The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena.

1. Mukesh sah, MD,JI
Virgen Milagrosa University Foundation

2. HYPERTENSIVE ENCEPHALOPATHY

3. General data
• Name: MRB
• Age: 5
• Sex: Female
• Race: Filipino
• Religion: Roman Catholic
• Present address: Pozzurubio, Pangasinan
• Admitted for the 1st time at the Region 1
medical center
• Informant: father

4. Chief complaint
• Difficulty of breathing
• Facial edema

5. History of present illness
• 15 days PTA, patient startd having skin rashes accompanied
with undocumented fever. Paracetamol was given and fever
was relieved.
• 10days PTA, patient started having facial edema,
accompanied by headache, and abdominal pain
• 6 day PTA, with persistent signs and symptoms above the pt
was brought to the community hospital and was referred to
a private doctor and was diagnosed with ACUTE RENAL
FAILURE.
• The patient was then admitted to a private hospital and
stayed there for 2 days.
• Few hours PTA, facial edema persisted, accompanied by
headache, abdominal pain, vomiting (6x), difficulty of
breathing, prompted the patient to be brought to our
institution hence admitted for the first time

6. Review of system
• General: weak, in cp distress + LOSS OF APPETITE
• Integumentary: (-) lesion; (-) pruritus
• Head and Neck: (-) ear discharge (-) nasal obstruction (-) sore
throat
• Respiratory: (-) hemoptysis (-) cough
• Cardiovascular: (-) chest pain (-) orthopnea (-)SOB
• Gastrointestinal: (-) diarrhea (-) constipation
• Genitourinary: (-) dysuria (+) hematuria (+) oliguria
• Musculoskeletal: (-) atrophy
• Endocrine: (-) heat or cold tolerance
• Hematologic: (-) pallor
• Muscuskeletal: (-) myalgia

7. Past medical history
• 2014 Pneumonia in Pozzorubio Community
Hospital
• No known allergies for food or drugs

8. Family history
• Father: 37 years old, appears to be healthy
smoker, occupation: buy and sell ( scrap)
• Mother: 34 yrs old appears to be healthy,
house wife
• Sibling : 1 sister 12 years old ,healthy
• Hypertension – grandparents on the paternal
side

9. Immunization history
• Patient had her immunizations done at the
barangay health center and was said to have
completed the scheduled immunization
program

10. Socio economic, environmental history
• Patient lives with parents and 1 sibling in a
one story house ( semi concrete house)
• Drinking water: mineral
• Garbage disposal: Burning
• Pt is exposed to 2nd hand smoking ( father)

11. • Pt is in kindergarten, active in school
• Diet mostly consists of rice vegetables and fish
• Loves to eat junk foods ,sweets and drinks
softdrinks

12. Physical examination
• General:
Weak looking, unconscious, Pt is cardiopulmonary
distress.
GCS 5 E1V1M3 (intubated) ER LEVEL
• Vital signs and Anthropometric Measurements
Temp: 37 C
PR:91 bpm
RR:26 cpm
BP: 180/120 mm Hg
Weight: 25kgs

13. • SKIN
(-) jaundice, (-) pallor, (-) rashes
• HEENT
pinkish palpebral conjunctivae ; anicteric
sclerae ; (-) circus senilis ; (-) xanthelasma ; (-)
alopecia ; (-) Tonsillopharyngeal congestion ;

14. • Chest/ Lungs : symmetrical ; (-) retractions ;(-)
lag; (-) spider angiomas; equal vocal and tactile
fremiti ; equally resonant on both lung
fields; equal breath sounds ; (-)rales ; (-)
wheezes
• Heart : Adynamic precordium ; Apex beat at the
4th or 5th intercostal space left midclavicular line ;
(-) thrills/ heaves ; (-); normal rate regular rhythm
; (-) murmurs
• Abdomen : flat ;normoactive bowel sounds ; soft;
tenderness on lower quadrant ; tymphanitic

15. • Extremities
(-) deformities ; ( -) clubbing ; (-) cyanosis
full equal pulses on extremities
• Motor :
Upper extremities: 5/5
Lower extremities 5/5
•DTR: normoreflexia

16. • Neurologic exam :
• Cerebrum : UNCONSCIOUS
• Cerebellum :
• Cranial nerves :
• I –
• II, III – pupils equally reactive to light
• III, IV, VI –
• V – intact corneal reflex , bilateral ;
• VII – (-) facial asymmetry
• VIII –
• IX, X –
• XI –
• (-) Babinski ; (-) nuchal rigidity ( -) Brudzinski (-) Kernig’s sign

17. admitting diagnosis
• HYPERTENSIVE ENCEPHALOPATHY SEC TO
NEPHROTIC SYNDROME

18. LABS
• URINALYSIS:
– Blood ++
– Protein +
– Leukocyte +++
– RBC 32
– Pus cells 124
– Epithelial 5
– Hyaline 4
– Bacteria 10
• CREATININE
– 53umol/L (nor)
• UREA
– 8 mmo/L ( n)
• GRAMS STAIN ETA:
– Pus cells +
– No microorganism seen
• CBC
– Wbc 23.6
– N 83.5
– L 10
– M 6.4
– E 0
– B 0.1
– Hgb 106 (dec)
– Hct 0.32 ( dec)
– Plt 519 (inc)
• Na 141 nor
• K 3.53 nor
• Cl 95.8 dec
• Ca 1.19 nor
• Triglycerides 1.45 mmol/L normal

19. Course in the ward
• 8/27 ( 1st hospital day)
• Diagnostics ordered
– Hgt
– S.electrolytes
– CBC
– Urinalysis
– S. albumin
– BUN Crea
– Triglycerides
– Plain CT scan
– ABG if with funds
– ETA GS/CS
– Serum C3 c/o Outside
• NPO
• Ivf: PNSS X 18-19 gtts/min (500/
BSA) M%
• Meds:
– Furosemide 20 mg IV q 8 hrs
– Paracetamol 250 mg IV q 4 hrs for
T> 37.8C
– Pen g 700000 m IU q 6hrs ANST
• Hook to nicardipine drip to run at
8cc/hr
– Nicardipine 10 cc
– D5W 90cc
• Ppv bagging at 10 lpm
• Referred to nephro

20. • 8/28 ( day 1 PICU)
Gcs 11 e4v1m6
+ facial edema + hematuria
No fever
BP: 110-120/80
SCE no retractions CBS
Full pulses
• Ivf: d5w(500cc)+ PNSS (500cc) X
18-19 gtts/min (500/ BSA) M%
• Meds:
– Furosemide 30 mg IV q 8 hrs
– Paracetamol 250 mg IV q 4 hrs for
T> 37.8C
– nicardipine drip to run at 16cc/hr
– PPV bagging at 10 lpm
• Repeat urinalysis
• Weigh pt

21. WORKING DIAGNOSIS
• HYPERTENSIVE ENCEPHALOPATHY
SEC TO NEPHROTIC SYNDROME

22. HYPERTENSIVE ENCEPHALOPATHY
• Hypertensive encephalopathy is most
commonly associated with renal disease in
children, including acute glomerulonephritis,
chronic pyelonephritis, and end-stage renal
disease
• is the initial manifestation of underlying renal
disease.

23. PATHOPHYSIOLOGY
• Marked systemic hypertension produces
vasoconstriction of the cerebral vessels, which
leads to vascular permeability, causing areas
of focal cerebral edema and hemorrhage.
• The onset may be acute, with seizures and
coma, or more indolent, with headache,
drowsiness and lethargy, nausea and
vomiting, blurred vision, transient cortical
blindness, and hemiparesis.

24. WORK UPS
• Examination of the eye grounds may be nondiagnostic
in children, but papilledema and retinal hemorrhages
may occur.
• MRI often shows increased signal intensity in the
occipital lobes on T2-weighted images, which is known
as posterior reversible leukoencephalopathy (PRES)
and may be confused with cerebral infarctions. PRES
may also be seen in children without hypertension.
• PRES manifests with generalized motor seizures,
headache, mental status changes, and visual
disturbances.
• CT may be normal in PRES; MRI is the study of choice.

25. TREATMENT AND MANAGEMENT
. Treatment is directed at restoration of a
normotensive state and control of seizures
with appropriate anticonvulsants.

26. • Nicardipine is a second-generation dihydropyridine-
derivative calcium channel blocker, which has high
vascular selectivity and strong cerebral and coronary
vasodilatory activity. It has been shown to increase
stroke volume and coronary blood flow.[9]
• Labetalol provides a steady consistent drop in blood
pressure without compromising CBF. It is frequently
used as initial therapy. Because of its nonselective
beta-blocking properties, labetalol should be avoided
in severe reactive airway disease and cardiogenic
shock.

27. • Nitroglycerin has been used to provide a rapid
reduction in elevated blood pressure complicating
myocardial ischemia. The reduction in blood pressure
may be severe and can cause further complications due
to venodilatory effects in volume-contracted
individuals.
• Nitroprusside sodium and hydralazine pose a
theoretical risk of intracranial shunting of blood.
Accordingly, these agents should be avoided in patients
suspected of having increased intracranial pressure
(ICP), because the potential intracerebral shunting of
blood can increase the ICP.

28. • Hydralazine has a limited role in this setting,
owing to reflex tachycardia, and it should not be
used in patients with suspected coronary artery
disease (CAD).
• Diuretics should also not be used in these
patients unless there is clear evidence of volume
overload. This is due to pressure natriuresis that
occurs and leaves these patients volume
depleted. Volume repletion by itself can
sometimes lower the blood pressure.

30. • THANK YOU