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    PPK Neurologi

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    Mutiara Kesuma Ningrum
    Henhen Heryaman is a specialist physician and lecturer at Padjadjaran University. He has taught courses in biochemistry and internal medicine. His research focuses on metabolic encephalopathy, including presentations on hepatic encephalopathy, uremic encephalopathy, hypoglycemia, and hyperglycemic crises. Metabolic encephalopathy is a reversible brain dysfunction caused by extracerebral processes. Specific causes include liver failure, kidney failure, electrolyte imbalances, and extreme blood sugar levels. Prompt diagnosis and treatment are important to prevent permanent brain damage.

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    PPK Neurologi

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    Mutiara Kesuma Ningrum
    139 views41 pages
    Henhen Heryaman is a specialist physician and lecturer at Padjadjaran University. He has taught courses in biochemistry and internal medicine. His research focuses on metabolic encephalopathy, including presentations on hepatic encephalopathy, uremic encephalopathy, hypoglycemia, and hyperglycemic crises. Metabolic encephalopathy is a reversible brain dysfunction caused by extracerebral processes. Specific causes include liver failure, kidney failure, electrolyte imbalances, and extreme blood sugar levels. Prompt diagnosis and treatment are important to prevent permanent brain damage.

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    PPK neurologi

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    Henhen Heryaman is a specialist physician and lecturer at Padjadjaran University. He has taught courses in biochemistry and internal medicine. His research focuses on metabolic encephalopathy, including presentations on hepatic encephalopathy, uremic encephalopathy, hypoglycemia, and hyperglycemic crises. Metabolic encephalopathy is a reversible brain dysfunction caused by extracerebral processes. Specific causes include liver failure, kidney failure, electrolyte imbalances, and extreme blood sugar levels. Prompt diagnosis and treatment are important to prevent permanent brain damage.

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    Download as pptx, pdf, or txt
    139 views41 pages

    PPK Neurologi

    Uploaded by

    Mutiara Kesuma Ningrum
    Henhen Heryaman is a specialist physician and lecturer at Padjadjaran University. He has taught courses in biochemistry and internal medicine. His research focuses on metabolic encephalopathy, including presentations on hepatic encephalopathy, uremic encephalopathy, hypoglycemia, and hyperglycemic crises. Metabolic encephalopathy is a reversible brain dysfunction caused by extracerebral processes. Specific causes include liver failure, kidney failure, electrolyte imbalances, and extreme blood sugar levels. Prompt diagnosis and treatment are important to prevent permanent brain damage.

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    CURRICULUM VITAE

    Nama : Henhen Heryaman,dr.,SpPD


    TTL : Garut, 17 November 1975
    Agama : Islam
    Jabatan Fungsional : Dosen Fakultas Kedokteran
    Akademik Universitas Padjadjaran
    Perguruan Tinggi : Fakultas Kedokteran Universitas
    Padjadjaran (UNPAD)
    RIWAYAT PENDIDIKAN
    Tahun Lulus Program Pendidikan Institusi
    1994 SMA SMAN 1 Garut
    2004 Dokter FK Unpad
    2014 Spesialis 1 FK Unpad
    PENGALAMAN MENGAJAR
    Program Institusi/Jurusan/Progr Sem/Tahun
    Mata Kuliah
    Pendidikan am Studi Akademik
    Biokimia Sarjana FK Unpad
    Kedokteran
    Ilmu Penyakit Dalam D3 Poltekes Kebidanan 2013-2015
    Kebidanan Bandung
    METABOLIC
    ENCEPHALOPATHY(ME)
    HENHEN HERYAMAN
    RANI W. PRASANTI
    SMF ILMU PENYAKIT DALAM
    RS BHAYANGKARA TK 1I SARTIKA ASIH
    BANDUNG
    LEARNING OBJECTIVE:

    • DEFINITION OF ME
    • PATHOPHYSIOLOGY OF ME
    • CLINICAL MANIFESTASION OF ME
    • SPECIFIC ETIOLOGIES OF ME
    • TREATMENT OF ME
    LEARNING OBJECTIVE:
    • DEFINITION OF ME
    • PATHOPHYSIOLOGY OF ME
    • SPECIFIC ETIOLOGIES OF ME
    • CLINICAL MANIFESTASION
    • TREATMEN OF ME
    • Metabolic encephalopathy is defined as a potentially reversible abnormality of
    brain function caused by processes of extracerebral origin
    • Confusion is clinically defined as the inability to maintain a coherent stream of
    thought or action.
    • Delirium is a confusional state with superimposed hyperactivity of the
    sympathetic limb of the autonomic nervous system with consequent signs
    including tremor, tachycardia, diaphoresis, and mydriasis.
    • Acute toxic-metabolic encephalopathy (TME), which encompasses
    delirium and the acute confusional state, is an acute condition of
    global cerebral dysfunction in the absence of primary structural brain
    disease
    • TME is common among critically ill patients.
    • Furthermore, TME is probably under-recognized and undertreated,
    especially when it occurs in patients who require mechanical
    ventilation
    • TME is usually a consequence of systemic illness, and the causes of TME
    are diverse.
    • Most TME is reversible, making prompt recognition and treatment
    important.
    • Certain metabolic encephalopathies, including those caused by
    sustained hypoglycemia and thiamine deficiency (Wernicke’s
    encephalopathy), may result in permanent structural brain damage if
    untreated.
    • Alcohol withdrawal syndromes must be excluded in patients with
    suspected TME.
    LEARNING OBJECTIVE:

    • DEFINITION OF ME
    • PATHOPHYSIOLOGY OF ME
    • CLINICAL MANIFESTASION OF ME
    • SPECIFIC ETIOLOGY OF ME
    • TREATMENT OF ME
    LEARNING OBJECTIVE:

    • DEFINITION OF ME
    • PATHOPHYSIOLOGY OF ME
    • CLINICAL MANIFESTASION OF ME
    • SPECIFIC ETIOLOGY OF ME
    • TREATMENT OF ME
    • Normal neuronal activity requires a balanced environment of
    electrolytes, water, amino acids, excitatory and inhibitory
    neurotransmitters, and metabolic substrates
    • normal blood flow, normal temperature, normal osmolality, and
    physiologic pH are required for optimal central nervous system
    function
    • Complex systems, including those mediating arousal and awareness
    and those involved in higher cognitive functions, are more likely to
    malfunction when the local milieu is deranged
    • All forms of acute TME interfere with the function of the ascending
    reticular activating system and/or its projections to the cerebral
    cortex, leading to impairment of arousal and/or awareness
    • Ultimately, the neurophysiologic mechanisms of TME include
    interruption of polysynaptic pathways and altered excitatory-
    inhibitory amino acid balance
    • The pathophysiology of TME varies according to the underlying
    etiology
    HEPATIC ENCEPHALOPATY (HE)

    • CHARACTERIZED :
    • ALTERATION COGNITION
    • MOTOR FUNCTION
    • CONSCIOUSNESS

    • COMPLICATION OF LIVER CIRRHOSIS


    • ACUTE LIVER FAILURE
    • THREE TYPES OF HE
    • TYPE A : ACUTE LIVER FAILURE
    • TYPE B : PORTO-SYTEMIC SHUNTS IN ABSENCE OF LIVER DYSFUNGTION
    • TYPE C : LIVER CIRRHOSIS
    HEPATIC ENCEPHALOPATY (HE)
    • GRADING :
    • HE 1 : ATTENTION DEFICITS AND PSYCOMOTOR SLOWING
    • HE II: LETAHARGY AND DISORENTATION
    • HE III : SOMNOLENCE AND SEMI-STUPOR
    • HE IV : COMA
    • WITH OR WITHOUT: EXTRAPYRAMIDAL, PYRAMIDAL AND CEREBELLAR SIGN
    • MOST CHARACTERISTICS ARE HYPOMIMIA, HYPOKINESIA, RIGOR, TREMOR, DYSARTIA,
    DYSDIADOCHOKINESIA AND ATAXIA .
    • HYPERREFLEXIA AND POSITIVE PYRAMIDAL SIGN ( III AND IV)
    • ASTERIXIS (II AND III)
    Butterworth et al. (2018)
    HEPATIC ENCEPHALOPATY (HE)

    • DIAGNOSIS
    • EXCLUDE OF OTHER POSSIBLE CAUSES OF BRAIN DYSFUNCTION
    • RESOLVE WITH HE THERAPY
    • DD/ WERNICKE’S ENCEPHALOPHATY
    • TOOLS :
    • PSE-SYNDROME TEST
    • CRITICAL FLICKER FREQUENCY (CFF)
    • EEG

    VILSTRUP et al.2014
    Butterworth et al. (2018)
    Journal of Liver and Clinical Research

    LOLA AND HE IN CIRRHOSIS


    • 370 patients with cirrhosis and bouts of OHE were screened. After exclusion, 193 (52.16%)
    patients were randomized to receive either intravenous infusions of LOLA (n = 98), 30 g daily, or
    placebo (n = 95) for 5 days. Standard of care treatment (including lactulose and ceftriaxone) was
    given in both groups
    • The grade of OHE was significantly lower in the LOLA group (compared to placebo) on days 1-4
    but not on day 5

