optometry is discussed here, eye diseases and disabilities are highlighted and management of such ocular conditions enumerated.
Friday, 27 July 2012
ABC of Ocular Pharmacology for Optometrists in Nigeria.
Drugs in pharmacology are chemical substances used in the treatment, cure, prevention and/or diagnosis of disease or used to otherwise enhance physical or mental well-being.
["Drugs." Dictionary.com Unabridged (v1.1)].
Stedman's Electronic Medical Dictionary denotes drug as a"Therapeutic agent; any substance, other than food, used in the prevention, diagnosis, alleviation, treatment, or cure of disease."
Ocular drugs are by implication therapeutic/chemical agents meant to prevent, treat, cure or diagnose eye diseases.
Clinical pharmacology studies the pharmacology of therapeutic agents in the treatment, cure, prevention, management or diagnosis of a disease.
Historically, clinical ocular pharmacology was developed in the early nineteenth century but advances in this field has since became the norm and drug therapy based mainly on empiric, palliative and often toxic outcomes are today being advanced to be curative, less toxic and better enhanced to actualize set objectives of the drugs. {Williams BP, et al. (abstract) . The birth of ocular Pharmacology in the 20th Century.}
The term ocular pharmacology or ocular clinical pharmacology on this blog discusses the pharmacokinetics and pharmacodynamics of drugs to manage, treat, cure, prevent or used for diagnosis purposes in the eye and its adnexa viz the lacrimal apparatus, the upper and the lower lid, the orbital fats and the orbital cavity and ocular vascular supplies.
The process of absorption, distribution, metabolism (biotransformation), and elimination of drugs by the body is known as pharmacokinetics. Pharmacodynamics of drug is the quantitative relationship between drug and effect (mechanism of drug action).
[Iain L.O. Buxton, (2006). The pharmacological basis of therapeutics.]
The cornea, the conjunctival epithelium, the sclera, the ocular blood barrier and the ocular brain barrier remains the most important barrier to drug interaction (topical or systemic) with the host site of action in the process of drug pharmacodynamics of ocular intended medications.
The ocular blood barrier is formed by the endothelium of the retinal vessels, the cilliary epithelium and the retinal pigment epithelium.
(Peiffer, et al., (2001). Small animal ophthalmology: problem oriented-approach. Elsevier Hlth Sci. p. 46).
Ocular drug therapy is administered via
a) Eye drops
b) Eye ointments
c) Ocular injections.
a) & b) above are known as topical route of drug administration in the sense that they come in contact with the cornea, the conjunctival epithelium and the sclera and most often effective on the anterior 1/6th of the ocular globe viz the the iris, the cilliary process & cilliary body, the aqueous humour, the cornea, the conjunctival body and other superfacial ocular vascular supplies.
To enhance their pharmakokinetics of eye drops & eye ointments, the following factors are considered:
1) Concentration of the drops
2) Solubility
3) Viscosity
4) Lipid/Aqueous affinity
5) Surfactants
6) Reflex tearing factor
7) Tissue Binding factor etc.
On the other hand, Ocular injections bypass the corneal barrier & the conjunctival epithelium to reach the posterior 5/6th of the globe. This route of drug administration usually results to more toxic than the eyedrops or the eye ointments but peak serum concentration is reached on time and efficacy of drugs is enhanced and prognosis of disease is often more clearer as therapeutic level of drug administered is usually high.
Ocular injections could be:
i) Peri-ocular {sub-conjunctival, sub-Tenon's & Retrobulbar}
ii) Intraocular {intercameral & intravitreal}
iii) Systemic.
Note: Usually refer to an experienced Ophthalmologist if you encounter conditions that require ocular injections.
Finally it should be noted that the corneal epithelium & corneal endothelium are hydrophobic while the corneal stroma is hydrophilic.
Thanks for your time... See you next time.
Dr Ezebuiroh Okwudiri Victor.
N/B: This write-up is a not-for-profit article.
Sunday, 3 June 2012
Diabetic Retinopathy, the role of the Optometrist!
Optom
Chronic hyperglycemia is characterized by a consistently elevated fasting blood sugar of at least 7 mmol/l (126 mg/dL) for a prolonged period to cause a systemic complication. Diabetes Mellitus is an example of chronic hyperglycemia. A Glycated hemoglobin HbA1c (the molecule of glucose in the cells of red blood cell in a period of 2 weeks to 1 month!) of more than 48 mmol/mol or 6.5% is diagnostic of Chronic hyperglycemia.
(Use of Glycated Hemoglobin (HbA1c) in Diagnosis of Diabetes Mellitus: Abbreviated report of WHO consultation, 2011)
Often times the body may develop hyperglycemia (an FBS level of at least 7mmol/l!) temporarily without inducing any body tissue damage. In other words, such elevated blood sugar level is not enough to disrupt the homeostasis of the body at that period of time and hence no metabolic imbalance complications are experienced by the body.
Chronic hyperglycemia has been reported to cause vascular microangiopathy and hence the various complications of Diabetes mellitus viz nephropathies, retinopathies and neuropathies. Vascular supply to various parts of the body provides the necessary nutrients to the human system and also provides systemic immunity and the oxygen necessary for life while at the same time removing wastes from the system.
Diabetes mellitus is best described as a metabolic disorder with heterogeneous etiologies which is characterized by chronic hyperglycemia and disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action (& in-action), or both.
{World Health Organization. Definition, Diagnosis and Classifications of Diabetes Mellitus and its complications. Part 1 : Diagnosis and Classification of Diabetes Mellitus. WHO/NCD/NCS/99.2 ed. Geneva, World Health Organization, 1999}.
The normal blood vessel has an enothelium lined von Willebrand factor (vWF)- a cell adhesion ligand that binds the endothelial cells with the vascular basement membrane and could be said to also reduce the tendency of blood leukocytes to aggregate on the endothelial surface. Also, the normal endothelium synthesizes Nitric oxide (NO), endothelial ADPase (which clears away platelet activator ADP {Adenosine 5'-diphosphate}) and PGI2 [postalglandin inhibitors 2] which inhibits blood leukocyte aggregation, abundance of growth factors like Vascular Endothelial Growth Factor (VEGF)and subsequent platelet activation.
In the normal state, the endothelium is in a state of homeostasis. This homeostasis could be disrupted by the presence of inflammation-inducing substance in the blood vessels or when the endothelium is been overwhelmed by oxidative stress or by direct influence of non-enzymatic absorption of glucose via the walls of the endothelium or by the effect of metabolic imbalance associated with Diabetes Mellitus or chronic hyperglycemia.
Endothelial activation is a precusor to endothelial dysfunction and subsequent atherosclerosis, retinopathies and nephropathies. Endothelial activation, secondary to the low inflammatory response, is a specific dysfunction of the endothelial intima of micro- and/or macro-vessels characterized by increased interaction of the intima with blood leukocytes and other inflammatory markers like postalglandins and complexly lead to vascular complications in Diabetes mellitus. Endothelial activation should be a primary criteria for identifying potential diabetic retinopathy complication. (Just saying!)
An injured endothelium secondary to oxidative stress on the intima, say, by blood clots or by oxidation of NO (Common in patients with chronic hyperglycemia) or from a torn thrombus or direct inhibition of endothelial homeostasis by non-enzymatic absorption of blood glucose, is characterized by an activated vWF factor, tissue factor (TF), VEGF, atherothrombus formation, subsequent activation of the fibrinogen cycle (which in Diabetics runs haywire with a poor fibrinolysis feedback!), micro- &/or macro- albuminuria etc. This leads to a cascade of complex reactions in platelet activation, adhesion, increased fibrinogen production, haphazard coagulation activations, formation of plagues in the presence of such risk factors like long term anabolic steroid use, hypercholesterolaemia, dyslipidaemia, smoking, high LDL {low density lipoprotein} cholesterol, hypertension and chronic hyperglycemia (very common in uncontrolled Diabetes Mellitus!).
Diabetic retinopathy results as a result of the endothelial insult and dysfunction.
There are two types of Diabetic retinopathy viz
(1) Wet Diabetic Retinopathy,
(2) Dry Diabetic Retinopathy.
(see my Blog [optometry.naija] on, "Pathogenesis of Retinopathies... In a bid to understanding the challenges it poses to the primary eye care Optometrist in the Nigerian setting!" to throw more light).
But among other things, a macular involvement in either wet or dry macular degeneration secondary to Diabetes is often classified as wet Diabetic Retinopathy cos of its tendency to be visually symptomatic!
To alter the effect of hyperglycemia on the endothelium and to return homeostasis in the vascular intima, insulin presence and insulin activation process must be restored; the hyperoxides that causes oxidative stress and hence subsequently inducing oxidative breakdown of endothelium anti-platelet by triggering activation of protein kinase C isoforms, increased hexosamine pathway, glucose autooxidation, increased methyl-glyoxal, formation of advanced gyceration products (AGEs) formation, and increased polyol pathway flux through a single process of over-production of mitochondrial superoxides should be altered by 'early' consistent use of antioxidants (even without evidence of retinal vascular microangiopathy).
[Maria Mohora et al., The sources and the targets of oxidative stress in the etiology of Diabetic complications. Romanian J. Biophys., Vol. 17, Bucharist, 2007.]
That been said, it becomes the sole priority of the Nigerian Optometrist to send patients for blood sugar screening, periodic Doppler ultrasonography (reduced blood flow rate and volume tends to decrease in diabetic patients), and to do a yearly dilated funduscopy to rule out subtle 'latent' diabetic retinopathies. Rubeosis Irides, cataract etc should be ruled out during ocular examinations. Tests to ascertain cholesterol levels should be done to rule out the role of cholesterol in the blood stream in forming plagues hence fast-forwarding atherothrombus formation in patients with chronic hyperglycemia. Co-management of diabetic morbidity with general physicians or with specialist endocrinologists in a bid to provide multi-approach system in tackling the syndrome should be our primary eye care priority.
We should emphasize on dieting, exercises, primary and secondary inhalation of smoke, hypertension control, obesity control and generally living a healthy lifestyle... It should stick to our memory that somehow obesity, comfortable living and sedentary lifestyle, with little or no exercise often provokes atherothrombus formations and could be said to trigger hexosamine pathway reaction that leads to pancreatic beta-cell destruction which begins with a resistance of insulin to circulating glucose, then glucose intolerance and finally glucose toxicity in the Islet of Langerhans... A vicious circle of chronic hyperglycemia common in type 2 diabetes becomes activated.
Type 1 Diabetes Mellitus on the other hand is an auto-immune condition that self-destructs the beta cells responsible for insulin secretion and presents with symptoms before 25 years.
