{"title":"Physical assessment and differential diagnosis of the poisoned patient.","authors":"K R Olson, P R Pentel, M T Kelley","doi":"10.1007/BF03259860","DOIUrl":"10.1007/BF03259860","url":null,"abstract":"<p><p>The rapid diagnosis and immediate intervention required in patients with serious drug overdose or poisoning makes toxicological screening of limited value to the emergency department physician. Instead, a careful clinical evaluation using the history, physical examination, and the more readily available laboratory tests may allow a tentative diagnosis and the initiation of life-saving treatment. Laboratory tests should include serum osmolality, electrolytes, glucose, BUN and an estimation of the anion and osmolar gaps. The ECG can also provide useful information. Clinical findings of important include altered blood pressure, pulse, respiration and body temperature, the presence of coma, agitation, delirium or psychosis, and muscular weakness. An ophthalmological examination is also of importance in the acutely poisoned patient. Oral burns or dysphagia may occur following ingestion of any strongly reactive substance, but the absence of oral burns does not preclude the possibility of oesophageal or stomach injury. Odours and skin colour may also contribute to the diagnosis. Comprehensive toxicology screening may not be immediately available, or may be inaccurate, thus adding little to the information obtained during the initial evaluation of the poisoned patient.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 1","pages":"52-81"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14669715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Treatment of human amatoxin mushroom poisoning. Myths and advances in therapy.","authors":"G L Floersheim","doi":"10.1007/BF03259857","DOIUrl":"https://doi.org/10.1007/BF03259857","url":null,"abstract":"","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259857","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14669913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neurological manifestations and toxicities of the antituberculosis drugs. A review.","authors":"M R Holdiness","doi":"10.1007/BF03259859","DOIUrl":"10.1007/BF03259859","url":null,"abstract":"<p><p>The neurological manifestations and toxicities of 12 antituberculosis drugs [isoniazid, rifampicin (rifampin), ethambutol, p-aminosalicylic acid, pyrazinamide, streptomycin, kanamycin, ethionamide, cycloserine, capreomycin, viomycin and thiacetazone] are reviewed. Their effects upon the central nervous system, cranial nerves, peripheral nerves and the neuromuscular junction are examined, and drug interactions of neurological concern are briefly discussed. Isoniazid is well known to increase the concentrations of gamma-aminobutyric acid in neural tissues. Although conflicting data have been published, isoniazid may play a limited future role in reducing the degree of adventitious movements noted in certain neurological diseases such as multiple sclerosis, spasmodic torticollis, and other segmental dystonic syndromes. With rifampicin neurological complications have been observed infrequently. Rifampicin penetrates into the CSF and has been shown to have useful activity against various micro-organisms in the CSF, including certain viruses; however, contrary to earlier suggestions, it appears to have no role in the treatment of subacute sclerosing panencephalitis. A number of studies have indicated that isoniazid is associated with a large number of accidental and intentional poisonings. The highest incidence has been observed with Southwestern American Indians in which this agent was involved in 7% of all suicide attempts and 19% of the suicide deaths. Degeneration of the optic chiasma and nerve is a well-known adverse effect of ethambutol; toxicity is manifested by impairment of visual acuity, marked loss of colour discrimination, constricted visual fields, and central and peripheral scotoma. Ototoxicity is a well known problem caused by streptomycin, kanamycin, capreomycin and viomycin. The use of streptomycin in pregnant mothers is associated with congenital deafness in newborns in certain cases. The aminoglycoside antibiotics are also associated with flaccid paralysis following neuromuscular blockade. Adverse reactions to cycloserine are mainly dose-related with neurological and psychiatric syndromes noted in up to 50% of patients. Recent data indicate that isoniazid, rifampicin, ethambutol, pyrazinamide, streptomycin, kanamycin, ethionamide, and cycloserine appear in measurable quantities in the cerebrospinal fluid. Five of these compounds (isoniazid, rifampicin, ethambutol, kanamycin, cycloserine) pass to some degree through non-inflamed meninges. Other than discontinuation of the therapeutic regimen and general supportive measures, very few methods are described in the literature for treatment of acute intoxications with antituberculosis drugs.