Uremic encephalopathy symptoms

Uremic encephalopathy occurs as a result of the effects of uremia on the central nervous system and is associated with symptoms including alterations in consciousness, thinking, memory, speech, psychomotor behavior, and emotion. Sensory and motor function may be altered, particularly affecting leg nerves, resulting in leg cramps and restless leg syndrome. Uremic encephalopathy is less common because of earlier initiation of dialysis in patients with Stage 5 CKD. 

The presenting symptoms of uremia are similar to many other encephalopathic states. The differential diagnosis is even more complex, since patients with renal failure are subjected to other intercurrent illnesses that may also induce other encephalopathic effects. In patients with renal failure, treatment with dialysis will restore more normal body fluid composition. Despite the possibility that multiple causes of encephalopathy might occur simultaneously, uremic encephalopathy may be successfully differentiated in most instances by means of the usual clinical methods. 

Uremic and dialysis encephalopathies. Patients with renal failure continue to manifest neuropsychiatric symptoms despite significant advances in therapeutics and management. Patients with renal failure who are not yet on dialysis develop an array of symptoms, including clouding of consciousness, disturbed sleep patterns, tremor and asterixis that may progress to coma and death. 

In all patients with chronic renal insufficiency, strict supervision of total aluminium intake is vital. The administration of aluminium should be stopped as soon as the serum concentration exceeds 150 pg/ml or at the appearance of the first symptoms of encephalopathy (81). According to current recommendations, dia-lysate solutions should contain less than 10 pg/l of aluminium (82). There is some controversy about the view that aluminium-containing medications used to control serum phosphate concentrations in uremic subjects should be replaced by calcium-containing phosphate binders (83). Another approach used to reduce the toxic risks of aluminium hydroxide may be to tailor doses to the phosphate concentration in serum, that is individualizing aluminium gel therapy (SED-12, 515). 

The dose of ammonium chloride can be calculated on the basis of the chloride deficit using the same method as for HCl, using the conversion of 20 g ammonium chloride providing 374 mEq of H . However, only half of the calculated dose of ammonium chloride should be administered so as to avoid ammonia toxicity. Ammonium chloride is available as a 26.75% solution containing 100 mEq in 20 mL, which should be further diluted prior to administration. A dilute solution may be prepared by adding 100 mEq of ammonium chloride to 500 mL of normal saline and infusing the solution at a rate of no more than 1 mEq/min. Improvement in metabolic stams is usually seen within 24 hours. CNS toxicity, marked by confusion, irritability, seizures, and coma, has been associated with more rapid rates of administration. Ammonium chloride must be administered cautiously to patients with renal or hepatic impairment. In patients with hepatic dysfunction, impaired conversion of ammonia to urea may result in increased ammonia levels and worsened encephalopathy. In patients with renal failure, the increased urea synthesis may exacerbate uremic symptoms. ... 

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