ABSTRACT
El nitrito de amilo, conocida como "poppers", se ha masificado como droga recreacional en parte por sus efectos con objetivos sexuales. Su consumo se asocia a complicaciones psiquiátricas y médicas. Reportamos el caso de un paciente que se presenta con metahemog-lobinemia moderada secundaria a la inhalación de nitrito de amilo asociado a alcohol. Al ingreso presenta cianosis peribucal y en extremidades, disociación entre oximetría de pulso y presión parcial de oxígeno en gases arteriales, además de metahemoglobinemia 29,9%. Se descartan otras intoxicaciones y causas primarias de metahemoglobinemia. Se maneja con oxigenoterapia, hidratación y ácido ascórbico, presentando una evolución favorable. Presentamos el primer caso en Chile de metahemoglobinemia secundaria al consumo de nitrito de amilo con fines recreativos.
Amyl nitrite, known as "poppers", has become popular as a recreational drug for sexual purposes. Its consumption is associated with psychiatric and medical complications. We report the case of a patient presenting with moderate methemoglobinemia secondary to amyl nitrite inhalation associated with alcohol. At admission, perioral and extremities cyanosis, a dissociation between pulse oximetry and partial pressure of oxygen in arterial gases, and methemoglobinemia 29.9% were present. Other intoxications and primary causes of methemoglobinemia were ruled out. The patient receives oxygen therapy, hydration, and ascorbic acid, presenting a favorable evolution. We report the first Chilean's case of methemoglobinemia secondary to amyl nitrite consumption for recreational purposes
Subject(s)
Humans , Male , Adult , Amyl Nitrite , Recreational Drug Use , Methemoglobinemia , Partial Pressure , Patients , Oximetry , HIV , Cyanosis , Clinical StudyABSTRACT
Cyanide poisoning can occur from industrial disasters, smoke inhalation from fire, food, and multiple other sources. Cyanide inhibits mitochondrial oxidative phosphorylation by blocking mitochondrial cytochrome oxidase, which in turn results in anaerobic metabolism and depletion of adenosine triphosphate in cells. Rapid administration of antidote is crucial for life saving in severe cyanide poisoning. Multiple antidotes are available for cyanide poisoning. The action mechanism of cyanide antidotes include formation of methemoglobin, production of less or no toxic complex, and sulfane sulfur supplementation. At present, the available antidotes are amyl nitrite, sodium nitrite, sodium thiosulfate, hydroxocobalamin, 4-dimethylaminophenol, and dicobalt edetate. Amyl nitrite, sodium nitrite, and 4-dimethylaminophenol induce the formation of methemoglobin. Sodium thiosulfate supplies the sulfane sulfur molecule to rhodanese, allowing formation of thiocyanate and regeneration of native enzymes. Hydroxocobalamin binds cyanide rapidly and irreversibly to form cyanocobalamin. Dicobalt edetate acts as a chelator of cyanide, forming a stable complex. Based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended for cyanide poisoning. Amyl nitrite and sodium nitrite, which induce methemoglobin, should be avoided in victims of smoke inhalation because of serious adverse effects.
Subject(s)
Adenosine Triphosphate , Aminophenols , Amyl Nitrite , Antidotes , Disasters , Edetic Acid , Electron Transport Complex IV , Equipment and Supplies , Fires , Hydroxocobalamin , Inhalation , Metabolism , Methemoglobin , Oxidative Phosphorylation , Oxygen , Poisoning , Polyphosphates , Regeneration , Smoke , Sodium , Sodium Nitrite , Sulfur , Thiocyanates , Thiosulfate Sulfurtransferase , Thiosulfates , Vitamin B 12ABSTRACT
Although sodium nitroprusside (SNP) is often used in pediatric intensive care units, cyanide toxicity can occur after SNP treatment. To treat SNP-induced cyanide poisoning, antidotes such as amyl nitrite, sodium nitrite, sodium thiosulfate, and hydroxycobalamin should be administered immediately after diagnosis. Here, we report the first case of a very young infant whose SNP-induced cyanide poisoning was successfully treated by exchange transfusion. The success of this alternative method may be related to the fact that exchange transfusion not only removes the cyanide from the blood but also activates detoxification systems by supplying sulfur-rich plasma. Moreover, exchange transfusion replaces cyanide-contaminated erythrocytes with fresh erythrocytes, thereby improving the blood's oxygen carrying capacity more rapidly than antidote therapy. Therefore, we believe that exchange transfusion might be an effective therapeutic modality for critical cases of cyanide poisoning.
Subject(s)
Humans , Infant , Amyl Nitrite , Antidotes , Natural Resources , Cyanides , Erythrocytes , Hydroxocobalamin , Intensive Care Units, Pediatric , Nitroprusside , Oxygen , Plasma , Sodium , Sodium Nitrite , ThiosulfatesABSTRACT
Acute catastrophic pulmonary vasoconstriction frequently leads to cardiovascular collapse. Rapid and selective pulmonary vasodilation is desired in order to restore haemodynamic stability. This pilot study examined the effectiveness of inhaled amyl nitrite as a selective pulmonary vasodilator. Nine adult swine were anaesthetized. Acute pulmonary hypertension with haemodynamic collapse was induced with a bolus administration of a thromboxane analogue, U46619. Six animals then received a capsule of amyl nitrite. The administration of inhaled amyl nitrite decreased mean pulmonary artery pressure from 42 +/- 3 to 22 +/ 3 mmHg at five minutes (p < 0.05), with a concomitant increase in cardiac output and mean arterial pressure. Pulmonary vascular resistance decreased from 4889 +/- 1338 to 380 +/- 195 dyne. sec. cm(-5) (by 92% from the maximal pulmonary hypertension change), with significant improvement in systemic haemodynamics. During acute thromboxane-mediated pulmonary hypertension with cardiovascular collapse, prompt administration of inhaled amyl nitrite was effective in restoring pulmonary and systemic haemodynamics within five minutes.