HYPERTENSIVE ENCEPHALOPATHY

by :Hasmawaty Basir
Hypertensive Encephalopathy

• syndrome of CNS dysfunction

• severe hipertension
• slowly,no spesific
• cephalgia, nausea, vomiting,mental changes
• funduskopy : bleeding, exudat and edema papil
Hipertension,classif JNC VII

• Pre hipertension: SBP 120-139 mmHg, DBP 80-89 mmHg

• Grd I HT: SBP 140-159 mmHG, DBP 90-99 mmHg
• Grd II HT: SBP >160mmHg, DBP>100 mmHg

Urgent HT : BP p ↑ ,suddenly, target organ

Damaged -,DBP > 120 mmHg

Emergensi HT: BP p ↑ suddenly ,with target

organ damaged +, DBP > 120 mmHg
•>>>> orang kulit hitam
• <<<< : orang kulit putih
• 60 juta America with HT,
< 1% HT emergensi
• 1 milyar penduduk HT, > 7,1 juta kematian per tahun
• HT Ensefalopati most <50 year
• HT risk :wanita 86-90%, laki-laki 81-83%,
Hipertensi Ensefalopati :
BP increase suddenly on chronic HT patient

HT predispotition:
• Chronic renal parenchymal disease
• Acute glomerulonephritis
• Renovascular hypertension
• Pheochromocytoma
• Eclampsia and preeclampsia
CLINICAL MANIFESTATION

• Commonly in patient with hystory of hypertension.

• BP > 240/140 mmHg
• normotension : target organ damaged : (160/100 mmHg)

• slowly, not spesifically

• Headache, nausea & vomit
• Onset usually in 24-48 hours
• Neurologic defisit > 24-48 hours
 Physical Examination
 BP measurement
 Blood sampling
 EKG
 EEG
 Chest X ray
 Urinalysis
 Arterial blood gas analysis
 Cranial scans & MRI
 Acut case ~ urgent treatment/
ICU(vital sign & EEG monitored )
 To decrease BP with
drug(monitored)
 Hydralazine,sodium nitropruside
 Anticonvulsan
 Promptly treated usually
recover wo deficit
 Blood pressure monitored ;
 Use anti hypertentension drug ,
avoid withdrawal
Funduscopy

retinopati HT grade IV
• papil edema,
• bleeding,
• eksudat,
• cotton-wool spots
HISTOPATOLOGI

Makroskopis
• Serebri normal ,
• local infarction

Mikroskopis
• lacunar infarction
HISTOPATOLOGI

Mikroskopis

Lesi vaskuler dan parenkim serebri.

• multipel , difus
• batang otak, utamanya basis pons,
• ganglia basal dan diencefalon,
• substansia alba serebri,
• kortex serebri dan medulla spinalis
 HISTOPATOLOGI……

Mikroskopis

Nekrosis fibrinoid
• 75% kasus,
• utamanya arteriole,
• Dindingnya bengkak,
• homogen, merah terang
• bag. Dalam : biru/ ungu
• Trombus fibrin sering
• deposit fibrin ekstravaskuler
HISTOPATOLOGI…..

Mikroskopis

Atherosklerosis dan arteriosklerosis :

 Perubahan hialin dgn iregularitas dinding PD

Mikroaneurisma Charcot-Bouchard :
 jarang ditemukan.
 Aneurisma di bagian luar dinding abnormal
 lumen dapat tertutupi : parsial /total
 perdarahan atau makrofag berisi homosiderin sering
 tidak spesifik untuk perubahan hipertensi.
HISTOPATOLOGI…..

Mikroskopis

Infark mikroskopik atau miliar

 deameter berkisar 100 mikron sampai 2 mm
 hipertensi maligna
 nekrosis fibrinoid dan oklusi fibrin
 dinding pembuluh darah ireguler secara fokal.

Perdarahan petekhi juga sering ditemukan

HISTOPATOLOGI……..

Histopatologi Mata

Dinding arteriole hialinisasi dan penebalan

 jarang nekrosis fibrinoid
 Mikroaneurisma pada beberapa kasus.
• Infark kecil pada retina (serabut saraf, lap. sel ganglion)
• dikelilingi oleh proliferasi sel glia.

