity from mild snoring to so call heroic or Olympic snoring. According to the Guinness Book of World Records, the loudest recorded snore measured 87.5 decibels, equivalent to the sound of traffic in a busy street. The word apnoea originates from the Greek word meaning want of breath. An apnoeic episode occurs when no air passes through the nose or mouth in a period of ten seconds. Sleep apnoea is characterized by periods of loud, gasping snoring followed by silence. This typically lasts between 30 and 100 seconds, during which struggling motions of the thorax and abdomen may be observed. Sleep apnoea syndrome is generally defined as 30 or more apnoeic episodes during a seven- hour sleep, or when there are five or more apnoeic episodes per hour.

Sleep apnoea may be characterized as: Central apnoea; Obstructive sleep apnoea Mixed apnoea, a combination of the

two.


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The focus of this article is obstructive sleep apnoea.

Mechanisms To understand the mechanisms behind

snoring and sleep apnoea, some knowledge of the neuro-physiology of sleep and alteration of body functions that occur during sleep is essential. There are two major sleep states, each with its own characteristic physiological and electrophysiological features. Normal sleep is a cyclical progression from sleep without rapid eye movements (non-REM sleep) to REM sleep through a period of between 90 and 120 minutes. Respiration during wakefulness and sleep differs, with wakefulness in itself being a powerful respiratory drive. The arousal system during non-REM sleep is very active, and asphyxia results in a rapid return to wakefulness. In comparison, arousal from REM sleep may be slow, as the arousal mechanisms are inhibited, and much lower levels of oxygen saturation are reached before arousal occurs. Thus in REM sleep there is a diminished response to airway obstruction, with a strong possibility of irregular respirations and occasional apnoeic episodes.

Respiratory response Also during sleep, reduced respiratory centre output to the muscles of the upper airway which normally dilate the oropharynx and larynx on inspiration - produces an increase in upper airway resistance. Relative hypotonia of the soft palate, genioglossus muscle, and posterior pharynx may cause a passive collapse of the upper airway. The arterial oxygen level drops, and the respiratory centre responds by increasing inspiratory drive. When the arousal is sufficient, the palate and pharyngeal tissues are pulled out of the way, and the apnoeic episode ends with a gasp.

Pulmonary response The response of the pulmonary circulation to hypoxia is vasoconstriction. Pulmonary hypertension, arrhythmia and (rarely) myocardial infarction are the sequelae to repeated hypoxic episodes.

Predisposing Factors

Bloom et al (1988) showed that snorers given alcohol or sedatives develop obstructive sleep apnoea. It is also thought that all snorers predispose to the development of obstructive sleep apnoea because stronger breathing efforts are needed to maintain adequate gas exchange. Chronic respiratory stimulation repeated nightly over a period of years may induce irreversible airway narrowing until the pharyngeal dilator muscles can no longer prevent the airways from complete collapse during sleep. This theory appears quite feasible, as the prevalence of sleep apnoea has been shown to be age-related, usually occurring in middle-aged subjects. Other identified predisposing factors to the syndrome are shown below:

Smoking Enlarged uvula Increasing age Enlarged oropharyngeal tissue Retrognathia Micrognathia Hypertrophic palatine tonsils Nasal deformity Macroglossia Marfans syndrome Acromegaly Pharyngeal neoplasms Myxoedema Craniofacial disproportions Downs syndrome Lymphoma Prader-Willi syndrome Guillain-Barr syndrome

Diagnostic When a patient initially presents at clinical

ENT examination with obstructive sleep apnoea, the following investigations are made:

Height and weight measurement - to calculate body mass, and collar size

Extensive otorhinolaryngologic examination

Overnight monitoring Otorhinolaryngologic examination.

The examination includes fibre optic rhinolaryngoscopy during voluntary snoring. In this manoeuvre, the nasendoscope is passed


14

into the postnasal space under local anaesthetic. The patient is asked to take a deep inspiratory effort with a closed nose and mouth in an attempt to simulate snoring conditions. To create a more natural snoring environment, a sleep nasendoscopy can be performed intra-venous midazolam. Anaesthetic monitoring is necessary throughout.

Overnight monitoring. Sleep studies are essential for a firm diagnosis of sleep apnoea. The ultimate investigation is polysomnography

which records the pattern of sleep and arousal measured by:

Electro-encephalography (EEG) Electromyography (EMG) Recording thoraco-abdominal

movements Recording oro-nasal flow Oximetry Electrocardiography (ECG)

Treatment Management of obstructive sleep apnoea

depends largely on the site/nature of obstruction: Nose - nasal polyps, deviated septum Pharynx - enlarged tonsils and adenoids,

nasopharyngeal tumours, macroglossia and micrognathia, acromegaly, dysfunction of pharyngeal airway

Larynx - tumours, laryngeal oedema Life style. Initially, patients are

advised to lose weight (if appropriate), avoid alcohol and sedatives, and avoid the supine position. Use of stimulants such as coffee and tea, and allowing the snorers bed partner to get to sleep first before the discordant snoring begins, may be advocated.

Continuous positive airways pressure. This is a widely used conservative intervention. It consists of a small mask connected to a pump that supplies positive pressure to the pharyngeal airway, acting as a pneumatic splint and preventing collapse.

However, it is cumbersome, expensive and often poorly tolerated. Long term compliance is reported to be only 58-69 per cent. Theoretical disadvantages of continuous positive airways pressure include reduced cardiac output and renal function. Other respiratory complications, such as pneumothorax, have also been documented.


15

Another option is to wear an oral appliance. It is used to move the jaw forward. It is usually made of soft plastic and fits over teeth like a sports mouth guard.

Nasal dilation. The nasal dilating clips decreased both the frequency and severity of obstructive breathing events in patients with obstructive sleep apnoea. However, their use has not been widely adopted.

Drug treatment - little value in the treatment of snoring or sleep apnoea.

For some patients, these options will not work. In these cases, surgery may be the best

and only choice. These patients have a physical abnormality that is blocking their airway. The surgery will be site-specific and will seek to eliminate the cause of the obstruction. Surgery.

May be used to help patients with obstructive sleep apnea. The most common options reduce or eliminate the excessive tissue in throat. This tissue collapses and blocks the airway during sleep.

Nasal surgery. Results of nasal surgery are largely controversial. It appears to be widely accepted that underlying nasal pathology, such as hypertrophic inferior turbinates, nasal polyps or deviated nasal septum, should be treated and the patient re-assessed before considering palatal surgery.

Uvulopalatopharyngoplasty (UVPP). This involves:

Removal of the tonsils (if present) Removal of the redundant folds of

tissue around the palatopharyngeus and palatoglossus muscles

Partial resection of the soft palate and uvula.


16

Patients must be carefully selected - many of them will already have intermittent airway obstruction, be overweight and may have coexisting respiratory or cardiovascular disease. They are at risk of post-operative oedema. If nasal surgery is performed at the same time, nasal packing may be required which will further compromise the airway.

