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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)
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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



Revista de medicin i psihologie aeronautic ___________________________ Volumul 12 Anul 2008 Nr. 2 (43)
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RONHOPATIA CRONIC: DIAGNOSTIC I TRATAMENT

Dr. Drago tefnescu
1


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.





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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.





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12



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
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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.

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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.



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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.
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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;
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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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18
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.



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19



SINDROMUL DE BURN-OUT AL MEDICULUI DE FAMILIE

Dr. Mihaela Popescu
1
, Dr. Magdalena Vinescu
1
, Dr. Daniela Cristovescu
1
,
Dr. Ctlin Arion
1
, Dr. Rzvan Popescu
2


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
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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.
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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:
context i situaie;
ntrirea suportului social;
comunicarea pe tipul de gndire
pozitiv;
crearea de cursuri;
dotarea cabinetelor de medicin de
familie, precum i gsirea unei soluii pentru
mai mult spaiu de organizare n cabinet;
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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22
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?

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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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24



BURN-OUT SYNDROME OF THE GENERAL PRACTITIONER

Mihaela Popescu M.D.
1
, Magdalena Vinescu MD
1
, Daniela Cristovescu MD
1
,
Ctlin Arion MD
2
, Rzvan Popescu MD
2


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.
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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.
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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:
context and situation;
increased social support;
positive thinking communication;
elaboration of courses;
instrumentation of the GPs
practice as well as a more efficient solution to
organize ones practice;
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.


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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?




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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.).





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29



ACTUALITI N TRATAMENTUL
HIPERTENSIUNII ARTERIALE

Dr. Mirela Anghel
1


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
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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:
diuretic tiazidic i inhibitor ECA
diuretic tiazidic i antagonist al
receptorilor AT
antagonist calciu i inhibitor ECA
antagonist calciu i antagonist al
receptorilor AT (R AT)
antagonist calciu i diuretic tiazidic
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,
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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.
Revista de medicin i psihologie aeronautic ___________________________ Volumul 12 Anul 2008 Nr. 2 (43)

32

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.












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

33



NEWS IN THE THERAPY OF ARTERIAL HYPERTENSION

Mirela Anghel M.D., PhD
1


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
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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:
thiazide diuretic and ACE
inhibitor
thiazide diuretic and
angiotensin receptor antagonist
calcium antagonist and ACE
inhibitor
calcium antagonist and
angiotensin receptor antagonist
calcium antagonist and thiazide
diuretic
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
receptor antagonist. Therefore, these drugs
should be a regular component of
combination treatment. Therapeutic strategy
should consider an intervention against all
cardiovascular risk factors, including a statin.
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35
Antihypertensive treatment in
patients with cerebrovascular disease
In patients with a history of stroke or
transient ischemic attacks, antihypertensive
treatment markedly reduces the incidence of
stroke recurrence and also lowers the
associated high risk of cardiac events. BP
goal should be < 130/80 mmHg. Because
evidence from trials suggests that the benefit
depends on BP lowering per se, all available
drugs in combination of priority use can be
used for starting. In observational studies,
cognitive decline and incidence of dementia
can be delayed by effective antihypertensive
treatment.
Antihypertensive treatment in
patients with coronary heart disease
and heart failure
BP goal is 130/80 mmHg. In patients
with a history of myocardial infarction, early
administration of beta-blockers, ACE
inhibitors or angiotensin receptor antagonists
reduces the incidence of recurrent myocardial
infarction and death. Antihypertensive
treatment is also beneficial in hypertensive
patients with chronic coronary heart disease,
using a combination therapy. Hypertension is
relatively rare in patients with congestive
heart failure. In these patients, treatment can
include thiazide and loop diuretics,
antialdosterone drugs, as well as beta-
blockers, ACE inhibitors, angiotensin
receptor antagonists; calcium antagonists
should be avoided unless needed to control
BP or anginal symptoms. Diastolic heart
failure is common in patients with a history of
hypertension and has an adverse prognosis. At
present there is no evidence on the superiority
of specific antihypertensive drugs.
Antihypertensive treatment in
patients with metabolic syndrome
Patients with metabolic syndrome have a
higher prevalence of microalbuminuria, left
ventricular hypertrophy and arterial stiffness
than those without the metabolic syndrome.
Their cardiovascular risk is also high, as well
as the chance of developing diabetes.
Treatment should start with a drug unlikely to
facilitate onset of diabetes. A blocker of the
renin-angiotensin system, followed, in
majority of cases, by the addition of a calcium
antagonist or a low-dose thiazide diuretic is
recommended. Ambulatory BP monitoring is
needed in the hypertension management of
these patients. A more in-deep assessment of
the target organs is recommended in order to
an early detection of subclinical organ
damage.
Antihypertensive treatment in
patients with resistant hypertension
Hypertension is usually defined resistant
or refractory to treatment when a therapeutic
plan that has included at least three drugs
(including a diuretic) in adequate doses has
failed to lower BP to goal. Resistant
hypertension is associated with subclinical
organ damage and a high cardiovascular risk.
First, we have look for potential causes of
resistant hypertension:
poor adherence to therapeutic plan
failure to modify lifestyle
concomitant intake of drugs that
raise BP (glucocorticoids, non-steroid anti-
inflammatory drugs, cocaine, etc)
obstructive sleep apnea
unsuspected secondary cause
irreversible organ damage
volume overload due to: inadequate
diuretic therapy, progressive renal insufficiency,
high sodium intake, hyperaldosteronism
Successful implementation of 2007
ESH/ESC Guidelines on management of
hypertension requires awareness of the
barriers interposed between recommendations
and clinical practice. One of these barriers is
knowledge and acceptance of the Guidelines
by physicians. We do not forget that the final
goal is the same: reducing of the
cardiovascular morbidity and mortality,
increasingly in our country in the last years.
The Revue of Aeronautical Medicine and Psychology________________________Volume 12 - Year 2008 Nr. 2 (43)

36

Bibliogrphy

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.





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

37



FEBRA DE ORIGINE NECUNOSCUT

Dr. otcan Mihai
1
, Dr. Popescu Drago
1
, Dr. Copaci Iulian
2
, Dr. Enache Mihaela
2
,
Dr. Duescu Victor
2
, Dr. Jurcu Ciprian
2
, Dr. Rusu Cristinel
2
, As.med.pr. Vasile Cornelia
1


REZUMAT

Cu toate progresele recente ale metodelor de diagnostic, febra de origine necunoscut (FON)
rmne o problem clinic deosebit. Medicul specialist de medicin intern este de obicei primul
care se confrunt cu aceast condiie. Frecvent este consultat un specialist n boli infecioase,
reumatologie sau hematologie-oncologie. O serie de teste standard pot stabili un diagnostic specific
sau cel puin o categorie mai larg n care este inclus diagnosticul. Cele trei mari categorii de cauze
ale FON infeciile, bolile de colagen i cele granulomatoase i tumorile - rmn nemodificate de
la primele studii efectuate de Petersdorf i Beeson n 1961.
Cuvinte cheie: febr, infecii, tumori, colagenoze.



1
Institutul Naional de Medicin Aeronautic i Spaial
2
Spitalul Clinic de Urgen Militar Central, secia Medical III
Febra de origine necunoscut (sau
sindromul febril prelungit), definit de
Petersdorf i Beeson n 1961, este
reprezentat de:
1) Febra documentat
(temperatura > 38.3C [101F]) la mai multe
determinri
2) Durata afeciunii mai mare
de 3 sptmni
3) Lipsa unui diagnostic dup o
sptmn de investigaii adecvate.
FON este cauzat de infecii (30-40%),
neoplasme (20-30%), boli de colagen i boli
granulomatoase (10-20%) i numeroase alte
cauze (15-20%). Datele din literatura de
specialitate relev faptul c n 4-15% din
cazurile de FON nu se poate stabili etiologia,
chiar dup examinri exhaustive.
Cele trei mari categorii de cauze ale
FON infecii, boli de colagen i boli
granulomatoase i tumori au rmas
nemodificate de la studiile clasice ale lui
Petersdorf i Beeson. Cu toate acestea,
tipurile de afeciuni care sunt incluse n aceste
categorii s-au modificat n ultimii 50 de ani.
De exemplu, lupusul eritematos sistemic, o
cauz frecvent de FON n trecut, este acum
mai uor diagnosticat prin testele serologice i
rareori se nscrie n cadrul FON. Afeciuni
care erau necunoscute sau insuficient descrise
cu cteva decade n urm, precum infeciile cu
HIV sau citomegalovirus, sunt cauze comune
de FON n zilele noastre. Multe boli care
cauzau FON n trecut (tumori, abcese) nu se
mai ncadreaz astzi n aceast categorie
datorit mbuntirii diagnosticului imagistic.
Cauzele de FON difer n cadrul
diferitelor grupe de pacieni. De exemplu,
sindroamele virale auto-limitate sunt cauze
rare de FON la pacienii vrstnici, dar arterita
temporal, tumorile i tuberculoza sunt mult
mai probabile n cazul persoanelor vrstnice
dect n populaia tnr.
Infeciile rmn cea mai frecvent cauz
de FON, constituind aproximativ o treime din
cazuri n studiile efectuate n ultimele cinci
decenii. Infeciile cel mai frecvent ntlnite
sunt abcesul, endocardita, tuberculoza,
osteomielita i infecia cu CMV.
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38
Abcesele au o frecven mai rar n
prezent datorit diagnosticrii precoce prin
metode imagistice.
Cele mai multe cazuri de endocardit
stafilococic sau streptococic sunt de
asemenea uor diagnosticate. FON apare mai
ales la pacienii cu endocardit cu culturi
negative datorit utilizrii necorespunztoare
a antibioterapiei sau organismelor dificil de
cultivat.
Tuberculoza trebuie ntotdeauna luat n
consideraie n cazul unei FON. Formele care
se prezint cel mai frecvent ca FON sunt
tuberculoza miliar i tuberculoza
extrapulmonar.
Unele infecii virale se pot prezenta ca
FON; cea mai frecvent cauz este infecia cu
CMV, dar i infeciile cu EBV sau HIV pot
avea o prezentare similar.
Tumorile erau considerate drept a doua
cauz de FON la aduli. Totui, n ultimele
studii, tumorile au avut o frecven de doar 7-
13% din cazurile de FON. Utilizarea de rutin
a tomografiei computerizate a condus la
diagnosticarea precoce a multor tumori, ceea
ce explic reducerea frecvenei acestei
categorii de afeciuni n etiologia FON.
Tumorile care se prezint cel mai frecvent
ca FON sunt malignitile hematologice, n
special boala Hodgkin i limfoamele non-
Hodgkin. Alte cauze mai rare sunt
reprezentate de mielomul multiplu i de
leucemii. Dintre tumorile solide, carcinomul
renal este cea mai frecvent cauz de FON;
mai rar pot fi ntlnite cancerul de colon,
hepatic, pulmonar sau cancerul de sn.
Mixoamele atriale sunt mai rar
menionate, probabil datorit utilizrii precoce
a ecocardiografiei transesofagiene.
Bolile de colagen, bolile granulomatoase
Studiile recente care au grupat bolile de
colagen i cele granulomatoase au evideniat
prevalena crescut a acestei categorii de
afeciuni fa de tumori n etiologia SFP.
Boala Still este cea mai frecvent cauz
de SFP la populaia sub 50 de ani; la pacienii
vrstnici arterita cu celule gigante i
polimialgia reumatic sunt cele mai frecvente
diagnostice.
Alte cauze de FON includ poliarterita
nodoas, crioglobulinemia, polimiozita,
sarcoidoza i boala inflamatorie intestinal cu
manifestri digestive minore.
Cauze diverse
Endocrine - Hipertiroidia i tiroidita subacut
sunt cele mai frecvente cauze endocrinologice
de FON
- Insuficiena adrenal este o
cauz rar, potenial fatal, de FON
Febra postmedicamentoas - cele mai
frecvente medicamente care pot cauza febr
postmedicamentoas sunt antibioticele de tip
betalactami, procainamida, izoniazida, chinidina
i difenilhidantoina. Oprirea administrrii
medicamentului suspectat conduce, n general,
la afebrilitate ntr-un interval de pn
la 48 de ore.
Bolile congenitale febra familial
mediteranean reprezint un diagnostic de
excludere
Alte cauze de FON:
emboli pulmonari periferici
tromboflebita ocult
hematoame neevideniate (de obicei
apar posttraumatic sau postoperator)
febra artificial - cel mai frecvent
ntlnit la adulii tineri cu experien
medical
FON nediagnosticat
Pacienii cu FON nediagnosticat au, n
general, o evoluie benign pe termen lung
(mai ales n cazurile n care febra nu se
asociaz cu scdere ponderal sau cu alte
semne ale unei afeciuni severe).
Scopul lucrrii
Evaluarea etiologiei actuale a febrei de
origine necunoscut pe un eantion de bolnavi
internai n secia Medical III SCUMC n
decurs de 24 de luni (ianuarie 2005 -
decembrie 2006).
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39
Metoda
Studiu retrospectiv n care au fost inclui
26 de pacieni care ndeplineau criteriile
Petersdorf-Beeson pentru FON, cu vrste
cuprinse ntre 18 i 66 ani (figura 1).
0
2
4
6
8
10
12
numar
pacienti
Figura 1- Distribuia pe varst
<20 ani
20-40 ani
41-60 ani
>60 ani


