Heroin-related noncardiogenic pulmonary edema : a case series.

STUDY OBJECTIVES: To examine the current clinical spectrum of noncardiogenic pulmonary edema (NCPE) related to heroin overdose. DESIGN: Retrospective chart review of all identified patients from August 1994 through December 1998. SETTING: Urban academic hospital. PATIENTS OR PARTICIPANTS: Heroin-related NCPE was defined as the syndrome in which a patient develops significant hypoxia (room air saturation < 90% with a respiratory rate > 12/min) within 24 h of a clinically apparent heroin overdose. This should be accompanied by radiographic evidence of diffuse pulmonary infiltrates not attributable to other causes, such as cardiac dysfunction, pneumonia, pulmonary embolism, or bronchospasm, and which resolve clinically and radiographically within 48 h. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Twenty-seven patients were identified during this 53-month period, with a majority being male patients (85%; average age, 34 years). Twenty patients (74%) were hypoxic on emergency department arrival, and 6 patients (22%) had symptoms develop within the first hour. One patient had significant hypoxia develop within 4 h. Nine patients (33%) required mechanical ventilation, and all intubated patients but one were extubated within 24 h. Eighteen patients (66%) were treated with supplemental oxygen alone. Hypoxia resolved spontaneously within 24 h in 74% of patients, with the rest (22%) resolving within 48 h. Twenty patients (74%) had classical radiograph findings of bilateral fluffy infiltrates, but unilateral pulmonary edema occurred in four patients (15%) and more localized disease occurred in two patients (7%). CONCLUSION: NCPE is an infrequent complication of a heroin overdose. The clinical symptoms of NCPE are clinically apparent either immediately or within 4 h of the overdose. Mechanical ventilation is necessary in only 39% of patients. The incidence of NCPE related to heroin overdose has decreased substantially in the last few decades.

Acute heroin overdose.

Acute heroin overdose is a common daily experience in the urban and suburban United States and accounts for many preventable deaths. Heroin acts as a pro-drug that allows rapid and complete central nervous system absorption; this accounts for the drug's euphoric and toxic effects. The heroin overdose syndrome (sensitivity for diagnosing heroin overdose, 92%; specificity, 76%) consists of abnormal mental status, substantially decreased respiration, and miotic pupils. The response of naloxone does not improve the sensitivity of this diagnosis. Most overdoses occur at home in the company of others and are more common in the setting of other drugs. Heroin-related deaths are strongly associated with use of alcohol or other drugs. Patients with clinically significant respiratory compromise need treatment, which includes airway management and intravenous or subcutaneous naloxone. Hospital observation for several hours is necessary for recurrence of hypoventilation or other complications. About 3% to 7% of treated patients require hospital admission for pneumonia, noncardiogenic pulmonary edema, or other complications. Methadone maintenance is an effective preventive measure, and others strategies should be studied.

Clinical course of gamma-hydroxybutyrate overdose.

STUDY OBJECTIVE: To describe the clinical characteristics and course of gamma-hydroxybutyrate (GHB) overdose. METHODS: We assembled a retrospective series of all cases of GHB ingestion see in an urban public-hospital emergency department and entered in a computerized database January 1993 through December 1996. From these cases we extracted demographic information, concurrent drug use, vital signs, Glasgow Coma Scale (GCS) score, laboratory values, and clinical course. RESULTS: Sixty-one (69%) of the 88 patients were male. The mean age was 28 years. Thirty-four cases (39%) involved coingestion of ethanol, and 25 (28%) involved coingestion of another drug, most commonly amphetamines. Twenty-five cases (28%) had a GCS score of 3, and 28 (33%) had scores ranging from 4 through 8. The mean time to regained consciousness from initial presentation among nonintubated patients with an initial GCS of 13 or less was 146 minutes (range, 16-389). Twenty-two patients (31%) had an initial temperature of 35 degrees C or less. Thirty-two (36%) had asymptomatic bradycardia; in 29 of these cases, the initial GCS score was 8 or less. Ten patients (11%) presented with hypotension (systolic blood pressure < or = 90 mm Hg); 6 of these patients also demonstrated concurrent bradycardia. Arterial blood gases were measured in 30 patients; 21 had a PCO2 of 45 or greater, with pH ranging from 7.24 to 7.34, consistent with mild acute respiratory acidosis. Twenty-six patients (30%) had an episode of emesis; in 22 of these cases, the initial GCS was 8 or less. CONCLUSION: In our study population, patients who overdosed on GHB presented with a markedly decreased level of consciousness. Coingestion of ethanol or other drugs is common, as are bradycardia, hypothermia, respiratory acidosis, and emesis. Hypotension occurs occasionally. Patients typically regain consciousness spontaneously within 5 hours of the ingestion.

Clinical course of crack cocaine body stuffers.

