The esophageal detector device. Does it work?

BACKGROUND: The esophageal detector device (EDD) is a diagnostic tool for confirmation of tracheal intubation. Capnography is the accepted standard for such confirmation. The purpose of this investigation was to determine whether results using the EDD and capnography agree. METHODS: Five hundred patients were divided into three separate studies. In study 1, with 300 consecutive patients, tracheal intubation was performed and tested with the EDD followed by capnography. In study 2, 100 patients had the esophagus intentionally intubated, and confirmation was tested similarly. The tube was then removed and the trachea intubated, and testing followed. Study 3 involved 100 patients and used a double-blind, randomized design. The tube was intentionally inserted into either the esophagus (n = 5) or trachea (n = 49), and testing followed. RESULTS: In study 1, the compressed EDD bulb reinflated 270 times and always agreed with capnography; in 20 of the 270 subjects (7%) bulb reinflation was delayed, taking from 5-30 s. In 30 instances, the bulb remained compressed, and there was no capnogram indicating esophageal intubation. In study 2, regardless of esophageal or tracheal intubation, agreement between EDD and capnogram was 100%. In study 3, the agreement between the two detecting instruments was 100%, but reinflation of the EDD bulb was delayed in 4% of tracheal intubations. In the 500 patients studied, results from the EDD and capnogram always agreed, but in 6% of all tracheal intubations, the EDD bulb inflated slowly. Of 181 esophageal intubations, the results from the EDD and capnogram always agreed, i.e., there was no reinflation or capnogram. The sensitivity, specificity, and predictive value for the EDD in all of these studies was 100%. CONCLUSIONS: The EDD is a valuable diagnostic technique for confirming tracheal intubation. Results using EDD agree with results using capnography; in 6% of instances there is a slow reinflation; and where there is no capnography, such as on hospital wards, EDD may be a useful diagnostic tool.

Desflurane versus isoflurane in patients with chronic hepatic and renal disease.

Forty patients with chronic hepatic (n = 20) and renal (n = 20) disease were studied randomly for the purpose of evaluating safety and laboratory values. These included alanine and aspartate aminotransferases, alkaline phosphatase, total bilirubin, creatinine, and blood urea nitrogen. Patients with hepatic disease received either desflurane (n = 9) or isoflurane (n = 11) and patients with renal disease received the two anesthetics in equal subsets. In the patients with hepatic and renal disease, there were no differences in laboratory values (P < 0.05). We conclude that, in patients with either hepatic or renal disease, laboratory values from pre- to postoperative state did not change significantly within 24 h of anesthesia, and no differences in these changes existed between desflurane or isoflurane.

The molecular basis for the two different clinical presentations of classical pyruvate carboxylase deficiency.

Eight cases of isolated human pyruvate carboxylase deficiency were examined from seven families. Although all patients presented with a chronic lacticacidemia, two particular patients presented with the added features of hyperammonemia, citrullinemia, and hyperlysinemia. When cultured skin fibroblasts from these patients were examined for their ability to synthesize [3H]biotin-containing proteins, it was found that the two patients who presented with hyperammonemia, citrullinemia, and hyperlysinemia did not synthesise a protein of the correct subunit molecular weight (Mr = 125 K daltons) corresponding to pyruvate carboxylase. In addition, when skin fibroblast proteins were labeled with [35S]methionine, cross-reacting material (CRM) corresponding to pyruvate carboxylase was immunoprecipitated by antipyruvate carboxylase antiserum in most patients, but again the two patients with the atypical presentation showed no CRM. We propose that the different clinical presentation of human pyruvate carboxylase deficiency is a manifestation of two different mutations in the pyruvate carboxylase gene, one that results in the synthesis of a relatively inactive pyruvate carboxylase protein CRM(+ve) and one that results in the lack of expression of the gene in the form of a recognizable protein CRM(-ve).

Variant maple syrup urine disease in mother and daughter.

Intermittent MSUD in a mother and her daughter is reported. Fibroblast cultures were studied for branched-chain keto acid decarboxylase and results show that the mother has approximately 12% while the daughter has 5% of the normal enzyme activity. Other key members in the family were also studied for enzyme activity. It appears that the child has inherited an abnormal gene from her homozygous mother and another abnormal gene from her heterozygous father.A classification based on the degree of residual enzyme activity and protein tolerance places the mother in grade III and the daughter in grade II category. Classical MSUD, where the enzyme activity is less than 2% of normal, belongs to grade I.