Algoritmul de investigaii a cuprins:
examen clinic, electrocardiogram, radiografie
toracic, ecografie abdomino-pelvin i
ecocardiografie transtoracic la toi pacienii.
Ecocardiografia transesofagian s-a efectuat
la 5 pacieni pentru confirmarea sau
infirmarea suspiciunii de endocardit ridicat
de examenul ecografic transtoracic.
Testele biologice uzuale, hemoculturi,
uroculturi, testare HIV i VDRL au fost
efectuate la toi pacienii. Unii pacieni au
necesitat teste biologice suplimentare (test la
procalcitonin, serologie CMV, EBV,
Borrelia burgdorferi, serologie pentru boli de
colagen AAN, ac anti ADN, FR, PCR,
complement).
n unele cazuri au fost necesare
investigaii paraclinice complexe: endoscopie
digestiv superioar, inferioar, computer
tomografie (torace, abdomen, pelvis),
rezonan magnetic (coloana vertebral).
Rezultate
Cele 26 de cazuri care s-au ncadrat n
definiia FON, au fost repartizate dup cum
urmeaz (figura 2):
infecii - 12 cazuri (infecie HIV - 2,
endocardite - 4, spondilodoscite - 4,
boal Lyme - 1, tuberculoz
peritoneal - 1);
neoplazii - 5 cazuri (cancer de colon 2,
prostatic - 1, ovarian - 1, leucemie cu
celule proase - 1);
boli de colagen - 2 cazuri (arterit
Takayashu, crioglobulinemie);
alte cauze - 5 cazuri (hipertiroidie/
tiroidite - 3, tromboz de sinus
cavernos - 1, alveolit alergic
extrinsec - 1);
nediagnosticate 2 cazuri.

Figura 2:Etiologia FON
46%
19%
8%
19%
8%
Infectii 12/26
Tumori 5/26
Boli de colagen
2/26
Alte cauze 5/26
FON
nediagnosticata

De remarcat c un procent important de
pacieni a primit tratament antibiotic anterior
internrii (prescris de ctre medicul de familie
sau n majoritatea cazurilor, autoadministrat)
cu toate c starea clinic general nu impunea
iniierea unui tratament antibiotic empiric
(figura 3). Aceast administrare nejudicioas
a antibioterapiei a condus la dificulti de
diagnostic n cazurile cu etiologie infecioas
(endocardite cu culturi negative, spondilodiscite).

Figura 3- Administrarea de tratament
antibiotic anterior internrii
58%
42%
Antibiotic 15
Fr antibiotic
11

Numrul mediu de spitalizri necesare
stabilirii diagnosticului (att n secia
Medical III ct i n alte uniti spitaliceti) a
Revista de medicin i psihologie aeronautic ___________________________ Volumul 12 Anul 2008 Nr. 2 (43)

40
fost de 1,7 (44 de internri pentru cei 26 de
pacieni) (figura 4). Numrul mediu de zile de
spitalizare a fost de 12,4 (547 zile pentru 44
internri n spital). Se poate uor observa
astfel ca FON reprezint o situaie clinic
mare consumatoare de timp i resurse.

Figura 4- Numrul de spitalizri
4%
15%
27%
54%
4 internri-1 caz
3 internari- 4
cazuri
2 internri- 7
cazuri
1 internare- 14
cazuri

Concluzii

FON reprezint o problem clinic
dificil, iar cauza poate fi greu de evideniat.
O evaluare diagnostic intensiv i raional
conduce de obicei la identificare majoritii
afeciunilor care se manifest iniial prin
FON. Investigaiile imagistice moderne
(ultrasonografia, examenul CT sau RMN)
precum i testele serologice sunt foarte utile
pentru identificarea bolilor care anterior erau
extrem de dificil de diagnosticat. Trebuie
reinut c FON este mai curnd cauzat de o
afeciune comun cu prezentare neobinuit
dect de o afeciune rar.
n unele situaii FON rmne
nediagnosticat chiar i dup evaluri
extensive. Aceti pacieni au de obicei o
evoluie benign pe termen lung, dar
urmrirea i reevaluarea sistematic sunt
eseniale. Nu sunt disponibile date care s
susin spitalizarea prelungit a pacienilor
care sunt clinic stabili i a cror investigare
este nondiagnostic.



Bibliografie

1. Barbado FJ, Vazquez JJ, Pena JM, et
al: Pyrexia of unknown origin: changing
spectrum of diseases in two consecutive
series. Postgrad Med J 1992 Nov.
2. Cunha BA: Fever of unknown origin.
Infect Dis Clin North Am 1996 Mar; 10(1):
111-27.
3. Chan-Tack K, Bartlett J: Fever of
unknown origin. Emedicine clinical reference,
2006 Mar.
4. Cunha BA: Fever of unknown origin
caused by adult juvenile rheumatoid arthritis:
the diagnostic significance of double
quotidian fevers and elevated serum ferritin
levels. Heart Lung 2004 Nov-Dec; 33(6):
417-21.
5. de Kleijn EM, van der Meer JW:
Fever of unknown origin (FUO): report on 53
patients in a Dutch university hospital. Neth J
Med 1995 Aug; 47(2): 54-60.
6. Ergonul O, Willke A, Azap A, Tekeli
E: Revised definition of 'fever of unknown
origin': limitations and opportunities. J Infect
2005 Jan; 50(1): 1-5.
7. Gaeta GB, Fusco FM, Nardiello S:
Fever of unknown origin: a systematic review
of the literature for 1995-2004. Nucl Med
Commun 2006; 27: 205-1.
8. Hirschmann JV: Fever of unknown
origin in adults. Clin Infect Dis 1997 Mar;
24(3): 291-300; quiz 301-2.
Revista de medicin i psihologie aeronautic ___________________________ Volumul 12 Anul 2008 Nr. 2 (43)

41
9. Kazanjian PH: Fever of unknown
origin: review of 86 patients treated in
community hospitals. Clin Infect Dis 1992
Dec; 15(6): 968-73.
10. Knockaert DC, Dujardin KS,
Bobbaers HJ: Long-term follow-up of patients
with undiagnosed fever of unknown
origin.Arch Intern Med 1996Mar25;
156(6):618-20.
11. Lopez Rodriguez M, Vazquez
Munoz E, Gomez Cerezo J, et al: [Cost-
effectiveness of computerized axial
tomography in the diagnosis of traditional
clinical picture of fever of unknown origin].
Rev Clin Esp 2005 Jan; 205(1):19-23.
12. Lortholary O, Guillevin L, Bletry
O: Fever of unknown origin: a retrospective
mulitcenter study of 103 cases, 1980-1988.
Eur J Intern Med 1992; 3: 109-20.
13. Luft FC, Rissing JP, White A,
Brooks GF: Infections or neoplasm as causes
of prolonged fever in cancer patients. Am J
Med Sci 1976 Jul-Aug; 272(1): 65-74.
14. Moret Ch, Meier P, Rotman S, et al:
[Fever of unknown origin with granulomatous
hepatitis, uveitis and acute renal failure].
Schweiz Rundsch Med Prax 2005 Jan 12;
94(1-2): 25-30.
15. Ozaras R, Celik AD, Zengin K, et
al: Is laparotomy necessary in the diagnosis of
fever of unknown origin? Acta Chir Belg
2005 Feb; 105(1): 89-92.
16. Petersdorf RG, Beeson PB: Fever of
unexplained origin: report on 100 cases.
Medicine (Baltimore) 1961 Feb; 40: 1-30.
17. Petersdorf RG: Fever of unknown
origin. An old friend revisited. Arch Intern
Med 1992 Jan; 152(1): 21-2.
18. Schattner A: The patient's history
remains a powerful tool in the diagnosis of
fever of unknown origin. Eur J Intern Med
2005 Feb; 16(1): 63.
19. Shoji S, Imamura A, Imai Y, et al:
Fever of unknown origin: a review of 80
patients from the Shin'etsu area of Japan from
1986-1992. Intern Med 1994 Feb; 33(2): 74-6.
20. Wagner AD, Andresen J, Raum E,
et al: Standardised work-up programme for
fever of unknown origin and contribution of
magnetic resonance imaging for the diagnosis
of hidden systemic vasculitis. Ann Rheum Dis
2005 Jan; 64(1): 105-10.