UVPP has a number of complications: Post-operative pain Velopharyngeal insufficiency

(manifested as nasal regurgitation and changes in voice quality)

Pharyngeal dryness Secondary haemorrhage Radiofrequency Volumetric Tissue

Reduction (RFVTR). This may also be called somnoplasty. Energy waves are used to shrink the soft palate and tongue base or to reduces or removes large turbinates and polyps.

Laser palatoplasty. A less radical surgical treatment, laser palatoplasty, is now being used in some centres. This apparently reduces snoring in 85 per cent of cases. A strip of inferior soft palate is excised, causing fibrosis and palatal stiffening. This procedure is said to have fewer side effects than UVPP.

Cervicofacial liposuction. Extra fatty tissue is removed below the chin. This reduces the weight pressing against the soft

tissue of the throat. It also helps lessen airway collapse behind the base of the tongue.

Craniofacial surgery. Advancement mandibular osteotomy and maxillary osteotomy have also been reported, but are only used for congenital craniofacial defects such as retrognathia.

Expansion hyoidoplasty. In cases where the tongue is the main site of obstruction, expansion hyoidoplasty and base of tongue resection have been developed.

Tracheostomy. It was first used for treatment of obstructive sleep apnoea syndrome in 1969, in a patient with Pickwickian syndrome. Wilson (1999) stated that: ln our present state of knowledge, tracheostomy is the only certain cure for life-threatening obstructive sleep apnoea in adults. Although technology has advanced considerably, cases of obstructive sleep apnoea still exist in which a permanent tracheostomy is indicated to ensure the patient survival. A tracheostomy can have a devastating impact on the patient, leaving him or her aesthetically disfigured and requiring strict hygienic care. It can result in inadequate voice production and exposes the patient to the risk of iatrogenic tracheal stenosis.

Gastric bypass. This form of bariatric surgery may be used as a last resort for people who cannot overcome obesity. It reduces the size of the stomach. This forces the patient to eat less.


17

Conclusions

The result of a surgery also may not be permanent. For some surgical patients, the sleep apnea problem may reoccur at a later time. They will need to follow-up with an ENT surgeon for a long time after the surgery.

The high cost of sleep studies and surgery may mean that many people are denied a fair evaluation and optimal treatment.

Clinical awareness and documentation of snoring and sleep apnoea have improved. However, many health professionals still do not realise that snoring (obstructive sleep apnoea) is a readily treatable condition. Failure

to recognise it may seriously impair the patients quality of life. Many patients, including pilots, are unaware of their sleeping disturbance and the symptoms are not easily recognized. Therefore, this condition may not be discovered during a regular health examination. However, this condition can be effectively treated.

In our opinion, pilots suffering from OSAHS do not necessarily have to lose their certificate. Diagnosis and treatment can be conducted, followed by regular check-ups.

Bibliography

1. Coleman SC, Smith T. Midline radiofrequency tissue reduction of the palate for bothersome snoring and sleep-disordered breathing: A clinical trial. Otolaryngol Head Neck Surg 2000; 122: 387-94.

2. Dalmasso F, Prota R. Snoring: analysis, measurement, clinical implications and applications. Eur Respir J 1996; 9: 146-159.

3. Guilleminault C, Eldridge FL, Demert WC. Insomnia with sleep apnea. A new syndrome. Science 1973; 181: 856-858.

4. Lugaresi E, et al. Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 1980; 3: 221-224.

5. Lugaresi E, Grignotta F, Montagna P, et al. Snoring: Pathophysiology and clinical consequences. Semin Respir Med 1988; 9:577-85.

6. Bloom JW, et al. Risk factors in a general population for snoring. Chest 1988; 93: 678-683.

7. Quesada JL, Mohammed A, Lorente J, Quesada P. Epidemiologa de la roncopata crnica. En: Quesada P, Perell E, Lorente J. Roncopata crnica. Sndrome de apnea obstructiva del sueo. Ponencia oficial de la SEORL. Ed. Garsi, Madrid 1998: 44-50.

8. Kauffmann F, Annesi I, Neukirch F, et al. The relation between snoring and smoking, body mass index, age, alcohol consumption and respiratory symptoms. Eur Respir J 1989; 2:599-603.

9. Wilson K, Stoohs RA, Mulrooney TF, Johonson LJ, Guilleminault C, Huang Z. The snoring spectrum. Chest 1999; 115:762-770.

10. Gislason T, Almqvist M, Eriksson G, Boman G, Taube A. Prevalence of sleep apnea syndrome among Swedish men-an epidemiological study. J Clin Epidemiol 1988; 41(6):571-6.


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11. Dickens Ch. The pothumous papers of the Pickwick club. Chapman and Hall, London 1837 (Cit. Fairbanks NF. Snoring and obstructive sleep apnea. Raven Press, New York 1987; 1-18).

12. Findley LJ; Unverzagt ME; Suratt PM. Automobile accidents involving patients with sleep apnea. Am Rev Respir Dis 1988; 138:337-40.

13. Coleman RM; Dement WC. Falling asleep at work: a problem for continuing operations. Sleep Res 1986; 15:265.

14. Ulfberg J, Carter N, Edling C. Sleep-disordered breathing and occupational accidents. Scand J Work Environ Health 2000; 26(3):237-42.

15. Hoffstein, V. Snoring. Chest 1996; 109: 201-222.

16. Hoffstein V. Blood pressure, snoring, obesity and nocturnal hypoxemia. Lancet 1994; 344:643-45.

17. Ohayon MM, Guilleminault C, Priest RG, Zulley J, Smirne S. Is sleepdisordered breathing an independent risk factor for hypertension in the general population (13.057 subjects)?. J Psychosom Res 2000; 48(6):593-601.

18. Silverberg DS, Oksenberg A. Are sleep-related breathing disorders important contributing factors to the production of essential hipertension?. Curr Hypertens Rep 2001;3(3):209-15.

19. DAlessandro R; Magelli C; Gamberini G; et al. Snoring every night as a risk factor for myocardial infarction: a case-control study. BMJ 1990; 300:1557-58.

20. Waller PC, Bhopal RS. Is snoring a cause of vascular disease? An epidemiological review. Lancet 1989; 1:143-46.


19

SINDROMUL DE BURN-OUT AL MEDICULUI DE FAMILIE

Dr. Mihaela Popescu1, Dr. Magdalena Vinescu1, Dr. Daniela Cristovescu 1, Dr. Ctlin Arion1, Dr. Rzvan Popescu2

REZUMAT

Sindromul de burn-out reprezint epuizarea mental i fizic prin implicarea n activitate, exagerat i de lung durat.

n 1974, H. Freundenberg redefinea stresul profesional prin sindromul de burn-out: uzura i epuizarea energiei, forelor i a resurselor care determin o scdere a ntregului potenial de aciune al individului; sindromul este indus de stresul cronic.

