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Biomedical subjects

C H Linden

Publications and source records attributed to C H Linden.

At least 19 recordsLinked to original sources
PubMed1997

Another hot tub hazard. Toxicity secondary to bromine and hydrobromic acid exposure.

We describe the clinical course of two patients who developed acute pneumonitis followed by reactive airways dysfunction syndrome after bathing in a hot tub. Additional findings were present and suggested that exposure to a corrosive agent was responsible. Bromine and hydrobromic acid generated from a widely used water disinfectant were implicated as the underlying cause. Physicians should be alert to the possibility that such exposures may initiate or exacerbate inflammatory pulmonary disease.

Acute Disease↗
PubMed1996

Unknown alcohol.

Explore the source record for details and available documents.

Alcoholic Intoxication↗
PubMed1991

Exclusion of cervical spine injury: a prospective study.

Trauma room lateral cervical spine radiographs (LCSR) may improve the safety of intubation and transportation of multiply injured patients by providing earlier recognition of spinal vertebral injuries. We prospectively evaluated 60 consecutive trauma admissions to determine the impact of clearance of cervical spine radiographs on patient care. Fifty-three patients had no cervical spine injury (CSI). Intubations, emergency head CT scan, aortography, or urgent operation (less than 6 hours after admission) were required in the majority of patients and preceded complete cervical spine clearance in all but one instance. The median time for radiologic clearance of the cervical spine was 15 hours (range, 1.5 to 181). LCSR failed to identify three of the seven acute CSI (all three had C7 fractures). The spine-injured were managed with cervical collars and no new neurologic injury developed. We conclude that: 1) LCSRs do not appear to alter urgent management of multiply injured patients during resuscitation and transportation; 2) chest radiographs and emergency investigations should not be delayed by repeated LCSR in the trauma room as it may be difficult to fully exclude CSI in many trauma patients; 3) we support the current ATLS guidelines, which suggest that all patients should be presumed to have an unstable CSI until the presence of cervical injury has been excluded.

Cervical Vertebrae↗
PubMed1990

Volatile substances of abuse.

Substances that are inhaled for the purpose of recreational self-intoxication include aliphatic hydrocarbons, alkyl halides, alkyl nitrites, aromatic hydrocarbons, ethers, and ketones. All have the ability to cause asphyxia, arrhythmias, cardiovascular depression, neurologic dysfunction, and mucosal, pulmonary, and skin irritation following acute exposure and permanent neurologic damage with chronic exposure. The acute effects of alkyl halides and alkyl nitrites also include carbon monoxide poisoning and hepatorenal toxicity, and methemoglobinemia, respectively. Chronic exposure to aromatic hydrocarbons and ketones can result in liver, kidney, and bone marrow injury; myopathy, rhabdomyolysis, metabolic acidosis, and electrolyte abnormalities are further complications of chronic aromatic hydrocarbon inhalation.

Drug Overdose↗
PubMed1987

Clinical effects of accidental levothyroxine ingestion in children.

Forty-one children, aged 1 to 5 years, who accidentally ingested levothyroxine sodium were studied. Symptoms possibly associated with the ingestion occurred in 11 patients (27%). These symptoms (tachycardia, hyperactive behavior, fever, vomiting, diarrhea, diaphoresis, and flushing) were categorized as minor and all resolved without treatment. Because observed effects were generally mild and often unrelated to either estimated amounts of hormone consumed or serum thyroxine levels, a conservative approach to patient treatment is recommended in cases of levothyroxine ingestion in children.

Administration, Oral↗
PubMed1986

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.

Acute Disease↗
PubMed1986

Cyanide poisoning from laetrile ingestion: role of nitrite therapy.

A 4-year-old child ingested laetrile and almost died of cyanide poisoning. Treatment with the Lilly cyanide antidote kit resulted in rapid, complete recovery. Extremely high whole blood cyanide levels were documented. The necessity for use of the antidote kit in serious cyanide poisoning has recently been questioned. This case demonstrates benefit from antidotal treatment.

Acute Disease↗
PubMed1985

Yohimbine: a new street drug.

Following the ingestion of an alleged aphrodisiac known as "yo-yo," a 16-year-old girl experienced an acute dissociative reaction accompanied by weakness, paresthesias, and incoordination. Subsequent symptoms included anxiety, headache, nausea, palpitations, and chest pain. Hypertension, tachycardia, tachypnea, diaphoresis, pallor, tremors, and an erythematous rash were noted on physical examination. Serum epinephrine and norepinephrine levels were found to be elevated. Symptoms resolved spontaneously but lasted approximately 36 hours. The ingested substance was identified as yohimbine. The pharmacology of yohimbine and the treatment of yohimbine poisoning are discussed.

Adolescent↗
PubMed1984

Monoamine oxidase inhibitor overdose.

Described is the clinical course of a 26-year-old woman who died following an overdose of the MAO inhibitor phenelzine. Signs and symptoms of toxicity were delayed in onset. Initial findings of excessive neuromuscular activity were followed by severe hyperthermia, coma, cardiovascular collapse, acute renal failure, hemolysis, rhabdomyolysis, and disseminated intravascular coagulation. A review of the literature suggests that these features are not unusual following MAO inhibitor overdosage. The pathophysiology and management of MAO inhibitor poisoning are discussed.

Acute Kidney Injury↗
PubMed1984

Acetaminophen overdose.

N-acetylcysteine (NAC) is the treatment of choice for acetaminophen overdose. With this therapy, morbidity from overdose can be held to a minimum. Mortality is rare in any case and virtually nonexistent in treated patients. Unless a high index of suspicion is maintained, the diagnosis may be missed until it is too late for effective antidotal treatment.

Acetaminophen↗