Uremic encephalopathy - Revision history

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Ostermayer: Created page with "==Background== Uremic encephalopathy is cerebral dysfunction caused by accumulation of uremic toxins due to acute kidney injury or chronic kidney diseaseOlano CG, Akram SM, Hashmi MF, et al. Uremic Encephalopathy. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024. Typically develops when eGFR falls below '''15 mL/min''' (CKD Stage G5), though can occur at higher eGFR in acute kidney injury where the rate of de..."

2026-03-10T01:02:16Z

Created page with "==Background== *Uremic encephalopathy is cerebral dysfunction caused by accumulation of uremic toxins due to acute kidney injury or chronic kidney disease<ref name="StatPearls">Olano CG, Akram SM, Hashmi MF, et al. Uremic Encephalopathy. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.</ref> *Typically develops when eGFR falls below '''15 mL/min''' (CKD Stage G5), though can occur at higher eGFR in acute kidney injury where the rate of de..."

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==Background==
*Uremic encephalopathy is cerebral dysfunction caused by accumulation of uremic toxins due to [[acute kidney injury]] or [[chronic kidney disease]]<ref name="StatPearls">Olano CG, Akram SM, Hashmi MF, et al. Uremic Encephalopathy. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.</ref>
*Typically develops when eGFR falls below '''15 mL/min''' (CKD Stage G5), though can occur at higher eGFR in acute kidney injury where the rate of decline is rapid<ref name="Rosner2022">Rosner MH, Husain-Syed F, Reis T, Ronco C, Vanholder R. Uremic encephalopathy. Kidney Int. 2022;101(2):227-241.</ref>
*Severity correlates with the '''rate of decline''' in kidney function — AKI causes more severe encephalopathy than progressive CKD at the same GFR, because chronic adaptation has not occurred
*'''Reversible with dialysis''' — this is both the treatment and the diagnostic confirmation; uremic encephalopathy is an '''absolute indication''' for emergent renal replacement therapy<ref name="StatPearls"/>
*'''Diagnosis of exclusion''' — there is no confirmatory test; the diagnosis is often made retrospectively when mental status improves after dialysis<ref name="Rosner2022"/>
*Pathophysiology is multifactorial: accumulation of uremic solutes (urea, guanidino compounds, indoxyl sulfate, p-cresol, PTH), disruption of the blood-brain barrier, neurotransmitter imbalances (↑ GABA, altered dopamine/serotonin), electrolyte derangements, and systemic inflammation
*Can also occur in dialysis patients receiving '''inadequate dialysis''' (noncompliance, AV fistula dysfunction, underdialysis)

==Clinical Features==
''The clinical spectrum ranges from subtle cognitive changes to coma. Progression is inevitable without treatment.''

===Early/Mild===
*Fatigue, malaise, poor concentration
*Insomnia, sleep-wake cycle disturbance
*Irritability, emotional lability
*Anorexia, nausea
*Impaired memory, difficulty with complex tasks
*Apathy, withdrawal

===Moderate===
*'''[[Altered mental status]]:''' confusion, disorientation, delirium
*[[Asterixis]] ('''flapping tremor''' — highly suggestive but not pathognomonic; also seen in hepatic encephalopathy, hypercapnia, drug toxicity)
*Myoclonus (multifocal muscle jerking)
*Tremor
*Dysarthria
*Ataxia, gait instability
*Hyperreflexia

===Severe===
*'''[[Seizures]]''' (generalized tonic-clonic or myoclonic; more common in AKI than CKD)
*Stupor
*'''Coma'''
*Opisthotonus (rare)

===ED Pearls===
*'''Asterixis + elevated BUN/creatinine + no prior known liver disease = think uremic encephalopathy'''
*Symptoms in CKD patients are often '''subtle and progressive''' — family may report gradual personality changes, forgetfulness, or increased confusion over days to weeks
*In AKI, encephalopathy can develop '''rapidly''' (hours to days) and may be the presenting feature
*A dialysis patient presenting with AMS should be evaluated for '''both''' uremic encephalopathy (inadequate dialysis) '''and''' dialysis disequilibrium syndrome (too-rapid dialysis) — timing relative to last dialysis session is key
*Uremic encephalopathy may '''paradoxically improve arthritis''' symptoms in patients with concurrent rheumatic disease — decreased activity is sometimes misinterpreted as clinical improvement
*'''Seizures''' in CKD/ESRD patients should prompt evaluation for uremia, but also for [[hypertensive encephalopathy]], [[hypoglycemia]], [[hyponatremia]], [[hypocalcemia]], [[hypermagnesemia]], and medication toxicity