Un studiu efectuat n Statele Unite, a ncercat s arate dac exist o legtur ntre gradul de stres al medicilor i randamentul muncii acestora. S-a plecat de la ideea c n Statele Unite ale Americii i Regatul Unit al Marii Britanii erorile medicale sunt destul de des ntlnite.

n aceast lucrare ne propunem s aducem n discuie cteva elemente legate de acest sindrom i afectarea medicului de familie. Cuvinte cheie: epuizare mental i fizic, factori de risc, consiliere, strategii de intervenie, hiperperseveren

1 Institutul Naional de Medicin Aeronautic i Spaial 2 Institutul Naional de Medicin Sportiv

Definiie Sindromul de burn-out reprezint

epuizarea mental i fizic prin implicarea exagerat i de lung durat. Apare fie prin supracompensare (cum randamentul este sczut, subiectul ncearc s creasc timpul de lucru pentru a realiza aceeai cantitate de munc), fie prin retragerea forat/programat pe parcursul creia medicul se gndete tot la problemele profesionale. Ambele sunt contraproductive, agravnd uneori problema. Epuizarea sau sindromul de burn-out reprezint o combinaie de stare avansat de oboseal emoional, depersonalizare i reducere a sentimentului de realizare personal. Acest sindrom poate aprea la persoanele care desfoar activiti profesionale ce impun relaionarea intens cu oamenii (dup C. Maslach i S. Jackson). Epuizarea se caracterizeaz printr-o apatie total i incapacitate de mobilizare a resurselor interioare, pentru a rspunde exigenelor exterioare. Unele persoane sunt mai mult supuse riscului de burn-out dect

altele; spre exemplu cele animate de un mare ideal de performan i de reuit, cele care se supraestimeaz datorit realizrilor profesionale, cele care nu au alt surs de satisfacie dect lucrul n sine sau cele care se ndeprteaz de alte sfere ale vieii nconjurtoare, refugiindu-se n munc.

De asemenea, exist i o faz care precede burn-out-ul caracterizat prin nemulumire difuz, oboseal cronic, sentiment de disconfort, insomnie, cinism, scheme negative de gndire, predispoziie la conflicte i accidente, denumit rust-out. Istoric

n 1974, H. Freundenberg redefinea stresul profesional prin sindromul de burn-out: uzura i epuizarea energiei, forelor i a resurselor care determin o scdere a ntregului potenial de aciune al individului. Sindromul este indus de stresul cronic n profesiile care presupun implicare direct n ajutorarea semenilor (sectorul social). La persoanele predispuse, stresul apare prin


20

dezechilibrul ntre ideal (ceea ce ateapt de la profesie) i real. Sindromul burn-out - este cel mai nalt nivel de stres determinat de munc i se caracterizeaz prin epuizare fizic i emoional.

O prezentare mai tehnic a sindromului burn-out a fost fcut de Maslach i Jackson (1986): un sindrom ce are 3 dimensiuni: a) depersonalizarea - persoana se distaneaz de ceilali, pe care ncepe s-i vad impersonal; b) reducerea realizrilor personale; c) epuizare emoional - persoana se simte golit de resurse emoionale personale i devine foarte vulnerabil la stresori. Starea de burn-out este cauzat de expunerea la stresul profesional i adesea este nsoit de depresie.

Instrumentul de evaluare al acestui sindrom este Maslach Burn-Out Inventory cu 4 scale: epuizare emoional, realizare profesional, depersonalizare, implicare.

Agenia European pentru Securitatea i Sntatea Muncii estimeaz c o treime dintre medici sufer de burn-out, iar 10% dintre ei ajung s aib deteriorri grave ale strii de sntate, cum ar fi depresia sever sau alte tulburri psihiatrice, boli degenerative, abuzul de alcool sau droguri. Cei mai afectai sunt cei cu tip comportamental A i hiperperseverenii. Poate fi considerat prognostic bun dac este recunoscut i tratat, ajungndu-se la un timp mediu de vindecare de aproximativ 7 luni.

Un studiu efectuat n SUA a ncercat s arate dac exist o legtur ntre gradul de stres al medicilor i randamentul muncii acestora. S-a plecat de la ideea c n SUA i Regatul Unit al Marii Britanii erorile medicale sunt destul de des ntlnite. Studiul a inclus 123 de medici pediatri, rezideni sau specialiti. Pe toat durata studiului medicii au fost supravegheai i s-a constatat c 20% dintre medici sufer de depresii, iar aproape 3/4 (74%) sufer de sindrom burn-out. Pe toat durata studiului s-au fcut 45 de prescripii medicale eronate. Concluzia a fost c sntatea mental a medicilor este mai important pentru sntatea pacienilor dect se credea pn acum. n SUA acest studiu a artat necesitatea reducerii orelor de lucru pentru medici (un factor foarte important n apariia stresului fiind lipsa de timp liber). De asemenea, n urma studiului, mbuntirea

condiiilor de munc pentru medici este considerat o prioritate.

Stresul nu afecteaz toi medicii. n acelai mediu, unii profesioniti vor experimenta un nivel maxim de stres, n timp ce alii se vor adapta mai uor. Cei predispui la stres sunt cei care au anumite caracteristici, precum: idealism, supraangajare n profesie, dorina de a performa, nevoia crescut de aprobare din partea celorlali, vulnerabilitatea n faa excesului de cereri, altfel spus, neputina de a le refuza, sentimentul de vin fa de ndeplinirea propriilor nevoi, nerbdare i grab.

Muli medici sufer de fantezia salvrii, adic fac tot felul de lucruri pentru pacieni, i asum majoritatea responsabilitilor n privina nsntoirii lor, vor cu orice pre s schimbe comportamentul pacientului, s-l vindece sau s-l salveze. Pentru ei este de neacceptat ideea c uneori chiar nu pot vindeca pacientul.

Atitudinea potrivit din partea medicului ar trebui s urmreasc aciuni de colaborare, empatie i ncurajare mai degrab, dect s urmreasc rezultatele. Numai aa relaia medic-pacient poate fi echilibrat, iar implicarea este reciproc.

Lupta declarrii celei mai stresante profesii poate fi ctigat de medicii de familie, confruntai cu cele mai multe tipuri de stresori cronici.

Putem chiar cuantifica civa factori de risc ce ar putea duce la acest sindrom:

1. Abundena consultaiilor, fie ele programate sau nu, prescriere de reete, concedii medicale, programul de evaluare a strii de sntate, anumite servicii, precum i programul informatizat de raportare ctre CASAOPSNAJ i minister.

