⚡Neurological deterioration in patients on Hemodialysis
⚡First described by Kennedy AC et al (Lancet, 1962)
⚡Waste basket❓
⚡Diagnosis of exclusion
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⚡Pathophysiology:
I. "Reverse urea" effect
🔺️Chronic uremia👉⬇️Brain urea transporters (50%) & ⬆️AQP4 (165%)
🔺️⬆️Brain osmolality👉 cerebral edema
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Pic- CKJ; Pediatric Nephrology
⚡Pathophysiology:
II. "Idiogenic osmoles" hypothesis
🔺️Generation of other osmotically active molecules
🔺️Inositol/ Glutamine/ Glutamate
🔺️Unidentified osmoles❓
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⚡Pathophysiology:
III.Paradoxical CSF acidosis
🔺️Rapid dialysis👉⬇️brain intra cellular/CSF pH
🔺️Altered solute/H2O transport regulation across BBB
🔺️Displacement of intracellular protein bound K/Na
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⚡Risk factor
🔺️Young age
🔺️Severe azotemia
🔺️Dialysis initiation
🔺️Low dialysate Na/HypoNa
🔺️Preexisting neurological diz
🔺️Trauma
🔺️Malignant HTN
🔺️Cardiac abnormality
🔺️Anemia
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⚡Clinical features (in order of progression)
🔺️Mild form- Restlessness/Headache
🔺️Nausea/ vomiting
🔺️HTN/ dizziness/ ms cramps
🔺️Disorientaion/ Tremors
🔺️Obtundation/ seizure/ coma
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⚡Look for other causes first‼
⚡Rare now-a-days
⚡Important D/D in developing countries where most dialysis units run without nephrologist supervision ‼
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Ref- Pediatr Nephrol(2012)27:2205
⚡Imaging:
👉Cerebral edema
👉Brain herniation: Look for empty bulb sign‼
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Pic- WJNU
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⚡Prevention:
🌀Early recognition of uremic states
🌀Sequential HD (Short initial t/t time with ⬇️Qb & smaller surface area dialyzer)
🌀Target initial blood urea reduction <30%
🌀Na modeling
🌀CRRT
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⚡Standard maneuvers (mannitol or hypertonic saline) to raise blood osmolality and to hyperventilate patient may be futile‼
⚡Better prevent it happening
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