==Differential Diagnosis==
''All other causes of [[altered mental status]] must be considered and excluded before attributing encephalopathy to uremia alone:''

===Metabolic/Toxic===
*'''[[Hyperkalemia]]''' (can cause weakness, paralysis, and obtundation in addition to cardiac effects)
*'''[[Hyponatremia]]''' or '''[[hypernatremia]]'''
*'''[[Hypoglycemia]]''' or '''[[hyperglycemia]]''' / [[hyperosmolar coma]]
*'''[[Hypercalcemia]]'''
*'''[[Hypermagnesemia]]''' (especially in CKD patients taking Mg-containing antacids)
*'''[[Hepatic encephalopathy]]''' (concomitant liver disease is common)
*'''Medication toxicity:''' [[opioids]] (accumulate in CKD), [[benzodiazepines]], [[gabapentin]]/[[pregabalin]], [[lithium]], [[metformin]] (lactic acidosis)
*'''Severe [[metabolic acidosis]]'''
*'''[[Wernicke encephalopathy]]''' (thiamine deficiency — may coexist in malnourished CKD patients)

===Structural/Vascular===
*'''[[Stroke (Main)|Stroke]]''' (CKD patients have high cerebrovascular risk)
*'''[[Subdural hematoma]]''' (uremic patients have impaired platelet function; anticoagulation for dialysis access)
*'''[[Intracranial hemorrhage]]'''
*'''[[Hypertensive encephalopathy]]''' / [[PRES]] (posterior reversible encephalopathy syndrome)

===Infectious===
*'''[[Sepsis (Main)|Sepsis]]''' (dialysis access infection, [[pneumonia]], [[UTI]]) — '''most important to exclude immediately'''
*'''[[Meningitis]]/[[encephalitis]]'''

===Dialysis-Related===
*'''[[Dialysis complications|Dialysis disequilibrium syndrome]]:''' Headache, nausea, AMS, seizures occurring '''during or shortly after''' dialysis (especially first sessions or aggressive ultrafiltration); caused by rapid osmolar shifts and cerebral edema
*'''Osmotic demyelination syndrome''' (from rapid correction of [[hyponatremia]])
*'''Aluminum toxicity''' (historical; rare with modern dialysate)

{{AMS DDX}}

==Evaluation==
===Workup===
''The workup is directed at confirming severe renal dysfunction AND excluding mimickers. It must be rapid.''

*'''BMP/CMP:''' BUN, creatinine (compare to baseline), electrolytes (K⁺, Na⁺, Ca²⁺, Mg²⁺, phosphorus), glucose, bicarbonate (anion gap)
**BUN is typically '''markedly elevated''' (often >100-150 mg/dL); however, there is no absolute BUN threshold that defines uremic encephalopathy
*'''CBC:''' Leukocytosis (suggests infection); anemia (baseline in CKD, acute worsening suggests bleed)
*'''VBG or ABG:''' Assess acid-base status and calculate anion gap; severe uremic acidosis may coexist
*'''[[Lactate]]:''' Evaluate for sepsis or tissue hypoperfusion
*'''Ammonia:''' If hepatic encephalopathy is also being considered (common in patients with combined liver/kidney disease)
*'''Fingerstick glucose:''' Immediate — rule out [[hypoglycemia]]
*'''[[ECG]]:''' Evaluate for [[hyperkalemia]] (peaked T waves, wide QRS), [[QT prolongation]]
*'''Toxicology screen:''' Exclude drug intoxication
*'''Serum osmolality:''' Assess for hyperosmolar states or osmolar gap (toxic alcohol)
*'''PTH, magnesium:''' Hyperparathyroidism and hypermagnesemia can both contribute to metabolic encephalopathy
*'''[[CXR]]:''' Evaluate for volume overload, infection
*'''Blood cultures:''' If any suspicion for [[sepsis]] (dialysis patients are high risk for bloodstream infection)
*'''[[CT head]] without contrast:''' To exclude [[intracranial hemorrhage]], [[subdural hematoma]], mass lesion, or signs of cerebral edema
**MRI is more sensitive (may show bilateral basal ganglia involvement — "lentiform fork sign" — or cortical/white matter changes) but is not required emergently
*'''[[LP]]:''' Not routinely needed; consider if clinical picture does not improve after dialysis or if there is concern for [[meningitis]]/[[encephalitis]]
*'''EEG:''' Not required in the ED; shows diffuse slowing proportional to the severity of renal dysfunction; may be useful if subclinical seizures are suspected