Nervus optik :
• Sclerosis dan hialinisasi kurang sering
• nekrosis fibrinoid ditemukan (arteriole nervus optik)
Edema papil :
• papil protrusi, edema dan tampak perluasan ke lateral
LABORATORIUM

Evaluasi penentuan tingkat kerusakan hipertensi.

• CBC Count : anemia hemolitik mikroangiopatik.

• Urinalisis, BUN, dan kreatinin : kreatinin, hematuria.
• Enzim jantung : eksklusi iskemia miokard
• Screening toksikologi urine :
eksklusi ensefalopati HT drug-induced
RADIOLOGI

CT scan kepala

• edema difus atau fokal

• bagian posterior substansia alba
• sel endotel PD oksipitoparietal mudah terkena cedera
• sensitif terhadap mediator vasoaktif
• Densitas bermakna inervasi simpatis
• arteri karotis interna sedang-besar
• autoregulasi maksimal
• resistensi pembuluh darah yang kecil
RADIOLOGI

MRI Brain

• P ↑ intensitas T2, bilateral

• edema substansia alba
• bagian posterior hemisfer.
• Tidak ada efek massa.
RADIOLOGI
MRI Brain

• Reversible posterior leukoencephalopathy

• sindrom
• sakit kepala,
• perubahan status mental,
• kejang,
• kehilangan penglihatan

• orang dewasa
• hipertensi, eklampsia, dan imunosupresi.
• P ↑ secara mendadak .
• Substansia alba sering
• MRI : AbN T2 Wi subs. alba oksipitoparietal
PATOFISIOLOGI

• Gagalnya autoregulasi normal

• peningkatan tiba-tiba resistensi vaskuler sistemik (SVR)
• lepasnya vasokonstriktor humoral dari dinding pd

• siklus kerusakan endotel,

• aktivasi cascade pembekuan intravaskuler lokal,
• nekrosis fibrinoid PD kecil
• lepasnya lebih banyak vasokonstriktor

• cedera vaskuler,
• iskemia jaringan
• disfungsi autoregulasi.
PATOFISIOLOGI

• ensefalopati hipertensi
• peningkatan perfusi serebri
• kerusakan integritas blood-brain barrier
• eksudasi cairan ke dalam serebri.

• normotensi,
• peningkatan TD > (60-125 mmHg)
• vasokonstriksi arteriol serebri,
• memelihara aliran darah serebral
• intaknya blood-brain barrier
PATOFISIOLOGI

• kronik hipertensi,
• autoregulasi serebral bergeser ke tekanan tinggi
• adaptasi dari elevasi kronik TD sistemik.
• Respon autoregulasi terjadi selama hipertensi emergensi
• kebocoran hidrostatik kapiler SSP
• kerusakan dan nekrosis pada arteriole
PATOFISIOLOGI

EDEMA
• Edema mengkompresi PD
• menurunkan aliran darah
• iskemia serebral.
• dilatasi arteriole
• peningkatan tekanan kapiler.
• edema secara progresif semakin bertambah.

• Penurunan aliran darah

• menurunkan pengiriman oksigen.
• meningkatkan permeabilitas kapiler,
• kebocoran bertambah
• menonaktifkan pompa natrium
PATOFISIOLOGI

Sistem Kardiovaskuler

• hipertensi kronik
• peningkatan kekakuan arteri,
• peningkatan tekanan darah sistolik,
• lebarnya tekanan nadi.

• menurunkan tekanan perfusi koroner,

• konsumsi oksigen miokard m↑
• hipertrofi ventrikel kiri.
• gagalnya ventrikel kiri
• edema paru atau iskemia miokard.
DIAGNOSIS DIFFERENSIAL

• EklampsiaEnsefalopati hepatik
• Ensefalopati uremik
• Perdarahan Subarachnoid
• Hematoma Subdural
• Feokromositoma
PENATALAKSANAAN

• TD basal harus dipertimbangkan

• mencegah turunnya TD berlebihan
• mencegah iskemia serebri.

Penurunan tekanan arteri rata-rata 25%

• Diastolik pada level 100-110 mmHg, aman.
• Pemantauan teliti di unit perawatan intensif
• titrasi obat
• memantau fungsi organ vital.