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 1","pages":"33-51"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14669711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adverse effects of hypolipidaemic drugs.","authors":"L C Knodel, R L Talbert","doi":"10.1007/BF03259858","DOIUrl":"10.1007/BF03259858","url":null,"abstract":"<p><p>Cholestyramine, colestipol, clofibrate, gemfibrozil, nicotinic acid (niacin), probucol, neomycin, and dextrothyroxine are the most commonly used drugs in the treatment of hyperlipoproteinaemic disorders. While adverse reaction data are available for all of them, definitive data regarding the frequency and severity of potential adverse effects from well-controlled trials using large numbers of patients (greater than 1000) are available only for cholestyramine, clofibrate, nicotinic acid and dextrothyroxine. In adult patients treated with cholestyramine, gastrointestinal complaints, especially constipation, abdominal pain and unpalatability are most frequently observed. Continued administration along with dietary manipulation (e.g. addition of dietary fibre) and/or stool softeners results in diminished complaints during long term therapy. Large doses of cholestyramine (greater than 32 g/day) may be associated with malabsorption of fat-soluble vitamins. Most significantly, osteomalacia and, on rare occasions, haemorrhagic diathesis are reported with cholestyramine impairment of vitamin D and vitamin K absorption, respectively. Paediatric patients have been reported to experience hyperchloraemic metabolic acidosis or gastrointestinal obstruction. Concurrent administration of acidic drugs may result in their reduced bioavailability. Serious adverse reactions to clofibrate will probably limit its role in the future. Of particular concern are ventricular arrhythmias, induction of cholelithiasis and cholecystitis, and the potential for promoting gastrointestinal malignancy which far outweigh the reported benefits in preventing new or recurrent myocardial infarction, cardiovascular death and overall death. Patients with renal disease are particularly prone to myositis, secondary to alterations in protein binding and impaired renal excretion of clofibrate. Drug interactions with coumarin anticoagulants and sulphonylurea compounds may produce bleeding episodes and hypoglycaemia, respectively. Nicotinic acid produces frequent adverse effects, but they are usually not serious, tend to decrease with time, and can be managed easily. Dermal and gastrointestinal reactions are most common. Truncal and facial flushing are reported in 90 to 100% of treated patients in large clinical trials. Significant elevations of liver enzymes, serum glucose, and serum uric acid are occasionally seen with nicotinic acid therapy. Liver enzyme elevations are more common in patients given large dosage increases over short periods of time, and in patients treated with sustained release formulations.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"2 1","pages":"10-32"},"PeriodicalIF":0.0,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14669713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Clinical features and management of self-poisoning with newer antidepressants.","authors":"P Crome, C Ali","doi":"10.1007/BF03259852","DOIUrl":"https://doi.org/10.1007/BF03259852","url":null,"abstract":"<p><p>Over the last decade a number of antidepressants have been introduced which differ either chemically, pharmacologically or toxicologically from established tricyclic and monoamine oxidase drugs. Of those presently available, maprotiline is similar in toxicity to tricyclic antidepressants perhaps causing convulsions more frequently. Lofepramine is metabolised to desmethylimipramine, but the limited clinical experience so far suggests that toxicity is less severe than with other tricyclic antidepressants. Amoxapine causes coma, convulsions and less frequently renal failure, but electrocardiographic abnormalities are uncommon. Mianserin and trazodone both cause drowsiness and more infrequently deeper grades of coma. Alprazolam produces the typical benzodiazepine overdose symptoms of drowsiness and floppiness. There is as yet insufficient clinical data to comment on the specific toxicity of fluoxetine and fluvoxamine. There are many more new antidepressants in various stages of development and it is likely that several of these will be marketed. Since their individual toxicities differ it is essential that monitoring of their overdose effects should be undertaken.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"1 6","pages":"411-20"},"PeriodicalIF":0.0,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259852","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14663031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Medication-induced oesophageal injury. Survey of the literature.","authors":"S J Bott, R W McCallum","doi":"10.1007/BF03259855","DOIUrl":"https://doi.org/10.1007/BF03259855","url":null,"abstract":"<p><p>This is a review of the 127 cases of drug-induced oesophagitis reported in the English language literature since 1970. The most common symptoms reported were retrosternal pain, odynophagia, and dysphagia. Most cases were self-limited and symptoms resolved in 7 to 10 days with symptomatic therapy. Occasionally, severe odynophagia or dysphagia necessitated hospitalisation. Emepronium bromide, tetracycline and its derivatives, potassium chloride, and quinidine account for 89% of the reported cases of medication-induced oesophageal injury. 14 other medications have been reported to injure the oesophagus. Serious sequelae, including death, have been linked to potassium-induced oesophageal injury. With other medications, however, serious complications were rare. The diagnostic study of choice is endoscopy; an air-contrast barium swallow may also detect the often subtle mucosal abnormalities produced by medication injury. However, the diagnosis does not require confirmation by radiographical or endoscopic means in all cases, and the history alone may be sufficient to make the diagnosis in uncomplicated cases. Medication-induced oesophageal injury is preventable if pills are taken with an adequate amount of fluid and if the practice of taking medications immediately before bedtime is avoided.