ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Black widow spider(Latrodectus mactans)envenomation is found throughout both the temperate and tropical latitudes, and is one of the leading causes of death from arthropod envenomations worldwide. The venom is highly neurotoxic, affecting the presynaptic motor endplate to allow massive noradrenaline (norepinephrine) and acetylcholine release into synapses causing excessive stimulation and fatigue of the motor end plate and muscle. Clinically, patients develop a bite site lesion and pain, abdominal pain and tenderness, and lower extremity pain and weakness within minutes to hours of envenomation. Symptoms progress over several hours, then subside over 2 to 3 days. The recommended treatment of ‘common’ envenomation is calcium gluconate 10% intravenously, titrated to relief of symptoms; antivenin, although effective, may cause hypersensitivity and serum sickness reactions, and should be restricted to life-threatening envenomations only.Brown recluse spider(Loxosceles reclusa)envenomations are seen in the Americas and in Europe, and are endemic to the south and central United States. The venom contains at least 8 enzymes, consisting of various lysins (facilitating venom spread) and sphingomyelinase D. which causes cell membrane injury and lysis, thrombosis, local ischaemia, and chemotaxis. Local envenomations begin as pain and itching that progresses to vesiculation with violaceous necrosis and surrounding erythema, and ultimately ulcer formation. Systemic envenomations may be life threatening, and present with fever, constitutional symptoms, petechial eruptions, thrombocytopenia, and haemolysis with haemoglobinuric renal failure. Treatment of local envenomations is conservative (local wound care, cryotherapy, elevation, tetanus prophylaxis, and close follow-up); systemic envenomation requires supportive care and treatment of arising complications, corticosteroids to stabilise red blood cell membranes, and support of renal function. Dapsone 100mg daily has emerged as a promising therapeutic agent in both animal studies and clinical trials.Over 650 species of scorpions are known to cause envenomation (mostly in children under 10 years); they are endemic mostly in arid and tropical areas. Different venoms and clinical presentations are seen across the different species. Most commonly, an inflammatory local reaction occurs with envenomation, which is treated with wound debridement and cleansing, tetanus prophylaxis, and antihistamines. Occasionally the venom is allergenic, and the resultant allergic reaction is treated in a standard fashion. Infrequently. Centruroides sculpturatusmay cause a severe cholinergic envenomation, with presentation of severe cholinergic toxicity (salivation, lacrimation, urination, defecation, bradycardia, bronchospasm, fasciculations). These patients need intensive care unit milieu, treatment of bronchospasm, and high dose anticholinergic therapy titrated to relief of symptoms.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Recent widespread abuse of cocaine has resulted in an alarming increase in emergency department admissions for acute treatment of this toxic drug. Highly publicised cocaine-associated deaths of prominent athletes have awakened both the medical community and the general public to the possible devastating effects of this so-called ‘champagne of drugs’. A potent central nervous system stimulant, cocaine produces symptoms that include changes in activity, mood, blood pressure, cardiac rhythm, respiration and body temperature. The adverse effects of cocaine, which may progress rapidly to death, include cerebrovascular accidents, myocardial infarction, sudden cardiac arrhythmias, pneumomediastinum, rhabdomyolysis with myoglobinuric renal failure and intestinal ischaemia. In addition, cocaine has been implicated in obstetric and neontal complications. Because of the exceedingly rapid progression of the ‘cocaine reaction’ to a fatal outcome, it is imperative that clinicians know how to recognise and manage the symptoms of cocaine overdose.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Acute pancreatitis has a high morbidity and significant mortality. Among its many causes ethanol is pre-eminent, but many other drugs have also been incriminated. This article begins with a definition of the mechanisms, pathogenesis and clinical features of acute pancreatitis; it then critically reviews the evidence for drugs, excluding ethanol, as being causative. The drugs which have been implicated are considered under 3 headings: definite associations, probable associations and unlikely associations. A brief outline of possible treatment, strategies and prognosis associated with acute pancreatitis concludes the article.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

In order to avoid inappropriate therapy and prolonged morbidity, it is important to recognise when a patient's rheumatic complaints are due to drugs. However, this is often difficult because of the large number of drugs that have been implicated and the diversity of clinical presentations.Arthropathy may be seen with several different syndromes, including drug-induced lupus erythematosus (DILE), serum sickness and gout. The most widely reported of these is DILE, which usually develops after some months or even years of drug therapy. While many authors do not specifically require their presence for the diagnosis of DILE, antinuclear antibodies have been detected in the great majority of reported patients with DILE, whatever the causative drug. In contrast, patients who develop arthropathy soon after commencing a drug rarely have antinuclear antibodies and appear to be distinct from patients with DILE.Apart from arthropathy, a number of other syndromes that appear to have an immunological basis may be induced by drugs. Cutaneous vasculitis is not uncommon and drugs are frequently considered to be the aetiological factor. Whether drugs may cause larger vessel systemic vasculitis is less certain. Rarely, polymyositis and scleroderma-like syndromes have been associated with drug therapy.Corticosteroid-induced osteoporosis is a complication of all the corticosteroid preparations that are widely used at present. However, the development of deflazacort, a so-called ‘bone-sparing’ steroid, has raised the possibility that the effect of corticosteroids on bone may be separable, at least in part, from the other actions of these drugs. Data have been conflicting with regard to whether there is a ‘safe’ dose of corticosteroid. Similarly, it is unclear whether prophylactic therapy with agents such as calcium, fluoride and vitamin D is beneficial. Nonetheless, recent findings suggest that approaches will be developed to minimise the risk of osteoporosis in patients who require corticosteroids.There are a number of other ways in which drugs may affect bones. Osteomalacia is a well-known but uncommon complication of treatment with anticonvulsants and occasionally other drugs. The mechanism probably relates to the induction of hepatic enzymes and the consequent increased metabolism of vitamin D in patients with borderline levels initially. Osteosclerosis may also result from drug therapy: usually with fluoride or retinol (vitamin A) and its analogues.With continued research, the true spectrum of drug-induced rheumatic syndromes should become more clearly defined. This will be of diagnostic assistance as well as being of value in studying the mechanisms behind these syndromes.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

We report 3 cases and review the published literature on sodium azide ingestion. A 38-year-old man intentionally ingested 2 tablespoonsful of sodium azide in water and developed seizures, coma, hypotension and fatal ventricular arrhythmias within 2 hours. A 33-year-old male ingested an unknown quantity of sodium azide. In the emergency department he was unconscious and underwent immediate intubation and gastric lavage. Nitrite therapy was instituted without improvement. He remained acidotic despite bicarbonate therapy and developed hypotension which was unresponsive to pressor agents. He died approximately 8 hours after admission despite resuscitative efforts. A 52-year-old male ingested 1.5 to 2g of sodium azide and survived for 40 hours. Nitrite therapy was ineffective.The role of sodium nitrite in treating sodium azide toxicity by producing methaemoglobin which complexes with azide is discussed.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS