case presentation

2. IDIOPATHIC INTRACRANIAL
HYPERTENSION
PRESENTED BY
BSS-101285 CAPTAIN RASHED-UL-HASAN
TRAINEE IN OPHTHALMOLOGY
AFMI, DHAKA

3. PARTICULARS OF THE PATIENT
Name : Mrs. Tuhina parvin
Age : 47 years
Sex : Female
Religion : Islam
Address (Present) : Dhaka
Date of admission : 05 Aug 2012

4. CHIEF COMPLAINTS
1. Transient blurring of vision on both eyes
for about 03 months

5. HISTORY OF PRESENT ILLNESS
 Patient states that she was reasonably well 03 months
back. Then she developed transient blurring of vision
on both eyes.
 No H/O double vision or deviation of eyes.
 No H/O headache, nausea, vomiting, seizures, fever,
weakness of limbs or tinnitus.
 No H/O trauma, head injury.

6. PAST OCULAR HISTORY
Not significant .
H/O PAST SYSTEMIC ILLNESS
She is hypertensive for 10 years.
No H/O DM, Bronchial asthma, IHD.
MENSTRUAL HISTORY
Menstrual cycle- Regular
PERSONAL HISTORY
FAMILY HISTORY
DRUG HISTORY - No H/O taking drugs like amioderone,
OCP, nalidixic acid, VIT-A etc.
TREATMENT HISTORY
Tab. Atenolol 50 mg 1+0+0
Tab. Amlodipine 10 mg 0+0+1
Not significant

7. GENERAL EXAMINATION
Appearance - Anxious Temp - 98 .40 F
Anaemia Pulse - 90/ min, regular
Jaundice BP - 160/95 mm of Hg
Cyanosis Resp.rate - 22/min.
Dehydration Absent
Oedema
Clubbing
Koilonychia
Neck rigidity
Lymph node - Not palpable

8. SYSTEMIC EXAMINATION
Cardio-vascular system
Respiratory system
Alimentary system
Nervous system - Higher psychic, motor ,sensory-NAD
All cranial nerves are normal except
Papilloedema in optic nerve head.
Nothing contributory

9. OCULAR EXAMINATION
POINTS RIGHT EYE LEFT EYE
Visual Acuity 6/6 (UA)
N-6
6/9(UA)
N-6
Colour vision Trichromatic Trichromatic
Visual field
(Confrontation)
Normal Normal
Ocular motility Normal in all gazes Normal in all gazes
Hirschberg reflex Central Central
Pupil Equally round &
reactive to light &
accommodation
Equally round &
reactive to light &
accommodation

10. Contd..
POINTS RIGHT EYE LEFT EYE
Eye lids NAD NAD
Eye lashes NAD NAD
Conjunctiva NAD NAD
Cornea NAD NAD
Anterior Chamber NAD NAD
Lens Clear Clear
IOP 14 mm of Hg 14 mm of Hg

11. DIRECT OPHTHALMOSCOPY
Fundus (Both eye)
Optic disc - Hyperaemic , swollen with
Elevated, blurred margin &
Parapapillary flame shaped haemorrhage.
Absence of venous pulse
Retinal blood vessels
Peripheral retina
Foveal reflex
Normal

12. SALIENT FEATURES
Mrs. Tuhina parvin, 47 yrs old having
Transient blurring of vision on both eyes for last 3
months .
Hypertensive for last 10 years
No H/O double vision, deviation of eyes.
No H/O trauma, head injury.
No H/O taking any medicine except anti hypertensive
drug

13. Contd..
 On general examination : BP-160/95 mm of Hg
 On ocular examination
V/A- 6/6(R/E ), 6/9 (L/E)
Ant Segment - NAD (B/E)
Fundoscopy-
Disc swelling with blurred margin
Parapapillary flame shaped haemorrhage
Absence of venous pulse
Retinal blood vessels , peripheral retina
Foveal reflex within normal limit.

