Cirurgia para controle do dano: uma revisão

Damage control surgery is one of the major advances in surgical practice in the last 20 years. The indications for damage control surgery are: the need to terminate a laparotomy rapidly in an exsanguinating, hypothermic patient who had developed a coagulopathy and who is about to die on the operating table; inability to control bleeding by direct hemostasis; and inability to close the abdomen without tension because of massive visceral edema and a tense abdominal wall. Damage control surgery has three phases: 1) laparotomy to control hemorrhage by packing, shunting, or balloon tamponade, or both; control of intestinal spillage by resection or ligation of damaged bowel, or both; 2) physiological resuscitation to correct hypothermia, metabolic acidosis, and coagulopathy. 3) planned reoperation for definitive repair. Damage control surgery is appropriate in a small number of critically ill patients who are likely to require substantial hospital resources. However, there are many questions that need to be answered. Who is the patient elected for this surgery? When is the ideal time to make the decision? Which are the parameters that indicate to the surgeons the moment to re-operate the patient? How to treat the long-term complications? In the present review we described some historical aspects, indications, technical aspects, advantages and disadvantages of this procedure, as well as its physiological consequences and morbidity and mortality rates of damage control surgery. Damage control surgery offers a simple effective alternative to the traditional surgical management of complex or multiple injuries in critically injured patients.

Experimental intoxication by the leaves of Melia azedarach (Meliaceae) in cattle

Green leaves of Melia azedarach were administered at single doses ranging from 5 to 30 g/kg bw to 11 calves. Clinical signs were depression, ruminal stasis, dry feces with blood, ataxia, muscle tremors, sternal recumbency, hypothermia and abdominal pain. Serum AST and CPK were increased. Signs appeared from 8 to 24 hours after dosing, and the clinical course lasted from 2 to 72 hours. Three calves dosed with 30g/kg bw died. The macroscopic findings included intestinal congestion, yellow discoloration of the liver, brain congestion and dry feces with blood in the rectum. The liver showed swollen and vacuolated hepatocytes. Necrotic hepatocytes were scattered throughout the parenchyma or concentrated in the periacinar zone. Degenerative and necrotic changes were observed in the epithelium of the forestomachs. There was also necrosis of the lymphoid tissue. Skeletal muscles showed hyaline degeneration and fiber necrosis. The necrotic fragments contained floccular or granular debris with infiltration by macrophages and satellite cells.

Effects of laparoscopy on the cardiorespiratory system of brown brocket deer (Mazama gouazoubira) anesthetized with ketamine/ xylazine/ midazolam combination and isoflurane

Laparoscopy is not widely used as a tool to perform assisted reproduction techniques in South American cervids; thus, scarce information in literature is available regarding its effects and appropriate anesthetic protocols to perform it. This study evaluated the effect of laparoscopy on heart rate (HR), respiration rate (RR), saturation of oxyhemoglobin (SpO2) and rectal temperature (RT) of six female brown brocket deer (Mazama gouazoubira) anesthetized with ketamine (5mg/kg), xylazine (0.3mg/kg), midazolam (0.5mg/kg) combination i.v. and isoflurane. Twelve laparoscopies were performed and each animal was used twice with a 40-day interval. After anesthetized, the animals were placed in dorsal recumbency to perform laparoscopy procedure using abdominal CO2 insufflations (14.2 ± 2.39mmHg; M ± SE). The main events of the laparoscopy procedure were divided into three periods: animal without (P1) and with abdominal insufflation (P2) and abdominal insufflation with the hips raised at 45º (P3). As a control, the animals were anesthetized again 40 days after the last laparoscopy, and were maintained in a dorsal recumbency for the same average duration of the previous anesthesia and no laparoscopy procedure was conducted. The period of anesthesia for the controls was also divided into P1, P2, and P3 considering the average duration of these periods in previous laparoscopies performed. Data were analyzed through the (ANOVA) variance analysis followed by Tukey test and values at P<0.05 were considered significant. No significant differences were observed in the parameters evaluated at P1, P2 and P3 between the animals submitted to laparoscopy and control. However, the RR mean between P1 (38.8 ± 4.42) and P3 (32.7 ± 4.81); and the RT mean between the P1 (38.2ºC ± 0.17), P2 (37.6ºC ± 0.19) and P3 (37.0ºC ± 0.21) varied significantly, independent of the laparoscopy. These data indicated that laparoscopy didn't cause any significant alterations in the cardiorespiratory parameters evaluated, even though the anesthetic protocol used can cause a reduction in the RT contributing to development of hypothermia during anesthesia.

Effects of a neuronal nitric oxide synthase inhibitor on lipopolysaccharide-induced fever

It has been demonstrated that nitric oxide (NO) has a thermoregulatory action, but very little is known about the mechanisms involved. In the present study we determined the effect of neuronal nitric oxide synthase (nNOS) inhibition on thermoregulation. We used 7-nitroindazole (7-NI, 1, 10 and 30 mg/kg body weight), a selective nNOS inhibitor, injected intraperitoneally into normothermic Wistar rats (200-250 g) and rats with fever induced by lipopolysaccharide (LPS) (100 µg/kg body weight) administration. It has been demonstrated that the effects of 30 mg/kg of 7-NI given intraperitoneally may inhibit 60% of nNOS activity in rats. In all experiments the colonic temperature of awake unrestrained rats was measured over a period of 5 h at 15-min intervals after intraperitoneal injection of 7-NI. We observed that the injection of 30 mg/kg of 7-NI induced a 1.5oC drop in body temperature, which was statistically significant 1 h after injection (P<0.02). The coinjection of LPS and 7-NI was followed by a significant (P<0.02) hypothermia about 0.5oC below baseline. These findings show that an nNOS isoform is required for thermoregulation and participates in the production of fever in rats.

Implications of ischemic penumbra for the diagnosis of brain death

The data reviewed here suggest the possibility that a global reduction of blood supply to the whole brain or solely to the infratentorial structures down to the range of ischemic penumbra for several hours or a few days may lead to misdiagnosis of irreversible brain or brain stem damage in a subset of deeply comatose patients with cephalic areflexia. The following proposals are advanced: 1) the lack of any set of clinically detectable brain functions does not provide a safe diagnosis of brain or brain stem death; 2) apnea testing may induce irreversible brain damage and should be abandoned; 3) moderate hypothermia, antipyresis, prevention of arterial hypotension, and occasionally intra-arterial thrombolysis may contribute to good recovery of a possibly large subset of cases of brain injury currently regarded as irreversible; 4) confirmatory tests for brain death should not replace or delay the administration of potentially effective therapeutic measures; 5) in order to validate confirmatory tests, further research is needed to relate their results to specific levels of blood supply to the brain. The current criteria for the diagnosis of brain death should be revised.

Dopaminergic profile of new heterocyclic N-phenylpiperazine derivatives

Dopamine constitutes about 80% of the content of central catecholamines and has a crucial role in the etiology of several neuropsychiatric disorders, including Parkinson's disease, depression and schizophrenia. Several dopaminergic drugs are used to treat these pathologies, but many problems are attributed to these therapies. Within this context, the search for new more efficient dopaminergic agents with less adverse effects represents a vast research field. The aim of the present study was to report the structural design of two N-phenylpiperazine derivatives, compound 4: 1-[1-(4-chlorophenyl)-1H-4-pyrazolylmethyl]-4-phenylhexahydropyrazine and compound 5: 1-[1-(4-chlorophenyl)-1H-1,2,3-triazol-4-ylmethyl]-4-phenylhexahydropyrazine, planned to be dopamine ligands, and their dopaminergic action profile. The two compounds were assayed (dose range of 15-40 mg/kg) in three experimental models: 1) blockade of amphetamine (30 mg/kg, ip)-induced stereotypy in rats; 2) the catalepsy test in mice, and 3) apomorphine (1 mg/kg, ip)-induced hypothermia in mice. Both derivatives induced cataleptic behavior (40 mg/kg, ip) and a hypothermic response (30 mg/kg, ip) which was not prevented by haloperidol (0.5 mg/kg, ip). Compound 5 (30 mg/kg, ip) also presented a synergistic hypothermic effect with apomorphine (1 mg/kg, ip). Only compound 4 (30 mg/kg, ip) significantly blocked the amphetamine-induced stereotypy in rats. The N-phenylpiperazine derivatives 4 and 5 seem to have a peculiar profile of action on dopaminergic functions. On the basis of the results of catalepsy and amphetamine-induced stereotypy, the compounds demonstrated an inhibitory effect on dopaminergic behaviors. However, their hypothermic effect is compatible with the stimulation of dopaminergic function which seems not to be mediated by D2/D3 receptors.

