Encephalopathy intravenous

Bihmbin oxidase [80619-01 -8] derived from Mjrothecium verrucaria was modified with polyethyleneglycol when this conjugate was injected intravenously to jaundiced rats, the plasma bihmbin dropped to normal levels. This approach might have potential in the treatment of hyperbihmbinemia, fulminant hepatitis, and neonatal bihmbin encephalopathy (177). 

Thiamin has a very low toxicity (oral LD5o of thiaminchloride hydrochloride in mice 3-15 g/kg body weight). The vitamin is used therapeutically to cure polyneuropathy, beri-beii (clinically manifest thiamin deficiency), and Wernicke-Korsakoff Syndrome ( Wernicke encephalopathy and Korsakoff psychosis). In mild polyneuropathy, 10-20 mg/d water-soluble or 5-10 mg/d lipid-soluble thiamin are given orally. In more severe cases, 20-50 mg/d water-soluble or 10-20 mg/d lipid-soluble thiamin are administered orally. Patients suffering from beri-beri or from early stages of Wernicke-Korsakoff Syndrome receive 50-100 mg of thiamin two times a day for several days subcutaneously or intravenously until symptoms are alleviated. Afterwards, the vitamin is administered orally for several weeks. 

Melarsoprol is a divalent arsenical. It reacts with sulfhydryl groups. Melarsoprol is used for the late stage of sleeping sickness. It has to be administered intravenously. Slow i.v. injection is recommended. It is widely distributed and enters the CNS. It has a very short elimination half-life as it is biotransformed to a pentavalent arsenical. Adverse effects include hypersensitivity reactions and gastrointestinal toxicity causing severe vomiting and abdominal pain. CNS reactions are most serious as the encephalopathy may be fatal. Hemolytic anemia may... 

Inadequate nutrition and conditions which are complicated by malabsorption may lead to thiamine deficiency. Beriberi, a diet-deficiency disease, is especially prevalent in those parts of the East where the diet consists mainly of polished rice. The disease is characterized by neuritis but may also lead to serious heart failure. Recovery is prompt when adequate amounts of vitamin B1 are restored to the diet. Severe deficiency as can occur in alcoholics may lead to Wernicke s encephalopathy, often accompanied by Korsakoff s syndrome. Care should be taken with intravenous substitution with thiamine in these cases to prevent serious complications like vascular collapse with hypotension, respiratory distress or an-gioedema. 

Where patients are at risk of Wernicke s encephalopathy - for example, because of chronic alcohol abuse, hyperemesis gravidarum, or malnutrition - they should be given thiamine. In many countries no intravenous preparation of thiamine alone is available, and the compound preparations that are available are prone to cause anaphylactoid reactions, so they should be given by slow infusion, and with adequate facilities for resuscitation. A high potency preparation (Pabrinex ) that contains thiamine 250 mg in 10 ml with ascorbic acid, nicotinamide, pyridoxine and riboflavin, can be given by intravenous infusion over 10 min. 

Larger volumes can only be safely removed if there is simultaneous albumin replacement intravenously (with about 8 g of albumin per litre of ascites). Synthetic plasma-expanders may not be greatly inferior to albumin in the short term. Transjugular intrahep-atic portal systemic shunting (TIPS) appears at least as effective as paracentesis in relieving refractory ascites without increasing mortality but with a raised risk of encephalopathy. 

Diazoxide is administered intravenously for the treatment of hypertensive emergencies, particularly malignant hypertension, hypertensive encephalopathy, and eclampsia. It is effective in 75 to 85% of the patients to whom it is administered and rarely reduces blood pressure below the normotensive range. 

Chemically it is trivalent arsenical used for advanced CNS African trypanosomiasis. It is administered intravenously in propylene glycol and after administration it rapidly excreted. It is highly toxic and used only in advanced trypanosomiasis when no alternative is there, these effects include vomiting, fever, abdominal pain, renal and cardiac disease and encephalopathy characterized by cerebral edema, seizures, coma (even death). 

The Wernicke-Korsakofi syndrome consists of both an acute (i.e., Wernicke s encephalopathy) and a chronic phase (i.e., Korsakoff s psychosis). The acute encephalopathy may be precipitated or worsened by carbohydrates (including intravenous glucose) unless thiamine is also replenished before or during administration. Wernicke s encephalopathy may first be manifested by the following ... 

Six unselected patients (four women), mean age 27 years, with acute liver failure and grade IV hepatic encephalopathy received terlipressin 0.005 mg/kg as a single intravenous bolus (16). There was an increase in cerebral blood flow 1 hour after the bolus, which returned to baseline at 5 hours, and an increase in intracranial pressure at 1 hour, which returned to baseline at 2 hours. The authors speculated that terlipressin could have a deleterious effect on cerebral hemodynamics in patients with severe hepatic encephalopathy. 

