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Introduction. Drug overdose (OD) is a frequent incident among opiate addicts. Survivors of ODs are at risk for additional and eventually fatal ODs. ODs may be classified as accidental (aOD) or deliberate (dOD). Investigations into the connection between OD and suicide attempts have led to insconsistent results. Purpose. (1) to determine how many non-fatal ODs were dODs and how many were aODs; (2) to determine how many cases of dODs were motivated by explicit or by ambivalent suicidal intentions; (3) to determine how many cases of aODs had causes that might respond to preventative measures; (4) to compare the addiction histories of dODs and aODs; (5) to compare the drugs causing the ODs; and (6) to compare the severity of the ODs in both groups. Methods. Prospective study utilizing a standardized questionnaire to evaluate opiate-addicted patients admitted to our treatment unit for OD. All cases underwent standardized drug testing to identify drug use patterns. Results. Seventy-four cases of OD underwent standardized interviews after awakening. Forty-three percent of the cases were dOD. Cases of dOD had significantly more OA in substitution programs, more previous ODs, and more often consumed methadone and cocaine. Among dODs, 22.5% had suicidal intention and 9.6% were ambivalent about committing suicide; background motivations were most often conflicts with spouses. Fifty-seven percent of the cases were aOD. Cases of aODs had significantly more potential lethal intoxications and had heroin detected more frequently, aODs happened with unexpected pure heroin (46%), in combination with alcohol (36%), as relapse after abstinence (40%) or after institutionalized treatment (19 %). This group should be accessible for targeted education. Keywords Non-fatal opiate overdose; opiate addicts; Deliberate overdose; Accidental overdose; Suicidal attempt; Methadone maintenance, INTRODUCTION Opiate-addicts have an annual mortality rate of 1.2% to 2.7%, which is up to 17-times higher than non-addicts in the same age groups (1-4). The most common causes of [...]

Objective: Acute oral poisonings with potassium dichromate are infrequent and have a high fatality rate. This report describes the clinical course and the analytical data of a severe acute potassium dichromate poisoning treated by hemofiltration, high-flux hemodialysis, albumin dialysis and liver transplantation. Case Report: A 49-year-old woman drank an aqueous solution containing approximately 16.8 g of potassium dichromate in a suicide attempt. The patient initially developed abdominal pain, nausea, vomiting and bloody diarrhea, followed by a bleeding disorder, renal and hepatic failure. On day 7 hepatic function deteriorated to such an extent that orthotopic liver transplantation had to be performed. The post-operative course was complicated by the development of a critical illness polyneuropathy. Four months after the ingestion the patient was discharged well with only a mild residual polyneuropathy. On admission the patient had a chromium level in whole blood of 13,000 [micro]g/L, in serum 7000 [micro]g/L and in urine 60,000 [micro]g/L. Before liver transplantation chromium concentration in whole blood and serum had decreased to 1900 [micro]g/L and 600 [micro]g/L, respectively. The majority of identified chromium elimination (183 mg) was due to extracorporeal elimination procedures including hemofiltration and albumin dialysis. Faecal excretion accounted for 21 mg chromium, exchange transfusion for 15 mg chromium and renal excretion for 6 mg chromium. In the first seven days chromium half-life in serum, whole blood and red blood cells was 38.9 hours, 66.6 hours and 92.4 hours, respectively. The hemofiltration clearance without DMPS ranged between 31.2 and 56.6 mL/min, the hemofiltration clearance with DMPS was between 21.3 and 46.0 mL/min. The albumin dialysis clearance amounted to 21.6 mL/min and hemodialysis clearance came to 22.4 mL/min. During renal failure the renal clearance for chromium was 1.17 mL/min but subsequently increased to 15.7 mL/min. Conclusion: In acute potassium dichromate poisoning acute hepatic failure may be the crucial life-threatening complication and liver transplantation may be the only life-saving treatment procedure. Of the extracorporeal elimination procedures used hemofiltration, albumin dialysis and high-flux hemodialysis appeared most effective. Chromium blood concentration fell to a level which did not harm the transplanted liver., Felgenhauer N(1), Pfab R(1), Stier A(2), Schramel P(3), Zilker T(1). (1) Toxikologische Abteilung, II. Medizinische Klinik, Klinikum r.d.Isar, Munchen; (2) Chirurgische Klinik, Klinikum r.d.Isar, Munchen; (3) GSF-Forschungszentrum, Neuherberg, [...]