Cardiopulmonary bypass alters the pharmacokinetics of propranolol in patients undergoing cardiac surgery

The pharmacokinetics of propranolol may be altered by hypothermic cardiopulmonary bypass (CPB), resulting in unpredictable postoperative hemodynamic responses to usual doses. The objective of the present study was to investigate the pharmacokinetics of propranolol in patients undergoing coronary artery bypass grafting (CABG) by CPB under moderate hypothermia. We evaluated 11 patients, 4 women and 7 men (mean age 57 ± 8 years, mean weight 75.4 ± 11.9 kg and mean body surface area 1.83 ± 0.19 m²), receiving propranolol before surgery (80-240 mg a day) and postoperatively (10 mg a day). Plasma propranolol levels were measured before and after CPB by high-performance liquid chromatography. Pharmacokinetic Solutions 2.0 software was used to estimate the pharmacokinetic parameters after administration of the drug pre- and postoperatively. There was an increase of biological half-life from 4.5 (95% CI = 3.9-6.9) to 10.6 h (95% CI = 8.2-14.7; P < 0.01) and an increase in volume of distribution from 4.9 (95% CI = 3.2-14.3) to 8.3 l/kg (95% CI = 6.5-32.1; P < 0.05), while total clearance remained unchanged 9.2 (95% CI = 7.7-24.6) vs 10.7 ml min-1 kg-1 (95% CI = 7.7-26.6; NS) after surgery. In conclusion, increases in drug distribution could be explained in part by hemodilution during CPB. On the other hand, the increase of biological half-life can be attributed to changes in hepatic metabolism induced by CPB under moderate hypothermia. These alterations in the pharmacokinetics of propranolol after CABG with hypothermic CPB might induce a greater myocardial depression in response to propranolol than would be expected with an equivalent dose during the postoperative period.

The effect of epidural and general anesthesia on newborn rectal temperature at elective cesarean section

Both epidural and general anesthesia can impair thermoregulatory mechanisms during surgery. However, there is lack of information about the effects of different methods of anesthesia on newborn temperature. The purpose of this study was to determine whether there are differences in newborn rectal temperature related to type of anesthesia. Sixty-three pregnant women were randomly assigned to receive general or epidural anesthesia. Maternal core temperature was measured three times with a rectal probe just before anesthesia, at the beginning of surgery and at delivery. In addition, umbilical vein blood was sampled for pH. The rectal temperatures of the babies were recorded immediately after delivery, and Apgar scores were determined 1, 5, and 10 min after birth. The duration of anesthesia and the volume of intravenous fluid given during the procedure (833 ± 144 vs 420 ± 215 mL) were significantly higher in the epidural group than in the general anesthesia group (P < 0.0001). Maternal rectal temperatures were not different in both groups at all measurements. In contrast, newborn rectal temperatures were lower in the epidural anesthesia group than in the general anesthesia group (37.4 ± 0.3 vs 37.6 ± 0.3°C; P < 0.05) immediately after birth. Furthermore, the umbilical vein pH value (7.31 ± 0.05 vs 7.33 ± 0.01; P < 0.05) and Apgar scores at the 1st-min measurement (8.0 ± 0.9 vs 8.5 ± 0.7; P < 0.05) were lower in the epidural anesthesia group than in the general anesthesia group. Since epidural anesthesia requires more iv fluid infusion and a longer time for cesarean section, it involves a risk of a mild temperature reduction for the baby which, however, did not reach the limits of hypothermia.

Effects of intracerebroventricular bombesin administration on local cerebral glucose utilization in the restrained and unrestrained rat

Intracerebroventricular (ICV) administration of bombesin (BN) induces a syndrome characterized by stereotypic locomotion and grooming, hyperactivity and sleep elimination, hyperglycemia and hypothermia, hyperhemodynamics, feeding inhibition, and gastrointestinal function changes. Mammalian BN-like peptides (MBNs), e.g. gastrin-releasing peptide (GRP), Neuromedin C (NMC), and Neuromedin B (NMB), have been detected in the central nervous system. Radio-labeled BN binds to specific sites in discrete cerebral regions. Two specific BN receptor subtypes (GRP receptor and NMB receptor) have been identified in numerous brain regions. The quantitative 2-[14C]deoxyglucose ([14C]20G) autoradiographic method was used to map local cerebral glucose utilization (LCGU) in the rat brain following ICV injection of BN (vehicle, BN O.1Jlg, O.5Jlg). At each dose, experiments were conducted in freely moving or restrained conditions to determine whether alterations in cerebral function were the result of BN central administration, or were the result of BN-induced motor stereotypy. The anteroventral thalamic nucleus (AV) (p=O.029), especially its ventrolateral portion (AVVL) (p

