1 ∂¶π∫∞πƒ√ £∂ª∞ CURRENT ISSUE °Ú›Ë ÙˆÓ ÙËÓÒÓ: ·ÂÈÏ‹ ÌÈ·˜ Ó¤·˜ ·Ó‰ËÌ›·˜; ª. ∆ÛÔÏÈ¿, π. §ÔÁÔı¤ÙË, ∞. ∫ˆÓÛÙ·ÓÙfiÔ˘ÏÔ˜ ¶ÂÚ›ÏË„Ë: ∫·Ù¿ ÙË ‰È¿ÚÎÂÈ· ÙÔ˘ 20Ô‡ ·ÈÒÓ· Ë ·ÓıÚˆfiÙËÙ· ‰ÔÎÈÌ¿ÛÙËΠ·fi ÙÚÂȘ ·Ó‰Ë̛˜ Áڛ˘. ™ÙËÓ ·˘Á‹ ÙÔ˘ 21Ô˘ ·ÈÒÓ·, Ë ÂÌÊ¿ÓÈÛË ÌÈ·˜ Ó¤·˜ ·Ó‰ËÌ›·˜ ÌÔÈ¿˙ÂÈ ·Ó·fiÊ¢ÎÙË. ∆· ÙÂ- ÏÂ˘Ù·›· ¯ÚfiÓÈ·, ¤Ó·˜ Û˘Ó¯Ҙ ·˘Í·ÓfiÌÂÓÔ˜ ·ÚÈıÌfi˜ ÂȉËÌÈÒÓ Áڛ˘ ÙˆÓ ÙËÓÒÓ ÂΉËÏÒÓÔÓÙ·È Î˘Ú›ˆ˜ ÛÙȘ ·ÛÈ·ÙÈΤ˜ ¯ÒÚ˜, ηıÒ˜ Î·È Û ¿ÏÏ· ̤ÚË ÙÔ˘ ÎfiÛÌÔ˘. ∞˘Ù¤˜ ÚÔηÏÔ‡ÓÙ·È ·fi ÈÔ‡˜ Ô˘ ¤¯Ô˘Ó ·˘ÍË̤ÓË ÏÔÈÌÔÁfiÓÔ ‰‡Ó·ÌË Î·È ÚÔηÏÔ‡Ó ˘„ËÏ‹˜ ·ıÔÁÔÓÈÎfiÙËÙ·˜ ÁÚ›Ë ÛÙ· ÙË- Ó¿. π‰È·›ÙÂÚË ·ÓËÛ˘¯›· ¤¯ÂÈ ÚÔηϤÛÂÈ Ë Â˘Ú›· ÂͿψÛË ÙÔ˘ ÈÔ‡ Ù˘ Áڛ˘ ∏5¡1 Û ¿ÁÚÈ· Î·È ÔÈÎfiÛÈÙ· ÙËÓ¿ ÛÙËÓ ∞Û›·. ∆Ô Û٤ϯԘ ·˘Ùfi ÌÔÚ› Ó· ÌÂÙ·‰Ôı› ·fi Ù· ÙËÓ¿ ÛÙÔÓ ¿ÓıÚˆÔ Î·È Ó· ÚÔηϤÛÂÈ Ïԛ̈ÍË Î·È ı¿Ó·ÙÔ. ∞Ó Î·È ¤¯ÂÈ ·Ú·ÙËÚËı› ÌÂÙ¿‰ÔÛË ÙÔ˘ ÈÔ‡ ·fi ¿ÓıÚˆÔ Û ¿ÓıÚˆÔ, Ê·›ÓÂÙ·È fiÙÈ ÙÔ Û٤ϯԘ ·˘Ùfi ‰ÂÓ ÌÔÚ› Ó· ÌÂÙ·‰Ôı› ‡ÎÔÏ· ÌÂٷ͇ ·ÓıÚÒˆÓ. øÛÙfiÛÔ, ÌÔÚ› Ó· ·ÔÎÙ‹ÛÂÈ ÙËÓ ÈηÓfiÙËÙ· ·˘Ù‹ Ì ·Ó¿ÌÈÍË Î·È ·ÓÙ·ÏÏ·Á‹ ÙÔ˘ ÁÂÓÂÙÈÎÔ‡ ÙÔ˘ ˘ÏÈÎÔ‡ (reassortment) Ì ÙÔ ÁÂÓÂÙÈÎfi ˘ÏÈÎfi ·ÓıÚÒÈÓÔ˘ ÛÙÂϤ¯Ô˘˜ ‹ Ì ‰È·‰Ô¯ÈΤ˜ ÌÂÙ·ÏÏ¿ÍÂȘ. ™Â ·˘Ù‹Ó ÙËÓ ÂÚ›ÙˆÛË, ÙÔ Û٤ϯԘ ∏5¡1 ı· Âͷψı› Û ÔÏfiÎÏËÚÔ ÙÔÓ ÎfiÛÌÔ Î·È ı· ÂΉË- ψı› ÌÈ· Ó¤· ·Ó‰ËÌ›·. °È· Ó· ÂÚÈÔÚÈÛÙ› Ë ÂͿψÛË ÙÔ˘ ÈÔ‡ Â›Ó·È ··Ú·›ÙËÙË Ë Û˘ÓÙÔÓÈṲ̂- ÓË ÚÔÛ¿ıÂÈ· ÙˆÓ Î˘‚ÂÚÓ‹ÛÂˆÓ ·ÏÏ¿ Î·È fiÛˆÓ ·Û¯ÔÏÔ‡ÓÙ·È Ì ÙËÓ ÂÎÙÚÔÊ‹ ÙËÓÒÓ ÒÛÙ ӷ ÂÊ·ÚÌÔÛıÔ‡Ó Ù· ηٿÏÏËÏ· ÂÎ·È‰Â˘ÙÈο ÚÔÁÚ¿ÌÌ·Ù· Î·È Ó· ‚ÂÏÙȈı› Ë ‚ÈÔÏÔÁÈ΋ ·ÛÊ¿ÏÂÈ·. ∫¿ı ¯ÒÚ· Ú¤ÂÈ Ó· ‰È·ı¤ÙÂÈ ¤Ó· Û¯¤‰ÈÔ ·ÓÙÈÌÂÙÒÈÛ˘ ÌÈ·˜ ÂӉ¯fiÌÂÓ˘ ·Ó‰ËÌ›·˜, fiˆ˜ ›- Û˘ Î·È ·fiıÂÌ· ÈηÓÒÓ ÔÛÔÙ‹ÙˆÓ ·ÓÙÈ-ÈÈÎÒÓ Ê·ÚÌ¿ÎˆÓ Ô˘ Ó· ·ÓÙ·ÔÎÚ›ÓÔÓÙ·È ÛÙȘ ·Ó¿ÁΘ ÙÔ˘ ÏËı˘ÛÌÔ‡. √ ÈÔ ·ÔÙÂÏÂÛÌ·ÙÈÎfi˜ ÙÚfiÔ˜, fï˜, ÁÈ· Ó· ÂÚÈÔÚÈÛÙ› Ë ·Ó‰ËÌ›·, ·Ú·Ì¤ÓÂÈ Ô ÂÌ‚ÔÏÈ·ÛÌfi˜. ™‹ÌÂÚ·, Á›ÓÂÙ·È ÂÓÙ·ÙÈ΋ ÂÚ¢ÓËÙÈ΋ ÚÔÛ¿ıÂÈ· ÁÈ· ÙËÓ ·Ó¿Ù˘ÍË ÂÌ‚ÔÏ›Ô˘ η- Ù¿ ÙÔ˘ ÛÙÂϤ¯Ô˘˜ ∏5¡1. §¤ÍÂȘ ÎÏÂȉȿ: °Ú›Ë, ÁÚ›Ë ÙËÓÒÓ, ·Ó‰ËÌ›·. Avian flu: a new pandemic threat? M. Tsolia, I. Logotheti, A. Konstantopoulos Abstract: During the course of the 20th century the world experienced three influenza pandemics. Today, at the dawn of the 21st century the emergence of a new pandemic seems inevitable. In recent years, an increasing number of epidemics caused by high pathogenicity avian influenza viruses have occurred, mainly in Asian countries but also in other parts of the world. The current widespread dissemination of H5N1 avian virus in wild and domestic birds in Asia is unprecedented and has caused global concern. What is more troubling is the fact that this virus has been transmitted from birds to humans causing disease and death. Although human-to-human transmission is known to have occurred, the virus cannot be transmitted between humans with great efficiency. However, it may acquire this capacity either by reassortment with a human strain or through adaptive mutations. In this case, the H5N1 strain will cause explosive global spread and a new influenza pandemic will occur. An effort should be made by governments and poultry producers to improve biosecurity and conduct education programmes with a view to restriction of the spread of avian influenza. An operational pandemic plan should be available in every country and an adequate amount of antiviral medication stockpiled. Immunization will be the most effective way to reduce the impact of a pandemic and researchers are currently trying to develop a vaccine against the H5N1 strain. Key words: Influenza, avian influenza, pandemic. µ’ ¶·È‰È·ÙÚÈ΋ ∫ÏÈÓÈ΋ ¶·ÓÂÈÛÙËÌ›Ô˘ ∞ıËÓÒÓ, ¡ÔÛÔÎÔÌÂ›Ô ¶·›‰ˆÓ “¶. Î·È ∞. ∫˘ÚÈ·ÎÔ‡” AÏÏËÏÔÁÚ·Ê›·: §ÔÁÔı¤ÙË πˆ¿ÓÓ· §˘Î›·˜ 5, ¡. ™Ì‡ÚÓË, ∆.∫. 171 23 e-mail: [email protected]2nd Paediatric Clinic, University of Athens, “P. & A. Kyriakou” Children’s Hospital Correspondence: Logotheti Ioanna 5 Lykeias Str., N. Smyrni, 171 23, Athens e-mail: [email protected]¶·È‰È·ÙÚÈ΋ 2006;69:1-9
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Abstract: During the course of the 20th century the world experienced three influenza pandemics.Today, at the dawn of the 21st century the emergence of a new pandemic seems inevitable. In recentyears, an increasing number of epidemics caused by high pathogenicity avian influenza viruses haveoccurred, mainly in Asian countries but also in other parts of the world. The current widespreaddissemination of H5N1 avian virus in wild and domestic birds in Asia is unprecedented and has causedglobal concern. What is more troubling is the fact that this virus has been transmitted from birds tohumans causing disease and death. Although human-to-human transmission is known to haveoccurred, the virus cannot be transmitted between humans with great efficiency. However, it mayacquire this capacity either by reassortment with a human strain or through adaptive mutations. In thiscase, the H5N1 strain will cause explosive global spread and a new influenza pandemic will occur. Aneffort should be made by governments and poultry producers to improve biosecurity and conducteducation programmes with a view to restriction of the spread of avian influenza. An operationalpandemic plan should be available in every country and an adequate amount of antiviral medicationstockpiled. Immunization will be the most effective way to reduce the impact of a pandemic andresearchers are currently trying to develop a vaccine against the H5N1 strain.
1. Treanor G. Influenza virus. In: Mandell GL, BennettJE, Dolin R (eds). Mandel, Douglas and Bennett'sPrinciples and practice of infectious diseases. 5thedition. Churchill Livingstone, Philadelphia, 2000:1823-1849.
2. Laver WG, Bischofberger N, Webster RG. Disarm-ing flu viruses. Sci Am 1999;280:78-87.
3. Osterhaus A. H5N1: the lessons to be learned. In:Zambon MC, ed. United Kingdom: Advances in in-fluenza. Blackwell Science; 1999. p. 11-17.
4. Laver G, Garman E. Virology. The origin and controlof pandemic influenza. Science 2001;293:1776-1777.
5. Hien TT, De Jong M, Farrar J. Avian influenza - AChallenge to global health care structures. N Engl JMed 2004;351:2363-2365.
7. Belshe RB. The Origins of Pandemic Influenza -lessons from the 1918 Virus. N Eng J Med 353;21:2209-2211.
8. Taubenberger JK, Reid AH, Lourens RM, Wang R,Jin G, Fanning TG. Characterization of the 1918 in-fluenza virus polymerase genes. Nature 2005;437:889-893.
