17 1(MD ) 1(MD ) 1(MD ) * 1(MD ) 1(MD ) –1(MD ) –1(PhD ) : * [email protected] : 95 08/ 05/ : 94 10/ 05/ : 94 07/ 26/ : : . . . 93 92 17 17 : . 17 1393 1392 : . 14 2 . SPSS Ver 19 . . Fisher Exact test (... ) 3 % 51 9/ % 25/6 . 36 ( % 37 % 63 ) 27 : % 37 . CSF CSF . % 74 .1/ . % 4/7 22 . . (. P>0.05 ) CSF . :

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80 17 1393 ( OPERON ) . RNA DNA . ) ) 38 37 2/ ( Roche applied science Glasgow Coma Scale ) ( . ) ( 14 Thermo )Nanodrop 2000c 13( )( 7 ) 24 ( DNA ( Scientific . . RNA 2 RNA cDNA 93 92 14 )Viva 2-steps RT -PCR Kit 17 ( Vivantis . . RNA Nanodrop cDNA . PCR . ( BIONEER ) . Eppendrof ) Eppendrof Mastercycler PCR . PCR ( BIO RAD ) : . . ( DNA ) transilluminator ( ) ( ( Vilber lourmat ) . MRI ) ( PCR ) ( CTscan ) ( 20 1. SPSS Ver 19 ( 24 ) (... ) Cool box . Fisher Exact test 80 . . CSF –RT-PCR PCR

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17 . % 63 . . (% )7/3 . 17 1( ) 27 1393 1392 . 1. ( ) 63( 17) 37( 10) 22( 6)2/ 12 – 24 ( ) 18( 5)5/ 24 36 29( 8)6/ 36 48 29( 8)6/ 48 1)7/3( 14( 4)8/ 44( 12)4/ 37( 10) . 62/2 ± % 25/6 2( ) 3 % 51 9/ 04/1 2 ( ) 11( 3)1/ 1 37( 10) 2 51( 14)9/ ≥3 19( 4) ( ) 62/2 ± 04/1 ( ) ± ) 38 46/ ± 43/0 ( )( ± ) 13 55/ ± 93/0 ( ± *) GCS * Glasgow Coma Scale CSF CSF % 74 1/ 3 3(. ) 20 1 4 ( 95% ) 19 7 % 29 6/ .(% )5 . 3 4

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3. ( ) (70 /4)19 (29 /6)8 0 CSF (74 /1)20 (25 /9)7 (74 /1)20 WBC 20 /81 ±6/97 ESR 4 . 17 % 14 8/ CSF ( )4 . . CT-Scan MRI 9 10 . 4 13 17 . (% 81 )4/ 22 . ( 10 37%) CSF % 92 6/ PCR . % 4/7 . ( 4 ) . Spastic Cerebral Palsy 27 . . 10 4 ( ) (92 /6)25

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59 66/ . .( 15 ) 12 1 Liu .( 18 ) % 88 CNS .( )7 Kolsk i .( 23 ) 3 50 . 6 % 7/3 .( 24 ) .( 16 ) 3 % 51 9/ GCS . 62/2 ± 04/1 . % 14 8/ 13 55/ ± 93/0 . Kolski . % 81 4/ . % 80 . .( 17 ) 12 . % 78 . % 78 . .( 18 ) .( 24 ) 2012 Sahni % 50 100 . % 80 .( 25 ) 18 1316 11 )1 CSF CSF . ( 22 80 Sahni . . . . AST (% )5 (% 90 ) 27 40% % 30 10 17 Fowler .( 25 ) . 4836 . 87 Beig . CSF % 55 12 6 .( 26 ) 35/4 Bokade .( )5 27/1 2012 2010

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% 40 . % 60 .( 29 ) . . 27 . . 10 4 . % 15 1% 17 .( 30 ) CSF Beig . % 21 8/ . % 42 1/ 7 . )5( HSV-1 Laman . % 92 6/ . . % 4/7 . . ( HHV ) . .( 27 ) Bokade . ( ) Fowler .( 28 ) . % 59 CSF .( 18 ) 3 1 HSV 2 5 Beig A EBV . .( 26 ) GCS . 2008 . 90 % 3/3 .( )5 RNA 37 % 41 11/ . 19 B5 . PCR . B4 .( 31 ) 5/6

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. . PCR . . 17 . .