For the record, Diabetes Mellitus is one of the most serious challenges to health care world-wide. According to recent projections it will affect 239 million people by 2010, doubling in prevalence since 1994. It is the 4th leading cause of blindness globally.
(Dr. David Kinschuck, Dr Robert H., Diabetic Retinopathy in primary care, Epidemiology, Pg 2., UK, 2010)
Diabetic retinopathy, especially at the advanced stage, leads to blindness. Go for diabetes screening today or get your blood sugar testing kit and watch what you eat. Happy new month.
Dr Okwudiri Victor Ezebuiroh
N/B: No financial interest is attached to this blog. It is primarily for education.
Chronic hyperglycemia is characterized by a consistently elevated fasting blood sugar of at least 7 mmol/l (126 mg/dL) for a prolonged period to cause a systemic complication. Diabetes Mellitus is an example of chronic hyperglycemia. A Glycated hemoglobin HbA1c (the molecule of glucose in the cells of red blood cell in a period of 2 weeks to 1 month!) of more than 48 mmol/mol or 6.5% is diagnostic of Chronic hyperglycemia.
(Use of Glycated Hemoglobin (HbA1c) in Diagnosis of Diabetes Mellitus: Abbreviated report of WHO consultation, 2011)
Often times the body may develop hyperglycemia (an FBS level of at least 7mmol/l!) temporarily without inducing any body tissue damage. In other words, such elevated blood sugar level is not enough to disrupt the homeostasis of the body at that period of time and hence no metabolic imbalance complications are experienced by the body.
Chronic hyperglycemia has been reported to cause vascular microangiopathy and hence the various complications of Diabetes mellitus viz nephropathies, retinopathies and neuropathies. Vascular supply to various parts of the body provides the necessary nutrients to the human system and also provides systemic immunity and the oxygen necessary for life while at the same time removing wastes from the system.
Diabetes mellitus is best described as a metabolic disorder with heterogeneous etiologies which is characterized by chronic hyperglycemia and disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action (& in-action), or both.
{World Health Organization. Definition, Diagnosis and Classifications of Diabetes Mellitus and its complications. Part 1 : Diagnosis and Classification of Diabetes Mellitus. WHO/NCD/NCS/99.2 ed. Geneva, World Health Organization, 1999}.
The normal blood vessel has an enothelium lined von Willebrand factor (vWF)- a cell adhesion ligand that binds the endothelial cells with the vascular basement membrane and could be said to also reduce the tendency of blood leukocytes to aggregate on the endothelial surface. Also, the normal endothelium synthesizes Nitric oxide (NO), endothelial ADPase (which clears away platelet activator ADP {Adenosine 5'-diphosphate}) and PGI2 [postalglandin inhibitors 2] which inhibits blood leukocyte aggregation, abundance of growth factors like Vascular Endothelial Growth Factor (VEGF)and subsequent platelet activation.
In the normal state, the endothelium is in a state of homeostasis. This homeostasis could be disrupted by the presence of inflammation-inducing substance in the blood vessels or when the endothelium is been overwhelmed by oxidative stress or by direct influence of non-enzymatic absorption of glucose via the walls of the endothelium or by the effect of metabolic imbalance associated with Diabetes Mellitus or chronic hyperglycemia.
Endothelial activation is a precusor to endothelial dysfunction and subsequent atherosclerosis, retinopathies and nephropathies. Endothelial activation, secondary to the low inflammatory response, is a specific dysfunction of the endothelial intima of micro- and/or macro-vessels characterized by increased interaction of the intima with blood leukocytes and other inflammatory markers like postalglandins and complexly lead to vascular complications in Diabetes mellitus. Endothelial activation should be a primary criteria for identifying potential diabetic retinopathy complication. (Just saying!)
An injured endothelium secondary to oxidative stress on the intima, say, by blood clots or by oxidation of NO (Common in patients with chronic hyperglycemia) or from a torn thrombus or direct inhibition of endothelial homeostasis by non-enzymatic absorption of blood glucose, is characterized by an activated vWF factor, tissue factor (TF), VEGF, atherothrombus formation, subsequent activation of the fibrinogen cycle (which in Diabetics runs haywire with a poor fibrinolysis feedback!), micro- &/or macro- albuminuria etc. This leads to a cascade of complex reactions in platelet activation, adhesion, increased fibrinogen production, haphazard coagulation activations, formation of plagues in the presence of such risk factors like long term anabolic steroid use, hypercholesterolaemia, dyslipidaemia, smoking, high LDL {low density lipoprotein} cholesterol, hypertension and chronic hyperglycemia (very common in uncontrolled Diabetes Mellitus!).
Diabetic retinopathy results as a result of the endothelial insult and dysfunction.
There are two types of Diabetic retinopathy viz
(1) Wet Diabetic Retinopathy,
(2) Dry Diabetic Retinopathy.
(see my Blog [optometry.naija] on, "Pathogenesis of Retinopathies... In a bid to understanding the challenges it poses to the primary eye care Optometrist in the Nigerian setting!" to throw more light).
But among other things, a macular involvement in either wet or dry macular degeneration secondary to Diabetes is often classified as wet Diabetic Retinopathy cos of its tendency to be visually symptomatic!
To alter the effect of hyperglycemia on the endothelium and to return homeostasis in the vascular intima, insulin presence and insulin activation process must be restored; the hyperoxides that causes oxidative stress and hence subsequently inducing oxidative breakdown of endothelium anti-platelet by triggering activation of protein kinase C isoforms, increased hexosamine pathway, glucose autooxidation, increased methyl-glyoxal, formation of advanced gyceration products (AGEs) formation, and increased polyol pathway flux through a single process of over-production of mitochondrial superoxides should be altered by 'early' consistent use of antioxidants (even without evidence of retinal vascular microangiopathy).
[Maria Mohora et al., The sources and the targets of oxidative stress in the etiology of Diabetic complications. Romanian J. Biophys., Vol. 17, Bucharist, 2007.]
That been said, it becomes the sole priority of the Nigerian Optometrist to send patients for blood sugar screening, periodic Doppler ultrasonography (reduced blood flow rate and volume tends to decrease in diabetic patients), and to do a yearly dilated funduscopy to rule out subtle 'latent' diabetic retinopathies. Rubeosis Irides, cataract etc should be ruled out during ocular examinations. Tests to ascertain cholesterol levels should be done to rule out the role of cholesterol in the blood stream in forming plagues hence fast-forwarding atherothrombus formation in patients with chronic hyperglycemia. Co-management of diabetic morbidity with general physicians or with specialist endocrinologists in a bid to provide multi-approach system in tackling the syndrome should be our primary eye care priority.
We should emphasize on dieting, exercises, primary and secondary inhalation of smoke, hypertension control, obesity control and generally living a healthy lifestyle... It should stick to our memory that somehow obesity, comfortable living and sedentary lifestyle, with little or no exercise often provokes atherothrombus formations and could be said to trigger hexosamine pathway reaction that leads to pancreatic beta-cell destruction which begins with a resistance of insulin to circulating glucose, then glucose intolerance and finally glucose toxicity in the Islet of Langerhans... A vicious circle of chronic hyperglycemia common in type 2 diabetes becomes activated.
Type 1 Diabetes Mellitus on the other hand is an auto-immune condition that self-destructs the beta cells responsible for insulin secretion and presents with symptoms before 25 years.
For the record, Diabetes Mellitus is one of the most serious challenges to health care world-wide. According to recent projections it will affect 239 million people by 2010, doubling in prevalence since 1994. It is the 4th leading cause of blindness globally.
(Dr. David Kinschuck, Dr Robert H., Diabetic Retinopathy in primary care, Epidemiology, Pg 2., UK, 2010)
Diabetic retinopathy, especially at the advanced stage, leads to blindness. Go for diabetes screening today or get your blood sugar testing kit and watch what you eat. Happy new month.
Dr Okwudiri Victor Ezebuiroh
N/B: No financial interest is attached to this blog. It is primarily for education.
Tuesday, 17 April 2012
Nigerian Optometry and the Role of Medication in Eye Care!
Optom
The scope of Optometry practice in Nigeria did not mention using medications to manage what it refers to 'minor ocular infection which does not pose a threat to integrity of the ocular or visual system'. But "manage" and "diagnosis" indirectly gives us access to using both diagnostics (drugs that help in diagnosis) and therapeutics (drugs that help in treating/managing disease conditions) without making us breakers of the law!
But come to think of this, what does this law refer to as, "minor" ocular infection that does not pose a threat to ocular or visual integrity? A patient of mine who I diagnose to have Angle closure Glaucoma viz positive family history of sudden and painful loss of sight, associated congestive cilliary injection around the corneo-limbal region, with a fixed & dilated pupil, whose intra-ocular pressure is way up the tonometric chart (@least 40 mm Hg on the affected eye!), with a reduced visual acuity of sudden onset and with so many other markers pointed at the culprit secondary Glaucoma, what do I do?
Of course we all know that the best thing to do is to find medical means to suppress the intra-ocular pressure at the same time providing him a referral service to a Glaucoma surgeon. In some cases, I give IV Mannitol or IV Diamox to facilitate reduction in IOP. I have been able to save many such eyes, subsequently send them to a Glaucoma surgeon to create filtration orifices in the eyes to ease the congestive tension ipsilaterally. Hypoxia is removed, patients sensory retina is preserved by the intervention I proffered, since asphyxiation of the sensory retina even for seconds could have apoptosis consequence on the neuro-retinal fibres.
This law sure needs to be reviewed as soon as possible! Yes the Cap 09 laws of the Federation!
Day to day practicing Optometrists are confronted by challenging eye conditions that require them, not only to diagnose but, to give urgent attention to the underlying cause of that eye conditions with the intention of removing the cause. Most of this attention given could be in form of medications or a combination of medication and glasses! It is therefore very important that basic knowledge of drugs especially those for diagnosing eye care conditions, those for managing eye conditions and those that might have visual side-effects.
Baring in mind that some systemic conditions presents ocular complications, it is not unwise to have basic knowledge of the disease pathology, identify medications that treat/manage these conditions, know the side-effects of these drugs both systemically and visually at the same time ensuring that the integrity of the eye is not compromised! Colleagues you will agree with me that such conditions like Diabetes and Hypertension are very chronic systemic conditions with obvious and sight threatening visual complications... Imagine an Optometrist managing the visual complications of these conditions without basic knowledge of the underlying conditions or the effect medications used for managing them may have on the entire visual apparatus. I see such systemic conditions with ocular complications almost on daily basis and I have to answer all their eye questions including those related to the systemic drugs used for managing those conditions, I have no other choice. What excuse would I give such patients if my knowledge of the diseases and the drugs are poor? I know that is not what they want to hear from their doctor! I have therefore fortified myself in anticipation of the inevitable.
