The effect of large-dose intrathecal opioids on the autonomic nervous system

Decreases in blood pressure after the spinal injection of opioids suggest that intrathecal (IT) opioids may have a sympatholytic effect similar to that of local anesthetic drugs. We compared two groups of patients aged 10-16 yr (n = 10 in each group). Group One (IT group) received IT opioids. Group Two (Epidural group) received 0.5% bupivacaine epidurally. The sympathetic effects of IT opioids and epidural bupivacaine were monitored by the changes in toe relative to calf temperature and by the changes in pulse wave gradients with digital plethysmography. Changes in temperature gradients comparing calf to toe and increases in pulse amplitude indicate vasodilatation caused by sympathetic blockade in this model. Calf to toe temperature gradients (Deltacalf-Deltatoe) were evaluated by subtracting the two measurements. Pulse wave plethysmography was recorded before and after spinal and epidural injection at intervals of 10 min for 40 min. All patients demonstrated changes in their calf to toe gradients after IT and epidural injections (-3.2 +/- 1.6). Systolic blood pressure decreased from a mean of 70 +/- 15 mm Hg to 55 +/- 10 mm Hg. Pulse wave plethysmography amplitude increased after the intrathecal opioid and epidural bupivacaine injection similarly. We conclude that the increases in pulse wave amplitude and decreases in calf-toe gradients indicate a sympatholytic effect after IT opioids similar to that of local anesthetics. IMPLICATIONS: The sympatholytic effects of neuraxial opioids were compared with those of local anesthetics. Two groups of patients were assigned to receive a neuraxial opioid or bupivacaine. Our results demonstrate that opioids cause hypotension and peripheral vasodilatation similar to bupivacaine. This finding suggests that neuraxial opioids have a sympatholytic effect comparable to that of local anesthetic drugs.     

Prolapse of intussusceptum through a perforated intussuscipiens

Two patients with prolapse of an intususceptum through a perforation in the intussuscipiens are described. There was little peritonitis at exploration. Prolapse of an intussusceptum is an occasional operative finding in patients with perforated intussusception.     

Psoas abscess: drainage through Petit's triangle

Thirteen cases of psoas abscess were treated by surgical drainage through Petit's triangle. This underutilized anatomic space provides a simple and effective route for drainage of retroperitoneal abscesses. Correspondence to: K. L. N. Rao     

Megacystis microcolon intestinal hypoperistalsis syndrome

Megacystis microcolon intestinal hypoperistalsis syndrome (MMIHS) is a rare cause of intestinal obstruction mainly affecting female neonates. We present a case of a newborn female infant with a history of abdominal distension, bilious vomiting and decreased urine output. Barium enema showed a microcolon. Patient died soon after admission and the autopsy revealed a shortened bowel, a microcolon with abundant ganglion cells in the myenteric plexus, and an enlarged urinary bladder. An interesting finding in this case was the presence of enlarged nerve bundles containing several large ganglion cells on the lateral wall of the cervix. The salient clinical and autopsy findings in this case are presented.     

ACUTE EFFECTS OF ORAL GLIBENCLAMIDE ON BLOOD PRESSURE AND FOREARM VASCULAR RESISTANCE IN DIABETICS

1. To determine the effects of an acute oral dose of glibenclamide on blood pressure (BP), basal forearm vascular resistance (FVR) and FVR responses to the K⁺atp channel activating vasodilator diazoxide, a placebo-controlled, double-blind cross-over study was performed in eight male volunteers with non-insulin-dependent diabetes mellitus. 2. Changes in vascular responses to progressively increasing concentrations of diazoxide (3.75–30 mg/kg per min) and nor-adrenaline (25–100 ngkg per min) were measured by venous occlusion plethysmography. 3. Glibenclamide significantly lowered plasma glucose levels compared with placebo (P < 0.02) and attenuated the decrease in FVR (P < 0.05) and the decrease in systolic BP (P < 0.05) that followed a meal. However, vasodilator responses to diazoxide were potentiated by the administration of oral glibenclamide (P < 0.01). 4. Acute administration of oral glibenclamide attenuates the normal decrease in FVR and systolic BP that follows a meal and potentiates rather than inhibits forearm vasodilator responses to intra-arterial diazoxide, probably via indirect humoral effects. These results suggest that glibenclamide has direct or indirect vasoconstrictor effects that antagonize the normal increase in forearm blood flow that follows a meal and that the inhibition of vascular K⁺ atp channels following acute oral glibenclamide administration is clinically insignificant compared with other indirect vascular effects of the drug.     

