1. fear of enhancing the CNS spread of the virus,
2. masking of adverse neurological sequelae of EBP by coexistent neurological complications of HIV.,
3. possible epidural infection in immuno-compromised patients, and
4. potential for HIV-associated coagulopathy to produce an epidural haematoma.
Only one study has looked at EBP's in this group of patients (1). It reviewed yearly physical examinations and biannual neuropsychological testing in six HIV seropositive males who had required an EBP for post-dural puncture headaches (PDPH). The authors were unable to identify morbidity attributable to the EBP in these patients who were followed for a period of six months to two years.
In another relevant study (6), Hughes et al reviewed the outcome of regional analgesia in eighteen parturients infected with HIV. The patients were followed for a period of 4-6 months post-partum. The authors found no neurologic or infectious complications related to the anaesthetic management.
Finally, three single case histories of EBP's (1, 2, 3) in HIV patients have likewise demonstrated no adverse sequelae. One of these patients was followed for a period of nineteen months, while a second had received two blood patches over a period of three years. The authors' own experience of EBP in an HIV positive patient concur with the above findings.
Background
HIV penetration of the CNS occurs early in the disease (perhaps with the first viraemic episode) and CNS complications are common (5). This explains why relatively frequent diagnostic or therapeutic lumbar punctures are needed in this group of patients.
Postulated mechanisms of spread include the central migration of systemically infected macrophages. Subsequent CNS dysfunction may occur as a result of:
1. direct disruption of brain structure and function,
2. opportunistic infections,
3. growth of tumours, and
4. peripheral neuropathies.
Subtle brain dysfunction can be detected in asymptomatic HIV patients using sophisticated neurophysiologic and neuropsychologic tests. Twenty five to thirty percent of asymptomatic (CDC stage 2 and 3) patients show evidence of minor cognitive/motor dysfunction, involving activities such as attention, memory and speed processing.
More severe dysfunction (dementia) occurs rarely in CDC stages 2 and 3, but has an incidence of 14% in CDC stage 4 infection.
Peripheral nervous system involvement also occurs in 15 - 20% of patients, resulting in sensory neuropathies, myopathies and Guillain-Barre syndrome.
In summary, the safety of EBP's in HIV patients remains to be fully evaluated. The patients' immuno-compromised status (with the possibility of occult infection and the potential for coexistent neurological dysfunction) may pose some hazard. However, evidence from the reports to date appears to demonstrate no associated morbidity.
Alternatives to EBP's (including conservative therapy and patching with saline or colloid) or even the use of homologous (HIV negative) blood for EBP may be considered.
References:
1. Tom DJ, Gulevich SJ, Shapiro HM, Heaton RK, Grant l. Epidural Blood Patch in the HIV Patient. Anesthesiology. 76: 943-947. 1992.
2. Frame WA, Lichtmann MW. Blood Patch in the HIV - positive Patient. Anesthesiology. 73:1297. 1990. Letter to the Editor.
3. Bevacqua BK, Slucky AV. Epidural Blood Patch in a Patient with HIV Infection. Anesthesiology. 74: 952. 1991. Letter to the Editor.
4. Gibbons JJ. Post Dural Puncture Headache in the HIV - positive patient. Anesthesiology. 74: 953. 1991. Letter to the Editor.
5. Shapiro HM, Grant I, Weinger M. AIDS and the Central Nervous System. Anesthesiology. 80:187-200. 1994.
6. Hughes SC, Dalley PA, Landers D, Dattel BJ, Crombleholme WR. Parturients Infected with Human Immunodeficiency Virus and Regional Anesthesia . Anesthesiology. 81: 32-37. 1995.