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   Table of Contents     
EDITORIAL  
Year : 2016  |  Volume : 8  |  Issue : 4  |  Page : 127-128
State of the globe: Acute febrile encephalopathy


1 Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Radiodiagnosis, King George's Medical University, Lucknow, Uttar Pradesh, India
3 Department of Obst and Gynae, King George's Medical University, Lucknow, Uttar Pradesh, India

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Date of Web Publication10-Nov-2016
 

How to cite this article:
Agarwal A, Gutch M, Kumar S, Agrawal S. State of the globe: Acute febrile encephalopathy. J Global Infect Dis 2016;8:127-8

How to cite this URL:
Agarwal A, Gutch M, Kumar S, Agrawal S. State of the globe: Acute febrile encephalopathy. J Global Infect Dis [serial online] 2016 [cited 2019 Sep 17];8:127-8. Available from: http://www.jgid.org/text.asp?2016/8/4/127/193748


Patients presenting with fever and altered sensorium should be treated as a medical emergency. Such presentation is very commonly seen in outpatient departments, as well as medical emergencies. We need to diagnose these promptly and administer antimicrobials and/or adjunctive therapies timely. Moreover, keeping in mind that irrational use of antibiotics has to be avoided in patients who will not be benefited by any such therapy (alternate etiology with similar clinical presentation-mimickers). Early recognition, efficient decision making, and early institution of therapy are the key to saving the life of the patient. The presence of fever by itself is not sufficient to make a diagnosis of infective etiology (like meningitis or encephalitis), and therefore careful evaluation is required to exclude the clinical mimickers of infection. In addition, encephalopathy can be precipitated by systemic infections/sepsis without cerebral infection per septic encephalopathy.[1] Hence, utmost cognizance of all these confounding factors is to be kept while dealing with such patients. Sepsis entails complications such as hypoglycemia, hyperpyrexia, hypovolemia, hepatic, or renal failure which can themselves cause alteration of sensorium.[1] There can also be severe rise in body temperature due to mechanisms such as overproduction of heat, impaired dissipation, or hypothalamic lesions due to noninfective central nervous system (CNS) diseases.[2] Patients with neuroleptic malignant syndrome have a fever along with altered sensorium, neck stiffness ± generalized rigidity even after the offending drug withdrawal; hence, these states should also be kept in mind while formulating the differential diagnosis of acute encephalitis.[3] Mostly, the presence of focal neurological signs can distinguish encephalitis from generalized (secondary) encephalopathy; however, this distinction may not always be possible clinically alone, and cerebrospinal fluid (CSF) analysis and imaging are required to rule out infection.[4],[5]

Herpes simplex virus (HSV) is one of the most common causes of sporadic encephalitis around the world.[6],[7] Postmonsoon Japanese encephalitis (JE) surge is well recognized, and more and more JE and other flavivirus encephalitis cases are being seen from many parts of India. Varicella encephalitis can be fatal in immunocompromised patients. Among other viruses, enterovirus, JE virus, and mumps are the important agents. More recently dengue, encephalitis is also being recognized and reported.[6],[7]

Cerebral malaria (CM) is a potentially fatal complication of falciparum malaria; it is also an important cause of altered sensorium in febrile patients particularly in endemic areas. CM should be an important differential diagnosis in patients presenting with acute fever and altered mental state in such areas. Postmonsoon surge is common to both malarial cases and viral encephalitis and therefore common symptomatology may be confusing to the treating physician, timely investigations are of help in such cases.[6],[7]

Dengue hemorrhagic fever presents as a short febrile duration, thrombocytopenia, it can present with altered sensorium.[8]

Sepsis-associated encephalopathy (SAE) is a sparsely understood CNS condition that is associated with manifestations ranging from lethargy, drowsiness to overt delirium in patients with sepsis. Importantly, according to a study, patients with SAE have higher mortality at 6 months; therefore, it carries serious prognostic implications for those who get admitted to Intensive Care Unit.[6],[7],[8],[9] A large number of patients present to an emergency in a tertiary care hospital with sepsis; therefore, it becomes an important differential diagnosis of AFE in adults.

