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Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
Acute poisoning caused by butazolidin (R) (phenylbutazone) has only been described in a few cases [l, 2, 5, 8, ll, 161. The poisoning can be serious, even fatal, unless quick and effective therapy is instituted.We therefore consider it is justified to publish a case of acute butazolidin poisoning in a 15-month-old child and refer to 8 similar cases from the literature. Case HistoryFifteen-month-old female child, healthy previous t o admission, 32 hours prior t o admission consumed 10-15 tablets butazolitlin (It) corresponding to 2-3 g phenylbutazone. The general practitioner who was summoned found the patient unaffected and prescribed a purgative cascara sagrada. Approximately 5 hours after the ingestion of the tablets a gradual deep quickening respiration developed and at the same time the patient became agitated, irritable and had passing jerky spasms in the arms and legs and also 4-5 periods of vomiting. After this she became increasingly lethargic with unchanged deep, rapid respiration.On admission the patient was agitated with slight stupor. The respiration was deep, approximately 50 per minute. Rectal temperature: 36.1", the pulse strong, 140 per minute. The skin was warm, dry and the turgor normsl. The liver could bc felt two fingers under the right curvature in the medio clavicular line, otherwise nothing abnormal was found. Weight was 9 kg.The blood analyses on admission werc: Hgb.: 12.8 g/100 ml, blood urea 50 mg/100 ml, sernm-sodium: 136 mN, scrnm-chloride: 108 mEq/L, serum potasiiim: 2.8 mEq/L, standard bicarbonate: 16.1 mMd/L, pH in capillary blood: 7.48, pC0,: 16 mm Hg.About 2 hours after admission an infusion was commenced through a cranial \-?in with 180 ml of electrolyte mixture (135 nil isotonic NaCL i-45 ml 10 yo glucosc). ,lft'er which 30 ml of blood were given and thc following 18 hours a tot>al of 600 in1 c-lectrolyte mixture (360 ml 8 yo glucose + 120 ml kalii na,tri chloridi 1 120 ml kalii chloridi e. glucoso). To t)he lat'ter soliition t'hcrc was in the beginning added a t,otnl of 5 mEq iVaHC0,. The treatment wit,h infusion was stopped ca. 24 hours aft>er admission as t,he necessary fluids could be givan by rnocit,h, in the beginning as ordinary fluid dict . I n t.he first samples of iirinc passcd 4 hoiirs after t,he commencement of t,hc infusion it slight proteinuria (1.3 %. ) and microscopic hemat#aria was found. Thc mean hour volume mas t'he following day 10-15 ml, t)ht. urine was acid (pH: 5.68-6.38).The general condition during t'hc first 2 days improved considerably, t h c pat~imt retjiirned t o consciousness, the respiration became normal and the pulse lower. At, the same time the pC0, became normidized
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