Pulmonary edema respiratory acidosis

The pulmonary toxicity of uranium compounds varies in animals. Reports of pulmonary toxicity in animals after acute-duration exposure to uranium are limited to experiments with uranium hexafluoride. Gasping and severe irritation to the nasal passages were reported after 10 minute exposures at 637 mg U/mg in rats and mice (Spiegl 1949) and nasal hemorrhage in rats after a 5 minute exposure to 54,503 mg/m (Leach et al. 1984). Uranium hexafluoride promptly hydrolyzes on contact with water to uranyl fluoride and hydrofluoric acid. Thus, the animals were potentially exposed to hydrofluoric acid, a potent toxicant to respiratory tract epithelium, which probably contributed to pulmonary tissue destruction (Leach et al. 1984 Spiegl 1949 Stokinger et al. 1953). In addition, exposure to fluoride ions can result in hypocalcemia, hypomagnesemia, pulmonary edema, metabolic acidosis, ventricular arrhythmia, and death (Meditext 1998). 

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

Because clove cigarettes also contain tobacco, they carry all of the hazards of regular tobacco smoking (Council on Scientific Affairs 1988). Several cases of serious medical illness have been associated with clove cigarettes in the United States (Guidotti et al. 1989). These include cases of hemorrhagic pulmonary edema, pneumonia, bronchitis, and hemoptysis. Because eugenol anesthetizes the respiratory tract, it inhibits the normal gag reflex and has led to aspiration pneumonia in at least one case. Accidental overdoses in children have led to CNS depression, urinary abnormalities, and anion-gap acidosis. These cases were treated successfully with supportive measures (Lane et al. 1991). 

Toxieology. Ethylene glycol aerosol causes irritation of the upper respiratory tract ingestion can cause central nervous system depression, severe metabolic acidosis, liver and kidney damage, and pulmonary edema. 

Nausea, vomiting, tinnitus, and hyperventilation are seen early in toxicity. As severity of toxicity increases, intractable vomiting, hyperthermia, hypotension, tachycardia, confusion, coma, seizures, pulmonary edema, acute renal failure, and death may occur. Hyperglycemia may be seen early, whereas hypoglycemia may occur later in toxicity. Acid-base disturbances such as respiratory alkalosis and/or metabolic acidosis may be noted. Signs and symptoms of salicylate toxicity may be noted as blood levels rise over 30mgdN. ... 

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... 

The toxicity of formaldehyde is related to its metabolic products and, as a result, individual variability in metabolism will determine toxic outcomes. Human ingestion of 118 ml of formaldehyde was fatal in some cases but not others. Systemic acidosis may appear upon ingestion along with corrosion and hemorrhaging of the digestive tract. Allergic sensitization may occur after exposure. This may lead to contact dermatitis after subsequent skin exposure, as well as asthmatic attack upon inhalation exposure. Inhalation may also result in irritation of the respiratory tract and pulmonary edema. 

Cardiac and respiratory stabilization are the first priorities following pentazocine poisoning. The patient s airway should be patent and adequate ventilation assured. If the patient has either inadequate ventilation or a poor gag reflex, then the patient may be at risk for subsequent CO2 narcosis with worsening acidosis or aspiration. If necessary, endotracheal tube intubation should be performed. Close monitoring of the patient s pulmonary exam should be performed to assure that pulmonary edema does not develop. The health care providers should place the patient on continuous cardiac monitoring with pulse oximetry and make frequent neurological checks. 

Sulfur dioxide is irritating to the eyes, mucous membranes, and respiratory tract. High levels of exposure produce cardiac arrest. Moderate exposure produces pulmonary edema. Low exposure results in systemic acidosis. Individuals who have hyperactive airway disease, including asthma, may be particularly sensitive. 

Respiratory acidosis with metabolic acidosis Example Cardiopulmonary arrest Severe pulmonary edema Drug ingestion with central nervous system depression... 

All patients developed a compensatory metabolic acidosis due to chronic hyperventilation. Respiratory alkalosis was thought to have developed because of capillary leak into the lungs producing borderline or frank pulmonary edema. After several days a superimposed normal anion gap acidosis developed from dilution by large volumes of saline fluid resuscitation. The authors found no defects in renal handling of calcium, phosphorous, or magnesium. There was no evidence of a renal acidification defect or renal tubular acidosis. 

HEALTH SYMPTOMS inhalation (cough, sneezing, dyspnea, tachypnea, vomiting, cyanosis, respiratory acidosis, bronchitis, bronchiolitis, pulmonary edema, emphysema, severe bronchiolar obstruction) skin contact (adhesions, foreign body granulomatas) ingestion (fever, vomiting, painful abdomen, presence of talc may be confirmed in the paracentesis fluid). 

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. 

A. Acute ingestion. Vomiting occurs shortly after ingestion, followed by hyper-pnea, tinnitus, and lethargy. Mixed respiratory alkalemia and metabolic acidosis are apparent when arterial blood gases are determined. With severe intoxication, coma, seizures, hypoglycemia, hyperthermia, and pulmonary edema may occur. Death is caused by central nervous system failure and cardiovascular collapse. 

Maintain an open ainway and assist ventilation if necessary (see pp 1-7). Warning Ensure adequate ventilation to prevent respiratory acidosis, and do not allow controlled mechanical ventilation to interfere with the patienf s need for compensatory efforts to maintain the semm pH. Administer supplemental oxygen. Obtain serial arterial blood gases and chest x-rays to obsenre for pulmonary edema (more common with chronic or severe intoxication). 

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