Pediatric spinal epidural abscess in an immunocompetent host without risk factors: Case report and review of the literature

Case

Report

Pediatric

spinal

epidural

abscess

in

an

immunocompetent

host

without

risk

factors:

Case

report

and

review

of

the

literature

Alessandra

Vergori

,

Alfonso

Cerase

,

Lucia

Migliorini

,

Maria

Grazia

Pluchino

,

Giuseppe

Oliveri

_,

_Umberto

_Arrigucci

_,

_Andrea

_De

_Luca

_,

_Francesca

_Montagnani

_*

UniversityDivisionofInfectiousDiseases,HospitalDepartmentofSpecializedandInternalMedicine,Siena,Italy

b

UnitofNeuroimagingandNeurointervention,HospitalDepartmentofNeurologicalandSensorialSciences,UniversityHospitalofSiena,Siena,Italy

c

UnitofNeurosurgery,HospitalDepartmentofNeurologicalandSensorialSciences,UniversityHospitalofSiena,Siena,Italy

d_{DepartmentofMedicalBiotechnologies,UniversityofSiena,Siena,Italy}

Introduction

Spinalepidural abscesses(SEAs) areunusualbacterial infec-tions requiring prompt diagnosis and management to prevent devastatingneurologicsequelae.

Theyrepresent about7% of vertebral infections and usually occur in subjects with predisposing underlying diseases or conditionssuchasdiabetesmellitus,chronicrenalfailure,cancer, advanced age, immunodeficiency,alcoholism, intravenous drug abuse, cauda equina, holocord syndrome, neurosurgery, spinal

anesthesia and acupuncture, mucocutaneous trauma, or by spreadingofaknowninfectionlocalizedatothersites.

Bacteriagainaccesstotheepiduralspacethroughcontiguous spread(primarySEA)orbyhematogenousdissemination (second-arySEA);thesourceofinfectionisnotidentifiedin20–40%ofcases

[1–4].

The most common causative agentis Staphylococcusaureus, both methicillin-susceptible (MSSA) or methicillin resistant (MRSA),accountingfor50–90%ofcases,followedbystreptococci (8–17%)andGramnegativebacteria(10–17%)[1,4,5].

SEAs have an insidious onset of pain and a progressively worseningclinicalpicturecharacterizedbyfeverandelevationof theindicesofinflammation.

Fourclinicalstageshavebeendescribed:stage1–lumbarpain, feverandlocaltenderness;stage2–radicularpain,nuchalrigidity and changes in the reflexes; stage 3 – sensory and motor

IDCases2(2015)109–115

ARTICLE INFO

Articlehistory: Received27July2015

Receivedinrevisedform29September2015 Accepted30September2015

Availableonline

Keywords:

Spinalepiduralabscess Management Staphylococcusaureus Children

ABSTRACT

Spinalepiduralabscesses(SEAs)areunusualbacterialinfections,withpossibledevastatingneurologic sequelae.Despiteabundanceofcaseseriesinadults,reportsinchildrenarescanty.

WedescribeaspontaneousSEAduetomethicillinsusceptibleStaphylococcusaureus(MSSA)ina previouslyhealthy15-yearoldmale,andweperformaliteraturereviewregardingmanagementof pediatricSEAswithoutriskfactors,from2001to2014.

Wefoundatotalof12cases(8males,averageage9.6years).Clinicalpresentationwasmainlyfever, back painand elevationof inflammation markers. All cases were initially misdiagnosed. Lumbar puncturewasperformedin36%ofpatients.Etiologicaldiagnosiswasobtainedin8cases.MSSAwas isolated in 4 patients, methicillin-resistant S. aureus in 1 patient, and S. aureus with unknown susceptibilitypatternsin2cases.Theaverageoftherapydurationwas6weeks.Patients’spinewas alwaysevaluatedbygadolinium-enhancedmagneticresonanceimaging;mostabscesseswerelocalized atthoracicandlumbararea,withoutosteomyelitis.In8cases,laminectomyand/orabscessdrainage were performed in association with medical therapy; 3 cases were successfully treated with antimicrobialtherapyonly;nodatawereavailableinonecase.Agoodoutcomewasobtainedinall patients,exceptareportedresidualheadacheandparaspinalpainlastingfor3years.

