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Fluid loss, hypotension caused

Immediate attention should be given to the management of hypotension caused by fluid loss Few drugs are effective... [Pg.122]

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. [Pg.631]

T Effects W/ antihypertensives, cliazoxicle, nitrates, EtOH T effects OF ACEIs, Li T risk of hypokalemia W/ amphotericin B, corticosteroids, mezlocillin, piperacillin, ticarcillin effects W/ cholestyramine, colestipol, NSAIDs EMS Monitor ECG for hypokalemia (flattened T waves) T risk of photosensitivity Rxns use caution w/ other diuretics, may T risk of electrolyte imbalances and dehydration may affect glucose (hyperglycemia) OD May cause dehydration, hypotension, drowsiness, headache, and fatigue symptomatic and supportive, do not do anything that would force greater fluid loss (ie, induce V)... [Pg.192]

Vomiting, abdominal pain, and bloody diarrhea are the most common signs seen after ingestion (Kopferschmitt et al, 1983 Malizia et al, 1977 Pillay et al, 2005). Tox-albumins cause severe gastrointestinal lesions of the oropharynx, esophagus, and stomach. The lesions are clinically similar to alkaline bums. Fluid losses can lead to dehydration, electrolyte disturbances, hypotension, and tachycardia (Ingle et al, 1966). [Pg.733]

Lmge exposures to Lewisite can cause Lewisite shock due to increased capillary membrane permeability and subsequent protein and plasma leakage across the capillary membranes. As a result, patients suffer intravascular fluid loss, hemoconcentration, hypovolemia, and hypotension (8,24). Cutaneous exposures can produce localized edema and pulmonary edema secondary to damage at the alveolm - capillary membrane (8). [Pg.134]

Depletional hyponatremia (excess loss of Na ) is almost always accompanied by a loss of ECF water, but to a lesser extent tlian the Na loss. Hypovolemia is apparent in the physical examination (orthostatic hypotension, tachycardia, decreased skin turgor). Loss of isosmotic or hypertonic fluid is the cause and this can occur through renal or extrarenal losses. If urine Na is low (generally <10 mmol/L), the loss is extrarenal (see Figure 46-2) because the kidneys are properly retaining filtered Na in response to increased aldosterone (stimulated by the hypovolemia and hyponatremia). Causes of extrarenal loss of Na" in excess of H2O include losses from the gastrointestinal tract or skin (see Figure 46-2). [Pg.1751]

A small amount of Lewisite on the skin will cause local edema because of the effects of this agent on local capillaries. With a large amount of Lewisite, the pulmonary capillaries are also affected there is edema at the site of exposure and pulmonary edema. With even larger amounts of Lewisite, all capillaries are affected, and proteins and plasma leak from the circulation into the periphery. Even after small amounts of Lewisite, the fluid loss can be sufficient to cause diminution of renal function and hypotension (Goldman and Dacre, 1989). [Pg.308]

Qiolera causes sudden onset of copious, non-bloody, watery rice-water diarrhoea with abdominal pain. Vomiting and fever are t)rpi-cally absent. Ciyptosporidiosis also causes severe watery diarrhoea and abdominal pain, and is commonly associated with a low-grade fever and vomiting. Cholera can result in rapid fluid loss of up to 1 litre per hour with concomitant losses of electrolytes. Dehydration due to large volume loss occurs later and can present with postural hypotension, tachycardia and shock in severe cases. [Pg.176]

Caution [C, /-] Contra Active varicella Infxn, serious Infxn except TB, fungal Infxns Disp Table VI-1 SE T Appetite, hyperglycemia, -i- K+, osteoporosis, nervousness, insomnia, steroid psychosis, adrenal suppression, fat redistribution, hypertension EMS Acute adrenal insufficiency can result w/ hypotension and shock if chronic steroids are abruptly stopped. Sxs can include abd pain, tach, confusion, hypotension, and chills. Support w/ IV fluids and steroid admin. GI perforation w/ chronic use. Can T Infxn risk and fracture risk from osteoporosis. Steroid psychosis can cause anxiety, agitation, euphoria, insomnia, mood swings, personality changes, depression, and memory loss usually at does of prednisone over 20 mg/d OD Acute hyperglycemia supportive care... [Pg.289]

The most frequent adverse reactions associated with the administration of proleukin include fever, chills, fatigue, malaise, nausea and vomiting. It has also been associated with capillary leak syndrome (CLS). CLS is defined as a loss of vascular tone and effusion of plasma proteins and fluids into the extravascular space. This leads to hypotension and decreased organ perfusion, which may cause sudden death. Other side effects include anaphylaxis, injection site necrosis and possible autoimmune and inflammatory disorders. [Pg.36]

A greater than 20% loss of ECF volume causes supine hypotension, usually after losing more than 4 L of fluid. [Pg.355]


See other pages where Fluid loss, hypotension caused is mentioned: [Pg.2057]    [Pg.362]    [Pg.103]    [Pg.184]    [Pg.222]    [Pg.184]    [Pg.222]    [Pg.300]    [Pg.456]    [Pg.1524]    [Pg.256]    [Pg.184]    [Pg.222]    [Pg.864]    [Pg.62]    [Pg.314]    [Pg.265]    [Pg.94]    [Pg.289]    [Pg.252]    [Pg.92]    [Pg.94]    [Pg.96]    [Pg.316]    [Pg.458]    [Pg.324]    [Pg.860]    [Pg.343]    [Pg.317]    [Pg.2306]    [Pg.92]    [Pg.94]    [Pg.289]    [Pg.316]    [Pg.68]    [Pg.348]   
See also in sourсe #XX -- [ Pg.16 ]




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