Pulmonary edema clinical presentation

A post-mortem examination and a rectal temperature of 41°C (106°F) were recorded. He had needle marks typical of intravenous drug abuse and pulmonary and cerebral edema. Abrasions and contusions of the ankles and wrists were evident from his struggling. Lidocaine was not administered to the victim during the resuscitative attempts. The clinical presentation of cocaine delirium... 

Chronic salicylism presents clinically in a similar fashion to the acute situation, although it is often associated with a delay in diagnosis, and a higher morbidity and mortality. Chronic salicylism is more often associated with pronounced hyperventilation, dehydration, pulmonary edema, renal failure, coma, seizures, and acidosis. Chronic salicylism can occur at serum salicylate levels as low as 15mgdl. ... 

Any amount of heroin can be potentially toxic, especially when the purity of this illicit drug is not known. Heroin depresses the CNS, thereby producing coma and respiratory depression. Pulmonary edema has been described following heroin overdose. Respiratory arrest may occur. Miosis is often present but may be absent in the presence of hypoxia or mixed drug over doses. With depression of the CNS, there is also a decrease in sympathetic tone and an increase in parasympathetic tone. This yields bradycardia and hypotension. Hypothermia may also occur as a result of peripheral vasodilation. Urine can be screened for heroin metabolic products. Blood heroin levels are not clinically useful. 

CNS depression is the most frequently reported clinical effect. The typical overdose patient may present with extreme somnolence that may progress to frank coma. Miosis is usually present unless the individual is acidotic or has suffered hypoxic brain injury. Respiratory depression can occur and may progress to respiratory arrest. Pulmonary edema may be seen. Bradycardia, hypotension, and hyperthermia can develop. Hydrocodone is often combined in products with acetaminophen therefore, patients should be evaluated for hepatotoxicity secondary to acetaminophen overdose. Available opiate immunoassays cross-react unreliably with hydrocodone. Peak therapeutic serum levels are 0.024 mg 1 toxic levels have been reported to reach 0.1-1.3 pgml , but are of little prognostic or therapeutic value. 

The clinical presentation of the patient is also important to consider when interpreting patterns of biochemical results. Patients with tumors that produce large amounts of epinephrine (and also metanephrine) may present with hyperglycemia, dyspnea, and pulmonary edema, signs and... 

B. Clinical Features. The disease begins 1-6 hours after exposure with a sudden onset of fever, chills, headache, myalgia, and nonproductive cough. In more severe cases, dyspnea and retrosternal chest pain may also be present. Fever, which may reach 103-106°F may last 2-5 days, but cough may persist 1-4 weeks. In many patients nausea, vomiting, and diarrhea will also occur. Physical findings are often unremarkable. Conjunctival injection may be present, and in the most severe cases, signs of pulmonary edema would be expected. In moderately severe laboratory exposures, lost duty time has been < 2 weeks, but, based upon animal data, it is anticipated that severe exposures will result in fatalities. 

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

III. Clinical presentation. Exposure to moderate concentrations of phosgene causes mild cough and minimal mucous membrane irritation. After an asymptomatic interval of 30 minutes to 8 hours (depending on the duration and concentration of exposure), the victim develops dyspnea and hypoxemia. Pulmonary edema may be delayed up to 24 hours. Permanent pulmonary impairment may be a sequela of serious exposure. 

IV. Diagnosis is based on a history of exposure and the clinical presentation. Many other toxic gases may cause delayed-onset pulmonary edema (see p 7). 

The clinical presentation of acute rejection and acute infection alone is nonspecific. Manifestations can include low-grade fever, shortness of breath, nonproductive cough, and changes in measured pulmonary function. In both entities, the chest radiograph may demonstrate perihilar infiltrates, interstitial edema. 

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