9. Tumpey TM. Basler CF, Aguilar PV, Zeng H,Solorzano A, Swayne DE et al. Characterization ofthe reconstructed 1918 Spanish influenza pandemicvirus. Science 2005;310:77-80.
10. Centers for Disease Control and Prevention Influen-za (flu): information about Avian influenza andAvian influenza A [Internet]. 2005: Webpage:http://www.cdc.gov/flu.
ation of influenza A virus from eight plasmids. Proc
Natl Acad Sci USA 2000;97:6108-6113.
23. Reichert TA. Preparing for the next influenza pan-
demic: lessons from multinational data. Pediatr In-
fect Dis J 2005;24(11 Suppl):S228-S231.
¶·È‰È·ÙÚÈ΋ 2006;69:1-9
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10 REVIEW ARTICLE
Director of Pediatric Nephrology, Children'sHospital of Pittsburghand the University of Pittsburgh School of Medicine
Correspondence:
Demetrius Ellis, M.D.Children's Hospital of Pittsburgh3705 Fifth AvenuePittsburgh, PA 15213e-mail: [email protected]
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Evaluation and management of hypertensive
crisis in childhood
D. Ellis
Abstract: Hypertensive crisis is relatively uncommon in the paediatric age group and many emer-gency departments are poorly prepared to manage children with this potentially lethal disorder. Thisreview provides guidelines aimed at facilitating the evaluation and management of children with thisdisorder.
Normal blood pressure (BP) levels differ byage, gender and height; accordingly no single BPlevel defines hypertension (HTN) in all children.Updated BP norms and definitions of HTN inchildren are provided in the latest of four com-prehensive reports (1). HTN is generally definedas the average of three manually obtained sys-tolic BP and/or diastolic BP measurements being≥95th percentile for age, gender and height.
There are several recent reviews of hyperten-sive crisis in adults (2-8), but the clinical ap-proach to this topic has been rarely addressedfor the paediatric age group (9,10). For purpos-es of this review, hypertensive crisis is a syn-drome classified as either a) hypertensive emer-gency if there are clinical manifestations of on-going organ injury, or, b) hypertensive urgencyif there are no acute clinical symptoms and evi-dence for end-organ damage is minimal or ab-sent. The implication is that the former requiresimmediate reduction in BP, while in the latterBP reduction may take place over hours or days.Although the large majority of children whopresent in the emergency department with hy-pertensive crisis have BP above the 99th per-centile, hypertensive crisis is not strictly definedby absolute BP levels.
In the absence of known preexisting renaldisorder, which often predisposes to hyperten-sive crisis, the possibility must be considered ofpreviously unrecognized cardiac and endocrino-
logic aetiologies of HTN, which may strongly in-
fluence the therapeutic choice for individuals in
the emergency department. This brief report de-
scribes a practical clinical approach to the diag-
nosis and immediate management of the child
presenting with hypertensive crisis, which may
be facilitated by means of an algorithm, along
with a table of potentially useful agents and
dosage guidelines suitable for the paediatric age
group. The goal of therapy is to prevent the cat-
astrophic consequences of this potentially lethal
disorder.
Symptoms and signs
Unlike adults, in whom hypertensive crises
usually occur in individuals with known and of-
ten severe preexisting HTN, in children the dis-
covery of HTN is often made at the time of pre-
sentation with a hypertensive crisis. Symptoms
of HTN in children depend on the acute nature
of the development of HTN as well as on the
magnitude of the BP elevation. Hence, in a child
with chronic HTN secondary to renal artery
stenosis, mild to moderate HTN is usually well
tolerated whereas the same BP level may cause
severe headache or seizures in a child with acute
glomerulonephritis. Similarly children with car-
diac outlet obstruction or cardiomyopathy may
become symptomatic despite mild HTN.
The most common symptoms of HTN in the
majority of older children who present in the
emergency department are those of hyperten-
sive encephalopathy, namely headache, nausea,
vomiting, mental confusion, blurred vision, ag-
itation or frank seizures. Other manifestations
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·10
11Hypertensive crisis in childhood
may include cerebral infarction, intracerebral or
retinal haemorrhage, congestive heart failure,
acute pulmonary oedema (with shortness of
breath), acute renal insufficiency, and microan-
giopathic haemolytic anaemia. Less common
sequelae of hypertensive crisis in children in-
clude myocardial infarction and aortic dissec-
tion. Newborns and infants with severe hyper-
tension may present with congestive heart fail-
ure, hypertensive retinopathy, respiratory dis-
tress, apnoea or cyanosis, extreme irritability,
hypotonia, convulsions or coma. Vomiting, di-
arrhoea and failure to thrive may be among the
chronic manifestations of hypertension in the
younger age group.
Causes of hypertensive crisis
Table 1 lists the main causes of hypertensive
crisis in children. Renal disorders predominate
and these include renovascular hypertension (in-
cluding renal artery stenosis and aortic coarcta-
tion), accelerated HTN in children with renal
failure and fluid overload together with pre-ex-
isting HTN, acute glomerulonephritis, haemolyt-
ic-uremic syndrome and other renal parenchy-
mal disorders. Less common causes are vasculi-
tis, head injury and phaeochromocytoma.
Pathophysiology of hypertensive
emergencies
The ability to maintain almost constant per-
fusion to an organ over a wide range of mean
arterial pressures ranging from 60-150 mmHg
is known as autoregulation of blood flow. This
process is mediated by multiple neurohumoral
mechanisms which affect vascular resistance,
and is particularly effective and well guarded in
the cerebral and renal circulations. Chronic
HTN leads to compensatory, functional and
structural changes in arterial vessels, which
maintain perfusion to these organs while pro-
tecting against injury that may otherwise result
from organ hyperperfusion due to HTN (11).
When the systemic BP surpasses the compen-
satory limits of autoregulation, arterial injury,
such as fibrinoid necrosis and organ ischaemia,
may follow (5, 12). Conversely when the BP is
suddenly reduced below the new steady state
limits of compensation, ischaemic injury may
be enhanced, particularly in individuals with
structural hypertensive arterial changes. Most
children with hypertensive emergencies do not
have structural vascular lesions and are, there-
fore, less susceptible to organ ischaemia after
lowering of the BP. Conversely, the lack of
adaptive responses in children with an acute
and rapid rise in BP may predispose to symp-
toms at BP levels which may not be gauged
as being sufficiently high to produce such
symptoms.
Evaluation of hypertensive emergencies
The algorithm shown in the Figure may facil-
itate the clinical assessment and management of
the symptomatic child with hypertensive emer-
gency. A similar approach may be applied in the
child with hypertensive urgency, in which case the
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Table 1. Causes of hypertensive crisis
ñ Abrupt increase in blood pressure in children withchronic hypertension (most common in those withrenal disorders or on dialysis)
ñ Renovascular hypertension, including renal arterystenosis, partial arterial thrombosis especially inneonates with umbilical arterial lines, aorticcoarctation
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·12
13Hypertensive crisis in childhood
glomerulonephritis. A history of illicit or pre-scribed drug use which may precipitate or aggra-vate pre-existing HTN may be helpful.
Urinalysis and measurement of BUN, serumcreatinine, electrolytes, calcium, phosphorus,magnesium and uric acid may provide evidenceof renal involvement. Because anti-hypertensivetherapy may alter plasma levels of renin, corti-sol and aldosterone, as well as urinary VMA ex-cretion, in undiagnosed cases, these measure-ments should be obtained before administeringanti-hypertensive drugs. A plasma toxicologyscreen may be useful in children with suspectedsubstance abuse. Chest X-ray and EKG orechocardiogram should also be done as early aspossible. Once the BP improves, children withsevere encephalopathy or focal neurologicdeficit may be escorted by an emergency depart-ment physician to the radiology department,where computerized cranial tomography maybe done to diagnose or eliminate thrombotic orhaemorrhagic events.
General principles of management
There have been no controlled clinical trialsof treatment of hypertensive emergencies or hypertensive urgencies in children. A review ofmultiple adult studies failed to produce statisti-cal superiority of any single therapeutic agentand the outcome was not uniform between stud-ies (6). Experience is accruing from clinical trialson adults with hypertensive emergencies of thecalcium channel inhibitor lacidipine or the ·1-adrenergic receptor blocker urapidil, adminis-tered for specific indications (6,13). However, itis the author's opinion that the newer vasculardopamine receptor agonist (DA1), fenoldopam(14) shows the most promise, particularly in re-placing intravenous nitroprusside in childrenwith renal dysfunction. Employment of the new-er agents may be more appropriate for hyperten-sive emergencies due to disorders not frequentlyencountered in childhood, such as atheroscle-rotic cerebrovascular and renal arterial disease,HTN associated with pregnancy, or aortic dis-section. Hence, reliance on older agents is stillpreferred.
As a general rule agents with a short durationof action are employed, so that if BP reduction isgauged as excessive, the effect can be quickly re-versed by stopping the agent and/or administer-ing normal saline. A major long-term objective
is to assure compliance with antihypertensive
therapy during follow-up (7,8).
The goal of emergency therapy is to achieve a
gradual decrease in systolic and diastolic BP to
near the 99th percentile, or to reduce the mean
arterial pressure (one third of the pulse pressure
difference added to the diastolic BP) by 25%.
With such reduction in BP over a period of min-
utes or hours the symptoms and signs of hyper-
tension tend to improve or resolve. Further low-
ering in BP may be effected more slowly over
several days or weeks in such a way that the BP
remains below the 90th percentile for age, gen-
der and height percentile (1).
Choice of oral vs. intravenous therapy in
hypertensive crisis
In general, if a renal aetiology for the HTN
can be readily ascertained and the child is capa-
ble of swallowing, the initial therapy in the
emergency department may consist of oral
agents. If the aetiology of HTN cannot be estab-
lished, the initial agent could be intravenous hy-
drallazine, with oral or trans-dermal clonidine
as an adjunctive agent. If HTN persists, the child
is admitted to the intensive care unit (ICU)
where more powerful parenteral agents may be
urgently administered and BP can be monitored
continuously and directly through an intra-arte-
rial transducer. A list of antihypertensive agents
and the recommended dosages for children with
hypertensive crisis are shown in Table 2.
Specific disorders such phaeochromocytoma
or drug-induced HTN from catecholamine ex-
cess (cocaine intoxication, monoamine oxidase
inhibitor crisis) may be managed with an alpha
adrenergic blocker such as phentolamine, while
avoiding initial use of beta blockers which may
potentiate the alpha adrenergic action of cate-
cholamines. Intravenous diuretics may be very
useful as adjunctive agents in the case of con-
gestive heart failure in disorders accompanied
by fluid overload, such as acute glomeru-
lonephritis.
Oral agents used to manage
hypertensive crisis
Assuming that the child does not have se-
vere neurological symptoms and is capable of
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·13
14 D. Ellis
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Table 2. Pharmacologic management of hypertensive crisis in infants and in children
Action Agents Dose Route Comments(trade names)
Vasodilator Hydrallazine 0.1-0.2 mg/kg IV Administer at <0.2 mg/kg/minute; (Apresoline, others) (maximum onset 5-20 minutes; lower dose can
20 mg/dose) be repeated after 5-20 minutes.Duration is 2-6 hours. Can cause reflex tachycardia. Available in 20 mg/ml ampoule.
Minoxidil 0.1-0.2 mg/kg Oral Onset ≤30 minutes; maximum effect (Loniten) (maximum @ 2-8 hours; long duration of effect,
50 mg/day) once daily dosing, contraindicated in phaeochromocytoma.
Diazoxide 1-3 mg/kg IV push Administer IV push over 10-30 (Hyperstat) (maximum seconds, maximum effect within
150 mg dose) 5 minutes, can be repeated after 5 minutes, duration of effect 3-12 hours. Available in 300 mg/30 ml ampule. Alternative dosage is 1 mg/kg every 5-15 minutes until BP control is achieved.
Sodium nitroprusside 0.25-8 mcg/kg/min IV drip Administer by continuous infusion (Nipride) only; onset within 2 minutes,
duration <10 minutes. Start at 0.25 mcg/kg/minute and increasedose by 25% every 5-10 minutes until BP control is obtained. Obtain thiocyanate levels if used for more than 48 hours; protect from light. Available in 50 mg/ 5 ml vial.
Adrenergic alpha Labetalol 0.2-0.5 mg/kg/dose IV Administer IV over 2-3 minutes; and beta (Normodyne, (maximum onset 2-5 minutes; maximum effect blocking agents Trandate) 1mg/kg) in 5-15 minutes, duration 2-4 hours;
lower dose can be doubled and repeated at 15 minute intervals x 2; can also be given at same dose by IV infusion over 1 hr. Avoid if child has history of asthma / bronchospasm. Contraindicated in congestive heart failure, sinus tachycardia, heart block. Available as 5 mg/ml.
Clonidine 5-10 mcg/kg/day Oral Divide dose and administer q 6-12 (Catapres) (maximum hours. Also available in transdermal
25 mcg/kg/day) formulation. Avoid in cerebrovascular disorders. May cause agitation, insomnia, drowsiness, rebound hypertension after rapid withdrawal.
Esmolol Loading dose: IV drip Use for postoperative hypertension; (Brevibloc) 500 mcg/kg IV, administer loading dose over 1
then use as minute; followed by continuous continuous infusion infusion; onset: beta blockade occurs 50-250 mcg/kg/min in 2-10 minutes; duration 10-30
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·14
15Hypertensive crisis in childhood
swallowing medications, the use of oral medica-tion may be limited to children with hyperten-sive emergencies or urgencies associated withknown or suspected renal disorders.
Short-acting nifedipine is currently a verypopular drug for use in this situation. Unlikeadults, where studies show that the use of thisagent may be associated with a precipitous fall inBP and increased risk of myocardial infarction,stroke and death (15), data on children indicatethat use of nifedipine is safe and effective (16,17). However, both the clinical situation and theinitial dose may modify safety. Guidelines foravoidance of the use of short acting nifedipine inchildren include:
1. Congestive heart failure, presence of my-ocardial ischaemia, after cardiac arrest, severeleft ventricular hypertrophy, left ventricular out-flow obstruction, or cardiac arrhythmia.
2. Acute hypertension with high cardiac out-
put states, such as sickle cell crisis or other chron-ic anaemias.
3. Cyanotic heart disease.4. Hypovolaemic states including children
with anasarca, those undergoing acute diuresis,or those with acute haemorrhage.
5. Acute hypertension associated with severepain. The BP should be reassessed after adminis-tration of appropriate analgesics such as mor-phine.
6. Acute central nervous system injury. 7. Children receiving large dosages of beta
blockers, such as atenolol or labetolol. 8. Infants less than one year of age. In the absence of such conditions, orthostatic
hypotension is usually avoided when the startingdose of nifedipine is 0.2 to 0.25 mg/kg bodyweight. Although it is often given sublingually,very little of the agent is actually absorbed via theoral mucosa. Thus, if the entire 10 mg nifedipine
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Table 2. Pharmacologic management of hypertensive crisis in infants and in children
Action Agents Dose Route Comments(trade names)
Isradipine 0.2-0.9 mg/kg/day Oral Available in capsules (2.5 and 5 mg) (DynaCirc) (maximum and in liquid formulation
0.6 mg/kg/day) (1 mg/mL). May cause tachycardia or congestive heart failure.
Calcium-channel Nifedipine 0.2-0.5 mg/kg Oral Swallow whole, or bite capsule and blocking agents (Procardia, others) (Initial dose should swallow, or remove liquid from
not exceed capsule with syringe; not effective by 0.25 mg/kg) sublingual route (actual effect due to
swallowing the drug with subsequent rapid oral absorption); initial dose can be repeated once within 30 minutes. Onset of effect within 1-5 minutes after bite and swallow, contraindicated in patients with heart disease; available in 10 and 20 mg capsules.
Nicardipine 1 mcg/kg/min IV drip Onset 10 minutes; duration (Cardene IV) (maximum 2-6 hours; available as 2.5 mg/ml
5 mcg/kg/min)
Alpha-adrenergic Phentolamine 0.05-0.1 mg/kg/dose IV Diagnostic test for blocker (Regitine) (maximum 5 mg) phaeochromocytoma. Onset
immediate; maximum effect in 2 minutes, duration 30 minutes; available in 5 mg vial.
ACE inhibitors Enalaprilat 5-10 mcg/kg/dose IV Administer undiluted over 5 minutes; onset ≤15 minutes; maximum effect in 1 hour; duration 4-6 hours. Severe hypotension can occur in sodium or volume depleted patients. Use lower dosages in neonates.
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·15
16 D. Ellis
capsule is to be used the “bite and swallow”
method is recommended. If lesser amounts are
needed, the contents of the 10 mg capsule are
drawn into a 1 mL graded syringe and the portion
needed (0.034 mL = 1 mg) may be administered
orally so as to speed up gastrointestinal uptake
and onset of action. This dose may be repeated
once within 30 minutes. All subsequent dosages
should not exceed 0.5 mg/kg body weight, with a
maximum of 10 mg, and the frequency of admin-
istration may be every 4-6 hours. Close BP moni-
toring is mandatory and such children should not
ambulate after receiving the medication unless
they are completely free of orthostatic hypoten-
sion, dizziness or mental disturbances.
Minoxidil is an alternative oral agent, with
properties of smooth arterial muscle relaxation
(leading to vasodilation), which may be effective
in overcoming hypertensive emergencies. Close
BP monitoring and avoidance of ambulation is
recommended after its use also.
Intravenous agents used to manage
hypertensive crisis
In children who are unable to take oral short-
acting nifedipine or minoxidil, or in those with
severe neurological symptoms, intravenous
medications are preferred. Diozoxide is rarely
used for this purpose because of unpredictable
or precipitous drops in BP. Hydrallazine has be-
come less popular because of the common side-
effects of flushing, tachycardia, nausea and
headache, although it is still useful in the emer-
gency department setting. With more severe or
refractory symptomatic HTN more potent intra-
venous medications are indicated.
In all instances in which intravenous medica-
tions other than hydrallazine are administered,
the child should have an arterial line inserted for
BP monitoring. In addition co-administered
medications must be reviewed for possible syn-
ergism or drug interaction, which may exacer-
bate adverse effects of antihypertensive agents.
The most useful parenteral agents in children
include sodium nitroprusside (9,18,19), nicardip-
ine (20-22), and labetalol (23,24); esmolol may be
a preferred drug for use in infants (9,23,25,26).
These agents may be given as a constant infusion
and have an onset of action of less than 5 minutes.
Generally, these medications should be started
with the lower dosages and increased stepwise by
25% every 5-10 minutes until the desired BP isreached.
Sodium nitroprusside may be the initial intra-venous agent in any child presenting with hyper-tensive emergency, with the exception of closedhead injury or suspected high intracranial pres-sure. With long-term use of this agent, accumula-tion of its metabolic end products, comprisingcyanide and thiocyanate, may cause nausea, vom-iting, neurological symptoms, hypothyroidism,dyspnoea and metabolic acidosis. Nicardipinemay be more suitable for use in individuals withrenal insufficiency who are unable to excretethese metabolites effectively. Less frequently,nicardipine may also be given as mini-boluses.Fenoldopan is a newer agent which is also effec-tive and uniquely suitable for managing HTN inthe case of renal insufficiency (5,6,14). Esmolol,labetalol (23,24) and enlaprilat (10,27) may beparticularly useful in infants. Esmolol can be giv-en by constant infusion while all three agents canbe administered on an intermittent basis. Intra-venous labetalol is particularly useful in the man-agement of HTN after transplantation, associatedwith cyclosporine or tacrolimus given in conjunc-tion with glucocorticoids. It can also be adminis-tered as an infusion over 1-hr. As with esmololand other beta blockers, labetalol should beavoided or be used with caution in children withreactive airway disease, and with consideration ofother contraindications to their use (Table 2). In-fants are particularly susceptible to enalaprilat-in-duced inhibition of angiotensin II, and may de-velop significant reduction in renal blood flowand glomerular filtration rate. Hence, enalaprilat(IV enalapril) should be used with caution in in-fants with known or suspected renal artery steno-sis. However, this agent may be used to managerenovascular HTN due to microthrombi associat-ed with intubation of the umbilical vessels.
Acknowledgements
My gratitude to Dr. Bill McGhee and for confirmingthe paediatric drug dosages shown in Table 2, and toMrs. Anne Spence who aided in the preparation of thealgorithm.
References
1. National High Blood Pressure Education ProgramWorking Group on High Blood Pressure in Chil-dren and Adolescents. The Fourth Report on the
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·16
17Hypertensive crisis in childhood
¶·È‰È·ÙÚÈ΋ 2006;69:10-17
Diagnosis, Evaluation and Treatment of High BloodPressure in Children and Adolescents. Pediatrics2004;114:555-576.
13. Alijotas-Reig J, Bove-Farre I, de Cabo-Frances F,Angles-Coll R. Effectiveness and safety of prehospi-tal urapidil for hypertensive emergencies. Am JEmerg Med 200;19:130-133.
14. Tumlin JA, Dunbar LM, Oparil S, Buckalew V, RamCV, Mathur V, et al. Fenoldopam, a dopamine ago-nist, for hypertensive emergency: a multicenter ran-domized trial. Fenoldopam Study Group. AcadEmerg Med 2000;7:653-662.
15. Grosssman E, Messerli FH, Grodzicki T, Kowey P.
Should a moratorium be placed on sublingualnifedipine capsules given for hypertensive emergen-cies and pseudoemergencies? JAMA 1996;276:1328-1331.
16. Egger DW, Deming DD, Hamada N, Perkin RM,Sahney S. Evaluation of the safety of short-actingnifedipine in children with hypertension. PediatrNephrol 2002;17:35-40.
17. Blaszak RT, Savage JA, Ellis EN. The use of short-acting nifedipine in pediatric patients with hyper-tension. J Pediatr 2001;139:34-37.
18. Gordillo Paniagua G, Velasquez Jones L, Martini R,Valdez Bolanos E. Sodium nitroprusside treatmentof severe arterial hypertension in children. J Pediatr1975;87:799-802.
19. Luderer JR, Hayes AH Jr, Dubnsky O, Cerlin CM.Long-term administration of sodium nitroprussidein childhood. J Pediatr 1977;91:490-491.
21. Flynn JT, Mottes TA, Brophy PD, Kershaw DB,Smoyer WE, Bunchman TE. Intravenous nicardip-ine for treatment of severe hypertension in children.J Pediatr 2001;139:38-43.
22. Michael J, Groshong T, Tobias JD. Nicardipine forhypertensive emergencies in children with renal dis-ease. Pediatr Nephrol 1998;12:40-42.
23. Sinaiko AR. Treatment of hypertension in children.Pediatr Nephrol 1994;6:603-660.
24. Bunchman TE, Lynch RE, Wood EG. Intravenouslyadministered labetalol for treatment of hyperten-sion in children. J Pediatr 1992;120:140-144.
25. Trippel DL, Wiest DB, Gillette PC. Cardiovascularand antiarrhythmic effects of esmolol in children. JPediatr 1991;119:142-147.
27. Hirschl MM, Binder M, Bur A, Herkner H, BrunnerM, Mullner M, et al. Clinical evaluation of differentdoses of intravenous enalaprilat in patients with hy-pertensive crisis. Arch Intern Med 1995;155:2217-2223.
