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    Encephalopathies: Zerlyn T. Leonardo, M.D., FPCP, FPNA

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    Janellee Daruca
    Encephalopathies refer to diffuse disturbances of brain function caused by failure of other organ systems. Some types discussed include hypoxic-ischemic encephalopathy from lack of oxygen to the brain, metabolic encephalopathy from organ failure or electrolyte imbalances, septic encephalopathy from sepsis, and Wernicke's encephalopathy from thiamine deficiency. Clinical manifestations range from mild confusion to coma and depend on the underlying cause and extent of brain injury. Treatment involves addressing the root cause while managing symptoms. Outcomes vary but complete recovery is possible if treated early.

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    Encephalopathies: Zerlyn T. Leonardo, M.D., FPCP, FPNA

    Uploaded by

    Janellee Daruca
    90 views50 pages
    Encephalopathies refer to diffuse disturbances of brain function caused by failure of other organ systems. Some types discussed include hypoxic-ischemic encephalopathy from lack of oxygen to the brain, metabolic encephalopathy from organ failure or electrolyte imbalances, septic encephalopathy from sepsis, and Wernicke's encephalopathy from thiamine deficiency. Clinical manifestations range from mild confusion to coma and depend on the underlying cause and extent of brain injury. Treatment involves addressing the root cause while managing symptoms. Outcomes vary but complete recovery is possible if treated early.

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    Enceph

    Original Title

    Encephalo Path i Es

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    Encephalopathies refer to diffuse disturbances of brain function caused by failure of other organ systems. Some types discussed include hypoxic-ischemic encephalopathy from lack of oxygen to the brain, metabolic encephalopathy from organ failure or electrolyte imbalances, septic encephalopathy from sepsis, and Wernicke's encephalopathy from thiamine deficiency. Clinical manifestations range from mild confusion to coma and depend on the underlying cause and extent of brain injury. Treatment involves addressing the root cause while managing symptoms. Outcomes vary but complete recovery is possible if treated early.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    90 views50 pages

    Encephalopathies: Zerlyn T. Leonardo, M.D., FPCP, FPNA

    Uploaded by

    Janellee Daruca
    Encephalopathies refer to diffuse disturbances of brain function caused by failure of other organ systems. Some types discussed include hypoxic-ischemic encephalopathy from lack of oxygen to the brain, metabolic encephalopathy from organ failure or electrolyte imbalances, septic encephalopathy from sepsis, and Wernicke's encephalopathy from thiamine deficiency. Clinical manifestations range from mild confusion to coma and depend on the underlying cause and extent of brain injury. Treatment involves addressing the root cause while managing symptoms. Outcomes vary but complete recovery is possible if treated early.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 50

    Encephalopathies

    Zerlyn T. Leonardo, M.D., FPCP, FPNA


    Encephalopathy
    • Acquired diffuse disturbance of cerebral
    function due to failure of some other
    organ system
     Heart /Circulation
     Lung/Respiration
     Kidneys
     Liver
     Endocrine glands
    Encephalopathies
    1. Hypoxic-Ischemic Encephalopathy
    2. Delayed Post-anoxic Encephalopathy
    3. Metabolic Encephalopathy
    4. Septic Encephalopathy
    5. Wernicke’s Encephalopathy
    Hypoxic-Ischemic Encephalopathy
    (HIE)
    Hypoxic-Ischemic Encephalopathy

    • Due to lack of Oxygen delivery to the


    brain secondary to:
     Respiratory Failure (Hypoxia)
    • Asphyxiation, paralysis of respiration, carbon
    monoxide or cyanide poisoning
     Hypotension (Ischemia)
    • Myocardial infarction, cardiac arrest, shock
    HIE: Clinical Manifestation

    Reversible --------------------------------Irreversible

    Impaired judgment, Persistent coma or


    Inattentiveness, vegetative state,
    Motor incoordination, Dementia,
    Euphoria Visual agnosia ,
    Parkinsonism,
    Choreoathetosis,
    Cerebellar ataxia,
    Myoclonus,
    Seizures,
    Amnestic state
    HIE: Clinical Manifestation

    Reversible --------------------------------Irreversible

    Duration of hypoxia or ischemia?


