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.

1. Levy MN, Schwartz PJ eds. Vagal control of the heart: Experimental basis and clinical implications. Armonk: Future 1994.

2. Lown B, Verrier RL.  Neural activity and ventricular fibrillation.N Engl J Med 1976; 294: 1165–70.

3. Dreifus LS, Agarwal JB, Botvinick EH et al. (American College of Cardiology Cardiovascular Technology Assessment Committee):- Heart rate variability for risk stratification of life-threatening arrhythmias.  J Am Coll Cardiol 1993; 22:948–50.

4. Malik M, Bigger JT, Cam AJ, Kleiger RE, Malliani A, Moss AJ, et al. Heart rate variability: Standards of measurement, physiological interpritation, and clinical use. Eur Heart J 1996; 17: 354–381

5. Hon EH, Lee ST. Electronic evaluations of the fetal heart rate patterns preceding fetal death, further observations. Am J Obstet Gynec.1965; 87: 814–26.

6. Hirsh JA, Bishop B. Respiratory sinus arrhythmia in humans; how breathing pattern modulates heart rate. Am J Physiol 1981; 241: H620–9.

7.  Sayers BM. Analysis of heart rate variability. Ergonomics 1973; 16: 17–32.

8. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Heart rate variability. Standards of measurement, physiological interpretation, and clinical use. Circulation,1996;93:1043-1065.

9. Bigger JT, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Frequency domain measures of heart period variability and mortality after myocardial infarction. Circulation  1992; 85: 164–71.

10. Kay SM, Marple, SL. Spectrum analysis: A modern perspective Proc IEEE.1981; 69: 1380–1419.

11.  Dietrich DF, Schindler C, Schwartz J et al. Heart rate variability in an ageing population and its association with lifestyle and cardiovascular risk factors: results of the SAPALDIA study.Europace. . 2006 ;8(7):521-9.

12. Schulnan SP, Lasorda D, Farah T, et al . Correlations between coronary flow reserve measured with a Doppler guide wire& treadmill exercise testing. Am Heart  J1997; 134:99

13. Kawasaki T, Azuma A, Kuribayashi Tet al. Enhanced vagal modulation and exercise induced ischaemia of the inferoposterior myocardium. Heart. 2006; 92(3): 325-30.

14. Boveda S, Galinier M,Pathak A,et al . Prognostic value of heart rate variability  in time domain analysis in congestive heart failure. J Interv Card Electrophysiol 2001;5:181-187.

15. Scolon P, Faxon D, Audei A.et al.ACC/AHA guideline for coronary angiography . J Am Coll Cardiol  1999;33:1765

16. Campeau L : Grading of angina pectoris. Circulation 54 : 522.1975.

17. Fearon WF, Lee DP, Froelicher VF The effect of resting ST segment depression on the diagnostic characteristics of exercise treadmill test .J Am Coll Cardiol 2000;35:1026.

18.  Gibbons RJ, Balady GJ, Bricker JT, et al ACC/AHA. guide line up date fore exercise testing. Summery article. A report of the ACC/AHA task force or practice guidelines (Committee to up date). (2002).

19. Hajiar I, Kotchen TA. trends in prevalence , awareness , treatment, and control of hypertension in the united states, JAMA 2003; 290:199.

20. Bigger JT, Fleiss JL, Rolnitzky LM, Steinman RC. The ability of several short-term measures of RR Variability to predict mortality after myocardial infarction. Circulation 1993; 88: 927–34.

21. De Ferrari GM, Vanoli E, Schwartz PJ. Cardiac vagal activity, myocardial ischemia and sudden death. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology. From cell to bedside. Philadelphia: W. B. Saunders, 1995: 422–34.

22. Lombardi F, Sandrone G, Mortara A et al. Circadian variation of spectral indices of heart rate variability after myocardial infarction. Am Heart J 1992; 123: 1521–9.

23. Merri M, Farden 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.    

24. Akselrod S, Gordon D, Madwed JB, Snidman NC, Shannon DC, Cohen RJ. Hemodynamic  regulation: investigation by spectral analysis. Am J Physiol 1985; 249: H867–75.

25. Saul JP, Rea RF, Eckberg DL, Berger RD, Cohen RJ . Heart rate and muscle sympathetic nerve variability during reflex changes of autonomic activity. Am J Physiol.1990; 258:H713–21.

26. Malik M, Camm AJ. Significant of long-term components of heart rate variability for the further prognosis after acute myocardial infarction. Cardiovasc Res 1990; 24: 793–803.

27. Cerati D, Schwartz PJ.  Single cardiac vagal fiber activity, acute myocardial ischemia, and risk for sudden death. Circ Res 1991; 69: 1389–1401.

