High-flow nasal cannula oxygen therapy was effective for dysphagia associated with respiratory muscle paralysis due to cervical spinal cord injury: A case report.

RATIONALE: Respiratory muscle paralysis due to low cervical spinal cord injury (CSCI) can lead to dysphagia. Noninvasive positive airway pressure (PAP) therapy can effectively treat this type of dysphagia. High-flow nasal cannula (HFNC) oxygen therapy can generate a low level of positive airway pressure resembling PAP therapy, it may improve the dysphagia. PATIENT CONCERNS: The patient was an 87-year-old man without preexisting dysphagia. He suffered a CSCI due to a dislocated C5/6 fracture, without brain injury, and underwent emergency surgery. Postoperatively (day 2), he complained of dysphagia, and the intervention was initiated. DIAGNOSIS: Based on clinical findings, dysphagia in this case, may have arisen due to impaired coordination between breathing and swallowing, which typically occurs in patients with CSCI who have reduced forced vital capacity. INTERVENTIONS: HFNC oxygen therapy was started immediately after the surgery, and swallowing rehabilitation was started on Day 2. Indirect therapy (without food) and direct therapy (with food) were applied in stages. HFNC oxygen therapy appeared to be effective because swallowing function temporarily decreased when the HFNC oxygen therapy was changed to nasal canula oxygen therapy. OUTCOMES: Swallowing function of the patient improved and he did not develop aspiration pneumonia. LESSONS: HFNC oxygen therapy improved swallowing function in a patient with dysphagia associated with respiratory-muscle paralysis following a CSCI. It may have prolonged the apnea tolerance time during swallowing and may have improved the timing of swallowing. HFNC oxygen therapy can facilitate both indirect and direct early swallowing therapy to restore both swallowing and respiratory function.

Adenosine, a hepato-protective component in active hexose correlated compound: its identification and iNOS suppression mechanism.

Supplementation of active hexose correlated compound (AHCC) improved the prognosis of postoperative hepatocellular carcinoma patients. Excess production of nitric oxide (NO) by inducible NO synthase (iNOS) is an inflammatory biomarker in liver injury. AHCC suppressed iNOS induction in hepatocytes, suggesting that AHCC has a potential liver-protective effect. However, the active component in AHCC responsible for NO suppressive activities has not been identified. The objective of this study was to identify this NO suppressive component and to investigate its mechanisms of action. AHCC was subjected to fractionation by cation exchanger, size exclusion chromatography, and normal- and reversed-phase HPLC. Aliquots of the fractions were added to primary cultured rat hepatocytes stimulated with interleukin (IL)-1ß, and NO production was assayed. By activity-guided fractionation and electron spray ionization mass spectrometry analysis, adenosine was identified as one of the NO suppressive components in AHCC. Adenosine inhibited NO production, and reduced the expression of iNOS protein and mRNA. It had no effects on IκB degradation, but it inhibited NF-κB activation. Adenosine also inhibited the upregulation of type I IL-1 receptor (IL-1RI). Experiments with iNOS promoter-luciferase constructs revealed that adenosine decreased the levels of iNOS mRNA at the promoter transactivation and mRNA stabilization steps. Adenosine decreased the expression of the iNOS gene antisense transcript, which is involved in iNOS mRNA stability. Adenosine in AHCC suppressed iNOS induction by blocking NF-κB activation and the upregulation of the IL-1RI pathways, resulting in the inhibition of NO production.

Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest.

BACKGROUND: Subarachnoid haemorrhage (SAH) is known as one of the aetiologies of out-of-hospital cardiac arrest (OHCA). However, the mechanisms of circulatory collapse in these patients have remained unclear. METHODS AND RESULTS: We examined 244 consecutive OHCA patients transferred to our emergency department. Head computed tomography was performed on all patients and revealed the existence of SAH in 14 patients (5.9%, 10 females). Among these, sudden collapse was witnessed in 7 patients (50%). On their initial cardiac rhythm, all 14 patients showed asystole or pulseless electrical activity, but no ventricular fibrillation (VF). Return of spontaneous circulation (ROSC) was obtained in 10 of the 14 patients (14.9% of all ROSC patients) although all resuscitated patients died later. The ROSC rate in patients with SAH (71%) was significantly higher than that of patients with either other types of intracranial haemorrhage (25%, n=2/8) or presumed cardiovascular aetiologies (22%, n=23/101) (p<0.01). On electrocardiograms, ST-T abnormalities and/or QT prolongation were found in all 10 resuscitated patients. Despite their electrocardiographic abnormalities, only 3 patients showed echocardiographic abnormalities. CONCLUSIONS: The frequency of SAH in patients with all causes of OHCA was about 6%, and in resuscitated patients was about 15%. The initial cardiac rhythm revealed no VF even though half had a witnessed arrest. A high ROSC rate was observed in patients with SAH, although none survived to hospital discharge.

