Acute Compartment Syndrome.

Acute compartment syndrome occurs most frequently in connection with injuries, terminal or chemical damage of tissues, ischemia, the activity of toxins or in patients with tissue ischemia or muscle necrosis. Clinical findings have found pronounced pain, followed by paresthesias, pallor, and paresis. Decreased pulsation of arteries has also been a frequent finding. In severe forms decompressive fasciotomy has been indicated within the first 12-24 hours after diagnosis. In the following paper, the authors present the case report of a 68-year woman who swallowed 1500 mg of trazodone as an attempt at suicide. After 12 hours her husband found her lying on the carpet with compression of the left arm under the trunk. The patient was treated conservatively and followed clinically, examined by ultrasonography, EMG and finally MRI.

Comportamiento suicida, intoxicación por drogas y lesiones cutáneas / Suicide behaviour, drug intoxication and skin lesions

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Bullous skin lesions with eccrine gland necrosis have been repeatedly described in drug-induced coma, while similar cutaneosus changes in patients with non-drugin-duced coma have only rarely been reported. We present one comatose patients with bullous skin lesión and eccrine gland necrosis on the dependent part of the body. These findings suggest that the hyperthermia, coupled with hy-poxia and local pressure could cause sweat gland fatigue and degeneration

Coma Reversal After Intravenous Lipid Emulsion Therapy in a Trazodone-Poisoned Patient.

A 77-year-old woman developed a deep coma (Glasgow Coma Scale score at 3/15) after a trazodone overdose (maximal ingested dose, 4500 mg), and orotracheal intubation was required for mechanical ventilation. In addition, she presented sinus bradycardia (<40/min) with QTc prolongation, whereas arterial blood pressure was preserved. The administration of intravenous lipid emulsion (1.5 mL/kg as a bolus followed by a continuous infusion of 0.5 mL/kg per minute for 30 minutes) resulted in a rapid improvement of her neurological condition, with a Glasgow Coma Scale score rising from 3 to 10/15 at the end of intravenous lipid emulsion infusion. A significant increase in heart rate (from 39 to 54/min) was also observed. The treatment was well tolerated, and the patient did not experience ventricular dysrhythmias. In addition, the patient was found to have a reduced metabolic activity related to cytochrome P450 2D6 polymorphism.

Chronic granulomatous pneumonia and lung rupture secondary to aspiration of activated charcoal in a French Bulldog.

A 4-year-old, spayed female French Bulldog was presented for respiratory distress and suspected aspiration pneumonia after oral administration of activated charcoal for possible ingestion of a suspected toxic dose of trazodone. The patient had a moderate volume of pleural effusion, which contained free and intracellular black particulate matter consistent with charcoal. Due to presumed charcoal aspiration with subsequent lung rupture, the right middle and right caudal lung lobes were surgically removed. Histology revealed abundant black debris consistent with charcoal and severe granulomatous inflammation. Based on the clinical, gross, and histologic findings, a diagnosis of severe, chronic, locally extensive, aspiration pneumonia and lung rupture with secondary pleuritis and mediastinitis due to charcoal aspiration was made. Aspiration pneumonia is the main complication of activated charcoal administration, which can incite extensive, granulomatous inflammation in the respiratory tract. To the authors' knowledge, this is the first report describing the cytologic and histologic findings associated with inadvertent charcoal aspiration in a veterinary species.

Unintentional trazodone overdoses in children ≤6 years of age: data from poison center over a period of 16 years.

CONTEXT: Trazodone is an atypical antidepressant with no established safety in children. Previous case reports showed no complications at doses 50-500 mg in children. Our study objective is to characterize the clinical effects, dose-related toxicity, and establish triage dose for acute trazodone ingestions in children ≤6 years of age. METHODS: Cases with acute trazodone ingestions in children ≤6 years of age between 2000 and 2015 were retrospectively reviewed. Data were analyzed for dose (mg/kg), clinical effects, management site, treatment, and outcome. Cases with coingestions, unknown outcome, or unknown dose were excluded. RESULTS: A total of 84 patients (mean age 26.7 months, 35 females, 49 males) were included. Of those, 52 (61.9%) had no clinical effects; 29 (34.5%) had minor effects (vomiting, dizziness, headache); and three (3.6%) had moderate effects (ataxia, slurred speech, priapism). No major effects or deaths were observed. Moderate effects were manifested at doses ≥6.9 mg/kg. Priapism occurred in a 2-year-old child at a dose of 6.9 mg/kg. Sixteen (19%) patients were managed at home and 68 (81%) patients were referred to a HCF. Among those referred to a HCF, three (4.4%) patients had moderate effects with ingested dose ≥6.9 mg/kg. However, 27 (39.7%) patients of those referred to a HCF had an ingested dose <6 mg/kg and none of them manifested symptoms beyond minor effects. All referred patients had uneventful recovery and no sequela. CONCLUSIONS: Children should be referred for further evaluation in acute unintentional trazodone ingestions with doses ≥6 mg/kg.