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.

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 (1^st and 2^nd 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.

3. Commission on Classification and Terminology of the International League against Epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989; 30(4):389–399.

4. Mosewich RK,So EL .A clinical approach to the classification of seizures and epileptic syndromes .Mayo Clin proc 1996;71:405-14.

5. Scott R A, Lhatoo S D. The treatment of epilepsy in developing countries: where do we go from here? Bull. World Health Organ 2001; 79(4):344-351.

6. Macdonald BK, Cockerell OC, Sander JW, Shorvon SD.The incidence and life time prevalence of neurological disorder in a prospective community-based study in the UK. Brain 2000; 23 (Pt 4): 665-676.

7. Bell GS,Sander JW .The epidemiology 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.

10. Hart YM, Shorvon SD.The nature of epilepsy in the general population ;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.

12. Aziz H, Akhtar 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 review of epidemiological, sociocultural and treatment aspects. Epilepsia 1988; 29 (suppl 1): 536–545.

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.

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

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 1^st January 2009 to 1^st 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.

2.  Loweski J. Mortality from acute respiratory infections in children less than 5 years of age: global estimates. World Health Stat Q 1986; 5: 247-252.

3.  Denny F, Loda FA. Acute respiratory infections are the leading cause of death in children in developing countries. Am J Trop Med Hyg 1986; 35: 1.

4.  Greenwood BM, Greenwood AM, Bradley AK, Tulloch S, Hayes R, Oldfield FSJ. Deaths in infancy and early childhood in a well-vaccinated, rural, West African population. Ann Trop Paediatr 1987; 7: 91-9.

5.  Organization program for the control of acute respiratory infections in children: case management in small hospitals in developing countries. Geneva: WHO/ARI/90.5,1990.       

6.  Onyango FE, Steinhoff MC, Wafula EM, Wariua S, Musia J, Kitonyi J. Hypoxaemia in young Kenyan children with acute lower respiratory infection. BMJ 1993; 306: 612-614.

7.  Levene S, Mckenzie SA. Pulse oxymetry in children. Lancet 1988; i: 415-416.

8. Reuland DS, Steinhoff MC, Gilman RH, et al.Prevalence and prediction of hypoxemia in children with respiratory infections in the Peruvian Andes. J Pediatr 1991; 119: 900-907.

9.  Lozano JM, Steinhoff M, Ruiz JG, Mesa ML, Martinez N, Dussan B. Clinical predictors of acute radiological pneumonia and hypoxaemia at high altitude. Arch Dis Child 1994; 71: 323-327.

10.  ShannF,BarkerJ,PooreP.Clinical signs that predict death in children with severe pneumonia.Pediatr Infect DisJ1989; 8: 852-855.

11.  Mulholland EK, Olinsky A, Shann FA. Clinical findings and severity of acute bronchiolitis. Lancet 1990; 335: 1259-1261.

12.  O'Dempsey TJD, Todd J. Respiratory rates are poor predictors of Hypoxaemia BMJ 1993; 306: 1342.  

13.  Reynolds EOR. Arterial blood gas tensions in acute disease of lower respiratory tract in infancy. BMJ 1999; 1: 1192-1195.

14.  Margolic PA, Ferloll T, Marrsocci S et al. Accuracy of the clinical          examination in detecting hypoxemia in infants with respiratory infections. J Pediatr, 1994:124(4):552-60

15.  Martin WW, Stanly U, Ayo P, Shabbar J, Mulholland Ek. Predictors of htpoxaemia in hospital admission with acute lower respiratory tract infection in developing countries. Arch Dis Child 1997; 76: p 310-314.

16.  Radish L ,Patrick S,AnoopV,et al .Can clinical signs or symptoms predict hypoxemia in children with acute lower respiratory tract infections.Indian Pediatrics 2004;41:129-135.

17.  Rogers MC, Wetzelel RC, Deshpande JK. Unusual causes of pulmonary edema, myocardial ischemia, and cyanoses in: Rogers, ed. Textbook of pediatric intensive care Williams and wilkens 1987, p389.

18.  Mai TV, Selby AM, Simpson JM, Issac D. Use of simple clinical parameters to assess severity of bronchiolitis:IJPediatr Child Health.1995 Oct.;31(5): p 465-8.

19.  Stanly U, Marten W, Kim M, et al. Clinical predictors of hypoxeamia in Gambian children with acute lower respiratory tract infection: prospective cohort study. BMJ 1999; 318: p 86-91.

20.  Dyke T, Brown N. Hypoxia in childhood pnemonia: Better detection and more oxygen needed in developing countries. BMJ1994; 308: p119-120.