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Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.58 no.4 Campinas July/Aug. 2008
Neuropathic pain after epidural needle trauma*
Dolor neuropático después del trauma con aguja de epidural
Gilson Cassem Ramos, TSAI; Eduardo Custódio de O. GomesII
de Especialista em Cardiologia da Sociedade Brasileira de Cardiologia; Doutor
em Medicina pela UnB-DF; Responsável pelo Serviço de Anestesia
do Hospital Samaritano de Goiânia
IICirurgião do Aparelho Digestivo; Responsável pelo Serviço de Cirurgia do Aparelho Digestivo do Hospital Samaritano de Goiânia
OBJECTIVES: Neurologic complications secondary to epidural block are uncommon.
Direct mechanical trauma to nerve roots may cause neuropathic pain that, usually,
has a favorable evolution; however, it is a potentially severe complication
that can evolve into a chronic disorder. The objective of this study was to
discuss acute traumatic neuropathic pain and, especially, its treatment.
CASE REPORT: A male patient was admitted for surgical treatment of gastroesophageal reflux via laparoscopy and scheduled to be discharged on the first postoperative (PO) day. He underwent epidural block associated with general anesthesia. During the localization of the epidural space, the patient complained of severe pain in the left lower limb. The needle was repositioned and the epidural space was located. In the PO, the patient developed allodynia and hyperesthesia. Neuropathic pain was diagnosed. Treatment included antidepressant, anticonvulsant, corticosteroids, tramadol, and vitamin B complex. On the 28th PO the patient was asymptomatic and presented a normal physical exam, being discharged from the hospital.
CONCLUSIONS: The patient presented a favorable evolution with the treatment instituted. Early diagnosis and treatment can avoid irreversible lesions, change the prognosis, and avoid social and medical-legal consequences.
Key Words: ANESTHETIC TECHNIQUES, Regional: epidural; COMPLICATIONS: neurologic; PAIN: neuropathic.
Y OBJETIVOS: Las complicaciones neurológicas provenientes de la anestesia
epidural no son comunes. El trauma mecánico directo en las raíces
nerviosas puede provocar un dolor neuropático que, habitualmente evoluciona
de forma favorable, sin embargo, se trata de una complicación potencialmente
grave que, bajo algunas circunstancias, puede progresar hacia un cuadro crónico.
El objetivo fue abordar el tema del dolor neuropático agudo y traumático,
estudiando principalmente su tratamiento.
RELATO DEL CASO: Paciente del sexo masculino, admitido para tratamiento quirúrgico de reflujo gastroesofágico, por la técnica laparoscópica y con alta hospitalaria prevista para el primer postoperatorio (PO). El paciente se sometió a un bloqueo anestésico epidural asociado a la anestesia general. Durante la localización del espacio epidural, el paciente refirió dolor muy intenso y parestesia en miembro inferior izquierdo. La aguja fue reposicionada y el e espacio epidural localizado. El paciente evolucionó en el PO con alodinia e hiperestesia. Fue firmado el diagnóstico de dolor neuropático. El tratamiento pautado constó de antidepresivo, anticonvulsivo, corticoide, tramadol y complejo vitamínico B. En el 28° PO el paciente estaba asintomático y con examen físico normal, cuando recibió el alta.
CONCLUSIONES: La evolución del cuadro con el tratamiento propuesto fue favorable. El diagnóstico y tratamiento precoces pueden evitar lesiones irreversibles, cambiar el pronóstico de los pacientes y evitar consecuencias de carácter social y médico-legal.
Neuropathic or deafferentation pain is triggered by direct damage of central or peripheral nervous tissue, i.e., the pain originates in the nervous system itself. Allodynia, hyperesthesia, sensorial deficit, and autonomic dysfunction (changes in skin color and temperature) are commonly seen 1. In this context, mechanical trauma to nervous tissue is the main cause of acute neuropathic pain.
Neurologic complications related with epidural block are rare, have a good prognosis, and permanent sensorial or motor sequelae are not seen 2-4. This scientific information coincides with those of the present case report, which describes a neurologic complication post-mechanical trauma of peripheral nerve tissue by an epidural needle. The patient developed acute neuropathic pain, which resolved a few days after institution of the treatment.
