ensefalopati
DESCRIPTION
Kuliah FK UNAND Angkatan 2008TRANSCRIPT
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ENCEPHALOPATHY
BASJIRUDDIN A.
Arsip FK UNAND Angkatan 2008 – Minggu 1
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• Encephalopathy is a term for any diffuse disease of the brain, that alters brain function or structure
• It can refer to a wide variety of:– degenerative brain disorders– different etiologies– prognoses– implications
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Types
Many types of encephalopathy :• Hypertensive encephalopathy : arising from acutely
increase blood pressure
• Hypoxic encephalopathy : severely reduced ogygen delivery to the brain
• Hepatic encephalopathy : arising from advanced cirrhosis of the liver
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Types cont...
• Uremic encephalopathy : arising from high levels of toxins normally cleared by the kidneys (rare, where dialysis is readily available)
• Toxic-metabolic encephalopathy : a catch-all for brain dysfunction caused by infection, organ failure, or intoxication
• Wernicke’s encephalopathy: arising from thiamine defficiency (alcoholism)
• Hashimoto’s encephalopathy: arising from an acute immune disorders
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Causes
May be caused by :• Acutely elevated blood pressure (BP)• an infection agent (bacteria, virus)• metabolic dysfunction• brain tumor• increased intracranial pressure• exposure to toxins : drugs, alcohol, chcemicals• lack of oxygen or cerebral blood flow• chronic progressive trauma
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Clinical Features
• Hallmark of encephalopathy is an altered mental state
• Common neurological symptoms depend on type and severity :– progressive loss of memory and cognitive ability– subtle personality changes– inability to concentrate– lethargy– progressive loss of consciusness
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May include :– Seizures, myoclonus– Involuntary twitching of muscles– Tremor– Nystagmus– Dementia– Loss of ability to speak or swallow
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Diagnosis
• Blood tests• Spinal fluid examination (lumbal puncture)• Electroencephalograms• Diagnosis for the various cases of
encephalopathy– Acute liver failure– Acute renal failure– Blood pressure– Imaging, etc.
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Therapy
• Treatment is symptomatic and varies, according to type/severity of the encephalopathy
• Anticonvulsants : to reduce or halt any seizures• Changes to diet and nutritional supplements• In severe cases, dialysis or surgery may be needed• In a special case maybe need liver transplantation
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Hypoxic encephalopathy
Definition• Hypoxic encephalopathy is a term refers to a lack of
oxygen supply and lack of cerebral blood flow to the cerebral hemispheres or the entire brain, can cause brain damage
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Causes and risk factors
Numerous causes, include:• Drowning• Asphyxiation (smoke inhalation)• Very low blood pressure• Strangling• Cardiac arrest• Carbon monoxide poisoning• High altitudes• Paralyze of the respiratory muscles
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• Brain cells : very sensitive to oxygen depriviationstart dying just under five minutes
after O2 supply is cut• Brain hypoxia can cause :
– Death– Severe brain damage
• Damage can occur within 5 minutes, once brain damage occurs, it is irreversible.
• This is an emergency condition need sooner oxygen supply restore
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Symptoms and sign
• In mild case:– Inattentiveness, poor judgment– Motor in-coordination
• Severe case:– Complete unawareness, unresponsiveness (pupillary
respone to light, breathing reflex)
• If lack of O2 is limited periode coma may be reversible
• Seizures may occur, which may be continous (status epilepticus)
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Diagnosis and test
• Clinical history• Physical examination• Include : - blood test
- Electroencephalography - EKG - Imaging
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Treatment
• Depends on the underlying cause• Importantly : basic life – support:
– Secure the air way– Blood pressure – supported with fluids,
medications– Controoled heart rate– Seizures treated
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Hypertensive encephalopathy (HTE)
HTE is an acute neurologic (cerebral) syndrome precipated by sudden severe hypertension (HT)
- Associate with crisis HT- HTE is a medical emergency recuiring
intensive/effective treatment : if untreated lead to coma and death
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HT Crisis
• HT emergency (Diast blood pressure > 140mmHg, syst blood
pressure > 250mmHg) with target organ damage (TOD) : encephalopathy, aortic dissection, acute renal failure, myocardial infarction, strokeNeed HT reduction with parenteral therapy and intensive monitoring
• HT urgency: without evidence of TOD : can be achieved by oral agents of anti HT
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JNC VI (The sevent of the Joint National Committee on prevention, Detection and treatment) classification of blood pressure :Stage 1 SBP of 140 to 159 mmHg or DBP of 90-99 mmHgStage 2 SBP of 160 to 179 mmHg DBP 100-109 mmHgStage 3 SBP > 180 mmHg > 110 mmHgStage 3 HT is also called severe HT or accelerated HT
