Pulmonary oedema, causes

Tlie respiratory system is tlie main target organ for vapour, gas or mist. Readily-soluble cheirticals, e.g. chlorine or phosgene, attack the upper respiratory tract less soluble gases, e.g. oxides of nitrogen, penetrate more deeply into the conducting airways and, in some cases, may cause pulmonary oedema, often after a time delay. 

Prolonged exposure may cause pulmonary oedema Systemic symptoms may occur in 0.5 to 1 hr Rapid collapse, respiratory paralysis imminent Immediately fatal... 

Ot and photo-oxidants Pulmonary oedema, emphysema, asthma, eye. nose, and throat irritation, reduced lung capacity. Vegetation damage, necrosis of leaves and pines, stunting of growth, photosynthesis inhibitor, probable cause of forest die-back, suspected cause of crop loss. Attack and destruction of natural rubber and polymers, textiles and materials. 

Despite being a wonder drug against malaria, quinine in therapeutic doses can cause various side-effects, e.g. nausea, vomiting and cinchonism, and in some patients pulmonary oedema. It may also cause paralysis if accidentally injected into a nerve. An overdose of quinine may have fatal consequences. Non-medicinal uses of quinine include its uses as a flavouring agent in tonic water and bitter lemon. 

These result from over-stimulation of the sympathetic nervous system anxiety, sweating, tachycardia, arrhythmia, hypertension, myocardial ischaemia, headache, cerebral haemorrhage, pulmonary oedema. Adrenaline may cause pupillary dilatation which must be distinguished from pupillary dilatation due to other causes, e.g. severe brain injury. 

Antimony pentachloride, in a case of acute poisoning, caused severe pulmonary oedema in the three victims, two of whom died.175 Antimony compounds form complexes with thiol groups (see Section 28.11.4), and in enzymes with thiol groups then these processes are blocked. 

Phosgene was used as a major CW agent in WW I and was responsible for the greatest number of CW induced mortalities. It causes a lethal pulmonary oedema after an asymptomatic lag phase of up to 24 h. Its specific mechanism of action is unknown, but is assumed to involve reactions with nucleophilic sites on macromolecules. 

Cloves can cause local skin irritation, pulmonary oedema, mouth sensitivity and sudden lower airway closure. In addition, smoking clove cigarettes can damage soft tissues and injure the airway finings (Fetrow and Avila, 1999). 

Profound first-dose hypotension can occur when ACE inhibitors are introduced to patients with heart failure. This effect may be particularly pronounced if the patient is taking a high dose of a loop diuretic. Temporary withdrawal of the loop diuretic could be considered but is not appropriate in this case as it may cause rebound pulmonary oedema. Therefore in this case the steps are to initiate the ACE inhibitor at low dose (e.g. ramipril 1.25 mg daily at night time while the patient is lying down) and then to monitor blood pressure hourly for the first 4 hours. 

The liver does not synthesise enough albumin and does not metabolise aldosterone. A lack of albumin in the vascular space reduces colloid oncotic pressure and water flows out of the blood vessels to form tissue oedema or ascites (oedema in the peritoneal cavity). Water oozing from the pulmonary arteries causes pulmonary oedema. 

Accumulation of fluid in tissues causes oedema, which can make facial skin look puffy and cause fluid accumulation in the alveoli (pulmonary oedema), reducing gas exchange. Oedema is observed in kidney disease, when large quantities of albumin are lost from blood and excreted in urine. 

Overdose. A moderate overdose (plasma salicylate 500-750 mg/1) will cause nausea, vomiting, epigastric discomfort, tinnitus, deafness, sweating, pyrexia, restlessness, tachypnoea and hypokalaemia. A large overdose (plasma salicylate > 750 mg/1) may result in pulmonary oedema, convulsions and coma, with severe dehydration and ketosis. Bleeding is unusual, despite the antiplatelet effect of aspirin. 

Exposure to very high levels of phosgene may lead to death before pulmonary oedema has developed. The cause of this is obscure, although the effect has been recorded in cases of exposure to high levels of other lung-damaging compounds, including chlorine. The hypothesis of reflex inhibition of respiration is often put forward in explanation of this effect. 

The compensatory mechanismfor rapidly restoring the plasma volume in rabbits appears to be detrimental to the life of the animal, for the more rapidly the plasma volume is restored, the more rapidly the oedema progresses. By partially dehydrating rabbits beforehand, the mortality can be decreased and haemoconcentration occurs. These observations would indicate that, in cases of haemoconcentration and fall in plasma volume due to a loss of fluid into the lungs, it would be better not to try to increase the plasma volume by transfusions, for anoxia due to pulmonary oedema is a more important factor in causing death than haemoconcentration and decreased plasma volume. 

Colourless liquid faint agreeable smell. Fumigant, used in fire extinguishers. Skin lesions look like 2nd-degree burns. Inhalation causes headache, vertigo, diplopia, convulsions, bron-chospasm, pulmonary oedema, death. 

Colourless liquid with high vapour pressure at room temperature. Exposure can occur during electroplating and nickel refining. Vapour is insoluble in water and penetrates deep into the lung, causing pulmonary oedema and cancer. 

Colourless or yellowish fuming liquid. Vesicant, causes pulmonary oedema. 0.01 ml applied der-mally to a rabbit causes death. 

---