Évaluation neurobiologique des souris spontanément hypertendues : Du vieillissement à la génomique comparative

Le but de cette thèse est premièrement d’évaluer l’effet du vieillissement sur les fonctions psychomotrices des souches de souris sélectionnées génétiquement en fonction de leur tension artérielle (TA); deuxièmement, de localiser les déterminants génétiques des phénotypes psychophysiologiques à partir de souches recombinantes congéniques (RCS). Ces travaux ont mené à la publication de 4 articles. Le premier article décrit l’évaluation des fonctions psychomotrices des souches avec une tension artérielle élevée (HBP), basse (LBP) et normale (NBP). La performance aux épreuves d’exploration, d’habiletés motrices et d’apprentissage spatial, a été mesurée sur deux cohortes âgées respectivement de 12 mois et de trois mois. Indépendamment de l’âge, les HBPs sont hyperactives dans l’open-field (OF), mais pas dans le test d’exploration de trous. Inversement, les LBP explorent moins d’espaces que les NBP et, à trois mois seulement, sont hypoactives dans l’OF. Par ailleurs, les HBPs et les LBP présentent des déficits précoces de coordination motrice et des fonctions visuo-motrices. Le second article concerne l’évaluation longitudinale de la coordination motrice, de l’anxiété et de l’apprentissage spatial des souches HBP, LBP et NBP, à l’âge de deux mois et de 12 mois. Le vieillissement accentue l’hyperactivité des HBPs dans l’OF. Par contre, l’hypoactivité des souris LBP est détectable seulement à l’âge de deux mois. Indépendamment de l’âge, les souris HBP et LBP montrent une perception réduite du danger dans l’épreuve d’anxiété et des dysfonctions visuo-motrices au labyrinthe aquatique. Enfin, des déficits précoces de coordination motrice se manifestent seulement chez les HBPs. Il reste à déterminer si les déficits observés sont liés à des déterminants génétiques indépendants ou secondaires aux altérations de la tension artérielle. Le troisième article présente la comparaison entre les souches consanguines A/J et C57Bl/6J (B6) aux épreuves de l’OF, de la planche à trous, du labyrinthe aquatique et du cintre (coordination motrice). Les B6 explore d’avantage l’OF et la planche à trous. Les B6 sont moins rapides sur le cintre, mais supérieurs aux A/J dans le labyrinthe aquatique, avec une plate-forme invisible ou visible. Ces résultats démontrent l’implication de déterminants génétiques. Cette thèse se termine par un quatrième article sur la localisation des déterminants génétiques de la susceptibilité au stress dans les RCS, dérivées de A/J et B6, et présentant un agencement spécifique de 12.5% du génome. La réactivité émotionnelle est évaluée dans l’OF et le plus-maze; la réponse de stress est mesurée par radio télémétrie de la température interne pendant le stress d’immobilisation (SI) sous diète régulière et riche en sel; l’excrétion des électrolytes urinaires est dosée après 24 heures de diète salée. Les loci les plus significatifs sont situés dans les régions suivantes: de l’émotionalité dans l’OF (Emo1) sur le chr. 1 (LOD=4.6) correspondant à la région homologue impliquée dans la cohorte d’hypertension familiale du Saguenay; de la dopa décarboxylase (ddc) sur le chr. 11 pour l’émergence du plus-maze (LOD=4.7); de la protéine liant l’endotoxine (lbp) sur le chr. 2 pour l’hypothermie initiale en réponse au SI (LOD=4); et de HSP90 sur le chr. 12 pour l’excrétion de Ca++ (LOD=4.6). Des banques de données sont ensuite interrogées pour recenser les polymorphismes des régions régulatrices ou codantes des gènes candidats chez les souches ancestrales A/J et B6, dont les séquences sont disponibles pour le génome entier. Des utilitaires web permettent de dévoiler les changements dans la structure secondaire de l’ARNm, l’interférence avec des microARN ou avec d’autres motifs de liaison. Plusieurs SNPs fonctionnels ont été identifiés pour le QTL du chr. 1, particulièrement dans les éléments de régulation; ceux-ci impliquant des gènes reliés avec les réponses inflammatoire/immunitaire ou avec le système cardiovasculaire. La quantification par la PCR confirme une régulation à la baisse d’atp1a2 dans le cœur et le cerveau des souches susceptibles à l’anxiété. Ces résultats confirment l’intrication des altérations de la susceptibilité au stress et de la régulation de la TA.

Cerebral edema and acute liver failure : pathophysiological mechanisms and new therapeutic approaches

L’encéphalopathie hépatique (EH) se développe chez les patients atteints d’une maladie du foie et se caractérise par de nombreuses anomalies neuropsychiatriques. L’insuffisance hépatique aiguë (IHA) se caractérise par une perte progressive de l’état de conscience, par une augmentation rapide de l’œdème cérébral et une augmentation de la pression intracrânienne entraînant une herniation cérébrale et la mort. Plusieurs facteurs sont responsables du développement de l’EH mais depuis une centaine d’années, l’hyperammonémie qui peut atteindre des concentrations de l’ordre de plusieurs millimolaires chez les patients atteints d’IHA aux stades de coma est considérée comme un facteur crucial dans la pathogenèse de l’EH. La présente thèse comprend 4 articles suggérant l’implication de nouveaux mécanismes pathogéniques dans le développement de l’EH et de l’œdème cérébral associés à l’IHA et tente d’expliquer l’effet thérapeutique de l’hypothermie et de la minocycline dans la prévention de l’EH et de l’œdème cérébral: 1. L’IHA induite par dévascularisation hépatique chez le rat se caractérise par une augmentation de la production de cytokines pro-inflammatoires cérébrales (IL-6, IL-1, TNF-). Cette observation constitue la première évidence directe que des mécanismes neuro-inflammatoires jouent une rôle dans la pathogenèse de l’EH et de l’œdème cérébral associés à l’IHA (Chapitre 2.1, articles 1 et 2). 2. L’activation de la microglie telle que mesurée par l’expression de marqueurs spécifiques (OX42, OX-6) coïncide avec le développement de l’encéphalopathie (stade coma) et de l’œdème cérébral et s’accompagne d’une production accrue de cytokines pro-inflammatoires cérébrales (Chapitre 2.1, article 1 et 2). 3. Un stress oxydatif/nitrosatif causé par une augmentation de l’expression de l’oxyde nitrique synthétase et une augmentation de la synthèse d’oxyde nitrique cérébral participe à la pathogénèse des complications neurologiques de l’IHA (Chapitre 2.3, articles 3 et 4). 4. Des traitements anti-inflammatoires tels que l’hypothermie et la minocycline peuvent constituer de nouvelles approches thérapeutiques chez les patients atteints d’IHA (Chapitre 2.1, article 1; Chapitre 2.2, article 2). 5. Les effets bénéfiques de l’hypothermie et de la minocycline sur les complications neurologiques de l’IHA expérimentale s’expliquent, en partie, par une diminution du stress oxydatif/nitrosatif (Chapitre 2.3, article 3; Chapitre 2.4, article 4).

