A Simple Surgical Technique for Correction of Macrotia with Poorly Defined Helical Fold

Macrotia is a relatively rare auricular deformity and few techniques for treatment have been described, most of which include skin and cartilage excisions. Effacement of the helical fold may accompany this deformity and should be reconstructed for aesthetic integrity. The authors present their ear reduction technique that achieves ear reduction and helical fold reconstruction through a posterior approach. The method is a simple procedure performed by incising and overlapping the cartilage and should be indicated for selected mild macrotia cases.     

Delayed traumatic intracerebral hematoma.

Although delayed traumatic intracerebral hematomas (DTICHs) have been frequently reported since 1970, the time interval from trauma to hemorrhage and diagnosis has not been well defined. Eight patients with DITCH were found among 1,320 head-injured patients admitted to the neurosurgical service through the emergency department from March 1989 to March 1990. The mean time interval between initial and follow-up CT scan was 22 h. The mean time interval between initial trauma and diagnosis of DITCH was 24 h. One patient was diagnosed incidentally by magnetic resonance imaging. Three patients underwent operation and five patients were managed conservatively. Three patients died, resulting in a case mortality rate of 37.5%. The time interval for DTICHs' development and pitfalls in its diagnosis were discussed.     

Comparison of tacrolimus and cyclosporin in renal transplantation by the protocol biopsies

Acute and chronic lesion scores on renal allograft protocol biopsies may predict long-term graft function. The aim of this study was to compare the effects of tacrolimus (Tac) and cyclosporine microemulsion (CsA) based immunosuppressive protocols using protocol biopsies from well-functioning renal allografts. 35 consecutive renal transplant patients were randomized to Tac (n: 17) versus CsA (n: 18) treatment arms. Patient age and sex, donor type and age, histocompatibility, cold ischemia time and prior delayed graft function were similar between the two groups. Treatment protocol consisted of prednisolone, azathioprine and Tac or CsA. Biopsies performed on the third, sixth and twelfth months were blindly evaluated by the same pathologist. The incidences of acute rejection (AR) episodes among CsA vs Tac groups were 33% vs 29%, respectively (NS). The Creatinine level was lower in Tac than CsA, although it was not significant (Table). Subclinical AR and subclinical chronic allograft nephropathy were detected on protocol biopsies in 3 (2 CsA, 1 Tac) and 12 (7 CsA, 5 Tac) patients, respectively. Acute lesion score at the third month PBx was significantly lower in the Tac group (p < 0.05). Chronic lesion scores in all biopsies were lower in the Tac group, although not significantly. The protocol biopsy findings suggest that graft injury may be less pronounced among the Tac group.     

Papilledema associated with dialysis disequilibrium syndrome

The purpose of this paper is to report a case of dialysis disequilibrium syndrome as an unusual cause of papilledema. A 38-year-old woman with type 1 diabetes mellitus presented with decreased visual acuity and bilateral optic nerve swelling associated with systemic signs and symptoms of dialysis disequilibrium syndrome. Repeated lumbar punctures revealed elevated intracranial pressures. She was placed on acetazolamide with some improvement in symptoms. After renal transplantation, the patient had complete resolution of headaches, nausea and the papilledema. Our conclusion is that patients with visual disturbance and focal neurological symptoms during and after hemodialysis should be suspected of having dialysis disequilibrium syndrome (DDS). DDS is thought to occur as a result of a rapid reduction in plasma osmolality during dialysis. As the shift of urea from cerebral spinal fluid (CSF) is delayed, the relative increase in CSF osmolality draws fluid into the brain. The ensuing cerebral edema is responsible for the characteristic neurological symptoms. We report the association of papilledema with this syndrome, and caution as to the possible concurrent risk of permanent visual impairment.     

Oral cyclic megadose methylprednisolone therapy for chronic immune thrombocytopenic purpura in childhood

The objectives of this study were to investigate the effectiveness of oral megadose methylprednisolone (OMMP) therapy in children with chronic immune thrombocytopenic purpura (ITP). Twenty-two patients were given oral methylprednisolone daily for 7 d (30 mg/kg for 3 d and then 20 mg/kg for 4 d). OMMP therapy was repeated once per month if the platelet count was less than 20,000/mm3 at the 30th day of therapy, for up to six courses. The number of platelets of all patients increased gradually during the OMMP therapy, with a peak number at the 7th day, then decreased until the 14th day, and remained relatively stable until 12 months. During the study no patient had a platelet count less than 20,000/mm3 at the 3rd day and 50,000/mm3 at the 7th day. Although the number of platelets was gradually decreased between the 7th and 14th days, it remained above 100,000/mm3 for at least 12 months in the nine patients, and above 20,000/mm3 in the four patients. None of these 13 patients required hospitalization or therapy during the follow-up period. All of the patients tolerated the medication well. None of them reported side-effects that were severe enough to discontinue therapy. We conclude that OMMP therapy is a safe, easy and effective therapy in children with refractory chronic ITP, and it may provide long-term remission in about two thirds of the patients.     

Neuronal Apoptosis in an in Vitro Model of Photochemically Induced Oxidative Stress

In neurons, oxidative stress can be triggered by neurotransmitter-linked mechanisms and may lead to apoptotic cell death. A simple and reproducible model of inducing oxidative stress is needed to elucidate mechanisms which link oxidative stress and neuronal apoptosis. We report here a method of inducing apoptosis in cell cultures by loading them with a photosensitive dye, rose bengal, and exposing the cultures to light, a procedure which generates reactive singlet oxygen. We used this model in primary culture of rat cerebellar granule neurons, and in a nonneuronal human embryonic kidney 293 cell line. We have measured the following: (a) metabolic activity of the mitochondria by quantitative staining with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), (b) DNA fragmentation by quantitative in situ terminal deoxynucleotidyl transferase assay, and (c) cell viability by a trypan blue exclusion test. The oxidative stress caused an early impairment of mitochondrial function (MTT assay). This was followed by DNA fragmentation and ultimately by cell death. Protection was obtained with an inhibitor of macromolecular synthesis, anisomycin, and with antioxidant, vitamin E. This model can be used to study the mechanism of oxidative stress-triggered neuronal apoptosis, and it may help in discovering new targets for neuroprotective drugs.