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Assessment of heart rate variability in patients with chronic stable angina
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1-5
Mohammed Hassan Alwan
Background and objectives: A prospective study performed in Ibn-Albitar hospital a tertiary center
to assess the effect of ischemic heart disease on heart rate variability.
Methods: Thirty nine consecutive patients all with history of chronic stable
angina &with positive treadmill test underwent 24 hours holter test to
assess heart rate variability. Compared it with 25 age & sex matched
control volunteer group.
Results: Thirty one
(79.48%) male of patients group& 20 (80%) male of control group . heart
rate variability expressed as (SDNN) standard deviation of normal to normal
interval, (RMSSD) square root of the mean squared differences of successive
normal to normal intervals& (pNN50) the
proportion derived by dividing (NN50) the number of interval differences of
successive normal to normal intervals greater than 50 milliseconds (ms.) by the
total number of normal to normal intervals all were significantly lower in
patients group.
Conclusion: This study showed that heart rate
variability significantly lower in patients with chronic stable angina.
Key words: Heart
rate, stable angina.
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JT, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Frequency
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cardiovascular risk factors: results of the SAPALDIA study.Europace. . 2006 ;8(7):521-9.
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134:99
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vagal modulation and exercise induced ischaemia of the inferoposterior
myocardium. Heart. 2006; 92(3): 325-30.
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variability in time domain analysis in
congestive heart failure. J Interv Card Electrophysiol 2001;5:181-187.
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effect of resting ST segment depression on the diagnostic characteristics of
exercise treadmill test .J Am Coll Cardiol 2000;35:1026.
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JT, et al ACC/AHA. guide line up date fore exercise testing. Summery article. A
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(2002).
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control of hypertension in the united states, JAMA 2003; 290:199.
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short-term measures of RR Variability to predict mortality after myocardial
infarction. Circulation 1993; 88: 927–34.
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ischemia and sudden death. In: Zipes DP, Jalife J, eds. Cardiac
electrophysiology. From cell to bedside. Philadelphia: W. B. Saunders, 1995:
422–34.
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indices of heart rate variability after myocardial infarction. Am Heart
J 1992; 123: 1521–9.
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DC, Mottley JG, Titlebaum EL. Sampling frequency of the electrocardiogram for the spectral analysis of
heart rate variability, IEEE Trans Biomed Eng 1990; 37: 99–106.
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Schwartz PJ. Single cardiac vagal fiber
activity, acute myocardial ischemia, and risk for sudden death. Circ Res 1991;
69: 1389–1401.
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Association between life-style factors and pulmonary tuberculosis in Erbil
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6-11
Ibrahim H. Mustafa & Badia M. Najib & Namir G. Al. Tawil
Background and objectives: The majority of individuals in a
population do not develop
tuberculosis, due either to lack of exposure or due to individual
characteristics that limit development of the disease after exposure. Evidences
suggested that there is an association between lifestyle variables and
tuberculosis. The main objective of this study was to study the association
between lifestyle characteristics and pulmonary tuberculosis.
Methods: A case-control study was carried out in
Erbil city during the period May 10, to December 28, 2009. A convenient sample
of 150 cases of TB attending the Consultation Clinic for Chest and Respiratory
Diseases was included in the study. A
sex and age matched, 150 patients were included in the study as a control
group. The control group was taken from patient of the Medical Wards of both
Rizgary and Hawler Teaching Hospitals who were free from chest infections and
lung cancer. Cases and controls were interviewed using a questionnaire designed
by the researchers.
Results: Around one quarter (24%) of the cases were smokers
compared with 14.7 % among the controls.
Significant difference of nutritional status between both groups was
detected. Controls eat more food and of better quality than cases. No
significant association between alcohol drinking, practicing of sports/
exercise and TB was detected.
Conclusion: TB was found to be associated with low
nutritional status and smoking.
Key words: pulmonary
tuberculosis, lifestyle, age and gender.
1. International Council of Nursing. Tuberculosis
Guideline. 2nd ed.
Geneva, Switzerland. 2004. P5-6.