Fatal Cerebral Edema, Seizures, and Hyponatremia After Trazodone Overdose.

Trazodone is a serotonin antagonist and reuptake inhibitor that is widely used for the treatment of depression and insomnia. Fatal overdose is rare and usually occurs when combined with other drugs or alcohol. Only a few lethal cases of pure trazodone overdose have been reported, all attributed to cardiotoxicity. We reported a 37-year-old woman who presented after ingesting 6.45 g of trazodone in a suicidal attempt. She was hyponatremic because of the syndrome of inappropriate antidiuretic hormone secretion and, shortly after, had a seizure and developed fatal cerebral edema. Others have described seizures and hyponatremia after pure trazodone overdose, but this is the first report of cerebral edema and death from a neurological complication. Careful monitoring and correction of sodium levels may be necessary in these patients.

Focal parietal necrosis of the sigmoid due to atypical neuroleptics: a case report.

We present the case of a 26-year-old man with schizoid personality disorder who suffered from a very focal and transparietal necrosis of the sigmoid after an overdose of atypical neuroleptics. This is a singular, rather unknown and potentially lethal side effect of these drugs. The physiopathology of this complication is multifactorial.

Prolonged delirium after quetiapine overdose.

Quetiapine is an atypical antipsychotic agent increasingly used to treat schizophrenia and bipolar disorder in pediatric patients. Few published data exist concerning quetiapine's effects in therapeutic settings or short-term overdose in pediatric and adolescent populations. In this report, we describe a 15-year-old adolescent girl who experienced continued delirium 5 days after an overdose of quetiapine, trazodone, and clonidine. The patient initially presented with sedation and stable vital signs. After 3 days of gradual improvement, she experienced episodes of delirium coinciding with an increase in resting heart rate. On the basis of suspicion for quetiapine-associated antimuscarinic effects, the patient was administered intravenously with physostigmine on the fifth day after ingestion. Treatment resulted in a brief resolution of symptoms. Serum quetiapine levels measured 1 day and 5 days after ingestion were 3400 and 4800 ng/mL, respectively. The use of physostigmine and interpretation of serum levels are discussed further.

QT Prolongation and delayed atrioventricular conduction caused by acute ingestion of trazodone.

Trazodone possesses minimal anticholinergic properties and, therefore, is generally regarded as having less cardiotoxic potential than other antidepressants. This report describes a young woman who developed significant QT prolongation and delayed atrioventricular nodal conduction after acute trazodone overdose. The case adds to the existing literature because it has a number of strengths, namely that confounding drugs and alcohol were lacking, trazodone exposure was confirmed by drug assay, and early presentation to hospital gave a valuable opportunity to study the time-course of the cardiac effects. This case reminds us to consider the possibility of cardiotoxic effects after trazodone overdose, even in young patients with no established cardiovascular disease.

Management of ventricular dysrhythmia secondary to trazodone overdose.

Torsades de pointes (TdP), a life-threatening ventricular dysrhythmia, was recorded in a 30-year-old woman who had taken a deliberate overdose of trazodone. The patient was successfully defibrillated to normal sinus rhythm and given intravenous magnesium sulfate according to Advanced Cardiovascular Life Support guidelines. The patient was discharged and experienced no further complications.

Suicide by multidrug ingestion: hypothesis on the role played by the self-administration of activated charcoal.

A fatal suicidal ingestion of drugs, together with activated charcoal, is reported. The death occurred 31 hours after the self-administration. The autopsy revealed a large amount of gastric content that appeared to be a compact mass of black color. Toxicologic analyses showed the presence of toxic levels of desalkylflurazepam and trazodone; metamizole and pridinol were also detected. The obtained results supported the hypothesis of a death due to acute intoxication delayed by the self-administration of activated charcoal, which elimination was probably hindered by the action of pridinol.

Investigation of a fatality due to trazodone poisoning: case report and literature review.

