[A case of acute fish gallbladder poisoning with multiple organ dysfunction].

Fish bile poisoning may damage human liver and kidney, causing degeneration and necrosis. Can also damage brain cells and heart muscle, resulting in nervous system and cardiovascular system lesions. This paper reports a case of a patient who developed multiple organ dysfunction syndrome (MODS) after oral administration of fish bile with Xiexin folk prescription for eye disease. In January 2020, he went to the poisoning and occupational diseases department of the emergency department of Qilu hospital. After receiving hemoperfusion, continuous renal replacement therapy (CRRT) and symptomatic support treatment, the patient was improved and discharged. CRRT combined with HP is one of the rapid and effective methods for the treatment of acute fish bile poisoning.

MYONECROSIS AND DEATH DUE TO PRESUMED MICROCYSTIN TOXICOSIS IN AMERICAN WHITE PELICANS (PELECANUS ERYTHRORHYNCOS).

Over a period of 5 mo, seven out of eight American white pelicans (Pelecanus erythrorhynchos) housed on a spring-fed pond at a zoo died or were euthanized. Clinical signs included inability to stand, anorexia, and weight loss. Clinicopathologic findings included heterophilic leukocytosis and elevated creatine kinase and aspartate aminotransferase. Histopathologic findings on all pelicans demonstrated severe, chronic, diffuse rhabdomyofiber degeneration and necrosis, making vitamin E deficiency a differential diagnosis despite routine supplementation. Based on tissue and pond water assays for the cyanobacterial toxin, microcystin, toxicosis is suspected as the inciting cause of death in these cases. We hypothesize that vitamin E exhaustion and resultant rhabdomyodegeneration and cardiomyopathy were sequelae to this toxicosis.

Assessment and Management of Toxidromes in the Critical Care Unit.

The most important diagnostic factor in uncovering a toxic etiology for delirium or critical illness is the clinician's openness to the possibility of its existence. Therefore, a consulting psychiatrist, already prepared to perform the detail-oriented work of sorting out behavioral manifestations of disease, can be a vital asset at the bedside if also attuned to the role of purposeful, accidental, and iatrogenic exposures in the intensive care unit. This article summarizes the presentation, evaluation, and treatment of toxidromes relevant to the work of acute psychosomatic medicine.

Chronic Toxic Metal Exposure and Cardiovascular Disease: Mechanisms of Risk and Emerging Role of Chelation Therapy.

Over the last few decades, there has been a growing body of epidemiologic evidence linking chronic toxic metal exposure to cardiovascular disease-related morbidity and mortality. The recent and unexpectedly positive findings from a randomized, double-blind, multicenter trial of metal chelation for the secondary prevention of atherosclerotic cardiovascular disease (Trial to Assess Chelation Therapy (TACT)) have focused the discussion on the role of chronic exposure to toxic metals in the development and propagation of cardiovascular disease and the role of toxic metal chelation therapy in the secondary prevention of cardiovascular disease. This review summarizes the most recent evidence linking chronic toxic metal exposure to cardiovascular disease and examines the findings of TACT.

Administración accidental de aceite puro esencial de arbol de té (Melaleuca alternifolia) en lactantes / Accidental pure essential tea tree oil (Melaleuca alternifolia) administration in two infants

El aceite de árbol de té es una sustancia que se obtiene mediante la destilación de las hojas y ramas frescas del árbol Melaleuca alternifolia. En los últimos años se ha popularizado su uso sobre todo como agente antiinfeccioso tópico en una gran variedad de enfermedades. Se trata de una sustancia natural que tiene un potencial efecto tóxico demostrado sobre todo si se ingiere. Presentamos dos casos de pacientes atendidos en nuestro Servicio de Urgencias tras administración e ingestión accidental de aceite esencial de árbol de té, en ambos casos los padres confundieron el envase con el de la vitamina D. La atención de estos pacientes nos llevó a realizar una búsqueda bibliográfica de casos publicados de intoxicación por ingesta de aceite de árbol de té y a poner de manifiesto la ausencia de advertencias de seguridad en los envases de aceite de árbol de té que actualmente se comercializan en nuestro país (AU)

Tea tree oil is an essential oil obtained by steam distillation of the leaves and terminal branches of Melaleuca alternifolia. In recent years, it has become popular as an antimicrobial agent against a large number of diseases. It is a natural substance that has a potential toxic effect especially if ingested. We report two cases of infants who came to our Emergency Department because they were accidentally given tea tree oil. In both cases parents mistook the tea tree oil bottle with the D vitamin bottle. The care of these patients led us to perform a literature search of published cases of tea tree oil poisoning and highlight the absence of safety warnings on tea tree oil packages currently marketed in our country (AU)

Meta-Analysis of the Effects of Xingnaojing Injection on Consciousness Disturbance.

