Purpose: Osmolar gap (OG) has been used for decades to screen for toxic alcohol levels. However, its reliability may vary due to several reasons. We validated the estimated ethanol concentration formula for patients with suspected poisoning and who visited the emergency department. We examined discrepancies in the ethanol level and patient characteristics by applying this formula when it was used to screen for intoxication due to toxic levels of alcohol. Methods: We retrospectively reviewed 153 emergency department cases to determine the measured levels of toxic ethanol ingestion and we calculated alcohol ingestion using a formula based on serum osmolality. Those patients who were subjected to simultaneous measurements of osmolality, sodium, urea, glucose, and ethanol were included in this study. Patients with exposure to other toxic alcohols (methanol, ethylene glycol, or isopropanol) or poisons that affect osmolality were excluded. OG (the measured-calculated serum osmolality) was used to determine the calculated ethanol concentration. Results: Among the 153 included cases, 114 had normal OGs (OG≤14 mOsm/kg), and 39 cases had elevated OGs (OG>14). The mean difference between the measured and estimated (calculated ethanol using OG) ethanol concentration was -9.8 mg/dL. The 95% limits of agreement were -121.1 and 101.5 mg/dL, and the correlation coefficient R was 0.7037. For the four subgroups stratified by comorbidities and poisoning, the correlation coefficients R were 0.692, 0.588, 0.835, and 0.412, respectively, and the mean differences in measurement between the measured and calculated ethanol levels were -2.4 mg/dL, -48.8 mg/dL, 9.4 mg/dL, and -4.7 mg/dL, respectively. The equation plots had wide limits of agreement. Conclusion: We found that there were some discrepancies between OGs and the calculated ethanol concentrations. Addition of a correction factor for unmeasured osmoles to the equation of the calculated serum osmolality would help mitigate these discrepancies.
In order to certify the diuretic mechanism of dopamine, this study was performed in dog. The following results were obtained. Dopamine, when given intravenously, produced diuresis, and increased glomerular filtration rate (GFR), renal plasma flow (RPF), and amount of sodium excreted in urine. When infused directly into a renal artery, dopamine elicited a marked diuresis confined only to the infused side, with concomitant rises in osmolar clearance and sodium excretion as well as a slight increase in free water clearance. Simultaneously total renal plasma flow and medullary plasma flow increased markedly with a increase of glomerular filtration rate and renal plasma flow. Medullary concentration gradient of sodium also markedly lowered in the infused kidney. These changes were not observed during mannitol diuresis and renal action of dopamine were not apparent in dog pretreated with haloperidol. From the above experimental results, it is thought that dopamine, when given into a vien or infused directly into a renal artery, induces diuresis, and the mechanism of its action is due to dual actions which are hemodynamic effect along with glomerular filtraction rate, and the increased response in the medullary blood flow.
In order to determine the extent of the placental transfer of Lithium ion, pregnant rabbits at $27{\sim}29$ days of gestation, which has hemochorial placenta similar to the human placenta, received 2 mM/Kg of $Li^+$ in the form of LiCl intravenously. Maternal arterial blood, placental sinus blood, fetal blood, amniotic fluid and maternal urine were drawn two hours after the single dose of LiCl. Concentrations of $Li^+$, $Na^+$, $K^+$ and osmolarity were measured in plasma of collected bloods, amniotic fluid and urine. Followings are the results obtained. 1) Evident level of $Li^+$ was detected in fetal blood, although fetal plasma concentration of $Li^+$ found to be almost one third of maternal plasma. 2) Plasma concentration of $Li^+$ in placental sinus blood was higher than that in fetal plasma but lower than that in maternal plasma. It means that downward concentration gradient of $Li^+$ from mother to fetus was still remarkable two hours after the injection. 3) Significant level of $Li^+$ was also detected in amniotic fluid. It seemed likely that $Li^+$, at least in part, excreted by the fetal urinary tract. 4) There were no differences in $Na^+$ and osmolar concentration between fetal and maternal blood. 5) From above results, it was concluded that $Li^+$ may transfer across the placenta but limited passage capacity through placental barrier for $Li^+$ is significant, beacause net transfer assumed to be going on even at two hours, at which time maternal equlibrium has been reached.
