Perioperative specific management of blood volume loss in craniosynostosis surgery

Accurate assessment and replacement of blood loss and fluid–electrolyte deficit during craniosynostosis repair is difficult owing to patient size and the diversity of surgical technique. Forty-three patients undergoing primary craniosynostosis repair over a 10-year period were studied retrospectively to determine blood loss and fluid deficit and to assess blood transfusion practices during both intraoperative and postoperative periods. Blood loss was calculated on the basis of estimated red cell mass (ERCM) and fluid-electrolyte imbalance was investigated with blood samplings. Blood transfusion was considered appropriate if the postoperative or posttransfusion ERCM was within 12% of the preoperative value. Estimated fluid requirement (EFR) was used in 4 ml kg^–1 h^–1 except for neonates. Intraoperatively, 80% of all patients were appropriately managed with respect to blood transfusion and EFR. Postoperatively only 20% of the patients receiving transfusions were transfused appropriately. In 23.3% of these patients (10/43) unexpected respiratory distress developed immediately after their recovery from the anesthesia. With the measurement of estimated blood volume and allowable blood loss, appropriate transfusion could be achieved for the successful treatment of the primary craniosynostosis. Received: 16 February 1998     

Ultrasensitive analysis of the intestinal absorption and compartmentalization of aluminium in uraemic rats: a 26Al tracer study employing accelerator mass spectrometry

BACKGROUND: Developments in accelerator mass spectrometry (AMS) now permit the determination of femtogram amounts of 26Al in blood and in various tissues with good precision and free of external contamination. METHODS: In the present study we used trace quantities of 26Al to investigate the intestinal absorption and compartmentalization of aluminium in rats with renal failure (Nx, 5/6 nephrectomy) and in pair- fed controls (C). Single oral doses of 20 ng 26Al were administered to six animals in each group and, subsequently, 24-h post-load 26Al was analysed in serum, urine, bone, liver, and spleen by means of AMS. RESULTS: Serum concentrations of 26Al were significantly lower in uraemic rats compared to controls, whereas urinary excretion was comparable (Nx, 7.11 +/- 5.78 pg/day vs C, 9.46 +/- 6.10 pg/day), suggesting a higher fraction of ultrafiltrable serum 26Al in uraemia. The target tissues of cellular transferrin-mediated 26Al uptake, liver and spleen, tended to show a larger degree of aluminium accumulation in controls (0.26 +/- 0.31 pg/g vs Nx, 0.14 +/- 0.10 pg/g and 0.37 +/- 0.27 pg/g vs Nx, 0.25 +/- 0.27 pg/g respectively). In contrast, in bone, a site of extracellular aluminium deposition, 26Al concentrations were more elevated in uraemia (1.22 +/- 0.59 pg/g vs C: 0.68 +/- 0.30 pg/g). Estimated total 26Al accumulation in all measured target tissues was significantly higher in uraemic rats (28.15 +/- 9.90 pg vs C: 17.03 +/- 7.03 pg) and total recovery of 26Al from tissue and urine was 26.58 +/- 6.74 pg in controls and 35.75 +/- 7.03 pg in uraemic animals, suggesting a fractional absorption of 0.133% and 0.175% respectively. CONCLUSIONS: Our data suggest that fractional absorption from a dietary level dose of 26Al is about 0.13%. Compartmentalization occurs in transferrin-dependent target tissues such as liver and spleen; however, in quantitative terms extracellular deposition in bone is more important. Uraemia has a significant effect on the intestinal absorption and compartmentalization of aluminium. It enhances fractional absorption and increases subsequent extracellular deposition of aluminium in bone. However, at the same time uraemia does not increase transferrin-dependent cellular accumulation of aluminium in liver and spleen.      

Ischemic necrosis of the entire femoral head and rapidly destructive hip disease: potential causative relationship

 Objective. Rapidly destructive hip disease (RDHD) is an uncommon disorder of the hip that has been considered a disease of unknown cause and distinct from ischemic necrosis of the femoral head. The objective of this study was to investigate ischemic necrosis of the femoral head as one potential cause of RDHD. Design and patients. In 600 patients who underwent MR imaging of the hip, 20 cases of ischemic necrosis involving the entire femoral head in 18 patients (3%) were retrospectively studied with routine radiography and MR imaging. All patients had surgically confirmed ischemic necrosis of the femoral head. Results and conclusions. All patients showed rapid destruction of the femoral head on routine radiography and MR imaging as compared with the gradual onset of clinical symptoms. Plain radiographs showed several bone fragments at the inferomedial aspect of the femoral head (75%), acetabular erosions (55%), eccentric depression at the lateral articular surface of the femoral head conforming to the adjacent acetabulum (35%), and mild osteoarthritis (15%). Bone sclerosis was often present at sites of impaction between the femoral head and the acetabulum. MR imaging showed marked distention of the joint capsule in all cases. In 14 of 20 cases, the contents of the joint space showed predominantly low or intermediate signal intensity on T1- and T2-weighted images. Ischemic necrosis involving the entire femoral head may represent one of the causes of RDHD.     

Substance P augments a persistent slow inward calcium-sensitive current in voltage-clamped spinal dorsal horn neurons of the rat

Rat spinal dorsal horn neurons in slice preparations perfused with Ringer solution containing 0.5-1 microM TTX and/or 10-20 mM tetraethylammonium at 29 degrees C, were studied by using a single microelectrode voltage-clamp technique. Slow persistent inward currents were recorded during depolarizing voltage commands to membrane potentials positive to about -40 mV. The inward current was depressed by removing external Ca, or by adding 0.1-0.2 mM Cd, 5 mM Co or 0.1 mM verapamil, and was increased by adding Ba or Bay-K 8644. Substance P (SP) augmented a persistent slow inward Ca-sensitive current in a dose-dependent manner. It is suggested that this effect may be instrumental in generating the SP-evoked slow depolarization, increase in membrane excitability, and the 'bursting' behavior in the immature rat dorsal horn neurons. In addition, in some neurons SP reduced the M-like current, which effect may contribute to, but not explain, generation of the SP-induced slow depolarization.