2. Stresul profesional nu se ncheie dup 8 sau 10 ore de munc. Medicul de familie trebuie s fie la dispoziia pacienilor si mereu, s acorde consultaii de urgen chiar i la domiciliul acestora i niciodat nu tie ce caz va urma. Nu poate stabili o rutin atta timp ct bolile pacienilor lui sunt diverse: de la o banal rceal, la afeciuni cardiace, la boli psihice sau cancer, iar medicul de familie este n linia nti. El trebuie s pun un prim diagnostic i s ndrume, dac e cazul, pacientul ctre specialistul potrivit.


21

3. Se ajunge ca linia ntre viaa profesional i cea personal a medicului de familie s fie extrem de fin. Or, acest fapt este un puternic declanator al strii de stres.

4. Pe lng solicitrile pacienilor, medicii de familie trebuie s fac faa i sarcinilor administrative, care nu sunt de neglijat. Astfel, ajung la stres cronic.

5. Medicul de familie asist la dramatismul evoluiei bolii.

Cum putem trata? Pentru acest sindrom exist unele

abordri terapeutice, pe baza unor terapii cognitiv-comportamentale sau consiliere individual. n terapia acestui sindrom pot fi implicai att psihiatrii ct i psihologii.

O metod alternativ o reprezint consilierea de grup, i anume Grupurile Balint i Ascona, adic psihoterapie comportamental care mprumut i elemente de psihanaliz (cele trei instane ale eului sine-eu-supraeu, cele trei niveluri incontient-subcontient-contient).

Grupurile Balint sunt formate din 8-13 persoane, unde participanii sunt aezai n cerc se tutuiesc i unde exist un lider din cadrul grupului (eventual prin rotaie) care coordoneaz discuiile i ncearc s le menin la subiect. Participanii se prezint pe rnd, una sau mai multe persoane pot anuna c doresc s prezinte un caz. Timpul acordat edinei (60-90 minute) se mparte n trei: prezentarea cazului, ntrebri pentru prezentator i discuii de tip brainstorming i evaluarea final. Nu se discut despre diagnostic pozitiv i diferenial ci se pune accentul pe relaia interpersonal medic-pacient (prin prisma conceptelor psihanalitice: rezisten, transfer, contratransfer).

n grupurile Ascona, elementul suplimentar fa de Balint este aducerea pacientului la edina de grup i discutarea de fa cu el a problemelor puse de caz.

Pentru a conchide, la finalul acestui articol propunem cteva strategii de intervenie, pentru sindromul de burn-out al medicului de familie:

I. Contientizarea problemei: consiliere psihologic n vederea

acceptrii realitii; creterea suportului social prin

discuii de grup; consiliere n vederea acceptrii

status rolului. II. Asumarea responsabilitii: introducerea unor pauze n

funcie de specificul activitii; ncurajarea iniiativei personale; completarea necesarului de

personal medical mediu, necesitatea echipei medic de familie-asistent;

educarea conducerii pentru un stil de munc recompensator.

III. Claritate cognitiv: sistem eficient de programri

pentru consultaii; numr de programri maxim plus

o marj pentru urgene (stabilirea de obiective realiste).

IV. Dezvoltarea unor mecanisme de coping:

nvarea unor noi abiliti i deprinderi realiste n funcie de:

9 context i situaie; 9 ntrirea suportului social; 9 comunicarea pe tipul de gndire

pozitiv; 9 crearea de cursuri; 9 dotarea cabinetelor de medicin de

familie, precum i gsirea unei soluii pentru mai mult spaiu de organizare n cabinet;

9 modificri n mediu (plante, aparat ap plat etc.).

Totui, amploarea acestui sindrom n Romnia nu este cunoscut, deoarece se minimalizeaz efectele acestuia, confundndu-se uor cu stresul vieii cotidiene i nelundu-se msuri concrete asupra individului (n cazul nostru medicul de familie) sau a factorilor de risc ce influeneaz producerea lui.


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Burnout Self-Check- Mind Tools Corporation, 2003

Instruciuni: pentru fiecare ntrebare punei un X n coloana corespunztoare. Punei un singur X pe fiecare rnd.

CHESTIONAR

ntrebare Nu ntotdeauna Rar Cteodat Des Foarte

des

1. Te simi prbuit i secat de energie psihic i fizic?

2. Gaseti c ai nclinaii negativiste despre meseria ta?

3. Crezi c uneori te compori prea dur cu persoanele care nu merit?

4. Crezi c te enerveaz uor micile probleme, colegii sau echipa?

5. Te simi nenteles i neapreciat de colegii ti?

6. Te simi singur?

7. Simi c ai realizat mai puin, dect ai fi putut?

8. Te simi sub un nivel neplcut de presiune?

9. Simi c nu ai obinut ce ai dorit de la slujba ta?

10. Simi c i-ai greit profesia?

11. ncepi s devii frustrat de anumite pri ale job-ului tu?

12. Simti c birocraia i structurile politice te mpiedic s faci meseria?

13. Simti c nu ai timp s faci multe lucruri, care ar fi importante pentru job-ul tu?

14. Te simi depit de sarcini?

15. Crezi c nu ai suficient timp s-i planifici viata aa cum doreti?


23

-1: Categorie

Numr Dificultate Total

Nu ntotdeauna 0 0 0

Rar 0 1 0

Cteodat 0 2 0

Des 0 3 0

F. des 0 4 0

0 0

>=

-1 Nici un semn de burn-out

5 Cteva semne de burn-out, doar dac civa factori nu sunt n mod particular evideniai

18 Fii atent! - poi avea risc de burn-out

35 Ai risc crescut de burn-out - f ceva urgent!

45 Ai risc sever de burn-out f ceva urgent! Bibliografie

1. Handbook of stress coping strategies, pag 92 (dup Jackson, S.E.-1984).

2. Derevenco, P., Anghel, I., Baban A. - Stresul n sntate i boala: de la teorie la practic, Editura Dacia, Cluj-Napoca, 1992.

3. Onody, S. - Sindromul Burn-out, apariia i posibilitile de soluionare, n Revista pedagogic nr. 5, 2001.

4. Psiholog Mirela Turc - Sindromul de burn-out, 2005.

5. Revista Medic.ro - Sindromul deburn-out al medicului 2006.

6. Anda Pacurar, Psihoterapeut formator Membru al Asociaiei pentru Psihologie i Psihoterapie Adlerian - Medicii de familie-de la stres la sindromul burn-out.


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BURN-OUT SYNDROME OF THE GENERAL PRACTITIONER

Mihaela Popescu M.D.1, Magdalena Vinescu MD1, Daniela Cristovescu MD1, Ctlin Arion MD2, Rzvan Popescu MD2

SUMMARY

Burn-Out Syndrome is the mental and physical exhaustion due to exaggerated and prolonged involvement. In 1974, H. Freundenberg redefined professional stress by burn out syndrome: the usage and exhaustion of energy, force and resources ultimately leading to a decrease of the entire potential of an individual.

One US study tried to establish a connection between the level of stress a physician is subject to and his work output. The main cause for the study was that in the US and the UK medical errors were more and more often.

