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

The plasma‐hydrocortisone level has been examined in ten patients with acute coronary occlusion and shock, in 12 patients with acute coronary occlusion without shock, in seven patients with congestive heart failure and in five control patients. Owing to the cir‐cadian rhythm of the plasma‐hydrocortisone level, the examinations have been carried out in five daily determinations on three consecutive days. As compared with the control patients, the average values were found to be significantly higher in patients with congestive heart failure and even higher in the patients with coronary occlusion with and without shock. No correlation was found between the plasma‐hydrocortisone concentration and the enzymes SGOT and SLDH, the morning temperature or the blood pressure in the patients with acute myocardial infarction. The plasma‐hydrocortisone level in the patients with coronary occlusion returned to the normal range within 48 hours after admission. The highest values were found in the patients who died, and the increased level was maintained until the last determinations before death.