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

42



FEVER OF UNKNOWN ORIGIN

otcan Mihai M.D.
1
, Popescu Drago M.D.
1
, Copaci Iulian M.D.
2
, Enache Mihaela M.D.
2
,
Duescu Victor M.D.
2
, Jurcu Ciprian M.D.
2
, Rusu Cristinel M.D.
2
, Vasile Cornelia, nurse
1

SUMMARY

Despite advances in diagnostic tools, fever of unknown origin (FUO) remains a challenging
clinical problem. The internal medicine physician is often the first to confront this condition.
Frequently, a specialist in infectious diseases, rheumatology, or hematology is consulted. A series
of standard tests can often establish a specific diagnosis or at least the broad category into which the
diagnosis falls. In most cases, the cause of FUO is a familiar disease with an uncommon
presentation, rather than a rare disorder. The three major categories of causes of FUO - infections,
collagen vascular and granulomatous diseases, and tumors - remain unchanged.
Key words: fever, infections, neoplasms, collagen disease.


1
National Institute of Aeronautical and Space Medicine
2
Emergency Clinical Military Hospital
FUOs are caused by infections (30-40%),
neoplasms (20-30%), collagen vascular and
granulomatous diseases (10-20%) and
numerous miscellaneous diseases (15-20%).
The literature also reveals that between 4-
15% of FUO cases defy diagnosis, despite
exhaustive studies.
The three major categories of causes of
FUO - infections, collagen vascular and
granulomatous diseases and tumors--remain
unchanged from the classic studies of
Petersdorf and Beeson. However, the types of
diseases that are noted in these categories
have changed over the last 50 years. For
example, systemic lupus erythematosus
(SLE), a common cause of FUO in the past, is
now more easily diagnosed by serologic tests
and rarely qualifies as an FUO. Diseases that
were unknown or not well described several
decades ago, such as HIV and
cytomegalovirus (CMV) infections, are
causes of FUO today. Many diseases that
previously caused FUO (tumors, abscesses)
no longer attain this status because of
dramatic improvements in diagnostic imaging
in the last several decades. The causes of
FUO differ among various patient groups. For
example, self-limited viral syndromes are an
uncommon cause of FUO in older adults, but
temporal arteritis, tumors and tuberculosis are
more likely in older persons than younger
ones.
Infections remain the most common
cause of FUO, constituting about a third of
cases in various case series over the last five
decades. The infections noted most often are
abscesses, endocarditis, tuberculosis,
osteomyelitis and CMV infection. Abscesses
are diminishing in importance, because they
are discovered earlier in the workup for fever,
before the definition of FUO is met. Most
cases of typical staphylococcal or
streptococcal endocarditis are easily
diagnosed. FUO is more likely to be
encountered in patients who have culture-
negative endocarditis due to inappropriate
prior antibiotic use or difficult-to-culture
organisms.
Tuberculosis, although less common now
than half a century ago, must always be
considered as a cause of FUO. Miliary and
extrapulmonary tuberculosis are the most
likely forms to present as FUO.
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43
Several viral infections can produce
prolonged fever and present as FUO; of these,
CMV infection is the most common, but
Epstein-Barr virus (EBV) and HIV infections
are also causes of FUO.
Tumors have classically been the second
most common cause of FUO in adults.
However, in recent reports, they have
accounted for only 7% to 13% of FUO cases.
The routine use of computed tomography
(CT) has led to earlier diagnosis of many
tumors, and they are not as common a cause
of FUO as they once were.
Tumors that present most often as FUO
are hematologic malignancies, especially
Hodgkin's disease and other lymphomas.
Other hematologic malignancies, such as
multiple myeloma and leukemias, are less
common causes of FUO.
Among solid tumors, renal cell
carcinoma is most often noted to cause FUO;
much less commonly, hepatomas and cancer
of the colon and gastrointestinal tract, lung,
and breast can cause FUO.
Atrial myxomas are mentioned less
frequently as enigmatic causes of fever,
probably because of the earlier use of
transesophageal echocardiography than in the
past.
Collagen and granulomatous diseases
Recent reviews of FUO that have
grouped collagen vascular diseases and
granulomatous diseases together have found
this category to be a more common cause of
FUO than tumors. Still's disease is the most
frequent diagnosis in adults younger than 50
years; in older adults with FUO, temporal
arteritis is the most common diagnosis.
Other causes of FUO include polyarteritis
nodosa, cryoglobulinemia, polymyositis and
sarcoidosis.
Inflammatory bowel disease may present
as FUO with few abdominal or
gastrointestinal complaints.
Miscellaneous causes
Endocrine: Hyperthyroidism and subacute
thyroiditis are the 2 most common
endocrinologic causes of FUO
Adrenal insufficiency is a rare,
potentially fatal cause of FUO
Drug fever - although a wide variety of
drugs can cause drug fever, the most common
are beta-lactam antibiotics, procainamide,
isoniazid, quinidine and diphenylhydantoin.
Inherited diseases - familial Mediterranean
fever- is a diagnosis of exclusion
Other causes of FUO - peripheral pulmonary
emboli, occult thrombophlebitis, undiscovered
hematoma (after trauma)
Factitious fever - most commonly
encountered among young adults with health
care experience or knowledge
Undiagnosed FUO
Patients with undiagnosed FUO generally
have a benign long-term course (especially
when fever is not accompanied by weight loss
or other signs of a serious underlying disease)
Purpose of the study
Evaluation of the etiology of FUO for the
patients admitted with this diagnosis in the
IIIrd Medical Department of Central Military
Hospital between January 2005 and
December 2006.
Method
Retrospective study which included 26
patients with ages between 18 and 66 years,
fulfilling the Petersdorf- Beeson criteria for
FUO (figure 1).

0
5
10
15
patients
number
Figure 1- Age distribution
<20 years
20-40 years
41-60 years
>60 years

The algorithm of investigations comprised
clinical examination, electrocardiography,
thoracic radiography, ultrasonography of
abdomen and pelvis, and transthoracic
echocardiography for all the patients.
Transesofageal echocardiography was
performed in five cases for the confirmation/
infirmation of endocarditis suspicion raised
by the trans thoracic examination.
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44
The usual biological tests, hemocultures,
urocultures, HIV and VDRL tests were
performed for all the patients. Some patients
needed other biological tests procalcitonin
test, serology for CMV, EBV, Borrelia
burgdorferi, serology for collagen diseases-
ANA, AND ds, RF, CPR, complement).
In some cases complex paraclinical
investigations were needed: superior and/or
inferior endoscopy, CT (thorax, abdomen,
pelvis), MRI (for the spine).

Results

The 26 cases fulfilling the definition of
FUO were parted as follows (figure 2):
infections - 12 cases (HIV infection -
2, endocarditis - 4, spondilodoscitis -
4, Lyme disease - 1, peritoneal
tuberculosis - 1)
tumors/neoplasms -5 cases (colom - 2,
prostate - 1, ovary - 1, hairy cell
leukemia - 1)
collagen and granullomatous diseases
- 2 cases (Takayashu arteritis - 1,
crioglobulinemia - 1)
miscellaneous - 5 cases (hipertiroidy/
tiroiditis - 3, cavernous sinus
thrombosis - 1, extrinsec allergic
alveolitis - 1)
undiagnosed - 2 cases

Figure 2:Etiology of FUO
46%
19%
8%
19%
8%
Infections 12/26
Tumors 5/26
Collagen
diseases 2/26
Miscellaneous
5/26
Undiagnosed

We want to remark that an important
percent of the patients received antibiotic
treatment prior to admission in the hospital
(prescribed by the primary care physician or,
in the majority of cases, self administrated),
although the general clinical state did not
required empirical initiation of antibiotherapy
(figure 3). This injudicious administration of
antibiotherapy leaded to difficulties in
establishing the diagnosis in the cases with
infectious etiology (culture - negative
endocarditis, spondilodiscitis).
Figure 3- Administration of antibiotic
treatment prior to admition
58%
42%
Antibiotic 15
No antibiotic 11

The medium number of hospitalizations
needed for establishing the diagnosis (both in
the IIIrd Medical Department of CMH and in
other medical departments) was 1,7 (44
admissions for 26 patients) (figure 4). The
medium period of hospitalization was 12,4
days (547 days for 44 admissions). It is easy
to observe that FUO represents a time and
resources- consuming clinical situation.

Figure 4- Number of hospitalisations
4%
15%
27%
54%
4 admissions-
1 case
3 admissions-
4 cases
2 admissions-
7 cases
1 admission-
14cases

Conclusions:

FUO can be an evasive clinical problem
and its cause difficult to detect
An intensive and rational diagnostic
evaluation usually results in the identification
of the most serious diseases that initially
manifest as FUOs
Modern imaging techniques (eg,
ultrasound, CT scan, MRI) and serologic tests
help revealing diseases that used to be
extremely difficult to diagnose.
Problems may arise in some patients
whose FUO remains undiagnosed, even after
extensive evaluations. These patients usually
have a benign long-term course, but close
follow-up and systematic reevaluation studies
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45
are essential to avoid missing potential
etiologies. No evidence supports prolonged
hospitalization in patients who are clinically
stable and whose workup is unrevealing.
In most cases, the cause of FUO is a
familiar disease with an uncommon
presentation, rather than a rare disorder.


Bibliography

1. Barbado FJ, Vazquez JJ, Pena JM, et
al: Pyrexia of unknown origin: changing
spectrum of diseases in two consecutive
series. Postgrad Med J 1992 Nov.
2. Cunha BA: Fever of unknown
origin. Infect Dis Clin North Am 1996 Mar;
10(1): 111-27.
3. Chan-Tack K, Bartlett J: Fever of
unknown origin. Emedicine clinical reference,
2006 Mar.
4. Cunha BA: Fever of unknown origin
caused by adult juvenile rheumatoid arthritis:
the diagnostic significance of double
quotidian fevers and elevated serum ferritin
levels. Heart Lung 2004 Nov-Dec; 33(6):
417-21.
5. Kleijn EM, van der Meer JW: Fever
of unknown origin (FUO): report on 53
patients in a Dutch university hospital. Neth J
Med 1995 Aug; 47(2): 54-60.
6. Ergonul O, Willke A, Azap A,
Tekeli E: Revised definition of 'fever of
unknown origin': limitations and
opportunities. J Infect 2005 Jan; 50(1): 1-5.
7. Gaeta GB, Fusco FM, Nardiello S:
Fever of unknown origin: a systematic review
of the literature for 1995-2004.. Nucl Med
Commun 2006; 27: 205-1.
8. Hirschmann JV: Fever of unknown
origin in adults. Clin Infect Dis 1997 Mar;
24(3): 291-300; quiz 301-2.
9. Kazanjian PH: Fever of unknown
origin: review of 86 patients treated in
community hospitals. Clin Infect Dis 1992
Dec; 15(6): 968-73.
10. Knockaert DC, Dujardin KS,
Bobbaers HJ: Long-term follow-up of patients
with undiagnosed fever of unknown
origin.Arch Intern Med 1996Mar25;
156(6):618-20.