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·17
The effect of air pollution and the effects of fine particulate matter
on the circulatory system
Z. Chalemis, G. Varlamis
Abstract: Inhaled air pollutants and especially ambient air particulate matter (PM) have beenidentified as causing respiratory problems, cancer and heart disease, in both adults and children, evento the extent that increased mortality is observed in periods of increased PM air pollution. Here a briefreview is made of PM and its effects in humans, with emphasis on the cardiovascular system. Specialemphasis has been given to the dangers in childhood, when the mechanisms of autoprotection are lesswell developed. The most dangerous particles are the “fine” (aerodynamic diameter <2.5 Ìm, PM2.5) andthe “ultrafine” (aerodynamic diameter <0.1 Ìm, PM0.1) particles, as they are solvable, can be transmittedeasily into the circulation and exert immediate action on various systems, including the heart. In thecardiovascular system they may cause arrhythmias, exacerbation of ST-segment, bradycardia, arterialvasoconstriction even myocardial infarction. The direct effect on the autonomic nervous system canlead to dangerous tachycardia or even inidism. When alveolar macrophages are exposed to PM producecytokines, which promote increase of the levels of endothelin-1 (ET-1) in the blood. This results invasoconstriction, a rise in blood pressure and increased risk of coronary heart disease and myocardialinfarction. Children, the elderly and patients with chronic cardiovascular disease are the groups mostsensitive to air pollution, but recently even intrauterine fetal death has been reported.
Key words: Air pollution, particulate matter, cardiovascular system.
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·18
19∏ ›‰Ú·ÛË Ù˘ ·¤ÚÈ·˜ Ú‡·ÓÛ˘ ÛÙÔ Î˘ÎÏÔÊÔÚÈÎfi
¶·È‰È·ÙÚÈ΋ 2006;69:18-24
∂ÈÛ·ÁˆÁ‹
∏ Û¯¤ÛË ÙˆÓ ·ÈˆÚÔ‡ÌÂÓˆÓ ÛˆÌ·Ùȉ›ˆÓ ÙÔ˘
·¤Ú· ÛÙËÓ ·ıÔÏÔÁ›· ÓfiÛˆÓ ÙÔ˘ ·Ó·Ó¢ÛÙÈ-
ÎÔ‡ Û˘ÛÙ‹Ì·ÙÔ˜ Î·È ÙÔ˘ ηÚΛÓÔ˘ ÙÔ˘ Ó‡ÌÔ-
Ó· ¤¯ÂÈ ·Ô‰Âȯı› Â‰Ò Î·È ·ÚÎÂÙ¿ ¯ÚfiÓÈ·
(1-4). ∆ËÓ ÙÂÏÂ˘Ù·›· ‰ÂηÂÙ›· ¤¯ÂÈ ·Ó·ÁÓˆÚÈ-
Ûı› Ô ÚfiÏÔ˜ ÙÔ˘˜ Î·È Û ·ı‹ÛÂȘ ÙÔ˘ ηÚ-
‰È·ÁÁÂÈ·ÎÔ‡ Û˘ÛÙ‹Ì·ÙÔ˜, ÙfiÛÔ Ì ÂȉËÌÈÔÏÔ-
ÁÈΤ˜ ÌÂϤÙ˜, fiÛÔ Î·È Ì ÂÈÚ·Ì·ÙÈΤ˜ ÂÚÁ·-
ۛ˜ (5-7), ÛÙȘ Ôԛ˜ ·Ô‰ÂÈÎÓ‡ÂÙ·È fiÙÈ Ë ·‡-
ÍËÛË Ù˘ ·¤ÚÈ·˜ Ú‡·ÓÛ˘ Û¯ÂÙ›˙ÂÙ·È Ì ·‡ÍË-
ÛË Ù˘ ÓÔÛËÚfiÙËÙ·˜, ÙˆÓ ÂÈÛ·ÁˆÁÒÓ Û ÓÔÛÔ-
ÎÔÌ›· Î·È Ù˘ ıÓËÛÈÌfiÙËÙ·˜ ·fi ηډȷÁÁÂÈ·-
ο ·›ÙÈ·. ∫¿ı ÁˆÁÚ·ÊÈ΋ ÂÚÈÔ¯‹ Î·È Î¿ıÂ
fiÏË ¤¯ÂÈ ÙË ‰È΋ Ù˘ ÔÈÎÈÏ›· Ú‡ˆÓ. ŒÙÛÈ ÔÈ
ı¿Ó·ÙÔÈ Ô˘ Û¯ÂÙ›˙ÔÓÙ·È Ì ÙËÓ ·¤ÚÈ· Ú‡·ÓÛË
‰È·Ê¤ÚÔ˘Ó ÛÙȘ ‰È¿ÊÔÚ˜ ÛÙ·ÙÈÛÙÈΤ˜ (2-7).
∂›‰Ë ۈ̷Ùȉ›ˆÓ
∆· ∞ȈÚÔ‡ÌÂÓ· ™ˆÌ·Ù›‰È· (∞™), Ù· ÔÔ›·
ÛÙË ‰ÈÂıÓ‹ ‚È‚ÏÈÔÁÚ·Ê›· ·Ó·Ê¤ÚÔÓÙ·È ˆ˜
Particulate Matter (PM), Â›Ó·È ÛÙÂÚ¿ ‹ ˘ÁÚ¿
ۈ̷ٛ‰È· (ÛÙ·ÁÔÓ›‰È·), Ô˘ ‚Ú›ÛÎÔÓÙ·È Û ‰È·-
ÛÔÚ¿ ÛÙËÓ ·ÙÌfiÛÊ·ÈÚ· Î·È Î·Ï‡ÙÔ˘Ó Â˘Ú‡
Ê¿ÛÌ· ÌÂÁÂıÒÓ, Ì ·ÂÚÔ‰˘Ó·ÌÈ΋ ‰È¿ÌÂÙÚÔ d
·fi <0,1 Ìm ̤¯ÚÈ >100 Ìm. ∞ÔÙÂÏÔ‡ÓÙ·È ·fi
Ì›ÁÌ· ÚÔ˚fiÓÙˆÓ Î·‡ÛˆÓ, ‚·Ú¤ˆÓ ÌÂÙ¿ÏψÓ,
¯ËÌÈÎÒÓ ·Ï¿ÙˆÓ Î·È ‚ÈÔÏÔÁÈÎÒÓ ˘ÏÈÎÒÓ fiˆ˜
ÌÈÎÚfi‚È·, ÈÔ› Î·È ÂÓ‰ÔÙÔ͛Ә (8). ∏ ¯ËÌÈ΋ ÙÔ˘˜
Û‡ÛÙ·ÛË ‰È·Ê¤ÚÂÈ ·Ó¿ÏÔÁ· Ì ÙËÓ ËÁ‹ ÂÎÔ-
Ì‹˜ ÙÔ˘˜. ¢È·ÎÚ›ÓÔÓÙ·È ·Ó¿ÏÔÁ· Ì ÙÔ Ì¤ÁÂıfi˜
ÙÔ˘˜ ·) Û “·Ó¿ÈÙ·”, Ì ÌÂÁ¿ÏÔ Ì¤ÁÂıÔ˜ (>10
Ìm) Î·È ÌÈÎÚfi ¯ÚfiÓÔ ·ÈÒÚËÛ˘, Ô˘ ηٷÎÚ·-
ÙÔ‡ÓÙ·È ·fi ÙÔÓ ÚÈÓÈÎfi ‚ÏÂÓÓÔÁfiÓÔ Î·È ‰ÂÓ ÂÈ-
Û¤Ú¯ÔÓÙ·È ÛÙÔÓ ÔÚÁ·ÓÈÛÌfi, ‚) Û “·Ó·Ó‡ÛÈ-
Ì·” (coarce, PM10 2,5-10 Ìm), Ù· ÔÔ›· ·Ó¿ÏÔÁ·
Ì ÙË ¯ËÌÈ΋ ÙÔ˘˜ Û‡ÛÙ·ÛË ÂÓÔ¯ÔÔÈÔ‡ÓÙ·È ÁÈ·
·ÛıÌ·ÙÈΤ˜ ÎÚ›ÛÂȘ, ̤¯ÚÈ Î·ÚΛÓÔ ÙÔ˘ Ó‡ÌÔ-
Ó·, Á) ÛÂ “ÏÂÙ¿” ‹ “ÌÈÎÚ¿” (fine PM2,5 <2,5 Ìm)
Î·È ‰) Û “Ôχ ÏÂÙ¿” ‹ “Ôχ ÌÈÎÚ¿” (ultra-
fine PM0,1 <0,1 Ìm) ۈ̷ٛ‰È·. √È ‰‡Ô ÙÂÏÂ˘Ù·›-
˜ ηÙËÁÔڛ˜ ۈ̷Ùȉ›ˆÓ ÂÓÔ¯ÔÔÈÔ‡ÓÙ·È ÁÈ·
ÙȘ ‚Ï¿‚˜ ÛÙÔ Î˘ÎÏÔÊÔÚÈÎfi Û‡ÛÙËÌ·, ηıÒ˜
Â›Ó·È ‰È·Ï˘Ù¿ Î·È ·fi ÙȘ ΢„ÂÏ›‰Â˜ ÌÂٷʤÚÔ-
ÓÙ·È ·Â˘ı›·˜ ÛÙË ÁÂÓÈ΋ ΢ÎÏÔÊÔÚ›· (8). ∆·
ÈÔ ÂÈΛӉ˘Ó· ∞™ Â›Ó·È ÙÔ˘ ÌÔχ‚‰Ô˘ (·fi
‚ÂÓ˙›Ó˜ Ì ·ÓÙÈÎÚÔÙÈο), ÙÔ˘ ·ÌÈ¿ÓÙÔ˘ (˘ÏÈο
ÊÚ¤ÓˆÓ ·˘ÙÔÎÈÓ‹ÙˆÓ) ηıÒ˜ Î·È ÛˆÌ·Ù›‰È· ¯Ë-
ÌÈÎÒÓ ·Ï¿ÙˆÓ Î·È ¿ÏÏˆÓ ÌÂÙ¿ÏÏˆÓ ·fi ‰Â˘ÙÂ-
ÚÔÁÂÓ›˜ ¯ËÌÈΤ˜ ·ÓÙȉڿÛÂȘ. ÕÏÏ· ÙÔÍÈο ∞™
Â›Ó·È ·˘Ù¿ Ô˘ ÂÚȤ¯Ô˘Ó ηÚÎÈÓÔÁfiÓÔ˘˜ Ô-
Ï˘·ÚˆÌ·ÙÈÎÔ‡˜ ˘‰ÚÔÁÔÓ¿ÓıڷΘ. √È ËÁ¤˜
Ú‡·ÓÛ˘ Ù˘ ·ÙÌfiÛÊ·ÈÚ·˜ Ì ∞™ Â›Ó·È ÔÈ ‚ÈÔ-
Ì˯·Ó›Â˜ (ÙÛÈÌÂÓÙÔ·Ú·ÁˆÁ‹˜, Ï·ÙÔÌ›·, ÂÚÁÔ-
ÛÙ¿ÛÈ· ·Ú·ÁˆÁ‹˜ ËÏÂÎÙÚÈÎÔ‡ Ú‡̷ÙÔ˜, ¯·Ï˘-
‚Ô˘ÚÁ›·), ÔÈ ÎÂÓÙÚÈΤ˜ ıÂÚÌ¿ÓÛÂȘ ÔÈÎÈÒÓ Î·È
ÔÏ˘Î·ÙÔÈÎÈÒÓ, ÔÈ ÂÍ·ÙÌ›ÛÂȘ ·˘ÙÔÎÈÓ‹ÙˆÓ, Ë
ÙÚÈ‚‹ ÂÏ·ÛÙÈÎÒÓ Î·È Ë ÛÎfiÓË ÙÔ˘ ‰¿ÊÔ˘˜. ∫˘-
ÚÈfiÙÂÚË ËÁ‹ ·ÛÙÈÎÒÓ Ú‡ˆÓ Â›Ó·È Ù· ·˘ÙÔΛÓË-
Ù· (ÔÛÔÛÙfi ·fi 46,7-64,3%) Î·È Ë Î·‡ÛË Â-
ÙÚÂÏ·›Ô˘ (ÔÛÔÛÙfi 8,4-28%) (9).