Sirolimus conversion after liver transplantation: improvement in measured glomerular filtration rate after 2 years

METHODS: We reviewed our prospectively maintained database of 2005 liver transplantations. Therapy was either started de novo or converted from calcineurin inhibitors (CNIs) to sirolimus as the main immunosuppressive agent for nephrotoxicity or rejection. Glomerular filtration rate (GFR) was determined with iodine 125-labeled sodium isthalamate (Glofil-125), and serum creatinine concentration was obtained before and 3 months after transplantation, and yearly in both groups. Sirolimus levels were 10 to 15 ng/mL in patients at less than 3 months after transplantations and 5 to 10 ng/mL in the remaining patients. All patients received mycophenolate mofetil as maintenance therapy. RESULTS: Data for 29 patients in the de novo group and 35 in the conversion group were reviewed. Patients in the de novo group demonstrated an acute cellular rejection rate of 17.2%, 40% of which were steroid resistant. In this group, 48.2% discontinuation of sirolimus was necessary because of adverse effects. Patients in the conversion group demonstrated an acute cellular rejection rate of 2.8% and a 34.3% rate of sirolimus discontinuation. Seventeen (56.7%) patients at 1 year and 8 (44.4%) patients at 2 years demonstrated continued improvement in GFR. In the conversion group, case-control analysis did not demonstrate a significant difference in GFR and serum creatinine concentration (P > .05) at 1 and 2 years after conversion. At the time of review, no patients in the conversion group required hemodialysis. CONCLUSIONS: Conversion to sirolimus therapy is an effective strategy in improving renal function in patients with CNI-induced nephrotoxicity and can be done without increased rejection. Most of our patients (65.7%) tolerated sirolimus conversion. Of these, 56.7% and 44.4% demonstrated continued increase in GFR with the CNI-free regimen at 1 and 2 years, respectively. Long-term, large-population, prospective, randomized, controlled studies should further validate these results.     

Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex

Apolipoprotein D (apoD) is elevated in Alzheimer's disease (AD) cortex, localizing to cells, blood vessels, and neuropil deposits (plaques). The role of apoD in AD pathology and the extent of its co-distribution with diffuse (amorphous) and compact (dense fibrillar) amyloid-beta (Abeta) plaques are currently unclear. To address this issue, we combined apoD and Abeta immunohistochemistry with ThioS/X-34 staining of the beta-pleated sheet protein conformation in temporal cortex from 36 AD patients and 12 non-demented controls. ApoD-immunoreactive, Abeta-immunoreactive, and ThioS/X-34-stained plaques were detected exclusively in AD tissue. Dual-immunolabeling showed that 63% of Abeta plaques co-localized apoD. All apoD plaques contained Abeta protein and ThioS/X-34 fluorescence. Compared to controls, AD cases showed elevated vascular and intracellular apoD immunostaining which localized primarily to cells clustered within plaques and around large blood vessels. ApoD-immunoreactive cells within plaques morphologically matched MHC-II- and CD-68-immunoreactive microglia, and did not contain the astrocytic marker GFAP, which labeled a subset of apoD-immunoreactive cells surrounding plaques. These data suggest that neuropil deposits of apoD localize only to a subset of Abeta plaques, which contain compact aggregates of fibrillar Abeta. Elevated apoD in AD brain may influence Abeta aggregation, or facilitate phagocytosis and transport of Abeta fibrils from plaques to cerebral vasculature.