2. European Center for Disease Prevention. Framework
action plan to fight tuberculosis in the
European Union. Stockholm ;2008.
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WHO. [database on
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nutrition. American Dietetic association: Jones and Bartlett publishers; 2003.
6. Dodoe A. Evaluation of nutritional status of new
tuberculosis patients at Effia- Nkwnta Regional Hospital. Ghana Med J 2008;
24(1):22-28.
7. Cegielski J P, McMurray D N. The
relationship between malnutrition and tuberculosis: evidence from studies in human and
experimental animal. Int J Tuberc Lung Dis2004, 8(3):286-298.
8. Karyadi E,
West C E, Nelwan R H, Dolmans W V, Meer J W. Social aspects of patients
with pulmonary tuberculosis in
Indonesia. Southeast Asian J Trop Med Public Health 2002;33(2.): 2254-264.
9. Hassmillr KM. The association between smoking and tuberculosis.
Salud Publica Mex 2006, 48(1):5201-5216.
10. Lönnroth K, Williams B, Stadlin S,
Jaramillo E, Dye C. Alcohol use
as a risk factor for tuberculosis – a systematic review. BMC Public Health 2008; 8(289): 289-299.
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Information. [homepage on the Internet]. University of Arizona. 2007[updated
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L., Critchley, J.A. Trends in Smoking and quitting in China from 1993 to 2003:
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Jan 10]. Available from: http://www.who.int/bulletin/volum/88/10/09-064-709/en/
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help.com/drinkingalcohol.asp
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[homepage on the Internet] . GUN Documentation License. c2010 [cited 2010 Nov
4] Available from: http://www.wordiq.com/definition/Sports.
15. Rao S. Tuberculosis and patient
gender: An analysis and its implications in tuberculosis control. Lung India J
2009; 26(2): 46-7.
16. Dhamgaye TM. Tobacco smoking and
pulmonary tuberculosis: A case- control study. J Indian Med Assoc 2008; 106(4): 216-9.
17. Boon S, Lill SP, Borgdorff MW,
Verver S, and Bateman ED. Association between smoking and tuberculosis
infection: a population survey in high tuberculosis incidence. BMJ 2005; 60(7): 43-53.
18. WordiQ.
[homepage on the Internet] . GUN Documentation License. c2010 [cited 2011 Jan
4] Available from:
http://www.wordiq.com/definition/tobacco_smoking.
19. Gajalakshmi V, Peto R. smoking
drinking and incidence tuberculosis in rural India: population-based
case-control study. Int J Epidemiol 2009; 38(4): 1018-1024.
20. Ministry of Youth and Sports Central
Organization for Statistics and Information Technology. Iraqi national youth
and adolescent. Baghdad: Iraq;2009.
21. Tocque K, Bellis MA, Beeching NJ,
Syed Q, Remmington T, and Davies PD. A
case control Study of lifestyle factors associated with tuberculosis in
Liverpool, North-west England. Eur.
Rspir 2001; (18): 959-964.
22. Schoeman JH, Westway MS, and Neething
A. Relationship between socio-economic factors
and pulmonary TB. Int J Epidemiol 2009; 20(2): 435-440.
23. Mustafa H, Najib BM, Al. Tawil NG.
Association between socio-demographic factors and pulmonary tuberculosis in Erbil city. 2010.
(Unpublished research).
24. Franca TD, Ishikawa LW, Pezavento SG,
Minicucci F, Cunha MS, and Sartori A. Impact of malnutrition on immunity and
infection. J. Venom. Anim. Toxins incl. Trop. Dis 2009;15(3): 230-6.
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Prevalence of epilepsy in Hawler city; a household survey
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12-18
Azad Hasan Khidr & Aso Sabir Sheikh-Bzeni
Background and
objectives: Epilepsy is a common neurological disorder and in spite of that, its
prevalence was not studied in Hawler city before. The objective of this study
is to know the prevalence of epilepsy in Hawler city.
Methods: A house hold survey was carried out in
Hawler city, Iraq 4623 persons selected as clustered random sample of the city population during period
of April 2007 to June 2008.