Why should an Optometrist have a sound knowledge of drugs with visual consequence? As rhetorical as the question might sound, it sure presents the present crop of Optometrist practicing in Nigeria with a moralistic dilemma! If my above patient was referred to the nearest Ophthalmologist (who probably stay thousands of kilometres away), it will take him another two (2) to three (3) weeks before getting prepared enough to go see the Doctor & imagine the snail pace of being able to see the Ophthalmologist! The eye would probably be gone before the Ophthalmologist in Nigeria, who is busy fighting its eye care colleague (the Optometrist) over futile issues.
To become an eye care medical professional in this country and in the African continent & in the world, Optometry in Nigeria had better develop its place in ocular pharmacology. We need to press for more legislation to change the status quo of our scope of practice. There is no legislation on drug use in Optometry, we need to advance on that course. We need to start from the ABC of pharmacology and that is what this blog is all about. What is our intellectual hold on what drugs are made of, how drug pass the obvious ocular barriers to reach the targeted ocular spaces? What are the components of the drugs? What are the pharmacodynamics, pharmacokinetics of those drugs and how do they interact in their target site of actions? Knowing all these does it profit the patient or are we just struggling to out-compete the Ophthalmologists in providing comphehensive eye care services for the growing number of visually challenged persons?
Without doubt, Optometrists in Nigeria constitute the bulk of eye care providers in Nigeria. As primary eye care providers, we treat with glasses and other medications that protect eyesight... Subsequent blog will elaborate on some pointers that will educate us on the necessity for fully legislated drugs prescription right by practicing Optometrists.
Thanks!
The scope of Optometry practice in Nigeria did not mention using medications to manage what it refers to 'minor ocular infection which does not pose a threat to integrity of the ocular or visual system'. But "manage" and "diagnosis" indirectly gives us access to using both diagnostics (drugs that help in diagnosis) and therapeutics (drugs that help in treating/managing disease conditions) without making us breakers of the law!
But come to think of this, what does this law refer to as, "minor" ocular infection that does not pose a threat to ocular or visual integrity? A patient of mine who I diagnose to have Angle closure Glaucoma viz positive family history of sudden and painful loss of sight, associated congestive cilliary injection around the corneo-limbal region, with a fixed & dilated pupil, whose intra-ocular pressure is way up the tonometric chart (@least 40 mm Hg on the affected eye!), with a reduced visual acuity of sudden onset and with so many other markers pointed at the culprit secondary Glaucoma, what do I do?
Of course we all know that the best thing to do is to find medical means to suppress the intra-ocular pressure at the same time providing him a referral service to a Glaucoma surgeon. In some cases, I give IV Mannitol or IV Diamox to facilitate reduction in IOP. I have been able to save many such eyes, subsequently send them to a Glaucoma surgeon to create filtration orifices in the eyes to ease the congestive tension ipsilaterally. Hypoxia is removed, patients sensory retina is preserved by the intervention I proffered, since asphyxiation of the sensory retina even for seconds could have apoptosis consequence on the neuro-retinal fibres.
This law sure needs to be reviewed as soon as possible! Yes the Cap 09 laws of the Federation!
Day to day practicing Optometrists are confronted by challenging eye conditions that require them, not only to diagnose but, to give urgent attention to the underlying cause of that eye conditions with the intention of removing the cause. Most of this attention given could be in form of medications or a combination of medication and glasses! It is therefore very important that basic knowledge of drugs especially those for diagnosing eye care conditions, those for managing eye conditions and those that might have visual side-effects.
Baring in mind that some systemic conditions presents ocular complications, it is not unwise to have basic knowledge of the disease pathology, identify medications that treat/manage these conditions, know the side-effects of these drugs both systemically and visually at the same time ensuring that the integrity of the eye is not compromised! Colleagues you will agree with me that such conditions like Diabetes and Hypertension are very chronic systemic conditions with obvious and sight threatening visual complications... Imagine an Optometrist managing the visual complications of these conditions without basic knowledge of the underlying conditions or the effect medications used for managing them may have on the entire visual apparatus. I see such systemic conditions with ocular complications almost on daily basis and I have to answer all their eye questions including those related to the systemic drugs used for managing those conditions, I have no other choice. What excuse would I give such patients if my knowledge of the diseases and the drugs are poor? I know that is not what they want to hear from their doctor! I have therefore fortified myself in anticipation of the inevitable.
Why should an Optometrist have a sound knowledge of drugs with visual consequence? As rhetorical as the question might sound, it sure presents the present crop of Optometrist practicing in Nigeria with a moralistic dilemma! If my above patient was referred to the nearest Ophthalmologist (who probably stay thousands of kilometres away), it will take him another two (2) to three (3) weeks before getting prepared enough to go see the Doctor & imagine the snail pace of being able to see the Ophthalmologist! The eye would probably be gone before the Ophthalmologist in Nigeria, who is busy fighting its eye care colleague (the Optometrist) over futile issues.
To become an eye care medical professional in this country and in the African continent & in the world, Optometry in Nigeria had better develop its place in ocular pharmacology. We need to press for more legislation to change the status quo of our scope of practice. There is no legislation on drug use in Optometry, we need to advance on that course. We need to start from the ABC of pharmacology and that is what this blog is all about. What is our intellectual hold on what drugs are made of, how drug pass the obvious ocular barriers to reach the targeted ocular spaces? What are the components of the drugs? What are the pharmacodynamics, pharmacokinetics of those drugs and how do they interact in their target site of actions? Knowing all these does it profit the patient or are we just struggling to out-compete the Ophthalmologists in providing comphehensive eye care services for the growing number of visually challenged persons?
Without doubt, Optometrists in Nigeria constitute the bulk of eye care providers in Nigeria. As primary eye care providers, we treat with glasses and other medications that protect eyesight... Subsequent blog will elaborate on some pointers that will educate us on the necessity for fully legislated drugs prescription right by practicing Optometrists.
Thanks!
Monday, 26 March 2012
Pathogenesis of Retinopathies... In a bid to understanding the challenges it poses to the primary eye care Optometrist in the Nigerian setting!
Optom
Retinopathy is a retinal disease that targets blood vessels in the retinal vasculature! Weakening of blood vessels is the focus of the disease while disruptions of vascular blood supply (ischaemia), leaking of tiny blood vessels (aneurysms), leaking of blood nutrients like lipids into the transparent retina (hard exudate/edematous macular), ischaemia-induced retinal nerve-ending apoptosis (soft exudate), blockage of blood vessels (thrombosis), formation of new blood vasculatures in non-vascular routes (neovascularization) like rubeosis iridis, rupture of neovascularized vessels due to mechanical pressure (retinal/sub-retinal/vitreous hemorrhages) are some of the common signs of most retinopathies.
It should not be disputed, this eye disease can easily cause irreversible or absolute blindness. Hence it is very important to know about this condition as early as an Optometrist can and be able to make a blindness' saving decision while not leaving any stone unturned.
Retinopathy can be proliferative or non-proliferative. A retinopathy is proliferative if blood vessel rupture is accompanied by neovascularization of blood vessels along the surface of the retina. A non-proliferate retinopathy is a type of retinopathy without rupture of blood vessels and without neovascularization of the retina.
Different systemic diseases like Diabetes, Hypertension, Sickle cell, etc, causes retinopathy; or it can be caused by pre-term delivery (Retinopathy of Prematurity), and due to idiopathic consequences (central serous retinopathy). Occlusions of any part of the central retinal arteries or veins can lead to retinopathy. By far, the most important Retinopathies are those caused by Diabetes or Hypertension, because of the classical picture they often leave behind in the acute phase of this disease and because they commonly affect alot of people all over the world.
Diabetes is a systemic disease characterised by chronic hyperglycemia. Diabetes retinopathy is a result of micro-vascular endothelial defect commonly referred as micro-angiopathy. Hyperglycemia promotes artherothrombosis process by making blood to form clots, to adhere to the endothelial plagues which results from age, nutrition and genetics. The formation of thrombus in the small retinal vessels and else where triggers aneurysms, occlusions of the retinal Vein or Artery, formation of neovascularization, formation of Vascular Endothelial Growth Factor (VEGF) in neovascularization and other inflammatory processes, subsequent degeneration of the retinal-blood barrier paints a picture of the classical signs of Diabetic retinopathy.
Hypertension breaks down vascular homeostasis by the increased wear and tear associated with elevated blood pressure for a prolonged period of time. Hypertension is a result of hardened (slerosing) blood vessels due to age (involutional sclerosis) or some other risk factors like smoking on the normal cardiovascular activity. The effect of the increasing 'pump' rate on the vessels to compensate for arterial resistance and the subsequent vaso-constriction of capillaries and other small vessels in the retina leads to increased vascular permeability and associated related retinopathy due to Hypertension. This high blood pressure also causes arteriolosclerosis (secondary to injury of on the endothelial surface of retinal arterioles) which is very important in formation of hypertensive retinopathy.
The pathogenesis of Retinopathy of Prematurity highlights the importance of Oxygen to the Retina. The Retina of the pre-term baby is characterised by under-developed retinal vessels. Due to oxygen treatment a poorly understood process leads to neovacularizations. The neovascularization seems to be a biological compensatory process that has gone viral. VEGF is a major factor in this disease process.
Sickle-cell retinopathy has its pathogenesis in the associated retinal hypoxia resulting from haemoglobinopathy, a feature of sickle-cell anaemia.
To be continued...
Thanks,
Dr Ezebuiroh Victor Okwudiri.
Retinopathy is a retinal disease that targets blood vessels in the retinal vasculature! Weakening of blood vessels is the focus of the disease while disruptions of vascular blood supply (ischaemia), leaking of tiny blood vessels (aneurysms), leaking of blood nutrients like lipids into the transparent retina (hard exudate/edematous macular), ischaemia-induced retinal nerve-ending apoptosis (soft exudate), blockage of blood vessels (thrombosis), formation of new blood vasculatures in non-vascular routes (neovascularization) like rubeosis iridis, rupture of neovascularized vessels due to mechanical pressure (retinal/sub-retinal/vitreous hemorrhages) are some of the common signs of most retinopathies.
It should not be disputed, this eye disease can easily cause irreversible or absolute blindness. Hence it is very important to know about this condition as early as an Optometrist can and be able to make a blindness' saving decision while not leaving any stone unturned.
Retinopathy can be proliferative or non-proliferative. A retinopathy is proliferative if blood vessel rupture is accompanied by neovascularization of blood vessels along the surface of the retina. A non-proliferate retinopathy is a type of retinopathy without rupture of blood vessels and without neovascularization of the retina.
