Delayed Onset Sciatic Nerve Palsy Secondary to Wound Hematoma following Anticoagulant Therapy Post-Bipolar Hemiarthroplasty - an Uncommon Complication: A Case Report

@#A 58-year old female patient presented to us with a three months’ old fracture of the neck of femur. She underwent bipolar hemiarthroplasty. In the immediate postoperative period, she developed deep vein thrombosis for which she was started on anticoagulant therapy. Patient had persistent discharge from the wound since then and underwent regular dressings. On the eighth post-op day, she developed sciatic nerve palsy secondary to wound haematoma. The haematoma was decompressed immediately and she had a dramatic improvement in pain but her neurological deficit persisted. The wound healed completely without any complications. At three months follow up, she had recovered completely with grade 5/5 power in ankle and foot and full sensory recovery in the sciatic nerve distribution. She was ambulating comfortably with a walker. At final follow up around 20 months post-operation, she was pain-free and walking without any support. The wound had healed completely.

Efeito do exercício resistido na redução do edema, nocicepção e regeneração nervosa em um modelo de compressão do nervo isquiático / Effect of resistance training on the reduction of edema, nociception, and nerve regeneration in a sciatic nerve compression model

OBJETIVOS: Analisar os efeitos do exercício físico resistido de subida em escada, sobre o edema, nocicepção e regeneração nervosa de ratos Wistar, submetidos à compressão do nervo isquiático. MÉTODOS: Foram estudados 24 ratos Wistar, divididos igualmente entre quatro grupos: Grupo Controle, Grupo Exercício, Grupo Lesão e Grupo Tratado ­ Lesão e Exercício. O Grupo Lesão e o Grupo Tratado foram submetidos à compressão do nervo isquiático com pinça hemostática por 30 segundos. A partir do terceiro dia após a lesão, iniciou-se o tratamento com exercício resistido de subida em escada para o Grupo Exercício e o Grupo Tratado. O tratamento consistiu em realizar duas séries de 10 subidas na escada, com sobrecarga de 100 gramas e intervalo de um minuto entre uma série e outra. O estudo foi conduzido por 22 dias e nesse tempo os animais foram avaliados quanto ao edema e à nocicepção. No 22º dia de pós-operatório, os animais foram anestesiados para retirada de um fragmento do nervo isquiático para análise do número de axônios e da densidade de fibras. Em seguida, ainda sob efeito da anestesia, os animais foram eutanasiados. Os nervos coletados seguiram protocolo de processamento histológico de rotina. As expressões do Fator de Crescimento Neural e do Fator de Crescimento Derivado do Cérebro foram avaliadas por Western blotting. RESULTADOS: Não houve diferença significativa entre os grupos no tamanho do edema. O Grupo Controle apresentou maior limiar nociceptivo comparado aos demais grupos. A análise morfométrica não revelou diferença significativa entre os grupos, quanto à quantidade de axônios e à densidade de fibras. A expressão do Fator de Crescimento Derivado do Cérebro foi maior no Grupo Lesão e no Grupo Tratado quando comparados ao Grupo Controle. CONCLUSÕES: O exercício físico resistido de subida em escada, nos parâmetros propostos, não foi eficaz para reduzir o edema, a nocicepção ou aumentar o número de axônios e a densidade de fibras nervosas após lesão do nervo isquiático.

AIMS: To analyze the effects of ladder-climbing resistance training exercise on edema, nociception, and regeneration of the sciatic nerve in Wistar rats subjected to sciatic nerve compression. METHODS: Twenty-four Wistar rats were divided into four groups: Control Group, Exercise Group, Injury Group, and Treated Group (injury and exercise). Injury Group and Treated Group were subjected to sciatic nerve compression with a hemostat for 30 seconds. On the third day after injury, Exercise Group and Treated Group began treatment with ladder-climbing resistance exercise. The treatment consisted in performing two series of 10 ladder climbs with a 100-gram overload and a one-minute interval between the series. The study was conducted for 22 days, during which time the animals were evaluated for edema and nociception. Twenty-two days after surgery, the animals were anesthetized for removal of a sciatic nerve fragment and analysis of the number of axons and fiber density. Thereafter, still under anesthesia, the animals were euthanized. Nerve sampling followed the routine histological processing protocol. Expressions of Neural Growth Factor and Brain-derived Neurotrophic Factor were evaluated by Western blotting. RESULTS: There was no significant difference in edema size between groups. Control Group showed the highest nociceptive threshold compared to the other groups. The morphometric analysis showed no significant difference in number of axons and fiber density between groups. The expression of Brain-derived Neurotrophic Factor was greater in the Injury Group and the Treated Group compared to the Control Group. CONCLUSIONS: The proposed ladder-climbing resistance training was not effective in reducing edema and nociception or in increasing the number of axons and fiber density after sciatic nerve injury.

