Christopher H. Linden

A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning

STUDY OBJECTIVE To compare the efficacy and safety of physostigmine with benzodiazepines for the treatment of agitation and delirium associated with anticholinergic poisoning. METHODS We conducted a retrospective study of 52 consecutive patients referred to a university hospital toxicology consultation service who were treated with physostigmine, benzo-diazepines, or both for anticholinergic agitation and delirium. Patients treated with physostigmine were compared with those treated with benzodiazepines with respect to demographics, severity of poisoning, response to treatment, side effects of treatment, and complications. RESULTS Physostigmine controlled agitation and reversed delirium in 96% and 87% of patients, respectively. Benzodiazepines controlled agitation in 24% of patients but were ineffective in reversing delirium. Initial treatment with physostigmine (n=30) resulted in a significant decrease in the incidence of agitation (P <.001) and level of central nervous system stimulation (P <.001), whereas initial treatment with benzodiazepines (n=22) did not (P =.03 and P =.05, respectively). Patients treated initially with physostigmine had a significantly lower incidence of complications (7% versus 46%; P <. 002) and a shorter time to recovery (median, 12 versus 24 hours; P =. 004) than those treated initially with benzodiazepines. There were no significant differences between these groups in the incidence of side effects (7% versus 14%; P =0.6) and length of stay (median, 32 versus 39 hours; P =.15). CONCLUSION Results suggest that physostigmine is more effective and safer than benzodiazepines for the treatment of anticholinergic agitation and delirium. A prospective controlled study is necessary to confirm such findings.

Acute ingestions of boric acid

Four patients with elevated serum boric acid levels after single, acute ingestions of 10 to 297 grams were reported to the Rocky Mountain Poison and Drug Center (RMPDC) between January 1983 and August 1985. Systemic effects were absent. In 1983-4, 364 cases of boric acid exposure were reported to the RMPDC with only one fatality from a probable chronic ingestion. Vomiting, nausea, diarrhea, and abdominal cramps were rather common. Systemic effects were notably absent in acute ingestions. Five of three hundred sixty-four patients had measured serum levels and were the only ones hospitalized. These observations suggest that significant poisoning is unlikely to result from a single, acute ingestion of boric acid. Serum boric acid levels appear to correlate poorly with clinical toxicity following acute ingestion.

Metabolic acidosis after acute ibuprofen overdosage

poster) presented at the American Association of Poison Control Centers/American Academy of Clinical Toxicology/ American Board of Medical Toxicology/Canadian Association of Poison Control Centres Annual Scientific Meeting, Sept. 25-30, 1986, Santa Fe, New Mexico. Submitted for publication March 31, 1987; accepted June 10, 1987. Reprint requests: Christopher H. Linden, MD, Assistant Professor, Department of Medicine, University of Massachusetts Medical Center, Worcester, MA 01605. another hospital. Inspection of the vomitus revealed both intact pills and pill fragments. Approximately 11/2 hours after ingestion, vital signs were as follows: pulse 120 beats/min, blood pressure 110/80 mm Hg, and respiratory rate 16/min. The child was flaccid, pale, and responsive only to pain. An intravenous infusion of dextrose 5% in water was started and oxygen was administered by nasal cannula. After gastric lavage with 0.9% saline solution through a size 12F nasogastric tube, the patient was given 5 g of activated charcoal and transferred to our institution. Approximately 3 hours after ingestion, vital signs were as follows: pulse 140 beats/min, blood pressure, t00/80 mm H g , respiratory rate 32/min, and rectal temperature 37 ~ C. CheyneStokes respirations with occasional periods of apnea lasting up to 10 seconds were noted. Rubbing of the sternum abruptly terminated the apnea and resulted in crying and withdrawal of the BUN SGOT SGPT LDH hpf Blood urea nitrogen Serum glutamic-oxaloacetic transaminase Serum glutamic-pyruvic transaminase Lactate dehydrogenase High-power field extremities. Results of the physical examination were otherwise urlchanged from those described above. Gastric lavage was repeated, and 15 g of activated charcoal with 15 ml of 70% sorbitol was administered by nasogastric tube. A Foley catheter was inserted, and the child was admitted to the intensive care unit. Laboratory evaluation yielded the following values: a[terial pH 7.27, Pr 36 mm Hg, and PO~ 110 mm Hg; serum sodium 140 mEq/L, potassium 3.6 mEq/L, chloride 106 mEq/L, bicarbonate 19 mEq/L, anion gap 15 mEq/L, and glucose 219 mg/dl (12.2 mmol/L). The complete blood cell count, the BUN, serum creatinine, SGOT, SGPT, LDH, and alkaline phosphatase levels, the prothrombin and partial thromboplastin times, and the urinalysis results were normal except for glucosuria (3+). Toxicologic analysis of blood and urine by thin-layer chromatography showed positive results only for ibuprofen. No salicylate was detected.