Canulacion arterial axilar versus femoral para cirugía del arco aórtico

Objetivo: Determinar si la canulación arterial axilar para perfusión selectiva anterograda cerebral (PSAC) con hipotermia moderada reduce la morbilidad, mortalidad y el pronóstico neurológico en pacientes llevados a cirugía del arco aórtico. Pacientes y métodos: Se hace una revisión retrospectiva de 2 cohortes de pacientes a quienes se les realizo cirugía del arco aórtico urgente o electiva, para comparar dos técnicas de canulación arterial diferente; la canulación axilar para perfusión selectiva anterograda cerebral con hipotermia moderada y la canulación femoral con hipotermia profunda, en un periodo de tiempo comprendido entre Diciembre del 2002 y Agosto del 2008 en el servicio de cirugía cardiovascular de la Fundación Cardioinfantil Instituto de Cardiología. Resultados: 68 pacientes, 50 hombres y 18 mujeres fueron llevados a cirugía de arco aórtico 19 pacientes (27%) con diagnóstico de aneurisma de aorta ascendente y arco aórtico y 49 pacientes (72%) con disección aortica tipo A aguda o crónica. A 55 pacientes (80.9%) se les hizo canulación axilar y a 13 pacientes (19,1%) se les hizo canulación femoral. No se encontraron diferencias en las variables preoperatorias entre los dos grupos. La mortalidad global fue de 13,2% (9 pacientes), todas las muertes se presentaron en pacientes con diagnóstico de disección aortica tipo A. El 55% de los pacientes (38/68) se operaron de urgencia. No se presentaron diferencias estadísticamente significativas en la mortalidad entre el grupo de canulación axilar, 8 muertes (14,5%) y el grupo de canulación femoral 1 muerte (7,7%) con (p=0.5). No se encontraron diferencias en la incidencia de déficit neurológico permanente entre los dos grupos, presentándose solamente dos pacientes con accidente cerebrovascular ambos en el grupo de canulación axilar (P=0.48). Conclusiones: la canulación axilar con perfusión cerebral selectiva anterograda en hipotermia moderada representa un método seguro de protección cerebral, con una mortalidad aceptable y una incidencia baja de complicaciones neurológicas permanentes, no encontramos diferencias en la mortalidad o la aparición de eventos neurológicos, cuando se comparo con la técnica de canulación arterial femoral. No se presentaron complicaciones asociadas al sitio de canulación en ninguno de los dos grupos.

Correlación entre saturación venosa, ruptura de anastomosis y formación de fístulas en pacientes con trauma abdominal en el Hospital Occidente de Kennedy

El manejo del trauma abdominal supone el reto de realizar una anastomosis o sutura intestinal en pacientes comprometidos hemodinámicamente. La decisión de cirugía de control de daños ante la presencia de acidosis, hipotermia y coagulopatía es evidente, sin embargo la situación no siempre es tan clara. En individuos con trauma se desarrollan cambios moleculares e inflamatorios por inadecuado balance entre aporte y demanda de oxígeno, que afectan el proceso de reparación de los tejidos con el riesgo de aparición de fístulas. Una forma rápida y práctica de detectar esta hipoperfusión es midiendo la saturación venosa de oxígeno (SVO2) y el Lactato Sérico. OBJETIVOS: Establecer correlación entre los valores de SVO2 transoperatorio y la aparición de fístulas intestinales en pacientes intervenidos por trauma abdominal. MATERIALES Y METODOS: Estudio de cohorte prospectivo que analiza diferentes variables en relación con la aparición de fistulas en pacientes con trauma abdominal que requieren suturas en el tracto gastrointestinal, haciendo énfasis en los niveles de SVO2. RESULTADOS: Los pacientes con falla anastomótica, presentaron un promedio de SVO2 más baja (60.0% ± 2.94%), versus los no fistulizados (69.89% ± 7.21%) (p =0.010). Todos los pacientes de la cohorte expuesta (SVO2<65%), presentaron dehiscencia de la anastomosis (RR =39.8, IC95%: 2.35,659.91, p<0.001, Test exacto de Fisher). El valor predictivo positivo de la saturación (<65%) fue de 57.14% (IC 95%: 13.34%, 100%) y el valor predictivo negativo fue de 100% (IC 95%:81.75%, 100%). La sensibilidad fue de 100% (IC 95%:87.50%, 100%) y especificidad de 91.89% (IC 95%: 81.75%, 100%). En el análisis bivariante determinó que el índice de trauma abdominal, el nivel de hemoglobina y el requerimiento de transfusión de glóbulos rojos, son factores de riesgo directamente relacionados con la falla de la anastomosis en pacientes con trauma abdominal CONCLUSIONES: - Hay una fuerte relación entre la falla en la reparación intestinal y SVO2 < 65%. - El pronóstico de una anastomosis intestinal está directamente relacionada con el estado hemodinámico y la perfusión tisular al momento de la intervención quirúrgica. - El nivel de SVO2 puede apoyar al cirujano en la decisión de realizar o no una reparación en víscera hueca al momento de intervención quirúrgica en un paciente con trauma abdominal.