In this work we discuss connection between Burn-out Syndrome affecting GPs and how important is mental health in doctors and of course how we can treat it.

Key words: mental and physical exhaustion, hyperperseverant, risk factors, counseling, intervention strategies.

1 National Institute of Aeronautical and Space Medicine 2 Institute of Sports Medicine

Definition Burn-Out Syndrome is the mental and

physical exhaustion due to exaggerated and prolonged involvement. It appears either by overcompensating (low output leads to an increased amount of time spent to achieve similar results) or by forced/programmed withdrawal during which the physician still thinks about his/hers professional problems. Both are counterproductive, sometimes even worsening the problem. The exhaustion or burn-out syndrome represents a combination between an advanced status of emotional fatigue, depersonalization and reduced sense of personal accomplishment, and can occur in persons undergoing professional activities that require relating profoundly with people.

The exhaustion is characterized by total apathy and the incapacity to mobilize internal resources in order to respond to external demands. Some persons are more prone to burnout than others; for example those, who are animated by a great ideal of performance and success, those who overestimate

themselves due to their professional accomplishments, those who except work have no other source of satisfaction or those who distance themselves from other aspects of life and take refuge in their work.

There is also, a preceding phase to the Burn-out syndrome called rust-out. Some of its characteristics are as follows: chronic fatigue, discomfort, insomnia, cynicism, negative thinking, predisposition to conflicts and accidents, diffuse discontent. History

In 1974, H. Freundenberg redefined professional stress by burn out syndrome: the usage and exhaustion of energy, force and resource ultimately leading to a decrease of the entire potential of an individual. The syndrome is induced by chronic stress in professions which involve direct implication in helping people (social component). In predisposed persons, the stress appears due to an imbalance between the ideal (whats expected) and the real.


25

The burn-out syndrome is the highest level of work-related stress characterized by emotional and physical exhaustion.

A more technical presentation of the syndrome was made by Maslach and Jackson in 1986: a syndrome with 3 dimensions: a) depersonalization one distances itself from others, who become impersonal; b) reduction of personal achievements; c) emotional exhaustion one feels emptied of personal emotional resources and becomes highly vulnerable to stress factors. The burnout state is caused by exposure to professional stress and is frequently associated with depression.

The evaluating instrument of the syndrome is the 4-scale Maslach Burn-Out Inventory: emotional exhaustion, personal accomplishment, depersonalization, involvement.

European Agency for Safety and Health at Work estimates that a 33% of all physicians suffer from burnout syndrome, and 10% tend to develop serious health problems such as severe depression or other psychiatric disorders, degenerative diseases, alcohol or drug abuse. The more affected are type-A individuals and the hyper perseverant. Recognizing and treating the syndrome is considered a good prognostic with a healing time of around 7 months.

One US study tried to establish a connection between the level of stress a physician is subject to and his work output. The main cause for the study was that in the US and the UK medical errors were more and more often.

The study included 123 pediatricians, residents or attendings. They were closely observed and the results showed that 20% suffer from depression and almost 3 quarters have developed burnout syndrome. During the duration of the trial there were 45 erroneous medical prescriptions.

The conclusion was that mental health in doctors is much more important to the health of the patients than it was believed. In the US the trial showed the necessity to reduce the number of work hours for doctors (one very important factor in the onset of stress-related problems being the lack of personal time).

Moreover, following the trial, the improvement of work conditions is considered a priority.

Stress does not affect all doctors in the same way. Given the same environment, some professionals will experiment a maximum level of stress, while others will adapt more easily. Those prone to stress are characterized by things such: idealism, the will to succeed, increased need for approval from peers, vulnerability in the face of overwhelming demands and the inability to refuse them, a feeling of guilt for accomplishing personal needs, impatience, rush and such.

Many doctors suffer from what is called the salvation fantasy, which means taking on the responsibilities for recuperating the patient. Theyll try to change the patients behavior patterns at any cost, to cure him or save him. The idea that sometimes patients are beyond salvaging is unacceptable to them.

The right attitude should lean more towards cooperation, empathy and encouragement than just obsessing about results. Only like this the relation doctor-patient can be balanced and the involvement mutual.

The fight for declaring the most stressful of all medical professions can easily be won by the General Practitioners (GPs). Without being perceived as top of the medical specialties and subspecialties, the GPs are confronted by most of the chronic stress factors.

We can actually quantify several of these factors, which ultimately lead to the onset of the burnout syndrome:

1. The abundance of consultations, either scheduled or not, prescriptions, medical leaves, the national program to evaluate health in the general population, certain services like the software for reporting to the ministry and Casa OPSNAJ.

2. Professional stress does not end when the work day ends. The GP has to be always on-call to respond to patients needs such as emergency consults at home. He can never know what the next case is going to be like.


26

He cannot establish a routine as long as his patients ailments are so diverse: from a common cold to cardiac problems, psychiatric disorders or cancer. The GP is in the front lines. He has to ascertain a first diagnosis and to guide the patient, as the case may be, towards the proper specialist.

3. Sometimes the line between the GPs private life and his professional life fades. This is a very powerful trigger for stress-related ailments.

4. Along with his patients demands, the GP must also cope with administrative tasks which are not negligible, thus chronic stress may develop.

5. The GP is witness to every dramatic change during the evolution of a medical condition. How can we treat it?

There are some therapeutic approaches based on cognitive-behavioral therapies or individual counseling. Both psychiatrists and psychologists can be involved in the therapy. An alternate method is group counseling, such as Balint groups or Ascona groups, which is behavioral psychotherapy that also borrows some elements of psychoanalysis: small groups consisting of 8 to 13 persons in which the participants talk to each other, elect a leader (usually by rotation) that coordinates discussions and tries to keep them in line with the topic at hand. The participants introduce themselves and one or more can announce the intention to present a case. The session time (60-90 minutes) is usually divided in three: presenting a case, Q & A, and a brainstorming session + the final evaluation. There will be no talking about right or wrong diagnosis or about differential diagnosis. Instead the emphasis shall be put on the doctor-patient relation (psychoanalysis wise: resistance, transference, counter transference).

In the Ascona groups, the supplemental element is bringing the patient to the group session and discussing the case in front of him.

In order to conclude, we propose several intervention strategies for the burn-out syndrome in the GP:

I. Acknowledging the problem: counseling to accept the reality; increased social support during

group sessions; counseling to accept status.

II. Assuming responsibility: introduction of breaks according

with the activity; encouragement of personal

initiative; fulfilling the necessary number of

mid-level medical personnel; educating the leadership towards a

compensatory work style. III. Cognitive clarity: a more efficient scheduling of

consultations; maximum number of appointments

plus a margin for emergencies. IV. Developing coping mechanisms:

Learning new abilities and real skills according to:

9 context and situation; 9 increased social support; 9 positive thinking communication; 9 elaboration of courses; 9 instrumentation of the GPs

practice as well as a more efficient solution to organize ones practice;

9 environnemental modifications (plants, coffee makers etc).