Xingnaojing (XNJ) is commonly extracted from Angongniuhuang, a classic Chinese emergency prescription, and widely used in the treatment of nervous system disorders including consciousness disturbance in China. To evaluate the beneficial and adverse effects of XNJ injection, on consciousness disturbance. Seven major electronic databases were searched to retrieve randomized controlled trials designed to evaluate the clinical efficacy of XNJ alone or combined with Western medicine in treating consciousness disturbance caused by conditions such as high fever, poisoning, and stroke. The methodological quality of the included studies was assessed using criteria from the Cochrane Handbook for Systematic Review of Interventions, and analyzed using the RevMan 5.3.0 software. Seventeen randomized controlled trials on XNJ were included in this study and the trials generally showed low methodological quality. The results revealed that XNJ alone or in combination with other medicines and adjuvant methods had a positive effect on patients with fever-, poisoning-, and stroke-induced coma. XNJ effectively treated consciousness disturbances that were caused by high fever, poisoning, or stroke.

Intoxicación aguda por anestésicos locales / Acute toxicity due to local anesthetics

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El monóxido de carbono y la neurología. Réplica / Carbon monoxide and neurology. Reply

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Neurotoxicity of metals.

Metals are frequently used in industry and represent a major source of toxin exposure for workers. For this reason governmental agencies regulate the amount of metal exposure permissible for worker safety. While essential metals serve physiologic roles, metals pose significant health risks upon acute and chronic exposure to high levels. The central nervous system is particularly vulnerable to metals. The brain readily accumulates metals, which under physiologic conditions are incorporated into essential metalloproteins required for neuronal health and energy homeostasis. Severe consequences can arise from circumstances of excess essential metals or exposure to toxic nonessential metal. Herein, we discuss sources of occupational metal exposure, metal homeostasis in the human body, susceptibility of the nervous system to metals, detoxification, detection of metals in biologic samples, and chelation therapeutic strategies. The neurologic pathology and physiology following aluminum, arsenic, lead, manganese, mercury, and trimethyltin exposures are highlighted as classic examples of metal-induced neurotoxicity.

Successful Rescue of a Patient with Acute Aconitine Poisoning Complicated by Polycystic Renal Hemorrhage.

INTRODUCTION: Aconitine is a highly toxic diterpenoid alkaloid, produced by plants of the Aconitum genus, that is still used in Chinese herbal medicines. Aconitine poisoning remains common in China and other parts of Asia. CASE REPORT: A 48-year-old man received a diagnosis of aconitine poisoning after ingesting herbal medicinal wine made with caowu, which is made from Aconitum kusnezoffii roots, and was admitted to our hospital' s emergency department. Electrocardiography and thoracoabdominal computed tomography showed cardiovascular toxicity from aconitine poisoning along with polycystic renal hemorrhaging. Because the arrhythmia was not controlled with lidocaine, blood purification with a reduced dosage of heparin was performed to treat the arrhythmia and to avoid increasing the bleeding of the polycystic renal hemorrhage. The patient recovered from aconitine poisoning and polycystic kidney hemorrhage. CONCLUSIONS: This case significantly advances our understanding of hemoperfusion with reduced heparin for the treatment of ventricular arrhythmia caused by aconitine poisoning.

Gloriosa superba poisoning mimicking an acute infection- a case report.

BACKGROUND: Gloriosa superba (GSb) is a highly poisonous plant and its toxicity is due to anti-mitotic effects of constituents such as colchicine and gloriosine on rapidly proliferating cells. Poisoning is known to cause very rapid and severe clinical manifestations due gastro intestinal, neurological, cardiac and bone marrow toxicity. CASE PRESENTATION: A young male presented with an acute onset febrile illness associated with diarrhoea, confusion, haematuria and aggressive behavior of 4 days duration. He developed subconjunctival haemorrhages, bleeding gums, neck stiffness, bilateral papilloedema, tender hepatomegaly and features suggestive of subacute intestinal obstruction. He had progressive reduction in white cell counts, platelets and derrangements in liver functions. The illness mimicked acute severe leptospirosis or dengue. On day 9 of illness he started to loose his hair and was totally alopecic by day 14. At this stage of illness, possibility of GSb poisoning was suspected. He admitted the act of self harm after repeated questioning. CONCLUSION: His presentation mimicked an acute severe tropical febrile illness such as leptospirosis or dengue until he started to loose his hair. Therefore we feel that Clinicians practicing in tropical setting where Gloriosa superba is endemic should be aware of its clinical presentations and should always consider the possibility of ingestion of Gloriosa superba when the patient has pancytopenia and develops shedding of hairs which results in total alopecia in a case of unexplained gastroenterocolitis, rather investigating.

