Preemptive diclofenac reduces morphine use after remifentanil-based anaesthesia for tonsillectomy

BACKGROUND: We investigated the effect of preincisional rectal diclofenac on pain scores and postoperative morphine requirements of children undergoing tonsillectomy after remifentanil-propofol anaesthesia in a randomized clinical trial. METHODS: Induction and maintenance of anaesthesia were with remifentanil and propofol. Forty children were randomly assigned into two groups before incision. The diclofenac group (n=20) received diclofenac suppositories (approximately 1 mg x kg(-1)) and the control group (n=20) received no treatment. Following discontinuation of remifentanil, patient-controlled analgesia (PCA) with morphine (a loading dose 50 micro g x kg(-1), a background infusion 4 micro g x kg(-1) x h(-1) and a demand dose 20 micro g x kg(-1) with 5-min intervals) was started. We assessed pain score [verbal analogue scales (VAS), 0-10] and sedation level at 5-min intervals and recorded the total morphine consumption of the first hour in the PACU. Patients were discharged to the ward with a new PCA morphine programme (a demand dose 20 micro g.kg-1 with a lockout time of 30 min, for 4 h), and total morphine consumption was recorded. RESULTS: The mean VAS score of the diclofenac group was significantly lower than the control group on arrival in the PACU (2.85 +/- 0.77, 7.60 +/- 0.83, respectively, P < 0.01) and it remained significantly lower in the PACU stay of the children. The mean total morphine consumption of the diclofenac group was less than the control group in the PACU (130.33 +/- 11.26 and 169.92 +/- 9.22, respectively, P=0.012) and the ward (50.80 +/- 11.38 and 87.77 +/- 10.55, respectively, P=0.021). CONCLUSIONS: Preemptive diclofenac given rectally reduced pain intensity and morphine requirements of children anaesthetized with remifentanil for tonsillectomy.     

Syncope as a first sign of seizure disorder

We studied the long-term follow-up of patients with the diagnosis of "syncope of unknown origin," and their progression to epilepsy to gain a better understanding of the relationship between syncope and epilepsy, and to determine whether findings of the first syncopal attack have prognostic significance in relationship to the onset of epilepsy or not. Eighteen patients with the diagnosis of syncope of unknown origin were evaluated for the possibility of becoming epileptic during a 4-year period, and four patients showed characteristic seizure disorder. There were no clinical or laboratory features that differentiated them from the nonepileptic group, except that they were all girls. The interval between the first syncopal attack and the typical epileptic seizure ranged between 7 and 19 months. Syncope of unknown origin could be the first sign of an epileptic disorder, especially in girls. Long-term follow-up extending up to 1 year is necessary to disclose the risk of becoming epileptic.     

Possible anatomic structures causing entrapment neuropathies of the median nerve: an anatomic study

This study aimed at identifying the anatomic structures which may be responsible for entrapment neuropathies of the median nerve. Thirty upper extremities of 15 formalin fixed adult cadavers were dissected from the axilla to the distal forearm under Zeiss Opmi 9--FC microscope. We encountered seven different anatomic structures that may compress the median nerve. These structures are the brachialis muscle, Struther's ligament, the bicipital aponeurosis, pronator teres, flexor digitorum superficialis, the accessory head of plexor pollicis longus (Gantzer's muscle) and vascular structures. The supracondylar process, which we did not encounter in our dissection, has been reported as another cause. Based on our dissection findings and on literature, the median nerve can be compressed by seven different structures from the axilla to the distal forearm. Knowledge of the course of the median nerve and its relations with the adjacent anatomic structures facilitates determination of the exact cause of entrapment and allows for a safe surgery.     

Expression of Fas, Bcl-2 and p53 molecules in glomerulonephritis and their correlations with clinical and laboratory findings

BACKGROUND AND AIM: Apoptosis plays a crucial role in glomerulonephritis (GN) as a regulatory mechanism and is controlled by various molecules including Fas antigen, Bcl-2 and p53 oncoproteins. The aim of the present study is to evaluate the correlation between the expression of these molecules and clinical and laboratory data in different types of GN. RESULTS: The expression of Fas antigen, Bcl-2 and p53 protein in five normal human kidney specimens and 55 tissues from patients with several types of GN were examined by immunohistochemistry and correlated with clinical and laboratory findings. The number of Fas-positive intraglomerular cells was significantly increased in proliferative GN when compared with non-proliferative cases. Numbers of Bcl-2- and p53-positive cells in proliferative GN were not different from the non-proliferative cases and there was no correlation between the changes in Fas, Bcl-2 and p53 themselves. Significant correlation of expression of these molecules with clinical and laboratory findings was not found, except between p53 and blood urea nitrogen levels. CONCLUSION: Apoptosis is a complex molecular process and the results of the present study should be supported with other methods to understand whether apoptosis contributes to progression or resolution of GN. Increased glomerular expression of Fas, Bcl-2 and p53 molecules in all types of GN might contribute new therapeutic approaches by modulating the expression of these molecules.     