However, the amplitude of the syndrome in Romania is still unknown, because its effects are ignored, being easily mistaken for day-to-day stress thus resulting in a lack of action towards an individuals problems (the GP in our case) and the risk factors leading to the syndrome.


27

Burnout Self-Check- Mind Tools Corporation, 2003

Instructions: For each question, put an 'X' in the column that most applies. Put one 'X' only in

each row.

Question Not at all Rarerly Some times Often

Very often

1. Do you feel run down and drained of physical or emotional energy?

2. Do you find that you are prone to negative thinking about your job?

3. Do you find that you are harder and less sympathetic with people than perhaps they deserve?

4. Do you find yourself getting easily irritated by small problems, or by your co-workers and team?

5. Do you feel misunderstood or unappreciated by your co-workers?

6. Do you feel that you have no-one to talk to?

7. Do you feel that you are achieving less than you should?

8. Do you feel under an unpleasant level of pressure to succeed?

9. Do you feel that you are not getting what you want out of your job?

10. Do you feel that you are in the wrong organization or the wrong profession?

11. Are you becoming frustrated with parts of your job?

12. Do you feel that organizational politics or bureaucracy frustrate your ability to do a good job?

13. Do you feel that there is more work to do than you practically have the ability to do?

14. Do you feel that you do not have time to do many of the things that are important to doing a good quality job?

15. Do you find that you do not have time to plan as much as you would like to?


28

Scoring:

0 valid interpretation: You have entered too few or too many Xs!

-1: Category Working

Number Weight

Weighted

Total

Not at all: 0 0 0

Rarely 0 1 0

Sometimes 0 2 0

Often 0 3 0

Very Often 0 4 0

0 0

>=

-1 No sign of burnout here!

5 Little sign of burnout here, unless some factors are particularly severe

18 Be careful - you may be at risk of burnout, particularly if several scores are high

35 You are at severe risk of burnout - do something about this urgently

45 You are at very severe risk of burnout - do something about this urgently

Bibliography

1. Handbook of stress coping strategies (Jackson, S.E. 1984).

2. Stress in health and illness: from theory to practice (Derevenco P., Anghel I., Baban A. - Cluj-Napoca, 1992).

3. Burn-Out Syndrome, appearance and solutions (Onody S. Pedagogical Magazine , no. 5, 2001).

4. Burn-Out Syndrome (Turc M. 2005).

5. Burn-Out Syndrome of GP ( Medic.ro Magazine, 2006).

6. GP From Stress to Burn-Out Syndrome (Pacurar A.).


29

ACTUALITI N TRATAMENTUL HIPERTENSIUNII ARTERIALE

Dr. Mirela Anghel1

REZUMAT

Ghidurile actuale recomand terapia combinat pentru controlul tensiunii arteriale la majoritatea pacienilor hipertensivi. Aceasta este aproape obligatorie la pacienii hipertensivi diabetici, renali i cu risc nalt i permite atingerea intelor tensionale mai repede dect cu monoterapie. Ghidurile recomand de asemenea abordri terapeutice specifice n condiii speciale.

Cuvinte cheie: hipertensiune, terapie, linii directoare.

1 Institutul Naional de Medicin Aeronautic i Spaial

Ghidurile pentru managementul hiper-tensiunii arteriale (HTA) elaborate n 2007 de ctre Societatea European de Hipertensiune (ESH) i Societatea European de Cardiologie (ESC) ofer o analiz minuioas a controlului tensiunii arteriale la pacienii hipertensivi, subliniind necesitatea utilizrii n practic a terapiei antihipertensive combinate.

Numeroase studii controlate au artat c tratamentul HTA este benefic. n toate cazurile de HTA, medicamentele care scad TA sistolic i/sau diastolic reduc morbiditatea i mortalitatea cardiovascular. Totui, acest efect este contrabalansat de dovezile care atest c managementul actual al HTA este incapabil s aduc riscul cardiovascular al pacienilor tratai la nivelul corespunztor persoanelor normotensive. Dei se crede c mai muli factori sunt responsabili de acest inconvenient, un candidat serios este controlul insuficient al HTA, nivelul TA al pacienilor hipertensivi tratai fiind mai mare dect al persoanelor normotensive martor. Aceast constatare poate fi depit printr-o strategie terapeutic bazat pe combinarea a dou sau mai multe medicamente antihipertensive care s permit obinerea unui mai bun control al TA (i implicit o protecie cardiovascular mai mare) la un numr mai mare de pacieni hipertensivi. Acesta este unul dintre motivele pentru care aceast abordare terapeutic a fost

recomandat de noile ghiduri elaborate de ESC/ESH.

Raionamentul terapiei antihipertensive combinate

n timp ce monoterapia iniial este eficient numai la un numr mic de pacieni hipertensivi, administrarea combinat de dou sau trei medicamente antihipertensive este eficient la 80%, respectiv 90% din cazuri. Terapia combinat joac un rol fundamental n tratamentul HTA i nu este limitat numai la practica clinic; a fost utilizat cu succes n studii controlate pentru obinerea unei TA optime la pacienii hipertensivi. Combinaiile optime de dou medicamente trebuie s ndeplineasc 5 cerine importante:

1) medicamentele trebuie s aib mecanisme diferite de aciune, dar complementare;

2) medicamentele administrate mpreun trebuie s aib un efect antihipertensiv mai mare sau egal cu suma efectelor antihiper-tensive ale fiecrui medicament, dei se accept i un efect care este doar mai mare dect al fiecrui medicament individual;

3) medicamentele combinate trebuie s determine o nsumare total sau parial a capacitii de a proteja organele lezate de HTA, de exemplu trebuie s produc regresia


30

hipertrofiei ventriculare stngi sau reducerea proteinuriei ntr-un grad mai mare dect acelai efect produs de fiecare medicament individual;

4) medicamentele trebuie s reduc (sau cel puin s nu creasc) reaciile adverse;

5) medicamentele nu trebuie s produc efecte nedorite (adverse) hemo-dinamice i umorale.

Iniierea terapiei antihipertensive combinate

Ghidurile ESH/ESC 2007 au elaborat o strategie clar a monoterapiei i terapiei combinate n HTA. n primul rnd, subliniaz c terapia combinat este necesar pentru a controla TA la majoritatea pacienilor hipertensivi, fcnd mai puin relevant alegerea medicamentului de prim intenie. De asemenea, precizeaz c terapia combinat este aproape obligatorie la pacienii hipertensivi diabetici, renali i cu risc nalt deoarece n toate aceste condiii clinice inta TA este 130/80 mmHg sau chiar mai redus, int care se poate atinge doar prin terapie combinat, aa cum dovedesc majoritatea studiilor clinice controlate.

