RESUMEN
PURPOSE: To evaluate the prevalence of dual platelet inhibition in cases of severe retrobulbar hemorrhage following retrobulbar and peribulbar anesthesia. SETTING: Department of Ophthalmology, Ludwig-Maximilans Universität, München, Germany. DESIGN: Retrospective study. METHODS: Two groups of patients were screened retrospectively over a 5-year period for the inclusion criterion of severe retrobulbar hematoma after retrobulbar or parabulbar injection. The first group consisted of emergency cases referred to the clinic. A second group of patients had received retrobulbar block at the hospital. All cases were collected and screened for the presence of antiplatelet therapy. RESULTS: Among roughly 160 000 patient records screened, 3 patients with grade IV retrobulbar hematoma were identified. Two of these patients were taking dual antiplatelet medications and 2 were on anticoagulation therapy during the time of retrobulbar or peribulbar anesthesia. None of the cases showed single medication platelet inhibition. The visual acuity of all patients stayed low at the 6-month follow-up (1.2 logMAR in 1 patient and no light perception in 2 patients). CONCLUSIONS: Retrobulbar hematoma is a rare but severe complication of retrobulbar anesthesia. With the high prevalence of dual platelet inhibition found in these cases, a prospective controlled trial seems unethical. In these high-risk patients, surgery should be performed under topical anesthesia if possible or general anesthesia if necessary. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.
Asunto(s)
Anestesia Local/métodos , Anticoagulantes/efectos adversos , Implantación de Lentes Intraoculares , Facoemulsificación , Inhibidores de Agregación Plaquetaria/efectos adversos , Hemorragia Retrobulbar/inducido químicamente , Anciano , Anticoagulantes/uso terapéutico , Arteriopatías Oclusivas/tratamiento farmacológico , Aspirina/efectos adversos , Aspirina/uso terapéutico , Procedimientos Quirúrgicos Cardíacos , Enfermedades Cardiovasculares/tratamiento farmacológico , Clopidogrel , Combinación de Medicamentos , Femenino , Humanos , Masculino , Inhibidores de Agregación Plaquetaria/uso terapéutico , Hemorragia Retrobulbar/diagnóstico , Hemorragia Retrobulbar/cirugía , Estudios Retrospectivos , Factores de Riesgo , Ticlopidina/efectos adversos , Ticlopidina/análogos & derivados , Ticlopidina/uso terapéutico , Warfarina/efectos adversos , Warfarina/uso terapéuticoRESUMEN
Long-term administration of PUFA is known to modulate immune functions and apoptotic pathways depending on the respective amount of n-6 and n-3 fatty acids (FA). Data on short-term effects on apoptotic pathways are rare. Apoptosis of splenic lymphocytes is the hallmark of detrimental sepsis. Therefore, we aimed to compare the immediate effects of parenterally administered n-6-enriched soyabean oil (SO)- and n-3-enriched fish oil (FO)-based lipid emulsions after laparotomy (LAP; sham procedure) and after induction of acute, severe sepsis by caecal ligation and incision. After 390 min of observation time, plasma was analysed for IL-1ß, IL-6 and NEFA. Apoptosis in splenic lymphocytes was quantified by Annexin-V expression. After LAP, infusion of both FO and SO did not change cytokine concentrations. Sepsis increased both cytokines. FO but not SO further augmented the rise. After LAP, SO increased NEFA, and both lipid emulsions reduced free arachidonic acid (AA). Sepsis resulted in a dramatic decrease in NEFA and AA. The drop in NEFA and AA was prevented by both SO and FO. In addition, FO resulted in an increased concentration of n-3 FA under both conditions. Infusion of both lipid emulsions induced apoptosis in splenic lymphocytes after LAP. Sepsis-induced apoptosis was not further enhanced by FO or SO. The present study shows that short-term administration of FO as opposed to SO caused pro-inflammatory effects during sepsis. Moreover, short-term administration of both SO and FO suffices to induce apoptosis in splenic lymphocytes. Finally, SO and FO do not further enhance sepsis-induced splenic apoptosis.