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NEUROLOGICAL COMPLICATIONS OF
HEMODIALYSIS
Rizzo, M. A., Frediani, F., Granata, A., Ravasi, B., Cusi, D., & Gallieni, M. (2012). Neurological complications of hemodialysis: state of the art. JN. JOURNAL OF NEPHROLOGY, 25(2), 170-182.
INTRODUCTION
 Hemodialysis can cause central or peripheral nervous system complication
 Collaboration between nephrologists, neurologists, and other fields are required
DIALYSIS DEMENTIA
 Subacute, progressive, fatal
 Chronic partially dialyzed patients > 3 years
 High alumunium level used in dialysis water
 Clinical manifestation: speec, cognition, movement
 Typical manifestations are dysarthria, mutism and facial grimacing.
 May progress to death in 6 months
 At first, the symptoms is intermittent, worsen during and after dialysis
 As the disorder progresses, symptoms become more constant
 Myoclonic jerks
DIALYSIS DEMENTIA
 EEG: bursts of high-voltage slowing in the frontal leads
 Patients with dialysis dementia have spongiform changes in the outer 3 cortical layers, with elevated
aluminum levels in the cerebral cortex. Other changes include neuronal loss, accumulation of lipofuscin
pigment and neurofibrillary degeneration in the motor cortex and in the red, dentate and olivary nuclei.
 Th/ diazepam and deferoxamine
DYSEQUILIBRIUM SYNDROME
 CNS disturbance due to cerebral edema
 Brain compartment more hyperosmolar, delayed urea shift to extracellular
 mild headache, nausea and muscle cramps to convulsions or delirium;
 Appear 3 to 4 hours after starting dialysis but may manifest themselves 8-24 hours later.
 The syndrome is usually self-limited, subsiding in hours, but delirium may persist for several days.
 Risk factors are first hemodialysis treatments, severe uremia in late referral patients, age, preexisting
neurological disorders and metabolic acidosis.
 Can be fatal
 Treatment of disequilibrium syndrome consists of preventive measures during hemodialysis which
include slow, gentle start of hemodialysis, increasing dialysate sodium levels and administration of
osmotically active substances.
WERNICKE’S ENCEPHALOPATHY
 Opthalmoplegia, ataxia, loss of consciousness
 Thiamin deficiency
 Th/ thiamine supplementation
CENTRAL PONTINE MYELINOLYSIS
 Etiology: too rapid sodium correction after hemodialysis
 Initial symptoms are progressive gait disturbance, postural instability, hallucinations and mild cognitive
dysfunction
 Progressing to paraparesis or quadriparesis, dysphagia, dysarthria, diplopia and loss of consciousness
CEREBROVASCULAR DISEASES
Ischaemic
 Vascular and tissue calcification due CKD-Mineral Bone Disorder, increase artery stiffness
 Usually in distal site
 CKD patients  hyperhomocysteinemia
Hemorrhagic
 Uremia causes platelet dysfunction and altered platelet–vessel wall interaction resulting in a bleeding
tendency
 Intradialytic anticoagulation
POSTERIOR LEUKOENCEPHALOPATHY SYNDROME
 Cerebral white matter
 Peculiar radiological findings in the posterior brain, which may spread to basal ganglia, brain stem, and
cerebellum
 Symptoms: headache, nausea, vomiting, visual disturbances, focal neurological deficits and seizures
 Potential etiological factors: hypertension, drugs, uremia itself and fluid/electrolyte disturbances
 Th/ treating hypertension
MONONEUROPATHY
CTS
AION
Ischaemic
monomelic
neuropathy
CARPAL TUNNEL SYNDROME (CTS)
 Very common
 Dialysis related amyloidosis,
 uremic calcinosis,
 AV fistula
ISCHAEMIC MONOMELIC NEUROPATHY
 Resulting from placement of forearm AV fistulas
 Risk factors: underlying stenotic or occlusive arterial disease, neuropathic diseases, calcifying accesses
from the brachial artery in the absence of collateral vessels, distal axonopathy and diabetic
polyneuropathy
 Medical emergency
 Th/ closure of AV fistula
 Alternative th/: distal revascularization interval legation (DRIL) and proximalization of arterial inflow (PAI)
ANTERIOR ISCHAEMIC OPTIC NEUROPATHY
 May be due to interference with the posterior ciliary artery blood supply to the optic nerves,
 Predisposing factors such as hypertension, hypotension, anemia and atherosclerosis.
 Start of dialysis, corticosteroid therapy, correction of anemia and adequate blood pressure control may
restore vision loss and make the syndrome reversible
HEMODIALYSIS HEADACHE
 Incidence: 5%
 Appears during the third hour of dialysis and lasts less then 4 hours in the majority of patients
 Moderate intensity, bilateral, throbbing or non-pulsatile
 The pathogenesis seems to be related to marked differences of pretreatment and posttreatment urea
levels, intradialytic hypotension and changes in magnesium levels
 Diagnostic criteria: headache developing during at least half of hemodialysis sessions, headache
resolving within 72 hours after each hemodialysis session and/or ceasing altogether after successful
transplantation
SUMMARY
 In hemodialysis patients, multiple neurological complications are commonly observed
 Cause morbidity and mortality
 Central vs peripheral nervous system
 Often underdiagnosed
 Can be prevented and managed
Neurological Complications of Hemodialysis

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Neurological Complications of Hemodialysis

  • 1. NEUROLOGICAL COMPLICATIONS OF HEMODIALYSIS Rizzo, M. A., Frediani, F., Granata, A., Ravasi, B., Cusi, D., & Gallieni, M. (2012). Neurological complications of hemodialysis: state of the art. JN. JOURNAL OF NEPHROLOGY, 25(2), 170-182.
