Heroin body packers.

Fourteen body packers carrying 2-112 heroin packages are reported. Nine people swallowed the packets, and five inserted them rectally. The ingested packages were large and radio-opaque; they consisted of hard lumps of concentrated heroin usually covered with glove latex, white adhesive tape, and a toy balloon. There were two complications in the 14 patients. One patient developed a bowel obstruction; at laparotomy 8 packages were found in the stomach and 27 at the ileo-cecal valve. Another patient, with heroin wrapped only with black electrician's tape and no latex inner or outer wrappings, developed heroin intoxication, noncardiogenic pulmonary edema, and a bowel obstruction. Eighteen packages were surgically removed from his stomach and 26 from his bowel. We recommend bisacodyl suppositories, activated charcoal mixed with a 3% sodium sulfate cathartic, and phosphosoda enemas for package removal; close observation for heroin toxicity or bowel obstruction; and surgical intervention for continuing toxicity, retention of packages in the stomach, or bowel obstruction.

Diphenoxylate-atropine (Lomotil) overdose in children: an update (report of eight cases and review of the literature)

Eight pediatric accidental overdoses of diphenoxylate-atropine (Lomotil) are reported, and 28 literature cases are reviewed. This overdose is primarily an opioid intoxication, occasionally associated with atropine toxicity. Only 6 of 36 children showed signs of atropine overdose (central nervous system excitement, hypertension, fever, flushed dry skin). Contrary to popular belief, atropine effects occur before, during, or after opioid effects. Opioid overdose (central nervous system and respiratory depression with miosis) predominated or occurred without any signs of atropine toxicity in 33 cases (92%). Diphenoxylate-induced hypoxia was the major problem and was associated with slow or fast respirations, hypotonia or rigidity, cardiac arrest, and in 3 cases cerebral edema and death. Respiratory depression recurred 13 to 24 hours after the ingestion in 7 cases and was probably due to accumulation of difenoxine, an active metabolite of diphenoxylate. Recommended treatment is intravenous naloxone for depressed or inadequate respirations, followed by continuous intravenous naloxone infusion, prompt gastric lavage, repeated administration of activated charcoal, and close monitoring for 24 hours.

Castor bean intoxication.

We report the cases of a child who ingested two or more castor beans and two adults who each ingested four beans. All three patients developed severe gastroenteritis and recovered without sequelae after receiving IV fluids. The literature contains reports of 424 cases of castor bean intoxication. Symptoms of intoxication include acute gastroenteritis, fluid and electrolyte depletion, gastrointestinal bleeding, hemolysis, and hypoglycemia. Delayed cytotoxicity has not been reported. Of the 424 patients, 14 died (mortality rates: 8.1% of untreated and 0.4% of treated). Deaths were due to hypovolemic shock. Recommended treatment for asymptomatic patients who have chewed one or more raw beans is emergency department evaluation, gastric decontamination, administration of activated charcoal, observation until four to six hours after ingestion, and discharge instructions to return if symptoms develop. After decontamination and activated charcoal, symptomatic patients require hospitalization for treatment with IV fluids, supportive care, and monitoring for hypoglycemia, hemolysis, and complications of hypovolemia. Monitoring for delayed cytotoxicity is unnecessary. Castor beans and their dust are highly allergenic and may cause anaphylaxis.

Confirmation of LSD intoxication by analysis of serum and urine.

Serum and urine specimens of 31 patients with suspected lysergic acid diethylamide (LSD) intoxication were analyzed for LSD by both radioimmunoassay (RIA) and high-pressure liquid chromatography (HPLC). The RIA assay, using 0.1 ng/mL as the limit of detection instead of the manufacturer's recommendation of 0.5 ng/mL, was positive for LSD in 13 blood and urine specimens from 14 patients. Results were compared to HPLC analysis using methysergide instead of lysergol as the internal standard and a limit of detection of 0.5 ng/mL. HPLC detected LSD in 9 of 13 serum specimens and 11 of 13 urine specimens that had tested positive by RIA. Of 18 patients with a final clinical diagnosis of LSD intoxication, LSD was detected by RIA in 14 patients and by HPLC in 11 patients. For 13 other cases in which the final diagnosis was a condition other than LSD intoxication, serum and urine assays for LSD were negative in all cases by both techniques. LSD assays have not been generally available in clinical laboratories. We conclude that the qualitative determination of LSD in either serum or urine by a commercially available radioimmunoassay has made it possible to provide reliable laboratory confirmation of LSD intoxication.