===Diagnosis===
*'''Diagnosis of exclusion''' — no single confirmatory test exists<ref name="Rosner2022"/>
*Clinical diagnosis is based on:
**'''Significantly impaired renal function''' (eGFR <15, markedly elevated BUN/creatinine)
**'''Compatible neurologic findings''' (progressive AMS, asterixis, myoclonus, seizures)
**'''Exclusion of other causes''' of altered mental status
**'''Improvement after initiation of dialysis''' (the most definitive diagnostic confirmation — but do not wait for this to begin treatment)
*'''ED diagnostic pearl:''' The combination of '''asterixis''' + '''BUN >100''' + '''no hepatic disease''' + '''no structural lesion on CT''' in a patient with known CKD or AKI is highly suggestive
*If neurologic status does not improve after 3-5 dialysis sessions, '''re-evaluate for alternative or additional diagnoses'''<ref name="Rosner2022"/>

==Management==
===Resuscitation and Stabilization===
*'''ABCs:''' Airway protection is critical — obtunded patients may need [[intubation]] (use medications that do not require renal clearance for RSI; consider [[rocuronium]] over [[succinylcholine]] if [[hyperkalemia]] is present or suspected)
*'''IV access:''' If patient does not already have dialysis access, '''emergent dialysis catheter placement''' will be needed
*'''Continuous monitoring:''' telemetry, pulse oximetry, frequent neuro checks
*'''Treat concurrent [[hyperkalemia]]:''' [[Calcium gluconate]], [[insulin]]/D50, nebulized [[albuterol]] (see [[Hyperkalemia]])
*'''Treat concurrent [[metabolic acidosis]]:''' [[Sodium bicarbonate]] for pH <7.1 or hemodynamic instability
*'''Treat concurrent volume overload:''' [[Nitroglycerin]], high-dose [[furosemide]], [[BiPAP]] (see [[Pulmonary edema]])

===Definitive Treatment: Emergent Dialysis===
*'''Uremic encephalopathy is an absolute indication for emergent renal replacement therapy'''<ref name="StatPearls"/>
*'''Hemodialysis''' is the most common modality in the ED setting
*Initiate with '''gentle parameters''' to reduce risk of '''dialysis disequilibrium syndrome:'''<ref name="Rosner2022"/>
**Lower blood flow rates (200-300 mL/min)
**Lower dialysate flow rates (400-600 mL/min)
**Shorter initial session (2-3 hours rather than standard 4 hours)
**Avoid large rapid shifts in plasma osmolality
*'''CRRT''' (continuous renal replacement therapy) may be preferred in hemodynamically unstable patients (ICU setting)
*'''Peritoneal dialysis''' is an alternative if hemodialysis is not available or vascular access cannot be obtained
*Clinical improvement is typically seen within '''24-48 hours''' of initiating adequate dialysis, though full neurologic recovery may take days to weeks
*EEG abnormalities may persist for months even after clinical improvement

===Seizure Management===
*'''[[Levetiracetam]]''' (Keppra) is the preferred antiepileptic in renal failure (dose-adjust; well tolerated)
*'''[[Benzodiazepines]]''' ([[lorazepam]], [[midazolam]]) for acute seizure termination
*'''Avoid [[phenytoin]]''' — highly protein-bound; levels are unreliable in CKD/ESRD (altered protein binding, renal clearance of metabolites); if must use, monitor free phenytoin levels
*Seizures may resolve with '''dialysis alone''' once uremia is corrected
*'''Do not use [[succinylcholine]]''' for intubation in seizing CKD patients — risk of exacerbating hyperkalemia

===Uremic Bleeding Considerations===
*If procedures are needed (dialysis catheter, LP, intubation), be aware of '''uremic platelet dysfunction'''
*'''[[DDAVP]]''' 0.3 mcg/kg IV — first-line to transiently improve platelet function
*See [[Chronic kidney disease]] for full uremic bleeding management

