A case is presented of a patient who developed paraplegia following the administration of epidural analgesia. Investigations including a myelogram, showed that a developmental laminar stenosis existed in this case. This is a progresssive condition which would have been expected to proceed to paraplegia later.The authors believe that it is important to draw the attention of other anaesthetists to the possibility of the existence of this kind of complication, because medicolegal consequences might have ensued if further investigations and treatment had not been carried out. Case reportA female patient aged 35 years, weighing 36 kg, presented for hysterectomy. She was clinically normal with a haemoglobin of 10.5 g%, urine examination was normal and the chest X-ray and electrocardiogram were within normal limits.The pre-operative blood pressure was 100/60 mmHg and pulse rate 92/min. Anaesthetic techniqueThe patient was premedicated with 0.6 mg atropine sulphate, intramuscularly, half an hour before surgery.The patient's back was prepared with 'Cetavlon', ether, iodine and spirit and the epidural space was located at L3-4 interspace with the patient in the right lateral and flexed position. Loss of resistance with a 10 ml syringe of air was used to locate the epidural space. Analgesia was achieved with 20 ml 1.5% lignocaine with 1 in 200 OOO adrenaline tartrate.The patient was placed in the lithotomy position for surgery. Morphine sulphate 7.5 mg was given intramuscularly after 15 min of epidural analgesia. There was no motor paralysis.The blood pressure was stable throughout the operation. The effect of the epidural started to wear off after 2.75 h and therefore light general anaesthesia was employed for the last half hour of surgery, using oxygen, nitrous oxide and trichloroethylene. Postoperative courseThe immediate postoperative course was uneventful. Pulse and blood pressure were stable and the patient was talking rationally.After 3 hours, on the evening of operation, she started to complain of radiating pain and weakness in the right leg.On examination the blood pressure was lOO/ 60 mmHg. and the pulse rate was IOO/min. The right hip flexors seemed weaker. There was no evidence of weakness in any other group of muscles. No sensory loss was evident. The spine was clinically normal. A self retaining catheter was in situ; therefore bladder function could not be assessed. This weakness of the right leg was

Context:Avanafil is a smooth muscle relaxant that is clinically used to treat erectile dysfunction. It is an inhibitor of phosphodiesterase-5 (PDE5), the enzyme that catalyzes the metabolism of cyclic guanosine monophosphate (cGMP). The inhibitory effect of avanafil on isolated detrusor muscle contractility has not been studied.Aims:This study investigated the inhibitory effect of avanafil on isolated caprine (goat) detrusor muscle contractility and the possible mechanisms involved.Settings and Design:80 mM potassium chloride (KCl)-induced contractility of the isolated goat detrusor was studied using a physiograph.Materials and Methods:Ten caprine detrusor strips were made to contract using 80 mM KCl before and after addition of three concentrations (10, 30, and 60 μM) of avanafil. Three reversal agents, ODQ, a guanylyl cyclase inhibitor; glibenclamide, an adenosine triphosphate (ATP)-sensitive potassium channel blocker; and iberiotoxin, a calcium-sensitive potassium (BKCa) channel blocker, were investigated for their ability to reverse the inhibitory effect of 30 μM avanafil on KCl-induced detrusor contractility.Statistical Analysis Used:The nonparametric statistical test, Kruskal–Wallis test, was used for the analysis of the data.Results:Avanafil caused a statistically significant inhibition of detrusor contractility at 30 and 60 μM concentrations. The inhibitory effect of 30 μM avanafil on detrusor contractility was significantly reversed by the addition of ODQ, glibenclamide, and iberiotoxin.Conclusions:Avanafil inhibits the contractility of the isolated detrusor by inhibiting PDE5, leading to raised cellular levels of cGMP. The raised levels of cGMP could have inhibited detrusor contractility by activating cGMP-dependent protein kinase, by opening ATP-sensitive potassium channels, and by opening BKCa. Avanafil could be evaluated for treating clinical conditions requiring relaxation of the detrusor like overactive bladder.

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