Therarityand thepossible differential diagnosis canlead to underestimateSEA occurrence in childrenwithoutriskfactors.ItseemsthereforeessentialtomaintainahighattentiontopediatricSEAs. Apromptdiagnosisandadequatetherapyareessentialprognosticfactorsforremission.

ß2015TheAuthors.PublishedbyElsevierLtd.ThisisanopenaccessarticleundertheCCBY-NC-ND license(http://creativecommons.org/licenses/by-nc-nd/4.0/).

* Correspondingauthorat:DepartmentofMedicalBiotechnologies,Universityof Siena,UniversityDivisionofInfectiousDiseases,PoliclinicoLeScotte,48lottopiano 0,vialeBracci,16,53100Siena,Italy.Tel.:+390577586562;fax:+390577233462.

E-mailaddress:francesca.montagnani@unisi.it(F.Montagnani).

ContentslistsavailableatScienceDirect

IDCases

j our na l h ome p a ge :w ww . e l se v i e r. co m/ l oc a te / i d cr

http://dx.doi.org/10.1016/j.idcr.2015.09.008

2214-2509/ß2015TheAuthors.PublishedbyElsevierLtd.ThisisanopenaccessarticleundertheCCBY-NC-NDlicense(http://creativecommons.org/licenses/by-nc-nd/ 4.0/).

abnormalities, with motor weakness and bowel and bladder dysfunction; stage 4 – paralysis with permanent sequelae. Alterationsarereversibleuptostage4. Itisthereforeessential toachieveanearlydiagnosis,starteffectiveantimicrobialtherapy and,ifrequired,proceedwithapromptneurosurgicalintervention

[2,3].

Severalcaseseriesofspinalepiduralabscessesinadultshave been reported in the scientific literature, whereas reports in childrenarescanty.WedescribeaspontaneousSEAduetoMSSAin a 15-year-old boy without risk factors, and have performed a review of publications in the scientific literature regarding management of pediatric SEAs published in the last 14 years. Two previous reviews, including reports on patients with risk factors, reported cases up to calendar year 2000 [6,7]. In the present work, we analyzed reports and reviews frompediatric patientspublishedfrom2001to2014which,asinourcase,didnot presentriskfactors.

A review of the English literature was performed by an exhaustive Pubmed search for case reports and reviews, with publicationdateJanuary2001–December2014,usingthe follow-ingterms:‘‘spinal subdural abscess’’, ‘‘spinal epidural abscess’’, ‘‘spontaneoussubduralabscess’’,‘‘spontaneousepiduralabscess’’, ‘‘spontaneousspinal epiduralempyema’’. The exclusion criteria were:(i)adultpopulation(age18years),(ii)incompleteclinical orageinformationor undistinguishabledata betweenpediatric andadultpatients,(iii)tubercularspinalepiduralabscesses,and (iv)anyunderlyingdiseaseinthemedicalorsurgicalhistory.A manualreviewofthepapersfoundbytheabovesearchmethod

wasperformedtoverify inclusionand exclusioncriteriaand to excludecaseswithriskfactorsforhematogenousspreading(e.g. impetigoinchickenpox,catscratch,mucocutaneoustrauma)and/ or underlingpredisposing diseases(e.g. caudaequina,holocord syndrome,neurosurgery).

Case

InJune2013,a15-year-oldmalewasreferredtotheEmergency Department of Siena University Hospital, Tuscany, Italy, from anotherregionalhospitalwithaprovisionaldiagnosisof meningi-tis.Hereportedahistoryoffever,headacheandbackpain,mainly in the lumbar-sacral region, during the previous 3 days. No previoustrauma,norminorormajorsurgerywasreportedbythe boyorhisparents.