===Consultations===
*'''Nephrology:''' Emergent — for dialysis initiation and ongoing management
*'''Critical care/ICU:''' Most patients with uremic encephalopathy require ICU admission
*'''Neurology:''' If diagnosis is uncertain, seizures are refractory, or mental status does not improve after dialysis
*'''Interventional radiology or surgery:''' If emergent dialysis catheter placement is needed

==Disposition==
*'''ICU admission''' for nearly all patients with uremic encephalopathy:
**Requires emergent dialysis with close hemodynamic monitoring
**Risk of seizures, airway compromise, arrhythmias from concurrent hyperkalemia
**Risk of dialysis disequilibrium syndrome during initial treatments
*'''Do not discharge''' patients with suspected uremic encephalopathy
*'''Reassess diagnosis''' if mental status does not improve after 3-5 dialysis sessions — consider structural lesion, ongoing infection, or alternative metabolic derangement<ref name="Rosner2022"/>
*For patients with known ESRD presenting with mild cognitive changes that improve after routine dialysis, discharge may be appropriate with '''close nephrology follow-up''' and evaluation for adequacy of dialysis (Kt/V measurement, access evaluation)

==See Also==
*[[Chronic kidney disease]]
*[[Acute kidney injury]]
*[[Dialysis complications]]
*[[Hyperkalemia]]
*[[Metabolic acidosis]]
*[[Altered mental status]]
*[[Hepatic encephalopathy]]
*[[Hypertensive emergency]]
*[[Seizure]]

==External Links==
*[https://www.ncbi.nlm.nih.gov/books/NBK564327/ StatPearls - Uremic Encephalopathy]
*[https://emedicine.medscape.com/article/239191-overview Medscape - Uremic Encephalopathy]

==References==
{{reflist|2}}

[[Category:Renal]]
[[Category:Neurology]]

← Older revision		Revision as of 09:26, 22 March 2026
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	==Background==		==Background==
	*Uremic encephalopathy is cerebral dysfunction caused by accumulation of uremic toxins due to [[acute kidney injury]] or [[chronic kidney disease]]<ref name="StatPearls">Olano CG, Akram SM, Hashmi MF, et al. Uremic Encephalopathy. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.</ref>		*Uremic encephalopathy is cerebral dysfunction caused by accumulation of uremic toxins due to [[acute kidney injury]] or [[chronic kidney disease]]<ref name="StatPearls">Olano CG, Akram SM, Hashmi MF, et al. Uremic Encephalopathy. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024.</ref>
	*Typically develops when eGFR falls below ~~'''~~15 mL/min~~'''~~ (CKD Stage G5), though can occur at higher eGFR in acute kidney injury where the rate of decline is rapid<ref name="Rosner2022">Rosner MH, Husain-Syed F, Reis T, Ronco C, Vanholder R. Uremic encephalopathy. Kidney Int. 2022;101(2):227-241.</ref>		*Typically develops when eGFR falls below 15 mL/min (CKD Stage G5), though can occur at higher eGFR in acute kidney injury where the rate of decline is rapid<ref name="Rosner2022">Rosner MH, Husain-Syed F, Reis T, Ronco C, Vanholder R. Uremic encephalopathy. Kidney Int. 2022;101(2):227-241.</ref>
	*Severity correlates with the ~~'''~~rate of decline~~'''~~ in kidney function — AKI causes more severe encephalopathy than progressive CKD at the same GFR, because chronic adaptation has not occurred		*Severity correlates with the rate of decline in kidney function — AKI causes more severe encephalopathy than progressive CKD at the same GFR, because chronic adaptation has not occurred
	*Reversible with dialysis — this is both the treatment and the diagnostic confirmation; uremic encephalopathy is an '''absolute indication''' for emergent renal replacement therapy<ref name="StatPearls"/>		*Reversible with dialysis — this is both the treatment and the diagnostic confirmation; uremic encephalopathy is an '''absolute indication''' for emergent renal replacement therapy<ref name="StatPearls"/>
	*Diagnosis of exclusion — there is no confirmatory test; the diagnosis is often made retrospectively when mental status improves after dialysis<ref name="Rosner2022"/>		*Diagnosis of exclusion — there is no confirmatory test; the diagnosis is often made retrospectively when mental status improves after dialysis<ref name="Rosner2022"/>
	*Pathophysiology is multifactorial: accumulation of uremic solutes (urea, guanidino compounds, indoxyl sulfate, p-cresol, PTH), disruption of the blood-brain barrier, neurotransmitter imbalances (↑ GABA, altered dopamine/serotonin), electrolyte derangements, and systemic inflammation		*Pathophysiology is multifactorial: accumulation of uremic solutes (urea, guanidino compounds, indoxyl sulfate, p-cresol, PTH), disruption of the blood-brain barrier, neurotransmitter imbalances (↑ GABA, altered dopamine/serotonin), electrolyte derangements, and systemic inflammation
	*Can also occur in dialysis patients receiving ~~'''~~inadequate dialysis~~'''~~ (noncompliance, AV fistula dysfunction, underdialysis)		*Can also occur in dialysis patients receiving inadequate dialysis (noncompliance, AV fistula dysfunction, underdialysis)