Five buffaloes kept in normal ambient temperature ($30^{\circ}C$) showed no significant changes in the heart rate, respiratory rate, packed cell volume, plasma constituents and renal hemodymics during intravenous infusion of urea for 4 h. The rate of urine flow, fractional urea excretion, urinary potassium excretion and osmolar clearance significantly decreased while the renal urea reabsorption markedly increased during urea infusion. The decrease of fractional potassium excretion was concomitant with the reduction of the rate of urine flow and urine pH. In animals exposed to heat ($40^{\circ}C$) the rectal temperature heart rate and respiratory rate significantly increased while no significant changes in GFR and ERPF were observed. An intravenous infusion of urea in heat exposed animals caused the reduction of the rate of urine flow with no changes in renal urea reabsorption, urine pH and fractional electrolyte excretions. During heat exposure, there were marked increases in concentrations of total plasma protein and plasma creatinine whereas plasma inorganic phosphorus concentration significantly decreased. It is concluded that an increase in renal urea reabsorption during urea infusion in buffaloes kept in normal ambient temperature depends on the rate of urine flow which affect by an osmotic diuretic effect of electrolytes. The limitation of renal urea reabsorption in heat stressed animals would be attributed to an increases in either plasma pool size of nitrogenous substance or body metabolism.
Ethylene glycol poisoning is treated mainly by alcohol dehydrogenase inhibition therapy and hemodialysis. Early recognition and initiation of treatment is important because toxic metabolites increase over time by hepatic metabolism; however, there is no confirmative diagnostic tool in our clinical setting. Therefore, diagnosis is dependent on history, high anion gap acidosis, high osmolal gap, etc.. Diagnosis and treatment are delayed in cases where history taking is not possible, such as a mental changed patient. Authors report on two cases of ethylene glycol poisoning by contrasting clinical outcomes, demonstrating the importance of early diagnosis and treatment for achievement of a good outcome.
Purpose: Toxic alcohols are responsible for accidental and suicide motivated poisonings, resulting in death or permanent sequelae for the afflicted patients. Major therapeutic modalities in these cases include treatment with alcohol dehydrogenase inhibitors and extracorporeal elimination. There have been a number of case reports of toxic alcohol intoxication in Korea. The purpose of this study was to review the clinical characteristics of patients suffering toxic alcohol intoxication. Methods: We retrospectively reviewed the medical records of patients who presented with toxic alcohol intoxication at 8 emergency departments (ED) from Jun 2005 to Nov 2011. Patients who ingested methanol, isopropyl alcohol, ethylene glycol, and other alcohols except ethanol, were included in this study. The clinical characteristics of these patients were analyzed to include anion and osmolar gap, and estimated concentration of alcohol in the body. Results: During the study period, 21 patients were identified who had ingested toxic alcohol (methanol; 12 patients, ethylene glycol; 9 patients). At ED arrival, the mean anion gap was $18.7{\pm}6.9$ and the osmolar gap was elevated in 13 patients. Oral and IV ethanol were administrated to 11 patients in order to inhibit alcohol dehydrogenase. Extracorporeal elimination procedures such as hemodialysis were performed in 9 patients. There were no fatalities, but the one patient suffered permanent blindness. Conclusion: This study found that ethylene glycol and methanol were the substances ingested which produced toxic alcohol intoxication. The patients presented with high anion gap metabolic acidosis and were typically treated with oral ethanol and hemodialysis.
Changes in handling of $Li^+$ by contralateral kidney during acute $Li^+$ loading were investigated immediately after unilateral ureteral obstruction. Carotid artery, jugular vein, renal vein and ureter of experimental animal were catheterized and renal venous flow was shunted to .external jugular vein. In experimental group right ureter was ligated. One to two hours after operation a single shot of LiCl solution (2 mEq/kg) was intravenously injected and then .arterial, renal venous blood and urine samples were taken sequentially for 1 to $1{\frac{1}{2}}$ hours. Urine volume, plasma and urinary concentrations of $Li^+$, $Na^+$ and $K^+$ were measured and urinary excretion of them were calculated. Results obtained were as follows: 1) In experimental group urine volume, urinary excretion of $Na^+$, and $K^+$ by contralateral kidney after unilateral ureteral obstruction were slightly larger than mean value of both kidney in control group. 2) During acute $Li^+$ loading contralateral kidney in experimental group showed limited $K^+$ excretion, but urinary flow and $Na^+$ excretion were comparable to mean value of both kidney in control group. 3) Urinary osmolar concentration in experimental group was much lower than that in control group, and it was maintained at low level even after Li loading. 4) In experimental group plasma$Li^+$ concentration decreased more slowly than in control group after a single shot of LiCl solution. 5) Urinary excretion of $Li^+$ in experimental group was markedly decreased, even lesseer than mean of both kidney in control group. 6) From the above results it was concluded that immediately after unilateral ureteral obstruction contralateral kidney showed normal water and $Na^+$ diuretic response to Li load but urinay $Li^+$ excretion was decreased and reclaimed $Li^+$ to systemic circulation.