Pentazocine (Talwin) intoxication: report of 57 cases.

Overdose of pentazocine (Talwin), an agonist/antagonist opioid analgesic, is relatively uncommon. Fifty-seven cases occurring over ten years are reported. Twenty-three patients (40%) had ingested only pentazocine and did not have the classic opioid toxidrome of CNS and respiratory depression with miosis. Most patients were awake, and no patient had a respiratory rate below 12/minute. Other findings included: grand mal seizures, hypertension, hypotonia, dysphoria, hallucinations, delusions, and agitation. Eleven of 23 patients received IV naloxone (0.4-2.4 mg), but only two showed improvement. Thirty-four patients (60%) had coingested pentazocine with one to five additional substances. Patients who had ingested pentazocine with alcohol, a sedative/hypnotic drug, or an antihistamine, showed increased toxicity, including apnea, deep coma, and recurrent seizures. One patient developed opioid pulmonary edema. One patient died. Three of five patients with coma and inadequate respirations responded to IV naloxone in doses of 0.4 to 1.2 mg.

Pine oil cleaner ingestion.

We report the cases of 22 patients who were hospitalized for pine oil cleaner ingestion. The toxic manifestations most commonly observed were mucous membrane and gastrointestinal irritation. Ataxia, which did not occur in adults, was a frequent presenting sign of intoxication in children. Fifty-nine percent of patients who ingested only pine oil cleaner developed central nervous system depression, and three of these developed coma. Three of five children and three of 17 adults developed acute hydrocarbon pneumonitis. Unlike aspiration pneumonitis, which follows petroleum distillate ingestion, chemical pneumonitis from pine oil cleaner may occur from gastrointestinal absorption of pine oil and deposition in lung tissue. However, recovery from pneumonitis in our patients was typically rapid and complete. Only two adults developed secondary bacterial pneumonia; no patient died. Ingestion of pine oil cleaner was rarely life threatening; most patients needed only gastrointestinal decontamination and minimal supportive care.

Ammonium nitrate cold pack ingestion.

Disposable ammonium nitrate cold packs are widely used in emergency departments instead of ice bags. Five confused or suicidal patients who tore open a pack and ingested from 64 to 234 grams of ammonium nitrate in a single dose, and another patient who attempted to do so, are reported. It is known that chronic ingestion of 6 to 12 grams/day of ammonium nitrate may cause gastritis, acidosis, isosmotic diuresis, and nitrite toxicity manifesting as methemoglobinemia or vasodilatation. None of these patients developed severe toxicity, although three had symptoms of gastritis, three had slight methemoglobinemia, and two had mild hypotension. The product was removed from the stomach promptly in three of the five patients. None had pre-existing renal or intestinal dysfunction, which are known to enhance ammonium nitrate toxicity.

Detection of phencyclidine usage by radioimmunoassay of saliva.

Paired serum and saliva samples, obtained from 100 emergency department patients suspected of phencyclidine (PCP) intoxication, were analyzed using a specific PCP radioimmunoassay (RIA). Seventy-four of the 100 saliva samples and 75 of the paired serum samples were positive for PCP. The final clinical diagnosis was PCP intoxication in 79 cases. Of these, both serum and saliva tests were positive in 70 cases, only serum was positive in two cases, and both serum and saliva samples were negative in seven cases. The concentration of PCP in the samples did not correlate with the severity of PCP intoxication. In the remaining 21 cases, with no clinical evidence of PCP intoxication, PCP assays were negative in both serum and saliva in 17 cases, three patients had positive saliva and serum tests, and one other patient had a positive PCP saliva assay. Thus, saliva would appear to be as reliable as serum as a specimen for PCP analysis.

The cocaine 'body packer' syndrome. Diagnosis and treatment.

The current recommended treatment for cocaine "body packers" is surgical removal of the drug packages to prevent death due to cocaine poisoning. We describe 47 patients treated successfully with purgation and one patient who required surgery to remove packages obstructing the small bowel. Treatment decisions depend on the physical findings, the location of the cocaine packages in the gastrointestinal (GI) tract, and the type of package. Twelve patients (25%) had packages highly susceptible to breakage or leaching cocaine; in two cases, pieces of wrapping sloughed in the GI tract, and in another, a bag broke as it was being passed. In 36 cases (75%), the packages were more resistant to breakage or leaching cocaine, and no complications occurred. The types of packages can often be distinguished roentgenographically; however, 12 patients who passed cocaine packages had abdominal roentgenograms that did not show these foreign bodies.

