An increased body mass index is no risk factor for postoperative nausea and vomiting. A systematic review and results of original data.

BACKGROUND: An increased Body Mass Index (BMI) is almost always mentioned as a fundamental risk factor for postoperative nausea (PN), vomiting (PV) or both (PONV). However, multivariate analyses were unable to detect any correlation. Therefore, we asked whether an increased BMI is really a risk factor for PONV. METHODS: For the systematic review, a search of electronic databases and a detailed manual search of reviews were carried out. For the analysis of the original data, 587 adult patients from a randomised controlled antiemetic trial (RCT) who underwent general anaesthesia were allocated to four weight groups: Underweight (BMI < 20), Normal Weight (BMI 20-25), Overweight (BMI 25-30) and Obesity (BMI > or = 30). RESULTS: Four publications with original data were found. Two described a positive relationship, although not clearly supported by the data. Despite this, most narrative reviews claimed a positive correlation between obesity and PONV by quoting again narrative reviews or misquoting originals. In the RCT, the calculated underlying risk profile for PONV was comparable between all groups. Incidences (95% confidence intervals) of PONV were 45.8% (34.0; 57.6), 41.7 (36.5; 46.9), 47.8 (38.4; 57.1) and 44.1 (31.0; 57.1), for the groups Underweight, Normal Weight, Overweight and Obesity, respectively (P=0.69). The incidences of PN and PV also did not differ with P=0.76 and P=0.36, respectively. CONCLUSION: Systematic search of the literature provides no evidence for a positive relationship. Furthermore, our data confirm that an increased BMI is not a risk factor for PONV. This negative finding is important as focussing on the relevant risk factors is needed to allow for an objective risk assessment of PONV.

Preliminary report: analgesia with Remifentanil for complicated eye muscle surgery.

The authors report a new anesthetic technique that is especially suitable for the surgery of complicated disorders of ocular motility. Analgesia is achieved by an intravenous dose of Remifentanil, an opioid that is normally used together with propophol as a form of total intravenous anesthesia (TIVA) for general anesthesia. The advantage of Remifentanil is a rapid increase (1-2 min.) and decrease (3-4 min.) of the effect. Eye muscle surgery can then be performed on a patient who is free of pain and slightly sedated. After the planned eye muscle surgery, while the patient is still under anesthesia, the muscle sutures are tied provisionally. Afterwards, the squint angle can be measured with a cover test and the patient is questioned about the presence of diplopia. If the position of the eye is not satisfactory, the knots can be loosened and the muscle can be fixated in another position.

Discordance, in a malignant hyperthermia pedigree, between in vitro contracture-test phenotypes and haplotypes for the MHS1 region on chromosome 19q12-13.2, comprising the C1840T transition in the RYR1 gene.

A point mutation in the gene encoding the skeletal muscle calcium release channel (RYR1) has been proposed as the probable cause of malignant hyperthermia (MH) in swine, where it segregates with the disease in all MH-prone strains investigated. The same C-to-T exchange in nucleotide position 1840 of the human RYR1 cDNA sequence was found in a few human MH pedigrees. We report a German MH pedigree where in vitro contracture test (IVCT) results and haplotypes of markers for the MHS1/RYR1 region including this base transition have yielded several discrepancies. The MH-susceptible phenotype was defined by IVCT performed according to the European standard protocol. Haplotypes were constructed for markers for the MHS1/RYR1 region on chromosome 19 and include the C1840T base exchange. Discussing the probabilities for a number of hypotheses to explain these data, we suggest that our results may challenge the causative role of this mutation--and possibly the role of the RYR1 gene itself--in human MH susceptibility, at least in some cases.

DNA aneuploidy and proliferation in spontaneous human and dimethylhydrazine-induced murine colorectal carcinogenesis.

DNA aneuploidy and proliferative abnormalities were studied by flow cytometry in 169 colorectal specimens from 162 patients. Of 37 adenomas, three showed aneuploidy and another seventeen revealed a "near diploid" DNA pattern. The rate of aneuploid and "near diploid" DNA changes in 92 carcinomas was 53.3% and 23.9%, respectively. No correlation was seen between the ploidy distribution and the stage or histologic grade of the carcinomas. The S-phase fractions of both adenomas and carcinomas significantly increased from the diploid (8.1 +/- 0.8% and 7.8 +/- 0.9% respectively; mean +/- SEM) to the "near diploid" (14.9 +/- 1.2% and 12.6 +/- 1.5%) and aneuploid (20.4 +/- 1.3% and 11.4 +/- 1.6%) lesions. To better understand neoplastic progression at very early stages, flow cytometry was also performed on 195 colonic specimens of 44 rats treated by weekly subcutaneous injections of 21 mg/kg Dimethylhydrazine. There was a single "near diploid" carcinoma in this group, and all other induced neoplasms (39 carcinomas and 27 adenomas) revealed a diploid DNA pattern. The S-phase fractions were as follows: controls (38 untreated animals) 8.6 +/- 0.1%, normal mucosa (of Dimethylhydrazine exposed rats) 10.1 +/- 0.25% (p less than 0.0001), adenomas 13.9 +/- 0.6% (p less than 0.01), and carcinomas 14.7 +/- 0.6% (p less than 0.01). These findings support the conclusion that genomic alterations and proliferative abnormalities may already be present in premalignant human colonic lesions. However, despite strong morphological similarities, major biological differences exist between the Dimethylhydrazine-induced murine intestinal carcinogenesis and spontaneously occurring human colorectal neoplasms.