STUDY OBJECTIVE: To describe the clinical course of a cohort of patients presenting to the emergency department with acute crack cocaine body-stuffer syndrome. METHODS: We conducted a retrospective cohort study in the ED of a county hospital with 75,000 visits per year. Our study cohort comprised all patients who presented between January 1993 and April 1995 and who met the definition of a crack cocaine body stuffer. We defined a crack cocaine body stuffer as anyone who admitted to or was strongly suspected of ingesting crack cocaine as a means of escaping detection by authorities, not for recreational purposes or as a means of transporting the drug across borders. RESULTS: We identified 98 cases; most such patients were brought to the ED by law enforcement agents. Most were male and younger than 30 years. Self-report by patients indicated that the amount of crack cocaine ingested ranged from 1 to more than 15 rocks. Most commonly the drug was unwrapped (28%) or wrapped in a plastic sandwich bag (29%). Generalized seizures developed in 4% of the patients; in all these patients seizures occurred within 2 hours of ingestion. In no patient did dysrhythmias develop. Many patients had minor signs of cocaine intoxication: 54% were tachycardic, 23% were hypertensive, 22% were agitated, and 19% required sedation. CONCLUSION: Mild cocaine intoxication is common in crack cocaine body stuffers, with seizures occurring within 2 hours of ingestion in a small percentage of patients.

Acetaminophen and salicylate serum levels in patients with suicidal ingestion or altered mental status.

Is universal screening of acetaminophen (APAP) and salicylate (SAL) necessary in patients with a suicidal ingestion or an altered mental status and suspected ingestion? This descriptive, retrospective chart review in an emergency department in a large urban county hospital examined all patients who presented with a history of suicidal ingestion or an altered mental status with a strong suspicion of ingestion from January 1992 through October 1993. APAP and SAL serum levels were measured in 1,820 patients, and charts of patients with APAP serum levels of > 1 microgram/mL or SAL serum levels of > 1 mg/dL were reviewed. The patient's history of ingesting APAP or SAL was recorded, as well as the clinician's interpretation of that level. Sixteen charts were not available. APAP levels of > 1 microgram/mL were found in 175 (9.6%) patients, 120 (6.5%) of whom were APAP history-positive and 55 (3%) APAP history-negative. None of the APAP history-negative group required therapy with N-acetylcysteine. Eight (0.3%) of the APAP history-negative group had potentially toxic levels of > 50 micrograms/mL. SAL levels of > 1 mg/dL were found in 155 (8.5%) patients, 44 (2.5%) of whom were SAL history-positive and 111 (6%) SAL history-negative. Three patients were SAL history-negative but had a significant chronic SAL intoxication. All these patients presented with an altered mental status and had an anion gap of > 20 mEq/L. Universal screening found that 0.3% of suicidal ingestions had a potentially toxic APAP intoxication not suggested by history. This incidence of infrequent but potentially life: threatening overdose should prompt clinicians to screen all of their patients with a suspected ingestion. Salicylate screening found that 0.16% of suicidal ingestions had a toxic SAL intoxication not suggested by history, although such intoxication should be suggested by an elevated anion gap and an altered mental status. Since this less severe intoxication is less frequent and usually suggested by commonly obtained laboratory data, universal screening is not indicated, but a more selective approach to screening could be taken.

Out-of-hospital treatment of opioid overdoses in an urban setting.

OBJECTIVES: To investigate clinical outcomes in a cohort of opioid overdose patients treated in an out-of-hospital urban setting noted for a high prevalence of i.v. opioid use. METHODS: A retrospective review was performed of presumed opioid overdoses that were managed in 1993 by the emergency medical services (EMS) system in a single-tiered, urban advanced life support (ALS) EMS system. Specifically, all patients administered naloxone by the country paramedics were reviewed. Those patients with at least 3 of 5 objective criteria of an opioid overdose [respiratory rate < 6/min, pinpoint pupils, evidence of i.v. drug use. Glasgow Coma Scale (GCS) score < 12, or cyanosis] were included. A response to naloxone was defined as improvement to a GCS > or = 14 and a respiratory rate > or = 10/min within 5 minutes of naloxone administration. ED dispositions of opioid-overdose patients brought to the county hospital were reviewed. All medical examiner's cases deemed to be opioid-overdose-related deaths by postmortem toxicologic levels also were reviewed. RESULTS: There were 726 patients identified with presumed opioid overdoses. Most patients (609/726, 85.4%) had an initial pulse and blood pressure (BP). Most (94%) of this group responded to naloxone and all were transported. Of the remainder, 101 (14%) had obvious signs of death and 16 (2.2%) were in cardiopulmonary arrest without obvious signs of death. Of the patients in full arrest, 2 had return of spontaneous circulation but neither survived. Of the 609 patients who had initial BPs, 487 (80%) received naloxone i.m. (plus bag-valve-mask ventilation) and 122 (20%) received the drug i.v. Responses to naloxone were similar; 94% i.m. vs 90% i.v. Of 443 patients transported to the country hospital, 12 (2.7%) were admitted. The admitted patients had noncardiogenic pulmonary edema (n = 4), pneumonia (n = 2), other infections (n = 2), persistent respiratory depression (n = 2), and persistent alteration in mental status (n = 2). The patients with pulmonary edema were clinically obvious upon ED arrival. Hypotension was never noted and bradycardia was seen in only 2% of our presumed-opioid-overdose population. CONCLUSIONS: The majority of the opioid-overdose patients who had initial BPs responded readily to naloxone, with few patients requiring admission. Noncardiogenic pulmonary edema was uncommon and when present, hypoxia was evident upon arrival to the ED. Naloxone administered i.m. in conjunction with bag-valve-mask ventilation was effective in this patient population. The opioid-overdose patients in cardiopulmonary arrest did not survive.