A 24 years old male patient, 1.90 m, 75 kg, physical status ASA I, was admitted for laparoscopic surgery for gastroesophageal reflux and scheduled to be discharged on the first postoperative day (PO). It was planned a lumbar epidural block associated with general anesthesia. After venipuncture, infusion of Ringer's lactate at 6 mL.kg-1 was instituted and 10 mg of intravenous diazepam was administered, preceded by 5 liters per minute of oxygen via face-mask. Monitoring included ECG on lead II derivation, non-invasive blood pressure, and pulse oximetry. The patient was placed on left lateral decubitus and 2% lidocaine (200 mg) was administered in the L1-2 space and adjacent paramedian areas to anesthetize the skin, subcutaneous tissue, and surrounding tissues. The epidural space was located on the paramedian approach with a 16G Tuohy needle with the bevel on a cephalad direction. During localization of the intervertebral space, the patient complained of severe pain and paresthesia, described as a shock-like sensation, in the entire length of the left lower limb (LLL); 10 mg of dexamethasone were administered intravenously. The needle was repositioned, the epidural space was injected, and 112.50 mg (30 mL) of 0.375% bupivacaine with epinephrine (1:200,000). The patient was, then, placed in horizontal dorsal decubitus and general anesthesia was induced with 190 mg of propofol, 40 mg of atracurium, and 200 µg of fentanyl. The patient was intubated with an 8.0 mm endotracheal tube, connected to a capnograph, and anesthesia was maintained with isoflurane (0.5%) and N2O-oxygen 1:1 mixture. The surgery evolved without intercurrences and lasted 65 minutes. Immediately afterwards, the patient presented clinical conditions to be extubated and was transferred to the recovery room. After a few minutes, the patient complained of severe burning pain and paresthesia in the entire length of the LLL. The initial physical exam detected paresis in both lower limbs secondary to residual epidural block, allodynia (pain to non-noxious stimuli) and hyperesthesia (pain disproportional to the triggering event) in the LLL, especially in the distribution of the femoral nerve (medial aspect of knee, leg, ankle, and foot) 5. Traumatic and iatrogenic neuropathic pain was diagnosed. At this moment, the patient received 25 mg of oral amytriptiline, and 100 mg of intravenous tramadol. The patient was re-evaluated two hours later, when he was no longer under the influence of the epidural block. He complained of severe pain in the LLL, presented facies of acute pain, muscle strength was preserved and he moved both lower limbs freely, but still maintained allodynia and hyperesthesia. He was discharged from the recovery room with an Aldrete-Kroulik index of 10 and transferred to the surgical ward with the following prescription: 4 mg of intravenous dexamethasone every 6 hours; 100 mg of intravenous tramadol every 12 hours; 25 mg of oral amytriptiline once a day; oral vitamin B complex containing B1 (thiamine, 100 mg), B6 (pyridoxine, 100 mg), and B12 (cyanocobalamin, 5,000 µg) every 6 hours, and bed rest. The patient was evaluated again the following day (first PO); the pain persisted and had increased in intensity overnight. Physical exam remained unchanged and hospital discharge was cancelled. Oral carbamazepine, 200 mg twice a day, was added to the prior prescription. On the second PO his pain had decreased, and on the fourth PO he referred a 70% improvement of his symptoms, with visible reduction in allodynia and hyperesthesia. He was discharged from the hospital and followed as an outpatient with the following prescription: 20 mg of oral prednisone every 12 hours for eight days; 50 mg of oral tramadol every 12 hours; 200 mg of oral carbamazepine twice a day; 25 mg of oral amytriptiline once a day; and oral vitamin B complex, B1 (100 mg), B6 (100 mg), and B12 (5,000 µg) every 6 hours. On the 9th day of treatment, 120 mg of oral etoricoxib once a day was prescribed. On the 28th PO the patient was asymptomatic and had a normal physical exam, being discharged from the outpatient follow-up.
Acute trauma to nerve tissue by the epidural needle damaged nerve fibers, especially those of the femoral nerve that also originates from the L2 segment of the spinal cord 5. This event was responsible for the development of classical neuropathic pain. Besides acute trauma, other causes of neuropathic pain include: infectious (herpes zoster, HIV), compressive (lumbar-sciatic pain), metabolic (diabetes mellitus), toxic-deficiencies (alcoholic), and chronic trauma (carpal tunnel syndrome).