1. Ginsberg L, Compston D A. Acute encephalopathy: 14. Whitley R. Infectious diseases. 2 ed. Viral diagnosis and outcome in patients at a regional infections of the central . 2004, neurological unit. Q J Med 1994. 87(3): 169-80 . London: Mosby . 2. Karmarkar S A , et al. A study of acute febrile 15. Glaser C A , et al. Beyond : clinical profiles encephalopathy with special reference to viral etiology. and etiologies associated with . Clin Infect IndianJPediatr2008;75(8):801 -5. Dis2006;43(12):1565 -77 . 3. Davison K L , et al. Viral encephalitis in England, 16. David G , Joseph R B, Avindra N. 1989-1998: what did we miss? . Emerg Infect Dis Neuropathogenesis of Viral Infections, in Clinical 2003;9(2):234 -40 . Neurovirology. Newyork;InformaHealthcare,2003. 4. Rantala, H, Uhari M. Occurrence of childhood 17. Ygberg S, Nilsson A. The developing immune encephalitis: a population-based study. Pediatr Infect system - fromfoetustotoddler.ActaPaediatr2012; DisJ1989;8(7):426 -30 . 101(2): 120-7. 5. Beig F K , et al. Etiology and clinico- 18. Bokade C , et al. Acute febrile encephalopathy in epidemiological profile of acute viral encephalitis in children and predictors of mortality. J Clin Diagn Res children of western Uttar Pradesh, India. Int J Infect 2014;8(8):c09 -11 . Dis2010;14(2):e141 -6. 19. Granerod J , et al. Causes of encephalitis and 6. Prober C . Central nervous system infections. In: differences in their clinical presentations in England: a NelsonTextbookofpediatrics.19ed.Philadelphia; multicentre, population-based prospective study. Saunders ,2011. LancetInfectDis2010;10(12):835 -44 . 7. Anga G , et al. The aetiology, clinical presentations 20. Le V T , et al. Viral etiology of encephalitis in and outcome of febrile encephalopathy in children in children in southern Vietnam: results of a one-year Papua New Guinea. Ann TropPaediatr2010;30(2): prospective descriptive study. PLoS Negl Trop Dis 109-18 . 2010;4(10):e854. 8. Bansal A , et al. Non traumatic coma. Indian J 21. Lesnicar G , et al. Pediatric tick-borne encephalitis Pediatr2005;72(6):467 -73 . in 371 cases from an endemic region in Slovenia, 1959 9. Hills S , et al. Evidence and rationale for the World to 20 00.PediatrInfectDisJ2003;22(7):612 -7. Health Organization recommended standards for 22. Ward K N , et al. Herpes simplex serious Japanese encephalitis surveillance. BMC Infect Dis neurological disease in young children: incidence and 2009;9:214. long-termoutcome.ArchDisChild2012;97(2):162 - 10. Kabilan L , et al. Japanese encephalitis in India: an 5. overview.IndianJPediatr2004;71(7) : 609-15 . 23. Liu X J , et al. [Clinical features and treatment of 11. Mizuguchi M , et al. Acute encephalopathy serious brainstem encephalitis caused by enterovirus 71 associated with influenza and other viral infections. infection]. Zhongguo Dang Dai Er Ke Za Zhi ActaNeurolScandSuppl2007;186:45 -56 . 2009;11(12):967 -9. 12. Gwer S , et al. Childhood acute non-traumatic 24. Kolski H , et al . Etiology of acute childhood coma: aetiology and challenges in management in encephalitis at The Hospital for Sick Children, resource-poor countries of Africa and Asia. Paediatr Int Toronto, 1994-1995. Clin Infect Dis 199 8;26(2):398 - Child Health2013;33(3):129 -38 . 409 . 13. Yeolekar M E, Trivedi TH. Febrile 25. Sahni G S. Recurring epidemics of acute encephalopathy: challenges in management. J Assoc encephalopathy in children in Muzaffarpur, Bihar. PhysiciansIndia2006;54:845 -7. IndianPediatr2012;49(6):502 -3.