    Rapidity of change of PaO2?
    Rule of thumb:
    •Hypoxia/Ischemia > 3-5 min
     Expect some degree of Permanent Brain Damage
    •Gradual decrease in PaO2  better tolerated
    HIE: Pathology
    HIE secondary to hypoxia
    • Brain cells most vulnerable to hypoxia
    1. Hippocampal pyramidal cells of CA1
    2. Layers 3 and 5 of the Neocortex
    3. Purkinje cells
    4. Striatal neurons (basal ganglia)
    HIE: Pathology
    • Hippocampal
    CA1 Atrophy

    Amnestic state,
    Dementia
    HIE: Pathology
    HIE secondary to hypoxia
    • Brain cells most vulnerable to hypoxia
    1. Hippocampal pyramidal cells of CA1
    2. Layers 3 and 5 of the Neocortex
    3. Purkinje cells
    4. Striatal neurons (basal ganglia)
    HIE: Pathology
    • Laminar Necrosis

    Inattention, Dementia, Poor judgment


    HIE: Pathology

    • Laminar Necrosis
    HIE: Pathology
    HIE secondary to hypoxia
    • Brain cells most vulnerable to hypoxia
    1. Hippocampal pyramidal cells of CA1
    2. Layers 3 and 5 of the Neocortex
    3. Purkinje cells
    4. Striatal neurons (basal ganglia)
    HIE: Pathology
    • Purkinje cell death

    Cerebellar Ataxia
    Motor Incoordination
    HIE: Pathology
    HIE secondary to hypoxia
    • Brain cells most vulnerable to hypoxia
    1. Hippocampal pyramidal cells of CA1
    2. Layers 3 and 5 of the Neocortex
    3. Purkinje cells
    4. Striatal neurons (basal ganglia)
    HIE: Pathology
    • Striatal Neuronal
    death

    Parkinsonism
    Choreoathetosis
    HIE: Pathology
    • HIE secondary to hypotension
     Result in Watershed Infarction
    HIE: Pathology

    • HIE secondary to
    hypotension
     Result in Watershed
    Infarction

    Visual Agnosia,
    “Man-in-a-barrel” weakness
    HIE: Diagnosis
    • Hx of hypoxic-ischemic event
     Cardiac Arrest
     Blood pressure < 70 mmHg systolic or
    PaO2 < 40 mmHg, and the duration
    • Elevated CarboxyHb level + Cherry Red
    skin color
     Carbon monoxide intoxication  hypoxia
    HIE: Treatment
    • Restore normal cardiorespiratory
    function
    • Hypothermia to target Temp of 32-34°C
    for 12-24 hours
    • Hyperbaric Oxygen for CO intoxication
    • Anticonvulsants for myoclonic seizures
     Clonazepam 1.5-10 mg daily
     Valproate 300-1200 mg daily
    HIE: Prognosis

    • For comatose survivors of


    cardiopulmonary resuscitation (CPR)
     Rule out confounders first:
    • Usage of Sedative
    • Usage of Neuromuscular blocking agents
    • Hypothermia therapy
    • Organ failure or shock
    Delayed Post-anoxic Encephalopathy
    Delayed Post-anoxic Encephalopathy

    • Uncommon phenomenon
     Patients with CO and Cyanide intoxication
    • No evident clinical impairment initially
    • Develop parkinsonian features (akinesia and
    rigidity but without tremors)
     Patients initially recovering from a hypoxic-
    ischemic event develop a relapse
    • Apathy, confusion, agitation
    Delayed Post-anoxic Encephalopathy
    • Progressive neurologic deficits
     shuffling gait, diffuse rigidity and spasticity
     persistent parkinsonism or myoclonus
    • Occasionally  coma and death after 1–2
    weeks
    • Pathology:
     Widespread cerebral demyelination may be
    present
     Damage to the basal ganglia
    Delayed Post-anoxic Encephalopathy
    Metabolic Encephalopathy
    Metabolic Encephalopathy
    • Disorders of cerebral function due to:
     Vital organ failure (liver, kidney)
     Electrolyte imbalances (sodium)
     Hypoglycemia
     Hyperglycemia
     Endocrine disorders (Thyroid storm,
    Myxedema, SIADH, Hashimoto, DI)
    Metabolic Encephalopathy:
    Clinical Manifestation
    • Varies:
     Mild confusional state  deep coma with
    decerebrate posturing
    • Delirium or acute confusional state
     usually the earliest recognized brain malfunction
     Patients may be:
    • agitated, usually with increased sympathetic nervous
    system activity, or
    • quiet and withdrawn
    Metabolic Encephalopathy:
    Diagnosis
    • Clues:
     Background of vital organ dysfunction or
    history of some event, e.g. toxic exposure
    that would upset the metabolic milieu of the
    brain
     Time course of symptoms:
    • Acute or recent in onset
    • Fluctuating level of consciousness
    • Coherent and obeying at one point, and a few hours
    later in a stupor
    Metabolic Encephalopathy:
    Diagnosis
    • Clues:
     PE: Jaundice, hyperventilation, tremors,
    asterixis, multifocal myoclonus
     Neuro exam:
    • Cranial nerve reflexes generally spared except
    in Wernicke’s encephalopathy (affects
    vestibuloocular reflex)
    Metabolic Encephalopathy:
    Treatment
    • Treat the underlying problem
    • Low dose neuroleptics for severe
    agitation
    Septic Encephalopathy
    Septic Encephalopathy:
    Pathophysiology
    Sepsis

