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- Acute Respiratory Arrest and Brain Sequale Ocurred after General Anesthesia in Diabetic Autonomic Neuropathy Patient: A Case Report
- Tae Hun An, Tae Hyeong Kim, Byung Sik Yu
- Korean J Crit Care Med. 2004;19(2):130-133.
- 1,554 View
- 9 Download
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Abstract
PDF - The incidence of autonomic neuropathy is high in diabetic patients. Cardiovascular complications including sudden cardiorespiratory arrest, bradycardia, hypotension can occur in diabetic patients complicated with autonomic neuropathy. The causes of sudden deaths in diabetics may not always be due to silent myocardial infarction but may also be due to autonomic neuropathy. Patients with diabetic autonomic neuropathy are less able to withstand hypoxia compare to normal people due to sympathetic nerve system damage. We present a case of acute respiratory arrest that occured in a 38 years old diabetic autonomic neuropathy patient after general anesthesia. Even though the patient was carried rapid and adequate airway management within 5 minutes, the patient had severe brain sequale. We conclude that the diabetic autonomic neuropathy patients require more careful monitoring and management for the hypoxia and cardiovascular status because they are more sensitive in hypoxia.
- The Use of Thiopental Sodium with BIS Monitoring in Hypoxic Brain Damage
- Jae Young Kwon, Sul Ki Song, Kyung Hoon Kim, Sang Wook Shin, Seong Wan Baik
- Korean J Crit Care Med. 2000;15(1):52-55.
- 1,436 View
- 10 Download
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Abstract
PDF
- Hypoxemia is a common and potentially serious postoperative complication. Hypoxic encephalopahty may occur in prolonged hypoxemia. This condition needs brain protection. There are many brain protective methods. The primary cental nervous system protective mechanism of the barbiturates is attributed to their ability to decrease the cerebral metabolic rate, thus improving the ratio of oxygen (O2) supply to O2 demand. The electroencephalogram-derived bispectral index system (BIS) is a promising new method to predict probability of recovery of consciousness. We experienced two cases of hypoxic brain damage in recovery room. The patients were treated with thiopental and monitored with BIS. The use of thiopental as brain protection during complete global ischemia after cardiac arrest was not effective.
Original Article
- Clinical Study of Diffusion Hypoxia in Early Period after Nitrous Oxide Anesthesia
- Hae Keum Kil, Won Oak Kim, Sung Jin Lee, Woo Kyung Lee
- Korean J Crit Care Med. 1998;13(1):55-60.
- 1,804 View
- 15 Download
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Abstract
PDF
- Introduction: Anesthesiologists have been aware of the dangers of diffusion hypoxia in the early postoperative period after nitrous oxide anesthesia, but it was suggested of a little clinical significance in healthy patients. Goal of this study is to re-evaluate the possibility of diffusion hypoxia.
METHODS
Eighty patients who were scheduled for vitrectomy were allocated to two groups by normal and abnormal chest X-ray findings and each group was divided into two subgroups by N2O concentration (1-a, 2-a; 50%, 1-b, 2-b; 60%). One and half hours after anesthesia, end-tidal alveolar concentration of oxygen (et-O2), N2O (et-N2O), and PaO2 were measured for 10 minutes after the inspired gases were changed to room air 2 L/minute with controlled ventilation in group 1-a. Those parameters were re-measured after re-administration of O2 and N2O of 50% of each for an hour and the inpired gases were changed to room air again.
RESULTS
In group 1-a, there was no significant differences of et-N2O and PaO2 after 5 minutes by air flow. And there was no differences of et-N2O and PaO2 between group 1-a and 1-b by et-N2O after 4 minutes. In group 1-b, PaO2 was in normal range at 10 minutes after, although et-O2 was decreased to 14.9%. However, group 2-b showed peripheral arterial saturation lower than 96% after 6 minutes and mild hypoxemia (PaO2 75.3 mmHg) at 10 minutes.
CONCLUSIONS
We suggest that hypoxemic episode during spontaneous breathing of room air in early postoperative period after nitrous oxide anesthesia may be occur due to decreased ventilatory function rather than diffusion of nitrous oxide. However, in patients with minimal abnormal chest X-ray findings even without clinical symptoms, it would be better to avoid high concentration of nitrous oxide.
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