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26. Fowler A, et al. Childhood encephalitis in Sweden: 29. Kumar A , et al. An epidemic of encephalitis etiology, clinical presentation and outcome. Eur J associated with human enterovirus B in Uttar Pradesh, PaediatrNeurol2008;12(6):484 -90 . India, 2008. J Clin Virol2011;51(2):142 -5. 27. Laman M , et al. Cryptococcal meningitis in 30. Fowlkes A L , et al. Enterovirus-associated immunocompetent Papua New Guinean children. Trop encephalitis in the California encephalitis project, Doct, 2010. 40(1): 61-3. 1998-2005.JInfectDis2008;198(11):1685 -91 . 28. Schubart C D , et al. Role of viruses in Kenyan 31. Khetsuriani N , et al. Neonatal enterovirus children presenting with acute encephalopathy in a infections reported to the national enterovirus malaria-endemicarea.AmJTropMedHyg2006; surveillance system in the United States, 1983-2003. 75(6): 1148-50 . PediatrInfectDisJ2006;25(10):889 -93

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Determination of Etiologic, Epidemiologic and Clinical Characteristics and Outcome of Children with Acute Febrile Encephalopathy in Rasht, 17-Shahrivar hospital

Hashemian H (MD) 1-*Mansoori M (MD) 1- Karambin M (MD) 1- Soltanipour S (MD) 1- Ghasemi Y (Ph.D) 1- Nemati K (MD) 1- Fallah Karkan M (MD) 1 Corresponding Address: Mansoori M ،Pediatric Growth Disorders Research Center, Guilan University of Medical* Sciences, Rasht, Iran

Email: [email protected]

Received: 18/Oct/2015 Revised: 26/Dec/2015 Accepted: 26/Oct/2016 Abstract Introduction: Acute encephalopathy is a condition in which brain function deteriorates rapidly and usually presents with loss of consciousness with or without focal neurologic symptoms. Some of its causes are infections, trauma, toxicities, and metabolic disorders and so on Objective: To evaluate etiologic, epidemiologic, clinical and para-clinical characteristics and outcomes in children with acute febrile encephalopathy during 2013-2014 in educational and remedial 17-Shahrivar hospital, Rasht . Materials and Methods: This is a case series and cross sectional study performed during 2013-2014 in 17-Shahrivar hospital, Rasht. All of children between 2 month and 14 years old with acute febrile encephalopathy enrolled in the study. Children with head trauma history or history of underlying metabolic or neurologic disease were excluded. Exact history was taken and clinical examination of neurologic system was done; Then laboratory examinations and related evaluation such as: Cell count and cerebro-spinal fluid, imaging and so on were performed. All of information was fulfilled in a checklist and data was entered in SPSS Ver 19 and analyzed with descriptive tests and Fisher Exact Test . Results: Twenty seven children including 63% male and 37% female were entered in the study which most of them were more than 36 month old. 6.25% of them had headache and 51.9% of them had history of fever for more than 3 days of fever. 74.1% of them had white blood cell changes. Blood, cell count and Cerebro Spinal Fluide(CSF) culture and CSF smear were not positive in any children. 37% of results were enterovirus in viral culture. Twenty two patients had , 4/7% of the children had improved with permanent side effect and none of them were died. Persistent complication of them was spastic cerebral palsy. There was no significant relation between treatment outcome and age group, season, gender and laboratory result of CSF (P>0.05). Conclusion: Our results showed that in our population one of important cause of acute febrile encephalopathy can be associated with enterovirus factors Conflict of interest: none declared .

Key words: Child \ Entrovirus \ ,Febrile ______Journal of Guilan University of Medical Sciences, No: 101, Pages: 20-29

Please cite this article as: Hashemian H, Mansoori M, Karambin M, Soltanipour S, Ghasemi Y, Nemati K, Fallah Karkan M. Determination of Etiologic, Epidemiologic and Clinical Characteristics and Outcome of Children with Acute Febrile Encephalopathy in Rasht, 17-Shahrivar hospital. J of Guilan Univ of Med Sci 2017;2 6(101):20-29. [Text in Persian]

1. Pediatric Growth Disorders Research Center, Guilan University of Medical Sciences, Rasht, Iran. 1396 / 101 / / 29