After it is triggered only some cases of acute traumatic neuropathic pain, including those of an infectious origin, evolve to chronic pain 6. Thus, 10% of the cases of herpes zoster turn into established post-herpetic neuralgia, for example. As for mechanical trauma to nerve fibers, less than 5% persist as complex regional pain syndrome (CRPS I) or as causalgia (CRPS II). More specifically, neurologic complications related with epidural block are rare (less than 0.1% incidence) 2-4. Factors that influence the development of acute pain into chronic pain are not fully understood; however, it is known that damage of the nervous system (mechanical trauma) and the psychological profile of the patient, such as mood disorders and anxiety, are potentially related with the evolution from acute to chronic pain 6.
Trauma of nerve cells causes changes in nociceptors, making them more sensible to algogenic substances (acetylcholine, histamine, leukotrienes, bradykinin, nitrous oxide, cytokines, etc) 7. Pain symptoms are sustained by those abnormalities associated with other factors, such as activity of the neurovegetative nervous system; hyperactivity of damaged neurons and their neuromata; hyperactivity of sensitive nerve root ganglia; the presence of ectopic foci of action potentials in peripheral nerve fibers and central units; and participation of central mechanisms. Therefore, in this new environment, pain sensations are referred by the patient as paresthesia, burning or shock-like sensations, and the physical signs of allodynia and hyperesthesia. Patients complain of worsening of symptoms at night (similar to the case presented here), due to a lack of competition from other stimuli or by mechanisms related with the low pain threshold, which is affected by the circadian rhythm. The painful syndrome remains as long as active tissue damage and inflammation are in progress. After trauma to nerve roots, neutrophils attract monocytes to the damaged areas, which differentiate into macrophages. Schwann cells react by phagocytosis of cell lesion residues and regenerating the myelin sheath around damaged axons. With the convergence of macrophages those cells, as well as Schwann cells and glial cells, release proinflammatory cytokines, resulting in hyperexcitability and spontaneous aberrant neural activity 8. Besides those abnormalities, functional changes of second order neurons in the posterior horn of the spinal cord gray matter are also observed (central mechanism) 9, an increase in the numbers of receptors, and increased size of the synapses of remaining nerve fibers after trauma to peripheral nerve fibers.
The painful stimulus is transmitted by two types of fibers: A-delta and C. Those fibers can be activated by mechanical, chemical, or thermal stimuli originating in the periphery, whose impulses are transmitted through the spinal cord. The two main pain conduction systems are: a) fibers from lamina V of the spinal cord that project to the lateral hypothalamus and somatosensorial cortex. This system seems to be responsible for the sensorial discrimination of the nociceptive signal; b) fibers originating in lamina I of the spinal cord, which project to the hypothalamus, amygdala, and singular nucleus (anterior region). This system mediates the affective component of pain. The signal can be modulated locally, within the spinal cord, or in supraspinal areas, which can facilitate or inhibit the transmission of the signal 10-12.
The drug of choice in neuropathic pain depends on its etiology. In general, antidepressants (tricyclic and selective inhibitors of serotonin reuptake), anticonvulsants, and opioids are the first, second, and third choice of drugs, respectively 13. In case of lancinating pain, as in trigeminal neuralgia, anticonvulsants (carbamazepine) are the drugs of first choice 14. Medications should be tried sequentially until the pain is under control with minimal side effects. Drug combination is usually necessary. Corticosteroids, non-steroidal anti-inflammatories, and B vitamin complex are adjuvant of the main drugs and can also be very useful, especially in neuropathic pain secondary to trauma, as it will be discussed later, and was prescribed to the patient presented here.
Tricyclic antidepressants (amytriptiline) potentiate the actions of noradrenaline by inhibiting its reuptake in the synaptic cleft, which increases the activity of the neuronal circuit. This mechanism is related with relief of neuropathic pain 15. Besides tricyclics, antidepressants that inhibit the reuptake of serotonin also show a favorable response in the treatment of neuropathic pain 13.
Among other mechanisms of action, anticonvulsants reduce the response of several mono- or polysynaptic pathways, inhibiting neuronal hyperactivity 16. They show a satisfactory response in acute neuropathic pain, and carbamazepine is the drug of choice in trigeminal neuralgia.
Opioids, including tramadol, can be considered second- or third-line agents in the treatment of neuropathic pain. They are effective in those painful situations 17, but are not considered the drugs of choice due to the risk of dependency, reduced cognitive capacity, tolerance, and possible hormonal dysfunctions, especially with chronic use 18. Tramadol has two mechanisms of action; it is a mu opioid receptor agonist and it inhibits the reuptake of noradrenaline and serotonin in the synaptic cleft 19.
