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Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.56 no.1 Campinas Jan./Feb. 2006
Sudorese profusa e hipotermia após administração de morfina por via subaracnóidea. Relato de caso*
Sudor profuso e hipotermia después de administración de morfina por vía subaracnoidea. Relato de caso
Gustavo Prosperi Bicalho, TSA; Carlos Henrique Viana Castro, TSA; Marcos Guilherme Cunha Cruvinel, TSA; Roberto Cardoso Bessa Júnior, TSA
Anestesiologista do Hospital Life Center
BACKGROUND AND OBJECTIVES:
Anesthesia and surgery often promote significant temperature changes. Hypothermia
during anesthesia is the most common perioperative thermal disorder. This report
describes an unusual body heat balance change associated to spinal morphine.
CASE REPORT: Female patient, 44 years old, physical status ASA I, with no previous diseases, admitted for abdominal hysterectomy due to uterine myomatosis. Spinal anesthesia was performed with 20 mg hyperbaric bupivacaine and 100 mg morphine and surgical procedure was eventless. In the post-anesthetic recovery unit (PACU), 3h30 minutes after blockade, patient presented excessive sweating, even leading to detachment of electrodes and adhesive tapes, mild sleepiness and decreased tympanic temperature to 35.2 ºC. Temperature was maintained below 36 ºC for the next 60 minutes and 90 minutes later temperature was 36.2 ºC with total remission of symptoms.
CONCLUSIONS: In addition to classic excessive heat loss mechanisms during neuraxial block, there may be direct disorders in the hypothalamic temperature control centers, in this case associated to spinal morphine.
Key Words: ANESTHETIC TECHNIQUES, Regional: spinal block; COMPLICATIONS: hypothermia
JUSTIFICATIVA Y OBJETIVOS:
La anestesia y cirugía con frecuencia causan alteraciones térmicas
importantes. La hipotermia durante la anestesia es la alteración térmica
más común en el perioperatorio. Este relato muestra un mecanismo no
usual de alteración de la temperatura, en este caso, asociado con el empleo
de morfina subaracnoidea. El objetivo de este relato fue describir el efecto
RELATO DEL CASO: Paciente femenina, de 44 años, estado físico ASA I, sin enfermedades previas, fue admitida para realizar histerectomía abdominal por miomatosis uterina. Recibió raquianestesia con 20 mg de de bupivacaína hiperbárica con 100 µg de morfina. Durante el procedimiento no presentó ninguna alteración. En la sala de recuperación post-anestésica, 3h30 minutos después de hecho el bloqueo, la paciente presento profusa sudoración en el tronco, que despega los electrodos y otros adhesivos, con leve somnolencia y disminución de la temperatura timpánica a 35,2 ºC. En los 60 minutos siguientes mantuvo temperatura debajo de 36 ºC pero a los 90 minutos la temperatura era de 36,2 ºC con remisión completa de los síntomas.
CONCLUSIONES: Aparte e los clásicos mecanismos de perdida de calor, pueden ocurrir perturbaciones directamente en los centros hipotalámicos de control de la temperatura corporal, que en este caso estuvo asociada a morfina subaracnoidea.
Hypothermia during anesthesia is the most common perioperative thermal disorder1. It results from the combination of anesthesia-induced thermoregulation changes, and exposure to cold environment and surgical factors which lead to excessive heat loss1. Thermal disorders during neuraxial block may be equal or even more severe than those observed during general anesthesia1. This report describes an unusual body heat balance change associated to spinal morphine.
Female patient, 44 years old, physical status ASA I, admitted for abdominal hysterectomy due to uterine myomatosis.
Monitoring in the operating room consisted of ECG, pulse oximetry, noninvasive blood pressure and venous access with 18G catheter. Spinal anesthesia was performed with patient in the sitting position in L2-L3 interspace, with 27G Withacre needle. Sensory block at T6 was obtained with 20 mg hyperbaric bupivacaine associated to 100 µg morphine. Patient was sedated with fractional midazolam doses (total 15 mg), droperidol (1.25 mg) and fentanyl (25 µg).
Patient received 10 mg dexametasone at surgery beginning and 4 mg ondansetron at surgery completion to prevent nausea and vomiting. During the procedure patient received 2500 mL pre-heated lactated Ringers. Solution is pre-heated in a microwave device resulting in crystalloid solutions of approximately 37 ºC. Operating room temperature is maintained by central air conditioning system, which maintains temperature in approximately 22 ºC. Patient was thermally isolated with blankets on chest and upper limbs. At the end of the surgery patient was referred to the PACU and perioperative monitoring was maintained.
At PACU admission, patient presented stable hemodynamic and ventilatory parameters and axillary temperature of 35.9 ºC.
Two hours after PACU admission (3h30 minutes after blockade), patient presented excessive body, head and arms sweating, even leading to detachment of electrodes and adhesive tapes, in addition to mild sleepiness and decreased axillary temperature to 35.2 ºC (equal to tympanic temperature). Initially, all venous access devices (catheter, device and serum bag) were replaced considering a possible pyrogenic reaction which was not confirmed because patient remained with low temperature. Capillary glycemia was within normal levels thus excluding the possibility of hypoglycemia.
No changes in vital signs, except for temperature, were observed during the episode. Temperature was maintained below 36 ºC for the next 60 minutes, still associated to excessive sweating, and 90 minutes later axillary temperature was 36.2 ºC with total remission of symptoms.
Anesthesia and surgery often promotes significant thermal disorders. Hypothermia is the most common phenomenon and results from anesthetic effects on body thermoregulatory control, usually associated to exposure to cold environment and to surgical factors leading to excessive heat loss1.