Hispastmedicalhistorywasunremarkable,buthereceiveda antigroupCmeningococcalconjugatevaccinedosetogetherwitha antidiphtheria-tetanusboosterdose2 weeksbefore admission; sevendaysofmyalgiasandlowgradefever(maximum37.58C) with spontaneous resolution were reported to after those immunizations.

On admission the patient was conscious complaining of headache and lumbar pain with bilateral leg weakness; on physical examination his BMI was 17.3 blood pressure 110/ 70mmHg, heart rate 92/min, respiratory rate 20/min, body temperature36.38C(hehadreceived1000mgofacetaminophen onehourbeforeadmission);hehadastiffneckwithalumbarpain arisingwhileattemptingtoflexhisneck,andpresenceofabilateral

Fig.1.Magneticresonanceimagingofthethoraco-lumbarspineatdiagnosis:unenhancedT2-weighted(a),shorttauinversionrecovery(STIR)(b),diffusion-weighted(DW) (c),apparentdiffusioncoefficient(ADC)map(d),andT1-weighted(e)sagittalandT2-weightedaxial(g)images,andgadolinium-enhancedT1-weightedsagittal(f)andaxial (h)images.Atthethoracolumbarjunction,aposteriormedian-leftparamedianepiduralcollectioncompressingthecaudalspinalcord,conusmedullaris,anduppercauda equinaisclearlyevident.Thelesionshowsirregularsignalintensityonunenhancedconventionalsequences(a,b,ande,blackarrows),restricteddiffusiononDWimagesand ADCmap(c,d,whitearrows),andperipheralgadolinium-enhancement(f,h).Notealsothatthelesionshowsextenttowardtheleftintervertebralforamen(g,h,arrowhead). STIRimagedoesnotshowassociatedabnormalsignalintensityofthebonemarrow.

A.Vergorietal./IDCases2(2015)109–115 110

straight leg raise sign, there was not any focal tenderness on palpationofthepatient’sspine.Neurologicalexaminationdidnot demonstrateanymotororsensorydeficit,butthepatientwasnot abletowalkduetotheseverepain.Therestofphysicalexamwas completely negative. Laboratory exams showed: leukocytes 11,300109_{/L (86.3% neutrophils), C-reactive protein (CRP)}

10.2mg/dl (upper normal value, upper limit of normal, ULN 0.5),procalcitonin0.18ng/ml(ULN0.5),PT71%(normalrange80– 120%),INR1.24.

Braincomputerassistedtomography(CT)wasnormal.Three setsofbloodcultureswerecollectedandlumbarpuncturewas performed.Cerebrospinalfluid(CSF)examinationrevealedaclear fluidwith pleocytosis (138leukocytes/mm3_{,67%polymorphs),}

glucoseconcentration67mg/dl(bloodglucose61mg/dl),protein concentration145.3mg/dl(normalrange20–40mg/dl). Empiri-caltreatmentwith intravenous(iv) ceftriaxone2gbidand iv acyclovir 500mg tid was prescribed and the patient was transferred to the Infectious Disease ward. The day after admission,lumbarpainwasprogressivelyworseningandlower and upper limbs weakness appeared. No peripheral nerve conductiondeficitsweredetectedonelectromyographyandno immunoglobulins type G in the alkaline region of CSF on isoelectrofocusingwererevealed.Urgentgadolinium-enhanced cerebralandspinalmagneticresonanceimaging(MRI)discloseda largeepiduralpurulentcollectionintheposteriorand median-paramedianleftspinalcanal,extendingfromT11toL2,withmass effectonspinalnerveroots(Fig.1).

