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  • Title: [Acute toxic encephalopathy in patients with tuberculosis].
    Author: Korniliva ZKh, Khokhlov IuK, Savin AA, Batyrov FA.
    Journal: Probl Tuberk; 2002; (12):42-6. PubMed ID: 12611336.
    Abstract:
    A hundred and thirty five patients admitted to Moscow Tuberculosis Hospital No. 7 for disseminated and progressive forms of tuberculosis were examined. Among neurological disorders in tuberculosis, acute toxic encephalopathy (ATE) should be placed in the first place in terms of their severity, problems of diagnosis and treatment. In patients with acutely progressive forms of tuberculosis, the development of ATE is brought about by two factors: 1) significant tuberculous toxemia concurrent, in 37% of cases, with severe alcoholic intoxication that leads to generalized toxic and allergic vasculitis and as a result DIC syndrome; 2) cerebral hypoxia with dyscirculatory disorders due to progressive cardiopulmonary failure. The status of patients with tuberculosis and ATE is generally critical or extremely critical. These are actually resuscitative patients. Most patients have disseminated bilateral lung lesions with multiple decay cavities, with massive bacterial isolation found at sputum bacterioscopy. With this, mycobacterial resistance to at least one antituberculous drug was found in 83% of cases. Primary multidrug resistance was detected in 29.6% of patients. The diagnosis of ATE in patients with tuberculosis is difficult and requires that tuberculous meningitis shall be excluded. Acute progression, no spinal fluid changes, significant signs of cooagulopathy and thrombcytopathy with multiorgan failure and progressive DIC syndrome may diagnose ATE in patients with acutely progressive tuberculosis. The specific features of treatment in patients with tuberculosis and ATE are intensive antituberculous therapy with predominantly parenteral administration of drugs and intensive therapy for the DIC syndrome. Despite the treatment, 48 (35.6%) patients died from progressive tuberculosis and ATE, in 40 (29.6%), therapeutic efficiency was low due to multidrug myobacterial resistance.
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