Different systemic diseases like Diabetes, Hypertension, Sickle cell, etc, causes retinopathy; or it can be caused by pre-term delivery (Retinopathy of Prematurity), and due to idiopathic consequences (central serous retinopathy). Occlusions of any part of the central retinal arteries or veins can lead to retinopathy. By far, the most important Retinopathies are those caused by Diabetes or Hypertension, because of the classical picture they often leave behind in the acute phase of this disease and because they commonly affect alot of people all over the world.
Diabetes is a systemic disease characterised by chronic hyperglycemia. Diabetes retinopathy is a result of micro-vascular endothelial defect commonly referred as micro-angiopathy. Hyperglycemia promotes artherothrombosis process by making blood to form clots, to adhere to the endothelial plagues which results from age, nutrition and genetics. The formation of thrombus in the small retinal vessels and else where triggers aneurysms, occlusions of the retinal Vein or Artery, formation of neovascularization, formation of Vascular Endothelial Growth Factor (VEGF) in neovascularization and other inflammatory processes, subsequent degeneration of the retinal-blood barrier paints a picture of the classical signs of Diabetic retinopathy.
Hypertension breaks down vascular homeostasis by the increased wear and tear associated with elevated blood pressure for a prolonged period of time. Hypertension is a result of hardened (slerosing) blood vessels due to age (involutional sclerosis) or some other risk factors like smoking on the normal cardiovascular activity. The effect of the increasing 'pump' rate on the vessels to compensate for arterial resistance and the subsequent vaso-constriction of capillaries and other small vessels in the retina leads to increased vascular permeability and associated related retinopathy due to Hypertension. This high blood pressure also causes arteriolosclerosis (secondary to injury of on the endothelial surface of retinal arterioles) which is very important in formation of hypertensive retinopathy.
The pathogenesis of Retinopathy of Prematurity highlights the importance of Oxygen to the Retina. The Retina of the pre-term baby is characterised by under-developed retinal vessels. Due to oxygen treatment a poorly understood process leads to neovacularizations. The neovascularization seems to be a biological compensatory process that has gone viral. VEGF is a major factor in this disease process.
Sickle-cell retinopathy has its pathogenesis in the associated retinal hypoxia resulting from haemoglobinopathy, a feature of sickle-cell anaemia.
To be continued...
Thanks,
Dr Ezebuiroh Victor Okwudiri.
Friday, 9 March 2012
A Reply to Kelechi Show!
Optom
Hey colleague! Am really very pleased that my blog is receiving attention from people like you in the North Americas. I saw your comment in my blog titled "Training Optometrists receive in Nigerian Universities".
First Optometry in Nigeria is still @ its teething stage but I must tell you that much water has crossed the bridge...
To start with, Nigerian Optometry has not fully been assimilated into the Ministry of Health & our regulatory Board (see my blog on "Legal codes for practicing Optometry in Nigeria?") is flexing its flabby muscles in a desperate bit that only takes us further down the path of 'isolation' from the public health care hierarchy in this country! It means that there is 90% chance of ending up in the private Optometry practice which often comes with little or no benefits (am not saying that private practice in Optometry is not lucrative but over sight duties of the Board in form of its disciplinary committee [See Part V section 22 of Decree 34 of December 1989 which in recent times is known as the popular Cap 09, Laws of the Federation of Nigeria 2004] is very much lacking for instance!) while the very few openings in the Federal health sector is lobbied with gusto!
The average Optometrist working in a private clinic in this country earns between N35, 000.00- N150, 000.00 ($ 250 dollars- $ 1, 000.00 dollars) per month! Most of the private clinics are under-equipped and sharp practices have become the order of the day partly because the Board is too lazy to effectively carry out her oversight duties... It's a more or less money collecting Board than professionally poised group. Partly its as a result of high costs of eye care equipments, the willingness of people accessing eye care for cost purposes, for ignorance purposes, lack of know how in the field and for myriads of other reason!
Though the Board in recent times is trying to show some courage! Under his watch, Dr Ntem, the current Registrar of the Board, continuing education (CE) as obtained in North America, Canada, Australia etc has come to stay! Every practicing Optometrist must obtain 15 units of their general yearly units from continuing education (C.E.) while the yearly organised General Conference fetches the remaining points.
I must tell you this, a semblance of professional audacity is claiming the entire ODORBN structure! Like for instance inter-school conferences of the Board student Board members known by its acronym NOSA aka Nigerian Optometrists students Association is taking a particular professional turn that encourages me on the future of this noble profession! In their third annual conference, NOSA Conference in IMSU (Imo state University Owerri) at the school of Optometry in the faculty of Medical and Health Education, I was there on humanitarian grounds and was pleased by the prevailing professional aura that presided the conference! Again, I will personally commend the professionalism being entrenched in Optometry in Nigeria since the CE became part of our requirements. Still its not yet time to start celebrating!
To this end, I will be very pleased if you decide to come practice here in Nigeria but, do not be fooled, its going be very challenging! There exists only minimal relationship between the Nigerian Optometrists and their counterpart eye care colleague, the Ophthalmologists, in terms of blindness prevention, inter-referral or co-managements. The later finds it very easier to work with ophthalmic nurses in their quest to achieve vision 2020 goals than to co-manage patients with us, except we work for them! This has resulted in many cases of unnecessary blindness in the Nigerian populace.
I do not all that blame the divisiveness between Ophthalmologists, General physicians etc with the Optometrists on the former as I blame it on the professional foundation in our schools! Most of our newly inductees often find it very challenging to perform acceptably without much baby-sitting by a senior colleague. More than 65% cannot perform a Retinoscope examination with 80% accuracy while 50% cannot view the optic nerve with 90% accuracy.
Our schools are understaffed with mostly dissatisfied Optometrists who might not be fully prepared to pass on knowledge to young Optometrists for the purpose of developing the profession. There is often no good remuneration and no means to go for oversea trainings as often required by law. Other lecturers might have other businesses that keeps distracting them from their professional calling or some others might be sit-at-home-do-nothing lecturers who are not practicing and yet others that can't even keep clinics afloat talk less of effectively training the leaders of tomorrow!
I was on hand in IMSU during the Conference's free eye treatment session and there was no supervising lecturer(s)! I was horrified at the whole lackadaisical posturing of some of our lecturers!Again, the Board's oversight on schools are condemnable! There was no day a single official from the Board visited my school and the school clinic for inspection (from 2000-2006), except during our induction in 2007 when a representative from ODORBN visited- not to inspect rather to preside in the induction. That's why some of our colleagues cannot boldly tell the minimum Blood pressure (BP) that defines hypertension! This CE introduced by the Dr Ntem's ODORBN is highly commendable or else I do not know what would have become of us.
Our ODORBN code of conduct states in Part 1 section 8, "Foreign-trained practitioners are expected to undego a professional Board assessment (i.e. proficiency test) of their qualification(s) before they can be registered with the Board..."
Again, in the Act of Parliament that established ODORBN (Optometrists and Dispensing Optician Registration board of Nigeria) in 1989, now famously known as Cap 09 of the laws of the Federation 2004, puts it thus:
"Where a person satisfies the Board- ...(b) that he holds or has passed examinations necessary for obtaining some qualification granted outside Nigeria which is for the time being accepted by the Board for the purposes of this section as respects the capacity in which, if employed, he is to serve; and
(c) he pays any fee prescribed for registration,
The Board may, if it thinks fit, give a direction that he shall be temporarily registered."
These are the necessary things required of you to come home and practice Optometry!
In Nigeria, the qualification(s) for registration as a member of Optometrists and Dispensing opticians Registration board of Nigeria [ODORBN] is outlined in Cap 09, Laws of the Federation 2004 in Schedule three [Section 10(1) and (4)]:
Accepted minimum qualification for the purpose of registration on the register established under this Act
For Optometry -
1) Diploma in Optometry obtained before 1976.
2) B.Sc. in Optometry.
3) O.D. (Doctor of Optometry).
4) Any equivalent qualification from a recognised institution.
For Dispensing Optics-
1) Certificate of the National Institute,
2) Diploma in Dispensing Optics,
3) Any equivalent qualification from a recognised institution.
I hope this article will be of help Dr Kelechi Show!
Thanks,
Dr Ezebuiroh Victor Okwudiri.
N/B: This blog attracts no financial assistance anywhere & the opinions here are technically mine!
Kelechi
ShowMar 4, 2012 01:46 PM
Wow, I am very moved by your statement. I
am a Nigerian but trained in the US as an optometrist. I will be going back to
Nigeria to practice but unaware of the eyecare climate back home.I wanted your
advice on what the most pressing issue is so that I'm prepared.
Kelechi Show
Kelechi Show
....
Hey colleague! Am really very pleased that my blog is receiving attention from people like you in the North Americas. I saw your comment in my blog titled "Training Optometrists receive in Nigerian Universities".
First Optometry in Nigeria is still @ its teething stage but I must tell you that much water has crossed the bridge...
To start with, Nigerian Optometry has not fully been assimilated into the Ministry of Health & our regulatory Board (see my blog on "Legal codes for practicing Optometry in Nigeria?") is flexing its flabby muscles in a desperate bit that only takes us further down the path of 'isolation' from the public health care hierarchy in this country! It means that there is 90% chance of ending up in the private Optometry practice which often comes with little or no benefits (am not saying that private practice in Optometry is not lucrative but over sight duties of the Board in form of its disciplinary committee [See Part V section 22 of Decree 34 of December 1989 which in recent times is known as the popular Cap 09, Laws of the Federation of Nigeria 2004] is very much lacking for instance!) while the very few openings in the Federal health sector is lobbied with gusto!
The average Optometrist working in a private clinic in this country earns between N35, 000.00- N150, 000.00 ($ 250 dollars- $ 1, 000.00 dollars) per month! Most of the private clinics are under-equipped and sharp practices have become the order of the day partly because the Board is too lazy to effectively carry out her oversight duties... It's a more or less money collecting Board than professionally poised group. Partly its as a result of high costs of eye care equipments, the willingness of people accessing eye care for cost purposes, for ignorance purposes, lack of know how in the field and for myriads of other reason!
Though the Board in recent times is trying to show some courage! Under his watch, Dr Ntem, the current Registrar of the Board, continuing education (CE) as obtained in North America, Canada, Australia etc has come to stay! Every practicing Optometrist must obtain 15 units of their general yearly units from continuing education (C.E.) while the yearly organised General Conference fetches the remaining points.
I must tell you this, a semblance of professional audacity is claiming the entire ODORBN structure! Like for instance inter-school conferences of the Board student Board members known by its acronym NOSA aka Nigerian Optometrists students Association is taking a particular professional turn that encourages me on the future of this noble profession! In their third annual conference, NOSA Conference in IMSU (Imo state University Owerri) at the school of Optometry in the faculty of Medical and Health Education, I was there on humanitarian grounds and was pleased by the prevailing professional aura that presided the conference! Again, I will personally commend the professionalism being entrenched in Optometry in Nigeria since the CE became part of our requirements. Still its not yet time to start celebrating!