A 70-year-old woman with a 2-year history of primary biliary cirrhosis confirmed by histological and immunological criteria took colestyramine sachets twice daily for 2 months and developed lethargy, confusion, and drowsiness (3). She had signs of chronic liver disease, portal hypertension, and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis, and a urinary pH of 4.85 together with tests of renal acidification excluded renal tubular acidosis. No other cause was found and she responded to 600 mmol of sodium bicarbonate intravenously over 36 hours. 

Injection of calcium disodium EDTA does not affect blood calcium levels but heavy metal ions in the body have a higher affinity for EDTA than does calcium, and hence these metals readily exchange in vivo to form soluble EDT A-heavy-metal complexes that are excreted in the urine. Because of its poor absorption from the alimentary tract, calcium disodium EDTA is usually injected intramuscularly or intravenously. These considerations led to its being used, initially in 195270), to treat lead encephalopathy. 

Developmental Effects. Studies in human infants indicate that only certain children are affected by aluminum. Excessive aluminum accumulation and encephalopathy may occur in premature infants with reduced renal function given dialysis with aluminum-containing intravenous fluid (Polinsky and Gruskin 1984 Sedman et al. 1985). Bone disease has also been reported in infants with renal failure who were treated orally with aluminum hydroxide (Andreoli et al. 1984). 

Diazoxide [dye az OX ide] is a direct-acting arteriolar vasodilator. It has vascular effects like those of hydralazine. For patients with coronary insufficiency, diazoxide is administered intravenously with a p-blocker, which diminishes reflex activation of the heart. Diazoxide is useful in the treatment of hypertensive emergencies, hypertensive encephalopathy, and eclampsia. Excessive hypotension is the most serious toxicity. 

Two premature neonates, who already had epileptic manifestations related to severe hypoxic ischemic encephalopathy, developed seizures (one tonic and the other tonic-clonic) within a few seconds of receiving intravenous midazolam (0.15 pg/kg) for sedation (25). In one, the seizure recurred after rechallenge on the same day. Benzodiazepines occasionally cause tonic seizures, especially after intravenous administration to children with Lennox-Gastaut syndrome. This seems to be the first report related to midazolam in newborns. 

In one study, no pharmacokinetic differences were noted when a single 0.15 mg/kg intravenous dose was given to six cirrhotic patients and six healthy subjects. However, tbe cirrhotic patients had no manifestations of end-stage disease, normal prothrombin times and relatively normal liver function tests. Four had experienced prior encephalopathy [58]. 

Analgesics. Opiates can precipitate hepatic encephalopathy in patients with decompensated liver disease. If required to control postoperative pain, doses should be reduced to 25-50% of normal. Constant intravenous infusions should be avoided if the patient is not to be insidiously overdosed. Codeine can precipitate hepatic encephalopathy by its constipating effect alone. Aspirin and other NSAIDs may exacerbate impaired renal function and fluid retention by inhibiting prostaglandin synthesis and may also precipitate gastrointestinal bleeding. 

Acyclovir is generally well tolerated whether administered topically, orally, or by the intravenous route. GI disturbances, headache, and rash may occur. Renal dysfunction due to crystalline nephropathy is more likely with IV administration, rapid infusion, in patients in the dehydrated state and with underlying renal disease, and in large doses. CNS effects are rare but include encephalopathy, tremors, hallucinations, seizures, and coma. Due to an elevated pH, intravenous administration may also cause phlebitis and inflammation at sites of extravasation (Wagstaff et al., 1994). 

There is a higher incidence of ifosfamide encephalopathy associated with the oral form compared with the intravenous form of ifosfamide this has been attributed to metabolic differences between the two (16). 

Buesa JM, Garcia-Teijido P, Losa R, Fra J. Treatment of ifosfamide encephalopathy with intravenous thiamin. Chn Cancer Res 2003 9(12) 4636-7. 

Stroke and ischemic encephalopathy, probably caused by cerebral vasospasm after intravenous immunoglobulin, have been reported as possible comphcations of intravenous immunoglobuhn (63). 

Sztajzel R, Le Floch-Rohr J, Eggimann P. High-dose intravenous immunoglobulin treatment and cerebral vasospasm A possible mechanism of ischemic encephalopathy Eur Neurol 1999 41(3) 153-8. 

Melarsoprol given intravenously in patients with trypanosomiasis can cause a peripheral neuropathy within 2-5 weeks (SEDA-14, 243). It also causes a reactive arsenical encephalopathy in 3-5% of patients with trypanosomiasis (SEDA-13, 834) (6). 

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