	==Clinical Features==		==Clinical Features==
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	===Moderate===		===Moderate===
	*[[Altered mental status]]: confusion, disorientation, delirium		*[[Altered mental status]]: confusion, disorientation, delirium
	*[[Asterixis]] (~~'''~~flapping tremor~~'''~~ — highly suggestive but not pathognomonic; also seen in hepatic encephalopathy, hypercapnia, drug toxicity)		*[[Asterixis]] (flapping tremor — highly suggestive but not pathognomonic; also seen in hepatic encephalopathy, hypercapnia, drug toxicity)
	*Myoclonus (multifocal muscle jerking)		*Myoclonus (multifocal muscle jerking)
	*Tremor		*Tremor
Line 36:		Line 36:
	===ED Pearls===		===ED Pearls===
	*Asterixis + elevated BUN/creatinine + no prior known liver disease = think uremic encephalopathy		*Asterixis + elevated BUN/creatinine + no prior known liver disease = think uremic encephalopathy
	*Symptoms in CKD patients are often ~~'''~~subtle and progressive~~'''~~ — family may report gradual personality changes, forgetfulness, or increased confusion over days to weeks		*Symptoms in CKD patients are often subtle and progressive — family may report gradual personality changes, forgetfulness, or increased confusion over days to weeks
	*In AKI, encephalopathy can develop ~~'''~~rapidly~~'''~~ (hours to days) and may be the presenting feature		*In AKI, encephalopathy can develop rapidly (hours to days) and may be the presenting feature
	*A dialysis patient presenting with AMS should be evaluated for ~~'''~~both~~'''~~ uremic encephalopathy (inadequate dialysis) ~~'''~~and~~'''~~ dialysis disequilibrium syndrome (too-rapid dialysis) — timing relative to last dialysis session is key		*A dialysis patient presenting with AMS should be evaluated for both uremic encephalopathy (inadequate dialysis) and dialysis disequilibrium syndrome (too-rapid dialysis) — timing relative to last dialysis session is key
	*Uremic encephalopathy may ~~'''~~paradoxically improve arthritis~~'''~~ symptoms in patients with concurrent rheumatic disease — decreased activity is sometimes misinterpreted as clinical improvement		*Uremic encephalopathy may paradoxically improve arthritis symptoms in patients with concurrent rheumatic disease — decreased activity is sometimes misinterpreted as clinical improvement
	*Seizures in CKD/ESRD patients should prompt evaluation for uremia, but also for [[hypertensive encephalopathy]], [[hypoglycemia]], [[hyponatremia]], [[hypocalcemia]], [[hypermagnesemia]], and medication toxicity		*Seizures in CKD/ESRD patients should prompt evaluation for uremia, but also for [[hypertensive encephalopathy]], [[hypoglycemia]], [[hyponatremia]], [[hypocalcemia]], [[hypermagnesemia]], and medication toxicity

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	===Metabolic/Toxic===		===Metabolic/Toxic===
	*[[Hyperkalemia]] (can cause weakness, paralysis, and obtundation in addition to cardiac effects)		*[[Hyperkalemia]] (can cause weakness, paralysis, and obtundation in addition to cardiac effects)
	*[[Hyponatremia]] or ~~'''~~[[hypernatremia]]~~'''~~		*[[Hyponatremia]] or [[hypernatremia]]
	*[[Hypoglycemia]] or ~~'''~~[[hyperglycemia]]~~'''~~ / [[hyperosmolar coma]]		*[[Hypoglycemia]] or [[hyperglycemia]] / [[hyperosmolar coma]]
	*[[Hypercalcemia]]		*[[Hypercalcemia]]
	*[[Hypermagnesemia]] (especially in CKD patients taking Mg-containing antacids)		*[[Hypermagnesemia]] (especially in CKD patients taking Mg-containing antacids)
Line 67:		Line 67:

	===Dialysis-Related===		===Dialysis-Related===
	*[[Dialysis complications\|Dialysis disequilibrium syndrome]]: Headache, nausea, AMS, seizures occurring ~~'''~~during or shortly after~~'''~~ dialysis (especially first sessions or aggressive ultrafiltration); caused by rapid osmolar shifts and cerebral edema		*[[Dialysis complications\|Dialysis disequilibrium syndrome]]: Headache, nausea, AMS, seizures occurring during or shortly after dialysis (especially first sessions or aggressive ultrafiltration); caused by rapid osmolar shifts and cerebral edema
	*Osmotic demyelination syndrome (from rapid correction of [[hyponatremia]])		*Osmotic demyelination syndrome (from rapid correction of [[hyponatremia]])
	*Aluminum toxicity (historical; rare with modern dialysate)		*Aluminum toxicity (historical; rare with modern dialysate)
Line 78:		Line 78:

	*BMP/CMP: BUN, creatinine (compare to baseline), electrolytes (K⁺, Na⁺, Ca²⁺, Mg²⁺, phosphorus), glucose, bicarbonate (anion gap)		*BMP/CMP: BUN, creatinine (compare to baseline), electrolytes (K⁺, Na⁺, Ca²⁺, Mg²⁺, phosphorus), glucose, bicarbonate (anion gap)
	**BUN is typically ~~'''~~markedly elevated~~'''~~ (often >100-150 mg/dL); however, there is no absolute BUN threshold that defines uremic encephalopathy		**BUN is typically markedly elevated (often >100-150 mg/dL); however, there is no absolute BUN threshold that defines uremic encephalopathy
	*CBC: Leukocytosis (suggests infection); anemia (baseline in CKD, acute worsening suggests bleed)		*CBC: Leukocytosis (suggests infection); anemia (baseline in CKD, acute worsening suggests bleed)
	*VBG or ABG: Assess acid-base status and calculate anion gap; severe uremic acidosis may coexist		*VBG or ABG: Assess acid-base status and calculate anion gap; severe uremic acidosis may coexist
Line 102:		Line 102:
	**Exclusion of other causes of altered mental status		**Exclusion of other causes of altered mental status
	**Improvement after initiation of dialysis (the most definitive diagnostic confirmation — but do not wait for this to begin treatment)		**Improvement after initiation of dialysis (the most definitive diagnostic confirmation — but do not wait for this to begin treatment)
	*ED diagnostic pearl: The combination of ~~'''~~asterixis~~'''~~ + ~~'''~~BUN >100~~'''~~ + ~~'''~~no hepatic disease~~'''~~ + ~~'''~~no structural lesion on CT~~'''~~ in a patient with known CKD or AKI is highly suggestive		*ED diagnostic pearl: The combination of asterixis + BUN >100 + no hepatic disease + no structural lesion on CT in a patient with known CKD or AKI is highly suggestive
	*If neurologic status does not improve after 3-5 dialysis sessions, '''re-evaluate for alternative or additional diagnoses'''<ref name="Rosner2022"/>		*If neurologic status does not improve after 3-5 dialysis sessions, '''re-evaluate for alternative or additional diagnoses'''<ref name="Rosner2022"/>