• ES minimal pada SSP

• Hindari klonidin, reserpin, dan metildopa.
• Diazoxide dihindari, efek penurunan aliran darah serebri.
PENATALAKSANAAN

Labetolol
•konsisten tanpa pengaruh aliran darah serebri.
•terapi awal.
•beta blocker non selektif
•tidak u penyakit saluran napas berat, syok kardiogenik.

Nitrogliserin
• cepat namun komplikasinya iskemia miokard.
• Efek venodilatasi pada kontraksi volume.

Obat yang dianjurkan : labetalol, nifedipin, esmolol.

KOMPLIKASI

Ensefalopati hipertensi

•defisit neurologik perdarahan dan stroke

•kematian

• koma,
Hipertensi •kematian,
•stroke,
•nefropati,
•iskemia atau infark miocard,
•retinopati,
•penyakit vaskuler perifer
KOMPLIKASI

•derajat kerusakan target organ.

•Tanpa pengobatan, mortality rate 6 bulan HT emergensi 50%
• mortality rate 1 tahun mencapai 90%.

Kematian karena peny. jantung iskemik & stroke m ↑

• Tiap kenaikan SBP 20 mmHg /DBP 10 mmHg
• TD > 115/75 mmHg,
• mortality rate dua kali lipat u peny. jantung iskemik & stroke
KESIMPULAN

• kegawatdaruratan medik
• diagnosis dan penanganan yang cepat.
• Gejala klinis bkembang lambat , tidak spesifik
• funduskopi : perdarahan, exudat dan papil edema.

Tanpa pengobatan stupor, koma dan kematian.

Diagnosis dan penatalaksanaan tepat & agresif
defisit neurologik mengalami perbaikan sempurna.
CASE REPORT
 REGISTRATION
Name : A.H
Age : 15 years old
Admission date : June 12, 2009
Registration number: 38.37.41
Sex : male
Occupation : Student
ANAMNESIS

Chief complain: headache

• A chronic progressive headache, 1 year

ago ,worsed 2 weeks before admission.
• felt continously in all area of his head, pulsatile,
particularly on the back of head at left side.
• didn’t worsen with activity ,particular food.
• projectile vomiting, 2 weeks before admission
ANAMNESIS

• History of being hospitalized inWahidin hospital at

June 5, 2009 for 5 days with the medicine were
PDAK capsul, ranitidine and discharged after
there’s was decreasing of headache
• On the second days after discharged home, the
patient had great headache.
• Eventually, the patient was hospitalized again in
Wahidin hospital.
ANAMNESIS

• History of being hospitalized in Wahidin hospital on

April 2009 for 17 days with seizure.
• Seizure occured at the whole body.
• It occured more than five times and ended less
than 5 the minutes.
• The patient was unconscious during the seizure.
ANAMNESIS

•The seizure was characterized by flexion of both

arms and extension of both legs rigidly, followed
by jerking of all of the limbs and from his mouth
came out foam and the patient had no fever.
• Interval of the series of the seizure were 3-5
minutes.
•When the patient had conscious, he was rage
violently.
ANAMNESIS

• The patient had undergone head CT Scan with

Cerebritis and got medicine cefotaxime,
metronidazole, dexamethasone, phenitoine,
ranitidine and discharged recovery.
• Before on april 2009 there were no history of
seizure, head injury nor ear infection.
ANAMNESIS

• There was a history of being hospitalized in

Maros Hospital at June 2008 with tiphoid fever and
was given tiphoid drugs for 2 weeks.
• Since tifoid fever, the patient felt headache worsen
therefore the patient always go to the practice
doctor.
ANAMNESIS

• History of increasing blood pressure

with BP 140/90 – 160/90mmHg, 2 months before
admission with irreguler treatment.
• There were no history of diabetes nor heart
disease.
• Micturation and defecation were wnl
 PHYSICAL EXAMINATION

 Blood pressure : 200/120 mmHg

 Body temperature : 37,5 0C
 Pulse : 102 /minute, regular
 Respiration rate : 24/minute,
 Thorax : wnl
 Abdomen : liver and spleen were
not palpabled
 PHYSICAL EXAMINATION

