Hyperglycemia seizures

Levels greater than 35 mcg/mL—hyperglycemia, hypotension, cardiac arrhythmias, tachycardia, seizures, brain damage... 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

Hyperglycemia Nephritis Seizures Disturbed color vision... 

Ventricular arrhythmias, hypotension, circulatory failure, seizures, hyperglycemia, and syndrome of inappropriate antidiuretic hormone (SIADH) have been reported. 

Side effects are usually associated with the increasing serum concentration of theophylline and includes nausea, vomiting, headache, insomnia, tachypnea, epigastric pain, palpitation, hypotension, irritability. Higher doses can cause persistent vomiting, cardiac arrhythmias, intractable seizures, tachycardia. Other side effects include alopecia, hyperglycemia, inappropriate ADH syndrome, rash. 

Toxicities are numerous and include nephrotoxicity, hypertension, hyperglycemia, liver dysfunction, hyperkalemia, altered mental status, seizures, and hirsutism. Cyclosporine causes very little bone marrow toxicity. While an increased incidence of lymphoma and other cancers (Kaposi s sarcoma, skin cancer) have been observed in transplant recipients receiving cyclosporine, other immunosuppressive agents may also predispose recipients to cancer. Some evidence suggests that tumors may arise after cyclosporine treatment because the drug induces TGF-B, which promotes tumor invasion and metastasis. 

Adverse Effects. Common side effects of tacrolimus include gastrointestinal disturbances (cramps, nausea, diarrhea, constipation), weakness, fever, and skin rashes and itching. More serious problems include renal and central nervous system (CNS) toxicity (headache, anxiety, nervousness, seizures).41 Tacrolimus is also associated with problems with glucose metabolism (hyperglycemia, glucose intolerance), and can cause diabetes mellitus in certain individuals.73... 

In addition to sinus tachycardia and tremor, vomiting is common after overdose. Hypotension, tachycardia, hypokalemia, and hyperglycemia may occur, probably due to -adrenergic activation. The cause of this activation is not fully understood, but the effects can be ameliorated by the use of B-blockers (see below). Cardiac arrhythmias include atrial tachycardias, premature ventricular contractions, and ventricular tachycardia. In severe poisoning (eg, acute overdose with serum level > 100 mg/L), seizures often occur and are usually resistant to common anticonvulsants. Toxicity may be delayed in onset for many hours after ingestion of sustained-release tablet formulations. 

Nausea, vomiting, tinnitus, and hyperventilation are seen early in toxicity. As severity of toxicity increases, intractable vomiting, hyperthermia, hypotension, tachycardia, confusion, coma, seizures, pulmonary edema, acute renal failure, and death may occur. Hyperglycemia may be seen early, whereas hypoglycemia may occur later in toxicity. Acid-base disturbances such as respiratory alkalosis and/or metabolic acidosis may be noted. Signs and symptoms of salicylate toxicity may be noted as blood levels rise over 30mgdN. ... 

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... 

Seizure activity should be initially treated with benzodiazepines. If benzodiazepines are not effective, phenytoin and barbiturates can be administered. Insulin replacement may be necessary to correct hyperglycemia. 

Hypertension and tachycardia are the primary toxic manifestations of pseudoephedrine overdose. An amount of more than three or four times the maximum daily dosage for adults or children may produce symptoms of jS-adrenergic stimulation. In severe poisonings, cardiac dysrhythmias and cerebral hemorrhage due to hypertensive crisis may occur. Anxiety, muscle tremor, and seizures may result from CNS stimulation. Hallucinations, drowsiness, and/or irritability are more common symptoms exhibited by children. Hypokalemia and hyperglycemia may be noted. Acute renal failure and rhabdomyolysis have occurred in rare instances with large overdoses. 

In acute overdose, peak serum levels > 100 pg ml may be predictive of arrhythmias and seizures. The use of sustained-release formulations and the presence of pharmacobezors in the gut may make it difficult to determine peak serum levels. Sinus tachycardia is the most common cardiac sign of theophylline toxicity. Ventricular and supraventricular tachycardia, ectopic beats, hypotension, and cardiac arrest may occur. Metabolic acidosis, hypokalemia, hypercalcemia, and hyperglycemia may be seen. Tremulousness and agitation frequently occur. Intractable seizures may occur in severe intoxications, probably secondary to adenosine receptor antagonism in the brain. Onset of seizures is a poor prognostic indicator. Persistent vomiting is commonly seen and may interfere with attempts at therapy. 

Nephrotoxicity, neurotoxicity (tremor, headache, motor disturbances, seizures), G1 complaints, hypertension, hyperkalemia, hyperglycemia, and diabetes are all associated with tacrolimus use. As with cyclosporine, nephrotoxicity is limiting. Tacrolimus has a negative effect on pancreatic islet beta cells, and glucose intolerance and diabetes melli-tus are well-recognized complications of tacrolimus-based immunosuppression. As with other immunosuppressive agents, there is an increased risk of secondary tumors and opportunistic infections. Notably, tacrolimus does not adversely affect uric acid or LDL cholesterol. 

Nephrotoxicity, neurotoxicity (tremor, headache, motor disturbances, seizures), GI complaints, hypertension, hyperkalemia, hyperglycemia, and diabetes are all associated with tacrolimus use. 

A. The earliest symptoms of acute caffeine poisoning are usually anorexia, tremor, and restlessness. These are followed by nausea, vomiting, tachycardia, and confusion. With serious intoxication, delirium, seizures, supraventricular and ventricular tachyarrhythmias, hypokalemia, and hyperglycemia may occur. Hypotension is caused by excessive beta-2-mediated vasodilation and is characterized by a low diastolic pressure and a wide pulse pressure. 

A critical aspect in post-TBI intensive care management is the avoidance of these secondary brain insults, which would otherwise be well-tolerated but can exacerbate neuronal injury in cells made vulnerable by the initial TBI. Of particular importance is the prevention of hypotension and hypoxia (which decrease substrate delivery of oxygen and glucose to injured brain), fever and seizures (which may further increase metabolic demand), and hyperglycemia (which may exacerbate ongoing injury mechanisms), as discussed in the following sections. 

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