Computed tomography (CT) scan brain is performed as the first imaging modality in all the patients with AFE to rule out contraindications for lumbar puncture. Enhancement of the meninges can be seen on contrast-enhanced CT scan in cases of bacterial meningitis, focal changes of viral encephalitis can also be seen. Imaging studies performed in patients with acute meningitis may sometimes provide normal findings, particularly in an early stage. Magnetic resonance imaging (MRI) of the brain is more specific and offers better results. Bilateral T2/fluid attenuated inversion recovery (FLAIR) thalamic hyperintensities, with or without hemorrhage, are the most common finding seen in patients with JE. MRI brain in patients with HSV encephalitis shows characteristic T2/FLAIR hyperintensities in the temporal and/or frontal lobes. Multiple hemorrhagic foci may be seen in dengue hemorrhagic encephalitis; other less common viral encephalitis may present with variable typical and atypical picture, serological, and CSF investigation correlation may be of help in such situation to differentiate among different viral categories. Bacterial meningitis presents as generalized or localized meningeal enhancement with or without associated cerebritis of underlying brain parenchyma. Tubercular basal meningitis has a predilection to form thick enhancing exudates in basal cisterns, complications such as hydrocephalus and infarcts may also be seen; tuberculomas may also be seen simultaneously. Bacterial abscesses may be seen as well-defined ring enhancing lesions showing diffusion restriction on diffusion weighted imaging.[6],[7]

Patients can make complete recovery provided the underlying cause is treated timely. Efficiency and skill are required to correctly and timely diagnose the underlying etiology. A small but significant number of patients die, and some of the patients are left with neurologic sequelae. Delayed neurologic recovery and sequelae are also well recognized.[6],[7],[8],[9] The fact that maximum mortality is seen in patients with AVE and SAE signifies that diffuse cerebral parenchymal involvement, lack of availability of specific drug for most of the viral infections, and multiorgan dysfunction in SAE possibly contribute to the overall increased mortality in these patients. Raised intracranial pressure in meningoencephalitis also contributes to mortality. Patients in whom a definitive diagnosis cannot be reached also show higher mortality.[6],[7],[8],[9]

 
   References Top

1.
Chaudhuri A, Kennedy PG. Diagnosis and treatment of viral encephalitis. Postgrad Med J 2002;78:575-83.  Back to cited text no. 1
    
2.
Dinarello CA, Gelfand JA. Fever and hyperthermia. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, editors. Harrison er SL, Longo DL, Jameson asper DL. 16 th ed. New York: McGraw-Hill; 2005. p. 104-8.  Back to cited text no. 2
    
3.
Amore M, Zazzeri N. Neuroleptic malignant syndrome after neuroleptic discontinuation. Prog Neuropsychopharmacol Biol Psychiatry 1995;19:1323-34.  Back to cited text no. 3
    
4.
Fitch MT, Abrahamian FM, Moran GJ, Talan DA. Emergency department management of meningitis and encephalitis. Infect Dis Clin North Am 2008;22:33-52, v-vi.  Back to cited text no. 4
    
5.
Davis LE. Diagnosis and treatment of acute encephalitis. Neurologist 2000;6:145-59.  Back to cited text no. 5
    
6.
Modi A, Atam V, Jain N, Gutch M, Verma R. The etiological diagnosis and outcome in patients of acute febrile encephalopathy: A prospective observational study at tertiary care center. Neurol India 2012;60:168-73.  Back to cited text no. 6
  Medknow Journal  
7.
Kumar S, Pandey AK, Gutch M, Razi SM, Gupta A, Jain N, et al. Acute viral encephalitis clinical features and outcome: Experience from a tertiary center of North India. Ann Trop Med Public Health 2015;8:262-6.  Back to cited text no. 7
  Medknow Journal  
8.
Jain N, Gutch M, Kumar V, Naik AK. A fatal combo of dengue shock syndrome with acute subdural hematoma. Neurol India 2012;60:105-6.  Back to cited text no. 8
[PUBMED]  Medknow Journal  
9.
Kumar R, Tripathi S, Tambe JJ, Arora V, Srivastava A, Nag VL. Dengue encephalopathy in children in Northern India: Clinical features and comparison with non dengue. J Neurol Sci 2008;269:41-8.  Back to cited text no. 9
    

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Correspondence Address:
Dr. Avinash Agarwal
Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-777X.193748

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2008 Journal of Global Infectious Diseases | Published by Wolters Kluwer - Medknow
Online since 10th December, 2008