<b>Treatment of Painful Muscle Cramp Due to Heat Injury Using Shakuyakukanzoto </b> / 日本東洋医学雑誌

We treated 5 patients with painful muscle cramp due to heat injury using Shakuyakukanzoto. According to their severities, 4 patients were classified with 1 st degree and 1 patient with 3rd degree heat injury. Painful muscle cramps in 4 patients with 1st degree were cured through a single dose of Shakuyakukanzoto. On the other hand, painful muscle cramps in 1 patient with 3rd degree was managed for 4 days after administration of Shakuyakukanzoto. No Shakuyakukanzoto complications were observed in any patient, nor contribution to rhabdomyolysis in 3 patients. Shakuyakukanzoto may be useful to prevent acute kidney injury due to rhabdomyolysis by controlling painful muscle cramps in heat injury.

Core temperature of a burning moxa ball and temperature when dropped from a moxa needle / 全日本鍼灸学会雑誌

[Objective]The aim of this study was to prevent accidental burns caused by touching a heated needle shaft or by a burning moxa ball falling from a moxa needle. Therefore, we measured the central temperature (Tc) of a burning moxa ball and the temperature at the landing point (Td) of a falling moxa ball.<BR>[Methods]Stainless steel acupuncture needles and unrefined moxa for moxa needles were used. The moxa balls weighed 0.15 g (diameter, 13± 1mm), 0.30 g (diameter, 16 ± 1mm), and 0.60 g (diameter, 24 ± 1mm). To measure the Tc of a moxa ball, a K-type thermocouple temperature probe was inserted into the centre of the ball. The Td of a moxa ball was measured by placing the probe 2 mm directly below the moxa ball. At each point in time, the moxa ball was forced to drop after ignition. Each measurement was repeated 5 times. The data were expressed as mean ±standard deviation.<BR>[Results]The maximum Tc of the 0.15, 0.30, and 0.60 g moxa balls was 569 ± 26°C at 72 ± 8s after ignition, 606 ± 26°C at 109 ± 4s, and 624 ± 48°C at 167 ± 14 s, respectively. Tc of each ball decreased to less than 45°C at 180 ± 8s, 225 ± 4s, and 345 ± 13s after ignition, respectively. When a 0.15 g moxa ball was dropped 30 s after ignition, Td measured 1, 5, and 10 s after the drop was 60 ± 6°C, 97 ± 7°C, and 137 ± 31°C, respectively. Td was less than 45 degrees 120 seconds after ignition. When a 0.30 g moxa ball was dropped 120 s after ignition, Td measured 1, 5, and 10 s after the drop was 66 ± 7°C, 96 ± 6°C, and 129 ± 2°C, respectively. Td was less than 40 degrees 120 seconds after ignition. Td was less than 45 degrees 180 seconds after ignition. When a 0.60 g moxa ball was dropped 180 s after ignition, Td measured 1, 5, and 10 s after the drop was 69 ± 3°C, 96 ± 14°C, and 135 ± 20°C, respectively. Td was less than 45 degrees 270 seconds after ignition.<BR>[Conclusion]For 0.15, 0.30, and 0.60 g moxa balls, if Tc, that is the temperature of the probe, is considered to be the temperature of the needle shaft, burns may be caused by touching the heated shaft up until about 180, 240, and 360 s after ignition, respectively. Furthermore, there is a risk of burns caused by dropping a burning 0.15, 0.30, or 0.60 g moxa ball before 120, 180, or 270 s after ignition, respectively.

Role of PPARβ in fibroblast response to heat injury.

Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear hormone receptor family of ligand-inducible transcription factors. Our previous study has shown that in human umbilical vein endothelial cells PPARβ initiates a protective mechanism that limits the extent of damage due to H2O2-induced injury. Although fibroblasts are one of the main cell types involved in wound repair, the role of PPARβ in the fibroblast response to heat injury has not been investigated. Thus, in this study, we examined possible protective role of PPARβ in fibroblasts from heat injury. We developed a novel dermal fibroblast heat injury model to characterize the mechanisms of the heat injury healing response that involved PPARβ. The specific PPARβ ligand GW0742, a PPARβ activator and a short hairpin RNA (shRNA) plasmid against PPARβ were used to reveal the action mechanism of PPARβ in heat injury-induced fibroblast changes in morphology and increased proliferation. In response to heat injury (52˚C for 30 s), fibroblast activation of PPARß, increased 1.56-fold. Administration of GW0742 significantly induced a protective effect on heat injury-induced fibroblasts by minimizing the structural damage and increasing the cell proliferation response. Likewise, inhinition of PPARß, usingh shRNA exacerbated the damage by inhibiting the de novo synthesis of PPARß. These results indicated that heat injury enhanced PPARß expression and PPARß protected fibroblast structure and proliferation.

Dolor en el trauma térmico / Pain in thermal trauma

La máxima agresión física que puede sufrir un ser humano son las quemaduras. Actualmente, en Chile se hospitalizan alrededor de 9.000 personas al año por quemaduras, con una tasa de mortalidad que ha ido en disminución en los últimos 20 años, por lo tanto la cantidad de pacientes sobrevivientes va en aumento. La IASP (Internacional Association for Study of Pain) definió el dolor en quemados como: "un dolor agudo y grave, que se produce al sufrir una quemadura y luego continuo con exacerbaciones que declinan gradualmente". El dolor en el trauma térmico está siempre presente, es de intensidad severa y prolongada en el tiempo, con una alta prevalencia de dolor crónico. Se sabe que el aumento en la intensidad se debe a que las quemaduras dañan gran cantidad de nociceptores, produciéndose una amplificación de la respuesta al dolor. Los opioides son el principal pilar en el tratamiento farmacológico. Es fundamental el buen manejo del dolor, para evitar el dolor patológico que aumentará el dolor crónico y con ello el desmedro de la vida personal de nuestros pacientes. Desafortunadamente el subtratamiento es una realidad, produciendo directamente un retraso en la recuperación de sus quemaduras y en la inserción social y laboral.

Burns are the greatest physical aggression that a human being can experience. In Chile, approximately 9000 patients are hospitalized annually due to burns, with a mortality rate that has decreased progressively in the last 20 years, which means that the amount of survivors is increasing. The IASP (International Association for Study of Pain) has defined pain in the burn patient as "an acute and severe pain produced by a burn that later continues with exacerbations that gradually decline". Pain in thermal trauna is always present, of severe intensity and prolonged in time, with a high prevalence of chronic pain. It is Known that the increase in intensity of pain is due to the damage of a great number of nociceptors, that produces an amplification of the response to pain. Opioids are the mainstay of pharmacologic treatment. Appropriate management of pain is fundamental to avoid pathologic pain that will increase the chronic pain and deteriorate the quality of life of our patients. Unfortunately undertreatment is a reality, retarding the healing of the burn wound, and the social and workplace reintegration.