 GCS : E4M6V5
 Higher cortical Fx : wnl
 Meningeal sign : neck stiffnes (-), KS -/-
 Cranial nerve : pupils were isocor 
2,5/2,5 mm, DLR +/+,
UDLR +/+
 Funduscopic examination: Edema papil -/+
 PHYSICAL EXAMINATION

 Motoric function:
 Movement Muscle
NN S Muscle
5 5T N N
NN 5 5 N N
 Physiologycal R. N NPathological R
- -
NN
- +
 Sensoric function : wnl
 Autonomic function : wnl
 COORDINATION TEST

 Romberg modified Test : (+) fall on the left

side
 Nose finger Test : wnl
 Knee Heel Test : wnl
 Diadokokinesis test : wnl
 Stepping test : wnl
 LABORATORY FINDINGS

 Hb 14,1 g/dl, WBC 12,75.103 /mm3, HCT 39,4 %, PLT 428.000

/mm3, MCV 74,8 fL, MCH 26,8 pg. MCHC 35,8 g/dl, Glucose at
random 100 mg/dl, SGOT 24 u/l, SGPT 49 u/l, ureum 25 mg/dl,
creatinine 0,6 mg/dl, Natrium 127 mmol/l, Kalium 2,9 mmol/l,
Chloride 97 mmol/l.
WORKING DIAGNOSIS

 Clinical : Chronic headache

 Topical : Cerebral hemisphere
 Etiological : Suspect Intracranial Tumor
 DD : Serebritis
 TREATMENT

 Corticosteroid
 Neuroprotector
 Analgetic
 H2 Reseptor antagonis
 Neurotropik
 Electrolite corection : NaCl 3% 12 drp/mnt
Suggestion
 Chest x-ray
 Head CT-Scan
 Consult to internist departement
 Consult to the opthalmology departement
 Imprs: Second grade Hypertension susp.Chonn syndr.
▪ DD : Renovascular Hypertension
GNA
Suggestion:
 Low salt diet
 Diltiazem 200 1x1
 Bisoprolol 2,5 mg 1x1
 Routine Urine, Blood Gas Analysis
 Abdominal USG
 Renalis artery Arteryography
 Impression : Retinopathy first grade of
hypertension
 Suggestion : Control to the Opthalmology
polyclinic if condition is getting better
 Follow Up
June 13, 2009 (2nd day)

 S : Headache , vas 10
 O : BP : 180/110 mmHg P : 104/mnt
 RR :48/mnt BT : 36,8 0C
 Neurological state: GCS: E4M6V5
 M MS MT PR PtR
NN 5 5 NN NN - -
NN 5 5 NN NN - +
 Thorax photo : No abnormality shows.
 Abdominal USG : Within normal limit
Follow Up
June 14, 2009 (3rd day)

Head CT Scan

•mass density 38,65 HU,

•Cerebellum
•Enlargement of lat, third ventr
•No mid line shift
•veiled maxillaris sinus
•paranasalis sinuses N
•Mastoid air cells N
•Cranium bones are intact
Imp:
• mass at Cerebellum,
•non communicating hydr,
•Bilateral Maxillaris Sinusitis
•Suggestion :
• Head CT Scan with Contrast
Follow Up
June 19, 2009 (8th day)

•Headache (±) , VAS 5

• BP : 180/100 mmHg,P : 70/mnt,RR :20/mnt,BT : 36,1 0C

The result from the Hypertension Kidney departement

Impression : Second Grade Hypertension ec. Susp
stenosis Renalis Artery (Renovascular Hypertension)
Suggestion :
•Low salt diet
•Diltiazem 200 0-0-1
•Check Complete urine, tot. chol., albumine, tot. protein.
•Planning for renalis artery arteriography
Follow Up
June 22, 2009 (11st day)

Headache (±) , VAS 4

BP:180/100mmHg,P:70/mnt,RR:20/mnt,BT:36,10C
Injection medicine are changed to oral medicine
Dexamethasone tab 3x2
PDAK capsul 3x1
Ranitidine tab 2x1
B1B6B12 tab 2x1
Diltiazem 200 0-0-1
Follow Up
June 25, 2009 (14thday)