Corticosteroids are anti-inflammatory agents that, among other properties, stabilize the membrane of the lisosomes and reduce the production of inflammatory substances by those organelles, decrease capillary permeability, which prevents loss of plasma to the tissues, and reduce leukocyte migration to the area of inflammation 20. Those potent anti-inflammatory agents are widely used in nerve tissue damage. Scientific protocols in animal models report the efficacy of those drugs on trauma-related neuropathic pain 21,22. Dexamethasone is a long-acting corticosteroid, which is 25 times more potent than short-acting corticosteroids 23, and it is frequently administered in cases of trauma to the nervous system.
Non-steroidal anti-inflammatories inhibit the activity of cyclooxygenase, reducing the synthesis and release of prostaglandins by the cells 24. They can also show good results in the treatment of neuropathic pain 25.
Vitamins B1, B6, and B12 influence the process of neural regeneration in peripheral neuritis and neuralgias, and are also indicated in this situation 26. The association of vitamin B complex, especially vitamins B1and B6, with dexamethasone can be very useful in the treatment of neuropathic pain 21.
Even though it is a rare occurrence, acute traumatic neuropathic pain, such as the one described here, has the potential to become chronic. Those cases can be associated with variable degrees of depression 27 and anxiety, and can turn into dramatic situations for the patient and family members, especially related with the social-economic and cultural conditions of those involved. In those circumstances, young patients in the height of their productive life can get involved in social situations, such as loss of a job, retirement, indemnifications, family separation, etc. All this can feed and perpetuate the pain syndrome 28. In this context, the physician can be sued, both in civil and criminal courts. This possibility is certainly reduced when the patient and his/her family consider they have been informed of the risks of the procedure as well as when the physician is able to establish a relationship of trust and professionalism with the patient.
In the present report, the initial conduct was the administration of amytriptiline associated with tramadol and other agents (dexamethasone and vitamin B complex). Antidepressants should be started in the lowest dose possible. Even though it is considered a second- or third-line drug, tramadol was administered along with the antidepressant. In this case, this conduct was justified because the patient presented severe acute neuropathic pain. Besides, possible opioid adverse effects would be minimized by the administration of low doses of tramadol for a limited period. On the following day, carbamazepine was added to the treatment. Its introduction was justified because the initial treatment was not effective. Thus, besides the persistence of the pain, its consequences, such as depression, uncertainty, and doubts, could affect the patient and his family, hindering even more the treatment. For this reason, it was decided to include the anticonvulsant early. The following day, the patient referred a considerable improvement in his condition.
Dexamethasone was discontinued when the patient was discharged from the hospital and it was substituted by prednisone, which was discontinued only after eight days of treatment to minimize the risk of adrenal insufficiency. Prednisone was, then, replaced by a non-steroidal anti-inflammatory (etoricoxib), which was continued until the end of the treatment.
Considering what has been discussed here on the social aspects of pain syndromes of the same nature, the physician tends to be more interventionist. Luckily, those cases have a favorable prognosis, especially due to the large arsenal of drugs available and that can be used in association. Early diagnosis and treatment can prevent irreversible lesions, change the prognosis, and avoid social and medical-legal consequences.
01. Albazaz R, Wong YT, Homer-Vanniasinkam S - Complex regional pain syndrome: a review. Ann Vasc Surg, 2008; 22:297-306. [ Links ]
02. Aromaa U, Lahdensuu M, Cozanitis DA - Severe complications associated with epidural and spinal anaesthesias in Finland 1987-1993. A study based on patient insurance claims. Acta Anaesthesiol Scand, 1997;41:445-452. [ Links ]