  • 2. INTRODUCTION  Hemodialysis can cause central or peripheral nervous system complication  Collaboration between nephrologists, neurologists, and other fields are required
  • 3.
  • 4. DIALYSIS DEMENTIA  Subacute, progressive, fatal  Chronic partially dialyzed patients > 3 years  High alumunium level used in dialysis water  Clinical manifestation: speec, cognition, movement  Typical manifestations are dysarthria, mutism and facial grimacing.  May progress to death in 6 months  At first, the symptoms is intermittent, worsen during and after dialysis  As the disorder progresses, symptoms become more constant  Myoclonic jerks
  • 5. DIALYSIS DEMENTIA  EEG: bursts of high-voltage slowing in the frontal leads  Patients with dialysis dementia have spongiform changes in the outer 3 cortical layers, with elevated aluminum levels in the cerebral cortex. Other changes include neuronal loss, accumulation of lipofuscin pigment and neurofibrillary degeneration in the motor cortex and in the red, dentate and olivary nuclei.  Th/ diazepam and deferoxamine
  • 6. DYSEQUILIBRIUM SYNDROME  CNS disturbance due to cerebral edema  Brain compartment more hyperosmolar, delayed urea shift to extracellular  mild headache, nausea and muscle cramps to convulsions or delirium;  Appear 3 to 4 hours after starting dialysis but may manifest themselves 8-24 hours later.  The syndrome is usually self-limited, subsiding in hours, but delirium may persist for several days.  Risk factors are first hemodialysis treatments, severe uremia in late referral patients, age, preexisting neurological disorders and metabolic acidosis.  Can be fatal  Treatment of disequilibrium syndrome consists of preventive measures during hemodialysis which include slow, gentle start of hemodialysis, increasing dialysate sodium levels and administration of osmotically active substances.
  • 7. WERNICKE’S ENCEPHALOPATHY  Opthalmoplegia, ataxia, loss of consciousness  Thiamin deficiency  Th/ thiamine supplementation
  • 8. CENTRAL PONTINE MYELINOLYSIS  Etiology: too rapid sodium correction after hemodialysis  Initial symptoms are progressive gait disturbance, postural instability, hallucinations and mild cognitive dysfunction  Progressing to paraparesis or quadriparesis, dysphagia, dysarthria, diplopia and loss of consciousness
  • 9. CEREBROVASCULAR DISEASES Ischaemic  Vascular and tissue calcification due CKD-Mineral Bone Disorder, increase artery stiffness  Usually in distal site  CKD patients  hyperhomocysteinemia Hemorrhagic  Uremia causes platelet dysfunction and altered platelet–vessel wall interaction resulting in a bleeding tendency  Intradialytic anticoagulation
  • 10. POSTERIOR LEUKOENCEPHALOPATHY SYNDROME  Cerebral white matter  Peculiar radiological findings in the posterior brain, which may spread to basal ganglia, brain stem, and cerebellum  Symptoms: headache, nausea, vomiting, visual disturbances, focal neurological deficits and seizures  Potential etiological factors: hypertension, drugs, uremia itself and fluid/electrolyte disturbances  Th/ treating hypertension
  • 11.
  • 13. CARPAL TUNNEL SYNDROME (CTS)  Very common  Dialysis related amyloidosis,  uremic calcinosis,  AV fistula
  • 14. ISCHAEMIC MONOMELIC NEUROPATHY  Resulting from placement of forearm AV fistulas  Risk factors: underlying stenotic or occlusive arterial disease, neuropathic diseases, calcifying accesses from the brachial artery in the absence of collateral vessels, distal axonopathy and diabetic polyneuropathy  Medical emergency  Th/ closure of AV fistula  Alternative th/: distal revascularization interval legation (DRIL) and proximalization of arterial inflow (PAI)
  • 15. ANTERIOR ISCHAEMIC OPTIC NEUROPATHY  May be due to interference with the posterior ciliary artery blood supply to the optic nerves,  Predisposing factors such as hypertension, hypotension, anemia and atherosclerosis.  Start of dialysis, corticosteroid therapy, correction of anemia and adequate blood pressure control may restore vision loss and make the syndrome reversible
  • 16.
  • 17. HEMODIALYSIS HEADACHE  Incidence: 5%  Appears during the third hour of dialysis and lasts less then 4 hours in the majority of patients  Moderate intensity, bilateral, throbbing or non-pulsatile  The pathogenesis seems to be related to marked differences of pretreatment and posttreatment urea levels, intradialytic hypotension and changes in magnesium levels  Diagnostic criteria: headache developing during at least half of hemodialysis sessions, headache resolving within 72 hours after each hemodialysis session and/or ceasing altogether after successful transplantation
  • 18.
  • 19.
  • 20. SUMMARY  In hemodialysis patients, multiple neurological complications are commonly observed  Cause morbidity and mortality  Central vs peripheral nervous system  Often underdiagnosed  Can be prevented and managed