Background Tibial tuberosity fractures in adolescents are uncommon. We retrospectively reviewed all tibial tuberosity fractures in adolescents (10-19) who presented to our level 1 pediatric trauma center over a 7-year period to review fracture morphology, mechanism of injury, fracture management including return to play, as well as complications. Additionally, we present a review of the literature and treatment algorithm. Methods We reviewed the clinical charts and radiographs of consecutive patients with tibial tuberosity fractures between

Poisoning by organophosphorus pesticides results from inhibition of acetylcholinesterase. The outcome and optimum treatment depend on properties which differ among individual compounds. Treatment consists of supportive care, especially aimed at respiratory complications, and specific antidotal treatment. Treatment with atropine and diazepam is well established, but there is controversy concerning treatment with oximes capable of forcing reactivation of inhibited acetylcholinesterase. Although all parameters have not been fully established, initial bolus doses followed by continuous intravenous infusion to achieve plasma concentrations of 85–170 μmol/L of pralidoxime or 10–20 μmol/L of obidoxime have been recommended. These are well above concentrations that were likely to have been achieved by many of the ineffective regimens reported in the literature. Several independent reasons for failure of attempts at oxime therapy are discussed in this overview. If nothing else, it is likely that maintenance of adequate levels of oxime will shorten the period that a patient requires assisted ventilation with its associated risks. Topics for further laboratory and clinical research are listed. It is important to seek further understanding and the introduction of better practice because death rates from this type of poisoning remain significant.

Mercury poisoning occurred after the acute, prolonged exposure of 53 construction workers to elemental mercury. Of those exposed, 26 were evaluated by clinical examination and tests of neuropsychological function. Patients received treatment with chelation therapy in the first weeks after exposure. Eleven of the patients with the highest mercury levels were followed in detail over an extended period. Observations included the evaluation of subjective symptoms of distress, using the 'Symptom Check List 90-Revised' (SCL-90R) and tests of visual-motor function such as 'Trailmaking Parts A and B', 'Finger Tapping', 'Stroop Colour Word Test' and 'Grooved Pegboard.' On day 85 ± 11 (mean±s.d.) after exposure, these 11 men again received either 2,3-dimercaptosuccinic acid (DMSA) or N-acetyl-D, L-penicillamine (NAP) in a short-term study designed to compare the potential to mobilize mercury and the incidence of drug-induced toxicity of these two chelating agents. Rapidly resolving metal fume fever was the earliest manifestation of symptoms. CNS symptoms and abnormal performance on neuropsychological tests persisted over the prolonged period of follow-up. There were significant correlations between neuropsychological tests and indices of mercury exposure. Serial mercury in the blood and urine verified the long half-life and large volume of distribution of mercury. Chelation therapy with both drugs resulted in the mobilization of a small fraction of the total estimated body mercury. However, DMSA was able to increase the excretion of mercury to a greater extent than NAP. These observations demonstrate that acute exposure to elemental mercury and its vapour induces acute, inorganic mercury toxicity and causes long-term, probably irreversible, neurological sequelae.

The measurement of plasma concentration, a prolonged QRS interval, and level of consciousness have all been recommended as useful indicators of toxicity following tricyclic antidepressant overdose. The aims of this study were firstly, to determine the relative prognostic value of each of these indicators and secondly, to assess when a patient can be discharged safely from the intensive care unit. Data were evaluated on 67 patients with tricyclic antidepressant overdose from four centers. Plasma tricyclic antidepressant concentrations were measured, coma grade was evaluated using the Matthew-Lawson Coma Scale and a ECG was obtained from 23 patients on admission. Complications such as convulsions, hypotension, arrhythmias, and need for intubation and ventilation were recorded. Thirty patients developed complications and no patient died. Coma grade was the best predictor of outcome. The development of serious complications is unlikely in patients whose level of consciousness is grade II or less and who are admitted to hospital more than 6 h after overdose. Plasma tricyclic antidepressant concentration was of no additional value in predicting toxic complications or deciding when the patient could leave the intensive care unit. Our study suggests that an alert and orientated patient with a QRS duration less than 100 ms is the best indicator for safe transfer to a medical or psychiatric ward.

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