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Cramping intravenous

A 27- year-old male with a three-year history of AIDS complains of progressive blurring of vision for two days. Eye examination reveals evidence of retinitis consistent with cytomegalic virus inclusion disease. Intravenous treatment is started, and within five days the patient complains of muscular weakness and cramping. Blood chemistries show a creatinine of. 5.2 mEq/L and a Ca of 6.9 mEq/L. [Pg.67]

Patients who present with heat exhaustion require fluid resuscitation. An attempt should be made to assess the amount of salt depletion and dehydration. This may be difficult clinically although the presence of symptoms such as muscle cramps in sodium depletion, and signs such as loss of tissue turgor may help. Laboratory measurement of sodium, urea, creatinine and haematocrit are the best guide. Pre-renal renal impairment is common. Treatment usually requires 5-10 1 of oral or intravenous isotonic fluids in the first 24 hours. In severe hyponatraemia the rapid correction of sodium should be carefully monitored with frequent sodium measurements and a reduction in fluid infusion rate if necessary to reduce the risk of osmotic demyelination (central pontine myelinol-ysis). [Pg.517]

Potentially severe adverse effects can result from systemic administration of cholinomimetic drugs, and none should be administered by intramuscular or intravenous injection. If significant amounts of these drugs enter the circulation, nausea, abdominal cramps, diarrhea, salivation, hypotension with reflex tachycardia, cutaneous vasodilation, sweating, and bronchoconstric-tion can result. Pilocarpine can cross the blood-brain barrier and affect cognitive function. Even the topical application of cholinomimetics to the eyes can present... [Pg.125]

These patients may also exhibit symptoms of excessive stimulation of muscarinic receptors (abdominal cramps, diarrhea, increased salivation, excessive bronchial secretions, miosis, bradycardia). Small doses of edrophonium (1-2 mg intravenously) will produce no relief or even worsen weakness if the patient is receiving excessive cholinesterase inhibitor therapy. On the other hand, if the patient improves with edrophonium, an increase in cholinesterase inhibitor dosage may be indicated. Clinical situations in which severe myasthenia (myasthenic crisis) must be distinguished from excessive drug therapy (cholinergic crisis) usually occur in very ill myasthenic patients and must be managed in hospital with adequate emergency support systems (eg, mechanical ventilators) available. [Pg.145]

Quinine is a cinchona alkaloid that acts rapidly against all four species of Plasmodium. It is used to treat protozoal infections and leg cramps, and as a bitter and flavoring agent. However, the drug is not used prophylactically for malaria. Quinines are contraindicated in patients with a history of hypersensitivity to quinine or quinidine. They should not be used in the presence of hemolysis and should be used with caution in patients with atrial fibrillation, cardiac conduction defects, or heart block. Quinine administration in myasthenia gravis may aggravate the disease, hence it should be avoided. Quinine can be used in pregnancy.37 Intravenous infusion of quinine should be slow, and the patient should be monitored for cardiotoxicity.38 Cinchonism, which is characterized by tinnitus, GI disturbances, and impaired vision may occur with therapeutic doses of quinine.39... [Pg.285]

SAFETY PROFILE A human poison by ingestion and possibly other routes. Moderately toxic by skin contact and subcutaneous routes in humans, Poison experimentally by inhalation and subcutaneous routes. Moderately toxic experimentally by intraperitoneal and intravenous routes. Human systemic effects anorexia, changes in kidney tubules, nausea or vomiting, wakefulness. Ingestion or absorption by other routes may also cause diarrhea, abdominal cramps, erj thematous lesions on skin and mucous membranes, circulatory collapse, tachycardia, cyanosis, delirium, convulsions, and coma. Death has occurred from ingestion of less than 5 g in infants, and from 5 to 20 g in adults. [Pg.204]

SAFETY PROFILE Poison by intravenous route. Moderately toxic by ingestion. A skin and severe eye irritant. Mutation data reported. Can cause cramps and diarrhea. Possibly similar to DDT. An FDA over-the-counter drug. An anthelmintic. When heated to decomposition it emits toxic fumes of Cr. See also DDT and CHLOROPHENOLS. [Pg.918]