To this end, I will be very pleased if you decide to come practice here in Nigeria but, do not be fooled, its going be very challenging! There exists only minimal relationship between the Nigerian Optometrists and their counterpart eye care colleague, the Ophthalmologists, in terms of blindness prevention, inter-referral or co-managements. The later finds it very easier to work with ophthalmic nurses in their quest to achieve vision 2020 goals than to co-manage patients with us, except we work for them! This has resulted in many cases of unnecessary blindness in the Nigerian populace.
I do not all that blame the divisiveness between Ophthalmologists, General physicians etc with the Optometrists on the former as I blame it on the professional foundation in our schools! Most of our newly inductees often find it very challenging to perform acceptably without much baby-sitting by a senior colleague. More than 65% cannot perform a Retinoscope examination with 80% accuracy while 50% cannot view the optic nerve with 90% accuracy.
Our schools are understaffed with mostly dissatisfied Optometrists who might not be fully prepared to pass on knowledge to young Optometrists for the purpose of developing the profession. There is often no good remuneration and no means to go for oversea trainings as often required by law. Other lecturers might have other businesses that keeps distracting them from their professional calling or some others might be sit-at-home-do-nothing lecturers who are not practicing and yet others that can't even keep clinics afloat talk less of effectively training the leaders of tomorrow!
I was on hand in IMSU during the Conference's free eye treatment session and there was no supervising lecturer(s)! I was horrified at the whole lackadaisical posturing of some of our lecturers!Again, the Board's oversight on schools are condemnable! There was no day a single official from the Board visited my school and the school clinic for inspection (from 2000-2006), except during our induction in 2007 when a representative from ODORBN visited- not to inspect rather to preside in the induction. That's why some of our colleagues cannot boldly tell the minimum Blood pressure (BP) that defines hypertension! This CE introduced by the Dr Ntem's ODORBN is highly commendable or else I do not know what would have become of us.
Our ODORBN code of conduct states in Part 1 section 8, "Foreign-trained practitioners are expected to undego a professional Board assessment (i.e. proficiency test) of their qualification(s) before they can be registered with the Board..."
Again, in the Act of Parliament that established ODORBN (Optometrists and Dispensing Optician Registration board of Nigeria) in 1989, now famously known as Cap 09 of the laws of the Federation 2004, puts it thus:
"Where a person satisfies the Board- ...(b) that he holds or has passed examinations necessary for obtaining some qualification granted outside Nigeria which is for the time being accepted by the Board for the purposes of this section as respects the capacity in which, if employed, he is to serve; and
(c) he pays any fee prescribed for registration,
The Board may, if it thinks fit, give a direction that he shall be temporarily registered."
These are the necessary things required of you to come home and practice Optometry!
In Nigeria, the qualification(s) for registration as a member of Optometrists and Dispensing opticians Registration board of Nigeria [ODORBN] is outlined in Cap 09, Laws of the Federation 2004 in Schedule three [Section 10(1) and (4)]:
Accepted minimum qualification for the purpose of registration on the register established under this Act
For Optometry -
1) Diploma in Optometry obtained before 1976.
2) B.Sc. in Optometry.
3) O.D. (Doctor of Optometry).
4) Any equivalent qualification from a recognised institution.
For Dispensing Optics-
1) Certificate of the National Institute,
2) Diploma in Dispensing Optics,
3) Any equivalent qualification from a recognised institution.
I hope this article will be of help Dr Kelechi Show!
Thanks,
Dr Ezebuiroh Victor Okwudiri.
N/B: This blog attracts no financial assistance anywhere & the opinions here are technically mine!
Tuesday, 6 March 2012
Legal codes for practicing Optometry in Nigeria?
Optom
This question came to me from a NOSA (Nigerian Optometric Student Association) colleague and I have surfed every strand of Google internet world, Ask.com internet world, Yahoo internet world... every bit of the internet globesphere only to come out with a ziltch- there is no mention of Optometric legal code on the internet! Lets try rephrasing the question to suit the discussion!
Any professional body must have sets of regulations to maintain its ethical standards in providing services to the public & Optometry is by no means different, despite many distractions militating against this noble profession!
In Nigeria, Optometry had been regulated by a statutory body known as Optometrists & Dispensing Opticians Registration Board of Nigeria (ODORBN) which was establish by an Act of Parliament, Cap 09 of the Laws of the Federation of Nigeria 2004 ( formerly known as Decree No 34 of December , 1989). Part 1 section 1 Establishment of Optometrists and Dispensing Opticians Registration Board of Nigeria
(1) There is hereby established for optometrists and dispensing opticians a body to be known as the Optometrsts and Dispensing Opticians Registration Board of Nigeria (in this Act referred to as "the Board").
In this Act, Optometry is defined by what I had come to realize is a generally accepted definition of this noble profession in this country. It reads, "optometry" means a health-care profession specialising in the art and science of vision care and whose scope of practice includes-
(a) eye examinations to determine refractive errors and other departures from the optimally healthy and visually efficient eye;
(b) correction of refractive errors using spectacles, contact lenses, low vision aids and other devices;
(c) correction of errors of binocularity by means of vision training (orthoptics);
(d) diagnosis and management of minor occular infections which do not pose a threat to the integrity of the occular or visual system; and
(e) occular first aid;
(section 29 : interpretations of the Act)
And our profession is refered to as 'the profession of optometry or dispensing optics (dispensing opticians);'
I think here lies the legal codes or ethical "red line" in the practice of Optometry in Nigeria. (this opinion is technically mine!).
That Act of Parliament which came into effect in the 1990s defined the function of "the Board" in Part 1 section 1 (2) (a) determining what standards of knowledge and skills are to be attained by persons seeking to become members of the profession of optometry and dispensing optics and improving those standards from time to time as circumstances may permit; [ see Part IV sections 18, 19 & 20]
(b) securing in accordance with the provisions of this Act, the establishment and maintenance of a register of persons registered under this Act as members of optometry and dispensing optics and the publication from time to time of lists of those persons; [see Part II sections 8, 9 & 10]
(c) conducting examinations in the relevant profession, and awarding certificates or diplomas to successful candidates as appropiate; and for such purpose the Board shall prescribe fees to be paid in respect thereof; and
(d) performing the other functions conferred on the board by this Act. [ Advising the Minister on qualifiaction standard Part IV section 20 (2); forming a Disciplinary commitee in a bid to ensure compliance to professional Optometric ethics Part V section 22, 23 & 24 etc]
To help us keep in line with the dos and don'ts of this noble profession here it became pertinent for a Code of Conduct for ODORBN members to be formulated. According to Dr Chinenye Timothy (OD) in her "The Optometrist's Sheperd" abstract, "Code of Conduct is a set of written rules outlining the responsibilities of or proper conduct for an individual, party or organisation." It should be pointed out here that the Code of Conduct for ODORBN was adopted in August, 2010 and it became Effective from January 1st, 2011. This set of rules mirrors the larger provisions and rules and regulations of the Act of the Parliament Cap 09, 2004.
Please colleagues lets grab a copy of our code of conduct and do better than only scan through it...lets make it the ten commandment in clinical ethics as we keep digging deep to keep afloat with the responsibilities if a Professional. Am of the view though that this Act should be reviewed to embrace advances in Optometry intrnationally.
I hope I was of help?
Thanks,
Dr Victor Ezebuiroh Victor
Note: This blog has not financial attachment anywhere and every opinion here are mine!
This question came to me from a NOSA (Nigerian Optometric Student Association) colleague and I have surfed every strand of Google internet world, Ask.com internet world, Yahoo internet world... every bit of the internet globesphere only to come out with a ziltch- there is no mention of Optometric legal code on the internet! Lets try rephrasing the question to suit the discussion!
Any professional body must have sets of regulations to maintain its ethical standards in providing services to the public & Optometry is by no means different, despite many distractions militating against this noble profession!
In Nigeria, Optometry had been regulated by a statutory body known as Optometrists & Dispensing Opticians Registration Board of Nigeria (ODORBN) which was establish by an Act of Parliament, Cap 09 of the Laws of the Federation of Nigeria 2004 ( formerly known as Decree No 34 of December , 1989). Part 1 section 1 Establishment of Optometrists and Dispensing Opticians Registration Board of Nigeria
(1) There is hereby established for optometrists and dispensing opticians a body to be known as the Optometrsts and Dispensing Opticians Registration Board of Nigeria (in this Act referred to as "the Board").
In this Act, Optometry is defined by what I had come to realize is a generally accepted definition of this noble profession in this country. It reads, "optometry" means a health-care profession specialising in the art and science of vision care and whose scope of practice includes-
(a) eye examinations to determine refractive errors and other departures from the optimally healthy and visually efficient eye;
(b) correction of refractive errors using spectacles, contact lenses, low vision aids and other devices;
(c) correction of errors of binocularity by means of vision training (orthoptics);
(d) diagnosis and management of minor occular infections which do not pose a threat to the integrity of the occular or visual system; and
(e) occular first aid;
(section 29 : interpretations of the Act)
And our profession is refered to as 'the profession of optometry or dispensing optics (dispensing opticians);'
I think here lies the legal codes or ethical "red line" in the practice of Optometry in Nigeria. (this opinion is technically mine!).
That Act of Parliament which came into effect in the 1990s defined the function of "the Board" in Part 1 section 1 (2) (a) determining what standards of knowledge and skills are to be attained by persons seeking to become members of the profession of optometry and dispensing optics and improving those standards from time to time as circumstances may permit; [ see Part IV sections 18, 19 & 20]
(b) securing in accordance with the provisions of this Act, the establishment and maintenance of a register of persons registered under this Act as members of optometry and dispensing optics and the publication from time to time of lists of those persons; [see Part II sections 8, 9 & 10]
(c) conducting examinations in the relevant profession, and awarding certificates or diplomas to successful candidates as appropiate; and for such purpose the Board shall prescribe fees to be paid in respect thereof; and
(d) performing the other functions conferred on the board by this Act. [ Advising the Minister on qualifiaction standard Part IV section 20 (2); forming a Disciplinary commitee in a bid to ensure compliance to professional Optometric ethics Part V section 22, 23 & 24 etc]
To help us keep in line with the dos and don'ts of this noble profession here it became pertinent for a Code of Conduct for ODORBN members to be formulated. According to Dr Chinenye Timothy (OD) in her "The Optometrist's Sheperd" abstract, "Code of Conduct is a set of written rules outlining the responsibilities of or proper conduct for an individual, party or organisation." It should be pointed out here that the Code of Conduct for ODORBN was adopted in August, 2010 and it became Effective from January 1st, 2011. This set of rules mirrors the larger provisions and rules and regulations of the Act of the Parliament Cap 09, 2004.