    Sidhu et al 2017. Hepatology Journal


    UREMIC ENCEPHALOPATHY

    • ACCUMULATE GUANIDINO COMPOUNDS DUE TO RENAL DYSFUNCTION


    • INTERFERE WITH GLUTAMATERGIC; GABA-ERGIC NEUROTRANSMISSION
    • INCREASES NEURONAL CALCIUM LEVEL AND NEUROEXICTATION (SECONDARY
    HYPER-PT)
    UREMIC ENCEPHALOPATHY

    • CLINICAL SYMTOMS :
    • EMOTIONAL ALTERATION : DEPRESSION, SLIGHT ATTENTION MEMORY DEFICITE,
    ALTERATION CONSCIOUSNES.
    • COGNITION ALTERATION : CONFUSION, PHYSICOSIS, SEIZURE AND COMA
    • HYPERREFLEXIA
    • ASTERIXIS
    • TREMOR
    • MYOCLONUS
    UREMIC ENCEPHALOPATHY

    • MANAGEMENT
    • HEMODIALYSIS
    • THIAMINE SUPPLEMENTATION
    • KETOANALOGS SUPPLEMENTATION
    SUBJECT SELECTION
    KETOANALOUGS SUPPLEMENTATION

    Che-Hsiung Wu et al 2017 PLoS ONE 12(5): e0176847.


    Che-Hsiung Wu et al 2017 PLoS ONE 12(5): e0176847.
    HYPOGLICEMIA

    • DD/; FOCAL NEUROLOGICAL SYMPTOMS IN ACUTE OR SUBACUTE ONSET


    • SEVERE HYPOGLICEMIA : SPEECH ARREST, HEMIPARESIS OR HEMICHOREA
    • MOST COMMON OCCURS : ADO, (SOLFUNILUREA) INSULIN
    • MEDICAL EMERGENCY
    2018 Diabetes Canada CPG – Chapter 14. Hypoglycemia

    HYPOGLICEMIA

    Neurogenic (autonomic) Neuroglycopenic

    Trembling Difficulty Concentrating

    Palpitations Confusion

    Sweating Weakness

    Anxiety Drowsiness

    Hunger Vision Changes

    Nausea Difficulty Speaking

    Dizziness
    2018 Diabetes Canada CPG – Chapter 14. Hypoglycemia

    Risk factors for severe hypoglycemia in people treated with sulfonylureas or insulin

    •Prior episode of severe hypoglycemia


    •Current low A1C (<6.0%)
    •Hypoglycemia unawareness
    •Long duration of insulin therapy
    •Autonomic neuropathy
    •Chronic kidney disease
    •Low economic status, food insecurity
    •Low health literacy
    •Preschool-age children unable to detect and/or treat mild hypoglycemia on their own
    •Adolescence
    •Pregnancy
    •Elderly
    •Cognitive impairment
    2018 Diabetes Canada CPG – Chapter 14. Hypoglycemia

    SEVERITY OF HYPOGLICEMIA
    • Mild
    – Autonomic symptoms present
    – Individual is able to self-treat

    • Moderate
    – Autonomic and neuroglycopenic symptoms
    – Individual is able to self-treat

    • Severe
    – Requires the assistance of another person
    – Unconsciousness may occur
    – Plasma glucose is typically <2.8 mmol/L
    2018 Diabetes Canada CPG – Chapter 14. Hypoglycemia

    TREATMENT SEVERE HYPOGLICEMIA


    UNCONSCIOUS PERSON WITH IV ACCESS
    1. Treat with 10-25 g (20-50 mL of D50W) of glucose intravenously over 1-3 minutes

    2. Retest in 15 minutes to ensure the BG >4.0 mmol/L and retreat with a further 15 g of carbohydrate if
    needed

    3. Once conscious, eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus
    protein
    HYPERGLICEMIA

    • HYPERGLICEMIA EMERGENCIES :
     DKA
     HHS

    • ALTERATION CONCIOUSNESS, SEIZURE AND FOCAL NEUROLOGICAL DEFICITES


    • STROKE MIGHT ACCOMPANY HSS
    • ASSOCIATED INFLAMATORY AND PROCOAGULANT STATE
    • PARTIAL EPILEPSIA AND HEMICHOREA
    MANAGEMENT OF CHRISIS HYPERGLICEMIA

    Abbas et al 2018: care.diabetesjournals.org


    CONCLUSION

    • ETIOLOGY OF ME STILL UNCLEAR


    • HYPOGLYCEMIA COMMON CAUSES OF SU AND INSULIN
    • CRISIS HYPERGLYCEMIA INDUCES STROKE (HSS)
    • LOLA DECREASES GRADING OF HE
    • KETOANALOGS DECRESES FREQUENCY OF HD AND DEATH

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