Troubleshooting obstetric spinal anaesthesia at district hospital level.

Obstetric spinal anaesthesia is routinely used in South African district hospitals for caesarean sections, providing better maternal and neonatal outcomes than general anaesthesia in appropriate patients. However, practitioners providing anaesthesia in this context are usually generalists who practise anaesthesia infrequently and may be unfamiliar with dealing with complications of spinal anaesthesia or with conversion from spinal to general anaesthesia. This is compounded by challenges with infrastructure, shortages of equipment and sundries and a lack of context-sensitive guidelines and support from specialised anaesthetic services for district hospitals. This continuous professional development (CPD) article aims to provide guidance with respect to several key areas related to obstetric spinal anaesthesia, and to address common concerns and queries. We stress that good clinical practice is essential to avoid predictable, common complications, and hence a thorough preoperative preparation is essential. We further discuss clinical indications for preoperative blood testing, spinal needle choice, the use of isobaric bupivacaine, spinal hypotension, failed or partial spinal block and pain during the caesarean section. Where possible, relevant local and international guidelines are referenced for further reading and guidance, and a link to a presentation of this topic is provided.

Anaesthesia for ruptured ectopic pregnancy at district level.

In South Africa, deaths as a result of ectopic pregnancies are increasing despite the overall improvements in maternal mortality. These deaths occur predominantly in district hospitals, with the final cause of death being hypovolaemic shock in almost all cases. In most cases, no anaesthesia was attempted despite the district hospitals having the clinical skills, equipment and infrastructure to provide a caesarean delivery service. It appears that there is a skills gap between the provision of anaesthesia for caesarean delivery and that of ruptured ectopic pregnancy. There is a growing recognition of the urgent need to prioritise the provision of emergency surgical care in rural settings. This should be viewed not as a luxury but as an absolute necessity. In this study, we aim to discuss the pathophysiology of a patient with a ruptured ectopic pregnancy briefly, outline district hospital requirements for safe surgery and then discuss a simple, safe method for the provision of anaesthesia in patients deemed too unstable to transfer to a referral facility.

Past adult lead exposure is associated with longitudinal decline in cognitive function.

OBJECTIVE: To determine whether adults with past exposure to neurotoxicants have progressive declines in cognitive function years after exposure has ceased, and whether tibia lead is a predictor of the magnitude of change. METHODS: A total of 535 former organolead manufacturing workers with a mean age of 55.6 years, a mean duration of 16 years since last occupational lead exposure, and low blood lead levels at the first study visit and 118 controls were evaluated with neurobehavioral tests two to four times over 4 years. "Peak" tibia lead levels, estimated from current levels measured by X-ray fluorescence, were used to predict changes in cognitive function over time. RESULTS: In former lead workers, peak tibia lead ranged from -2.2 to 98.7 microg Pb/g bone mineral. Compared to controls, former lead workers performed worse over time for three tests of visuo-constructive ability and verbal memory and learning (p < 0.05). In former lead workers, peak tibia lead predicted declines for six tests of verbal memory and learning, visual memory, executive ability, and manual dexterity (p < 0.05 for four tests and < 0.10 for two additional tests). On average, for these six tests, an increase of 15.7 microg/g of peak tibia lead was equivalent in its effects on annual test decline to 5 more years of age at baseline. CONCLUSIONS: These are the first data to suggest that cognitive function can progressively decline due to past occupational exposures to a neurotoxicant.

Infection with adeno-associated virus may protect against excitotoxicity.

Gene therapy has developed as a promising approach for therapy in a broad variety of conditions. Viral vectors have been developed that may replace a defective gene, prevent expression of a mutant gene, or deliver a protective gene and thereby delay cellular loss. Using adeno-associated virus containing green fluorescent protein (AAV-GFP) we were able to specifically transduce cells located in the inner retina and induce over-expression of GFP in adult rat retinae. The delivery and expression of GFP had no influence themselves on retinal ganglion cell survival. Administration of the reporter vector AAV-GFP provided retinal ganglion cells with slight but significant protection from intravitreal NMDA. This was a locally mediated phenomenon; greater protection was seen in regions with more transduced cells. Any evaluation of the efficacy of a putative viral vector should consider the possible protective or toxic effect of the native virus.

Thy-1 is critical for normal retinal development.

In the mammalian retina, Thy-1, the most abundant mammalian neuronal surface glycoprotein, is found predominantly if not exclusively on retinal ganglion cells. We hypothesized that Thy-1 plays a significant role in retinal development. Neurite outgrowth of retinal ganglion cells from Thy-1(-) mice over multiple substrates was compared to that seen with wild-type controls. Adult mouse retinas were histologically compared between Thy-1(-) and three strains of Thy-1 positive mice. Thy-1(-) retinal ganglion cells had significantly less neurite outgrowth than controls. The inner nuclear, inner plexiform, ganglion cell and outer segment/pigment epithelium layers were thinner in Thy-1(-) retinae than in controls. Thy-1 appears to be critical for normal retinal development.

bcl-2 gene therapy exacerbates excitotoxicity.

The protooncogene bcl-2 can block neuronal death from both naturally occurring apoptosis and exogenous insults. bcl-2 is therefore a promising candidate for the prevention of excitotoxic neuronal death. Using an adeno-associated viral vector, we delivered the bcl-2 gene to the ganglion cell layer of the rat eye. We hypothesized that infection with bcl-2 would protect ganglion cells against excitotoxic cell death. However, retinal infection with bcl-2 increased ganglion cell susceptibility to both axonal injury and intravitreal NMDA. Our study--intended to explore the possibility of bcl-2 transduction as an in vivo therapeutic approach--revealed a deleterious effect of bcl-2 transduction.