Paradigm shift redefining molecular, metabolic and structural events in Alzheimer's disease involves a proposed contribution by transition metals. Defined lengthy preclinical stage provides new hope to circumvent advancement of disease- and age-related neurodegeneration.

It is estimated that 5.5 Million North Americans suffer from varying degrees of Alzheimer's disease (AD) and by the year 2050 it may be one in 85 people globally (100 Million). It will be shown that heavy metal toxicity plays a significant role in sporadic AD. Although current literature speaks to involvement of metal ions (via Fenton reaction), studies and reviewers have yet to link cellular events including known structural changes such as amyloid plaque development to this metal toxicity the way it is proposed here. Contrary to the current AD model which positions BACE1 (ß-secretase) as an aberrant or AD-advancing enzyme, it is proposed herein that the neuron's protective counteraction to this metal toxicity is, in fact, a justified increase in BACE1 activity and amyloid precursor protein (APP) processing to yield more secreted APP (sAPP) and ß-amyloid peptide in response to metal toxicity. This new perspective which justifies a functional role for APP, BACE1 enzyme activity and the peptide products from this activity may at first appear to be counterintuitive. Compelling evidence, however, is presented and a mechanism is shown herein that validate BACE1 recruitment and the resulting ß-amyloid protein as strategic countermeasures serving the cell effectively against neuro-impeding disease. It is proposed that ß-amyloid peptide chelates and sequesters free heavy metals in the extracellular medium to aggregate as amyloid plaque while unchelated ß-amyloid migrates across the cell membrane to chelate intracellular free divalent metals. The sequestered intracellular metal is subsequently chaperoned as a metallo-peptide to cross the plasma membrane and aggregate as amyloid plaques extracellularly. The BACE1 countermeasure is not genetic or metabolic aberration; and this novel conclusion demonstrates that it must not be inhibited as currently targeted. APP, BACE1, ß-amyloid peptide, and sAPP play positive roles against the preclinical oxidative load that predates AD symptoms for as long as 20 years. A healthy neuron may tolerate free metal toxicity, such as iron in the case of injury-induced amyloid, for as long as twenty years due to this very BACE1 activity. In later stages, the uncontrolled metals and ROS are compounded by other factors which together overcome this BACE1/ß-amyloid protein countermeasure. This results in a sudden increase in IL-1 leading to Tau's hyperphosphorylation as cited and eventually to Tau dissociation from the microtubule cytoskeleton interrupting cell trafficking. At this later stage of AD the ß-amyloid protein which once served as a vehicle to escort toxic metals to the extracellular medium and a trap to form a relatively benign extraneuronal disposal site is no longer translocated due to interruption of trafficking and now accumulates intracellularly facilitating hyper-oxidative ROS levels and contributes to irreversible neuron apoptosis.

Management of cyanide toxicity in patients with burns.

The importance of cyanide toxicity as a component of inhalational injury in patients with burns is increasingly being recognised, and its prompt recognition and management is vital for optimising burns survival. The evidence base for the use of cyanide antidotes is limited by a lack of randomised controlled trials in humans, and in addition consideration must be given to the concomitant pathophysiological processes in patients with burns when interpreting the literature. We present a literature review of the evidence base for cyanide antidotes with interpretation in the context of patients with burns. We conclude that hydroxycobalamin should be utilised as the first-line antidote of choice in patients with burns with inhalational injury where features consistent with cyanide toxicity are present.

Toxin-induced cardiovascular failure.

Adverse cardiovascular events comprise a large portion of the morbidity and mortality in drug overdose emergencies. Adverse cardiovascular events encountered by emergency physicians treating poisoned patients include myocardial injury, hemodynamic compromise with shock, tachydysrhythmias, and cardiac arrest. Early signs of toxin-induced cardiovascular failure include bradycardia, tachycardia, and specific ECG findings. Treatment of toxicologic tachycardia relies on rapid supportive care along with proper use of benzodiazepines for sedation. Treatment of toxicologic bradycardia consists of the use of isotonic fluids, atropine, calcium salts, and glucagon. High-dose insulin euglycemia should be used early in the course of suspected severe poisoning and intravenous lipid emulsion given to patients who suffer cardiac arrest.

Personalization of multiple sclerosis treatments: using the chelation therapy approach.

