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Case ReportACase ofHerpes Simplex Virus-1 Encephalitis from aMedicolegalPoint of View

Alessandro Feola ,1 Anna Mancuso,1 and Mauro Arcangeli2

1Department of Biomedicine and Prevention, University of Rome “Tor Vergata”, Rome, Italy2Department of Life, Health and Environmental Sciences, University of L’Aquila, L’Aquila, Italy

Correspondence should be addressed to Alessandro Feola; [email protected]

Received 25 January 2018; Accepted 26 April 2018; Published 10 June 2018

Academic Editor: Benedetto Bruno

Copyright © 2018 Alessandro Feola et al. 'is is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

We present a case of herpes simplex virus-1 encephalitis (HSVE) and discuss the difficulty of early diagnosis and the possibility ofa wrong or delayed diagnosis and treatment of this encephalitis. We show the importance of considering HSVE to pursue everycase of suspicious medical liability.

1. Introduction

Herpes simplex virus-1 (HSV-1) encephalitis (HSVE) isa rare viral infection of the human central nervous system(CNS) entailing neurological dysfunction. However, it is thecommonest infectious cause of sporadic encephalitis. 'eannual incidence of HSVE worldwide is estimated to be 1–4cases/1,000,000 [1, 2].

HSVE has a bimodal age distribution, with peak in-cidences in children less than 3 years old and those aged50 years or more. Most cases occur in subjects older than50 years of both sexes. HSVE is difficult to diagnose and hasa poor prognosis. Morbidity and mortality are greater iftreatment is delayed or inadequate. In these cases, therecould be medicolegal consequences, particularly legal lia-bility for medical malpractice and nervous system injuryassessment. We report the case of a 60-year-old man withHSVE.

2. Case Presentation

A 60-year-old diabetic patient with chronic kidney disease,and treatment with corticosteroids for nephrotic syndrome,came into our emergency room. He presented with fever,dyspnea, and disorientation and was in a fugue state with

naming difficulties and aphasia. A complete blood countshowed a white blood cell count of 14,630/ml and his C-re-active protein was 1.2mg/dl (normal range, 0–0.5mg/dl). Acomputed tomographic scan was negative for brain injury.Cerebrospinal fluid (CSF) tests were positive: the fluidwas turbid, glycorrhachia was 141mg/dl (normal range,50–80mg/dl), proteinorrachia was normal, and the CSFwhite cell count was 135/UI (normal range, 0–5/UI) witha left shift (90%neutrophils and 10% lymphocytes).'e patientwas given broad-spectrum antibiotic therapy while awaitingthe CSF culture results. Two days later, the patient was co-matose, with right hemiplegia. He did not obey simple com-mands and opened his eyes only after painful stimulation. 'eCSF culture was negative for bacteria, but viral DNA corre-sponding to HSV-1 was detected in the fluid. Magnetic res-onance imaging detected diffuse signal changes in the corticaland subcortical matter, especially in the frontal-temporal re-gion and the parietal region in both cerebral hemispheres, butparticularly in the left hemisphere. Doctors diagnosed herpeticencephalitis. 'ey prescribed acyclovir treatment at a dose of750mg/250ml in 3h three times a day for 21 days because thepatient’s glomerular filtration rate ranged from 10ml/min to50ml/min. 'e patient was moved to a rehabilitation facilityafter 21 days. At discharge from the rehabilitation facility, thepatient had a percutaneous endoscopic gastrostomy (PEG)

HindawiCase Reports in MedicineVolume 2018, Article ID 3764930, 3 pageshttps://doi.org/10.1155/2018/3764930

mailto:[email protected]://orcid.org/0000-0002-9666-2636https://doi.org/10.1155/2018/3764930

and experienced hyperactivity of the muscle stretch reflex withextension of the knee on the right side. He was able to movehis right foot, extend his right knee, and walk unassisted, buthe had some problems with his dynamic balance.

Six months later, the patient underwent brain MRI,which showed a large unenhanced signal alteration. 'isalteration was consistent with a malacic area of gliosis in theleft temporal lobe and to a lesser extent in the left frontallobe, in the corona radiata, and in the centrum semiovale.'ere was also ex vacuo dilatation of the right-left ventricle.On the right side, the signal was iperintense in the temporal,frontal, and parietal periventricular white matter.

Ten months after the onset of encephalitis, the patientwas treated with PEG for recurrent dysphagia. He hada mask-like face and double incontinence. He was able toobey simple commands but was unable to speak. He hadjoint limitations in the shoulders, elbows, and hands, withextrapyramidal side effects and pyramidal hypertonia of theupper limbs. 'e patient had lost all motor function and wastotally dependent.

3. Discussion

'ere are two main types of HSVE, primary and recurrent.In more than 70% of cases, HSVE is caused by the reac-tivation of a latent virus in individuals who have previouslybeen infected. Once reactivation has occurred, viral particlesare transported via the anterograde axonal transport via theolfactory and trigeminal pathways to the CNS [3]. In 30% ofcases, HSVE is caused by a primary infection, and the virusalso reaches the CNS by the olfactory and trigeminal nerves.In immunocompetent hosts, HSVE affects brain regionssuch as the limbic system, mesial temporal and frontal re-gions (amygdala, hippocampus, parahippocampal gyrus,temporal uncus, insula, and cingulate gyrus) earlier andmost severely. 'e putamen and basal ganglia are usuallyunaffected [3].

