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a 7 year old MALE child presented to ALMANAQIL PEDIATRICS HOSPITAL acutely with QUININE ASSOCIATED BLINDNESS.
The child was diagnosed with P. falciparum MALARIA (no cerebral component) .
the child was inadvertently administered nearly 4 times RECOMMENDED QUININE dose via home I.M. route.
Within 30 minutes, the child was noted bumping into furniture and was shortly completely BLIND. Within 60-90 minutes, the child was brought into the hospital by a very concerned Mother.
Unfortunately, obtaining a serum QUININE LEVEL not possible.
ADDITIONALLY, by physical inspection, the child could not detect light nor forms.
Pupils were fixed , dilated and non-responsive to light.
He was afebrile and normotensive. Other of physical exam was non contributory.
.
Ophthalmolgic examination not performed.
CBC: WBC 9 , Hgb 11.9 , PLT 351
ULTRAFILTRATION was being considered for the child however, given this war crises, it would be delayed.
THEREFORE, we came up with combination of SYSTEMIC GLUCOCORTICOID and ORAL NIFIDIPINE.
This was based upon review of the literature (in keeping with theory that QUININE TOXICITY induces a RETINAL ARTERY SPASM)combined with easy assess and low toxicity of the medication.
THEREFORE, 10mg DEXAMETHASONE given IV to the child by ME , DR.RAHMA .
10 min later, the child could see figures in visual field.
30 minutes thereafter, NIFEFIPINE 5mg po given, At which point the child was seeing light.
The Nifedipine 5mg PO 8hrs continued for 2 more doses inhospital.
the DEXAMETHASONE 5mg IV also was continued on a12 hr basis , the child was discharged on only ORAL PREDNISOLONE for next 5 days.
The child had return of complete sight, within 16 hours, in house.
_ POTENTIAL TOXICITIES AND ADVERSE REACTIONS WITH QUINONE INCLUDE :
Idiopathic thrombocytopenia purpura (ITP) and thrombotic thrombocytopenic purpura (TTP) with chronic renal impairment, disseminated intravascular coagulation (DIC), Neutropenia, hemolytic uremic syndrome (HUS) ,Optic neuritis and atrophy,QTC prolongation,
Tinnitus cinchonism (risk of cinchonism is directly related to dose and duration of therapy).
_ Serious HYPERSENSITIVITY reactions include:
anaphylactic shock, anaphylactoid reactions, urticaria.
_ serious skin RASHES, include:
Stevens-Johnson syndrome and toxic epidermal necrolysis, angioedema, facial edema and bronchospasm.
QUININE RELATED BLINDNESS :
there is mean time of onset of blurred vision of 6 to 15 hours.
while usually gradual, it can also be sudden .
It may last up to 10 W but generally recovery up to 3 W .
however patient may become permanently blind.
_ OPHTHALMIC FINDINGS during the acute phase is :
dilated pupils and unresponsiveness to light .
_OPHTHALMOSCOPIC APPEARANCE :
- In some cases the retinal vessels have appeared narrowed early.
- In another cases the retina appeared edematous and the papilla hyperemic.
- In yet other cases the fundi appeared normal at an early stage while the patient was already losing vision.
FUNDUSCOPIC CHANGES due to QUININE TOXICITY appear to be seen only when vision is improving,suggesting a direct toxic effect to the neuro retina layers.
ELECTRORETINOGRAPHIC CHANGES suggest quinine directly affects the photoreceptor and ganglion cell layers.
FURTHER, Quinine has a CURARE-LIKE action on neuromuscular junctions, which includes an anticholinergic action such as mydriasis.
PUPILLARY DILATATION (MYDRIASIS) is a consistent feature of quinine toxicity.
In some patients the pupillary changes may be so extreme that the patient is left with dilated atrophic pupils.
most cases left with permanent retinal and neurological damage from QUININE, in setting of serum Quinine levels more than 10.
REGARDING TREATMENT for QUININE ASSOCIATED BLINDNESS :
_ FOR years believed to be ONLY SUPPORTIVE.
_NOW there are several suggested treatments aimed at REDUCING the SERUM QUININE LEVELS and the RETINAL ARTERY SPASM including:
1.ULTRAFILTRATION.
2. NIFEDIPINE .
3.STELLATE GANGLION BLOCK.
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