The serotonin syndrome. Implicated drugs, pathophysiology and management.

The serotonin syndrome has increasingly been recognised in patients who have received combined serotonergic drugs. This syndrome is characterised by a constellation of symptoms (confusion, fever, shivering, diaphoresis, ataxia, hyperelflexia, myoclonus or diarrhoea) in the setting of the recent addition of a serotonergic agent. The most common drug combinations causing the serotonin syndrome are monoamine oxidase inhibitors (MAOIs) and serotonin selective reuptake inhibitors (SSRIs), MAOIs and tricyclic antidepressants, MAOIs and tryptophan, and MAOIs and pethidine (meperidine). This syndrome is caused by excess serotonin (5-hydroxytryptamine; 5-HT) availability in the CNS at the 5-HT1A-receptor. There may also be some interaction with dopamine and 5-HT2-receptors. This syndrome probably has a low incidence, even among patients taking these drug combinations, and there is likely to be some other as yet unidentified inciting factor causing some patients to develop a full serotonin syndrome. Because fatalities and severe complications have accompanied the serotonin syndrome, the previously described drug combinations should be used cautiously or not at all. The serotonin syndrome is usually mild and, if managed with drug withdrawal and supportive therapy, generally improves within hours. Patients who develop hyperthermia should be treated aggressively with external cooling and paralysis. Methysergide and cyproheptadine appear to be useful adjuncts in treating the serotonin syndrome.

Massive ingestion of sustained-release verapamil with a concretion and bowel infarction.

Gastric concretions secondary to a drug overdose are uncommon but potentially fatal if not recognized and treated. They may continue to release drug into the stomach for hours or days after the ingestion, complicating diagnosis and treatment. We describe the case of a man with the previously unreported association of bowel infarction with a verapamil ingestion and concretion. This case illustrates the need for a heightened awareness of this potential complication.

The incidence of ethanol-induced hypoglycemia.

The purpose of the study was to determine the incidence of ethanol-induced hypoglycemia. All nondiabetic patients who had blood alcohol levels above 0.10% and a random serum chemistry drawn (including glucose) were included. Over a 6-month study period, 378 patients were included in the study. Fifteen patients (4%) presented with hypoglycemia (glucose less than 67 mg%). Of these, four (1%) were profoundly hypoglycemic (glucose less than 50 mg%). Two hundred and fifty three patients (67%) patients were normoglycemic (glucose 67-106 mg%) and 110 patients (29%) were hyperglycemic (glucose greater than 106 mg%). Nonfasting glucose measurements from a control group of 96 nondiabetic, nonintoxicated patients were compared with those of the study group. Two patients (2%) presented with hypoglycemia and none (0%) presented with profound hypoglycemia. Forty-five patients (47%) presented with normoglycemia, and 49 (51%) with hyperglycemia. There were no statistically significant differences found in the hypoglycemia rate between the intoxicated patients and nonintoxicated control population (odds ratio of 0.75; P greater than .05). Four of 378 intoxicated patients (1%) had profound hypoglycemia (less than 50 mg/dL) compared with none (0%) of the 96 nonintoxicated patients. Intoxicated patients had a statistically significant lower rate of hyperglycemia in comparison with the nonintoxicated control group (29% versus 51%; P less than .0001). Age, sex, race, ethanol level, and serum electrolyte measurement had no predictive value for hypoglycemia in intoxicated patients. The anion gap was consistently elevated in hypoglycemic patients in comparison with normoglycemic patients (P less than .05). Hypoglycemia appears to occur as frequently in an ethanol-intoxicated population as in a population without elevated ethanol levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Saltpeter ingestion.

A 37-year-old man presented to the emergency department after an attempt to self-treat his priapism with saltpeter (K+NO3). Initially he had a potassium of 7.6 with electrocardiographic changes and a markedly elevated CO2. The potassium and carbon dioxide normalized in less than 24 hours with standard treatment for hyperkalemia. Hyperkalemia is expected with large oral potassium ingestion; and the elevated CO2 was spurious, caused by the misreading of serum nitrates by the Ektachrom 700 system. Ingestion of K+NO3 should be added to the differential of hyperkalemia with a markedly elevated CO2.

Carbidopa-levodopa overdose.

A 57-year-old woman ingested 15 to 17 tablets of carbidopa-levodopa 10/100 tablets (carbidopa 150 mg and levodopa 1,500 mg) along with ibuprofen, carisoprodol, hydrocodone, and acetaminophen. The patient developed choreiform movements that persisted despite obtundation and attempts to extinguish them with naloxone, morphine, and diazepam. When the patient developed a rising level of creatine phosphokinase and myoglobinuria, she was treated with ventilatory support and pancuronium. She required paralysis for 60 hours, when her chorea resolved.