Ghidurile precizeaz c iniierea terapiei antihipertensive cu o combinaie de dou medicamente permite reducerea mai rapid a nivelului TA dect cu monoterapie. Acest fapt are o importan particular la pacienii cu risc cardiovascular nalt, la care studiul VALUE (Valsartan Antihypertensive Long-term Use Evaluation) a artat c o lips a scderii prompte a TA poate fi asociat cu o rat mai mare a evenimentelor cardiovasculare.

Combinaiile prioritare de medicamente antihipertensive

Conform ghidurilor ESH/ESC 2007, combinaiile prioritare de medicamente antihipertensive sunt:

9 diuretic tiazidic i inhibitor ECA 9 diuretic tiazidic i antagonist al

receptorilor AT 9 antagonist calciu i inhibitor ECA 9 antagonist calciu i antagonist al

receptorilor AT (R AT)

9 antagonist calciu i diuretic tiazidic 9 beta blocant i antagonist calciu

(dihidropiridine) n practica clinic, alegerea combinaiei

preferate de medicamente antihipertensive trebuie s fie bazat pe mai muli factori, incluznd vrsta pacientului, profilul de risc cardiovascular i metabolic, prezena leziunilor organelor int, tolerabilitatea medicamentelor din combinaia aleas, existena unei patologii asociate.

Terapia antihipertensiv n condiii speciale

Pacienii vrstnici Studii clinice controlate la pacienii

hipertensivi peste 60 ani au artat c tratamentul antihipertensiv eficient determin scderea marcat a morbiditii i mortalitii cardiovasculare. Tratamentul poate fi iniiat cu diuretice tiazidice, antagoniti de calciu, IECA, antagoniti ai R AT i beta blocante. inta TA este aceeai ca i la pacienii hipertensivi tineri, i anume 140/90 mmHg, daca este tolerat. Muli pacieni necesit dou sau mai multe medicamente pentru controlul TA. Datorit riscului crescut de hipotensiune postural, TA trebuie ntotdeauna msurat i n ortostatism.

Pacienii diabetici inta TA este < 130/80 mmHg, fiind

necesar terapia antihipertensiv combinat. Dovezile indic faptul c scderea TA exercit un efect protector asupra apariiei i progresiei leziunilor renale. O protecie adiional este obinut prin administrarea unui inhibitor al ECA sau blocant al R AT. De aceea, aceste medicamente trebuie s constituie unul dintre componentele schemei terapiei combinate. Strategia terapeutic trebuie s se adreseze tuturor factorilor de risc cardiovascular, incluznd astfel i o statin.

Pacienii cu boli cerebrovasculare La pacienii care au avut accident

vascular cerebral sau atac ischemic tranzitor,


31

tratamentul antihipertensiv reduce marcat incidena recurenei AVC i, de asemenea, scade riscul nalt asociat de evenimente cardiace. inta TA este < 130/80 mmHg. Deoarece studiile evideniaz c beneficiul depinde de scderea per se a TA i mai puin de medicamentul ales, iniierea terapiei se poate face cu oricare dintre combinaiile prioritare. Studii observaionale reliefeaz c declinul cognitiv i incidena demenei pot fi ntrziate de terapia antihipertensiv eficient.

Pacienii cu boal coronarian ischemic i cu insuficien cardiac

inta TA este 130/80 mmHg. La pacienii care au un istoric de infarct miocardic, administrarea precoce de beta blocante, inhibitori ECA sau blocani ai R AT reduce incidena recurenei infarctului i a decesului. Tratamentul antihipertensiv este de asemenea benefic la pacienii cu boal ischemic coronarian cronic, fiind utilizat o schem de terapie combinat. Pacienii cu insuficien cardiac congestiv au rareori i HTA. La aceti pacieni, tratamentul antihipertensiv trebuie s includ diuretice tiazidice i/sau de ans i antialdosteronice, beta blocante, inhibitori de ECA sau blocani de receptor AT; blocantele de calciu trebuie evitate dac nu sunt imperios necesare pentru controlul TA sau al simptomelor anginoase. Insuficiena cardiac diastolic este frecvent la pacienii cu istoric de HTA i are un prognostic rezervat; pn n prezent nu exist dovezi care s ateste superioritatea unui anumit medicament antihipertensiv.

Pacienii cu sindrom metabolic Pacienii cu sindrom metabolic au o

prevalen mai mare a microalbuminuriei, hipertrofiei ventriculare stngi i a rigiditii arteriale dect persoanele fr sindrom metabolic. Riscul cardiovascular este de asemenea ridicat, ca i dezvoltarea diabetului zaharat. Tratamentul antihipertensiv trebuie iniiat cu un medicament care nu faciliteaz apariia diabetului; sunt recomandate un

blocant al sistemului renin-angiotensin, urmat de multe ori de adugarea unui antagonist de calciu sau diuretic tiazidic n doz mic. Este necesar monitorizarea ambulatorie a TA n managementul HTA la aceti pacieni. De asemenea, este recomandat o evaluare detaliat a organelor int pentru depistarea unor eventuale leziuni subclinice.

Pacienii cu HTA rezistent la tratament

HTA este de obicei definit rezistent sau refractar la tratament atunci cnd un plan terapeutic care a inclus cel puin trei medicamente (inclusiv un diuretic) n doze adecvate nu a reuit s aduc TA la valorile int. HTA rezistent este asociat cu leziuni subclinice ale organelor int i cu risc cardiovascular nalt. n primul rnd, trebuie cautate posibile cauze de HTA rezistent:

aderen slab la planul terapeutic; insuficienta modificare a stilului de

via; administrarea concomitent de

medicamente care cresc TA (glucocorticoizi, antiinflamatorii nesteroidiene, cocain etc.);

apneea obstructiv n somn; o cauz secundar de HTA

nesuspectat iniial; leziuni de organ int ireversibile; suprancrcare volemic prin: terapie

diuretic insuficient, insuficien renal progresiv, aport crescut de sodiu, hiperaldosteronism.

Implementarea cu succes a liniilor directoare n managementul HTA elaborate de ESH i ESC n 2007 necesit contientizarea barierelor interpuse ntre recomandri i practica clinic. Una dintre aceste bariere o reprezint cunoaterea i acceptarea acestor ghiduri de ctre medic. Nu trebuie s uitam c scopul final este acelai: scderea morbiditii i mortalitii cardiovasculare, n continu cretere n ara noastr.


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Bibliografie

1. MacMahon S, Rodgers A. The effects of antihypertensive treatment on vascular disease: reappraisal of evidence in 1994. J Vasc Med Biol 1993;4:265-271.

2. Grassi G, Antihypertensive combination treatment and new European guidelines, www.escardio.org.

3. Struijker-Boudier HA, Ambrosioni E, Holzgreve H, et al. The need for combination antihypertensive therapy to reach target blood pressures: what has been learned from clinical practice and morbidity-mortality trials? Int J Clin Pract 2007;61:1592-1602.

