Hemodynamic Response to a Rapid Fluid Challenge in End-Stage Liver Disease / 대한마취과학회지

BACKGROUND: Patients with end-stage liver disease have a hyperdynamic circulatory state complicated by a high right ventricular end-diastolic volume index (RVEDVI) and a low ventricular performance. These changes often make if difficult to evaluate volume status and preload. In this study, we analyzed hemodynamic profiles after a rapid fluid challenge in the recipients of a liver transplant. METHODS: Hemodynamic responses were evaluated before and after 200 ml of a 5% albumin challenge in forty patients, recipients of a liver transplant with a Swan-Ganz right-heart ejection fraction oximetry thermodilution cathether. Patients were divided into two groups, group A (responders, n=12, >or= 10% increase in stroke volume index (SVI) after fluid challenge) and group B (non-responders, n = 28, decrease or < 10% increase in SVI after fluid challenge). We analyzed hemodynamic data obtained from the two groups before and after the fluid challenge. RESULTS: Group B had a lower baseline right ventricular ejection fraction (REF) (49.9+/-5.9% vs 42.8+/-5.7%), a higher RVEDVI (120.8+/-19.4 ml/m2 vs 143.6+/-26.3 ml/m2), and a higher right ventricular end-systolic volume index (RVESVI) (60.8+/-14.0 ml/m2 vs 82.8+/-20.5 ml/m2) than group A. In group B, the cardic index (CI) and right ventricular stroke work index (RVSWI) were not increased after the fluid challenge. There was a mild decrease in the mean arterial pressure (MAP) in group B after the fluid challenge. There was a moderate negative correlation between the fluid-induced change in SVI and the baseline RVEDVI in all patients (r =-0.40, P<0.05). CONCLUSIONS: Our study suggests that there is no improvement of hemodynamic profiles after a rapid fluid challenge in many patients with end-stage liver disease, especially those with a high RVEDVI.

Paraplegia Following Percutaneous Nephrolithotomy under General Anesthesia: A case report / 대한마취과학회지

We present a case of paraplegia, compatible with spinal cord ischemia, following percutaneous nephrolithotomy in a 58-year-old male under the diagnosis of left renal stone. After retroperitoneal operative procedures in the prone position, sensory loss below the level of T4, paraplegia and transient loss of visual acuity were developed. These clinical findings reflect ischemia of the anterior spinal cord with complete motor paralysis and sensory loss to T4 dermatomal level resulting from an anterior spinal artery syndrome. The initial treatment was started with intravenous heparin and corticosteroid. At present, sensory loss is almost recovered and motor deficit is remarkably improved to a level of ambulation with cane. The patient is still treated with oral coumadine and neuromotor rehabilitation. The cause of spinal cord ischemia is unknown, but we speculate ischemia of the spinal cord was associated with embolism and spasm or trauma of feeding artery (ies) of Adamkiewicz.

The Effect of Selective Muscarinic Receptor Antagonists on Antiallodynic Action in a Rat Model of Neuropathic Pain / 대한마취과학회지

BACKGROUND: Peripheral nerve injury may produce a syndrome consisting of spontaneous pain, allodynia and hyperpathia. In previous study, we examined the antiallodynic action produced by intrathecal (i.t.) cholinesterase inhibitors (ChEi) in a neuropathic pain rat model and the reversal of antiallodynic state by i.t. atropine, muscarinic antagonist, but not by nicotinic antagonist mecamylamine. The purpose of this study was to determine the selective antagonistic action of four subtypes of muscarinic receptor on antiallodynic state by i.t. ChEi in a rat model of neuropathic pain. METHODS: Sprague Dawley rats were prepared with tight ligation of left L5/L6 spinal nerves with 6-0 black silk and chronic lumbar intrathecal catheters. After obtaining the baseline hindpaw withdrawal scores, edrophonium (100 microgram) or neostigmine (10 microgram) was administered intrathecally. Tactile allodynia was measured using von Frey filaments and allodynic threshold was calculated by the up-down method. Allodynic changes were tested at 15, 30, 45, 60, 90, 120 and 180 minutes. To examine the reversal of antiallodynia and to compare the antagonizing action of antiallodynic state produced by i.t. administration of ChEi, non-selective muscarinic receptor antagonists atropine (10 microgram), M1 antagonist pirenzepine (3 microgram), M2 antagonist methoctramine (3 microgram), M3 antagonist 4-DAMP (3 microgram) and M4 antagonist tropicamide (3 microgram) were injected intrathecally respectively 5 minutes prior to the injection of edrophonium or neostigmine. RESULTS: Antiallodynia produced by i.t. edrophonium was reversed by pretreatment with i.t. methoctramine, 4-DAMP, tropicamide and pirenzepine (P<0.05). On the contrary, antiallodynic state made by i.t. neostigmine was not antagonized by methoctramine, 4-DAMP and tropicamide. M1 antagonist pirenzepine had a moderate, statistically significant (P<0.05) effect on reversal of increased allodynic threshold while atropine showed a complete antagonism. CONCLUSION: These experiments suggest that antialllodynic action of cholinesterase inhibitors is likely due to mediation of spinal muscarinic system and M1 receptor subtype is more likely involved in this mechanism.