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Accelerated and malignant HT: describe the retinal findings :• Accelerated HT
– Associated with group 3 Keith Wegner (KW) retinopathy
– Characterized by retinal hemorrhages and exudates• Malignant HT
– Associated with group 4 KW retinopathy– Characterized by papill edema, heralding– i.cran pressure
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• JNC VII Classification of Blood Pressure
BP Classification SBP mmHg DBP mmHg
Normal < 120 and < 80
Prehypertension 120-139 Or 80-89
Stage 1 hypertension 140-159 Or 90-99
Stage 2 hypertension > 160 Or > 100
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The presence of acut or ongoing end organ damage
Requirement of reduction in BP
Anti hypertensive agents
A few hours
Intravenous Oral, possible
24-48 hours
NoYes
Hypertensive emergency
Hypertensive urgency
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Pathophysiology
- In chronically HT: cerebral autoregulatory range shifted to high pressure
Adaptation of systemic blood pressure (BP)
- Increase cerebral perfussion from the loss of BBB integrity
Exudation of fluid into the brain
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Acute HT emergency
Disruption of BBB
Hydrastatic leakage across the capillaries
Arterioler damageNecrosis
Generalizad vasodilatation
Cerebral edema, papill edema
Neurologic deficitsAltered mentation
Pathophysiology
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Clinical Features
• HTE may present as any age (commond in 3-4th decades)
• History of chronic HT• Headache
– nausea, vomiting– confussion, agitated
• Sometimes develop in the setting of– renal failure– Vasculitis– Pheochromocytoma
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Clinical Features cont...
• Visual symptoms– bluring– scotoma– cortical blindness– nystagmus
• Seizures focal or generalized• Confusion agitate coma• Funduscopy : grade III-IV Keith Wagner (KW) retinal changes,
exsudate, hemorrhage• Head CT Scan : bilateral areas of low attenuation of the brain
(reversible with reduction of BP)
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Normal Fundus
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Grade II Retinopathy
Widened light reflex
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Grade III Retinopathy
Edema; cotton wool patches; hemorrhages
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Grade IV Retinopathy
Papilledema
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Diagnosis- Acutely elevated BP- Clinical feature of neurologic syndrom- Acute or ongoing end organ damage
- brain- renal- heart- retinal
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Lab Studies• CBC for presence of microangiopathic
hemolitic anemia hemolytic anemia• BUN creatinine • Hematuria, proteinuria• Cardiac enzymes to exclude myocardial
ischemia
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Imaging Studies• CT scan to evaluate : stroke infart or
hemorrhage• Perform chest x-ray : to evaluate complication
of HTE• Other tests : electrocardiogram cardiac
ischemia ?
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Treatment
• Directed toward lowering arterial BP :– avoid excessive BP lowering– prevent cerebral ischemia– lowering DBP to 100-110mmHg
• Acute monitoring in ICU– Mean Arterial Pressure (MAP)monitoring required for
adequate titration of pharmac. agents– End organ function
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Treatment
Anti HT– Nitroprusside : first line therapy rapid onset, short duration
of action reduces peripheral resistance– Nitroglycerin : rapid reduction BP decreases coronary
vasospasm– Labetalol : steady consistent drop in BP without
compromissing CBF– Nicardipine : potent, rapid onset of action ease titration,
lack of toxic metabolitest– Electrolite, acid-base balance
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Treatment
Anti convulsants• Administer phenitoin. Dose : 18-20mg/kg iv• Diazepam. Dose 5-10mg iv 10-20 min, not to exceed
30mg/kg. • Lorazepam. Dose 4mg iv slowly at 2mg/min : if
seizure continues after 10-15 min additional 4mg iv slowly at 2 mg/min.
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Further Care• Routinely : Monitoring MAP-adequate titration of
pharmac.agents: Perform neurologic reassessment due to
inadequate treatment: Progression neurologic result
Further Care
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ENCEPHALITIS
• Encephalitis is as acute inflamation of the brain, commonly caused by viral infection
• It can be caused by a bacterial such as :– meningitis – encephalitis suprative or cerebral absces– or a complication of other infections disease :
• Parasitic: toxoplasmosis, amoebic
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Symptoms• Fever, headache, photophobia, seizures,
weakness• Stiffness of the limbs, slowness in movement• Seizure
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DIAGNOSIS
• Acute onset of fever, headache confusion• Seizures• Irritability• LP : protein ↑
cell (wbc) ↑ glucose normal
• EEG : sharp waves• Detection of antbodies in CSF againts specific viral
agent (herpes, varicella, etc)
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TREATMENT
• Usually symptomatic• Anti viral agent (acyclovir etc)• Antibiotic for bacterial encephalitis• Anti convulsant• Supportive treatment such as mechanical
ventilation etc