The direct effect of isoproterenol on renal function, when given intravenously, is usually obscured by its potent hypotensive action. To obviate the latter action, isoproterenol was infused directly into one renal artery of the dog, the other kidney serving as a control for the general action. And following results were obtained. In the first series of experiments, the directic action of isoproterenol was ascertained. $1.0\;{\mu}g/kg/min$. reduced on both kidneys the urine flow, clearances of PAH and creatinine, as well as the amount of sodium excreted, but the effect was weaker on the experimental side than on contralateral side. With $0.1\;{\mu}g/kg/min$., two cases among 6 experiments showed marked diuresis, two cases no apparent effect, and another two marked antidiuresis on the experimental kidney, whereas the contralateral kidney exhibited antidiuresis in all cases. Further reducing the dose unmasked the diuretic action on the ,experimental kidney. In another series, the effects of isoproterenol on the blood flow distribution within the kidney and on sodium concentration gradient within the kidney tissue were observed. $0.05\;{\mu}g/kg/min$ isoproterenol markedly increased the medullary plasma flow and slightly increased total renal plasma flow and glomerular filtration rate, along with concomitant increase in the amount of sodium excreted and osmolar clearance, and decrease in reabsorption of free water. Sodium concentration gradient markedly decreased in the experimental kidney, reaching 2/3 of the value observed in the contralateral kidney at the papilla. It is thus concluded that isoproterenol exerts a diuretic action, when infused directly into a renal artery, and the mechanism of the action rests on its hemodynamic action, substantiated as the increase in glomerular filtration and in the medullary blood flow, resulting in washout of hyperosmolality produced by the coutercurrent multiplier system.
To study the regulation of amniotic fluid volume and electrolyte concentration by the Membranes surrounding the amniotic fluid, the rate of $Li^+$ disappearance from amniotic sac of expired fetuses were examined while increasing the amniotic volume and osmolarity in rabbits. After intraamniotic injection of 1 ml isosmotic saline (about 20% of the amniotic fluid volume) containing 15 mM LiCl and 0.5 g/L Censored, the time courses of $Li^+$ and Censored disappearance were determined. From there the $Li^+$ clearance through the extrafetal routes was estimated and compared with that obtained from living fetuses. The volume, $Na^+$ concentration and osmolarity of amniotic fluid were measured and their relationships with $Li^+$ disappearance were evaluated. The fellowing results were obtained: 1. The rate of disappearance from amniotic fluid of living fetuses during the first 30 minutes was strikingly higher for $Li^+$ than for Censored, suggesting that extrafetal routes exist. At 60 and 90 minutes, however, the disappearance rate of $Li^+$ was less than that of Censored, suggesting the possibility of $Li^+$ reentry through fetal urination. 2. The disappearance of $Li^+$ from the amniotic fluid of the expired fetus was substantial, although lower than that of living fetuses, throughout the experimental period. 3. The $Na^+$ concentration and the osmolarity of the amniotic fluid of expired fetus measured 30 minutes after an intraamniotic injection of isoosmotic saline showed wide variation, but thereafter they changed gradually towards the normal extracellular fluid level. 4. When the amniotic fluid was iso- or hyposmolar, the rate of $Li^+$ disappearance from the amniotic fluid of the expired fetuses showed little variation. However, when the amniotic fluid was hyperosmolar, the rate at 30 minutes was markedly lower than those of isosmotic or hyposmotic amniotic fluid. At 90 minutes, the rate of $Li^+$ disappearance in hyperosmolar fluid reached a similar level to the rate in isosmolar fluid. 5. The intraamniotic injection of 400 mOsm/L saline solution decreased the disappearance rate of $Li^+$ from expired fetuses, while the injection of mannitol into the maternal vein induced no significant change. From these results it is concluded that: 1) a significant amount of $Li^+$ may leave the amniotic fluid via filtration through the membranes surrounding the amniotic fluid, 2) during hyperosmolar challenge to amniotic fluid, osmotic bulk flow might counteract the filterable loss, and 3) $Li^+$ disappearance might continue even after the volume and osmolarity of the amniotic fluid have recovered to control values.
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