14. PROVISIONAL DIAGNOSIS
Bi-lateral Papilloedema
with
Essential Hypertension

15. DIFFERENTIAL DIAGNOSIS
 Intracranial space occupying lesion (ICSOL)
 Idiopathic intracranial hypertension (IIH)
 Malignant hypertension

16. Name of
disease
Points in favour Points in against
ICSOL Bilateral disc
swelling
No H/O headache, nausea,
vomiting ,seizure
No focal localizing signs.
IIH  Bilateral disc
swelling
Normal Retinal
blood vessels
No H/O headache.
Malignant
hypertension
Bilateral disc
swelling
BP is not too high
In retina- generalized
vasoconstriction or segmental
dilatation are absent & retinal
background is normal.

17. INVESTIGATIONS
CBC
 Hb % - 13.4 g/dl
 ESR - 30 mm in 1st hr
 WBC - 7.4x109/L
 Platelet - 228x109/L
Blood Sugar(F) - 6.2mmol/L
ECG - WNL
Urine for R/E - Normal

18. Blood for lipid profile
 S. Cholesterol - 227 mg/dl
 S. TG - 101 mg/dl
 HDL cholesterol - 34 mg/dl
 LDL Cholesterol - 134 mg/dl
Serum FT4, TSH
Serum Electrolytes WNL
Serum Urea, Creatinine
Lumbar puncture - Flow - normal

19. MRI OF THE BRAIN & OPTIC NERVE

20. MRI OF THE BRAIN & OPTIC NERVE

21. MRI OF THE BRAIN & OPTIC NERVE

22. MRV OF THE BRAIN

23. VISUAL FIELD ANALYSIS
RIGHT EYE
LEFT EYE

24. FINAL DIAGNOSIS
IDIOPATHIC INTRACRANIAL HYPERTENSION
with
ESSENTIAL HYPERTENSION

25. TREATMENT
 Weight reduce.
 Tab . Acetazolamide 250 mg
1+1+1
 Tab . Potassium chloride 600 mg
1+1+1 (after meal)
 Tab . Amlodipine 5 mg
0+0+2
 Tab . Atenolol 50 mg
1+0+0

26. On discharge
 V/A- 6/6 (un aided); N-6 (both eye)
 No double vision
 Pupil (both eye): Equally round & reactive to light
& accommodation
 Fundus
- Papilloedema
- Venous congestion Reduced
- Venous dilatation

27. FOLLOW-UP
Patient was properly counseled about the
recurrence & complication of IIH. She was
advised to report to us after 2 weeks for further
follow up.

28. Colour Fundus Photography
Hyperemia
Dilated blood vessels
Blurred margin
02-09-2012
04-11-2012

30. IDIOPATHIC INTRACRANIAL HYPERTENSION
Pseudotumor Cerebri
Benign Intracranial Hypertension

31. DEFINITION
It may be defined as
 Raised intracranial pressure
** >250mm water .
 In the absence of
** Space occupying lesion.
** Enlarged Ventricle .
** Abnormal CSF .

32. EPIDEMIOLOGY
 General population - 1 / 100,000 / yr
 Women aged 15 – 44 years - 3.5 / 100,000 / yr
 Women BMI >29 - 20 / 100,000 / yr

33. DIAGNOSTIC CRITERIA
Dandy criteria (1937)
Symptoms and signs of increased intracranial
pressure
No localizing neurologic signs.
CSF show increased pressure, but no cytologic or
biochemical abnormalities
Normal to small symmetric ventricles

34. Subsequent additions :
 The diagnostic lumbar puncture should be done with
the patient in the lateral decubitus position.
 Magnetic resonance imaging (MRI) or Venography
should be included to rule out intracranial space
occupying lesion or dural venous sinus thromboses.
 Other causes of intracranial hypertension should be
ruled out.