Various musculoskeletal symptoms have been reported with bumetanide, including pain, cramping, and weakness (SEDA-22, 236). The symptoms are usually mild and self-limiting, with an incidence of less than 2%, but disabhng reactions have occurred after oral administration and intravenous injection, and severity correlates with dose. The onset is usually 2-4 hours after dosing the onset may be slower during infusion. [Pg.567]

Deferoxamine is only used parenterally. It is more toxic when used in patients with a low iron burden. After subcutaneous infusion many patients have some local irritation and swelling. Rapid intravenous injection can be followed by flushing, wheals, tachycardia, hypotension, acute adult respiratory distress, and renal insufficiency shock or convulsions can also occur. Headache, blurred vision, dysuria, diarrhea, and leg or hand cramps have been reported. Intramuscular injection can be painful. Hypersensitivity reactions occasionally occur, with rash, fever, and edema anaphylactic shock has been encountered (SEDA-7, 262) (7,8). As a test dose in patients with aluminium storage... [Pg.1059]

There have been reports of leg cramps after intravenous administration of encainide (24). [Pg.1214]

Intravenous erjdhromycin should be restricted to as few patients as possible. It can cause severe abdominal cramps, probably by a direct action on smooth muscle (36-38). [Pg.1238]

The case once made against use of iron dextran in pregnancy because of a supposed risk of possible uterine cramps (SED-9, 377) or a greater risk of systemic reactions (SED-8, 513) has not been substantiated. However, in one case a pregnant woman had anaphylactic shock as a reaction to intravenous iron, and this resulted in fetal cerebral damage (SEDA-22, 246). [Pg.1916]

Cisplatin can cause anaphylactic shock, asthma, or urticaria (236). Hypersensitivity reactions, probably of type I, have also been reported after the administration of cisplatin, carboplatin, and oxaliplatin (237-243). Life-threatening allergy to cisplatin has also been reported after 16 doses of cisplatin 20 mg/m /week (244). These allergic reactions can include respiratory dysfunction (for example wheezing, dyspnea), gastrointestinal discomfort (for example abdominal cramps, diarrhea), and rashes (for example pruritus, urticaria, facial erythema, and swelling). The risk of exfoliative dermatitis is very low. In most patients, the first signs of hypersensitivity reactions usually occurred after the administration of multiple intravenous courses... [Pg.2862]

The acute form of diarrhea is short-lived and can be effectively prevented or rapidly suppressed by concomitant atropine. The cholinergic symptoms are accompanied by abdominal cramps (36%), sweating (57%), salivation (11%), visual disturbances (15%), lacrimation (12%), and piloerection (3%). The recommended dose of atropine is 0.25 mg intravenously for prevention or 0.25-1.0 mg for acute treatment of patients with early cholinergic symptoms. As cholinergic symptoms have not been observed with other camptothecin derivatives, it can be speculated that these adverse effects are restricted to irinotecan, whose piperidino group bears some structural similarity to the potent nicotine receptor stimulant dimethylphenylpiperazinium (106). [Pg.3459]

Amphetamines have also been associated with a syndrome of acute kidney injury and rhabdomyolysis. Several series have described patients following intravenous injection of methamphetamine or phenmetrazine who presented with hyperactivity, fever, chills, sweats, abdominal cramps, diarrhea, and hypotension [177,178]. The patients have developed acute kidney injury which is usually oliguric and associated with classic rhabdomyolysis, similar to cases of cocaine-induced rhabdomyolysis. Several patients have had disseminated intravascular coagulation and liver function abnormalities as well. Methamphetamine abuse has also been associated with accelerated hypertension, unexplained chronic renal failure, acute lead poisoning (a common reagent used in its production utilizes lead acetate) and at least one case of biopsy proven interstitial nephritis the latter patient responded to intravenous corticosteroids but whether the nephritis was truly due to amphetamines remains unproven [179]. [Pg.608]

Human studies with VX began in 1959 when an investigator, Dr Van M. Sim, volunteered to be the first subject. VX, 0.04 ig kg-1, was given intravenously over 30 s with no untoward effects and no change in erythrocyte cholinesterase activity. Three and a half hours later, 0.08 ug kg-1 was administered by the same method. He developed a headache, felt sweaty and lightheaded, and complained of abdominal cramps, but blood cholinesterase activity was normal. For regulatory and approval reasons, a year intervened before the study continued. [Pg.232]


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