∞ÙÌÔÛÊ·ÈÚÈÎÔ› Ú‡ÔÈ
√È Î˘ÚÈfiÙÂÚÔÈ ·ÙÌÔÛÊ·ÈÚÈÎÔ› Ú‡ÔÈ Â›Ó·È ÙÔ
‰ÈÔÍ›‰ÈÔ ÙÔ˘ ı›Ԣ (SO2, ηÙ' ÂÍÔ¯‹Ó ‚ÈÔÌ˯·-
ÓÈÎfi˜ Ú‡Ô˜), Ù· ·˙ˆÍ›‰È·, Ô˘ ‰È·ÎÚ›ÓÔÓÙ·È
Û ÓÈÙÚÈο ÔÍ›‰È· (NOx) Î·È ‰ÈÔÍ›‰ÈÔ ÙÔ˘ ·˙Ò-
ÙÔ˘ (NO2) Î·È Â›Ó·È Î˘Ú›ˆ˜ ÚÔ˚fiÓÙ· η‡ÛˆÓ,
ÙÔ ÌÔÓÔÍ›‰ÈÔ ÙÔ˘ ¿Óıڷη (C√, ÚÔ˚fiÓ Î·‡-
ÛÂˆÓ Â›Û˘), Ë Ù¤ÊÚ· (ÂÚȤ¯ÂÈ ÔÍ›‰È· ÌÂ-
Ù¿ÏÏˆÓ ·fi η‡ÛË ÏÈÁÓ›ÙË ÁÈ· ·Ú·ÁˆÁ‹ ËÏÂ-
ÎÙÚÈÎÔ‡ Ú‡̷ÙÔ˜), ÔÈ ˘‰ÚÔÁÔÓ¿ÓıڷΘ (∏C,
·fi ·ÙÂÏ‹ η‡ÛË ·˘ÙÔÎÈÓ‹ÙˆÓ) Î·È ÙÔ fi˙ÔÓ
(O3, ÚÔ˚fiÓ ÊˆÙÔ¯ËÌÈÎÒÓ ·ÓÙȉڿÛÂˆÓ ÛÙËÓ
·ÙÌfiÛÊ·ÈÚ· ·fi NOx, O2 Î·È ËÏȷ΋ ·ÎÙÈÓÔ‚Ô-
Ï›·). √ ηı¤Ó·˜ ·fi ÙÔ˘˜ Ú‡Ô˘˜ ·˘ÙÔ‡˜ ¤¯ÂÈ
‰È·ÊÔÚÂÙÈ΋ ›‰Ú·ÛË ÛÙÔÓ ·ÓıÚÒÈÓÔ ÔÚÁ·-
ÓÈÛÌfi (¶›Ó·Î·˜ 1).
∞Ó·Ó¢ÛÙÈÎfi
∏ Û¯¤ÛË ÙˆÓ ·ÙÌÔÛÊ·ÈÚÈÎÒÓ Ú‡ˆÓ Î·È ÙˆÓ
∞™ Ì ·ı‹ÛÂȘ ÙÔ˘ ·Ó·Ó¢ÛÙÈÎÔ‡ ¤¯ÂÈ ÌÂÏÂ-
ÙËı› Î·È ÂÚÈÁÚ·Ê› ‰ÈÂÍÔ‰Èο. ∆· ÌÂÁ·Ï‡ÙÂ-
Ú· ∞™ Ô˘ ηٷÎÚ·ÙÔ‡ÓÙ·È ÛÙÔÓ ÚÈÓÈÎfi ‚ÏÂÓ-
ÓÔÁfiÓÔ, ÙËÓ ÙÚ·¯Â›· Î·È ÙÔ˘˜ ‚ÚfiÁ¯Ô˘˜ ÚÔη-
ÏÔ‡Ó ·ÏÏÂÚÁÈ΋ ÚÈÓ›Ùȉ·, ÙÚ·¯ÂÈ›Ùȉ·, ¯ÚfiÓÈ·
‚ÚÔÁ¯›Ùȉ· Î·È ‚ÚÔÁ¯ÈÎfi ¿ÛıÌ·. √È ÂÚÂıÈÛÙÈΤ˜
Ô˘Û›Â˜ fiˆ˜ SO2, NOx, O3 Î·È ·ÏÏÂÚÁÈÔÁfiÓ·
ۈ̷ٛ‰È· ÚÔηÏÔ‡Ó ¿ÛıÌ· Î·È ¯ÚfiÓȘ ·Ô-
ÊÚ·ÎÙÈΤ˜ Ó¢ÌÔÓÔ¿ıÂȘ, ÂÓÒ ÙÔ ‚ÂÓ˙fiÏÈÔ,
Ô ·Ì›·ÓÙÔ˜ Î·È ¿ÏÏ· ‚·Ú¤· ̤ٷÏÏ· ÚÔη-
ÏÔ‡Ó Î·ÚΛÓÔ ÙÔ˘ Ó‡ÌÔÓ· (∂ÈÎfiÓ· 1) (1).
∆· ۈ̷ٛ‰È· Ì ‰È¿ÌÂÙÚÔ <10 Ìm ‰ÈÂÈÛ‰‡-
Ô˘Ó ÛÙÔÓ ‰È¿ÌÂÛÔ ÈÛÙfi Î·È ÚÔηÏÔ‡Ó ›ÓˆÛË Î·È
‰ËÌÈÔ˘ÚÁ›· ÎÔÎÎȈ̿وÓ. ∆· ÌÈÎÚ¿ (<2,5 Ìm)
Î·È Ù· Ôχ ÌÈÎÚ¿ ∞™ (<0,1 Ìm) Â›Ó·È Î·È Ù· ÈÔ
ÂÈΛӉ˘Ó·, ÁÈ·Ù› ·ÊÂÓfi˜ ‰ÈÂÈÛ‰‡Ô˘Ó ·Â˘ı›·˜
ÛÙËÓ Î˘ÎÏÔÊÔÚ›· ÙÔ˘ ·›Ì·ÙÔ˜ Î·È ‰ÚÔ˘Ó ÛÂ
‰È¿ÊÔÚ· fiÚÁ·Ó·, ·ÊÂÙ¤ÚÔ˘ Û¯ÂÙ›˙ÔÓÙ·È Ì ÙË
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·19
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38. Raaschou-Nielsen O, Hertel O, Thomsen BL, OlsenJH. Air pollution from traffic at the residence of chil-dren with cancer. Am J Epidemiol 2001;153:433-443.
41. Gourgoulianis KI, Brelas N, Hatziparasides G, Pa-payianni M, Molyvdas PA. The influence of altitudein bronchial asthma. Arch Med Res 2001;32:429-431.
42. Priftis K, Panagiotopoulou-Gartagani P, Tapratzi-Potamianou P, Zachariadi-Xypolita A, Sagriotis A,Saxoni-Papageorgiou P. Hospitalizations for child-hood asthma in Athens, Greece, from 1978 to 2000.Pediatr Allergy Immunol 2005;16:82-85.
43. Anthracopoulos M, Karatza A, Liolios E, Triga M,Triantou K, Priftis K. Prevalence of asthma amongschoolchildren in Patras, Greece: three surveys over20 years. Thorax 2001;56:569-571.
44. Mihailidou H, Paspalaki P, Skalidaki M, Katakis E,Smyrnaki P, Mantzouranis E. Decreasing morbidityof childhood asthma by regular outpatient follow-up, in Crete. Minerva Pediatr 2004;56:197-206.
45. Haines A, McMichael AJ, Epstein PR. Environmentand health: Global climate change and health. CMAJ2000;163:729-734.
46. ∂˘Úˆ·˚΋ ∂ÈÙÚÔ‹ ∫·ı·ÚÔ‡ ∞¤Ú· ÁÈ· ÙȘ ¶fiÏÂȘÙ˘ ∂˘ÚÒ˘ - Swiss Participation in European Re-search Programmes. APHEA 2: Short-term effects ofair pollution on health - A European approach tomethodology, dose response assessment and evalua-tion of public health significance. [Abstract, Inter-net]. Webpage: http://www.sbf.admin.ch/htm/services/publikationen/international/frp/eu-abstracts/html/fp/fp4/env97.0477.html.
¶·È‰È·ÙÚÈ΋ 2006;69:18-24
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·24
Is there or not vitamin D deficiency in children and adolescents in
Greece?
D. Lapatsanis1, A. Moulas2, V. Cholevas2, P. Soukakos3, Z. Papadopoulou1, A. Challa2
Abstract
Background: Season and changes in the way of living significantly modify exposure to the sun,which is important for vitamin D synthesis in the skin. Children and adolescents who have high boneturnover may comprise a high-risk population for vitamin D deficiency.
Methods: A sample of 210 clinically healthy children aged 3 to 18 years, were assigned into three agegroups: 3-10, 11-14 and 15-18 years of age. Blood samples were taken during winter and summer fordetermining calciotropic hormones, calcium, phosphate (Pi) and biochemical markers of bonesynthesis.
Results: The 47% of the subjects aged 15-18 years, and 13-14% of the 3-14 years, had 25OHD levels<10 ng/ml in the winter. In the summer all had 25OHD>10 ng/ml. The prevalence ofhypovitaminosis D was higher in the older girls, accompanied by lower Pi concentrations in thewinter (win.: 1.19±0.03, sum.: 1.39±0.03 mmol/l, p<0.001). The 24,25(OH)2D levels in the oldersubjects were lower by 2/3 in the winter than in the summer (0.73±0.10 vs 2.41±0.20 ng/ml, p<0.001).The biochemical markers of bone synthesis, osteocalcin (OC) and total alkaline phosphatase (ALP)were significantly lower in the older girls in both winter and summer, respectively (OC: 5.8±0.3 vs
1 Department of Paediatrics,Medical School, University of Ioannina
2 Laboratory of Paediatrics,Medical School, University of Ioannina
3 Department ofOrthopedics, MedicalSchool, University of Ioannina
Correspondence:
Anna ChalaDepartment of Paediatrics, Medical School, University of Ioannina451 10, IoanninaE-mail: [email protected]
Date of submission: 03-09-2004Date of approval: 28-11-2005
Pediatr Jan-Feb 06 final allges 27-01-06 15:34 ™ÂÏ›‰·25
26 ¢. §··ÙÛ¿Ó˘ Î·È Û˘Ó.
¶·È‰È·ÙÚÈ΋ 2006;69:25-36
8.7±0.6 and 4.6±0.3 vs 7.3±0.5 ng/ml, p<0.001; ALP: 108±5 vs 212±28 and 116±7 vs 248±31 IU/l,p<0.001).
Conclusions: In Greece young people aged 15-18 years, are at increased risk of vitamin D deficiencyduring the winter. Vitamin D supplementation of milk and popular beverages would be of help incounteracting this.
Key words: Vitamin D deficiency, children and adolescents.
27. Manios Y, Babaroutsi E, Bletsa M, Rammata M, Si-
dossis S, Yannakoulia M, Sidossis LS. Physical Activ-
ity, calcium intake and bone mineral density in a se-
mi-representative sample of Greek pupils and adults
[Abstract]. 2nd Congress of the European Chapter
of the American College of Nutrition; 2002 Novem-
ber 15-16; Athens, Greece.
28. Bletsa M, Babaroutsi E, Sidossis S, Manios Y, Sidos-
sis LS. Prevalence of osteopenia and osteoporosis in
Greece [Abstract]. 2nd Congress of the European
Chapter of the American College of Nutrition; 2002
November 15-16; Athens, Greece.
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30. McKenna MJ. Differences in vitamin D status be-
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31. Lehtonen-Veromaa M, Mottonen T, Irjala K,
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yvitamin D is a metabolite of vitamin D essential for
bone formation. Nature 1978;276:517-519.
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sue Int 1997;61:104-109.
37. Douglas AS, Miller MH, Reid DM, Hutchison JD,
Porter RW, Robins SP. Seasonal differences in bio-
chemical parameters of bone remodeling. J Clin
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38. Round JM. Plasma calcium, magnesium, phospho-
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schoolchildren. Brit Med J 1973;3:137-140.
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40. Kristinsson JO, Valdimarsson O, Sigurdsson G,
Franzson L, Olafsson I, Steingrimsdottir L. Serum
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sity in 16-20-year-old girls. Lack of association. J In-
tern Med 1998;243:381-388.
