Uremic Encephalopathy
Definisi
Uremic encephalopathy is an organic brain disorder. It develops in patients with acute or chronic renal failure, usually when the estimated glomerular filtration rate (eGFR) falls and remains below 15 mL/min.
Manifestasi Klinis
mild symptoms
severe signs
lassitude & fatigue
seizures & coma
Patofisiologi
One contributing factor to uremic encephalopathy may involve imbalances of neurotransmitter amino acids within the brain. During the early phase of uremic encephalopathy, plasma and cerebrospinal fluid (CSF) determinations indicate that levels of glycine increase and levels of glutamine and gamma-aminobutyric acid (GABA) decrease. As uremia progresses, it has been proposed that the accumulation of guanidino compounds results in activation of excitatory N-methyl-D-aspartate (NMDA) receptors and inhibition of inhibitory GABA receptors, which may cause myoclonus and seizures. In addition, alterations occur in metabolism of dopamine and serotonin in the brain, which may lead to early symptoms (eg, sensorial clouding).
Etiologi
Chronic renal failure
Faktor risiko
loss medication of CRF
DM & Hypertension
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Vomiting
Emotional volatility
Decreased cognitive function
Disorientation
Confusion
Bizarre behavior
Stupor, coma
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Anorexia
Nausea
Restlessness
Drowsiness
Diminished ability to concentrate
Slowed cognitive functions
CMD
History
The clinical presentation is variable and is determined by the rate of progression of the underlying kidney disease. In patients with a slow decline in eGFR, fatigue, anorexia, weight-loss, and nausea are the presenting signs. Cognitive dysfunction is slow, progressive, and subtle. Psychometric testing is required to identify the involvement of the central nervous system. At the other end of the spectrum are patients with a rapid decline in eGFR. These patients can present with confusion, delirium, seizures, and coma.
Physical
physical exam reveals cognitive dysfunction in the form of abnormalities in memory, judgment, and ability to perform calculations. Hyperreflexia, asterixis, papilledema, and nystagmus are frequently present. Neuropathy and myopathy may be present.
Laboratory Studies
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Renal function studies – Markedly elevated blood urea nitrogen (BUN) and creatinine levels are seen in uremic encephalopathy
Serum electrolyte and glucose measurements To rule out hyponatremia, hypernatremia, hyperglycemia, and hyperosmolar syndromes as the cause of encephalopathy
Complete blood cell count –To detect leukocytosis, which may suggest an infectious cause, and to determine whether anemia is present (anemia may contribute to the severity of mental alterations)
Serum calcium, phosphate, and parathyroid hormone (PTH) levels –To assess for hypercalcemia, hypophosphatemia, and severe hyperparathyroidism, which cause metabolic encephalopathy
Serum magnesium level –This may be elevated in a patient with renal insufficiency, particularly if the patient is ingesting magnesium-containing antacids; hypermagnesemia may manifest as encephalopathy
Toxicology screen
Medication levels
Tatalaksana
Address the following factors when treating uremic encephalopathy, which are also included in the standard care of any patient with ESRD
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Adequacy of dialysis
Correction of anemia
Regulation of calcium and phosphate metabolism