35. RISK FACTORS
 Age & sex : Mostly younger obese women.
 Exposure to or withdrawal from certain exogenous
substances
 Systemic diseases
 Disruption of cerebral venous flow
 Certain endocrine or metabolic disorders

36. SYMPTOMS OF IIH
1. Headache (90%)
2. Visual loss
 Transient (70%) or persistent (30%)
 Loss of contrast sensitivity
3. Pulsatile Tinnitis (60%)
4. Others (photopsia, diplopia)

37. OCULAR EXAMINATION
1. V/A - 6/6 in Both eye
2. Colour test - Trichromatic
3. Anterior segment - NAD
4. Adnexa - Within normal limit
5. Ocular motility - Full in all gazes , occasionally limited
abduction of one or both eye .
6. Fundus - Bi-lateral Papilloedema

38. Normal fundus Fundus of IIH

39. LABORATORY STUDIES
Blood test
a. Complete blood count (CBC)
b. Serum iron and iron-binding capacity
c. Antinuclear antigen (ANA) profile (e.g. anti- DNA)
d. Full procoagulant profile
CSF studies
It include :
a. Pressure
b. Cytology
c. Biochemistry

40. MRI AND MRV OF THE BRAIN
 The findings on neuroimaging studies include
o Normal or small slit like ventricles
o Enlarged optic nerve sheaths
o An empty sella
o Transverse sinus stenosis

41. VISUAL FIELD ANALYSIS
 Initially enlargement of blind spot and
gradually constriction of Visual Field(VF).
 Other VF defects (nasal defects, central
defects )

42. TREATMENT
Indication :
Severe symptoms
 Headache
 Visual loss

43. MEDICAL MANAGEMENT
 Weight control
For overweight patients.
 Oral medication
i. Carbonic anhydrase inhibitor (acetazolamide)
Orally 500mg bid for 4-5 weeks
ii. Frusemide (Lasix )
iii. To reduce headache
Amitriptyline, Propranolol or Topiramate
o If there is no response, consider Steroids

44. Steroids
 It is used to hasten recovery in patients who present
with severe papilloedema and a progressive loss of
visual field in one or both of the eyes.
 I/V Dexamethasone 4mg 6 hourly for 1-2 weeks.
 If vision is deteriorate, consider surgery.

45. SURGICAL MANAGEMENT
 Optic nerve sheath fenestration
(decompression)

46.  Cerebrospinal fluid (CSF)
diversion
 Lumbo-peritoneal shunt
 Ventriculo-peritoneal shunt

47. PROGNOSIS
 Spontaneous remission (3-12 months)
May be remitting and relapsing or develop into
chronic condition.
 Recurrence (10%)

48. “Idiopathic Intracranial Hypertension?”
- Vision loss no longer!
If untreated ultimately may lead to irreversible
vision loss .
Papilloedema Optic atrophy

49. FOLLOW-UP
It depends on:
 Initial visual function of the patient
 Underlying disease causing increased ICP
 Perceived compliance of the patient with medical
therapy
The patient can be observed every 3-4 weeks to look
 V/A
 Pupil
 Fundus
 VFA

50. CONCLUSION
Idiopathic intracranial hypertension (IIH) is a
disorder of unknown etiology that may lead to
progressive optic atrophy & blindness.
Although IIH may appear to be self-limiting, it is
considered to be a chronic disorder; patients should
be instructed to return to an ophthalmologist if
symptoms of increased ICP occur.

51. Idiopathic intracranial hypertension (IIH) is a
disorder of unknown etiology that predominantly
affects obese women of childbearing age. It may
lead to progressive optic atrophy and blindness.It
is essential to educate patients regarding the
potential for disabling blindness. Although IIH
may appear to be self-limiting, it is considered to
be a chronic disorder; therefore, once the
medications given to treat it are tapered off,
patients should be instructed to return to an
ophthalmologist if symptoms of increased ICP
recur.

53. 1. Symptoms and signs of increased intracranial
pressure is present
2. Localizing neurologic signs are present
3. Mostly occur in younger obese women
4. MRI should be included to rule out intracranial
space occupying lesion .

54. 2. Localizing neurologic signs are present

56. Fundus of IIH Fundus of Malignant Hypertension