WithadiagnosisofSEAevolvinginstage3,intheeveningof the 2nd day from admission, neurosurgeons performed an L2

laminectomyandabscessdrainage.Antimicrobialtreatmentwas modified withdiscontinuation ofceftriaxoneand acyclovir, and empiricalswitchtomeropenem2gtidandvancomycin1gbid., choosing a wider spectra coverage due to the aforementioned neurological deteriorationand tothe large amountofobtained purulent material, Histological analysis of the surgical tissue samplesshowedchronicpurulentinflammation,without neoplas-tic changes.AbscessculturerevealedMSSA;thestrain wasalso fullysusceptibletoalltestedantimicrobials.Onthebasisofthe aboveinvitrosusceptibilityresults,thetreatmentwasmodified againwithiv ceftriaxone2gbidandivclindamycin 900mgtid Negativeresultswereobtainedfrombloodcultures,CSFculture andpolymerasechainreactiononCSFforBorreliaspp., mycobac-terialandviralgenomes;serumagglutinationtestsfortyphoidand brucellosiswerenegative;nocongenitaloracquired immunodefi-ciencywasrevealed.NormalvaluesofCRPandwhitebloodcell count were obtained respectively on the 7th and 18th day; remissionofthefeverwasobtainedwithin72hafteradmission and a progressive improvement of the clinical condition was observed. Lumbarpain disappearedand thepatient underwent rehabilitation with a complete recovery. On the 21st day, the patientwasdischargedfromhospitalwiththefinaldiagnosisof SEA by MSSA and with the advice to continue antimicrobial therapywithivceftriaxone2gdailyandoralclindamycin600mg tidLumbarspinalMRI,performedapproximatelyonemonthafter surgery(Fig.2a,b),showedcompleteresolutionoftheabscessand gadolinium-enhancing postoperative reactive changes in the fascialmuscularplanes.Heartandabdomenultrasoundandchest radiographywerenegative.

Fig.2.Magneticresonanceimagingfollow-upbySTIR(upperline)andgadolinium-enhancedfat-suppressedT1-weighted(lowerline)sagittalimagesobtained24daysafter surgery(a)andonemonth(b),threemonths(c),andsevenmonths(d)later.Besidescompleteremovalandabsenceofrelapseoftheepiduralabscess,aclearcutreductionof gadolinium-enhancingreactivechangesisevident.NotealsotheprogressivedevelopmentofkyphosiswithfulcrumatL1–L2level,togetherwithincreaseoflumbarlordosis. A.Vergorietal./IDCases2(2015)109–115 111

Table 1

Clinical, instrumental and laboratoristic findings in the reviewed SEAs cases. Patient Year of study

[reference]

Gender, age Spine level Locationa

Symptoms at admission Primary

Diagnosisa CSFc WBC/mmc (% PMN) CRP Levelb Positive blood culturea 1 2001 [8]

F, 7 weeks T10–12 N/A Flaccid paraplegia N/A N/P Normal Normal N/A

2 2011

[9]

M, 15 years T3–T8 Right

Postero-lateral

Right scapular pain, fever, chills with night sweats, headache, photophobia

Right rhomboid muscle strain with spasm, acute febrile illness

Normal N/A 84.5 mg/L

(n.v. <10) Yes

3 2011

[10]

F, 11 years T11–L4 Posterior Fever, lumbar pain Back pain N/P 13,770 (82%) 27.2 mg/dl

(n.v. <0.5) No 4 2012 [11] M, 16 days C1/2 – lumbosacral Posterior+ Right side (plusParaspinal collection C3–T4, right pleural space and right kidney collection)

Fever, nervousness N/A 180 PMN, 9900 red

blood cells 21,200 (43%) 232 g/L (n.v. N/A) Yes 5 2012 [12]

M, 15 years L2–L3 Posterior Urinary retention,

Backpain, Fever

Low back pain and Not specified urinary retention N/P 18,600 (70%) ++ (value N/A) N/A 6 2013 [13]

M, 13 years C7–T1 Posterior, on both

sides

Transient fever, neck and upper back pain, tingling sensation in hands and feet, urine incontinence, abdominal distension, inability to sit and walk