11. Lopez Rodriguez M, Vazquez
Munoz E, Gomez Cerezo J, et al: [Cost-
effectiveness of computerized axial
tomography in the diagnosis of traditional
clinical picture of fever of unknown origin].
Rev Clin Esp 2005 Jan; 205(1):19-23.
12. Lortholary O, Guillevin L, Bletry
O: Fever of unknown origin: a retrospective
mulitcenter study of 103 cases, 1980-1988.
Eur J Intern Med 1992; 3: 109-20.
13. Luft FC, Rissing JP, White A,
Brooks GF: Infections or neoplasm as causes
of prolonged fever in cancer patients. Am J
Med Sci 1976 Jul-Aug; 272(1): 65-74.
14. Moret Ch, Meier P, Rotman S, et
al: [Fever of unknown origin with
granulomatous hepatitis, uveitis and acute
renal failure]. Schweiz Rundsch Med Prax
2005 Jan 12; 94(1-2): 25-30.
15. Ozaras R, Celik AD, Zengin K, et
al: Is laparotomy necessary in the diagnosis of
fever of unknown origin? Acta Chir Belg
2005 Feb; 105(1): 89-92.
16. Petersdorf RG, Beeson PB: Fever
of unexplained origin: report on 100 cases.
Medicine (Baltimore) 1961 Feb; 40: 1-30.
17. Petersdorf RG: Fever of unknown
origin. An old friend revisited. Arch Intern
Med 1992 Jan; 152(1): 21-2.
18. Schattner A: The patient's history
remains a powerful tool in the diagnosis of
fever of unknown origin. Eur J Intern Med
2005 Feb; 16(1): 63.
19. Shoji S, Imamura A, Imai Y, et al:
Fever of unknown origin: a review of 80
patients from the Shin'etsu area of Japan from
1986-1992. Intern Med 1994 Feb; 33(2): 74-6.
20. Wagner AD, Andresen J, Raum E,
et al: Standardised work-up programme for
fever of unknown origin and contribution of
magnetic resonance imaging for the diagnosis
of hidden systemic vasculitis. Ann Rheum Dis
2005 Jan; 64(1): 105-10.

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46



POSIBILITI DIAGNOSTICE I EXPLORRI BIOCHIMICE
ALE FUNCIEI HEPATICE MODIFICATE

Dr. Florica Nftnil
1
, Dr. Mariana Jinga
2
, Dr. Florin Nftnil
2
, Dr. Maria Dumitru
1
,
Dr. Magdalena Vinescu
1

REZUMAT

Articolul prezent are n vedere dou situaii frecvent observate n practic, atunci cnd
ntlnim rezultate anormale ale testelor biochimice care investigheaz funcia hepatic. Lucrarea
i propune s prezinte posibile capcane ale investigaiilor paraclinice hepatice n particular
biochimice i sintetizarea investigaiilor suplimentare care s-ar justifica sau nu.

Cuvinte cheie: carcinom hepatocelular, steatoz hepatic non-alcoolic, boala de ficat gras,
hemocromatoz.


1
Institutul Naional de Medicin Aeronautic i Spaial
2
Spitalul Clinic de Urgen Militar Central
Steatoza hepatic non alcoolic (non-
alcoholic liver disease = NAFLD) este o
cauz comun de cretere a transaminazelor.
Unul din cinci pacieni cu steatoz hepatic
non-alcoolic (NASH = nonalcoholic
steatohepatitis) au semne histopatologice
necroinflamatorii i fibroz care poate evolua
spre complicaii ca ciroz i insuficien
hepatic sau carcinom hepatocelular.
Pacienii cu ficat gras alcoolic evolueaz
spre complicaii obinuite tip ciroz alcoolic,
dar au fost raportate i cazuri de decese
asociate cu interval Q-T lung i posibil
disfuncie autonom. Oricum, la pacienii cu
NAFLD i NASH, ntrebarea n legtur cu
intervalul prelungit QT ca i posibil cauz de
deces la aceti pacieni urmeaz s primeasc
rspunsuri dup studii aflate n desfurare.
Relativ frecvent n practic observm
rezultate anormale ale funciei hepatice la
pacienii investigai pentru afeciuni non-acute
(bilirubin, transaminaze, gamaglobuline)
ceea ce pune sub semnul ntrebrii necesitatea
i momentul efecturii unor analize
suplimentare.
Valorile anormale ale testelor hepatice
pot aprea i din alte motive dect afectarea
funciei hepatice i uneori este dificil a se
stabili situaiile care impun efectuarea
investigaiilor suplimentare i n special
secvenialitatea acestora.
O analiz a celor mai apreciate articole
despre practica medical publicate n Journal
of Clinical Pathology, relev existena unor
dovezi importante care susin respectivele
recomandri.
Indicarea investigaiilor suplimentare, n
cazul unor rezultate anormale la testele
hepatice, uzuale, este fundamentat, n
special, de studiile observaionale efectuate la
pacienii cu teste biochimice modificate i pe
rezultate obinute la biopsia hepatic.
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47

Tabel 1 - Investigaii recomandate n cazurile cu modificri ale testelor hepatice


Cel mai des n practica de zi cu zi
ntlnim pacieni cu valori crescute ale
enzimelor hepatice ( 2 3xN) i care se
asociaz cu modificri histologice relevate de
puncia hepatic (la noi practicndu-se n scop
diagnostic uzual doar n hepatopatiile cronice
virale).
Valori mari ale transaminazelor la un
pacient diabetic i/sau obez, fr infecie
viral hepatic, sunt datorate deseori steatozei
hepatice non-alcoolice, rezultat prin depunerea
de lipide, secundar hipertrigliceridemie i
rezistenei la insulin. Nu exist nici un
tratament medicamentos pentru steatoza
hepatic non-alcoolic, dar exerciiul fizic i
scderea n greutate amelioreaz rezultatele
testelor funcionale hepatice. Investigarea
unor astfel de pacieni pare s se bazeze, n
principal, pe identificarea cauzelor ce pot fi
tratate i pe ipoteza c stabilirea
diagnosticului de steatoz hepatic va
ameliora prognosticul i va permite tratarea
ulterioar.
Repetarea analizelor se justific n
cazurile care impun diferenierea unei
afeciuni stabile de una progresiv. Referitor
la intervalul dintre testri exist mai multe
ghiduri, ns puine dintre ele sunt bazate pe
dovezi. n cazul pacienilor asimptomatici i
situaia unei patologii cu caracter lent
evolutiv, se recomand ca n situaia unor
creteri moderate (pn la valori de dou-cinci
ori mai mari dect limita maxim a
normalului), testele s fie repetate la un
interval de 1 la 3 luni i nu mai devreme
(sptmni). Ceea ce este considerat normal
variaz n funcie de originea etnic i de
vrst; aceast confuzie poate fi rezolvat prin
stabilirea unor intervale specifice fiecrui
grup particular.
n continuare vom exemplifica modificri
ale testelor hepatice i 2 situaii diagnostice:

Cazul 1
C.M., sex masculin n vrst de 46
ani, diagnosticat n urm cu 4 ani cu diabet
zaharat tip II (echilibrat prin diet) i
hipercolesterolemie, fiind n tratament cronic
cu atorvastatin 20 mg/zi. De asemenea
pacientul recunoate consum zilnic, moderat
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48
de alcool. La o evaluare de rutin a prezentat
hemoglobina glicozilat 7,3, colesterol total
182 mg%, HDL-colesterol 41 mg%,
trigliceride 178 mg%, enzimele hepatice au
fost: ALAT: 252 ui/l, valori normale < 72 ui/l,
fosfataza alcalin 92 ui/l, bilirubina, proteine
tot. 7,4 g%, albumina 3,6 g%, fr alte
modificri biochimice (uree, creatinina, Na/K
normale).
Reevaluat dup 3 luni: ALAT 288
ui/l, fosfataza alcalin 80 ui/l, bilirubina
total, electroforeza normal, markeri virali
AgHBs, Ac anti HCV negativi, autoanticorpi
antimitocondroali, antinucleari - negative,
L1-antitripsina a avut valori normale,
sideremie 206 mg/l, feritina 1008 mg/l
(normal <250 mg/l). ndrumat ctre o clinic
de hepatologie biopsia hepatic a confirmat
diagnosticul de hemocromatoz cu fibroz
hepatic F3.
Discuii
Valorile anormale ale testelor
hepatice pot fi ntlnite n diverse afeciuni,
altele dect hepatice.
Ocazional, n practic, ntlnim
modificri ale testelor hepatice (bilirubina,
enzime hepatice crescute). Situaiile care
impun lrgirea investigaiilor suplimentare
sunt dificil de apreciat.
Valorile crescute ale transami-
nazelor la un diabetic sunt deseori datorate
steatozei hepatice chiar non-alcoolice,
rezultat din depunerea de lipide secundar
hipertrigliceridemiei i rezistenei la insulin.
ntr-o era a prescrierii tratamentului cu statine
se poate presupune c nivelul crescut al
transaminazelor poate fi datorat acestui
medicament, fapt nesusinut de studiile clinice
cu control statistic care urmreau efectul
cardio-protector al statinelor i care nu a
evideniat dect rar ascensionarea
transaminazelor dar nu la valori mai mari
de 1-2 xN.
Diabetul zaharat poate fi
manifestarea de debut a hemocromatozei la
20% din pacieni, ns cele doua afeciuni
coexist. n cazul steatozei hepatice alcoolice
sau non-alcoolice se asociaz frecvent
creterea feritinei i mai rar suprancrcare cu
fier, dei pot fi evideniate i depozite mici cu
fier intrahepatic. n tabelul 1 sunt prezentate
investigaiile care se recomanda n cazurile cu
modificri ale testelor hepatice.