Though Multiple Sclerosis (MS) sufferers are probably genetically predisposed, toxic metal poisoning (TMP) does seem an increasingly likely environmental trigger. The technique for measuring and clearing TMP was chelation therapy using ethylene-diamine-tetracetic acid (EDTA), which revealed aluminum accumulation in both cases. The first patient, initially benefiting from removing dental fillings that had leaked mercury, also showed gadolinium accumulation from scan contrast medium, and a genomic deficiency of glutathione transferase M1. Glutathione production was impaired and hence also liver detoxification functions. The personal protocol involved glutathione administration and deutrosulfazyme to enhance oxygenation and alleviate oxidative stress. As aluminum began to clear with EDTA infusion, the extracellular/intracellular water ratio was carefully monitored, and carbohydrates limited. In the second case, aluminum poisoning responded to EDTA chelation therapy with eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA), multivitamins, and glutathione administration, again followed by deutrosulfazyme, water ratio control, and dietary correction. The two personalized protocols presented here tend to confirm the hypothesis of TMP as an environmental or iatrogenic trigger for MS, especially when inadequate detoxification lies at the root. Cleansing by chelation therapy, properly understood, can be efficacious, especially bearing in mind the altered cellular water ratio.

Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes.

Ketoacidotic syndromes are frequently encountered in acute care medicine. This article focuses on ketosis and ketoacidotic syndromes associated with intoxications, alcohol abuse, starvation, and certain dietary supplements as well as inborn errors of metabolism. Although all of these various processes are characterized by the accumulation of ketone bodies and metabolic acidosis, there are differences in the mechanisms, clinical presentations, and principles of therapy for these heterogeneous disorders. Pathophysiologic mechanisms that account for these disorders are presented, as well as guidance regarding identification and management.

Cyanide poisoning caused by ingestion of apricot seeds.

AIM: To report diagnostic, clinical and therapeutic aspects of cyanide intoxication resulting from ingestion of cyanogenic glucoside-containing apricot seeds. METHODS: Thirteen patients admitted to the Pediatric Intensive Care Unit (PICU) of Erciyes University between 2005 and 2009 with cyanide intoxication associated with ingestion of apricot seeds were reviewed retrospectively. RESULTS: Of the 13 patients, four were male. The mean time of onset of symptoms was 60 minutes (range 20 minutes to 3 hours). On admission, all patients underwent gastric lavage and received activated charcoal. In addition to signs of mild poisoning related to cyanide intoxication, there was severe intoxication requiring mechanical ventilation (in four cases), hypotension (in two), coma (in two) and convulsions (in one). Metabolic acidosis (lactic acidosis) was detected in nine patients and these were treated with sodium bicarbonate. Hyperglycaemia occurred in nine patients and blood glucose levels normalised spontaneously in six but three required insulin therapy for 3-6 hours. Six patients received antidote treatment: high-dose hydroxocobalamin in four and two were treated with a cyanide antidote kit in addition to high-dose hydroxocobalamin. One patient required anticonvulsive therapy. All patients recovered and were discharged from the PICU within a mean (SD, range) 3.1 (1.7, 2-6) days. CONCLUSION: Cyanide poisoning associated with ingestion of apricot seeds is an important poison in children, many of whom require intensive care.

Intoxicación letal por inhalación accidental de fosfuro alumínico / Fatal poisoning by accidental inhalation of aluminium phosphide

Se describen los casos de 2 hermanas de 6 y de 9 años con intoxicación letal por inhalación de fosfuro alumínico, tras su uso inadecuado en el medio rural. La clínica consistió en la rápida instauración de vómitos, arritmias cardíacas, shock, disnea, edema pulmonar/distrés respiratorio agudo, acidosis metabólica y disfunción hepática. Las pacientes fallecieron pese a la instauración de medidas de soporte vital avanzado. Aunque teóricamente un diagnóstico precoz podría mejorar el pronóstico, la alta tasa de letalidad y la ausencia de un antídoto específico para este tóxico deben dirigir los esfuerzos a la prevención, a la restricción de su uso como plaguicida y a alertar acerca de su toxicidad (AU)

The cases of two 6 and 9-year-old sisters with lethal poisoning by inhalation of aluminium phosphide, after its inadequate use in a rural environment, are described. The clinical symptoms consisted of sudden vomiting, cardiac arrhythmias, shock, dyspnea, pulmonary edema/acute respiratory distress, metabolic acidosis and hepatic dysfunction, and the patients died in spite of advanced life support. Although an early diagnosis might theoretically improve the poisoning outcome, its high lethality rate and the absence of a specific antidote, efforts must be directed towards prevention and restricting its use as pesticide and being aware of its toxicity (AU)