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Christian Tomaszewski

Publications and source records attributed to Christian Tomaszewski.

4 recordsLinked to original sources

Optic nerve sheath diameter does not change with patient position.

OBJECTIVES: Optic nerve sheath diameter (ONSD) has been proposed as a marker for increased intracranial pressure. Trendelenburg's position is often used in hypotensive patients and reverse Trendelenburg's position (30 degrees head up) is often used in head injury patients. We asked if there would be any change in OSND in healthy human adults between the supine, Trendelenburg's, and reverse Trendelenburg's positions. METHODS: Prospective case-control blinded study using consenting healthy adults. Three separate investigators measured the ONSD in each eye of 10 separate volunteers in the supine, Trendelenburg's, and reverse Trendelenburg's positions with 30 degrees angulation from the horizontal. Data were analyzed using the paired t test. RESULTS: In the supine position, the mean ONSD was 4.6 +/- 0.71 (SD) mm in the right eye and 4.5 +/- 0.56 (SD) mm in the left eye. In Trendelenburg's position, the mean ONSD was 4.4 +/- 0.72 (SD) mm in the right eye and 4.7 +/- 0.53 (SD) mm in the left eye. In reverse Trendelenburg's position, the mean ONSD was 4.4 +/- 0.49 (SD) mm in the right eye and 4.8 +/- 0.76 (SD) mm in the left eye. There was no significant difference in OSND between positions for either eye by analysis of variance. Interobserver agreement was +/-1 mm in at least 90% of the subjects regardless of position. CONCLUSION: Optic nerve sheath diameter measurement by ultrasound does not significantly change with Trendelenburg's or reverse Trendelenburg's position in comparison with the supine position in healthy individuals.

Adult↗

Evaluation of a rapid bedside toxicology screen in patients suspected of drug toxicity.

Although rapid bedside toxicological screening is reliable, it has not been validated in the emergency department (ED) setting. We assessed the accuracy of a 10-min bedside immunoassay, Triage Panel (TP), for 7 drugs of abuse and tricyclic antidepressants (TCA) in ED patients suspected of drug toxicity. This was a prospective observational study conducted at an urban teaching ED (100,000 visits/year) of patients suspected of drug toxicity during a 7-month period. The assay was compared for agreement with combined SYVA EMIT and TLC. GC/MS or HPLC was used for analyzing sensitivity and specificity in discordant findings. A total of 172 cases (ages 0.6-73 years) were screened with TP, and 100 (58%) were found to be positive for at least one drug. Sensitivity (proportion and 95% CI) was as follows: cocaine 30/31 (90.6-100%), phencyclidine no cases, THC 21/24 (80.1-94.3), opiates 14/14 (100), amphetamines 1/1 (NA), barbiturates 10/10 (100), benzodiazepines 20/21 (90.5-99.9), and TCA 13/13 (100). Specificity was above 98% for every drug except TCAs (which was 95%), partly due to interference from iminostilbene (a carbamazepine metabolite) in three cases. Agreement between TP and hospital laboratory was over 90% for every drug class. Both benzodiazepines and THC showed significant disagreement between the two testing modalities. In conclusion, in a series of ED patients suspected of drug toxicity, the TP was an accurate tool to rule out the presence of seven drugs of abuse and TCAs. Further testing will be required to verify the efficacy of the test in populations with a higher prevalence of phencyclidine and amphetamine abuse.

Adult↗

Formate kinetics in methanol poisoning.

OBJECTIVE: We sought to describe the kinetics, dialysis clearance, and laboratory markers of formate (FA), the toxic metabolite of methanol (meOH). METHODS: Data were obtained from a prospective, multicenter study of fomepizole +/- dialysis for methanol poisoning. Inclusion criteria confirmed methanol exposure or suspicion of exposure plus either acidemia or abnormal osmolar gap. Dialysis indications were [meOH] > 50 mg/dL, pH < 7.1, refractory acidosis, or visual toxicity. Serial plasma formate, methanol, pH, and electrolyte measurements were made. Formate was determined by gas chromatography. Endogenous and dialysis elimination half-lives were calculated as t(1/2) = 0.693/Ke, with Ke (elimination constant) derived from the slope of log (FA) vs. time. Half-lives were compared with an unpaired Student's t-test. Dialysis clearance was calculated using the Fick Principle. Pearson correlation analysis compared initial formate with initial pH, serum bicarbonate, and anion gap. RESULTS: Eleven patients were treated in the study. Eight had detectable formate with mean [FA] of 15.1 mmol/L (range 0.5-34.8). Endogenous elimination half-life was 205 +/- 90 minutes. Elimination half-life during dialysis (n = 5) was 150 +/- 37 minutes, which was not different (t = 0.22; NS). The overall dialysis formate clearance rate was 223 +/- 25 mL/min. Correlation coefficients were: pH vs. formate r2 = 0.93; bicarbonate vs. formate r2 = 0.81; and anion gap vs. formate r2 = 0.76 (all p < 0.05). CONCLUSIONS: Although dialysis clears formate, it did not significantly enhance endogenous elimination in our series of patients. Low pH, low bicarbonate, and elevated anion gap correlate independently with formate presence.

Adult↗

Hyperbaric oxygen does not prevent neurologic sequelae after carbon monoxide poisoning.

UNLABELLED: Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. OBJECTIVE: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. METHODS: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. RESULTS: Carbon monoxide poisoning induced significant memory deficits (SDL(CO) = 156 sec; SUL(CO) = 75%) compared with nonpoisoned (NP) animals (SDL(NP) = 272 sec; SUL(NP) = 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. CONCLUSIONS: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity.

Analysis of Variance↗