Cazul 2
A.S. 32 ani, sex masculin se
prezint pentru stare febril de aproximativ 7
zile i stare general modificat.
Clinic obiectiv febril 38,2
o
C,
subicter conjunctival fr semne de faringita,
fr tuse, normal clinic i radiologic
pulmonar, fr alte modificri la examenul
clinic.
Biologic:HL: - hemoglobina 13,9 g%,
leucocitoza 10600/mm
3
cu limfocitoza
5500/mm
3
, bilirubina totala 2,8 mg%,
bilirubina indirect 2,5 mg%, frotiul periferic
evideniaz limfocite atipice, reticulocite
normale, enzime hepatice i restul testelor n
limite normale, VSH 29/57. ndrumat ctre
Spitalul de boli infecioase este diagnosticat
cu mononucleoz infecioas (Ac anti virus
Ebstein-Barr pozitiv) i nu s-a considerat
necesar continuarea investigaiilor.
Discuii
Infecia cu virusul Ebstein-Barr se
poate prezenta sub form de hepatit (valori
crescute ale transaminazelor, n special dup
vrsta de 20 ani sau se poate manifesta prin
hemoliza autoimun care asociaz valori
crescute ale bilirubinei neconjugate, creterea
lactat-dehidrogenazei, reticulocitelor i
modificri caracteristice frotiului periferic.
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49
Pacientul prezentat a beneficiat de
tratament simptomatic; reevaluat dup
2 sptmni era afebril, stare general bun,
iar din punct de vedere biochimic teste
normale cu excepia persistenei unei bilirubine
indirecte moderat crescute (1,3mg%) fiind
diagnosticat cu sindromul Gilbert.
Creterea bilirubinei neconjugate la
adult este puin probabil asociat unei
afeciuni hepatice deoarece majoritatea
proceselor obstructive sau hepatice sunt
nsoite de creterea bilirubinei conjugate sau
anomalii ale probelor hepatice.


n loc de concluzii

Cele mai multe teste hepatice
convenionale nu fac o evaluare a funciei, iar
majoritatea rezultatelor nu sunt specifice
pentru ficat.
Prezena sindromului Gilbert creeaz
premisele creterii izolate a nivelului
bilirubinei neconjugate. Valorile mari ale
transaminazelor (peste dublul valorilor
normale) apar frecvent n contextual afectrii
hepatice dovedite histologic i justific
efectuarea unor investigaii suplimentare.



Transaminazele cresc, cel mai frecvent,
secundar steatozei hepatice alcoolice sau non-
alcoolice, dar trebuie avute n vedere i alte
posibile etiologii.
La pacienii asimptomatici: valorile
enzimelor hepatice sunt crescute de aproximativ
3 ori peste nivelul maxim al normalului se
impune repetarea lor dup 1-3 luni.
Dac persist acest nivel la dou
determinri se impun investigaii suplimen-
tare (vezi tabelul 1).
La pacienii cu factori asociai de risc sau
manifestri clinice de boala hepatic: - se
recomand investigaii suplimentare (vezi tabel).



Bibliografie


1. Journal of Hepatology vol 18
nr.1 January 2008.
2. Green R.M.Flamns, AGA tehnical
review on the evalution of the liver functions
test, gastroenterology 2002.
3. Hearty Protection Study
Collaborative Group.
4. Smellie WSA, Forth J, Ryder Set
al. Best practice in primary care pathology-
J.Clin.Pathol.5-July 2006.
5. American Gastroenterological
Association medical position statement
Evaluation of liver Chemistry tests
Gastroenterology 2002.





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50



THE POSSIBLE WAYS OF DIAGNOSTIC AND BIOCHEMICAL
EXPLORATION OF MODIFIED HEPATIC FUNCTION

Florica Nftnil M.D.
1
, Mariana Jinga M.D.
2
, Florin Nftnil M.D.
2
,
Maria Dumitru M.D.
1
, Magdalena Vinescu M.D.
1


SUMMARY

This article brings to your attention two situations that are often observed in current practice,
when we meet abnormal results of biochemical tests which study the hepatic function. The
purpose of this article is to present the possible tricks of biology hepatic testes particularly the
biochemical ones- and to gather the supplementary investigations that will be or not justified.

Key words: hepatocellular carcinoma, non-alcoholic steatohepatitis, alcoholic fatty liver
disease, hemocromatosis



1
National Institute of Aeronautical and Space Medicine
2

2
Emergency Clinical Military Hospital
Non-alcoholic liver disease (NAFLD) is a
common cause of increasing the level serum
of amino/alanine transferase. One of five
patients that are suffering from non-alcoholic
steatohepatitis shows hystopatological
necroinflamatory signs and fibroses that can
develop complications such as cirrhosis,
hepatic failure and hepatocellular carcinomas.
Patients with fat alcoholic liver develop
ordinary complications such as alcoholic
cirrhosis, but it has been reported cases of
deceases associated with a long Q-T interval
(Quick time), and possible autonomies
dysfunctional. Anyway, at the patients with
NAFLD and NASH exist the possibility that a
long Q-T interval to be a cause for decease,
but the answer will be given when current
ongoing studies will be completed.
Relatively frequent, in current practice it
has been noticed abnormal results of
hepatic functions to patients investigated for
non acute diseases (total bilirubin,
gammaglobulines, aminotransferases) which
rise the question of the proper time and
necessity of performing supplementary
investigations.
Abnormal values of hepatic tests can be
determined by other reasons than malfunction
of hepatic function and, sometimes, it is
difficult to establish situations when
supplementary investigations are required,
and the sequence of these investigations.
A review of one of the best known
articles about medical practice, published in
The Journal of Clinical Pathology, shows the
existence of important evidences in support of
the recommendations mentioned above.
Using supplementary investigations, in
case of abnormal hepatic usual tests results, is
of a crucial importance, especially for
observational studies are done to the patients
with modified values of biochemical test, and
based on results obtain from hepatic biopsy.
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51
Table 1 The recommended investigations in the patients
with modified hepatic laboratory tests

Test Normal results Interpretation
First investigation
recommended

haemoleucogram Macrocitosis



Trombocitopeny
Suggest excessive
consumption of alcohol if
glutamil transferasis is
increased
Possible hypersplenism
(portal hypertnesion)
Autoantibodies AMA positive, IgM ASM or

ANA positive, IgG
Probable incipient biliar
ciroses
Suggest autoimun hepatic
Ferititine High Possible hemocromatosis,
ask investigation
Antigen HBs Positive Probable chronic infection
Antibodies anti-hepatitis C Positive Possible chronic infection
If no diagnosis was
established

Hepatic echography Hepatic mass or.. Tumor/caliculi
Antibodyes anti-
endomisium
Positive Suggest celiac disease





Most often patients meet on daily basis
have a high level of hepatic enzymes (approx
2-3xN) associated with evident histological
modifications revealed by hepatic function (in
our case, this is usually used only for
diagnosis of chronic viral hepatitis).
In many cases, high values of
amino/alanine transferase to a patient diabetic
and/or overweight, without viral hepatic
infection, are due the fact that, non-alcoholic
steatohepatitis, are resulted from lipids
deposits, secondary hypertriglycerides and
insulin resistance. There is no drug treatment
for non-alcoholic steatohepatitis, but physical
exercises and weight loosing can improve the
of results hepatic functional tests.
Investigations of such patients seems to be
based, mainly, on the identification of causes
that can be healed, and on the presumption of
establishing the steatohepatitis diagnosis will
improve the chances and will allow later
treatment.
Repeating the analysis is justified in
cases where is needed to make a clear
difference between stable affections and
progressive ones. There are many guides for
establishing the interval between tests, but
most of them have no practical support. In
case of patients with low level of pathological
evolution (up to 2 5 times of maximum
normal), it is recommended that tests to be
repeated not earlier than 1 to 3 months. The
normal values depend on the age and ethnical
origin; this confusion can be solved by
establishing specific intervals for each
particular group.
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52
We will exemplify changes of hepatic
tests in 2 cases:

Case 1
CM, male, 46 years old, diagnosed
4 years ago with diabetes type II, stabilized
through diet and hypercholesterolemia,
treated with atorvastatine 20mg/day, daily
moderate alcohol consumption. On a routine
investigation there were the following results:
glicozidic haemoglobine 7, 3; total cholesterol
182 mg%, HDL-cholesterol 41 mg%,
triglyceride 178%, hepatic enzyme: ALAT:
252 ui/l, normal values<72 ui/l, alkaline
phosphates 92 ui/l, total bilirubin, total
proteins 7,4%, albumine 3,6%, with no other
biochemical modifications (urea, creatinin,
Na/K normal);
Reevaluation after 3 months:
ALAT 288 ui/l, alkaline phosphates 80 ui/l,
total bilirubin and normal electoforeyis, viral
markers HBsAg, Ac, HCV negative,
antimitocondrial/ antinuclears autoantibodies
negatives, L1 - normal antitripsine, serum
iron 206, ferritin 1008 mg/l (normal values <
250 mg/l). Sent to a hepatic clinic hepatic
biopsy confirmed diagnosis of
hemocromatosis with hepatic fibrosis F3.

Discussion
Abnormal values of hepatic tests
can be meeting in many diseases, other than
hepatic ones. Occasionally we can meet
changes of hepatic tests (bilirubine, high
values of hepatic enzymes), which requires
supplementary investigations.
High level of transferases to a
patient with diabetes is often due to alcoholic
or even non-alcoholic steatohepatitis, resulted
from lipids deposits, secondary
hypertriglycerides and insulin resistance. In a
period with statines treatment we can assume
that high level of transaminases occurs
because of this medicine (drug), but this
option has not been confirmed yet by any
clinical studies statistic controlled for
discovering the cardio-protection effect of
statines. These studies underlined that very
rare transferases level was increased, but not
more that 1 -2 x N.
The diabetes can be the first of
haemocromotosis, as was noticed at 20% of
the patients, but the two diseases can exist
together. In alcoholic or non-alcoholic
steatohepatitis cases, frequently can be notice
increase level of ferritin and, rarely, high level
of iron, but sometimes can be discovered
small deposits of intra hepatic iron. In table
are presented recommended investigations in
cases of changes the hepatic tests.

Case 2
A.S 32 years old, male, has showed
up with fever over the period of seven days
and changes in general healthy status;
Clinic objective fever of 38.2
0
C,
conjunctival subicter with no signs of
faringitis, no coughing, clinical and
radiological normal, and no other changes at
clinical exam;
Biological: haemoglobine 13.9%,
leucociytoses 10600/mm
3
, lymphocytoses
5500/mm
3
, total bilirubin 2.8mg%, indirect
bilirubin 2.5 mg%, peripheral blood shows
atypically lymphocytes, normal retyculocites,
hepatic enzymes and the rest of the test within
normal limits, VSH 29/57. It was directed to
Infectious Diseases Hospital, where he was
found with infectious mononucleosis (Ac anti
Ebstein-Barr positive) and not further
investigations were done.

Discussion
The infection with Ebstein-Barr
virus can be meeting as hepatitis (high level
of transferases, especially after age of 20) or
by autoimun hemolizys, that associates
increased values of indirecte bilirubin,
increase values of lactate-dehidrogenasys,
retyculocitis and changes of characteristics of
peripheral blood frotilium.
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53
Symptomatic treatment was given
to the patient; the evaluation performed after
2 weeks has shown no sign of fever, normal
values of biochemical tests, with the
exemption of an increased level of indirect
bilirubin (1.3%)- being diagnosed with
Gilbert syndrome.
At adult people, increased level of
indirecte bilirubin is not likely to be
connected with a hepatic disorder because
the majority of obstructive or hepatic
processes are associated with high level of
conjugate bilirubin are abnormal values of
hepatic tests.

