Acute pulmonary oedema

Lee CH, Guo YL, Tsai PJ, et al Fatal acute pulmonary oedema after inhalation of fumes from polytetrafluoroethylene (PTFE). Eur RespirJ 10(6) 1408-1411, 1997... 

Angina pectoris, hypertension, congestive heart failure, acute myocardial ischaemia, acute pulmonary oedema, unstable coronary syndromes especially when associated with elevated filling pressures. Nitrate therapy may exaggerate outflow obstruction in hypertrophic obstructive cardiomyopathy. 

Uses. Frusemide is very successful for the relief of oedema. Progressively increasing the dose of frusemide increases urine production. Taken orally it acts within an hour and diuresis lasts up to 6 hours. Enormous urine volumes can result and overtreatment may lead to hypovolaemia and circulatory collapse. Given i.v. it acts within 30 minutes and can relieve acute pulmonary oedema, partly by a vasodilator action which precedes the diuresis. An important feature of frusemide is its efficacy... 

Oedema states associated with sodium overload, e.g. cardiac, renal or hepatic disease, and also without sodium overload, e.g. acute pulmonary oedema following myocardial infarction. Note that oedema may also be localised, e.g. angioedema over the face and neck or aroimd the ankles following some calcium channel blockers, or due to low plasma albumin, or immobility in the elderly in none of these circumstances are diuretics indicated. 

Acute pulmonary oedema left ventricular failure... 

Ethacrynic acid is normally used in the treatment of fluid retensive conditions due to congestive heart failure, cirrhosis of the liver, renal disease, and the nephrotic syndrome. It is invariably employed for the control and management of ascites due to lymphoedema, idiopathic oedema and malignancy. It is also recommended through i.v in an emergency situation of acute pulmonary oedema. 

It has been known for many years that the inhalation of nitrous fumes may cause acute pulmonary oedema and death in man. In the United Kingdom, nitrous fume poisoning is listed under occupational diseases prescribed under the National Insurance Act, 1965 (P.D. 17). Kennedy (1972) summarised some of the many situations where nitrous fumes may occur. In another paper (Kennedy 1972,1974) he listed animal studies on the toxicology of nitrous fumes. In rabbits, Kleinerman and Wright (1961) found macrophage infiltration 4 days after an exposure of 25 ppm for 2 h. 

Overactivation of glutamate receptors can contribute to a wide variety of lesions, including acute pulmonary oedema (Said et al. 1996), airway hyperesponsiveness (Said 1999) and inflammation. Blocking of the N-methyl-D-aspartate subtype of glutamate receptors by dizocilpine maleate (MK-801 10 pM) attenuated oxidant injury induced by paraquat (100 mg/kg to the pulmonary circulation) or by xanthine oxidase (Said et al. 2000). 

Higher amounts of tryptophan (its degradation produd skatole) in feeds of ruminants may cause acute pulmonary oedema (a buildup of fluid in the spaces outside the blood vessels of the lungs) and emphysema (a chronic respiratory disease causing a decrease in lung function and often breathlessness). 

Quinine is known to cause a variety of hypersensitivity reactions including cinchonism, fever, angioedema, pruritus, acute renal failure and thrombocytopenia. Acute pulmonary oedema and transient pulmonary infiltrates have also been reported. BOOP after quinine therapy is a rare adverse reaction. 

Laboratory evaluation [241] of acute and chronic toxicity of prenylamine indicates that, in high doses, convulsions accompanied by respiratory paralysis (often with pulmonary oedema) led to death. Doses inadequate to produce this result led only to phenomena characteristic of reserpine-like dmgs. Chronic administration failed to produce recognizable changes in any organs or tissues studied. No toxic effects, unattributable to amine depletion, have appeared during several years clinical use. 