In general, body heat balance is a three-stage system: one afferent, one central and one efferent. The integration of these three stages maintains core temperature within very narrow levels2.
The afferent stage corresponds to skin, deep tissues, spinal cord and brain thermal receptors. These receptors send signals which ultimately are integrated in the hypothalamus, especially in the anterior pre-optic region. When the integration of such signals in the hypothalamus shows a deviation from a temperature level, the hypothalamus generates a thermoregulatory response aiming at increasing or decreasing body heat loss to the environment, thus returning to balance.
When there is core temperature down-deviation, the hypothalamus generates responses to maintain heat and major responses are initially peripheral vasoconstriction and then muscle shivering. On the other hand, when there is temperature up-deviation, the hypothalamus generates a response to increase heat loss and may increase in up to 10 times body heat loss. Temperature interval between these two responses is called inter-threshold range and in general is just 0.2 ºC2. In fact, it is known that the integration of thermal information is highly complex involving polysynaptic pathways with the participation of ascending reticular formation, locus sub-ceruleus and raphe nucleus magnum, among others. However, most investigators accept that the hypothalamus pre-optic region is the dominant thermoregulatory center in mammalians3-6.
It is known that the inter-threshold range is highly increased during anesthesia, as well as responses to maintain or generate heat are decreased. This way, anesthetized patients are much more vulnerable to core temperature changes.
It is known that patients submitted to neuraxial block are at risk of developing intraoperative hypothermia, with core temperature decreases similar to those observed during general anesthesia3. However, hypothermia mechanisms are somewhat different.
During neuraxial blocks, there are three primary mechanisms in charge of decreasing core temperature. The first is heat redistribution by sympathectomy and vasodilation of the anesthetized territory, transferring heat from core to peripheral compartment, being it the primary mechanism seen in the first post-blockade hour. This initial redistribution may decrease core temperature in 1 to 2 ºC. Then, there is thermoregulatory vasoconstriction loss in anesthetized territories decreasing a lot the efficacy of heat maintenance. Finally, there is a decrease of vasoconstriction and shivering thresholds in patients with neuraxial block even in non-anesthetized regions1.
At PACU admission, our patient presented axillary temperature of 35.9 ºC. A significant heat loss decrease was expected after PACU admission as compared to the intraoperative period, due to some factors. First, room temperature is higher as compared to the operating room since air temperature in this sector where between 24 and 26 ºC. Patient received a better thermal isolation with blankets covering almost all her body. And finally, there was no longer heat loss by the surgical area. Temperature decreased two hours after PACU admission when additional temperature decrease is no longer expected due to above-mentioned reasons.
However, the phenomenon indicating a possible physiological thermoregulatory response disorder is the association with an unexpected autonomic response. The situation was a patient with mild hypothermia (axillary temperature of 35.2 ºC) and excessive sweating in unblocked segments. As mentioned, sweating is a mechanism operating in the upper limit of the inter-threshold range, a limit which triggers heat loss in a situation where core temperature is increasing.
It is known that opioids interfere with body thermoregulation. The typical effect is a decrease in vasoconstriction and a change in muscle shivering thresholds6. They are usually administered in the clinical practice to inhibit muscle shivering caused by postoperative hypothermia exactly because they modify its threshold. This effect is present in all µ agonists. It has to be stressed with regard to this effect that meperidine is more effective as compared to other opioids in equipotent doses for more markedly decreasing muscle shivering6. This higher efficacy may be due to k receptors-mediated effects. However, in our case, these classic opioid effects did not correspond to the observed phenomenon, that is, excessive sweating in a mildly hypothermal patient.
This phenomenon has already been reported by other authors. Sayyid et al. have reported a case of hypothermia of 33.6 ºC associated to excessive sweating in a pregnant patient receiving 100 µg spinal morphine for postoperative analgesia4. Symptoms started three hours after blockade. Two hours later patient received 400 µg naloxone with prompt reversion of symptoms and increased temperature.
Wishaw also reports a case of hypothermia (tympanic temperature of 33.6 ºC) associated to spinal morphine in a parturient submitted to Cesarean delivery under spinal anesthesia5.
One may consider in our case that neuraxial morphine has reached, by dispersion, opioid receptors of the hypothalamic region after approximately 3h30 minutes. A thermoregulatory center disorder was then generated with the possible definition of a new hypothalamic temperature balance level, that is, the inter-threshold range as a whole was above this new upper temperature threshold generating excessive sweating with consequent heat loss to the environment and hypothermia. This response was only seen in regions above the umbilical line because more distal segments were still under residual sympathetic block.
This case has shown that interactions of anesthetic, surgical and environmental factors for the development of intraoperative thermal disorders may be even more complex. In addition to classic excessive heat loss mechanisms during neuraxial block, there may be direct disorders of hypothalamic temperature control centers, in our case associated to spinal morphine.
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04. Sayyid SS, Jabbour DG, Baraka AS - Hypothermia and excessive sweating following intratecal morphine in a parturient undergoing cesarean delivery. Reg Anesth Pain Med, 2003;28: 140-143. [ Links ]
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06. De Witte J, Sessler DI - Perioperative shivering: physiology and pharmacology. Anesthesiology, 2002;96:467-484. [ Links ]
Dr. Gustavo Prosperi Bicalho
Address: Rua Alvarenga Peixoto, 711/1301
ZIP: 30180-120 City: Belo Horizonte, Brazil
Submitted for publication January 27, 2005
Accepted for publication December 14, 2005
* Received from Departamento de Anestesiologia do Hospital Life Center, Belo Horizonte, MG