RESUMEN
BACKGROUND: Recognition of a cervical spine injury is important to prevent further injury and in planning for future care. The management of the patient with a possible cervical spine injury who remains unresponsive is controversial. METHODS: A retrospective evaluation of obtunded trauma patients admitted to the surgical intensive care unit who underwent bedside fluoroscopic cervical spine evaluation. Fluoroscopic findings and all complications were noted. RESULTS: Twenty obtunded patients with possible cervical spine injuries underwent bedside fluoroscopic cervical spine evaluation. All patients had at minimum a normal three-view cervical spine series before fluoroscopy. Thirteen patients (65%) had the fluoroscopic examination completed at the bedside and were cleared. The complete cervical spine could not be evaluated in six patients (30%). One patient (5%) was found to have a C4-5 subluxation in the bedside examination. None of the patients had progression of their neurologic symptoms after cervical spine flexion/extension, and none developed evidence of spinal cord injury after being cleared during their hospital course. Cervical collars remained in place for 5.7+/-1.41 days (range, 1- 26 days). Three patients (15%) were noted to have decubiti under the cervical collar. CONCLUSION: In this small study, the use of bedside fluoroscopy to evaluate the cervical spine appears safe and easy to perform. One unrecognized injury was identified. The technique is usually successful and gives reassurance that a significant cervical spine injury is not present.
Asunto(s)
Vértebras Cervicales/lesiones , Fluoroscopía , Sistemas de Atención de Punto , Traumatismos Vertebrales/diagnóstico por imagen , Adulto , Vértebras Cervicales/diagnóstico por imagen , Femenino , Fluoroscopía/métodos , Escala de Coma de Glasgow , Humanos , Masculino , Estudios Retrospectivos , InconscienciaRESUMEN
OBJECTIVE: To investigate the physiologic effects of nitric oxide synthase inhibition with N-nitro-L-arginine methyl ester in an acute resuscitated model of porcine septic shock. DESIGN: Randomized control trial. SETTING: Animal research facility. STUDY SUBJECTS: Domestic Yorkshire swine. INTERVENTIONS: Twenty-four animals were randomly divided into one of four treatment groups as follows: normal saline resuscitation (NSR) (control group); NSR plus 200 micrograms/kg of lipopolysaccharide (LPS) at 1 hour after baseline (LPS group); NSR, LPS, and a continuous infusion of 50 micrograms/kg per minute of N-nitro-L-arginine methyl ester (NAME) at 1 hour after baseline (LPS/NAME group); and NSR and NAME (NAME group). All animals received NSR at 1 mL/kg per minute starting at baseline. MAIN OUTCOME MEASURES: Mean arterial pressure (MAP), systemic vascular resistance index (SVRI), mean pulmonary arterial pressure (MPAP), and pulmonary vascular resistance index (PVRI) were measured at baseline and hourly for 4 hours. Values at baseline and 3 hours are given below as mean (+/- SE). RESULTS: All variables remained unchanged in the control group. The administration of LPS produced a systemic hyperdynamic response characterized by a decrease in MAP and SVRI from 66.0 +/- 3.9 to 55.0 +/- 2.8 mm Hg (P < .05) and from 422.0 +/- 22.0 to 272.0 +/- 29.0 mm Hg.min.kg/L (P < .05), respectively. The administration of LPS produced an increase in MPAP and PVRI from 16.3 +/- 0.8 to 30.0 +/- 1.3 mm Hg (P < .05) and from 37.0 +/- 5.3 to 119.0 +/- 13.0 mm Hg.min.kg/L (P < .05), respectively. In the LPS/NAME group, NAME infusion normalized MAP and increased SVRI from 506.0 +/- 40.0 to 642.0 +/- 72.0 mm Hg.min.kg/L (P < .05). Infusion of NAME potentiated LPS-induced pulmonary hypertension, increasing MPAP and PVRI from 16.8 +/- 0.6 to 36.0 +/- 2.8 mm Hg (P < .05) and from 59.0 +/- 3.5 to 319.0 +/- 64.0 mm Hg.min.kg/L (P < .05), respectively. Infusion of NAME alone increased MAP from 74.0 +/- 1.3 to 100.0 +/- 4.1 mm Hg (P < .05) and had no significant effect on MPAP and PVRI. CONCLUSIONS: The potentiation of LPS-induced pulmonary hypertension following NAME infusion suggests that inhibition of nitric oxide synthase may have a limited role in the treatment of septic shock.
Asunto(s)
Aminoácido Oxidorreductasas/antagonistas & inhibidores , Arginina/análogos & derivados , Óxido Nítrico/antagonistas & inhibidores , Choque Séptico/fisiopatología , Animales , Arginina/farmacología , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Presión Venosa Central/efectos de los fármacos , Escherichia coli , Femenino , Frecuencia Cardíaca/efectos de los fármacos , Hemodinámica/efectos de los fármacos , Lipopolisacáridos/efectos adversos , Masculino , NG-Nitroarginina Metil Éster , Óxido Nítrico Sintasa , Consumo de Oxígeno/efectos de los fármacos , Presión Esfenoidal Pulmonar/efectos de los fármacos , Resucitación , Cloruro de Sodio , Porcinos , Resistencia Vascular/efectos de los fármacosRESUMEN
Improved and reliable methods for assessing glomerular filtration rate (GFR) in intensive care patients are needed in light of known deficiencies using creatinine clearance. We compared simultaneous two-hour clearances of inulin (CIn), creatinine (CCr), and 99mTc-diethylenetriaminepentaacetic acid (CDTPA) in 18 medical or surgical intensive care patients (range, 49 to 92 years old) with blood urea nitrogen (BUN) levels greater than 17.9 mmol/liter (0.5 mg/ml), serum creatinine levels greater than 150 mumol/liter (0.02 mg/ml), or estimated Cockcroft clearance less than 60 ml/min. Patients had severe renal dysfunction with average GFR of 35 ml/min (range, 2 to 69 ml/min). CDTPA and CCr correlated significantly with CIn, although CDTPA tended to provide a closer approximation. Cockcroft clearance (32 +/- 4 ml/min) was grossly similar to CDTPA and CIn and correlated significantly, especially when weight was calculated using actual as opposed to ideal body weight. In a subset of 13 patients with CIn less than 30 ml/min, only CDTPA was significantly correlated with CIn. In patients in the intensive care unit, CDTPA provides a rapid, accurate, and inexpensive clinical assessment of GFR, even at very low GFRs.