The three main types of altitude illness, characterised initially by nausea, headache, sleep disturbance and stomach upset, are acute mountain sickness (AMS) high altitude pulmonary oedema (HAPE) and high altitude cerebral oedema (HACK). They occur after rapid ascent to altitudes greater than 2,500 m (about 8,000 feet) in unacclimatised people. In unacclimatised mountaineers, the prevalence of AMS at 4,559 metres (15,000 feet) is approximately 50% and HAPE 4%. Risk depends on individual susceptibility, rate of ascent and pre-exposure to high altitude. AMS is not a pre-requisite for HAPE. 

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. 

Acute poisoning may result from inhalation of cadmium dusts and fumes (usually cadmium oxide) and from the ingestion of cadmium salts. The major toxic effects are due to local irritation. In the case of oral intake, these include nausea, vomiting, salivation, diarrhoea and abdominal cramp. Cadmium is more toxic when inhaled. Signs and symptoms, which appear after a few hours, include irritation of the upper respiratory tract, chest pains, nausea, dizziness and diarrhoea. Permanent lung damage may occur in the form of emphysema and peribronchial and perivascular fibrosis. Death is usually due to massive pulmonary oedema. 

High concentration oxygen therapy is reserved for a state of low PaOj in association with a normal or low PaCO (type I respiratory failure), as in pulmonary embolism, pneumonia, pulmonary oedema, myocardial infarction, and young patients with acute severe asthma. Concentrations of up to 100% may be used for short periods, since there is little risk of inducing hypoventilation and CO retention. 

In the treatment of acute myocardial failure with associated pulmonary oedema, the objectives are to improve gas exchange, increase myocardial contractility and reduce the workload of the left ventricle. Dobutamine, a somewhat selective pi -adrenoceptor agonist, produces a pronounced inotropic effect that results in an increased cardiac output (where contractility is the limiting factor) and an elevation of arterial blood pressure. The drug preparation, following appropriate dilution, is administered by continuous intravenous infusion at a rate of 1-5 (ig/kg min. An intravenous dose (0.5 mg/kg) of furosemide (loop diuretic) increases venous capacitance by redistributing venous blood from the lungs to the peripheral circulation, which... 

X-ray examination still plays some role especially in the acute phase (heart enlargement and pulmonary oedema) and in the detection of aneurysms and calcifications, visualisation of heart valves, pacemakers, etc. 

Figure 13.3 (A) A diagram showing a normal and an abnormal negative component of the P wave in V1. When the product of the width in seconds by the height in millimetres of the negative mode exceeds (in negativity) -0.03, it is considered abnormal. (B) An example of pulmonary oedema (a) in acute phase of myocardial...

Focal haemorrhage and pulmonary oedema are typical of the acute toxic effects, but there does not appear to be extensive permanent damage from non-fatal doses. However, residual focal emphysema and interstitial fibrosis remaining after the initial lesions have cleared are possible long term results of the injury [1794,2235]. 

Clinical manifestation. It includes several syndromes a) pulmotoxic and irritative syndrome - expressed by catarrhal changes on the contact mucosa and respiratory tract, toxic pulmonary oedema b) hemotoxic syndrome - expressed by severe hemolysis of different degrees, in the severe forms - hemolytic shock and anaemia c) hepatal syndrome - characterised by subicterus or icterus, increased liver and bilirubinaemia d) renal syndrome - by oliguria or anuria, pathological deviations in the urine and acute kidney insufficiency. In the extremely severe forms consciousness is disordered. Laboratory blood and urine chemical tests show evidence of phenol metabolites, data for blood damage (increased values of free hemoglobin, reduced number of erythrocytes), positive liver tests etc. 

Respiratory syndrome - strongly expressed with acute dispnea toxic pulmonary oedema ... 

Late complications of acute CN poisoning have included pulmonary oedema (Graham etal., 1977), acute renal failure (Megarbane and Baud, 2003), rhabdomyolysis (Brivet etal., 1983), CNS degenerative changes and early diffuse cerebral oedema (Fligner etal., 1987 Vamell etal., 1987) and neuropsychiatric manifestations including paranoid psychosis (Kales etal., 1997). 

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