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amin D metabolites in puberty: Effect of sexual mat-
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docrinol Metab 1982;55:94-101.
42. Mora S, Pitukcheewanont P, Kaufman FR, Nelson
JC, Gilsanz V. Biochemical markers of bone
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43. Seydewitz HH, Henschen M, Kuhnel W, Brandis M.
Pediatric reference ranges for osteocalcin measured
by the Immulite analyzer. Clin Chem Lab Med
2001;39:980-982.
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wald R. Calcium accretion in girls and boys during
puberty: A longitudinal analysis. J Bone Miner Res
2000;15:2245-2250.
45. Price PA, Baukol SA. 1,25-Dihydroxyvitamin D3 in-
creases synthesis of the vitamin K-dependent bone
protein by osteosarcoma cells. J Biol Chem
1980;255:11660-11665.
46. Matkovic V. Calcium metabolism and calcium re-
quirements during skeletal modeling and consolida-
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47. Guillemant J, Cabrol S, Allemandou A, Peres G,
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tion of PTH in growing male adolescents. Bone
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48. Dawson-Hughes B, Harris SS, Dallal GE. Plasma
calcidiol, season, and serum parathyroid hormone
concentrations in healthy elderly men and women.
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49. Heaney RP, Dowell MS, Hale CA, Bendich A. Calci-
um absorption varies within the reference range for
serum 25-hydroxyvitamin D. J Am Coll Nutr
2003;22:142-146.
50. DeLuca HF, Cantorna MP. Vitamin D: its role and
uses in immunology. FASEB J 2001;15:2579-2585.
51. Mathieu C, Waer M, Laureys J. Rutgeerts O, Bouil-
lon R. Prevention of autoimmune diabetes in NOD
mice by 1,25 dihydroxyvitamin D3. Diabetologia
1994;37:552-558.
52. Cantorna MT, Hayes CE, DeLuca HF. 1,25-Dihy-
droxyvitamin D3 reversibly blocks the progression of
relapsing encephalomyelitis, a model of multiple scle-
rosis. Proc Natl Acad Sci USA 1996;93:7861-7864.
53. Cantorna MT, Hayes CE, DeLuca HF. 1,25 Dihy-
droxyvitamin D3 inhibits the progression of arthritis
in murine models of human arthritis. J Nutr 1998;
128:68-72.
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·35
36 ¢. §··ÙÛ¿Ó˘ Î·È Û˘Ó.
54. Hyppönen E, Läärä E, Reunanen A, Järvelin MR,Virtanen SM. Intake of vitamin D and risk of type 1diabetes: a birth-cohort study. Lancet 2001;358:1500-1503.
55. Krause R, Buhring M, Hopfenmuller W, Holick MF,Sharma AM. Ultraviolet B and blood pressure.Lancet 1998;352:709-710
56. Holick MF. Vitamin D: importance in the preven-tion of cancers, type I diabetes, heart disease, and os-teoporosis. Am J Clin Nutr 2003;79:362-371.
57. Grant WB. An estimate of premature cancer mortal-ity in the U.S. due to inadequate doses of solar ul-traviolet-B radiation. Cancer 2002;94:1867-1875.
¶·È‰È·ÙÚÈ΋ 2006;69:25-36
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·36
Morbidity and clinical manifestations of brucellosis in Greece
M. Mavrokosta, E. Galanakis
Abstract: Despite the preventive efforts, brucellosis remains endemic in many areas worldwide. ∆helong-term morbidity of the disease in Greece was investigated in the present study, with an emphasison childhood morbidity. The study was based on the data reported from 1979 through 2003 by theGreek National Statistical Service and in the relevant published studies. During the 1980s, brucellosispresented with a decrease in morbidity, but a reemergence was observed in the mid 1990s. Theaverage annual incidence was 4.38 reported cases and 7.76 admissions / 100,000 population. Amongthe hospitalized patients, 11,2% were children aged less than 14 years, and average annual incidencewas calculated at 5.08 admissions / 100,000 child population. The morbidity in childhood andadolescence increased with age. Male and female infants and toddlers were equally affected, but malespresented with a considerably higher morbidity during late childhood and adolescence. Endemicareas were identified, mainly in Northern Greece. The lowest incidence rates were observed in theislands and in urban areas. The protean clinical manifestations of brucellosis were confirmed in theGreek published studies. The persistence and the recent reemergence of brucellosis in Greece stressthe need of animal control and pasteurization of milk and dairy products, and of screening thefamilies of index cases. Physicians should think of brucellosis when caring for patients who reside inor have traveled to endemic areas and who present with atypical manifestations.
1. Vassalo DJ. The saga of brucellosis: controversy overcredit for linking Malta fever with goats’ milk.Lancet 1996;348:804-808.
2. Young EJ. An overview of human brucellosis. ClinInfect Dis 1995;21:283-290.
3. Corbel MJ. Brucellosis: an overview. Emerg InfectDis 1997;3:213-221.
4. Sauret JM, Vilissova N. Human brucellosis. J AmBoard Fam Pract 2002;15:401-406.
5. Taleski V, Zerva L, Kantardjiev T, Cvetnic Z, Erski-Biljic M, Nikolovski B et al. An overview of theepidemiology and epizootology of brucellosis inselected countries of Central and Southeast Europe.Vet Microbiol 2002;90:147-155.
69. Benecos P, Spingou T, Galanakis E, Lapatsanis PD.
Thrombocytopenic purpura secondary to brucellosis.Eur J Pediatr 1998;157:698.
70. Apostolova E, Papadopoulos V, Leptidou-KerestetziT. Branchial cyst empyema due to Brucella melitensisinfection as a form of focal Brucellosis. J Infect2002;44:271.
2 Laboratory of Radiology,“Ippokration” GeneralHospital Thessaloniki
3 Department of Nutrition,“Ippokration” GeneralHospital Thessaloniki
4 Department ofOphtalmology,“Ippokration” GeneralHospital Thessaloniki
5 Laboratory of Pathology,“Ippokration” GeneralHospital Thessaloniki
6 Dept. of Clinical Chemistry,Sahlgrenska UniversityHospital, Gothenburg,Sweden
¶·È‰È·ÙÚÈ΋ 2006;69:45-51
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·45
46 ¶. ∞˘ÁÔ˘ÛÙ›‰Ô˘-™·‚‚ÔÔ‡ÏÔ˘ Î·È Û˘Ó.
Correspondence:
P. Augoustides-SavvopoulouBiochemistry-MetabolismLaboratory1st Paediatric Clinic of Aristotle University“Ippokration” General Hospital Thessaloniki49, Konstantinoupoleos Str., 546 42, Thessaloniki ∂-mail: [email protected]
Date of submission: 21-03-2005Date of approval: 28-11-2005
¶·È‰È·ÙÚÈ΋ 2006;69:45-51
with NTBC, the patient is in excellent clinical condition. As far as we are aware, he is the firsttyrosinaemia type I patient on a therapeutic regimen of NTBC in Greece.
Key words: ∆yrosinaemia type I, therapy, NTBC, hepato-renal.
Schimke immuno-osseous dysplasia. Case report and review of the
literature
S. Psoni1, H. Georgaki2, A. Kapogiannis2, A. Salavoura3, M. Kanariou3, F. Sotsiou4, H. Fryssira1
Abstract: Schimke immuno-osseous dysplasia (SIOD) [(Schimke immuno-osseous dysplasia -SIOD, Online Mendelian Inheritance In Man, website: http://www.ncbi.nlm.nih.gov/htbin-post/OMIM; OMIM:242900)] is a rare autosomal recessive disorder characterized by spondylo-epiphyseal dysplasia, renal failure, defective cellular immunity and distinct phenotype withdisproportionate short stature, triangular face, bulbous nose and abdominal pigmented spots. Theresponsible gene has been mapped recently. SIOD must be included in the differential diagnosis ofcases with growth retardation and osseous dysplasia, as the prognosis can be poor, because of severedamage of the cellular immunity and renal insult. A case of a three year-old boy with short stature andproteinuria, characteristic features in this condition, is described.
£ÂṲ́˜ ¢¯·ÚÈÛٛ˜ ÛÙÔÓ Assistant Professor C.F.Boerkoel ·fi ÙÔ ∆Ì‹Ì· ªÔÚȷ΋˜ °ÂÓÂÙÈ΋˜ ÙÔ˘∞ÓıÚÒÔ˘ ÙÔ˘ Baylor College of Medicine, USA.
µÈ‚ÏÈÔÁÚ·Ê›·
1. Lou S, Lamfers P, McGuire N, Boerkoel CF. Longevi-ty in Schimke immuno-osseous dysplasia. J MedGenet 2002;39:922-925.
2. Schimke RN, Horton WA, King CR, Martin NL.Chondroitin-6-sulfate mucopoly-saccharidosis inconjunction with lymphopenia, defective cellular im-munity and the nephrotic syndrome. Birth DefectsOrig Artic Ser 1974;10:258-266.
3. Sigurdardorttir S, Myers SM, Woodworth JM, Ray-mond GV. Mental retardation and seizure disorder inSchimke immunoosseous dysplasia. Am J Med Genet2000;90:294-298.
5. Boerkoel CF, Takashima H, John J, Yan J, StankiewiczP, Rosenbarker L et al. Mutant chromatin remodelingprotein SMARCAL1 causes Schimke immuno-os-seous dysplasia. Nat Genet 2002;30:215-220.
6. Boerkoel CF, O'Neill S, Andre JL, Benke PJ, Bog-danovic R, Bulla M et al. Manifestations and treat-ment of Schimke immuno-osseous dysplasia: 14 newcases and a review of the literature. Eur J Pediatr2000;159:1-7.
8. Ludman MD, Cole DE, Crocker JF, Cohen MM Jr.Schimke immuno-osseous dysplasia: case report andreview. Am J Med Genet 1993;47:793-796.
9. Saraiva JM, Dinis A, Resende C, Faria E, Gomes C,Correia AJ et al. Schimke immuno-osseous dysplasia:case report and review of 25 patients. J Med Genet1999;36:786-789.
10. Tylki-Szymanska A, Pyrkosz A, Krajewska-WalasekM, Michalkiewicz J, Kowalska A, Rokicki D. Schimkeimmuno-osseous dysplasia: two cases. Pediatr Radiol2003;33:216-218.
11. Stormon M, Friedman J, King S, Cutz E, Furuya KN.An unusual case of diarrhea in schimke immuno-os-seous dysplasia. J Pediatr Gastroenterol Nutr2002;35:369-371.
12. Petty EM, Yanik GA, Hutchinson RJ, Alter BP, Sch-malstieg FC, Levine JE et al. Successful bone marrowtransplantation in a patient with Schimke immuno-osseous dysplasia. J Pediatr 2000;137:882-886.
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·58
The importance of vision tests in pre-school and school age children
in the primary paediatric setting
A. Xekalaki, I. Antoniadou - Koumatou
Abstract: Undetected vision problems in children can lead to a variety of adverse consequences. Themost serious of these are amblyopia and inadequate school performance. Vision assessment shouldbe carried out as part of the regular paediatric examination. Screening tests for vision need to beappropriate for the various ages of children.
1. Appelboom TM. A history of vision screening. J SchHealth 1985;55:138-141.
2. Hartmann EE, Dobson V, Hainline L, Marsh-TootleW, Quinn GE, Ruttum MS, et al. Preschool visionscreening: summary of a Task Force report. Behalfof the Maternal and Child Health Bureau and theNational Eye Institute Task Force on Vision Screen-ing in the Preschool Child. Pediatrics 2000;106:1105-1161.
3. The Official Website of the Nobel Foundation. The1981 Prize in Physiology or Medicine. [Webpage, In-ternet]. The Nobel Assembly of Karolinska Institutet.www.nobel.se/medicine/laureates/1981/press.html.
4. Snowdon SK, Stewart Brown SL. Preschool visionscreening [Executive Summary]. Health TechnolAssess 1997;1:1-83.
6. Moseley MJ. Preschool vision screening: a recent re-port calls for a halt [Commentary]. Br J Opthalmol1998;82:722-723.