Results: Out of the 4623 persons studied, only 45
patients (23 female and 22 male) were found to be epileptic, with a life time
prevalence of 9.7/1000 population. The commonest age group affected was
childhood age (1st and 2nd decade). This study showed that partial epilepsy was more common than
generalized epilepsy. There is no marked difference between genders in the
disease pattern (51.1% were females, 48.9% were males).
Conclusion: Epilepsy is a common disorder in Hawler city. There was no significant
difference between genders in the disease pattern. In our locality children
were more affected with epilepsy than other age groups.
Key words: Epilepsy,
Hawler city, Prevalence.
1. Fisher RS, van Emde Boas W, Blume W. Epileptic
seizures and epilepsy: definitions proposed by the International League Against Epilepsy
(ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia 2005; 46(4):
470-472.
2. Chang BS,Lowenstein DH .Epilepsy Engl J Med2003;
349:1257.
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life time prevalence of neurological disorder in a prospective community-based
study in the UK. Brain 2000; 23 (Pt 4): 665-676.
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of epilepsy: the size of the problem. Seizure 2001; 10(4), 306-314.
8.
Sander JWAS, Shorvon SD. Epidemiology of the epilepsies.J Neurol Neurosurg
Psychiatry 1996; 61:433—43.
9.
Lisle JR, Waldron HA.Employees with epilepsy in the NHS.Br Med J 1986; 292:305—6.
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;Characteristics of patients receiving medication for epilepsy.Epilepsy Res
1995; 21:43—9.
11.Jacoby A, Buck D, Baker G, McNamee P, Graham JS, Chadwick DW .Uptake and
costs of care for epilepsy: findings from a UK regional study.Epilepsia 1998;
39:776—86.
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SW, Hasan KZ. Epilepsy in Pakistan: stigma and
Psychosocial problems. A population-based epidemiologic study. Epilepsia 1997;
38:1069—73.
13. Gilliam F.Optimizing health outcomes
in active epilepsy. Neurology 2002; 58 (Suppl. 5): 59–520.
14. Baker GA, Spector S, McGrath Y, Soteriou H. Impact of epilepsy in
adolescence: a UK controlled study. Epilepsy Behav 2005; 6:556—62.
15. Jorge G, Jose T, Samuel W. Understanding the burden of epilepsy in Latin
America: A systematic review of its prevalence and incidence. Epilepsy Research 2005; 66:63–74
16. Jessica M U, Robert F H. Mind on
Statistics. Thomson brooks /Cole2007.
17. Al Atta F A. The prevalence of epilepsy in Baghdad –door to door study.
F.I.C.M.S.dissertation . Iraqi commission for medical specializations 2001.
18.Onal AE, Tumerdem Y, Ozturk MK,Gurses
C .Epilepsy prevalence in a rural area
in Istanbul. Seizure 2002; 11:397-401.
19. Aziz H, Guvener A, Akhtar SWl.
Comparative epidemiology of epilepsy in Pakistan and Turkey: population based
studies using identical protocols. Epilepsia 1997; 38: 716–22.
20. Haerer A F, Anderson D W,
Schoenberg B S. Prevalence and clinical features of epilepsy in a
biracial United States population. Epilepsia 1986; 27: 66–75.
21.Li S , Schoenberg B S , Wang C , Cheng X , Zhou S ,Bolis C L .Epidemiology of epilepsy in urban
areas of the Peoples’Republic of China. Epilepsia 1985; 26: 391–394.
22. Heaney DC, Macdonald BK, Everitt A .Socioeconomic variation in incidence
of epilepsy: prospective community based study in south east England. Br Med J
2002; 325(7371): 1013-1016.
23. AL Rajeh S., Awada A, Bademost O., Oguniyi A. The prevalence of epilepsy and other seizure
disorders in an Arab population: a community-based study .Seizure 2001; 10:
410–414.
24.Mac T L , Tran D S ,
Fabrice Q , Peter O , Pierre M P,Tan C (2007). Epidemiology, aetiology, and
clinical management of epilepsy in Asia: a systematic review Lancet Neurol; 6:
533–43.
