Pulmonary involvement from animal toxins: the cellular mechanisms.

Venomous animals and their venom have always been of human interest because, despite species differences, coevolution has made them capable of targeting key physiological components of our bodies. Respiratory failure from lung injury is one of the serious consequences of envenomation, and the underlying mechanisms are rarely discussed. This review aims to demonstrate how toxins affect the pulmonary system through various biological pathways. Herein, we propose the common underlying cellular mechanisms of toxin-induced lung injury: interference with normal cell function and integrity, disruption of normal vascular function, and provocation of excessive inflammation. Viperid snakebites are the leading cause of envenomation-induced lung injury, followed by other terrestrial venomous animals such as scorpions, spiders, and centipedes. Marine species, particularly jellyfish, can also inflict such injury. Common pulmonary manifestations include pulmonary edema, pulmonary hemorrhage, and exudative infiltration. Severe envenomation can result in acute respiratory distress syndrome. Pulmonary involvement suggests severe envenomation, thus recognizing these mechanisms and manifestations can aid physicians in providing appropriate treatment.

Pulmonary involvement from animal toxins: the cellular mechanisms

Abstract Venomous animals and their venom have always been of human interest because, despite species differences, coevolution has made them capable of targeting key physiological components of our bodies. Respiratory failure from lung injury is one of the serious consequences of envenomation, and the underlying mechanisms are rarely discussed. This review aims to demonstrate how toxins affect the pulmonary system through various biological pathways. Herein, we propose the common underlying cellular mechanisms of toxin-induced lung injury: interference with normal cell function and integrity, disruption of normal vascular function, and provocation of excessive inflammation. Viperid snakebites are the leading cause of envenomation-induced lung injury, followed by other terrestrial venomous animals such as scorpions, spiders, and centipedes. Marine species, particularly jellyfish, can also inflict such injury. Common pulmonary manifestations include pulmonary edema, pulmonary hemorrhage, and exudative infiltration. Severe envenomation can result in acute respiratory distress syndrome. Pulmonary involvement suggests severe envenomation, thus recognizing these mechanisms and manifestations can aid physicians in providing appropriate treatment.

Alprazolam and lorazepam overdose and the absence of brainstem reflexes.

Benzodiazepines (BZDs) rarely cause respiratory depression and death. On the other hand, high-dose BZDs may lead to profound sedation and diminished brainstem functions that mimic other structural brain lesions as described in our case: a 70-year-old unresponsive woman. She was hypothermic and had rapid shallow breathing. Her Glasgow Coma Scale score was E1V1M4, with pinpoint pupils and absent corneal, oculocephalic and oculovestibular reflexes. Other physical exams, laboratory testing and brain imaging were unremarkable. After two doses of 0.4 mg naloxone and intravenous thrombolytics were given, there were no significant responses, and the diagnosis remained a mystery. The cause of her unconsciousness was uncovered when her husband found empty bags of 80 tablets of alprazolam and lorazepam. Her consciousness and brainstem reflexes improved dramatically after 0.25 mg of intravenous flumazenil. The blood for BZDs concentration showed alprazolam 268 ng/mL (20-40 ng/mL), lorazepam 861 ng/mL (20-250 ng/mL) and their metabolites.

Escitalopram, bupropion, lurasidone, lamotrigine and possible vortioxetine overdose presented with serotonin syndrome and diffuse encephalopathy: A case report.

BACKGROUND: Psychotropic drugs can cause neurological effects when overdosed. This study reports a case of psychotropic drugs overdose presenting with serotonin toxicity and encephalopathy. CASE PRESENTATION: A 20-year-old female with major depression presented with agitation 3 h after an overdose on multiple medications. Her current medications were vortioxetine, lamotrigine, lurasidone, and bupropion (extended-release). Vital signs showed hyperthermia and tachycardia. Neurological examination was remarkable for mydriasis and hyperreflexia with inducible ankle clonus. The electrocardiography showed sinus tachycardia with QTc 480 ms. Twelve hours later, she became obtunded and developed subcortical myoclonus. The electroencephalogram demonstrated a diffuse encephalopathy pattern without epileptic activities. She was diagnosed with serotonin syndrome based on Hunter Serotonin Toxicity Criteria. Myoclonus and abnormal vital signs resolved within hours after cyproheptadine administration, but she remained unconscious for 3.5 days. Urine drug screening was positive for benzodiazepines and metabolites, lamotrigine, escitalopram, and hydroxybupropion. This suggested she had overdosed on escitalopram which had been previously prescribed. Unfortunately, vortioxetine and lurasidone could not be detected by our current facilities. CONCLUSION: This case exhibited serotonin syndrome and encephalopathy from overdose of multiple psychotropic agents. Her prolonged depressed consciousness could be explained by the half-life of the drugs and possible drug interactions.

Alterations of body composition patterns in pre-dialysis chronic kidney disease patients.

PURPOSE: Body mass index (BMI) might be an inaccurate estimate of detailed body composition because it does not differentiate muscle from fat mass. We sought to understand the effect of kidney function decline on alterations of body composition patterns among pre-dialysis CKD patients. METHODS: Body composition was measured by multi-frequency bioelectrical impedance analysis (BIA). Low muscle mass was defined as appendicular muscle mass (kg) adjusted to the square of height in meters < 7.0 and 5.7 kg/m2 in men and women, respectively. The designation of obesity by percent body fat was ≥ 25% in men and ≥ 30% in women. Alternative definition of obesity by BMI was ≥ 25 kg/m2. Visceral fat area cut point was > 100 cm2 as indication of abdominal obesity. RESULTS: Mean age of participants was 61.3 ± 13.8 years (n = 103). The average glomerular filtration rate (GFR) was 34.0 ± 24.2 mL/min/1.73 m2. By BIA, the prevalence of low muscle mass was 16.5% and was comparable between both sexes. Obesity by percent body fat was identified in 71.8% of patients and 38.2% had abdominal obesity. Using BMI criteria, the prevalence of obesity was less common (55.3%) and associated with under-identification of obesity by 27.0%. Low muscle mass and obesity by percent body fat were more prevalent in the more advanced stages of CKD. By multivariable regression analysis, a 10 mL/min/1.73 m2 decline in GFR was associated with a 0.59 kg reduction of total body muscle mass (p = 0.01), but not fat mass or BMI, after adjusting for confounders. CONCLUSION: Low muscle mass was prevalent among pre-dialysis CKD patients. BMI commonly classified obese CKD individuals by percent body fat criteria as non-obese. The reduction of muscle mass was associated with GFR decline.

Ergotism unresponsive to multiple therapeutic modalities, including sodium nitroprusside, resulting in limb loss.

Unlike epidemics in past centuries, patients suffering from peripheral vascular ischemia related to ergotism now rarely lose a limb because of vasodilator therapies. We report a patient with ischemia from ergotamine tartrate who failed to recover with medical therapy, resulting in limb amputation.