Patterns of Nerve Conduction Blockade by Different Combinations of Lidocaine-bupivacaine Mixture / 대한마취과학회지

BACKGROUND: A mixture of local anesthetics such as lidocaine and bupivacaine has frequently been used in clinical practice. The rationale behind this is to take advantage of lidocaine's rapid onset and bupivacaine's perpetuation in anesthesia. The purpose of this study was to examine the changes in the onset and recovery of nerve blocking action exerted by the different combinations of these two in the mixture. METHODS: Isolated sciatic nerve preparations obtained from adult male Sprague-Dawley rats were used in this study. Recordings of A-fiber compound action potentials (A-CAPs) were made at the end of the isolated nerve while single pulse stimuli (0.5 msec, supramaximal intensity, 2 Hz) were applied to the opposite end of the nerve. Seven different composition of lidocaine-bupivacaine mixtures were prepared (0 : 6, 1 : 5, 2 : 4, 3 : 3, 4 : 2, 5 : 1, 6 : 0 vol./vol.), where basal concentrations of lidocaine and bupivacaine were 0.2% and 0.05%, respectively. Amplitudes of A-CAPs were measured before, during and after perfusion of mixture solution. The time needed for A-CAPs amplitude to decrease to 10% of the basal value after starting perfusion (onset time) and that needed to reach to 50% of the basal value after ceasing the perfusion (recovery time) were measured. RESULTS: With increasing concentration ratios of lidocaine to bupivacaine in the mixture as mentioned above, the following onset and recovery times were obtained (6.0 +/- 0.3, 5.6 +/- 0.3, 6.0 +/- 0.5, 8.3 +/- 0.5, 7.3 +/- 0.6, 7.8 +/- 0.3, and 10.8 +/- 0.8, minutes; 38 +/- 4, 63 +/- 12, 87 +/- 19, 100 +/- 13, 104 +/- 18, 137 +/- 27, and 157 +/- 18 minutes, respectively). CONCLUSION: Onset times were, in general, exponentially decreased with the increase in the lidocaine concentration. However, recovery times were lineary increased with the increase in the bupivacaine concentration. So, it should be kept in mind that rapid onset can only be obtained with the expense of substantial reduction in the duration of local anesthetic effect of the mixture, and vice versa.

The Effect of Adrenaline on the Blockade of Compound Action Potential by Local Anesthetics in Rat Sciatic Nerves / 대한마취과학회지

BACKGROUND: Adrenaline has often been used to prolong the local anesthetic effect during surgical procedures. As a possible explanation for this, a local vasoconstriction caused by adrenaline has been proposed. However, in a recent study, clonidine, an alpha2 adrenergic receptor agonist, was reported to block the conduction of mammalian nerves in vitro. Thus, there is a possibility that adrenaline may block nerve conduction by acting on the adrenergic receptor. The present study is performed to see : (1) If adrenaline directly affects nerve conduction ; (2) If adrenaline affects conduction blockade caused by local anesthetic. METHODS: Recordings of compound action potentials (CAPs) of A- and C-components were obtained from isolated sciatic nerves of adult male Sprague-Dawley rats. Dose-response curves of lidocaine and adrenaline regarding depression of CAPs were determined. Effects of adrenaline on the lidocaine-induced nerve block was assessed by comparing the effect of lidocaine (3.5x 10 5) with a lidocaine-epinephrine mixture (Lido-Epi, 3.5 x10 5 lidocaine with 1:100,000 epinephrine). RESULTS: Adrenaline, near the clinical concentrations, had no effect on the size of either A- or C-component of CAPs. The ED50 of lidocaine was 3.5x 10 5. Lidocaine depressed A-CAP 45.9+/- 7.0 when compared with baseline value, and the Lido-Epi solution depressed A-CAP to 41.7+/- 5.0 (P > 0.05). Lidocaine depressed C-CAP 59.8 +/- 3.4 when compared with the baseline value, and the Lido-Epi solution depressed C-CAP to 60.5 8.1 (P > 0.05). Consequently, adrenaline did not augment lidocaine induced nerve blockade. CONCLUSION: This study confirmed that adrenaline applied to the peripheral nerve has no effect either on nerve conduction itself or on conduction block produced by lidocaine.