Please colleagues lets grab a copy of our code of conduct and do better than only scan through it...lets make it the ten commandment in clinical ethics as we keep digging deep to keep afloat with the responsibilities if a Professional. Am of the view though that this Act should be reviewed to embrace advances in Optometry intrnationally.
I hope I was of help?
Thanks,
Dr Victor Ezebuiroh Victor
Note: This blog has not financial attachment anywhere and every opinion here are mine!
Saturday, 3 March 2012
Retinopathies & the challenges it presents to the Primary Eyecare Optometrist in The Nigerian Setting
Optom
The Retina is the light sensitive portion of the eye located posterior to the cornea. It is an exension of the central nervous system that processes the sense of sight. It consist lots of motor and sensory neural pathways, pigment proteins, and blood vessels. Anatomically, it sits on the Brush's membrane of the Choroid while been bathed by the vitreous body ventrally!
Diseases of the Retina could involve inflammations (as in uveitis etc) , weakening of blood vessels (as in Retinopathies) or formation of thrombosis (embolus embedded in the weakened retinal blood vessels!) or idiopathic retinal neural fibre cell apoptosis (as in Glaucoma) or degenerations of the rods & cone (as in Retinitis pigmentosa or Albinoic retina).
Retinopathy is a disease of the blood vessels of the retina which subsequently affects the other components of the retina by the formation of aneurysms, formation of retinal & sub-retinal haemorrhages, formation of new retinal vessels (neovascularizations), sipping of lipids or other intra-vascular fluids into the surrounding intra-retinal surroundings (hard exudates), apoptosis of retinal nerve endings (soft or cotton wool exudates) or the the formation of vitreous traction and subsequent retinal detarchment or retinal tear etc. This retinal disease can show symptoms almost immediatly or can take very long periods of time especially if it does not affect the macula.
Retinopathy could either be caused by Diabetes, Hypertension, Syphilis or as a result of premature delivery or due to unknown cause. Its very common in adults from 30 years and above and in preterms. Retinopathies can cause various vision problems ranging from low vision to outright blindness. Macula edema is one of the most important cause of low vision in patients with retinopathy. A detarched retina is one hell of a consequence of Retinopathy.
Retinopathy could be quiet but a comorbid condition of the disease causing condition can exaggerate the symptoms. The management of retinopathy with glasses is greatly affected by the presence of co-morbidity. A proliferative kind of retinopathy gives off a poor prognosis for glasses and other invasive procedures. Referal to a Retinal surgeon will suffice it but meanwhile patients are adviced to go for regular eye checks, they are made to understand the need to clinically reduce the primary disease and do alot of adjustments in their lives like to quit smoking etc.
The prevailing picture puts the Optometrist in a very tight corner when it comes to interventions against Retinopathies. It should be understood that any patient with Retinopathy who visits an Optometrist with reduced vision, sudden or delayed, expects sight restoration. Eye glass option is often the patient's first instincts, these patients are by now low vision patients. At this point it seems the uninformed Optometrist is merely walking the tight rope. If the Retinopathy is either proliferative or that the patient's macula was involved, the prognosis for glasses will look even more gloomier! It is therefore expected of us (Practicing Optometrists) to understand the pathogenesis of Retinopathy and hence play the card of preventive medicine as early as possible before the ugly sequela of this retinal disease but it should be understood that nothing will equate regular eye checks by risk group. Such persons that are 30 years and above are of high risk, patients suffering from Hypertension, Diabetes or combiniation of the two whose chronic disease conditions are not managed properly increases the chances of Retinopathy, patients with positive family history of Retinopathy are also at higher risk etc.
Finally, I will discuss different types of Retinopathy and how the Optometrist factors in in the different types of this retinal disease in subsequent blogs! Happy new month folks!
Dr Ezebuiroh Okwudiri Victor
N/B: No financial interest is attached to this blog...it's principally & technically free!
The Retina is the light sensitive portion of the eye located posterior to the cornea. It is an exension of the central nervous system that processes the sense of sight. It consist lots of motor and sensory neural pathways, pigment proteins, and blood vessels. Anatomically, it sits on the Brush's membrane of the Choroid while been bathed by the vitreous body ventrally!
Diseases of the Retina could involve inflammations (as in uveitis etc) , weakening of blood vessels (as in Retinopathies) or formation of thrombosis (embolus embedded in the weakened retinal blood vessels!) or idiopathic retinal neural fibre cell apoptosis (as in Glaucoma) or degenerations of the rods & cone (as in Retinitis pigmentosa or Albinoic retina).
Retinopathy is a disease of the blood vessels of the retina which subsequently affects the other components of the retina by the formation of aneurysms, formation of retinal & sub-retinal haemorrhages, formation of new retinal vessels (neovascularizations), sipping of lipids or other intra-vascular fluids into the surrounding intra-retinal surroundings (hard exudates), apoptosis of retinal nerve endings (soft or cotton wool exudates) or the the formation of vitreous traction and subsequent retinal detarchment or retinal tear etc. This retinal disease can show symptoms almost immediatly or can take very long periods of time especially if it does not affect the macula.
Retinopathy could either be caused by Diabetes, Hypertension, Syphilis or as a result of premature delivery or due to unknown cause. Its very common in adults from 30 years and above and in preterms. Retinopathies can cause various vision problems ranging from low vision to outright blindness. Macula edema is one of the most important cause of low vision in patients with retinopathy. A detarched retina is one hell of a consequence of Retinopathy.
Retinopathy could be quiet but a comorbid condition of the disease causing condition can exaggerate the symptoms. The management of retinopathy with glasses is greatly affected by the presence of co-morbidity. A proliferative kind of retinopathy gives off a poor prognosis for glasses and other invasive procedures. Referal to a Retinal surgeon will suffice it but meanwhile patients are adviced to go for regular eye checks, they are made to understand the need to clinically reduce the primary disease and do alot of adjustments in their lives like to quit smoking etc.
The prevailing picture puts the Optometrist in a very tight corner when it comes to interventions against Retinopathies. It should be understood that any patient with Retinopathy who visits an Optometrist with reduced vision, sudden or delayed, expects sight restoration. Eye glass option is often the patient's first instincts, these patients are by now low vision patients. At this point it seems the uninformed Optometrist is merely walking the tight rope. If the Retinopathy is either proliferative or that the patient's macula was involved, the prognosis for glasses will look even more gloomier! It is therefore expected of us (Practicing Optometrists) to understand the pathogenesis of Retinopathy and hence play the card of preventive medicine as early as possible before the ugly sequela of this retinal disease but it should be understood that nothing will equate regular eye checks by risk group. Such persons that are 30 years and above are of high risk, patients suffering from Hypertension, Diabetes or combiniation of the two whose chronic disease conditions are not managed properly increases the chances of Retinopathy, patients with positive family history of Retinopathy are also at higher risk etc.
Finally, I will discuss different types of Retinopathy and how the Optometrist factors in in the different types of this retinal disease in subsequent blogs! Happy new month folks!
Dr Ezebuiroh Okwudiri Victor
N/B: No financial interest is attached to this blog...it's principally & technically free!
Saturday, 18 February 2012
Follicular Kerato-Conjuntivitis in this boy of 3 years 2
Optom
Continuing on this discuss, in a previous blog I discussed the challenges I faced in managing this 3 year old boy with an Adenoviral type of Kerato-Conjunctivitis with heaps of periauricular lymph nodes superimposing the peripheral cornea of the left eye.
On the last two visits the young boy's eyes had shown a good prognosis. I am currently using a tappered dosing of the topical NSAID, an additional gutt: Ciprofloxacin i every 1hr.
Why did I not use steroids that immuno-suppresses such activitis? Why did I opt for an NSAID that would typically counteract the effect of prostalglandins on the compromised LE but wont influence immune responses? (Note the immune responses against allergens in the eyes manifests in the symptoms common with allergic conjunctivitis?). I might have been awed @ the corneal infiltrates & the exagerated dilatation of conjunctival vessels. I might have been too cautious in using a topical steroid because this hyper-active boy might be mechanically causing corneal abrassion whenever his eyes irritate him. (His parent said he does not itch his eyes, but who can tell?). I might have weighed the toxic/therapeutic consequences hence my choice of the NSAID over the corticosteroids.
I must have been too careful with the hazy cornea & the age of the boy, hence the use of Gutt: Ciprofloxacin to prophylactically check for opportunistic infection on the cornea. I did a flouresin examination of the cornea in each visit to ensure that the young boy's cornea remains intact.
It should come to our knowledge that allergic conjunctivitis of any type might not respond to a specific regimen of drug(s) but knowing its triggering factor is definately an important step in the right direction.
I have also noticed that prescribing glasses, when indicated, using cooling compresses & applying lubricants either in form of eyedrops or in form of ointments (like I used Chloramphenicol eye ointment both for its broad spectrum antibacterial property & for the viscous nature of the ointment), using antihistamines like Keturtifen Fumerates etc to reduce symptomatic itching, an immune response by the host eye to percieved allergens, have been shown to have tremendous influence in managing adenoviral Kerato-conjunctivitis...remember that type of conjunctivitis that could develop real membrane over the conjunctiva & even threatening to invade cornea itself? Recently, some researchers in clinical practice even suggested using 5% Betadine topical solution to flush off the adenoviral load on the surface of the eye! Betadine is a brand name for Povidone iodine known for its very strong antiseptic & antimicrobial charactaristics. It is often used in cataract surgery to sterilize the adnexa of the eyes in fight against opportunistic bacterias that causes Endophthalmitis.
I saw the young boy yesterday & his parents were very happy. His eyes was clearer. His vision has improved & the lustre of the eye was better. But I adviced her on keeping a close look out for any symptom on the boy's right eye & to gradually lower the dosage of all administered eyedrops... It was so good to be of help! Thanks
Dr Ezebuiroh Victor Okwudiri.
Note: This article is devoid of any financial requirements. Feel free to comment, it makes me feel better.
Our free Glaucoma screening exercise is still going on @Opposite Shell Pipeline. Happy weekend.
Continuing on this discuss, in a previous blog I discussed the challenges I faced in managing this 3 year old boy with an Adenoviral type of Kerato-Conjunctivitis with heaps of periauricular lymph nodes superimposing the peripheral cornea of the left eye.
On the last two visits the young boy's eyes had shown a good prognosis. I am currently using a tappered dosing of the topical NSAID, an additional gutt: Ciprofloxacin i every 1hr.