Conclusions

Most of conventional hepatic tests do not
make an evolution of function, and majority
of results are not specifically for liver.
The presence of Gilbert syndrome makes
chances for isolate increase of the level of
indirecte billirubin. High level of transferases
(double than normal values) is frequently
connected with a hepatic malfunction,
histological confirmed, and justify further
investigations.
Normally high values of transferases are
associated with secondary hepatic steatosis
alcoholic or non-alcoholic, but other
etiologies should be considered as well. At
asymptomatic patients: values of hepatic
enzymes are 3 times higher than maximum
level of normal ones and these should be
repeated after 1 3 months. If this high level
persists after the second test, further
determinations are required (see table).
Further investigations are recommended to
the patients with risk factors or clinical signs
of hepatic disease (see table).



Bibliography

1. Journal of Hepatology vol 18
nr 1 January 2008.
2. Green R.M. Flamns, AGA
technical review on the evaluation of liver
functions tests, gastroenterology 2002.
3. Hearty Protection Study
Collaborative Group.
4. Smellie WSA, Forth J, Ryder Set
al. Best practice in primary care pathology
J. Clin. Pthol.5 July 2005.
5. American Gastroenterological
Association medical position statement
Evaluation of liver Chemistry tests -
Gastroenterology 2002.
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54



INTERVENIA PSIHOLOGIC DE SUPORT
N STRESUL TRAUMATIC
- METODE DE REDUCERE A REACIILOR LA STRES -

Psih. Doina Trandafir
1


REZUMAT

Stresul postraumatic (posttraumatic stress disorder, PTSD) este o entitate clinic ce descrie
un complex de reacii i triri psihice consecutive supunerii la un incident critic (eveniment
traumatizant). Nu oricine triete o traum dezvolt PTSD ns majoritatea oamenilor are nevoie de
asisten psihologic pentru a face fa situaiei. Pentru a preveni instalarea simptomelor de stres
postraumatic se cere intervenia, n primele 72 de ore de la evenimentul traumatizant, cu ajutorul
unor tehnici simple cu caracter nonterapeutic, adresate unor persoane normale aflate n situaii
anormale. Numeroase studii arat beneficiile unor astfel de intervenii.
Cuvinte cheie: Posttraumatic Stres Disorder, stres traumatic, debriefing, defusing.


1
Institutul Naional de Medicin Aeronautic i Spaial
Pe data de 2 august 2005, de pe
aeroportul Charles de Gaulle din Paris,
decoleaz cursa Air France 358, cu destinaia
Toronto, avnd la bord 297 pasageri. Avionul,
un Airbus A-340, este una din cele mai sigure
aeronave din lume, lansat n 1993, foarte
fiabil; are de parcurs cteva mii de km
distan. Zborul dureaz 8 ore. Alain Rosaye,
pilot comandant, 57 ani, lucreaz de peste 20
de ani la Air France. Este secondat de
Frederic Naud, copilot, 43 ani.
Cu cteva minute nainte de ora 14,
comandantul efectueaz decolarea.
Era o zi superb, soarele strlucea, cerul
era albastru, norii erau albi...o zi splendid
(Joann, pasager).
Eram servii ireproabil, mncarea era
excelent, nsoitorii de bord erau foarte buni
(Eddie, pasager).
Zborul este unul obinuit. Dirijarea se
trece pe pilot automat. Buletinul meteo anun
nori la Toronto, ploaie, posibil furtun. Ceva
mai trziu, un alt raport meteo informeaz c
pe aeroportul din Toronto s-a declarat alert
roie (furtun, ploaie, pericol de fulgere).
Aterizarea este ntrziat. Avionul intr pe
culoarul de ateptare. Furtun violent la
Toronto. Fulgerele pun n pericol aterizrile.
nainte de cursa Air France, 2 avioane
aterizaser pe aceeai pist. Piloii primesc
informaia c se frneaz greu. Se pregtete
aterizarea.
Se ntuneca tot mai mult, parc eram
ntr-o mare de fulgere ce loveau n fiecare
secund n jurul nostru. Pasagerii ncepeau
s aib emoii, inclusiv eu. Coborrea pentru
aterizare a fost de comar. Eram nconjurai
de fulgere, turbulenele erau enorme, se
simea cum pilotul se lupt s menin
avionul pe poziie pentru a ateriza. Fiului
meu i era fric iar fata noastr era departe
de noi (Philippe, pasager).
Mi-am legat i mai strns centura,
ateptndu-m la o aterizare dur, ca pilotul
s nfig avionul pe pist sau s decoleze
din nou, fiindc mi-am dat seama c
aterizarea nu va fi una normal. Aceast
aterizare a fost mai intens i mai dur din
toate cte am trit (Joann).
A fost o aterizare foarte dificil. Lumea a
nceput s aplaude. in minte ca doamna de
lng mine a zis: ce aterizare uimitoare!.
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55
Imediat dup ce a terminat propoziia s-a
instaurat haosul. (Eddie)
La cteva minute dup contactul cu solul,
la 146 km/h, cursa 358 depete pista.
Pasagerii sunt puternic zglii. Se aude:
Foc! Evacuai imediat avionul!. Se
instaureaz panica. Fumul i flcrile se
rspndesc rapid.
n acel moment am crezut c vom muri cu
toii. Era clar, nimeni nu avea cum s
supravieuiasc. Toi eram siguri c avionul
va exploda. (Philippe)
Pasagerii sar dei sunt aproape de flcri
i de fumul motorului. Plou.
Nu aveai alternativ, dect s sari. Mi-
am spus rapid o rugciune, am nchis ochii,
am srit. (Eddie)
Echipele de intervenie ajung n
52 secunde, dar din cauza focului nu se pot
apropia prea mult. Nu se vede mai nimic din
cauza ploii. Fragmente desprinse din avion:
roi, poriuni de arip.
Nu-mi venea a crede ochilor. Am vzut
bagaje i alte lucruri aruncate n aer. Mi-am
dat seama c puteam s avem i noi aceeai
soart (Phillipe).
Avionul este cuprins de flcri. Pasagerii
se ndeprteaz. Confuzie. Sunt uzi i murdari
de noroi. Unii plngeau, alii i cutau rudele
i prietenii.
Eram 25- 30 de oameni. M-am ntrebat:
doar atia am supravieuit?(Joann)
Angajaii aeroportului ncearc s dea de
urma celor prezeni la bord.
Timp de or rudele au crezut c am
murit. Noi eram cuprini de panic, speriai
de moarte. Cnd ne-am revzut ne-am simit
norocoi. Am simit c am cptat o nou
ans. A fost un moment frumos, emoionant
(Philipe).
Buletinul de tiri anun la scurt vreme
c toi pasagerii cursei 358 au scpat cu via.
Au fost clipe de comar dar i un adevrat
miracol.
*
Dac ne-am fi aflat n acel avion, cu
siguran lectura textului de mai sus ne-ar fi
produs amintiri neplcute, chiar nsoite de
unele simptome fizice i mentale. S-a
constatat c 80% din cei ce sufer impactul
unui incident traumatic dezvolt reacii
cognitive, fizice sau emoionale n 24 h dup
eveniment. Fr intervenia de suport psihic,
n 22% din cazuri acestea se prelungesc de la
6 luni la 1 an. 4% din tulburrile de stres
posttraumatic duc la incapacitare
profesional.
Stresul postraumatic (posttraumatic
stress disorder, PTSD) este o entitate clinic
ce descrie un complex de reacii i triri
psihice consecutive supunerii la un incident
critic (eveniment traumatizant). Acesta poate
fi orice situaie cu efect negativ asupra strii
fizice, cognitive, emoionale i comportamen-
tale, care are un caracter neobinuit i apare
brusc. n aviaie, astfel de evenimente
traumatice pot fi accidente i incidente
nsoite de rnii i/sau pagube materiale,
participarea la aciunile de investigare a unui
accident etc. n mediul non-aeronautic, PTSD
poate fi declanat de violene grave, abuzuri,
accidente, moartea neateptat a unei
persoane apropiate, catastrofe naturale .a.
Nu oricine triete o traum dezvolt
PTSD. Unii oameni gsesc sprijin la prieteni,
familie, biseric. Majoritatea ns are nevoie
de asisten psihologic de specialitate. Pentru
a preveni instalarea simptomelor PTSD

se
cere intervenia, n primele 72 de ore de la
evenimentul traumatizant, cu ajutorul unor
tehnici simple cu caracter nonterapeutic,
adresate unor persoane normale aflate in
situaii anormale. Din datele furnizate de
Eurocontrol reiese c efectele a dou

pentru a diagnostica PTSD, durata tulburrilor psihice


trebuie s fie mai mare de o lun (DSM-IV)
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56
accidente similare (ca numr de victime i
amploare), au fost diferite n funcie de
acordarea suportului psihic imediat
consecutiv evenimentului critic, astfel:
n 1978, fr suport psihic, au existat
29 pierderi, i 31% apeluri la servicii de
sntate mental; n 1986, cu suport psihic,
s-au nregistrat o singur pierdere i
1% apeluri la servicii specializate.
Principala problem a implementrii
programelor de suport in situaii de stres
posttraumatic o constituie prejudecile din
rndul profesionitilor (prejudeci generate
n mare parte de orgoliul profesional i de
experiena de ignorare a problemelor). Cele
mai frecvente prejudeci sunt:
programele de suport psihic se
adreseaz doar celor implicai n eveniment.
De fapt, reaciile de stres traumatic apar i la
martori (controlori de trafic aerian, persoane
din echipele de intervenie);
oamenii devin mai puin vulnerabili
pe msur ce se confrunt cu evenimente
traumatice. n realitate, incidente repetate pot
crete probabilitatea de a dezvolta reacii de
stres traumatic;

relativizarea i minimizarea
evenimentului au efect pozitiv. Formulri de
genul ai avut noroc, putea fi mai ru
produc n realitate durere, iritare, suferin.
cei care reacioneaz calm pe
durata unui accident traumatic risc mai puin
s dezvolte reacii de stres traumatic. Acest
lucru nu este de fapt o garanie pentru evoluia
viitoare. O mam ce acord primul ajutor
copilului su poate claca imediat ce situatia
copilului devine sigur;
discuiile legate de un incident
critic anterior nrutesc situaia. Realitatea
este c reaciile de stres traumatic nu se evit
prin evitarea confruntrii cu emoiile generate
de acesta. Adesea acest tip de stres se
consider risc profesional i se crede c e mai
bine s te ntorci ct mai repede la lucru. Un
pilot, dup un zbor de noapte cu incident
tehnic - aterizare fr aparatur de bord - a
fost pus de eful su pe planul de zbor pentru
a doua zi. Nendrznind s refuze, a efectuat
acel zbor (fr nici un fel de incident) dar a
recunoscut: acel zbor a fost cel mai greu din
viaa mea. Dac ar fi aprut o problem, cu
greu a fi fost n stare s-i fac fa.
Evaluarea psihologic i implicit
intervenia de suport dup un eveniment
traumatizant se realizeaz n trei etape
(vezi Fig.1).