Glycosaminoglycan excretion in children with nephrotic syndrome

Although most childhood nephrotic syndromes respond to steroid treatment, steroid resistant nephrotic syndrome (SRNS) is also common and is particularly difficult to treat. This study investigated the role of glycosaminoglycans (GAG) in the pathogenesis and clinical course of nephrotic syndrome in children. Thirty-four children (21 males and 13 females, mean age 3.7±1.6 years) with steroid-sensitive nephrotic syndrome and 20 children with steroid-resistant nephrotic syndrome (12 males and 8 females, mean age 10.9±3.8 years; of the twenty, four had primary SRNS (FSGS) and the others had secondary SRNS) were included the study. Mean urine levels of GAG relative to creatinine (U_GAG/U_Cr) in patients with SRNS (n=20, 113.01±78.46 mg g^–1 Cr) and in patients experiencing the nephrotic period of steroid-sensitive nephrotic syndrome (n=34, 132.15±101.55 mg g^–1 Cr) were both significantly higher than mean U_GAG/U_Cr for control subjects (n=30, 51.83±47.66 mg g^–1 Cr) (P<0.01 for both). Patients excreted significantly more GAG during the nephrotic period of steroid-sensitive nephrotic syndrome than during remission (132.15±101.55 vs 39.11±42.73 mg g^–1 Cr, respectively; P<0.01). There was, however, no significant difference between U_GAG/U_Cr for patients with steroid-resistant nephrotic syndrome and U_GAG/U_Cr in the nephrotic period of steroid-sensitive nephrotic syndrome. Urine GAG excretion correlated significantly with the severity of proteinuria. The results suggest that GAG play a significant role in the pathogenesis of nephrotic syndrome but that GAG excretion is not a marker for response to steroid treatment in pediatric patients with this condition.     

Mitral annular calcification and brown tumor of the rib in a child with chronic renal failure

Mitral annular calcification and liquefaction necrosis of this lesion mimicking intracardiac tumor because of secondary hyperparathyriodism have been described in adult patients with chronic renal failure, but have not been reported in children. Chronic renal failure is one of the predisposing factors of this condition. We report the case of a 13-year-old patient with continuous ambulatory peritoneal dialysis with severe hyperparathyroidism who was found to have intracardiac and rib lesions considered to be brown tumors.     

Incidence of nocturnal enuresis and nocturia in children with tuberculosis

Nocturnal enuresis is a common problem and occurs in 15 to 20 percent of 5-year-old children. The etiology of nocturnal enuresis remains unknown and is probably multifactorial. In this study 52 children aged between 6-17 years with tuberculosis were questioned for nocturia and nocturnal enuresis, retrospectively. Nocturnal, enuresis was found in 12 (23%) and nocturia in 22 (42%) of the children, respectively. After specific treatment with antituberculosis drugs nocturnal enuresis and nocturia were improved in 5 and 21 children, respectively. However, it could not be explained why these disorders were much higher in children with tuberculosis than healthy children. The findings suggest that nocturnal enuresis and nocturia may be in a high frequency in children with tuberculosis; however, the authors think that prospective and more extensive studies should be performed to clarify these preliminary findings.     

Nitric oxide involvement in seizures elicited by pentylentetrazol and sex dependence

It has been known that susceptibility to some types of epilepsy is affected by sex. In addition, the role of NO in epileptogenesis is still unclear; NO has been suggested to be either an anticonvulsive or a proconvulsive agent. In an attempt to elucidate both the role of NO and sex differences in sensitivity to seizures, male and female Wistar rats were treated intraperitoneally (i.p.) by pentylentetrazol (PTZ)(80 mg/kg) and by a nitric oxide synthase(NOS) inhibitor N-omega-nitro-L-arginine-mthylester(L-NAME)(50mg/kg) and a NO precursor sodium-nitroprusside(SNP)(2.5mg/kg)- applied 15 min. before PTZ injection. Latency, frequency, severity, and duration of generalized clonic and clonic-tonic convulsions were recorded. Furthermore, alterations in severity, latency, frequency, and duration of convulsions were observed to correlate with NO. Both sexes, injected with PTZ, showed repetitive seizure patterns. Seizures were found to be more severe in females. L-NAME and SNP pretreatment produced paradoxical effects on PTZ-induced seizures in both sexes. L-NAME completely prevented PTZ-induced seizures in male rats, whereas increased severity, frequency, duration, and significantly shortened the latency in female rats. Unexpectedly, SNP increased convulsion severity, frequency, duration, and shortened latencies in male, whereas it decreased convulsion severity, frequency, and duration and prolonged latency in females. These results indicate that endogenous NO is involved in the regulation of convulsive action suggesting a role depending on sex.