Ordering of laboratory tests in a teaching hospital. Can it be improved?

A review of ordering patterns for thyroid function tests and for measurements of creatine kinase (CK) isoenzyme and lactate dehydrogenase (LDH) isoenzyme levels indicated considerable misuse. We employed an educational program for both types of tests, but changed the request form only for ordering the thyroid function tests. No changes were made in the forms for ordering CK and LDH isoenzyme tests. The effect was a prompt decrease in ordering triiodothyronine radioimmunoassay and thyrotropin tests to 38% and 61%, respectively, of baseline rates. There was no effect on rates of ordering CK and LDH isoenzyme tests, which were 102% and 96%, respectively, of baseline rates. The improved use of thyroid function tests was likely because of the change in the laboratory request form, since the educational strategy by itself had no effect on the ordering of CK and LDH isoenzyme tests.

Quantitation of phencyclidine in serum by enzyme immunoassay: results in 405 patients.

Phencyclidine (PCP) in serum (5 ng/mL and higher) was quantitated by a homogeneous enzyme immunoassay procedure. Precision and accuracy data indicate that the procedure meets the requirements for a clinical assay. The short turnaround time for the assay makes it superior to other available methods for the emergency determination of PCP in serum. The analytical results were comparable to those by GC/MS on 70 samples tested. The serum concentration of PCP was determined in 500 specimens from 405 patients. In 216 patients with "pure" PCP intoxication, the serum concentration did not show a direct relationship to either the clinical pattern of intoxication or to the history of the route of PCP use.

A case of neuroleptic malignant syndrome successfully treated with amantadine.

A paranoid schizophrenic patient developed the neuroleptic malignant syndrome after receiving three doses of fluphenazine HCl and two doses of thioridazine while he was recovering from major trauma. Treatment with diphenhydramine and benztropine mesylate was ineffective. Administration of amantadine HCl resulted in resolution of all symptoms within 24 hours. After 2 days, the amantadine was discontinued. The following day, the neuroleptic malignant syndrome appeared. Readministration of amantadine again resulted in prompt remission of symptoms.

Acute phencyclidine intoxication: clinical patterns, complications, and treatment.

We describe four major and five minor clinical patterns of acute phencyclidine (PCP) intoxication and give the incidence of findings in each pattern. Major patterns were acute brain syndrome (248 cases; 24.8%), toxic psychosis (166 cases; 16.6%), catatonic syndrome (117 cases; 11.7%), and coma (106 cases; 10.6%). Minor patterns included lethargy or stupor (38 cases; 3.8%), and combinations of bizarre behavior, violence, agitation, and euphoria in patients who were alert and oriented (325 cases; 32.5%). Patients with major patterns of PCP toxicity usually required hospitalization and accounted for most complications. In general, patients with minor patterns had mild intoxication and did not require hospitalization except for the treatment of injuries or autonomic effects of PCP. Various types of injuries occurred in 16%, and aspiration pneumonia occurred in 1.0% of all cases. There were 22 cases of rhabdomyolysis (2.2%), with three patients requiring dialysis for renal failure. One patient who had been comatose from PCP died suddenly. A fresh pulmonary embolism was found at autopsy.

Acute yellow phosphorus poisoning from pesticide pastes.

Ten cases of ingestion of yellow phosphorus rat poison, including four cases that occurred during the past 3 years, are reported. Comparison of these cases with 82 others from the literature showed that ingestion of yellow phosphorus paste often results in clinical findings that are different from those described for acute yellow phosphorus poisoning in current toxicology texts. The time lag between swallowing of the poison and onset of symptoms varied from a few minutes to 24 h. Garlic odor, mucosal burns, and phosphorescent vomitus or feces occurred in only a small percentage of cases. Diarrhea was not a presenting complaint. Initial symptoms were referable to the gastrointestinal tract, central nervous system, or both. Mortality rates were 23% for patients who had early symptoms of vomiting or abdominal pain; 73% for those where the first manifestation of intoxication was restlessness, irritability, drowsiness, stupor, or coma; and 47% for patients who had a combination of these GI and CNS symptoms initially. Applying standard diagnostic criteria for yellow phosphorus poisoning to patients who have consumed yellow phosphorus pastes may result in serious diagnostic errors.