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EDITORIAL
J Res Med Sci 2020,  25:68

Central nervous system infections versus lead toxicity in the differential diagnosis of encephalopathy


1 Medical Toxicology and Drug Abuse Research Center, Birjand University of Medical Sciences, Birjand, Iran
2 Medical Toxicology and Drug Abuse Research Center, Birjand University of Medical Sciences, Birjand; Department of Persian Medicine, School of Persian and Complementary Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
3 Medical Toxicology and Drug Abuse Research Center; Deputy of Research and Technology, Student Research Committee, Birjand University of Medical Science, Birjand, Iran
4 Addiction Medicine Program, Wake Forest School of Medicine, Winston-Salem, NC, USA
5 Medical Toxicology and Drug Abuse Research Center, Birjand University of Medical Sciences, Birjand, Iran; Department of Medical toxicology, Rocky Mountain Poison and Drug Safety, Denver Health and Hospital Authority, CO, USA

Date of Submission23-Oct-2019
Date of Decision16-Feb-2020
Date of Acceptance03-Apr-2020
Date of Web Publication27-Jul-2020

Correspondence Address:
Dr. Omid Mehrpour
Rocky Mountain Poison and Drug Safety, Denver Health and Hospital Authority, CO

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrms.JRMS_810_19

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How to cite this article:
Nakhaee S, Mehrpour M, Mortazavi B, Weiss ST, Mehrpour O. Central nervous system infections versus lead toxicity in the differential diagnosis of encephalopathy. J Res Med Sci 2020;25:68

How to cite this URL:
Nakhaee S, Mehrpour M, Mortazavi B, Weiss ST, Mehrpour O. Central nervous system infections versus lead toxicity in the differential diagnosis of encephalopathy. J Res Med Sci [serial online] 2020 [cited 2020 Nov 1];25:68. Available from: https://www.jmsjournal.net/text.asp?2020/25/1/68/291017



Currently, lead toxicity is a major health problem in Iran, with lead encephalopathy being the most serious presentation of lead poisoning. It is not common in adults and may occur at high blood concentrations of lead.[1] The signs and symptoms of lead encephalopathy include headache, delirium, hallucinations, lethargy, agitation, tremor, memory loss, and single or recurrent seizures.[1],[2],[3] A tonic–clonic seizure is the most typical seizure type in these patients.[3] Delirium induced by lead may increase over a period of several days.[1] Coma is an uncommon presentation of lead encephalopathy, and progressive cerebral edema and increased intracranial pressure may result in death.[1]

The differential diagnosis of encephalopathy includes several central nervous system (CNS) infections, such as subacute meningitis, intracranial abscess, and encephalitis, along with lead encephalopathy. At least one report suggests that lead encephalopathy can present with a pattern similar to meningitis and encephalitis.[4] The failure to recognize any one of these serious etiologies can lead to significant morbidity and mortality.

Since the presentation of lead encephalopathy may mimic the presentations of serious CNS infections, distinguishing between them can be challenging. Both CNS infections and lead encephalopathy may present with a history of delirium, headache, and seizure, and both may be associated with increased intracranial pressure. We therefore point out some differences between these two scenarios to help with the decision-making process. Although fever is usually noted in CNS infections, it is infrequent in lead encephalopathy. In contrast, lead encephalopathy may be accompanied with loss of memory and disturbances in attention, processing, visual-spatial capabilities, and cognitive and behavioral problems that are not typically seen with CNS infections.[4]

Cerebrospinal fluid (CSF) analysis may allow the diagnosis of lead encephalopathy or rule out other differential diagnoses. In patients with either lead encephalopathy or CNS infection, the hallmark characteristics of lumbar puncture include an increase in the opening pressure and increased CSF protein concentration.[5],[6] However, the CSF white blood cell count in lead encephalopathy is slightly increased or even normal, while it is typically greatly increased in CNS infections (pleocytosis).[5],[7]

The complete blood count may also help differentiate between the diagnoses. Anemia, especially hypochromic microcytic anemia, is a common finding in patients with lead encephalopathy.[8] Although some viral causes of encephalitis may induce bone marrow depression,[9] the frequency of anemia is higher, more specific to the red blood cell line, and more chronic in patients with lead encephalopathy.

Finally, the co-occurrence of gastrointestinal symptoms may help in the differentiation of lead encephalopathy from CNS infections.[4] Some specific indicators of lead poisoning that are not typically seen with CNS infections include abdominal pain (lead colic), constipation, and weight loss.[10] In cases where a blood lead concentration is not readily available, positive abdominal imaging results may help physicians diagnose lead encephalopathy and start treatment expeditiously.[11] The distinguishing features between lead encephalopathy and CNS infections are summarized in [Table 1].
Table 1: Typical presentation features distinguishing lead encephalopathy from central nervous system infection

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  References Top

1.
Mason LH, Harp JP, Han DY. Pb neurotoxicity: Neuropsychological effects of lead toxicity. Biomed Res Int 2014;2014:840547.  Back to cited text no. 1
    
2.
George M, Heeney MM, Woolf AD. Encephalopathy from lead poisoning masquerading as a flu-like syndrome in an autistic child. Pediatr Emerg Care 2010;26:370-3.  Back to cited text no. 2
    
3.
Talbot A, Lippiatt C, Tantry A. Lead in a case of encephalopathy. BMJ Case Rep 2018;2018:bcr-2017-222388.  Back to cited text no. 3
    
4.
Shabani M, Nasiri M, Aminzadeh Z, Hassanian Moghaddam H. A challenge between central nervous system infection and lead toxicity: Opioid case reports from Iran. Iran J Med Sci 2019;44:168-71.  Back to cited text no. 4
    
5.
Whitfield CL, Ch'ien LT, Whitehead JD. Lead encephalopathy in adults. Am J Med 1972;52:289-98.  Back to cited text no. 5
    
6.
Coffin R, Phillips JL, Staples WI, Spector S. Treatment of lead encephalopathy in children. J Pediatr 1966;69:198-206.  Back to cited text no. 6
    
7.
Al Khayat A, Menon NS, Alidina MR. Acute lead encephalopathy in early infancy—Clinical presentation and outcome. Ann Trop Paediatr 1997;17:39-44.  Back to cited text no. 7
    
8.
Alinejad S, Aaseth J, Abdollahi M, Hassanian-Moghaddam H, Mehrpour O. Clinical aspects of opium adulterated with lead in Iran: A review. Basic Clin Pharmacol Toxicol 2018;122:56-64.  Back to cited text no. 8
    
9.
Binder D, Fehr J, Hengartner H, Zinkernagel RM. Virus-induced transient bone marrow aplasia: major role of interferon-alpha/beta during acute infection with the noncytopathic lymphocytic choriomeningitis virus. J Exp Med 1997;185:517-30.  Back to cited text no. 9
    
10.
Hayatbakhsh MM, Oghabian Z, Conlon E, Nakhaee S, Amirabadizadeh AR, Zahedi MJ, et al. Lead poisoning among opium users in Iran: An emerging health hazard. Subst Abuse Treat Prev Policy 2017;12:43.  Back to cited text no. 10
    
11.
Zamani N, Hassanian-Moghaddam H, Bahrami-Motlagh H, Ahmadi S, Phillips S. Lead poisoning due to ingestion of lead-contaminated opium: A diagnostic study on patients' imaging findings. J Trace Elem Med Biol 2019;55:26-32.  Back to cited text no. 11
    



 
 
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