Fig. 1. Fazele evalurii persoanelor afectate de catastrofe (sursa: tefnescu, 2008).




Impact
catastrof
Faza
imediat
Faza
acut
Faza
sechelelor
Echipele de salvare
Promptitudine
Proximitate
Simplitate
Echipele de profesioniti n sntate mental
Intervenii posterioare
Locaii specifice
Tehnici specifice
Persistena
simptomatologiei
Prevenirea
sechelelor
posttraumatice
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57
Imediat dup incidentul critic, persoana
este ndeprtat de locul evenimentului.
Echipele de salvare asigur primul ajutor,
fiind focalizate pe urgenele vitale.
Prevenirea apariiei PTSD ncepe cu
interveniile profesionitilor n sntate
mental, din faza acut de stres, avnd drept
obiectiv restabilirea echilibrului psihic.
Filozofia acestor tehnici se bazeaz pe ideea
c o intervenie rapid poate mpiedica
dezvoltarea unei patologii ulterioare.
n aceast etap, intervenia poate fi de
tipul unu-la-unu sau de grup. Alegerea
aparine consilierului, care ine cont de timpul
scurs de la eveniment, factori culturali,
personalitatea celor implicai, compatibilitatea
lor etc. Cele dou tipuri de tehnici urmeaz
acelai principiu de baz: discutarea cu
victima, pentru a diminua impactul crizei.
Principala diferen dintre tehnicile amintite
este aceea c tehnica unu-la-unu ofer
posibilitatea gsirii unei soluii particularizate
la caracteristicile individuale ale persoanei n
cauz, n timp ce sesiunile de grup pun
accentul pe normalizarea experienelor trite
(prin faptul c participanii la discuii i
mprtesc gnduri i emoii similare).
Tehnicile de grup se adreseaz unui
numr de minim trei persoane care au trit
experiena aceluiai incident critic.
Principalele intervenii sunt cunoscute sub
denumirile de defusing i debriefing.
Termenul defusing (de la eng. defuse,
dezamorsare) se refer la procesul de
dezactivare a unei bombe emoionale
(situaia exploziv). Acesta permite victimelor
s ventileze emoiile legate de dezastrul prin
care au trecut (amintiri, pierderi, metode de a
face fa situaiei). Aceast ventilare are loc
ntr-un mediu securizat i suportiv. Procesele
de defusing implic n mod obinuit edine
imediate informale realizate ad-hoc. Deoarece
timpul alocat acestor ntlniri este adesea prea
scurt, edinele de defusing reprezint doar un
punct de plecare. Sunt necesare intervenii
ulterioare, care pot consta fie n simpla oferire
de suport psihologic (grupuri de terapie
suportiv), fie n programe elaborate i
formale de debriefing.
Durata unei edine de defusing este
de 20 pn la 60 de minute i se adreseaz de
obicei unor grupuri mai mici dect n cazul
debriefingului. Etapele generale urmrite
sunt: prezentarea participanilor la discuie,
explorarea faptelor i gndurilor asociate,
enumerarea simptomelor i reaciilor i
normalizarea acestora. Se pot recomanda
consilieri ulterioare.
Defusingul nu este o form de tratament
ci mai degrab un mod de ncurajare i
clarificare a persoanei n cauz.
Debriefingul psihologic este adesea un
prim pas bun pentru a ajuta persoanele
implicate n evenimente traumatice. Este
vorba de ntlniri formale, individuale sau n
grupuri mici, n general la scurt timp dup un
incident critic, cu scopul precis de a aborda
reziduurile emoionale consecutive incidentului
critic. Debriefingul poate fi desfurat n orice
loc, suficient de ncptor i care poate
asigura intimitatea. Durata unei edine poate
fi de pn la cteva ore.
Este bine ca, ori de cte ori este posibil,
orice individ aflat n criz s beneficieze de
debriefing. Multe organizaii recomand sau
chiar cer sesiuni de debriefing sau defusing
consecutiv apariiei unui incident. Crucea
Roie american ofer, de pild, astfel de
servicii.
Exist cteva modele de debriefing.
Organizaii precum NOVA (National
Organization for Victim Assistance) prefer
un model de debriefing prin care se instruiete
personalul din echip i voluntarii. Dei
modelele de debriefing difer ca numr i tip
de faze (stadii), ele se bazeaz pe aceleai
elemente de baz, adresndu-se tuturor
aspectelor care alctuiesc ceea ce numim
reacie normal la stres (elemente de vz, auz,
gust, gnduri, emoii, amintiri).
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58
n tabelul de mai jos am rezumat principalele etape de intervenie de tip debriefing i
momentele aferente acestora.

Tabelul 1. Etape ale debrifingului.

ETAPE MOMENTE NTREBRI
Prezentare
Se prezint membrii echipei, se anun scopurile i
regulile de desfurare. Scop: destinderea atmosferei,
crearea unui climat de ncredere i cooperare.

cine suntem?
Fapte

ce s-a ntmplat, care este
evenimentul critic?
care a fost rolul tu n raport
cu evenimentul?
Gnduri ce ai gndit n acel moment?
Reacii

care a fost prima reacie? ce
ai simit? care a fost cel mai
ru moment?
Explorare
Simptome (cognitive, emoionale, fizice,
comportamentale)

ce simptome au aprut?
nvminte
Se explic normalitatea reaciilor i
anormalitatea situaiei
ce ai nvat din aceast
situaie?
Informare
Revenire (reinserie)
Sinteza celor discutate, rspunsuri la
ntrebri, recomandri



Principalele avantaje ale debriefingului
sunt: explicarea nenelegerilor, recunoaterea
emoiilor negative, schimb de experien,
suport interpersonal, sprijin pentru depirea
momentelor critice, mbuntirea comunicrii
n echipaj, creterea coeziunii grupului,
pregtirea pentru noi situaii.
Au fost dezvoltate diverse programe de
intervenie n stresul postraumatic. Dintre
cele mai cunoscute, amintim:
After Action Stress Debriefing - program
iniiat de aviaia militar german, se
adreseaz echipajelor ce revin din misiuni de
lupt. Este un prim ajutor psihologic n
mediul operaional, avnd ca scop
compensarea emoional. Debriefingul este
asigurat de echipe n componena crora intr
psihologi, medici, comandani, preoi.
Intervenia urmeaz civa pai:
explicarea scopului i regulilor, reconstrucia
verbal a evenimentului, obinerea unui
consens de grup despre ce s-a ntmplat,
restaurarea responsabilitii, validarea
tririlor, prevenirea acuzaiilor, evocarea
manifestrilor emoionale, nvminte.
Critical Incident Stress Debriefing -
program propus de Eurocontrol pentru
acordarea asistenei controlorilor de trafic
aerian confruntai cu situaii critice. n
maximum 3 ore au loc discuii ce vizeaz
eliberarea emoional. Etapele sunt similare
modelului anterior, urmrindu-se trecerea de
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59
la nivelul cognitiv al analizei la cel emoional.
Consilierii sunt alei din rndul colegilor
controlori de trafic, pe baza unor caliti
precum experien profesional, capacitatea
de ascultare i nelegere, maturitate i
echilibru psihic s.a.
La finalul sesiunilor de defusing i
debriefing pot fi recomandate intervenii
psihologice specifice (n faza sechelelor) ce se
bazeaz n principal pe abordri cognitiv-
comportamentale, care vor face subiectul unor
abordri ulterioare.

n concluzie, se remarc necesitatea unui
prim ajutor psihologic, n cazul apariiei unui
eveniment traumatic (prin tehnici de defusing
i debriefing), n vederea reducerii riscului de
apariie a PTSD. Nefiind tehnici terapeutice,
acestea pot fi nsuite cu uurin de consilieri
pregtii special pentru astfel de intervenii.
Una din nemulumirile pasagerilor care trec
printr-un astfel de eveniment este dat de
neacordarea acestui ajutor. n exemplul de la
nceputul articolului, unul din pasageri
remarca totala lips de organizare i faptul c
nimeni nu ne spunea ce s-a ntmplat, nimeni
nu s-a ocupat de noi. Efortul pentru a asigura
intervenia psihologic n faza acut este
minor n comparaie cu beneficiile aduse, att
pentru persoanele implicate ct i pentru
companie (de transport aerian, n acest caz).



Bibliografie

1. Eurocontrol (2005), Critical
Incident Stress Management prezentarea
tehnicii la Bucureti, februarie.
2. Holdevici, I., Licu, M. (2004),
Asistena psihologic n tulburarea de stres
postraumatic. Metode de intervenie
terapeutic, n Psihologie aplicat n forele
armate, Ed. Universitii Naionale de
Aprare, Bucureti, 2004 (p. 87-102).
3. Popa, M. (2005), Psihologie
aeronautic, Ed. Universitar Carol Davila,
Bucureti.
4. tefnescu, D. (2008), Curs de
intervenie psihologic n situaii de stres
postraumatic (material nepublicat).
5. Cazul prezentat a fost preluat din
documentarul Clipe de comar difuzat pe
Discovery Channel.





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60



PSYCHOLOGICAL SUPPORT IN CASE OF TRAUMATIC
STRESS - METHODS FOR STRESS REACTIONS REDUCING -

Doina Trandafir, psychologist
1


SUMMARY

Posttraumatic stress disorder (PTSD) is a clinical disorder made of psychological reactions
consecutive of a critical event exposure. PTSD is not necessarily the result of some trauma. People
can find support in friends, family or Church. Still, many of them need specialized psychological
assistance. In order to prevent the appearance of PTSD symptoms, intervention is needed within 72
hours from the traumatic event, by means of simple non-therapeutic techniques on normal persons
confronted with abnormal situations. Many researches show the benefits of these interventions.

Keywords: Posttraumatic Stress Disorder, traumatic stress, debriefing, defusing.