Why did I not use steroids that immuno-suppresses such activitis? Why did I opt for an NSAID that would typically counteract the effect of prostalglandins on the compromised LE but wont influence immune responses? (Note the immune responses against allergens in the eyes manifests in the symptoms common with allergic conjunctivitis?). I might have been awed @ the corneal infiltrates & the exagerated dilatation of conjunctival vessels. I might have been too cautious in using a topical steroid because this hyper-active boy might be mechanically causing corneal abrassion whenever his eyes irritate him. (His parent said he does not itch his eyes, but who can tell?). I might have weighed the toxic/therapeutic consequences hence my choice of the NSAID over the corticosteroids.
I must have been too careful with the hazy cornea & the age of the boy, hence the use of Gutt: Ciprofloxacin to prophylactically check for opportunistic infection on the cornea. I did a flouresin examination of the cornea in each visit to ensure that the young boy's cornea remains intact.
It should come to our knowledge that allergic conjunctivitis of any type might not respond to a specific regimen of drug(s) but knowing its triggering factor is definately an important step in the right direction.
I have also noticed that prescribing glasses, when indicated, using cooling compresses & applying lubricants either in form of eyedrops or in form of ointments (like I used Chloramphenicol eye ointment both for its broad spectrum antibacterial property & for the viscous nature of the ointment), using antihistamines like Keturtifen Fumerates etc to reduce symptomatic itching, an immune response by the host eye to percieved allergens, have been shown to have tremendous influence in managing adenoviral Kerato-conjunctivitis...remember that type of conjunctivitis that could develop real membrane over the conjunctiva & even threatening to invade cornea itself? Recently, some researchers in clinical practice even suggested using 5% Betadine topical solution to flush off the adenoviral load on the surface of the eye! Betadine is a brand name for Povidone iodine known for its very strong antiseptic & antimicrobial charactaristics. It is often used in cataract surgery to sterilize the adnexa of the eyes in fight against opportunistic bacterias that causes Endophthalmitis.
I saw the young boy yesterday & his parents were very happy. His eyes was clearer. His vision has improved & the lustre of the eye was better. But I adviced her on keeping a close look out for any symptom on the boy's right eye & to gradually lower the dosage of all administered eyedrops... It was so good to be of help! Thanks
Dr Ezebuiroh Victor Okwudiri.
Note: This article is devoid of any financial requirements. Feel free to comment, it makes me feel better.
Our free Glaucoma screening exercise is still going on @Opposite Shell Pipeline. Happy weekend.
Tuesday, 14 February 2012
Follicular Kerato-conjunctivitis in this boy of 3 year plus!
Optom
Happy Valentine Day folks!
Wow its just like yesterday, this time last year! What was I doing self in my last year valentine? I have forgotten... Okey I was googling, facebooking & optometry.naija was still a baby! Its really reasuring to know that somehow last year's love is still enough to go round this year...
Lets discuss a current clinical issue which I observed in managing a three year old boy whose mother brought to my clinic last week ( 7th February 2012). A boy of 3 years old presenting with a monocular redness on the L.E. the mother noticed in the child's eye the penultimate day. He had unilateral epiphora of the ipsilateral eye, mild edematous lids slightly warm & soft to feel. The was marked echymosis, perilimbal conjunctival membrane was masking early follicular infiltrations on the corneal surrounding.
There was no previous history of ill health. Child still goes to school but parents concern stems from the marked hyperemia on the left eye- it was like a pool of crimson redness!
On further observation, patient was very stubborn cos he uses his feet to kick me during diagnosis, there was no conjuntival membrane but lots of scattered papillae adorned the cul du sac like a flower wreath or just scattered. Parent said there was no associated itchiness, no discharges but strands of ropy discharge could be noticed. Cornea was slightly hazy & the follicular infiltrations on the perilimbal area, with @ least one follicular infiltration on the superior corneal area of the ipsilateral eye! These follicular infiltrations are hedge by heaps of periauricular lymph nodes that suddenly exagerated on patient's subsequent clinical appontment 3/7 days later.
The boy was very restless, not necessarily because of the eye condition. I think the boy could be hyper-active, just like many kid's of his age. The parent reports that there was no other sibling who had such similar conditions & this was patient's first eye care visit!
The boy could not identify any visual acuity chart neither was he paynig any attention to other cues. I went straight to applying Gutt: Procaine ii in 5 minutes interval for 15 minutes. This was to numb his over-sensitive L.E. cornea to give patient some soothing relief & prepare patient for the application of flouresin sodium strip on the affected eye for another 1 minute. I had to ensure that the infiltration had not invaded the epithelium of the cornea. The young boy barely allowed my torchlight close to him, hence I could check for the presence of keratic precipitate. The picture depicted a unique likelihood of Epidemic Keratoconjunctivitis.
Adenoviral infection in the eye is the cause of Epidemic Keratoconjunctivits. Treatment of this condition with steroids, topical NSAID, eye lubricant, cyclosporine, cold compress etc is tailored to the symptoms associated with the conjunctivitis. It is usually self-limiting but could cause consequenses!
I followed the typical treatment pattern but only that I replaced steroid with a combination of NSAID & gentamicin (Gutt: Diclogenta i every hour for 3 days & tapered to, Gutt: Diclogenta i qds 1/52). I applied gutt: Mydracyl 1% ii on the Right Eye . I prescribed oint: Chloramphenicol i noct, to soothe the eye & provide a lubricating cover. I added Tab:Vit C ii tds 1/52, Tab: Yeast ii tds 2/52.
In their return visit, I observed a marked improvement in child's vision. I have currently placed her on Gutt: Ciprofloxacin i every 1 hour. Their second visit was better, patient's eye has stopped tearing & the lid edema has gone down & the redness is reducing!
Thanks,
Dr Ezebuiroh Victor.
Note: 1) There is no financial attachment to this article!
2) Pan-Oj clinic & Diagnostic service limited opposite Shell pipeline is organizing a FREE GLAUCOMA screening from 14th february to 18ths february.
Thanks.
Happy Valentine Day folks!
Wow its just like yesterday, this time last year! What was I doing self in my last year valentine? I have forgotten... Okey I was googling, facebooking & optometry.naija was still a baby! Its really reasuring to know that somehow last year's love is still enough to go round this year...
Lets discuss a current clinical issue which I observed in managing a three year old boy whose mother brought to my clinic last week ( 7th February 2012). A boy of 3 years old presenting with a monocular redness on the L.E. the mother noticed in the child's eye the penultimate day. He had unilateral epiphora of the ipsilateral eye, mild edematous lids slightly warm & soft to feel. The was marked echymosis, perilimbal conjunctival membrane was masking early follicular infiltrations on the corneal surrounding.
There was no previous history of ill health. Child still goes to school but parents concern stems from the marked hyperemia on the left eye- it was like a pool of crimson redness!
On further observation, patient was very stubborn cos he uses his feet to kick me during diagnosis, there was no conjuntival membrane but lots of scattered papillae adorned the cul du sac like a flower wreath or just scattered. Parent said there was no associated itchiness, no discharges but strands of ropy discharge could be noticed. Cornea was slightly hazy & the follicular infiltrations on the perilimbal area, with @ least one follicular infiltration on the superior corneal area of the ipsilateral eye! These follicular infiltrations are hedge by heaps of periauricular lymph nodes that suddenly exagerated on patient's subsequent clinical appontment 3/7 days later.
The boy was very restless, not necessarily because of the eye condition. I think the boy could be hyper-active, just like many kid's of his age. The parent reports that there was no other sibling who had such similar conditions & this was patient's first eye care visit!
The boy could not identify any visual acuity chart neither was he paynig any attention to other cues. I went straight to applying Gutt: Procaine ii in 5 minutes interval for 15 minutes. This was to numb his over-sensitive L.E. cornea to give patient some soothing relief & prepare patient for the application of flouresin sodium strip on the affected eye for another 1 minute. I had to ensure that the infiltration had not invaded the epithelium of the cornea. The young boy barely allowed my torchlight close to him, hence I could check for the presence of keratic precipitate. The picture depicted a unique likelihood of Epidemic Keratoconjunctivitis.
Adenoviral infection in the eye is the cause of Epidemic Keratoconjunctivits. Treatment of this condition with steroids, topical NSAID, eye lubricant, cyclosporine, cold compress etc is tailored to the symptoms associated with the conjunctivitis. It is usually self-limiting but could cause consequenses!
I followed the typical treatment pattern but only that I replaced steroid with a combination of NSAID & gentamicin (Gutt: Diclogenta i every hour for 3 days & tapered to, Gutt: Diclogenta i qds 1/52). I applied gutt: Mydracyl 1% ii on the Right Eye . I prescribed oint: Chloramphenicol i noct, to soothe the eye & provide a lubricating cover. I added Tab:Vit C ii tds 1/52, Tab: Yeast ii tds 2/52.
In their return visit, I observed a marked improvement in child's vision. I have currently placed her on Gutt: Ciprofloxacin i every 1 hour. Their second visit was better, patient's eye has stopped tearing & the lid edema has gone down & the redness is reducing!
Thanks,
Dr Ezebuiroh Victor.
Note: 1) There is no financial attachment to this article!
2) Pan-Oj clinic & Diagnostic service limited opposite Shell pipeline is organizing a FREE GLAUCOMA screening from 14th february to 18ths february.
Thanks.
Thursday, 9 February 2012
Refracting the young child!
Optom
In Optometric clinical services refraction is amongs the most relevant clinical procedure carried out. Here in Nigeria, Optometry practice revolve around refraction, management of chronic eye conditions like Glaucoma and/or co-managing co-morbid conditions with other healthcare providers etc one cannot fail to agree that refraction becomes a routine tool in the hand of the Optometrist to identify early ocular manifestation of some systemic diseases like Diabetes; to manage ametropia; to treat refractive errors, anisometropias, some kind of squints, especially those that are not beyond 22 prism dioptres etc; to break suppression; to manage low vision; to check the prognosis of a cataract extraction surgery... Refraction can help treat binocular difficulties associated with accommodation anomalies. Refraction should be as routine as, say, routine blood pressure check in adults!
Refraction procedure carried out in adults is pretty straight forward, except in individuals with very poor cognitive background or in adults with poorly managed Diabetes, Glaucoma, Cataract, hypertension etc. It involves-
a) Checking visual Acuity (VA) in Right eye then left the left eye.
b) Using retinoscopy in a dark room to determine refractive error of the eyes.
c) Doing subjective refraction to get the final prescription of the individual.
Its a very simple procedure in adults but somehow in children we always wary ourselves by the prospect of hyper-active accomodative facility. Attentional span is another matter while compliance with refractionist's instruction is one of the major challenge in refracting a child. The younger the child, the less likely to comply in refraction and vice versa. What do I do?