7. Rahi JS, Dezateux C. The future of preschool visionscreening services in Britain [Editorials]. BMJ 1997;315:1247-1248.
8. Ciner EB, Schmidt PP, Orel-Bixler D, Dobson V,Maguire M, Cyert L, et al. Vision screening ofpreschool children: evaluating the past, looking to-ward the future. Optom Vis Sci 1998;75:571-584.
9. Wasserman RC, Croft CA, Brotherton SE. Preschoolvision screening in pediatric practice: A study fromthe pediatric research in office setting (PROS) Net-work. Pediatrics 1992;89:834-838.
10. Newman DK, Hitchcock A, McCarthy H, Keast-Butler J, Moore AT. Preschool vision screening: out-come of children referred to the hospital eye service.Br J Ophthalmol 1996;80:1077-1082.
11. Preslan MW, Novak A. Baltimore Vision ScreeningProject. Ophthalmology 1996;103:105-109.
12. Bolger PG, Stewart-Brown SL, Newcombe E, Star-buck A. Vision screening in preschool children: com-parison of orthoptists and clinical medical officers asprimary screeners. BMJ 1997;303:1291-1294.
13. Yang YF. Visual acuity testing in schools: what needsto be done [Paper]. BMJ 1996;313:1053.
14. Hall DBM, ed. Health for all children. Report of the
¶·È‰È·ÙÚÈ΋ 2006;69:59-64
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·63
64 ∞. •ÂηϿÎË, π. ∞ÓÙˆÓÈ¿‰Ô˘-∫Ô˘Ì¿ÙÔ˘
third joint working party on child Health Surveil-lance. 3rd ed. Oxford: Oxford University Press;1996. p. 164.
15. AAP Policy statement: Eye examination and Visionscreening in infants, children and young adults. Pe-diatrics 1996;98:153-157.
17. American Optometric Association. Pediatric eyeand vision examination. Reference guide for clini-cians. Prepared by the American Optometric Asso-ciation Consensus Approved by the AOA Board ofTrustees. 1994 June 23, 2nd ed. 1997.
22. Salt AT, Sonksen PM, Wade A, Jayatunga R. Thematuration of linear acuity and compliance with theSonksen-Silver Acuity System in young children.Dev Med Child Neurol 1995;37:505-514.
23. Jayatunga R, Sonksen PM, Bhide, A, Wade A. Mea-sures of acuity in primary-school children and their
ability to detect minor errors of vision. Dev MedChild Neurology 1995;37:515-527.
24. Hered RW, Murphy S, Clancy M. Comparison ofthe HOTV and LEA Symbols charts for preschoolvision screening. J Ophthalmic Nurs Technol 1997;16:68-73.
25. Wade AM, Ades AE, Salt AT, Jayatunga R, SonksenPM. Age-related standards for ordinal data: model-ing the changes in visual acuity form 2 to 9 years ofage. Stat Med 1995;15,14(3):257-266.
26. Lea Huvärinen MD. Precision Vision. InstructionManual for vision testing products. http://www.lea-test.sgic.fi ‹ http://med-apos.bu.edu/leaweb/index.html. 2001; p. 4.
27. Newman, East MM. Preschool vision screening: neg-ative predictive value for amblyopia. Br J Opthalmol1999;83:676-679.
28. Simons K. Preschool vision screening: rationale,methodology, and outcome. Surv Ophthalmol 1996;41:3-30.
29. Morad Y, Werker E, Nemet P. Visual acuity tests us-ing chart, line and single optotype in healthy ambly-opic children. J AAPOS 1999;3:94-97.
30. Fern KD, Manny RE. Visual acuity of the preschoolchild: a review. Am J Optom Physiol Opt 1986;63:319-345.
31. Kohler L. Early detection and screening evaluationof preventive programmes. Pediatriki 1983;46 (Sup-pl):S337-S341.
32. U.S. Department of Health and Human Services.Agency for Healthcare Research and Quality. Screen-ing for Visual Impairment in Children Younger thanAge 5 Years. Systematic Evidence Review for the U.S.Preventive Services Task Force. May 2004.
33. Lindstedt E. What is a vision test. Presented Oct26th 1991 at the opening of the Eva Lindstedt EarlyIntervention Programme at the Eye Clinic-SantaCasa Hospital-SaoPaulo, Brazil.
¶·È‰È·ÙÚÈ΋ 2006;69:59-64
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·64
Red reflex examination in newborn babies and infants as a basic
part of the physical examination
A. Nikolaidou, G. Tsolas
Abstract: The red reflex examination is recommended for all newborn babies and infants. This articledescribes the indications for and the technique of performing this examination, including the indicationsfor dilation of the pupils before examination and the indications for referral to an ophthalmologist.
Key words: Red reflex, retinal abnormalities, vision screening, eye examination.
1. Calhoun JH. Consultation with the specialist. Eyeexaminations in infants and children. Pediatr Rev1997;18:28-31.
2. Mills MD. The eye in childhood. Am Fam Physician1999;60:907-916.
3. Olitsky SE, Nelson LB. Common ophthalmologicconcerns in infants and children. Pediatr Clin NorthAm 1998;45:993-1012.
4. Curnyn KM, Kaufman LM. The eye examination inthe pediatrician's office. Pediatr Clin North Am2003;50:25-40.
5. American Academy of Pediatrics, Committee onPractice and Ambulatory Medicine, Section onOphthalmology. Eye examination and visionscreening in infants, children, and young adults. Pe-diatrics 1996;98:153-157.
6. American Academy of Pediatrics, Section on Oph-thalmology. Red reflex examination in infants. Pedi-atrics 2002;109:980-981.
8. Ogut MS, Bozkurt N, Ozek E, Birgen H, KazokogluH, Ogut M. Effects and side effects of mydriatic eye-drops in neonates. Eur J Ophthalmol 1996;6:192-196.
9. Fraunfelder FT. Pupil dilation using phenylephrinealone or in combination with tropicamide. Ophthal-mology 1999;106:4.
10. Gaynes BI. Monitoring drug safety; cardiac events inroutine mydriasis. Optom Vis Sci 1998;75:245-246.
11. Resano A, Esteve C, Fernandez Benitez M. Allergiccontact blepharoconjunctivitis due to phenylephrineeye drops. J Investig Allergol Clin Immunol 1999;9:55-57.
Recommendation on administration of Palivizumab (Synagis) for the
prevention of disease caused by respiratory syncytial virus (RSV)
Hellenic Society of Neonatology
Abstract: The aim of this article is to make recommendations about the use of Palivizumab(Synagis) for the disease caused by respiratory syncytial virus (RSV), according to the literatureaccessible to the Hellenic Society of Neonatology at the present time.RSV is the main cause of lower respiratory tract infection in the first two years of life. Seventy per centof infants are infected during their first year of life and 95% by the end of their second year. Of thoseinfected, 15-22% will present with bronchiolitis, pneumonitis or pneumonia, and 0.5-2% will needhospitalization. The mortality from RSV ranges between 0.5-3.5% (1,2). Reinfection occurs in 50%of infants. The presentation of RSV is seasonal, differing between countries. In Greece it is reportedmainly from November until March. The infants at highest risk are premature infants ≤28 weeks of gestation, with or without chronicbronchopulmonary disease (BPD), or more mature infants with BPD, congenital heart disease orimmunodeficiencies. Synagis is a monoclonal antibody against RSV.The prophylactic administration of Synagis at a dose of 15 mg/kg i.m. during the season of RSVinfection has been reported to reduce the rates of hospitalization for RSV infections by 55%.According to this information, Synagis is recommended for the following groups:
a) Infants ≤2 years of age with BPD, if they have been on treatment in the last 6 months before thestart of the RSV season.
b) Premature infants without BPD, if they have been born at:1. gestational age ≤28 weeks and are aged <1 year during the RSV season2. gestational age 29-32 weeks and are aged <6 months during the RSV season3. gestational age 33-35 weeks, if they have additional risk factors and are aged <6 months during
the RSV season.c) Infants with congenital heart disease, with or without cyanosis, if they are aged <1 year, or if
they need surgery or hospitalization during the RSV season. Also infants with cardiomyopathies, ifthey are aged <1 year of age during the RSV season.
d) Infants with immunodeficiencies.
Editor:
Dr Sofia Petmezaki Paediatrician-NeonatologistHead of Neonatal ICU,“Mitera” Maternity Clinic
Date of submission: 27-06-2005Date of approval: 15-09-2005
Pediatr Jan-Feb 06 final allges 27-01-06 15:35 ™ÂÏ›‰·69
70 ∂ÏÏËÓÈ΋ ¡ÂÔÁÓÔÏÔÁÈ΋ ∂Ù·ÈÚ›·
¶·È‰È·ÙÚÈ΋ 2006;69:69-71
‰È·Ê¤ÚÂÈ ·fi ¯ÒÚ· Û ¯ÒÚ·. ™ÙËÓ ∂ÏÏ¿‰· ÂÌÊ·-
Ó›˙ÂÙ·È Î˘Ú›ˆ˜ ÌÂٷ͇ ¡ÔÂÌ‚Ú›Ô˘ Î·È ª·ÚÙ›Ô˘.
¶Ï¤ÔÓ ÂÈÚÚ‹ ÁÈ· ÛÔ‚·Ú‹ ÓfiÛËÛË ·fi
ÙÔÓ RSV ›ӷÈ:
- Ù· ÚfiˆÚ· Î·È Î˘Ú›ˆ˜ ÂΛӷ Ô˘ ÂͤگÔ-
ÓÙ·È ·fi ÙË ªÔÓ¿‰· ∂ÓÙ·ÙÈ΋˜ ¡ÔÛËÏ›·˜ ¡Â-
ÔÁÓÒÓ, ÙËÓ ÂÔ¯‹ Ù˘ ¤Í·ÚÛ˘ ÙÔ˘ ÈÔ‡
- ·È‰È¿ Ì ¯ÚfiÓÈ· Ó¢ÌÔÓÈ΋ ÓfiÛÔ, .¯.
‚ÚÔÁ¯ÔÓ¢ÌÔÓÈ΋ ‰˘ÛÏ·Û›· (B¶¢), ΢ÛÙÈ΋
›ÓˆÛË, ‰È·ÊÚ·ÁÌ·ÙÔ΋ÏË
- ·È‰È¿ ÌÂ Û˘ÁÁÂÓ‹ ηډÈÔ¿ıÂÈ·
- ·È‰È¿ Ì ڈÙÔ·ı‹ ‹ ‰Â˘ÙÂÚÔ·ı‹ ‰È·-
Ù·Ú·¯‹ ÙÔ˘ ·ÓÔÛÔÔÈËÙÈÎÔ‡ Û˘ÛÙ‹Ì·ÙÔ˜
- ·È‰È¿ Ì ·ÓÔÛÔηٷÛÙÔÏ‹
- ·È‰È¿ Ì Ó¢ÚÔÌ˘˚΋ ÓfiÛÔ (3)
∂ÈϤÔÓ ·Ú¿ÁÔÓÙ˜ ÎÈÓ‰‡ÓÔ˘ ÁÈ· ÓfiÛËÛË
·fi RSV ›ӷÈ: (2,4)
- ŒÍÔ‰Ô˜ ·fi ªÔÓ¿‰· ∂ÓÙ·ÙÈ΋˜ ¡ÔÛËÏ›-
·˜ ¡ÂÔÁÓÒÓ, ÚÈÓ ‹ ηٿ ÙËÓ ÂÔ¯‹ ¤Í·ÚÛ˘
ÙÔ˘ RSV
- ¶·ÚÔ˘Û›· ¿ÏÏˆÓ ·‰ÂÏÊÒÓ - Û˘Á¯ÚˆÙÈÛÌfi˜
- ∞Ó ËÁ·›ÓÂÈ ÛÂ ‚ÚÂÊÔÓËÈ·Îfi ÛÙ·ıÌfi
- ∞Ó ÚÔ¤Ú¯ÂÙ·È ·fi Ôχ‰˘ÌË Î‡ËÛË
- ∞Ó ÚfiÎÂÈÙ·È Ó· ¯ÂÈÚÔ˘ÚÁËı› ÁÈ· ηډÈÔ-
¿ıÂÈ·
- ¡Â˘ÚÔÏÔÁÈΤ˜ ·ı‹ÛÂȘ
- ªÂÁ¿ÏË ·fiÛÙ·ÛË ·fi ÓÔÛÔÎÔÌÂ›Ô (·˘-
ÍË̤ÓË ÓÔÛËÚfiÙËÙ·)
- ¶·ıËÙÈÎfi οÓÈÛÌ·
- ÷ÌËÏfi ÎÔÈÓˆÓÈÎÔ-ÔÈÎÔÓÔÌÈÎfi ›‰Ô
£Âڷ¢ÙÈο, ÛÙË ÓfiÛËÛË ·fi RSV ¤¯Ô˘Ó
¯ÚËÛÈÌÔÔÈËı› ÂÎÙfi˜ ·fi Ù· ÎÔÈÓ¿ ̤ÙÚ· ·Ô-
Ê˘Á‹˜ ‰È·ÛÔÚ¿˜ ÏÔÈÌÒÍÂˆÓ (χÛÈÌÔ ¯ÂÚÈÒÓ,
Ì¿ÛΘ, ·ÔÊ˘Á‹ Û˘Á¯ÚˆÙÈÛÌÔ‡) Î·È ‚ÚÔÁ¯Ô-
‰È·ÛÙ·ÏÙÈο, ÛÙÂÚÔÂȉ‹, O2, πgGIV, ¯ˆÚ›˜ ȉȷ›-
ÙÂÚ· ηϿ ·ÔÙÂϤÛÌ·Ù·.
