ABSTRACT
CONTEXT: Hydrofluoric acid (HF) is widely used in industry and at home. Severe lesions can occur after contact with highly concentrated solutions, leading to tissue necrosis and bone destruction. Specific treatment is based on neutralization of fluoride ions with calcium or magnesium solutions. CASE REPORT: A 41-year-old male was seen at the emergency department 35 minutes after skin contact with 70 percent HF, showing whitened swollen lesions on the middle and fourth fingers of his right hand with severe pain starting immediately after contact. 2.5 percent calcium gluconate ointment was applied. Twenty-four hours later, the patient was still in severe pain and the lesions had worsened. Considering the high concentration of the solution, early start of severe pain, lesion characteristics and impossibility of administering calcium gluconate subcutaneously because of the lesion location, the radial artery was catheterized and 2 percent calcium gluconate was administered via infusion pump for 36 hours, until the pain subsided. No adverse effects were seen during the procedure. Ten days later, the lesions were stable, without bone abnormalities on X-rays. Six months later, a complete recovery was seen. CONCLUSIONS: Intra-arterial calcium gluconate might be considered for finger burns caused by concentrated HF. Complete recovery of wounded fingers can be achieved with this technique even if started 24 hours after the exposure. However, controlled clinical trials are needed to confirm the effectiveness and safety of this intervention.
CONTEXTO: Ácido fluorídrico é largamente usado na indústria e no ambiente doméstico. Lesões graves podem ocorrer depois de contato com soluções altamente concentradas levando a necrose tecidual e destruição óssea. O tratamento específico é baseado na neutralização dos íons de flúor com soluções de cálcio ou magnésio. RELATO DE CASO: Homem de 41 anos foi atendido na sala de urgência 35 minutos depois de contato da pele com ácido fluorídrico a 70 por cento, apresentando lesões esbranquiçadas e edemaciadas nos dedos médio e quarto da mão direita com dor intensa que iniciou logo após o contato. Pomada de gluconato de cálcio a 2,5 por cento foi aplicada. Depois de 24 horas, o paciente continuava com dor mais intensa e as lesões haviam piorado. Considerando a concentração da solução, o início precoce da dor intensa, as características das lesões e a impossibilidade de administrar gluconato de cálcio no subcutâneo devido ao local da lesão, foi inserido cateter na artéria radial para infusão de gluconato de cálcio a 2 por cento com bomba de infusão por 36 horas até melhora da dor. Nenhum efeito adverso foi observado durante o procedimento. Dez dias depois as lesões encontravam-se estáveis, sem alterações dos ossos vistas nos raios-X. Seis meses depois houve recuperação completa. CONCLUSÃO: Gluconato de cálcio intra-arterial pode ser considerado em queimaduras digitais por ácido fluorídrico. Recuperação completa dos dedos acometidos pode ser obtida com essa técnica mesmo que iniciada 24 horas após a exposição. Porém, ensaios clínicos controlados são necessários para confirmar a efetividade e a segurança desta intervenção.
Subject(s)
Adult , Humans , Male , Burns, Chemical/drug therapy , Calcium Gluconate/therapeutic use , Finger Injuries/drug therapy , Hydrofluoric Acid/toxicity , Accidents, Occupational , Burns, Chemical/etiology , Finger Injuries/chemically induced , Infusions, Intra-Arterial/methods , Infusions, Intra-Arterial/standardsABSTRACT
PURPOSE: To study the effects of total hepatic ischemia, and reperfusion on the accumulation of neutrophils in the brain of rats submitted to normovolemic conditions as well as to controlled hemorrhagic shock state. METHODS: Thirty two adult male Wistar rats, were divided into four groups: the Control group, was submitted to the standard procedures for a period of 60 min of observation; Shock group, was submitted to controlled hemorrhagic shock (mean arterial blood pressure=40mmHg, 20min) followed by volemic resuscitation (lactated Ringer's solution + blood, 3:1) and reperfusion for 60min; Pringle group, was submitted to total hepatic ischemia for 15min and reperfusion for 60min. The total group was submitted to controlled hemorrhagic shock for 20min followed by volemic resuscitation (lactated Ringer's solution + blood, 3:1), total hepatic ischemia for 15min and reperfusion for 60min. Measurements of serum lactate and base excess were used to characterize the hemorrhagic shock state with low tissue perfusion. The counting of neutrophils on the brain was performed after the euthanasia of animals. RESULTS: The values for the counting of neutrophils on the brain indicate that did not occur difference among studied groups (p=0.196) (Control 0.12± 0.11, Shock 0.12± 0.13, Pringle 0.02± 0.04, Total 0.14± 0.16). CONCLUSION: Hemorrhagic shock associated to total hepatic ischemia for 15 minutes, followed by 60 minutes of reperfusion, did not causes significant neutrophils accumulation in the brain of rats