1
National Institute of Aeronautical and Space Medicine
On 2 august 2005, from Charles de
Gaulle airport took off an Air France airplane
with 297 passengers with Toronto destination.
Airbus A 340 is one of the securest planes,
released in 1993, very reliable. Period of the
flight: 8 hours. Alain Rosaye, pilot, 57 years
old, has a 20 years fly experience. Copilot
was Frederic Naud, 43 years old.
Few minutes before 2 a.m., the plane took
off.
It was a wonderful day, the sun was
shining, the sky was blue, the clouds were
white...a splendid day (Joann, passenger).
We were impeccable served, the food was
great, the stewards was very good (Eddie,
passenger).
The flight was a ordinary one. Automatic
pilot is on. Weather forecast announces
clouds in Toronto, rain, possible storm. Later,
another weather report informs red alert on
Toronto airport (storm, rain, lightings).
Landing is delayed. The plain is waiting for
landing permission. Toronto is under a violent
storm in. The lightning put the landings into
danger. 2 planes have landed on the same
runway before the Air France aircraft. Pilots
are informed about landing difficulties.
The sky was darken and darken. It seems
like we were in a sea of lightings. The
passengers were excited, me as well. The
descend was like a bad dream. We were
surrounded by lights, turbulences was
prodigious. We all felt the pilot s difficulty to
maintain the position of the plane. My son
was terrified and my daughter was far from
us (Philippe, passenger).
I tight my belt and I was sure that could
be a harsh landing. I was expecting a new
take off because I realized that the landing
could t be a common one. That landing was
severest I lived (Joann).
The landing was very difficult and the
passengers acclaimed. I remember that lady
next to me said: what amazing landing! Right
after that the chaos established (Eddie).
Few minutes after the ground contact,
with 146 km/h speed, the airplane get out of
the runway. The passengers were violent
shaken. Somebody cried: fire! Get out
immediately! The fire and flames are fast
spreaded.
In those moments we thought we die.
Nobody was able to survive, that was for sure.
We all were undoubted of explosion (Philippe).
The passengers were next to the fire of
the engine. It was raining.
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We had no choice beside to plunge. I said
a prayer, I closed my eyes and I jumped
(Eddie).
The intervention team arrived in 52
seconds but fire disable approaching. I saw
thins flying in the air and I realized that we
could suffer the same (Philippe).
The plane was on fire. Everybody was
confused. People were wet and dirty. Some
was crying, some were looking for their
relatives and friends.
About a half an hour our relatives
considered us to be dead. We were alarmed
and scarred of death. When we met our
friends and relatives we felt lucky. I thought I
was gifted with another chance (Philippe).

*

If we were in that plane, reading the
upper text would bring unpleasant memories
for us, for sure, even some physical and
mental symptoms. It was shown that in 80%
of cases, people who suffer a trauma could
develop cognitive, physical or emotional
reactions in 24 h from event. Without
psychological support, in 22% of cases these
symptoms may last from 6 months to 1 year.
4% of posttraumatic stress disorder leads to
professional disability.
Posttraumatic stress disorder (PTSD) is a
clinical disorder made of psychological
reactions consecutive of a critical event
exposure. This could be any unusual and
unexpected situation that has a negative
impact on human states (physical, emotional,
cognitive, and behavioral). In aviation this
kind of situation may be an incident or
accident or implication, as a member of team,
in accidents investigation. Beside aviation,
PTSD may appear after serious injury and
violence, natural calamity, unexpected deaths
so on.
PTSD is not necessarily the result of some
trauma. People can find support in friends,
family or Church. Still, many of them need
specialized psychological assistance. In order to
prevent the appearance of PTSD symptoms,
intervention is needed within 72 hours from the
traumatic event, by means of simple non-
therapeutic techniques on normal persons
confronted with abnormal situations. Data
provided by Eurocontrol show that the effects of
two similar accidents (in terms of casualties and
amplitude/damages) have been different,
function of psychic aid provided consecutively
right after the critical event. A few examples: in
1978, without psychic support, there were 29
losses and 31% appeals to mental health
services; in 1986, with psychic support, there
was only one loss and 1% appeals to specialized
services.
The main issue in implementing the
support in posttraumatic stress situations
programs are the preconceived ideas among
professionals (which are mainly generated by
professional self-importance and by the
experience with issues ignoring, the most
frequent being:
- psychological support programs are
meant for those implied in the event. In fact,
reactions of traumatic stress appear also on
witnesses (air traffic controllers, staff of
intervention teams);
- people become less vulnerable while
exposed to traumatic events. In reality,
repeated incidents may increase probability to
develop reactions to traumatic stress;
- relativization and minimization of the
event have a positive effect. Actually, syntagms
such as you were lucky, it could have been
worse may hurt, irritate, or bring sufferance.
- persons who react calmly during a
traumatic accident have fewer chances to
develop reactions to traumatic stress. This is
not a guarantee for his/her future development.
The mum giving first aid to her child may fail
immediately right after this one is stabilized.
- discussions on a previous critical
incident worsen things. The reality is that
reactions to traumatic stress cannot be avoided
by avoiding/dodging confrontation with stress
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62
generated emotions. Often, this kind of stress is
considered to be professional risk and it is
believed that it would better to come back to
work as soon as possible. After a night flight
marked by a technical incident landing under
non functional flight instruments -, a pilot has
been requested to fly again the next day. Unable
to refuse, he carried it out (with no incident this
time); in the end, he admitted that that flight had
been the hardest task ever and that, any problem
survened by that time; he would have been
unable to surpass it.
Psychological evaluation and, thus,
support intervention after a traumatic event is
covered in 3 steps (see Figure 1):


Figure 1: Steps in evaluation of subjects affected by catastrophes (source: tefnescu, 2008)















Right after the critical incident, the
person is moved away the event place. The
rescue teams offer the first aid, with focus on
vital emergencies. Prevention of PTSD starts
with the acute stress phase, by the interventions
of the mental health professionals. The goal is
reestablishing psychic balance. These
techniques philosophy relies on the fact that
rapid interventions could prevent further
pathology development.
At this level, there can be either one-by-
one, or group interventions. The choice
belongs to the (psychological) counselor who
takes into account the time passed since the
event, the cultural factors, the personality of
the patients implied, their compatibility etc.
The two types of techniques follow the same
main principle: discussions with the victim, to
diminish the impact of the crisis. The main
difference between the above techniques is
that the one-by-one way gives the possibility
to find particularized solutions to individual
characteristics of the affected person, while
group sessions stress upon normalization of
lived experiences (by the fact that participants
to the discussion share similar thoughts and
emotions).
Group techniques are meant for at least 3
persons who lived the experience of the same
critical incident. The most important
interventions are defusing and debriefing.
Defusing is the term given to the process
of talking it out - taking the fuse out of an
emotional bomb (explosive situation). It
involves allowing victims and workers the
opportunity to ventilate about their disaster
related memories, stresses, losses, and
methods of coping, and be able to do so in a
safe and supportive atmosphere. The defusing
process usually involves informal and
impromptu sessions.
Because the allotted time is often too
brief, the defusing session is simply a starting
point. Further intervention is often required
and this can be anything from offering
ongoing support (e.g., briefly touching base
with the persons/groups in the coming
Calamity
impact
Immediate
stage
Acute
stage
After effects
stage
First help intervention
team
readiness
proximity
simplicity
Mental health intervention team
Subsequent interventions
Special places
Specific techniques
After effects
prevention
Persistence of
symptoms
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63
days/weeks) to scheduling and providing
formal debriefing sessions.
The length of a defusing session is 20-60
minutes; this technique is applied to a smaller
group than debriefing does. The common steps
are: introduction of the participants, discussing
about facts and associated thoughts,
enumerating the symptoms and reactions and
their normalizing. The counselor can
recommend further psychological treatment.
Defusing is not a therapeutic form of
treatment but rather a way to encourage and to
explain the facts for the persons involved.
The psychological debriefing (PD) is
often a good first step for helping people
process their direct involvement with
traumatic events. The PD is a formal meeting,
done individually or in small groups. It is
generally held shortly after an unusually
stressful incident, strictly for the purpose of
dealing with the emotional residuals of the
event. Any location that is large enough to
accommodate the group, and which can be
secured so as to assure privacy, is appropriate
for use. This session may require a block of
time that is several hours in length.
Whenever it is possible, everyone involved
in the crisis should attend the debriefing(s).
Many organizations recommend or even require
attending defusing or debriefing sessions,
whenever certain types of incidents occur. For
instance, the American Red Cross formerly
offered defusing.
There are now several debriefing models.
Organizations like the National Organization
for Victim Assistance (NOVA) may favor a
model which they teach their volunteers and
staff members. While the various models
differ in the number and type of phases (or
stages), they all get at the same basic
elements. This is done to help people cope
with the sights, sounds, and smells, thoughts,
feelings symptoms, and memories that are all
part of a normal stress reaction to a traumatic
event.

Table below shows the phases of debriefing model and their main moments.

Table 1. Phases of debriefing

ETAPE MOMENTS QUESTIONS
Introduction
Introduction of the team member, explaining the
purpose of the meeting and its rules. Aim: to obtain
relaxation and trust.

Who are we?
Facts


What happened? What is the
traumatic event? What was
your role in that event?
Thoughts

What was in your mind in
those moments?
Reactions

What was your first reaction?
What did you felt? Which was
the worst moment?
Exploration
Symptoms (cognitive, emotional,
physical, behavioral)
What symptoms appear?
Conclusions
Explaining the normality of reactions
and abnormality of the situation.
What did you learn from the
situation?
Informing
Return
Synthesis, answers to the questions,
recommendations.


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64
The main advantages of debriefing are:
explaining the misunderstandings, negative
emotions recognition, experiences changes,
interpersonal and coping support, crew
communication and cohesion improvement,
training for new situations.
Programs for post traumatic intervention:

After Action Stress Debriefing
AACD was developed by German
military aviation and it is addressed to after
fight mission team. It is a psychological first
aid initiated to reduce emotional trauma.
Debriefing is done by team of physicians,
psychologists, priests and people in
command.
The main phases of intervention are:
elucidation of debriefing purpose, verbal
reconstruction of the trauma, obtaining an
accord on what happened, discussing the
responsibilities, explaining the normality of
the feelings, charging preventions,
conclusions.

Critical Incident Stress Debriefing
CISD is a Eurocontrol release addressed
to air traffic controllers in critical situations.
Technique consists in discussion about what
happened (maximum 3 hours). There is a
similarity of steps with AACD. The
counselors are selected from ATC colleagues.
This selection is based on some personal
characteristics (professional background,
capacity of listening and understanding,
psychological maturity and balance).
The persons who suffer debriefing and
defusing may receive an advice about further
psychological interventions. These
interventions are based on a cognitive
approach.
In conclusion, debriefing and defusing
are important means of psychological first
help, useful for reducing PTSD. Easy to learn,
these techniques assure benefits for
individuals and company.



Bibliography

1. Eurocontrol (2005), Critical
Incident Stress Management prezentarea
tehnicii la Bucureti, februarie.
2. Holdevici, I., Licu, M. (2004),
Asistena psihologic n tulburarea de stres
postraumatic. Metode de intervenie
terapeutic, n Psihologie aplicat n forele
armate, Ed. Universitii Naionale de
Aprare, Bucureti, 2004 (p. 87-102).
3. Popa, M. (2005), Psihologie
aeronautic, Ed. Universitar Carol Davila,
Bucureti.
4. tefnescu, D. (2008), Curs de
intervenie psihologic n situaii de stres
postraumatic (material nepublicat).
5. Presented case were showed on
Discovery Channel as a documentary.




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