03. Auroy Y, Narchi P, Messiah A et al. - Serious complications related to regional anesthesia. Anesthesiology, 1997;87:479-486. [ Links ]
04. Dahegren N, Törnebrandt K - Neurological complications after anaesthesia. A follow-up of 18.000 spinal and epidural anaesthetics performed over three years. Acta Anaesthesiol Scand, 1995;39:872-880. [ Links ]
05. Gardner E- Coxa e Joelho, em: Gardner E, Gray DJ, Rahilly RO - Anatomia. Rio de Janeiro, Guanabara Koogan, 1985;213. [ Links ]
06. Rowbotham MC - Síndromes Dolorosas Específicas, em: Goldman L, Ausiello D Cecil - Tratado de Medicina Interna, 22ª Ed, Rio de Janeiro, Elsevier, 2005;2599-2601. [ Links ]
07. Loeser JD, Melzack R - Pain: an overview. Lancet, 1999;353: 1607-1609. [ Links ]
08. Watkins LR, Maier SF, Goehler LE - Immune activation: the role of pro-inflammatory cytokines in inflammation, illness responses and pathological pain states. Pain, 1995;63:289-302. [ Links ]
09. Amano N, Hu JW, Sessle BJ - Responses of neurons in feline trigeminal subnucleus caudalis (medullary dorsal horn) to cutaneous, intraoral, and muscle afferent stimuli. J Neurophysiol, 1986; 55:227-243. [ Links ]
10. LaMotte C - Distribution of the tract of Lissauer and the dorsal root fibers in the primate spinal cord. J Comp Neurol, 1977;172: 529-561. [ Links ]
11. Basbaum AI, Fields HL - Endogenous pain control systems: brainstem spinal pathways and endorphin circuity. Annu Rev Neurosci, 1984;7:309-338. [ Links ]
12. Besson JM, Chaouch - A Peripheral and spinal mechanisms of nociception. Physiol Rev, 1987;67:67-186. [ Links ]
13. Finnerup NB, Otto M, Jensen TS et al. - An evidence-based algorithm for the treatment of neuropathic pain. MedGenMed, 2007;9:36. [ Links ]
14. Finnerup NB, Otto M, McQuay HJ et al. - Algorithm for neuropathic pain treatment: an evidence based proposal. Pain, 2005;118:289-305. [ Links ]
15. Rosenblatt RM, Reich J, Dehring D - Tricyclic antidepressants in treatment of depression and chronic pain: analysis of the supporting evidence. Anesth Analg 1984;63:1025-1032. [ Links ]
16. Hays H, Woodroffe MA - Using gabapentin to treat neuropathic pain. Can Fam Physician 1999;45:2109-2112. [ Links ]
17. McQuay H, Carroll D, Jadad AR et al. - Anticonvulsant drugs for management of pain: a systematic review. BMJ, 1995;311: 1047-1052. [ Links ]
18. Gilron I, Bailey JM, Tu D et al. - Morphine, gabapentin, or their combination for neuropathic pain. N Engl J Med, 2005;352:1324-334. [ Links ]
19. Budd K - Chronic pain-challenge and response. Drugs, 1994; 47(Suppl 1):33-38. [ Links ]
20. Parrillo JE, Fauci AS - Mechanisms of glucocorticoid action on immune processes. Annu Rev Pharmacol Toxicol, 1979;19:179-201. [ Links ]
21. Caram-Salas NL, Reyes-García G, Medina-Santillán R et al. - Thiamine and cyanocobalamin relieve neuropathic pain in rats: synergy with dexamethasone. Pharmacology, 2006;77:53-62. [ Links ]
22. Wang S, Lim G, Zeng Q et al. - Expression of central glucocorticoid receptors after peripheral nerve injury contributes to neuropathic pain behaviors in rats. J Neurosci, 2004; 24:8595-8605. [ Links ]
23. Zoorob RJ, Cender D - A different look at corticosteroids. Am Fam Physician, 1998;58:443-450. [ Links ]
24. Metz AS - Anti-inflammatory agents as inhibitors of prostaglandin synthesis in man. Med Clin North Am, 1981; 65:713-757. [ Links ]
25. Herrero JF, Romero-Sandoval EA, Gaitan G et al. - Antinociception and the new COX inhibitors: research approaches and clinical perspectives. CNS Drug Rev, 2003;9:227-252. [ Links ]
26. Sacramento EF, Silva BB - Vitaminas e Minerais, em: Silva P - Farmacologia, 6ª Ed, Rio de Janeiro, Guanabara Koogan, 2002;979-984. [ Links ]
27. Thielke SM, Fan MY, Sullivan M et al. - Pain limits the effectiveness of collaborative care for depression. Am J Geriatr Psychiatry, 2007;15:699-707. [ Links ]
28. Oliveira JT - Aspectos comportamentais das síndromes de dor crônica. Arq Neuropsiquiatr, 2000;58:360-365. [ Links ]
Correspondence to: Submitted em 11
de novembro de 2007 *
Received froms Serviço de Anestesia do Hospital Samaritano de Goiânia,
Dr. Gilson Cassem Ramos
Rua 8, 74/402 - Setor Oeste
74115-100 Goiânia, GO
Accepted em 1º de abril de 2008
Submitted em 11
de novembro de 2007
* Received froms Serviço de Anestesia do Hospital Samaritano de Goiânia, GO