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UREMIC ENCEPHALOPATHY - Coggle Diagram
UREMIC ENCEPHALOPATHY
DEFINITION, ETIOLOGY
& RISK FACTOR
Etiology
- Many compounds have been implicated in the pathogenesis of UE, and they are known as uremic toxins (UT). Urea is the most studied UT.
- While severe cognitive changes of uremic encephalopathy develop when the estimated glomerular filtration rate (eGFR) falls below 15mL/min, frequently cognitive changes can be identified at eGFR in the range of 40-60 mL/min.
Risk Factor
- Acute Kidney Injury
- Chronic Kidney Injury
- TTP
Definition
- Uremic encephalopathy (UE) is defined as cerebral dysfunction due to the accumulation of toxins resulting from acute or chronic renal failure.
PATHOPHYSIOLOGY
- No common pathway has been identified, but overall, three processes may be contributing. These include an imbalance in the inhibitory and excitatory neurotransmitters, neuronal degeneration, and vascular inflammation.
DIFFERENTIAL DIAGNOSIS
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Fluid and Electrolyte disturbances, such as hyponatremia and hypermagnesemia
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TREATMENT
- UE is an absolute indication to initiate renal replacement therapy (RRT).
- Management of CKD should be implemented simultaneously, such as the use of erythropoiesis-stimulating agents, phosphate binders, calcium replacement, and nutrition modification.
- There is clinical evidence that intermittent hemodialysis (HD) is more effective than continuous ambulatory peritoneal dialysis (CAPD).
- However, there is a danger to precipitating dialysis disequilibrium syndrome (DDS) due to the risk of rapid osmotic changes at the start of HD.
- Mannitol is used to prevent DDS in the first few HD sessions. Twenty-five grams of mannitol can be given before starting hemodialysis for the first three sessions
Primary Survey
- Airway -> Oropharyngeal tube
- Breathing -> Oxygen
- Circulation -> IV line
- Dissability
- Exposure
Secondary Survey
- AMPLE anamnesis
- Examination from head to toe
COMPLICATIONS
- Some of the complications of UE are seizures, coma, and death. Upon initiation of renal replacement therapy, UE may be partially reversed.
- However, some cognitive changes may become permanent.
PROGNOSIS
- With the initiation of RRT, the clinical syndrome of UE improves. This process may occur in days to weeks.
- The EEG changes take several months to recover and may not return to baseline.
- Some cognitive changes in the brain may be irreversible.
- That is one more reason to initiate RRT before the onset of UE.
DIAGNOSIS APPROACH
History & Physical
- 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.
- These patients can present with confusion, delirium, seizures, and coma.
- A 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.
Evaluation
- Laboratory Evaluation -> Such as complete blood count (CBC), comprehensive metabolic panel (CMP), magnesium level, phosphorus level, lactic acid level, and toxicology screen should be ordered.
- Neurological Evaluation -> EEG findings in UE include a loss of alpha frequency waves and slowing overall all, and intermittent bursts of theta and delta waves with slow background activity.
- Neuroimaging -> CTscan of the brain can exclude focal lesions. Abnormalities are found in the cortex, subcortical white matter, basal ganglia, and hippocampus.