Ketoprofen and tramadol for analgesia during early recovery after tonsillectomy in children.

BACKGROUND: Pain following tonsillectomy is often intense. Nonsteroidal anti-inflammatory drugs and opioids are effective, but both can cause adverse effects. Tramadol may be a viable alternative for post-tonsillectomy pain. This study was designed to compare the analgesic effects of ketoprofen and tramadol during the early recovery period after tonsillectomy. METHODS: Forty-five ASA class I children (9-15 years) were randomized to receive either saline, ketoprofen (2 mg.kg(-1)) or tramadol (1 mg.kg(-1)) after induction of anesthesia. Upon completion of surgery, the study treatment was continued as a 6 h intravenous (i.v.) infusion of another dose of saline, ketoprofen (2 mg.kg(-1)) or tramadol (1 mg.kg(-1)). Postoperatively, each patient received rescue analgesia with patient-controlled analgesia (PCA) device programmed to deliver 0.5 microg.kg(-1) bolus doses of fentanyl. Postoperative pain was assessed using Visual Analog Scale (VAS) during swallowing. Intraoperative blood loss was measured. RESULTS: The total number of requests of PCA-fentanyl was significantly less in ketoprofen group compared with tramadol and placebo groups (P = 0.035 and P = 0.049, respectively, in pairwise comparisons) and the VAS scores for pain were significantly lower in ketoprofen group compared with tramadol (P = 0.044) or placebo groups (P = 0.018) during the first six postoperative hours. Measured intraoperative blood loss was greater in ketoprofen-treated patients than in those receiving placebo (P = 0.029). CONCLUSION: A dose of 4 mg.kg(-1) of i.v. ketoprofen provided good pain relief with moderate supplemental PCA-fentanyl requirements during the first six postoperative hours after tonsillectomy in children whereas the effects of 2 mg.kg(-1) of i.v. tramadol did not differ from those of placebo.

Craniofacial features in osteogenesis imperfecta: a cephalometric study.

Osteogenesis imperfecta (OI) is a heterogeneous group of connective tissue diseases that mainly manifest as bone fragility and skeletal deformity. In most families it segregates as a dominant trait and results from mutations in type I collagen genes. In this study we analyzed the size and form of the bony structures in heads of 59 consecutive patients with OI types I, III, or IV (Sillence classification), using lateral radiographs. Paired controls were matched for gender and age. The purpose was to obtain baseline information of craniofacial development in OI patients that have not received bisphosphonate treatment. In OI type I we found smaller than normal linear measurements, indicating a general growth deficiency, but no remarkable craniofacial deformity. In OI types III and IV, the growth impairment was pronounced, and the craniofacial form was altered as a result of differential growth deficiency and bending of the skeletal head structures. We found strong support both for an abnormally ventral position of the sella region due to bending of the cranial base, and for a closing mandibular growth rotation. Vertical underdevelopment of the dentoalveolar structures and the condylar process were identified as the main reasons for the relative mandibular prognathism in OI. Despite of the widespread intervention with bisphosphonates, the facial growth impairment will probably remain characteristic for many OI patients, and their orthodontic treatment should be further developed.

Lack of correlation between the type of COL1A1 or COL1A2 mutation and hearing loss in osteogenesis imperfecta patients.

Osteogenesis imperfecta (OI) is caused by mutations in COL1A1 and COL1A2 that code for the alpha1 and alpha2 chains of type I collagen. Phenotypes correlate with the mutation types in that COL1A1 null mutations lead to OI type I, and structural mutations in alpha1(I) or alpha2(I) lead to more severe OI types (II-IV). However, correlative analysis between mutation types and OI associated hearing loss has not been previously performed. A total of 54 Finnish OI patients with previously diagnosed hearing loss or age 35 or more years were analyzed here for mutations in COL1A1 or COL1A2. Altogether 49 mutations were identified, of which 41 were novel. The 49 mutations represented the molecular genetic background of 41.1% of the Finnish OI population. A total of 38 mutations were in COL1A1 and 11 were in COL1A2. Of these, 16 were glycine substitutions and 16 were splicing mutations in alpha1(I) or alpha2(I). In addition, 17 null allele mutations were detected in COL1A1. A total of 32 patients (65.3%) with a mutation had hearing loss. That is slightly more than in our previous population study on Finnish adults with OI (57.9%). The association between the mutation types and OI type was statistically evident. Patients with COL1A1 mutations more frequently had blue scleras than those with COL1A2 mutations. In addition, patients with COL1A2 mutations tended to be shorter than those with COL1A1 mutations. However, no correlation was found between the mutated gene or mutation type and hearing pattern. These results suggest that the basis of hearing loss in OI is complex, and it is a result of multifactorial, still unknown genetic effects.

Stapes surgery in osteogenesis imperfecta in Finland.

We present the surgical findings and audiometric results of ear surgery performed between 1961 and 2002 on 33 Finnish patients (43 operations) with osteogenesis imperfecta (OI). The mean age at the time of the first operation was 30.1 years. The typical surgical findings were a thick, fixed, or obliterated footplate, thick and vascular mucosa with an excessive tendency to bleed, and elastic, fractured, or atrophic stapes crura. As compared with previous studies, the hearing gain was poorer and the remaining postoperative gap was greater for the 43 operations analyzed. The results of this nationwide study, however, may not be directly comparable with operative results of non-population studies. On the other hand, the hearing gain in our study was better in university hospitals than in central hospitals and, furthermore, was comparable with that of previous studies after surgery performed by a single surgeon in a university hospital. Conductive hearing loss related to OI may be successfully treated with surgery in most patients. The rarity of the disease, leading to small annual numbers of operations, the variable surgical findings, and the profuse bleeding tendency of the middle ear, as well as the audiometric results in this study, support centralization of ear surgery in OI patients.

Hearing loss in Finnish adults with osteogenesis imperfecta: a nationwide survey.

Hearing loss, bone fragility, and blue sclerae are the principal clinical features in osteogenesis imperfecta (OI), a genetic disorder of connective tissue. In a nationwide search, an audiometric evaluation of 133 adult patients was performed. According to the criteria introduced by Sillence, type I was the most common form of OI. Of the patients with normal hearing on audiometry, 17.1% reported subjective hearing loss, and 19.1% of the patients with impaired hearing did not recognize it. On audiometry, 57.9% of the patients had hearing loss, which was progressive, often of mixed type, and mostly bilateral, and began in the second to fourth decades of life. The frequency or severity of the hearing loss was not correlated with any other clinical features of OI. Hearing loss is common, affecting patients with all types of OI. Subjective misjudgment of hearing ability supports the need for repeated audiometry in all OI patients. A baseline study at the age of OI years followed by audiograms every third year thereafter is recommended.