Upper airway obstruction during midazolam/nitrous oxide sedation in children with enlarged tonsils.

PURPOSE: The purpose of this nonrandomized, case-control study was to examine the incidence and severity of upper airway obstruction (UAO) in children with enlarged tonsils during inhalation of nitrous oxide (N2O). METHODS: Following premedication with oral midazolam, 0.5 mg/kg, measurements were collected during a 3-minute control period followed by 3 minutes of breathing 50% N2O in oxygen. An unblinded anesthesiologist held a facemask over the child's mouth and nose without supporting the head or neck, or attempting to maintain airway patency. Every 20 seconds, the degree of airway obstruction was graded as none, partial, or complete. Twenty-five children presenting for tonsillectomy and 25 controls without enlarged tonsils participated. RESULTS: During 50% N2O inhalation, 14 children (56%) in the tonsillectomy group, and four children (16%) in the control group demonstrated partial UAO. One child in the tonsillectomy group with partial UAO developed hypoxemia (SpO2 72%). One child in the tonsil group developed complete UAO during inhalation of 50% N2O. CONCLUSION: Children who receive sedation with oral midazolam and 50% N2O inhalation may exhibit significant UAO, especially in the presence of enlarged tonsils. Presedation physical exams should evaluate the presence of tonsil size during examination of the mouth and airway.

Chloral hydrate sedation: the additive sedative and respiratory depressant effects of nitrous oxide.

UNLABELLED: The combination of chloral hydrate and nitrous oxide (N2O) is often used for sedation in pediatric dentistry. The purpose of this study was to determine the extent to which N2O increases the level of sedation and respiratory depression in children sedated with chloral hydrate. Thirty-two children, 1-9 yr, received chloral hydrate, 70 mg/kg (maximum 1.5 g), and then received N2O (30% and 50%). Hypoventilation (maximal PETCO2 > 45 mm Hg) occurred in 23 (77%) children during administration of chloral hydrate alone, in 29 (94%) breathing 30% N2O (P = 0.08 versus control), and in 29 (97%) breathing 50% N2O (P = 0.05 versus control). Mean PETCO2 was increased during 30% (P = 0.007) and 50% (P = 0.02) N2O administration. Using chloral hydrate alone, 8 (25%) children were not sedated, 10 (31%) were consciously sedated, and 14 (44%) were deeply sedated. Using 30% N2O, 2 children (6%) were not sedated, 0 were consciously sedated, and 29 (94%) were deeply sedated (P < 0.0001). Using 50% N2O, 1 child (3%) was not sedated, 0 were consciously sedated, 27 (94%) were deeply sedated, and 1 (3%) had no response to a painful stimulus (P < 0.0001). We conclude that the addition of 30% or 50% N2O to chloral hydrate often causes decreases in ventilation and usually results in deep, not conscious, sedation in children. IMPLICATIONS: Pediatric sedation in the dental office often consists of nitrous oxide (N2O) after chloral hydrate premedication. We found that the addition of 30% or 50% N2O to chloral hydrate often causes decreases in ventilation and usually results in deep, not conscious, sedation in children.

Breathing patterns and levels of consciousness in children during administration of nitrous oxide after oral midazolam premedication.

PURPOSE: The combination of midazolam and nitrous oxide is commonly used to achieve sedation and analgesia during pediatric oral procedures, yet there are few, if any, data that illustrate the ventilatory effects of N2O in children, especially when used in combination with additional central nervous system (CNS) depressants. It was hypothesized that the addition of N2O inhalation to oral midazolam premedication would enhance the sedative effects of the midazolam and add analgesia without causing significant respiratory depression. The purpose of this study was to test this hypothesis. MATERIALS AND METHODS: Thirty-four healthy children about to undergo restorative dental treatment under general anesthesia were premedicated with oral midazolam, 0.7 mg/kg, and were then exposed to 40% N2O for 15 minutes after a 5-minute control period. The effect of adding N2O on SpO2, respiratory rate, PETCO2, VT, and VT/TI was examined and the levels of consciousness (conscious vs deep sedation) before and during N2O inhalation were determined. RESULTS: During the course of the study, no child developed hypoxemia (SpO2 < 92%) nor clinically significant upper airway obstruction. Four children who did not develop hypoventilation (defined as PETCO2 > 45 mm Hg) during the control period did so after initiation of N2O. Overall, there were no significant differences in SpO2, PETCO2, VT, or VT/TI between the control and study periods. However, respiratory rates were significantly higher in the first 10 minutes of N2O inhalation when compared with the control period. Before starting N2O administration, 14 children were not clinically sedated, 19 children met the criteria for conscious sedation, and one child met the criteria for deep sedation. At the end of 15 minutes of N2O inhalation, 12 children were not clinically sedated, 17 children met the definition of conscious sedation, three were deeply sedated, and one child had no response to IV insertion, implying a state of general anesthesia. There were no differences in sedation scores between the control and study periods (P = .6). Overall, seven children had an increase in their sedation score while breathing N2O, four had a decrease in their sedation score, and 22 had no change. CONCLUSIONS: The addition of 40% N2O to oral midazolam, 0.7 mg/kg, did not result in clinically meaningful respiratory depression nor upper airway obstruction, but did, in some children, cause an increase in the level of sedation beyond simple conscious sedation.

Retroperitoneal fibrosis.

Retroperitoneal fibrosis is an uncommon inflammatory disease that leads to extensive fibrosis throughout the retroperitoneum. The majority of cases are idiopathic. The characteristic perivascular distribution of the idiopathic form supports the theory that the disease is an immune-mediated response to severe atherosclerosis. Evidence suggests that idiopathic retroperitoneal fibrosis may be part of a systemic fibrosing disease. Other less common forms include methysergide-related and malignant retroperitoneal fibrosis. The signs and symptoms of the disease are vague and nonspecific, and therefore the diagnosis relies heavily on radiologic findings. Once the diagnosis is suggested, the distinction must be made between malignant and nonmalignant retroperitoneal fibrosis, because the prognosis is dismal for malignant retroperitoneal fibrosis, but very good for other forms of the disease. Surgical biopsy remains the only way to definitively establish this diagnosis. Treatment may be surgical or medical, with the best outcome observed in patients receiving both.

The structure of the urokinase-type plasminogen activator receptor gene.

The cellular receptor for urokinase-type plasminogen activator (uPAR) is a glycosylphosphatidylinositol (GPI)-anchored membrane protein that plays a central role in pericellular plasminogen activation. It contains 313 amino acid residues, including 28 cysteine residues in a pattern of three homologous repeats. The cysteine residue pattern suggests that uPAR belongs to a superfamily of proteins including CD59, murine Ly-6, and a variety of elapid snake venom toxins. A novel 1.7-kb uPAR cDNA was isolated that is missing exon 5 and that contains 380 bp not previously reported at the 5' end. This cDNA was used to probe a human genomic library from which three clones were isolated and analyzed. The uPAR gene consists of 7 exons spread over 23 kb of genomic DNA. Exons 2, 4, and 6 code for homologous domains within the mature protein, as do exons 3, 5, and 7; CD59-like homologous pairs are encoded by exons 2-3, 4-5, and 6-7, respectively. The structure of the gene for uPAR further confirms the relationship of this molecule to the superfamily containing CD59, Ly-6, and the elapid snake venom toxins.