25. Kotsopoulos I A, van M T, Kessels F G, de K M, Knottnerus J A
.Systematic review and meta-analysis of incidence studies of epilepsy and
unprovoked seizures. Epilepsia 2002; 43: 1402—1409.
26. Tran DS, Odermatt P, Le TO .Prevalence of epilepsy in a rural district
of central Lao PDR. Neuroepidemiology 2006; 26: 199–206.
27. Hauser W A, Annegers, John F, Kurland L T. Incidence of epilepsy and
unprovoked seizures in Rochester, Minnesota: 1935-1984. 1935–1984. Epilepsia
1993; 34: 453–468.
28.Annegers
J F, Hauser W A, Lee J, Rocca W .Incidence of acute symptomatic seizures in
Rochester, Minnesota, 1935–1984. Epilepsia 1995; 36: 327–333.
29.DeLorenzo
R J, Hauser W A,Towne A R , Boggs J G,Pellock Penberthy L, Garnett L, Fortner C
A. A prospective, population-based
epidemiologic study of status epilepticus in Richmond, Virginia. Neurology
1996; 46: 1029–1035.
30.
Loiseau J, Loiseau P, Duche B. A survey of epileptic disorders in Southwest
France: seizures in elderly patients. Ann Neurol 1990; 27:232.
31.
Stephen LJ,Brodie MJ.Epilepsy in elderly people. Lancet 2000; 355:1441.
32.
Vignatelli L, Tonon C, D’Allessandro R, Bologna Group for the study of Status
Epilepticus. Incidence and short-term prognosis of status epilepticus in adults
in Bologna, Italy. Epilepsia 2003; 44:964–968.
33.Logroscino G , Hesdorffer D C, Cascino G , Annegers J
F, Hauser WA .Time trends in incidence, mortality, and case-fatality after first episode of status epilepticus.
Epilepsia 2001; 42, 1031–1035.
34.Cowan L D ,Bodensteiner J B , Leviton A ,Doherty
L.Prevalence of the epilepsies in children and adolescents. Epilepsia 1989; 30:
94-106.
35.Christensen J , Kjeldsen
M J , Andersen H , Friis M L ,
Sidenius. Gender differences in epilepsy. Epilepsia 2005; 46:956-960.
36. Christensen J, Mogens V, Marianne G P, Carsten B, Per
Sidenius. Incidence and prevalence of epilepsy in Denmark Epilepsy Research
2007; 76:60—65.
37. Picot M C, Michel B M, Jean PD, Pierre D, Arielle C .The
prevalence of epilepsy and macoresistant epilepsy in adults: A population-based
study in a Western European country. Epilepsia 2008; 9(7):1230–1238.
38. Almu S, Zerihun T, Paul C, Richard H. The prevalence of
epilepsy in the Zay Society, Ethiopia–—an area of high prevalence.Seizure 2006;
15: 211—213.
39. Nyame PK, Biritwum RB .Epilepsy: knowledge, attitude and
practice in literate urban population, Accra, Ghana. West Afr J Med 1997;
16:139—45.
40.Mung’ala-Odera V , White S, Meehan R , Otieno G O , Njuguna
P , N Mturi T,Edwards B G,Neville, Newton C R J C (2008). Prevalence, incidence
and risk factors of epilepsy in older children in rural Kenya. Seizure 2008;
66:396—404.
41. Shorvon SD, Farmer PJ. Epilepsy in developing countries: A
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29 (suppl 1): 536–545.
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Detection of Anti-CMV IgM and Anti-Toxoplasma gondii IgG in Pregnant Women with History of Abortion
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19-23
Saeed Kholam Husain & Zagros Kamal Al-Barzanjy & Amin Aziz Bakir & Rezan Kamal Ahmad
Background and
objectives: Several infection are
associated with abortion among them toxoplasmosis and cytomegalovirus
infection. Toxoplasma gondii causes congenital toxoplasmosis along with HCMV a highly teratogenic
virus that interfere emberyogenesis. Both infections are almost asymptomatic
thus, diagnosis depends primarily on serological tests namely ELISA to detect
antibodies in serum of pregnant women.
