Subarachnoid Spread of Epidural Anaesthetic Following Dural Puncture

1989 ◽  
Vol 9 (1) ◽  
pp. 48
Author(s):  
A. Leach ◽  
G. B. Smith
1998 ◽  
Vol 26 (3) ◽  
pp. 256-261 ◽  
Author(s):  
A. Vartis ◽  
C. B. Collier ◽  
S. P. Gatt

A combined spinal epidural anaesthetic (CSE), by design, produces a deliberate multicompartment block across a breached dural membrane. Since the lateral holes of the epidural catheter may lie in close proximity to the dural puncture site, a bolus solution of drug injected via the epidural catheter has the potential to leak through the dural puncture into the subarachnoid space. The aim of this study was to determine the incidence of intrathecal leak by performing an epidurogram. Fifteen patients undergoing surgery with a CSE anaesthetic using a 16 gauge Tuohy/26 gauge pencil point needle were studied. Within three hours of catheter insertion, 12 ml of contrast (iohexol 300 mg/ml) was injected via the epidural catheter under fluoroscopic control with screen recording and exposure of lateral and anteroposterior X-ray plates. All films were later reviewed for evidence of intrathecal spread. We did not observe any evidence of intrathecal spread of contrast. However, caution should be observed during administration of an intraoperative bolus dose of analgesic agent via a catheter inserted as part of a combined spinal epidural anaesthetic technique, particularly with the use of hydrophilic opiods.


1985 ◽  
Vol 53 (01) ◽  
pp. 095-098 ◽  
Author(s):  
C R Jones ◽  
R McCabe ◽  
C A Hamilton ◽  
J L Reid

SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline.Alpha2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response- to increased circulating catecholamines during birth.


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