    • Action of • Reduced cerebral


    inflammatory blood flow and
    mediators on the oxygen extraction by
    cerebrovascular the brain
    endothelium • Cerebral edema
    • Impaired astrocyte • Disruption of the
    blood-brain barrier
    function

    Multiorgan
    Failure Septic Encephalopathy
    Septic Encephalopathy: Diagnosis

    • Background of sepsis + encephalopathy


    (diffuse brain dysfunction without focal
    findings)
     Varies from acute confusional state to
    coma
     Fluctuating level of consciousness
     Abnormal movements like tremors,
    asterixis and myoclonus
    Septic Encephalopathy: Diagnosis

    • Patients dying from severe sepsis or


    septic shock may have:
     elevated levels of the serum brain injury
    biomarker S-100
     neuropathologic findings of neuronal
    apoptosis and cerebral ischemic injury
    Septic Encephalopathy: Prognosis

    • Septic encephalopathy presenting as


    coma  50% mortality rate
    • Successful treatment of underlying
    sepsis almost always result in complete
    resolution of encephalopathy
    • Profound long-term cognitive disability
    is uncommon
    Wernicke’s Encephalopathy
    Wernicke’s Encephalopathy
    • Due to Thiamine (Vit B1) deficiency
     Alcoholism
     Malnutrition due to:
    • hyperemesis, starvation, renal dialysis, cancer, AIDS, or
    rarely gastric surgery
    • Characteristic triad:
     Confusion
     Ophthalmoplegia all 3 present only in 1/3 of
     Ataxia patients
    Wernicke’s Encephalopathy
    • If untreated:
     stupor  coma  death
    • If treated:
     Ocular palsies improve within hours of thiamine
    administration
    • Horizontal nystagmus may persist
     Ataxia improves more slowly
    • ½ recover incompletely (persist as wide-based, shuffling
    gait, unable to tandem walk)
     Confusion improve more gradually
    Wernicke’s Encephalopathy
    • With treatment  confusion recede  an
    amnestic state with impairment in recent
    memory and learning may become more
    apparent (Korsakoff's psychosis)
    • Korsakoff's psychosis
     frequently persistent
     characterized by:
    • Gaps in memory
    • Confabulation
    • Disordered temporal sequencing
    Wernicke’s Encephalopathy:
    Pathology
    • Endothelial proliferation, demyelination, and some
    neuronal loss
    Acute cases
     Periventricular lesions surround the third ventricle, aqueduct,
    and fourth ventricle, with petechial hemorrhages
    Chronic cases
     Atrophy of the mamillary bodies
    • These changes may be detected by MRI scanning
    • Amnestic defect is related to lesions in the dorsal
    medial nuclei of the thalamus
    Wernicke’s Encephalopathy:
    Pathogenesis
    • Thiamine
     Enzyme co-factor in glucose and glutamate
    metabolism
     Deficiency produces
    • Diffuse decrease in cerebral glucose utilization
    and results in mitochondrial damage
    • Excitotoxic cell damage due to glutamate
    accumulation
    Wernicke’s Encephalopathy:
    Treatment
    • Thiamine 100mg IV or IM ASAP then
    daily until normal diet is resumed
     Given before IV glucose solutions are
    started
    Central Pontine Myelinolysis
    Central Pontine Myelinolysis
    • Typically presents as quadriplegia and
    pseudobulbar palsy
    • Predisposing factors
     severe underlying medical illness or
    nutritional deficiency
     most cases are associated with rapid
    correction of hyponatremia or with
    hyperosmolar states
    Central Pontine Myelinolysis:
    Pathology
    • Demyelination without inflammation in
    the base of the pons, with relative
    sparing of axons and nerve cells
    • Occasionally present as lesions outside
    the brainstem
    Central Pontine Myelinolysis:
    Prevention
    • Therapeutic guidelines for the
    restoration of severe hyponatremia
    should aim for gradual correction
     10 mmol/L (10 meq/L) within 24 h
     20 mmol/L (20 meq/L) within 48 h

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