Acute myelitis, diskitis, meningitis 800 cells/mmc, 2% PMN, glucose 21 mg/dl 7,100 (N/A) ++ (value N/A) No 7 2013 [14]

M, 1.2 years L3–L4 Posterior Refusal to walk, irritability,

weakness

N/A N/P 13,800 (N/A) N/A No

8 2013

[14]

M, 3 years T1–L2 Posterior Fever, stomachache N/A N/P 20,000 (N/A) 82.2 mg/L Yes

9 2013

[14]

F, 17 years L1–L4 Posterior Fever, nausea, vomiting N/A N/P 15,800 (N/A) 182 mg/L No

10 2013 [Present

report]

M, 15 years T11–L2 Left and posterior Fever, headache, back pain Meningitis, myelitis 138 cells/mmc, 67% PMN, glucose 67 mg/dl, proteins 145.30 mg/dl 11,300 (86.3%) 10.20 mg/ dl (n.v. <0.5) No 11 2014 [16]

M, 21 months L4–L5 Right into the

spinal canal

Fever, refuse to walk Septic arthritis N/P N/A 200.1 mg/L No

a

N/A, not available.

b

CRP, C-reactive protein; n.v., normal value.

c _{CSF, cerebrospinal fluid; N/P, lumbar puncture not performed.}

A. Vergori et al. / IDCases 2 (2015) 109–115 112

Table 2

Etiology, therapy and outcome in the reviewed SEAs cases. Patient Year of study

[reference]

Etiologya

Source of isolate

Osteomyelitisa

Surgery Empiric therapy Targeted therapyb

Duration of therapyb Outcome 1 2001 [8] Staphylococcus aureus Pus Absent T9–T12 laminectomy

N/A Not specified iv

anti-staphylococcal antibiotics

N/A No deficit after

18 months follow up

2 2011

[9]

MSSA Blood Absent Thoracic

laminectomy-drainage

Cefotaxime Ceftriaxone 4 weeks Residual headache

and paraspinal pain for subsequent 3 years

3 2011

[10]

MSSA Pus Absent Drainage Vancomycin + Ceftriaxone Clindamycin+

Ceftriaxone iv then Clindamycin + Cefuroxime per os 7.5 weeks No deficit 4 2012 [11]

MSSA Pus and

Blood

Absent Right sided

laminectomy drainage

Ampicillin + Gentamicin Then Vancomycin + Meropenem

Flucloxacillin + Ampicillin 8 weeks (Note: E. faecalis from urine and renal abscess) No deficit 5 2012 [12] Staphylococcus aureus Pus N/A L2–L3 laminectomy drainage N/A Cefazolin Then Cephalexin 6 weeks No deficit 6 2013 [13]

Unknown – Absent None Ceftriaxone + Vancomycin N/A 6 weeks No deficit

7 2013

[14]

Unknown – Absent None Nafcillin, Vancomycin

Then

Clindamycin (+Vancomycin on readmission)

N/A N/A Standing with

assistance on discharge

8 2013

[14]

MRSA Blood Absent Left

laminectomy T5–L2 Clindamycin iv+ Vancomycin iv+ Rifampin iv Clindamycinperos + Rifampinperos N/A No deficit 9 2013 [14]

Unknown – Absent None Daptomycin iv+

Doripenem iv+ Doxycycline

ThenDoxycycline + Doripenem

N/A N/A No deficit

10 2013 [Present

report]

MSSA Pus Absent L2

Laminectomy-abscess drainage

Vancomycin + meropenem Ceftriaxone + Clindamycin iv, Then amoxicillin/clavulanate + rifampicin per os 8 months No deficit 11 2014 [16] Group A beta-hemolytic Streptococcus Pus Absent L4–L5, Partial S1 Laminectomy and drainage

N/A Ceftriaxone 6 weeks No deficit

a

MSSA, methicillin-susceptible Staphylococcus aureus; MRSA, methicillin resistant Staphylococcus aureus; where not specified: not reported.

b

N/A, Not available.