Proporción de pacientes que presentan hipotermia peri operatoria durante un reemplazo articular de cadera, rodilla u hombro

Introducción: La hipotermia perioperatoria se ha documentado como factor de riesgo para el aumento de la morbimortalidad de los pacientes aumentando morbilidad miocárdica, riesgo de infección, pérdidas sanguíneas y tiempo de hospitalización. La aplicación de anestésicos toma relevancia ya que causa la pérdida de control central de la temperatura. Nuestro objetivo con este estudio fue describir la proporción de casos de hipotermia en la población sometida a un reemplazo articular durante un periodo de cuatro meses. Materiales y métodos: Se realizó un estudio de cohorte prospectivo. La población a estudio fueron los pacientes que fueron sometidos a un reemplazo total de cadera, rodilla u hombro. Se registró la temperatura central en el momento previo a la inducción anestésica, 30, 60 y 90 minutos después, al finalizar el procedimiento y al ingresar a recuperación. Se reportó el porcentaje de pacientes con hipotermia en cada tiempo. Resultados: Se analizaron en total 88 pacientes, el 55,7% fue llevado a cirugía de cadera, 39,7% de rodilla y 4,5% de hombro. El tipo de anestesia más utilizado fue general y la duración promedio de anestesia fue 164 minutos. La medición de la temperatura central se realizó en nasofaringe, esófago o tímpano. La proporción de pacientes que presentaron hipotermia en la inducción fue 21,6%, a 30 minutos 83%, a 60 minutos 73,9%, a 90 minutos 68,2%, al finalizar 59,1% y en recuperación 58%. Se realizó una prueba Chi cuadrado comparando las proporciones entre la inducción y los cinco periodos posteriores, se encontró que la proporción de pacientes con hipotermia en los cinco tiempos posteriores tuvo una diferencia estadísticamente significativa (p=0,00) comparada con la proporción de pacientes con hipotermia durante la inducción. Conclusión: En los pacientes sometidos a un reemplazo articular la hipotermia fue una condición prevalente posterior a la aplicación de los anestésicos sistémicos. Los dispositivos de calentamiento intraoperatorio usados actualmente son insuficientes para evitar la hipotermia, lo que indica concordancia con la literatura en cuanto a las recomendaciones de calentamiento perioperatorio, con énfasis en el precalentamiento, para prevenir la caída significativa de la temperatura y la morbimortalidad asociada.

Diacylglycerol-induced protection against injury during ischemia and reperfusion can be achieved without activation of protein kinase C in the rat heart: Comparative studies with ischemic preconditioning

The role of protein kinase C (PKC) activation in ischemic preconditioning remains controversial. Since diacylglycerol is the endogenous activator of PKC and as such might be expected cardioprotective, we have investigated whether: (i) the diacylglycerol analog 1,2-dioctanoyl-sn-glycerol (DOG) can protect against injury during ischemia and reperfusion; (ii) any effect is mediated via PKC activation; and (iii) the outcome is influenced by the time of administration. Isolated rat hearts were perfused with buffer at 37°C and paced at 400 bpm. In Study 1, hearts (n=6/group) were subjected to one of the following: (1) 36 min aerobic perfusion (controls); (2) 20 min aerobic perfusion plus ischemic preconditioning (3 min ischemia/3 min reperfusion+5 min ischemia/5 min reperfusion); (3) aerobic perfusion with buffer containing DOG (10 μM) given as a substitute for ischemic preconditioning; (4) aerobic perfusion with DOG (10 μM) during the last 2 min of aerobic perfusion. All hearts then were subjected to 35 min of global ischemia and 40 min reperfusion. A further group (5) were perfused with DOG (10 μM) for the first 2 min of reperfusion. Ischemic preconditioning improved postischemic recovery of LVDP from 24±3% in controls to 71±2% (P<0.05). Recovery of LVDP also was enhanced by DOG when given just before ischemia (54±4%), however, DOG had no effect on the recovery of LVDP when used as a substitute for ischemic preconditioning (22±5%) or when given during reperfusion (29±6%). In Study 2, the first four groups of study were repeated (n=4–5/group) without imposing the periods of ischemia and reperfusion, instead hearts were taken for the measurement of PKC activity (pmol/min/mg protein±SEM). PKC activity after 36 min in groups (1), (2), (3) and (4) was: 332±102, 299±63, 521±144, and 340±113 and the membrane:cytosolic PKC activity ratio was: 5.6±1.5, 5.3±1.8, 6.6±2.7, and 3.9±2.1 (P=NS in each instance). In conclusion, DOG is cardioprotective but under the conditions of the present study is less cardioprotective than ischemic preconditioning, furthermore the protection does not appear to necessitate PKC activation prior to ischemia.