In many cases, the presentation of encephalitis ismonolateral in the beginning, but the lesions graduallybecome widespread and bilateral, and they affect the con-tralateral temporal lobe asymmetrically. HSVE sometimesaffects the occipital cortex. 'e lesions are uneven andasymmetrical. Herpetic encephalitis is marked by necrotic-hemorrhagic lesions, with perivascular lymphocytic in-filtration in the necrotic tissues and the meninges [4]. 'eseresult in broad malacic areas as a result of tissue destructionand secondary atrophy [5]. Infected patients develop pro-dromal symptoms, such as malaise, fever, headache, andnausea, followed by the acute or subacute onset of neuro-logical symptoms, which can include lethargy, confusion,and delirium. However, the commonest symptoms are fever(90%), headache (81%), psychiatric symptoms (71%), con-vulsions (67%), vomiting (46%), weakness (33%), andmemory loss (24%) [6]. HSVE has no diagnostic features.Focal neurological deficits, lymphocytic pleocytosis in theCSF, and neuroimaging-detected changes may initially belacking. During evaluation, it is important to exclude otherpossible causes of encephalitis [7]. HSV-1 encephalitis hashigh morbidity and mortality. 'e mortality rate in

untreated patients is approximately 70%, and normal neu-rological function is not restored to 97% of the survivingpatients, who experience sequelae [8–11]. 'e complicationsof HSVE can be divided into the acute effects, includingcerebral edema, intracranial hypertension, cerebral hernia-tion and seizures, and chronic complications, which dependupon the areas affected and can also include anti-NMDA(N-methyl-D-aspartate) receptor encephalitis.

In most patients, encephalitis develops monophasically.In some cases, the patients return to their doctors aftertreatment, with an apparent clinical relapse. 'ese patientscan be of any age, with a large variety of neurologicalmanifestations, including behavioral or personality changes,memory loss, and seizures. Negative prognostic factors areadvanced age, coma or a depressed level of consciousness atonset, and a delayed specific antiviral treatment. Normalelectroencephalography predicts survival independently ofpossible confounders [12]. An early diagnosis and timelytreatment with acyclovir are very important in optimizingthe outcome [13]. Delayed treatment with acyclovir is thenegative prognostic factor that can be changed most easily.'e prognosis can also be affected by immunosuppression,severe comorbidities, a history of alcohol abuse, lack of fever,and CSF leucocytes

brain,” Journal of the Neurological Sciences, vol. 54, no. 2,pp. 209–226, 1982.

[5] J. A. Dudgeon, “Herpes encephalitis. II. Pathology of herpesencephalitis,” Postgraduate Medical Journal, vol. 45, no. 524,pp. 386–391, 1969.

[6] R. J. Whitley, S. J. Soong, C. Linneman Jr., C. Liu, G. Pazin,and C. A. Alford, “Herpes simplex encephalitis. Clinical as-sessment,” JAMA, vol. 247, no. 3, pp. 317–320, 1982.

[7] F. Magurano, G. L. Marella, A. Marchi et al., “A case offulminant subacute sclerosing panencephalitis presenting withacute myclonic-astatic epilepsy,” Annali dell’Istituto Superiore diSanità, vol. 53, no. 2, pp. 167–169, 2017.

[8] I. Steiner and F. Benninger, “Update on herpes virus in-fections of the nervous system,” Current Neurology andNeuroscience Reports, vol. 13, p. 414, 2013.

[9] K. L. Tyler, “Herpes simplex virus infections of the centralnervous system: encephalitis and meningitis, includingMollaret’s,” Herpes, vol. 11, no. S2, pp. 57A–64A, 2004.

[10] D. W. Kimberlin, “Management of HSV encephalitis in adultsand neonates: diagnosis, prognosis and treatment,” Herpes,vol. 14, no. 1, pp. 11–16, 2007.

[11] R. J. Whitley, “Herpes simplex encephalitis: adolescent andadults,” Antiviral Research, vol. 71, no. 2-3, pp. 141–148, 2006.

[12] R. Sutter, P. W. Kaplan, M. C. Cervenka et al., “Electroen-cephalography for diagnosis and prognosis of acute en-cephalitis,” Clinical Neurophysiology, vol. 126, no. 8,pp. 1524–1531, 2015.

[13] F. Raschilas, M. Wolff, F. Delatour et al., “Outcome of andprognostic factors for herpes simplex encephalitis in adultpatients: results of a multicenter study,” Clinical InfectiousDiseases, vol. 35, no. 3, pp. 254–260, 2002.

[14] A. R. Tunkel, C. A. Glaser, K. C. Bloch et al., “'emanagementof encephalitis: clinical practice guidelines by the InfectiousDiseases Society of America,” Clinical Infectious Diseases,vol. 47, no. 3, pp. 303–327, 2008.

[15] C. Sagnelli, F. Di Martino, N. Coppola, A. Crisci, andE. Sagnelli, “Acute liver failure: a rare clinical presentation ofvisceral leishmaniasis,” New Microbiologica, vol. 35, no. 1,pp. 93–95, 2012.

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