Case report: A 23-year-old male after having dissolved 13 sparklers in water drank this solution of 5.8 g of barium nitrate in a suicide attempt. He experienced nausea, vomiting, generalized muscular weakness. He complained about tingling paresthesiae in his hands and feet. He was unable to stand upright or to sit. In an upright position he could not hold his head nor raise his arms for more than four seconds. Ventilation was not compromised with a peak flow of 400 L/sec. He showed no signs of shock. The EGG showed no abnormality. Under potassium substitution at admission he still exhibited hypokalemia and hypophosphatemia. Abdominal X-ray revealed no opaque deposits. Treatment consisted of symptomatic measures and replacement of potassium 240 mmol/24 h. Symptoms resolved within 28 hours after ingestion. Toxicokinetics of barium: Barium concentrations in serum declined according to a two compartment kinetic. The [Alpha]-half life was 5 hours, the [Beta]-half life 14 hours. In urine not more than 10 mg barium could be found within 36 hours. Barium excreted in the stool amounted to 57 mg in this time. Even if the bioavailability of barium after barium nitrate ingestion is low the barium recovery was tiny in this case. Discussion: Intoxications with soluble barium salts leads to muscular weakness, hypokalemia and hypophosphatemia. Paresthesiae and cardiac dysrhythmias are common. Most of the barium is excreted with the stool, renal clearance is very low. From our case it is likely that most of the barium may be retained in the body. Possibly barium is stored in bones, like strontium which is a ion with similar physicochemical properties. Pfab R, Gerber-Zupan G, Zilker Th. Toxikologische Abteilung II. Med. Klinik, Klinikum r.d. Isar, TU Munchen, Germany

Case reports: We observed two cases of severe long lasting diabetes insipidus after an iatrogenic cumulative lithium intoxication. Pat.1: A 56-year-old female developed all signs of a lithium intoxication under lithium treatment for a psychotic disorder. Lithium concentration at admission was 3.56 mmol/L, 1.68 mmol/L after the first and 0.7 mmol/L after the second hemodialysis. Polyuria began on day one after admission with 6180 ml/24 h and reached a maximum of 19,050 mL/L at day 9. Intravenous substitution of fluids was necessary. Thirst tests on day 9 and day 21 led to an increase in serum osmolality with little increase in urine osmolality. 30 days after the onset the 24 h urine volume was still 6L. 60 days after the onset of diabetes insipidus the patient showed near normal 24 h urine output. Pat.2: A 45-year-old female under lithium medication developed an unintentional lithium intoxication. Lithium concentration at admission was 2.5 mmol/L. Without hemodialysis the lithium levels decreased to 1.7 (2.day), 0.8 (3.day) and 0.2 (4.day). Polyuria started on day 3 with 8,400 mL and reached a maximum of 51,000 mL (!!) on day 17. Treatment with a high dose of desmopressin, indomethacin and amiloride improved the polyuria to 14,390 mL on day 29. But this medication did not bring long lasting success. On day 43 the urine output was back to 30,750 mL. Thirst test always led to a severe increase in serum osmolality. After day 53 it was possible to reduce the volume input. The patient left the hospital after 57 days still with polyuria (5-6 L). 71 days after admission she was able to concentrate her urine under water restriction. Conclusion: Cumulative lithium intoxication can lead to nephrogenic diabetes insipidus. Desmopressin can only temporarily improve the urinary output. The disturbance seems irreversible for several months. Wetzel D, Felgenhauer N, Pfab R, Zilker Th. Toxikologische Abteilung II. Med. Klinik, Klinikum r.d. Isar, TU Munchen, Germany