Beneficial effect of a prone position for patients with hypoxemia after transthoracic esophagectomy.

OBJECTIVE: Although the prone position has been reported to improve arterial oxygenation in patients with acute respiratory distress syndrome, there have been no reports on its efficacy in patients with hypoxemia after transthoracic esophagectomy with three-field lymphadenectomy. This study was undertaken to assess the efficacy of the prone position on hypoxemia after three-field lymphadenectomy for thoracic esophageal carcinoma. DESIGN: Prospective randomized clinical study. SETTING: General intensive care unit at a university hospital. INTERVENTIONS AND MEASUREMENTS: Sixteen patients who underwent three-field lymphadenectomy and showed hypoxemia (PaO2/FiO2 ratios of <200 under positive end-expiratory pressure of >5 cm H2O) on the fifth postoperative day were randomly assigned to prone (eight patients) and nonprone (eight patients) groups. Prone position for 6 hrs was carried out for four consecutive days. The PaO2/FiO2 ratio, the duration of ventilatory support, and length of stay, were measured. RESULTS: Oxygenation: The PaO2/FiO2 ratio markedly increased by 32% +/- 22% in seven of eight patients (p <.05) when the patients were moved from the supine to the prone position. The PaO2/FiO2 ratio after the fourth prone position (238 +/- 55, p <.05) was significantly higher than that before the first trial of prone position (166 +/- 25) in these seven patients. Duration of ventilatory support and intensive care unit length of stay: Both the ventilation period (11.6 +/- 2.2 vs. 14.0 +/- 1.6 days, p =.0029) and the length of stay in the intensive care unit (12.8 +/- 4.4 vs. 17.2 +/- 3.4 days, p =.0032) were significantly shorter in the prone group compared with the nonprone group. The PaO2/FiO2 ratio at the time of cessation of prone positioning was significantly higher than the corresponding value in the nonprone group. CONCLUSION: In hypoxemic patients after three-field lymphadenectomy, the prone position improved arterial oxygenation without any deleterious effects. The beneficial effect of the prone position is possibly attributable to opening of the bronchi obstructed by secretions.

The influence of nicardipine-, nitroglycerin-, and prostaglandin E(1)-induced hypotension on cerebral pressure autoregulation in adult patients during propofol-fentanyl anesthesia.

UNLABELLED: We investigated the influence of drug-induced hypotension at a mean arterial pressure (MAP) of 60-70 mm Hg on cerebral pressure autoregulation in 45 adult patients during propofol-fentanyl anesthesia. Time-averaged mean blood flow velocity in the right middle cerebral artery (Vmca) was continuously measured at a PaCO(2) of 39-40 mm Hg by using transcranial Doppler ultrasonography. Hypotension was induced and maintained with a continuous infusion of nicardipine, nitroglycerin, or prostaglandin E(1). Cerebral autoregulation was tested by a slow continuous infusion of phenylephrine to induce an increase in MAP of 20-30 mm Hg. From the simultaneously recorded data of Vmca and MAP, cerebral vascular resistance (CVR) was calculated as MAP/Vmca. Furthermore, the index of autoregulation (IOR) was calculated as DeltaCVR/DeltaMAP, where DeltaCVR = change in CVR and DeltaMAP = change in MAP. The test was performed twice for each condition on each patient: baseline and hypotension. The IOR during baseline was similar among the groups. During nitroglycerin- and prostaglandin E(1)-induced hypotension, IOR was not different from baseline. In contrast, during nicardipine-induced hypotension, IOR significantly decreased compared with baseline (0.37 +/- 0.08 versus 0.83 +/- 0.07, P < 0.01). In conclusion, nicardipine, but not nitroglycerin or prostaglandin E(1), significantly attenuates cerebral pressure autoregulation during propofol-fentanyl anesthesia. IMPLICATIONS: Vasodilators may influence cerebral autoregulation by changing cerebral vascular tone. Nicardipine, but not nitroglycerin or prostaglandin E(1), attenuated cerebral pressure autoregulation in normal adult patients during propofol-fentanyl anesthesia.