¶ÚÔÏËÙÈο, ¯ÔÚËÁ‹ıËΠÂȉÈ΋ RSV IgGIV,
·ÏÏ¿ ··ÈÙ›ÙÔ IV ÌfiÓÔ ¯ÔÚ‹ÁËÛË, ÂÌÊ¿ÓÈÛÂ
ÙÔ˘˜ ÎÈÓ‰‡ÓÔ˘˜ ÙˆÓ ·Ú·ÁÒÁˆÓ ·›Ì·ÙÔ˜ ηÈ
ÂÓ›ÔÙ ·Ú·ÙËÚ‹ıËÎÂ Î·È ‚·Ú‡ÙÂÚË ÓfiÛËÛË ÛÂ
·ӷÌfiÏ˘ÓÛË ÛÙ· ·È‰È¿ Ô˘ ›¯·Ó Ï¿‚ÂÈ RSV
IgGIV (2).
∆Ô 1998, ÙÔ FDA ¤ÙÚ„ ÙË ¯Ú‹ÛË Ù˘
palivizumab (Synagis) ÁÈ· ÚfiÏË„Ë ÌfiÏ˘ÓÛ˘
·fi ÙÔÓ RSV. ∏ ¯Ú‹ÛË ÙÔ˘ Synagis Ì›ˆÛ η-
Ù¿ 55% ÙËÓ ·Ó¿ÁÎË ÁÈ· ÂÈÛ·ÁˆÁ‹ ÛÙÔ ÓÔÛÔÎÔ-
ÌÂ›Ô ÁÈ· Ïԛ̈ÍË ·fi RSV (5). ™Ù· ÚfiˆÚ· ¯ˆ-
Ú›˜ B¶¢, ÙÔ ÔÛÔÛÙfi Ì›ˆÛ˘ ‹Ù·Ó 78% ÂÓÒ ÛÂ
·˘Ù¿ Ì B¶¢ ‹Ù·Ó 39% (1).
∆Ô Synagis Â›Ó·È ÂÍ·ÓıÚˆÔÔÈË̤ÓÔ ÌÔÓÔ-
ÎψÓÈÎfi ·Óٛۈ̷ ÂÓ·ÓÙ›ÔÓ Ù˘ F-ÁÏ˘ÎÔÚˆ-
Ù½Ó˘ ÙÔ˘ RSV. ∏ ¯ÔÚ‹ÁËÛË ÙÔ˘ Synagis ˘ÂÚ-
ÙÂÚ› Ù˘ RSV IgGIV, ‰ÈfiÙÈ ·Â‰Â›¯ıË ·ÔÙÂ-
ÏÂÛÌ·ÙÈÎfiÙÂÚË ÛÙËÓ ÚfiÏË„Ë, Â›Ó·È Â‡ÎÔÏË
ÛÙËÓ ¯ÔÚ‹ÁËÛ‹ Ù˘, ‰ÂÓ ¤¯ÂÈ ÙÔ˘˜ ÎÈÓ‰‡ÓÔ˘˜
ÙˆÓ ·Ú·ÁÒÁˆÓ ·›Ì·ÙÔ˜ Î·È Â›Û˘, ‰‡Ó·Ù·È
Ó· ¯ÔÚËÁËı› Û˘Á¯ÚfiÓˆ˜ Ì ÂÌ‚fiÏÈ· Ì ˙ÒÓÙ˜
ÈÔ‡˜ .¯. ªªR (6,7).
∆o Synagis ¯ÔÚËÁÂ›Ù·È πª Û ‰fiÛË 15 mg/kg
·Ó¿ Ì‹Ó· Û maximum 5 ‰fiÛÂȘ, ÛÙËÓ ÂÔ¯‹
¤Í·ÚÛ˘ ÙÔ˘ RSV. ™Â ‚·ÚȤ˜ ÂÚÈÙÒÛÂȘ ÌÔ-
Ú› Ó· ¯ÚÂÈ·ÛÙ› ¯ÔÚ‹ÁËÛË Î·È ÛÙÔÓ 2Ô ¯ÚfiÓÔ
˙ˆ‹˜, ÛÙËÓ ÂÔ¯‹ ¤Í·ÚÛ˘ ÙÔ˘ ÈÔ‡ (4).
™˘ÌÂÚ·ÛÌ·ÙÈο, ‚¿ÛÂÈ ÙˆÓ ·ÓˆÙ¤Úˆ, Ë
∂ÏÏËÓÈ΋ ¡ÂÔÁÓÔÏÔÁÈ΋ ∂Ù·ÈÚ›· ÂÈÛËÁÂ›Ù·È ÙË
¯ÔÚ‹ÁËÛË ÙÔ˘ Synagis:
·) ™Â ·È‰È¿ ≤2 ÂÙÒÓ, ·Ó ¿Û¯Ô˘Ó ·fi ¯Úfi-
ÓÈ· Ó¢ÌÔÓÔ¿ıÂÈ· (µ¶¢) Î·È Ï·Ì‚¿ÓÔ˘Ó
ıÂڷ›· ÁÈ' ·˘Ù‹, ÙÔ˘˜ ÙÂÏÂ˘Ù·›Ô˘˜ 6 Ì‹Ó˜
ÚÈÓ ÙËÓ ¤Í·ÚÛË ÙÔ˘ RSV.
‚) ™Â ÚfiˆÚ· ¯ˆÚ›˜ µ¶¢ ·Ó ›ӷÈ:
1. ∏.∫. ≤28 ‚‰. Î·È ÙËÓ ÂÔ¯‹ Ù˘ ¤Í·ÚÛ˘
ÙÔ˘ RSV Â›Ó·È ËÏÈΛ·˜ ≤1 ¤ÙÔ˘˜,
2. ∏.∫. 29-32 ‚‰. Î·È ÙËÓ ÂÔ¯‹ Ù˘ ¤Í·ÚÛ˘
ÙÔ˘ RSV Â›Ó·È ËÏÈΛ·˜ <6 ÌËÓÒÓ,
3. ∏.∫. 33-35 ‚‰. ·Ó Û˘Ó˘¿Ú¯Ô˘Ó ÂÈϤ-
ÔÓ ÂÈ‚·Ú˘ÓÙÈÎÔ› ·Ú¿ÁÔÓÙ˜ Î·È ·Ó ÙËÓ ÂÔ¯‹
Ù˘ ¤Í·ÚÛ˘ ÙÔ˘ RSV Â›Ó·È ËÏÈΛ·˜ <6 ÌËÓÒÓ.
Á) ™Â Û˘ÁÁÂÓ›˜ ηډÈÔ¿ıÂȘ Ì ·ÈÌÔ‰˘-
Ó·ÌÈο ÛËÌ·ÓÙÈ΋ ·ÓˆÌ·Ï›·, Ì ΢¿ÓˆÛË ‹ ÌË,
·Ó Â›Ó·È <1 ¤ÙÔ˘˜ ÛÙËÓ ÂÔ¯‹ ¤Í·ÚÛ˘ ÙÔ˘
RSV. ∂›Û˘, ÛÂ Û˘ÁÁÂÓ›˜ ηډÈÔ¿ıÂȘ Ô˘
ÚfiÎÂÈÙ·È Ó· ¯ÂÈÚÔ˘ÚÁËıÔ‡Ó ‹ ¯ÚÂÈ¿˙ÔÓÙ·È ÓÔ-
ÛÔÎÔÌÂȷ΋ ÂÚ›ı·Ï„Ë ÙËÓ ÂÔ¯‹ ¤Í·ÚÛ˘
ÙÔ˘ RSV, fiˆ˜ ›Û˘ Û ηډÈÔÌ˘Ô¿ıÂȘ
Ô˘ ¯ÚÂÈ¿˙ÔÓÙ·È ıÂڷ›· Û ‚Ú¤ÊË ËÏÈΛ·˜ <1
¤ÙÔ˘˜ ÙËÓ ÂÔ¯‹ ¤Í·ÚÛ˘ ÙÔ˘ RSV (8).
‰) ™Â ·È‰È¿ ÌÂ Û˘ÁÁÂÓ‹ ‹ ›ÎÙËÙË ‰È·Ù·-
Ú·¯‹ ÙÔ˘ ·ÓÔÛÔÔÈËÙÈÎÔ‡ Û˘ÛÙ‹Ì·ÙÔ˜.
√È Û˘ÛÙ¿ÛÂȘ ·˘Ù¤˜ ÂÊ·ÚÌfi˙ÔÓÙ·È ÛÙȘ
∏¶∞ (4), IÛ·Ó›· (1), πÙ·Ï›· (5), µÚÂÙ·Ó›· (3),
∂˘ÚÒË (6), ∫·Ó·‰¿˜ (7), °ÂÚÌ·Ó›· (9), §·ÙÈÓÈ-
΋ ∞ÌÂÚÈ΋ (2), √ÏÏ·Ó‰›· (10), ¶Ôψӛ· (11),
√˘ÁÁ·Ú›· (12).
µÈ‚ÏÈÔÁÚ·Ê›·
1. Spanish Consensus Committee: Prevention of Res-
piratory Syncytial Virus Infection in Spain. Pediatric
Edwin A et al. Guidelines for the use of Palivizumab
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in the prevention of RSV disease. A consensus opin-ion. Pediatrics in Review en Espan
~ol, Abril 2000;
21(2):62-68.3. U.K. Guidelines for the use of Synagis. Document is-
sued by Abbott U.K., 1999.4. American Academy of Pediatrics Committee on In-
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5. Giovannini M, Giuffre L, Marini A, Rondini G, Ros-si G, Salvioli GP. Respiratory Syncytial Virus Infec-tions in children. State of the Art. Neonatologica1999;13(2):89-92.
6. Carbonell-Estrany X, Giuffre L, Kimpen Jan LL,Adan D, Calenius H, Devlieger H et al. Guidelinesfor the use of Synagis® (Palivizumab), a HumanisedMonoclonal Antibody for the prevention of Respi-ratory Syncytial Virus (RSV) Disease in High RiskInfants. A consensus opinion. Supplement to Infec-tions in Medicine, December 1999;16(G):29-33.
7. A joint statement of the Canadian Paediatric Societyand the Fetus and Newborn Committee. Palivizum-ab and respiratory syncytial virus immune globulinintravenously for the prophylaxis of respiratory syn-cytial virus infection in high risk infants. Paediatricsand Child Health 1999;4(7):474-480.
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