Objective: Intoxications are frequent complications in drug users. These overdoses lead to coma or loss of physical control. Within 10 years 50% of all drug addicts have at least one overdose leading to hospitalization. 12% of drug dependent patients die from such an overdose. We therefore conducted a prospective study--still going on--to evaluate the motives and reasons which lead to intoxications in drug addicts. Methods: 20 patients (14 male and 6 female) all polydrug abusers who were admitted to our unit with an overdose were studied. After recovery from the intoxication the patient underwent standardized psychiatric interviews to assess the motives and circumstances that led to the intoxication. 4 questionnaires were used for each patient: Europ ASI (European Addiction Severity Index), AMDP (Arbeitsgemeinschaft fur Methodik u. Dokumentation in der Psychiatrie) IPC (Control of Reinforcement) and a test for judgment for potential suicide. The patients were scrutinized if an intentional intoxication seemed likely. Did the patient expect no harm to his health (risky behavior), did he expect to damage himself, did he expect to die? In self-inflicted harm the conflict that caused this action was looked at. In unintentional overdose it was investigated if the reasons were abstinence, underestimation of the dosage, an unusual combination of drugs or a previous consumption of ethanol. Results: In 12 patients (60%) the intoxication was intentional. In 8 patients (40%) an accidental overdose could be diagnosed. Of the 12 intentional intoxications two were severe suicidal attempts. 5 patients did not mind to die, 5 would not give reasons but were aware of having taken an overdose (risky behavior). In 8 patients the cause was a severe partner conflict (separation or divorce), 2 had general stress and two had other reasons. Of the 8 unintentional intoxications, 6 were under the influence of ethanol and doxepin, 2 took the wrong dose after abstinence. Conclusion: Overdoses in drug users are intentional in about 60%. Psychiatric investigation and intervention is imperative. Unintentional overdoses are due to a combination of substances of unknown interaction for the user. Overdoses after a period of abstinence are also seen. Muller R(1), Pfab R(2), Zilker Th(2) (1) Psychiatrische Klinik (2) Toxikologische Abteilung II. Med. Klinik, Klinikum r. d. Isar TU Munchen, Germany

Objective: Investigating thyroid function during opiate withdrawal under general anesthesia precipitated by an opiate antagonist, we observed a suppression of TSH and a fall in [TT.sub.3]. Former studies on the influence of opiates on the hypothalamic--pituitary--thyroid gland axis revealed conflicting results. To answer the question if opiate withdrawal or the opiate antagonist suppresses TSH secretion we performed two studies, one in opiate addicts during withdrawal and one in healthy volunteers receiving the opiate-antagonist naltrexone. To differentiate between an effect of naltrexone on the hypothalamic or pituitary level we studied naltrexone alone, naltrexone + dopamine antagonist metoclopramide and performed a TRH-Test with and without medication. Methods: TSH and [TT.sub.3] were measured in 20 opiate addicts before, during and after `cold' withdrawal. 20 healthy volunteers were used as control group. In each of 12 healthy volunteers (informed consent) four different tests were performed: a. Blood was taken at 9:00 and 13:00, 14:30 before and 15:00 after TRH (no medication), b. Same blood sampling as under a. (100 mg naltrexone orally after first blood sampling), c. Same blood sampling as under a. metoclopramide was given IV after 13:00 blood sampling, d. Same blood sampling as under a. naltrexone was given at 9:00 after first blood sampling, metoclopramide was given IV after 13:00 blood sampling. The statistical comparison was calculated by the Wilcoxon Test. Results: during opiate withdrawal TSH levels in serum ([micro]U/mL) fell from 1.53 [+ or -] 0.23 (at admission) to 0.25 [+ or -] 0.19 (height of the withdrawal) and rose again to 1.01 [+ or -] 0.47 (after withdrawal). These were significantly different to the controls (p [is less than] 0.0001). [TT.sub.3] followed the same pattern. In the volunteers TSH fell from (9:00) 1.39 [+ or -] 0.79 to (13:00) 1.20 [+ or -] 0.53 [circadian rhythm (a)]. If naltrexone was given (b) TSH fell from 1.4 [+ or -] 0.73 to (13:00) 0.77 [+ or -] 0.6. If metoclopramide (c) was given and compared to naltrexone (b) at 14:30 TSH was significantly higher [0.67 [+ or -] 0.22 (N) vs 1.11 [+ or -] 0.57 (M)]. In experiment d. the TSH suppression by naltrexone was reversed by metoclopramide, the TRH-Test showed no significant difference in the TSH release (a-d). Conclusion: Opiate withdrawal suppresses TSH secretion naltrexone inhibits TSH secretion. Metoclopramide can reverse the inhibitory effect of naltrexone. Opiate thus inhibits hypothalamic dopamine release. Therefore during opiate withdrawal a lack of endorphins allows hypothalamic dopamine release which suppresses TSH secretion. Pfab R(1), Knoth K(1), Natale B(1), Bottermann P(2), Born P(2), Rohlfing U(2), Zilker Th. (1) Toxikolgische Abteilung II. Med. Klinik, (2) II. Med. Klinik, Klinikum r.d. Isar TU Munchen, Germany