Headache (-) , VAS 1

BP:180/100mmHg,P:70/mnt,RR:20/mnt,BT:36,1 0C
Head CT Scan with contras :
Impression : There is no abnormality show at this CT
Scan as the first CT Scan
Suggestion : Brain MRI
Final Diagnosis
Clinical : Chronic headache + Second grade
hypertension
Topical : Posterior Fossa
Etiological : Hypertensive Encephalopathy +
Non Communicating Hydrocephalus
DISCUSSION

• Headache developed chronic progressive 1 year

before admission and it did not worsen by physical
activity and particular food.
• The headache was pulsatile especially on the back
of head at left side with projectile vomiting.
• This is a possibly of an Increasing of Intracranial
Pressure (↑ ICP) and it was thought of a Space
Occupaying Lesion.
Discussion……….

• The patient had a seizure since 2 months before admission

with no fever.
•Occured at the whole body (a Tonic Clonic Seizure).
• The patient had undergone head CT Scan with Cerebritis
and got medicine cefotaxime, metronidazole,
dexamethasone, phenitoine, ranitidine and discharged
recovery.
•Before april 2009 there were no history of seizure, head
injury nor ear infection.
Discussion……….

• The patient then admitted to the hospital on June 2009 with

the same complaint of headache.
•On the physical examination, we found Babinsky Reflex (+) in
the left leg, Romberg modified Test : (+) fall on the left side
but the other coordination tests were within normal limit.
• The head CT Scan without contrast showed a mass at
cerebellar lobe and non communicating hydrocephalus. So
we concluded there was a lesion at the cerebellar lobe.
Discussion……….

This patient has a history of increasing blood pressure with

blood pressure average 140/90 – 160/90 mmHg occurred 2
months before admission with irreguler treatment. On the
funduscopic examination found papil oedema at the left eye.
So we conclude retinopathy hypertension. The consultation
result from the Hypertension Kidney departement is Second
Grade Hypertension ec. Susp stenosis Renalis Artery
(Renovascular Hypertension).
Discussion……….

During treatment with corticosteroid and antihypertensive

drugs about 14 days, much improvement on the clinical
manifestation and the head CT Scan with contrast. The
impression of head CT Scan with contrast showed no
abnormality.
So we concluded the final diagnosis is :
Primary hypertension-induced cerebellar
encephalopthy causing obstructive
hydrocephalus.
Discussion……….

• SY Lee et al report a patient presenting with acute onset

progressively worsening headache and confusion associated
with uncontrolled hypertension.
• CT and MRI revealed acute non-communicating
hydrocephalus secondary to cerebellar and pontine oedema.
Discussion……….

M Verrees report on two cases of isolated edema of the

cerebellar hemispheres, which occurred in the setting of
hypertensive crisis and led to complete obstruction of or
significant impingement on the fourth ventricle and
potentially lethal hydrocephalus.
Discussion……….

•Kuang-Lin-Lin et al describe an 11-year-old male who

presented with edema and a cerebellar lesion, with acute
obstructive hydrocephalus resulting from hypertensive
encephalopathy.
•The cerebellar lesion had been initially diagnosed as a
glioma.
Discussion……….

 In children, a cerebellar lesion occurring with

acute obstructive hydrocephalus and
hypertensive encephalopathy is rare but
reversible.
 Clinicians should be aware of this condition
because it might be misdiagnosed as a tumor
of the posterior fossa.
Discussion……….

•Treatment with steroid, glycerol, and

antihypertensive drugs resulted in a slow decrease in
the brain swelling and cerebral edema.
• Treatment consists of measures that promptly reduce
arterial blood pressure, but antihypertensive drugs
must be used cautiously; a safe target is a pressure of
150/100 mmHg.
Discussion……….

One may use intravenous sodium nitroprusside, 0.5 to 0.8

mg/kg/min; a calcium channel blocker such as nifedipine, 10 to
20 mg sublingually; or intravenous beta-adrenergic blockers
(labetalol, 20 to 40 mg intravenously followed by an infusion at
2 mg/min, or esmolol are favored).
These must be followed by longer-acting antihypertensive
agents such as ACE inhibitors or calcium channel blockers.

•Hydrocephalus and intracranial HT persisted, requiring a

shunt operation.