Methods: A
semi-quantitative Elisa technique is applied for detection of anti-toxoplasma
IgG and anti-CMV IgM in sera of 348 pregnant women tested in Rezan Private Lab
who have previously experienced abortion.
Results: The
seropositivity rates are 29.05% for Toxoplasma-IgG and 45.25% for CMV-IgM. The
increasing age is associated with increasing times of abortion (p ≤ 0.0001).
Cases with co-infection are more likely to have multiple abortions. The number
of abortions is statistically not highly associated with socioeconomic status
of pregnant women (p ≥ 0. 1364).
Conclusion: Through this
study a plain connection can be figured out between chance of multiple times of
abortion and infections caused by CMV and Toxoplasma
gondii. Similarly, this association is verified
more with increasing age while the socioeconomic status of cases is not
indicative for the possibility of multiple miscarriages. All these results are
rationally expected and in agreement with most other studies.
Key words: Abortion,
Congenital Toxoplasmosis, Cytomegalovirus Infections.
1. Bergström S.
Infection-Related Morbidities in the Mother, Fetus and Neonate. J Nutr. 2003;
133:1656-60
2. Mara Depino
A. Maternal Infection and the Offspring Brain. The Journal of Neuroscience.
2006; 26(30):7777-8
3. Ross D. S, Jones J L, Lynch M. Toxoplasmosis,
Cytomegalovirus, Listeriosis, and Preconception Care. Matern Child Health
J.2006; 10:187-91
4. Pappas G, Roussos N, Falagas
M. Toxoplasmosis snapshots: Global status of Toxoplasma gondii seroprevalence
and implications for pregnancy and congenital toxoplasmosis. International
Journal for parasitology. 2009; 39:1385-94
5. Halonen S. K. and Weiss L. M.
Toxoplasma gondii Presentations at the 10th International Workshops on
Opportunistic Protists: 100 Years and Counting. Eukaryotic Cell. 2009;
8(4):437-40.
6. Stray-Pedersen
B. Toxoplasmosis in pregnancy. Baillière's Clinical Obstetrics and Gynaecology.
1993; 7(1):107-37
7. Garry D J, Elimian A, Wiencek V, and Baker D A.
commercial laboratory IgM testing for Toxoplasma gondii in pregnancy: A 20-year
experience. Infectious Diseases in Obstetrics and Gynecology. 2005;
13(3):151-53
8. Kravetz J D and Federman D G. Toxoplasmosis in
pregnancy. The American Journal of Medicine. 2005; 118:212-16
9. Gilbert R E, Peckham C S. Congenital toxoplasmosis in
the United Kingdom: to screen or not to screen. J. Med. Screen. 2002; 9:135-41
10. Landolfo S, Gariglio M, Gribaudo G, Lembo D. The Human Cytomegalovirus. Pharmachology and
Therapeutics. 2003; 98(3):269-97
11. Malm G, Engman M. Congenital cytomegalovirus
infections. Seminars in Fetal and Neonatal Medicine. 2007; 12:154-59
12. Munro S. C. Hall B. Whybin L. R. Leader L.
Robertson P. Maine G. T. and Rawlinson W. D. Diagnosis of and Screening for Cytomegalovirus
Infection in Pregnant Women. Journal of Clinical Microbiology. 2005;
43(9):4713-18
13. Ornoy A, Diav-Citrin O, Fetal effects of primary and
secondary cytomegalovirus infection in pregnancy. Reproductive Toxicology.
2006; 21(4):399-409
14. McCarhy F.P. Jones C. Rowlands S. Giles M. Primary and
secondary cytomegalovirus in pregnancy. The Obstetrician & Gynaecologist.