4. Isles CG, Walker LM, Beevers GD, et al. Mortality in patients of the Glasgow Blood Pressure Clinic.J Hypertens 1986;4:141-156.

5. Mancia G. Blood pressure reduction and cardiovascular outcomes: past, present, and future. Am J Cardiol 2007;100:3J-9J.

6. Mancia G, De Backer G, Dominiczak A, et al.; Management of Arterial Hypertension of the European Society of Hypertension; European Society of Cardiology. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).J Hypertens. 2007 ;25:1105-1187.

7. Nesbitt SD. Antihypertensive combination therapy: optimizing blood pressure control and cardiovascular risk reduction. J Clin Hypertens 2007;9:26-32.

8. Burt VL, Cutler JA, Higgins M, e coll. Trends in the prevalence, awareness, treatment, and control of hypertension in the adult US population. Data from the health examination surveys, 1960 to 1991. Hypertension 1995;26:60-69.

9. Chobanian AV, Bakris GL, Black HR, et al. National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:12061252.

10. Swales JD. Current clinical practice in hypertension: the EISBERG (Evaluation and Interventions for Systolic Blood pressure Elevation-Regional and Global) project. Am Heart J 1999; 138:231-237.

11. Julius S, Kjeldsen SE, Weber M, et al.; VALUE trial group. Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipine: the VALUE randomised trial. Lancet 2004;363:2022-2031.


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NEWS IN THE THERAPY OF ARTERIAL HYPERTENSION

Mirela Anghel M.D., PhD1 SUMMARY

Current guidelines recommend combination treatment to control blood pressure in the majority of hypertensive patients. It is almost mandatory in diabetic, renal and high risk hypertensive patients and may allow blood pressure targets to be reached earlier than with monotherapy. Guidelines also recommend specific therapeutic approach in special conditions.

Key words: hypertension, therapy, guidelines.

1 National Institute of Aeronautical and Space Medicine

The New European Society of Hypertension/ European Society of Cardiology (ESH/ESC) Guidelines on hypertension, issued in 2007, offer an in-depth examination into the problem of blood pressure (BP) control during treatment, emphasizing the need in current clinical practice for combination drug treatment.

A large number of controlled studies have conclusively shown that the treatment of hypertension is beneficial. In virtually all hypertensive conditions, drugs that lower diastolic and/or systolic blood pressure reduce cardiovascular morbidity and mortality. However, this is counterbalanced by the evidence that current management of hypertension is unable to bring the cardiovascular risk of the treated hypertensive patients back to the level of the normotensive individuals. Although several factors are believed to be responsible for this finding, a likely candidate is poor blood pressure control, i.e. the fact that blood pressure levels of treated hypertensives remain, almost invariably, higher than those of normotensive controls. This limitation can be overcome by a therapeutic strategy based on a combination of two or more antihypertensive drugs, which allows achieving a better blood pressure control (and thus greater cardiovascular protection) in a much larger fraction of hypertensive patients. This is one of the reason for which this therapeutic approach has been recommended by the 2007 European

Society of Hypertension/European Society of Cardiology Guidelines.

Reasoning of antihypertensive combination treatment

Whereas initial monotherapy effectively lowers blood pressure in only a limited fraction of the hypertensive population, combined administration of two or three drugs achieves a successful antihypertensive response in about 80% and 90% of cases, respectively. Combination therapy plays a fundamental role in the overall treatment of hypertension that is not limited to clinical practice; combination treatment with two and three drugs has also been commonly employed to achieve optimal blood pressure in controlled studies. Optimal two-drug combinations are characterized by five main requirements:

1) drugs to be combined should display mechanisms of action that are different but complementary;

2) drugs should, when given together, produce an antihypertensive effect that is greater than, or equal to, the sum of the antihypertensive effect of the individual combination components, although an effect that is just greater than that of either drug alone may also be acceptable;

3) drugs should also be total or partial summation of their ability to protect against the organs that are damaged by hypertension, e.g. they should produce a regression of left


34

ventricular hypertrophy or a reduction in proteinuria greater than what can be achieved with the individual combination components;

4) drugs should reciprocally reduce (or at least not increase) their side effects;

5) drugs should not have untoward (adverse) haemodynamic and humoral effects.

Starting antihypertensive combination treatment

ESH/ESC 2007 Guidelines make a clear statement on the use of monotherapy and combination drug therapy strategy. They first emphasize that combination treatment is needed to control blood pressure in the majority of patients, making the issue related to the drug of first therapeutic choice less relevant. They also recognize that combination treatment is almost mandatory in diabetic, renal and high risk hypertensive patients because in all these clinical conditions blood pressure goal is set at 130/80 mmHg or even lower, target that can be reached only by combination therapy, as the majority of controlled clinical studies have shown.

Guidelines make a further point in favor of combination therapy, underling the concept that starting treatment with a two-drug combination may allow blood pressure targets to be reduced earlier than with monotherapy. This is of particular importance in high-risk patients, in the light of the evidence provided by the Valsartan Antihypertensive Long-term Use Evaluation (VALUE) study that a lack of a prompt blood pressure control may be associated in these individuals with a higher cardiovascular events rate.

Combination therapy of priority use

According to 2007 ESH/ESC Guidelines combination of priority use includes the following:

9 thiazide diuretic and ACE inhibitor

9 thiazide diuretic and angiotensin receptor antagonist

9 calcium antagonist and ACE inhibitor

9 calcium antagonist and angiotensin receptor antagonist

9 calcium antagonist and thiazide diuretic

9 beta-blocker and calcium antagonist (dihydropiridine)

In practical terms the choice of the preferable combination of drugs regimen should be based on a number of factors, including the patients age, metabolic and cardiovascular risk profile, the presence of target organ damage, tolerability and side effects of the combinations used, associated pathology.

Therapeutic approach in special conditions

Antihypertensive treatment in elderly Randomized trials in hypertensive patients aged 60 years have shown that a marked reduction in cardiovascular morbidity and mortality can be achieved with effective antihypertensive treatment. Drug treatment can be initiated with thiazide diuretics, calcium antagonists, angiotensin receptor antagonists, ACE inhibitors, and beta-blockers. BP goal is the same as in younger patients, i.e. < 140/90 or below, if tolerated. Many elderly patients need two or more drugs to control blood pressure. Because of the increased risk of postural hypotension, BP should always be measured also in the erect posture.

Antihypertensive treatment in diabetics Goal BP should be < 130/80 mmHg,

being necessary combination treatment. Available evidence indicates that lowering BP also exerts a protective effect on appearance and progression of renal damage. Some additional protection can be obtained by the use of an ACE inhibitor or an angiotensin recept

revista de medicina si psihologie aeronautica_vol.12_nr.2_2008

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