Trazodone is an antidepressant agent used in Spain since 1975. There are few documented reports of fatalities solely attributed to trazodone and none in which the main metabolite is analyzed. A fatal case of self-poisoning following oral ingestion is reported along with a description of the validated analytical methods involved, a discussion of poisoning characteristics, and a review of reports describing trazodone overdose cases with analytical results. The deceased was an 86-year-old man with cancer, who suffered depression. He went to see his doctor in a primary health care unit and told him he had just taken an unknown amount of tablets of Deprax to commit suicide. The doctor induced emesis as a first emergency measure. His death occurred before arriving to the hospital, and he left a suicide note nearby. Systematic toxicological analysis of postmortem blood used routinely in our laboratory revealed the presence of trazodone 4.9 mg/L and m-chlorophenyl-piperazine (m-CPP) 0.6 mg/L, its active and major metabolite. In addition, metamizol 19.6 mg/L and 4-methyl-amino-antipyrine (4-MAA) 40.7 mg/L, its active metabolite, were also found in blood. All drugs and metabolites involved in the case were detected using gas chromatography-nitrogen-phosphorus detection (GC-NPD) and confirmed using gas chromatography-mass spectrometry (GC-MS) mode total ion chromatogram. An additional high-performance liquid chromatography-diode array detection (HPLC-DAD) screening also obtained the same results. Quantitation of trazodone together with its metabolite in blood was carried out using GC-NPD, while quantitation of metamizol was performed using HPLC-DAD. Limits of detection for trazodone and m-CPP were 33 and 11 microg/L, respectively, absolute recoveries were more than 86% and 75%, respectively, intra-assay precisions less than 4%, interassay precisions less than 5%, and linearity up to 2.0 mg/L. Limit of detection for metamizol was 1117 microg/L, absolute recovery more than 84%, intra-assay precision less than 8%, interassay precision less than 12%, and linearity up to 48 mg/L. Based on the autopsy findings, patient history, toxicology results, and previously reported trazodone intoxications, the forensic pathologists ruled that the cause of death was due to an overdose of trazodone, and the manner of death was listed as suicide.

An unusual presentation of sertraline and trazodone overdose.

OBJECTIVE: To report an unusual and life-threatening presentation of an overdose of sertraline and trazodone. CASE SUMMARY: A patient with a history of depression ingested sertraline 6,000 mg and trazodone 1,300 mg in a suicide attempt. Twenty-four hours after antidepressant administration, the patient presented with symptoms of selective serotonin-reuptake inhibitor (SSRI) overdose and serotonin syndrome, and later developed an enlarged tongue consistent with angioedema. A compromised airway resulted and endotracheal intubation was necessary. After intubation, the symptoms subsided and the patient recovered. DISCUSSION: Although SSRIs and trazodone are generally considered to be relatively safe in single-agent overdose, serious delayed reactions can occur, especially if several agents are involved. In this case the patient initially presented with symptoms typical of an SSRI overdose that did not appear to be exceptionally dangerous. Over time, symptoms consistent with angioedema appeared that necessitated intubation. Although previous reports of angioedema have been reported with SSRIs, this is the first report, to our knowledge, of a presentation this severe. CONCLUSIONS: This case demonstrates that overdose with the newer antidepressants can result in unusual and delayed presentations and must be treated with caution.

Fatal overdose with trazodone: case report and literature review.

A fatal case of suicide with trazodone alone in a 40-year-old patient is reported. Life-threatening arrhythmias, such as torsades de pointes and complete AV block, are recorded. Blood collected at admission contained a trazodone toxic concentration of 25.4 micrograms/mL. The patient developed multiple organ failure and died less than 24 hours after his admission to the emergency department. The authors discuss the effects of overdose of trazodone, a well-known safe antidepressant drug.

Postmortem forensic toxicology of trazodone.

Trazodone is a popular antidepressant medication that has been available for approximately 30 years. It has a reputation as a safe drug with relatively few reported fatalities attributed solely to it. We review the pharmacology and forensic toxicology of trazodone and report toxicology and cause and manner of death in a series of 37 deaths in which trazodone was detected. Although the normal upper therapeutic blood concentration for trazodone is about 2 mg/L, fatalities are rarely attributed solely to it at blood concentrations below 9 mg/L. Considering the pharmacology of the drug, potential interactions between other drugs with serotonin reuptake properties need to be considered, as does the increased susceptibility to the toxic effects in patients with pre-existing heart disease. In the cases reviewed, none were attributed solely to trazodone, although trazodone was frequently present together with other serotonergic drugs, such as the selective serotonin reuptake inhibitors like fluoxetine and sertraline. Ten cases had blood trazodone concentrations above 2 mg/L. Of these cases, trazodone played a primary role in the death of three subjects, with blood concentrations all greater than 9 mg/L. We confirm the conclusions of others that trazodone is a relatively safe drug except in massive overdose, although its toxicity may be influenced by the presence of other drugs and underlying pathophysiology.