2009; 11(2):96-100
15. Gibson L, Piccinini G, Lilleri D, Revello M G, Wang Z,
Markel S, Diamond D J, Luzuriaga K. Human Cytomegalovirus Proteins pp65 and
Immediate Early protein 1 are Common Targets for CD8+ Cell Responses in
Children with Congenital or Postnatal Human Cytomegalovirus. Infection. The Journal
of Immunology. 2004; 172:2256-64
16. Fujikawa T, Numazaki K, Asanuma H, Tsutsumi H. Human
cytomegalovirus infection during pregnancy and detection of specific T cells by
intracellular cytokine staining. Int J Infect Dis. 2003; 7:215-21
17. Chou D, Ma Y, Zhan J, McGrath C, Parry S. Cytomegalovirus
infection of trophoblast cells elicits an inflammatory response: A possible
mechanism of placental dysfunction. American journal of Obstetrics and
Gynecology. 2006; 194:535-41
18. Sinclair J and Sissons P, Latancy and reactivation of
human cytomegalovirus. Journal of General Virology. 2006; 87:1763-79
19. Numazaki K and Fujikawa T, Prevalence of serum
antibodies to cytomegalovirus in pregnant women in Sapporo. Japan. Int J Infect
Dis. 2002; 6:147-8
20. Meyer U. The Neurodevelopmental Impact of Prenatal Infections at
Different Times of Pregnancy: The Earlier the Worse? Neuroscientist. 2007;
13(3):241-56
21. Lazzarotto T. The Best Practices for Screening,
Monitoring, and Diagnosis of Cytomegalovirus Disease, Part II. Clinical
Microbiology Newsletter. 2010; 32(2):9-15
22. Ali S A, Sharef T Y. Serological Study of
Cytomegalovirus (CMV) in Spontaneous Abortion. Zanco J. Med. Sci. 2007;
11(1):31-6
23. Mombrò M, Perathoner
C, Leone A, Buttafuoco V, Zotti C,
Lievre MA, Fabris C. Congenital toxoplasmosis: assessment of risk to
newborns in confirmed and uncertain maternal infection. Eur J Pediatr. 2003; 162(10):703-6
24. Pechaham C, Tookey P, Logan S, Giaquinto C. Screening
options for prevention congenital cytomegalovirus infection. J Med Screen.
2001; 8:119-24
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Clinical predictors of hypoxemia in children with acute lower respiratory tract infections
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Kawes O.Zangana & Dlair A.K.Chalabi
Background and objectives: Acute
lower respiratory tract infections (ALRI) are the leading cause of morbidity
and mortality among children in developing countries. Pulse oxymetry is a
simple technique to determine the oxygen saturation. However, the detection of
hypoxemia by use of pulse oxymetry is not available in most situations in
developing countries; in addition, the availability of supplementary oxygen is
inadequate. It is therefore, important to identify hypoxemia accurately in
children by using of clinical signs. The objective of this study was to find
out the clinical signs and symptoms that predict hypoxemia in acute lower
respiratory tract infection.
Methods:
A well matched case control study
was performed on 120 children from 2 months to 5 years of age admitted with
acute lower respiratory tract infections (ALRI)
to the emergency department of Raparin Pediatric Teaching Hospital
-Erbil, from 1st January 2009 to 1st April 2010.Clinical
symptoms and signs were recorded .Hypoxemia was defined as oxygen saturation
less than 95%. A
portable oxymeter was used to measure oxygen saturation with an appropriately
sized sensor on the finger or the toe. The reading was taken while the child
was breathing room air. The clinical symptoms and signs to predict the presence
of hypoxemia were evaluated.
Results: Sixty (50%) children were hypoxemic. The median O2
saturation was 91.2%with a range of 72-93.8%. Physical signs including
intercostal and subtotal retractions, supraclavicular recessions, grunting,
nasal flaring, cyanosis, head nodding, were statistically associated with
hypoxemia.
Conclusion: None of the clinical features
either alone or in combinations has sufficient sensitively and specificity to
predict hypoxemia in children with acute lower respiratory tract infections,
therefore pulse oxymetry is desirable for identification of hypoxemia.
Key words: Predictors; Hypoxemia; Acute lower respiratory tract
infection.
1.
British Thoracic Society standards of care committee. BTS guide lines for the management of community acquired
pneumonia in childhood. Thorax 2002;
57:51.
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Evaluation of vitamin c & malondialdehyde levels in type 2 diabetes mellitus
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