Line 108:		Line 108:
	===Resuscitation and Stabilization===		===Resuscitation and Stabilization===
	*ABCs: Airway protection is critical — obtunded patients may need [[intubation]] (use medications that do not require renal clearance for RSI; consider [[rocuronium]] over [[succinylcholine]] if [[hyperkalemia]] is present or suspected)		*ABCs: Airway protection is critical — obtunded patients may need [[intubation]] (use medications that do not require renal clearance for RSI; consider [[rocuronium]] over [[succinylcholine]] if [[hyperkalemia]] is present or suspected)
	*IV access: If patient does not already have dialysis access, ~~'''~~emergent dialysis catheter placement~~'''~~ will be needed		*IV access: If patient does not already have dialysis access, emergent dialysis catheter placement will be needed
	*Continuous monitoring: telemetry, pulse oximetry, frequent neuro checks		*Continuous monitoring: telemetry, pulse oximetry, frequent neuro checks
	*Treat concurrent [[hyperkalemia]]: [[Calcium gluconate]], [[insulin]]/D50, nebulized [[albuterol]] (see [[Hyperkalemia]])		*Treat concurrent [[hyperkalemia]]: [[Calcium gluconate]], [[insulin]]/D50, nebulized [[albuterol]] (see [[Hyperkalemia]])
Line 117:		Line 117:
	*'''Uremic encephalopathy is an absolute indication for emergent renal replacement therapy'''<ref name="StatPearls"/>		*'''Uremic encephalopathy is an absolute indication for emergent renal replacement therapy'''<ref name="StatPearls"/>
	*Hemodialysis is the most common modality in the ED setting		*Hemodialysis is the most common modality in the ED setting
	*Initiate with ~~'''~~gentle parameters~~'''~~ to reduce risk of ~~'''~~dialysis disequilibrium syndrome:~~'''~~<ref name="Rosner2022"/>		*Initiate with gentle parameters to reduce risk of dialysis disequilibrium syndrome:<ref name="Rosner2022"/>
	**Lower blood flow rates (200-300 mL/min)		**Lower blood flow rates (200-300 mL/min)
	**Lower dialysate flow rates (400-600 mL/min)		**Lower dialysate flow rates (400-600 mL/min)
Line 124:		Line 124:
	*CRRT (continuous renal replacement therapy) may be preferred in hemodynamically unstable patients (ICU setting)		*CRRT (continuous renal replacement therapy) may be preferred in hemodynamically unstable patients (ICU setting)
	*Peritoneal dialysis is an alternative if hemodialysis is not available or vascular access cannot be obtained		*Peritoneal dialysis is an alternative if hemodialysis is not available or vascular access cannot be obtained
	*Clinical improvement is typically seen within ~~'''~~24-48 hours~~'''~~ of initiating adequate dialysis, though full neurologic recovery may take days to weeks		*Clinical improvement is typically seen within 24-48 hours of initiating adequate dialysis, though full neurologic recovery may take days to weeks
	*EEG abnormalities may persist for months even after clinical improvement		*EEG abnormalities may persist for months even after clinical improvement

Line 131:		Line 131:
	*[[Benzodiazepines]] ([[lorazepam]], [[midazolam]]) for acute seizure termination		*[[Benzodiazepines]] ([[lorazepam]], [[midazolam]]) for acute seizure termination
	*Avoid [[phenytoin]] — highly protein-bound; levels are unreliable in CKD/ESRD (altered protein binding, renal clearance of metabolites); if must use, monitor free phenytoin levels		*Avoid [[phenytoin]] — highly protein-bound; levels are unreliable in CKD/ESRD (altered protein binding, renal clearance of metabolites); if must use, monitor free phenytoin levels
	*Seizures may resolve with ~~'''~~dialysis alone~~'''~~ once uremia is corrected		*Seizures may resolve with dialysis alone once uremia is corrected
	*'''Do not use [[succinylcholine]]''' for intubation in seizing CKD patients — risk of exacerbating hyperkalemia		*'''Do not use [[succinylcholine]]''' for intubation in seizing CKD patients — risk of exacerbating hyperkalemia

Line 152:		Line 152:
	*'''Do not discharge''' patients with suspected uremic encephalopathy		*'''Do not discharge''' patients with suspected uremic encephalopathy
	*Reassess diagnosis if mental status does not improve after 3-5 dialysis sessions — consider structural lesion, ongoing infection, or alternative metabolic derangement<ref name="Rosner2022"/>		*Reassess diagnosis if mental status does not improve after 3-5 dialysis sessions — consider structural lesion, ongoing infection, or alternative metabolic derangement<ref name="Rosner2022"/>
	*For patients with known ESRD presenting with mild cognitive changes that improve after routine dialysis, discharge may be appropriate with ~~'''~~close nephrology follow-up~~'''~~ and evaluation for adequacy of dialysis (Kt/V measurement, access evaluation)		*For patients with known ESRD presenting with mild cognitive changes that improve after routine dialysis, discharge may be appropriate with close nephrology follow-up and evaluation for adequacy of dialysis (Kt/V measurement, access evaluation)

	==See Also==		==See Also==