ENCEPHALOPATHY BASJIRUDDIN A. Arsip FK UNAND Angkatan 2008 – Minggu 1
Nov 01, 2014
ENCEPHALOPATHY
BASJIRUDDIN A.
Arsip FK UNAND Angkatan 2008 – Minggu 1
• 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
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
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
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
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
May include :– Seizures, myoclonus– Involuntary twitching of muscles– Tremor– Nystagmus– Dementia– Loss of ability to speak or swallow
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.
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
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
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
• 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
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)
Diagnosis and test
• Clinical history• Physical examination• Include : - blood test
- Electroencephalography - EKG - Imaging
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
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
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
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
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
• 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
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
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
Acute HT emergency
Disruption of BBB
Hydrastatic leakage across the capillaries
Arterioler damageNecrosis
Generalizad vasodilatation
Cerebral edema, papill edema
Neurologic deficitsAltered mentation
Pathophysiology
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
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)
Normal Fundus
Grade II Retinopathy
Widened light reflex
Grade III Retinopathy
Edema; cotton wool patches; hemorrhages
Grade IV Retinopathy
Papilledema
Diagnosis- Acutely elevated BP- Clinical feature of neurologic syndrom- Acute or ongoing end organ damage
- brain- renal- heart- retinal
Lab Studies• CBC for presence of microangiopathic
hemolitic anemia hemolytic anemia• BUN creatinine • Hematuria, proteinuria• Cardiac enzymes to exclude myocardial
ischemia
Imaging Studies• CT scan to evaluate : stroke infart or
hemorrhage• Perform chest x-ray : to evaluate complication
of HTE• Other tests : electrocardiogram cardiac
ischemia ?
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
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
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.
Further Care• Routinely : Monitoring MAP-adequate titration of
pharmac.agents: Perform neurologic reassessment due to
inadequate treatment: Progression neurologic result
Further Care
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
Symptoms• Fever, headache, photophobia, seizures,
weakness• Stiffness of the limbs, slowness in movement• Seizure
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)
TREATMENT
• Usually symptomatic• Anti viral agent (acyclovir etc)• Antibiotic for bacterial encephalitis• Anti convulsant• Supportive treatment such as mechanical
ventilation etc