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"1 6","pages":"449-57"},"PeriodicalIF":0.0,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259855","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14662949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lead intoxication.","authors":"L S Ibels, C A Pollock","doi":"10.1007/BF03259851","DOIUrl":"https://doi.org/10.1007/BF03259851","url":null,"abstract":"<p><p>Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout. Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000 mg, and in adults 1000 mg administered intravenously or 2000 mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 micrograms/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"1 6","pages":"387-410"},"PeriodicalIF":0.0,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259851","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14663030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Vincristine neurotoxicity. Pathophysiology and management.","authors":"S S Legha","doi":"10.1007/BF03259853","DOIUrl":"https://doi.org/10.1007/BF03259853","url":null,"abstract":"<p><p>Vincristine is an antineoplastic drug with a broad spectrum of activity against haematological malignancies and childhood sarcomas. Besides useful activity, it lacks the usual emetic and myelotoxicity of anticancer drugs, but its use is limited by neurotoxicity. The neurotoxicity commonly manifests as reduced motility of the intestines resulting in constipation, and peripheral neuropathy which is predominantly sensory in nature. The early symptoms include numbness and tingling of hands and feet which is accompanied by loss of deep tendon reflexes. In its more severe form, muscle weakness develops which is more marked in distal muscles of the hands and feet. Other manifestations of neurotoxicity include ocular palsies, hoarseness of voice, and autonomic neuropathy in the form of postural hypotension and atony of the urinary bladder. The neurotoxicity is dose related and cumulative with repeated dosage such that the drug therapy has to be stopped after a cumulative dose of 30 to 50 mg. The neurotoxicity is usually reversible on interruption of the therapy, but the recovery is slow and takes several months. There are no specific antidotes which have established usefulness against neurotoxicity.</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"1 6","pages":"421-7"},"PeriodicalIF":0.0,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF03259853","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14663033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Drug-induced psychiatric disorders and their management.","authors":"L E Hollister","doi":"10.1007/BF03259854","DOIUrl":"10.1007/BF03259854","url":null,"abstract":"<p><p>Psychiatric disorders induced by drugs are of most concern when they occur in the context of therapeutic use of a drug. Such iatrogenic psychiatric disturbances may interfere considerably with the treatment of the primary illness and may cause concern to patients, their relatives and the medical staff. Because many drugs are often used simultaneously in seriously ill patients, it may be difficult to be sure which drug may have been responsible. The best procedure is to remove those drugs which are most probable causes of the psychiatric disturbances as well as any drugs that are not truly essential for the treatment of the patient. Problems involved in evaluating the relationship between use of drugs and psychiatric disorders are considerable. Many reports are isolated cases and the denominators which might provide some idea of the potential risk are unknown. Many relationships are still controversial, such as the association of depression with sedatives, antihypertensives and oral contraceptives. Areas of uncertainty are great. Psychomotor impairment may be caused by a drug that can alter consciousness, or any drugs that can produce more delineated psychiatric syndromes. Sedative drugs are those most commonly associated with psychomotor impairment, and may include psychotherapeutic drugs, sedative antihistamines, narcotic analgesics and, of course, the widely used social drug, alcohol. Delirious states are most often associated with drugs that possess central anticholinergic actions. These include not only drugs clearly identified as anticholinergics, but also tricyclic antidepressants and anti-Parkinson drugs. Cimetidine, which is often used parenterally in seriously ill patients, is also a prominent cause. Delirium is most often seen in elderly patients and in those who have received rather large doses of drugs. The association of schizophrenic-like psychoses with dopaminomimetic drugs tends to support the prevailing dopamine hypothesis of schizophrenia. Levodopa, the dopamine precursor, and bromocriptine, a direct dopamine agonist, are examples of such relationships. Abuse of social drugs has also been thought to provide a useful model of schizophrenia. Hallucinogens are probably a rather poor model, abuse of amphetamines may provide a better model, and possibly the best is the psychotic state elicited by phencyclidine. Manic reactions are clinically difficult to differentiate from schizophrenic-like psychoses and are often produced by similar drugs. Corticosteroids may produce either manic or schizophrenic-like disorders, as well as occasionally confusion and depression.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77871,"journal":{"name":"Medical toxicology","volume":"1 6","pages":"428-48"},"PeriodicalIF":0.0,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14662948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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