A. Vergori et al. / IDCases 2 (2015) 109–115 113

Atmonthlyfollow-upexaminations,whitebloodcellsandCRP were constantly normal but the patient complained general asthenia and mild occasional lumbar pain and the same antimicrobial regimen with ceftriaxone and clindamycin was prolongedforfurther4weeks.

Twomonthsafterhospitaldischarge,spinallumbarMRI(Fig.2c) showedreductionofreactivechangesandthepatientcomplained persistentmildlumbarpainduringsubsequentclinicalevaluation; amoxicillin/clavulanate 1gtid plusrifampicin 600mg perdaily orallywasprescribedduringthesubsequent6months.

Aftertotal8monthsofantimicrobialtreatment,lumbarspinal MRIshowedfurtherreductionofreactivechanges(Fig.2d),despite development of thoracolumbar kyphosis and lumbar lordosis. Antimicrobialtherapywasfinallystopped.Nosymptomsneither sequelaewerereportedinthesubsequent1yearclinicalfollowup. Discussion

Includingourreport,wefoundatotalof12pediatricSEAcases without predisposing factors: 8 were males, average age was 9.6years[range16days–17years].ThepatientdescribedbyPrasad andDeVere[15],masqueradingasanacuteabdomen,wasexcluded from subsequent analysis, due to lack of complete clinical information (paper submitted as ‘‘Visual Diagnosis’’). In the remaining11patients,clinicalpresentation was:feverandback pain,withelevationofCSFcellcounts(average,15,196cells/mm3₎

and CRP levels, except in a single case. Lumbar puncture was performedin4/11cases(36.3%),withanabnormalresultofCSF’scell countin3 cases.Responsible microorganismswereidentified in 8cases(72%):in1caseagroupAbeta-hemolyticStreptococcuswas isolatedfromapurulentcollection,intheremaining7casesS.aureus wasculturedfrompurulentcollection(n=4),fromblood(n=2)or frombothsites(n=1).MSSAwasreportedin4patients,MRSAin 1patient,whileintheremaining2casesdrugsusceptibilitywasnot reported.Inoneofthesetwolattercases,evenifnotspecifiedinthe originalpaper,a presumptivediagnosisofMSSAcanbeinferred basedonresponsetoantimicrobialtherapy(cefazolin,cephalexin). Theaverageoftherapydurationwas6 weeks.Infour casesthe durationwasnotspecified.

All the patients, were initially misdiagnosed as: back pain, meningitis(eveninabsenceoftheclassicalmeningealsyndrome), acutemyelitis,diskitis,cordcompressionbyaneoplasticmassand septicarthritis;patients’spinewasalwaysevaluatedby gadolini-um-enhancedMRI.Mostabscesses(N=10/11)werelocalizedat thethoracicandlumbararea,withoutsignsofosteomyelitis.

In 8/11 cases, laminectomy and abscess drainage were performedinassociationwitheffectivemedicaltherapy;onlyin twocases,bothwithoutanaetiologicaldiagnosis,treatmentwas successful with antimicrobial therapy only [13,14]. A good outcome, defined as a complete recovery, was obtained in all patients,withtheexceptionofthereportofRook etal.[9]who describedresidualheadacheandparaspinalpainlastingfor3years. Completedataofthereviewedliteraturereportsaresummarized inTables1and2.

Tothebestofourknowledge,thiscasereportisoneoftherare descriptionsofpediatricSEA,withoutunderlyingriskfactors.Ina previousliteraturereviewcoveringreportsfrom1980to2000[6], 12pediatricpatientswithSEAwithoutanyriskfactorswerefound: nocomplicationsorassociatedosteomyelitiswerereportedanda favorableoutcome wasobtainedafter medical(n=1/12,8%)or combinedsurgicalplus medical(n=11/12,92%) therapy.MSSA wasthepredominantdetectedpathogen(n=7/12,58%)[6].

Accordingtoourreviewofrecentliteraturefrom2001to2014, SEA in pediatric age is confirmed to be very rarely reported, especiallyintheabsenceofpredisposingriskfactors:inthelast 14yearsonly12casesweredescribed.

Osteomyelitiscomplication wasneverreported. A combined surgical and medical therapy was usually performed with favorable outcome and MSSA was confirmed to be the main aetiological agent. Despite this prominent etiology, given the potential for serious sequelae, anti-MRSA therapy should be considered mandatoryin theempiric antimicrobialregimenfor pediatric SEA in areas with high rates of MRSA, awaiting microbiologicalidentificationanddrugsusceptibilityresults.

Aninterestingmatter ofdiscussionis thepossiblesourceof staphylococcal bacteremia in pediatric patients without risk factors:asnaresandskinaretheprimarycolonizationsites,these shouldbeconsideredtheprimarysources.Inourcasereport,no previoustraumacouldbelinkedtoabacteremiaby microorgan-isms colonizing the skin, not even acupuncture procedures as previouslyreportedforadultpatients[19].

The required duration of antimicrobial therapy remains an issue:ameandurationof6weekswasreportedinthereviewed cases;thepreviousmostrecentreview[14]suggesteda4–6weeks regimen.In thecasereported herein,antimicrobialtherapywas indeedprolongeduntil8months,withasuccessfuloutcomeand withoutsideeffects.Theadoptedregimenanditsdurationcanbe matterofdiscussion:despiterapidfeverremissionand normali-zationofCRP,clinicianschosethislonglastingdualregimendueto unusualpresentationinanotherwisehealthyadolescentandto long term persistence of mild referred back pain. It has been previouslystatedthataprolongedmedicaltherapyisadvisablein cases without surgical interventions and its duration should dependonthelevelofimmunecompetence,clinicalimprovement andresponsetotreatmentdemonstratedbysubsequentreduction of inflammation at MRI [14,17]. In the only previous report describingresidual3yearsofheadacheandparaspinalpain[9],the durationoftherapywastheshortestdescribed(4weeks).

It should be noted that MRI follow-up is reported to overestimateinflammatorychanges,mainlywhenbone involve-ment is present: MRI follow-up has been usually reported as unnecessaryinspondylodiscitiswhentheclinicalandlaboratory abnormalitiesrespondtotreatment[18].Despitetheabsenceof specific statementsin the literature, this should bereasonably validalsofor patients withSEA.Thepatient withSEAreported hereindidnotshowaboneinvolvement,howeverhecomplained ofalonglastinglowbackpain.MRIfollow-upshowedcomplete removaloftheabscess,followedbyregularreductionofnormal postoperativereactivefindings,anddevelopmentof thoracolum-barkyphosistogetherwithincreasedlumbarlordosis.

Thecasedescribedherein,alongwiththereviewedliterature, underlinethediagnosticcomplexityofthiscondition,particularlyat itsonset.Manyclinicalfeaturesmaybenon-specificforSEAandthe classicalones(fever,back painandneurologicaldeficits) canbe incompletely present at the early stages. Headache and neck stiffnessarerarelyreported,buttheirpresence,asdescribedalsoin ourpatient,cancontributetomisdiagnosis:in100%ofthereviewed cases,adiagnosisotherthanSEAwaspostulatedonadmissionanda lumbarpuncturewasthereforefrequentlyperformed,withpossible dangerousconsequencesdependingonSEAlocation.

Inconclusion, itseemsessentialtomaintaina highindexof suspicion for SEA in children: the rarity and the possible differentialdiagnosisonthebasisoftheearlysignsandsymptoms can lead clinicians to underestimate its occurrence, but an as prompt as possible diagnosis is an essential prognostic factor, allowinganimmediatemedicalandsurgicalinterventionbefore thedevelopmentofnon-reversiblesequelae.

Conflictofinterest

Onbehalfofallauthors,thecorrespondingauthorstatesthat thereisnoconflictofinterest.

A.Vergorietal./IDCases2(2015)109–115 114

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