After eliciting visual acuity information from the child, case history from the child and parent, I do a dark room objective refraction on the child looking out for induced accomodation by the light of my retinoscope. I start with the right eye and end up with the left eye. I almost always follow it up with a wet refraction and my drug of choice is Gutt: Mydracyl 1% ii ou for like 10 minutes. After my wet refraction, I compare my dry & wet refraction under the spectrum of the child's chief complaint and make my final "Doctor's" judgement.
I do not normally give oblique angles for children with such manifest refractions except in situations where there are obvious reasons to prescribe it. I approximate to the nearest 180 degree or 90 degree cylinders! I find it very skeptical fully correcting a child, but I do devout lots of interest in doing followup refractions every 3-6 months to monitor obvious refractive changes! I can even give a child of nine months glasses but I never forget that the vision in a child's eye is dynamic... it changes with time.
Thanks,
Dr Ezebuiroh Victor Okwudiri
Note: We do not have any financial consideration attached this article.
In Optometric clinical services refraction is amongs the most relevant clinical procedure carried out. Here in Nigeria, Optometry practice revolve around refraction, management of chronic eye conditions like Glaucoma and/or co-managing co-morbid conditions with other healthcare providers etc one cannot fail to agree that refraction becomes a routine tool in the hand of the Optometrist to identify early ocular manifestation of some systemic diseases like Diabetes; to manage ametropia; to treat refractive errors, anisometropias, some kind of squints, especially those that are not beyond 22 prism dioptres etc; to break suppression; to manage low vision; to check the prognosis of a cataract extraction surgery... Refraction can help treat binocular difficulties associated with accommodation anomalies. Refraction should be as routine as, say, routine blood pressure check in adults!
Refraction procedure carried out in adults is pretty straight forward, except in individuals with very poor cognitive background or in adults with poorly managed Diabetes, Glaucoma, Cataract, hypertension etc. It involves-
a) Checking visual Acuity (VA) in Right eye then left the left eye.
b) Using retinoscopy in a dark room to determine refractive error of the eyes.
c) Doing subjective refraction to get the final prescription of the individual.
Its a very simple procedure in adults but somehow in children we always wary ourselves by the prospect of hyper-active accomodative facility. Attentional span is another matter while compliance with refractionist's instruction is one of the major challenge in refracting a child. The younger the child, the less likely to comply in refraction and vice versa. What do I do?
After eliciting visual acuity information from the child, case history from the child and parent, I do a dark room objective refraction on the child looking out for induced accomodation by the light of my retinoscope. I start with the right eye and end up with the left eye. I almost always follow it up with a wet refraction and my drug of choice is Gutt: Mydracyl 1% ii ou for like 10 minutes. After my wet refraction, I compare my dry & wet refraction under the spectrum of the child's chief complaint and make my final "Doctor's" judgement.
I do not normally give oblique angles for children with such manifest refractions except in situations where there are obvious reasons to prescribe it. I approximate to the nearest 180 degree or 90 degree cylinders! I find it very skeptical fully correcting a child, but I do devout lots of interest in doing followup refractions every 3-6 months to monitor obvious refractive changes! I can even give a child of nine months glasses but I never forget that the vision in a child's eye is dynamic... it changes with time.
Thanks,
Dr Ezebuiroh Victor Okwudiri
Note: We do not have any financial consideration attached this article.
Saturday, 4 February 2012
Cataract, its treatment & the role of Optometry in Nigeria 4
Optom
Cataract is a condition of the crystalline lens that renders it opaque. Opaqueness of the crystalline lens is subjectively interpreted as loss of visual acuity or functional vision loss measurable by missing of letters on the visual acuity chart. The aim of treating cataract disease non-surgically, as I discussed in the previous part of this blog, was to reduce or remove or manage deterioration of vision in early cataract disease. When neither drugs or glasses are no longer helpful in managing vision deterioration secondary to cataract disease, cataract surgery becomes the final management option. There is almost a total (100%) recovery of visual functions in a 'normal' eye after undergoing a cataract extraction surgery. The surgical options like the Extra-capsular cataract extraction (ECCE) or Intra-capsular cataract extraction (ICCE) or the more recent small incision cataract surgery (SICs) or the Phaco-emulsification cataract surgery methods are available to the cataract surgeon.
Before the Nigerian Optometrists refer patients for surgery, its very important to pay attention to the following:
1) The patient's vision has reduced to @least 6/24 & becomes incapable of functioning normally for activities of daily living.
2) The patient is at risk of inducing diseases like glaucoma as a result of the cataract.
3) The patient has only one functional eye and @ the same time the eye is cataractous.
4) The patient has a comobid condition like a retinopathy and cataract in, say, diabetes. or
5) The patient is in 'good' health condition. (People with Diabetes, Hypertension, Cardiac arrest etc are very risky to perform the cataract surgery, unless when they are in very stable conditions as ascertained by their general physician).
6) The patient must be willing to do the surgery.
7) Who is the performing Ophthalmologist?
8) What drugs are the individual on e.g. Anticoagulants, anti-platelets, systemic alpha-1a antagonists, ophthalmic and systemic steroids etc?
9) Did you discuss the likely outcomes of the surgery with the patient?
It should be known that the knowledge of the performing surgeon by the refering Optometrists build confidence in the patient and in the refering Optometrist. Its the ethical goal of the Nigerian Optometrist to restore eye sight of its patients including making the proper refferal for ocular surgery procedures.
We are therefore calling on the Nigerian Ophthalmologists to give us informations on how to access their colleagues & let them come together with Optometric representatives to discuss bilaterally with the aim of finding a common ground in cataract surgery management & in post-surgical management of this crystalline lens disease. If such relationship is officially established cataract surgery rate will rise...so too will reduced post-cataract complications!
The role of Nigerian Optometrist in eyecare service provision is indisputable; same too can be said of the high prevalence of cataract in Nigeria & in the world. If there could be a flexible relationship between the Ophthalmologists and the Optometrist as it affects management of cataract patients. We all have a stake in this. Post surgical prognosis is partly dependent on surgical procedure, patients general health condition, how 'good' the surgery was; & partly on co-management by an Optometrist.
Note that after seven(7) days post cataract extraction surgery the chances of developing endophthalmitis reduces exponentially. A stable refraction on a post cataract eye is partly dependent on prognosis following cataract extraction & partly dependent on time, in 3 weeks to 4 weeks after surgery refraction is usually stable. Management of comorbid conditions are managed appropiately after surgery wound has healed. Children less than 5 years are very difficult to implant IOLs, even if it becomes implanted, they still need to wear bifocals since IOL do not induce accomodation. Slit Lamp is very important during post cataract surgical care. Always ensure that IOP is measured in an eye following catarct surgery. Comorbid conditions like amblyopia, maculopathies, Retinopathies, Glaucomas, Uveitis etc should be managed after cataract extraction. 80-90 % of normal cataract eyes that undergo surgery have successful prognosis.
That said, Optometrists managing post cataract surgery patients should look out for:
a) Conjunctival hyperemia, subconjunctival injection, cilliary injections around the limbus.
b) Profuse discharge exceeding 7 days after surgery.
c) Continous ocular hypotension or persistant ocular hypertension.
d) Uveitis or Keratitis or Episcleritis or scleritis.
e) Associated photophobia exceeding 3 weeks to 1 month following surgery.
f) Chronic Epiphora following surgery.
g) Itching in the eye.
h) Visual acuity improvement following surgery.
i) Bleb healing.
j) Any complaint from the patient leading to reduced functional vision.
Finally, there are about 17 million persons with cataracts and unless a very good working relationship is built amongs the eye care experts (The Ophthalmologists & the Optometrists) we might not be able to reduce or eliminate the epidemic of functional blindness this disease would cause in the coming years! Shadow boxing is a mere waste of valuable time. Every day someone somewhere becomes blind. We might lose the fight if we do nothing. We can still plant a tree now, though we would have had a tree today if we had planted it 20 years ago! We still can.
Concluded...
Dr Ezebuiroh Okwudiri Victor.
Cataract is a condition of the crystalline lens that renders it opaque. Opaqueness of the crystalline lens is subjectively interpreted as loss of visual acuity or functional vision loss measurable by missing of letters on the visual acuity chart. The aim of treating cataract disease non-surgically, as I discussed in the previous part of this blog, was to reduce or remove or manage deterioration of vision in early cataract disease. When neither drugs or glasses are no longer helpful in managing vision deterioration secondary to cataract disease, cataract surgery becomes the final management option. There is almost a total (100%) recovery of visual functions in a 'normal' eye after undergoing a cataract extraction surgery. The surgical options like the Extra-capsular cataract extraction (ECCE) or Intra-capsular cataract extraction (ICCE) or the more recent small incision cataract surgery (SICs) or the Phaco-emulsification cataract surgery methods are available to the cataract surgeon.
Before the Nigerian Optometrists refer patients for surgery, its very important to pay attention to the following:
1) The patient's vision has reduced to @least 6/24 & becomes incapable of functioning normally for activities of daily living.
2) The patient is at risk of inducing diseases like glaucoma as a result of the cataract.
3) The patient has only one functional eye and @ the same time the eye is cataractous.
4) The patient has a comobid condition like a retinopathy and cataract in, say, diabetes. or
5) The patient is in 'good' health condition. (People with Diabetes, Hypertension, Cardiac arrest etc are very risky to perform the cataract surgery, unless when they are in very stable conditions as ascertained by their general physician).
6) The patient must be willing to do the surgery.
7) Who is the performing Ophthalmologist?
8) What drugs are the individual on e.g. Anticoagulants, anti-platelets, systemic alpha-1a antagonists, ophthalmic and systemic steroids etc?
9) Did you discuss the likely outcomes of the surgery with the patient?
It should be known that the knowledge of the performing surgeon by the refering Optometrists build confidence in the patient and in the refering Optometrist. Its the ethical goal of the Nigerian Optometrist to restore eye sight of its patients including making the proper refferal for ocular surgery procedures.
We are therefore calling on the Nigerian Ophthalmologists to give us informations on how to access their colleagues & let them come together with Optometric representatives to discuss bilaterally with the aim of finding a common ground in cataract surgery management & in post-surgical management of this crystalline lens disease. If such relationship is officially established cataract surgery rate will rise...so too will reduced post-cataract complications!
The role of Nigerian Optometrist in eyecare service provision is indisputable; same too can be said of the high prevalence of cataract in Nigeria & in the world. If there could be a flexible relationship between the Ophthalmologists and the Optometrist as it affects management of cataract patients. We all have a stake in this. Post surgical prognosis is partly dependent on surgical procedure, patients general health condition, how 'good' the surgery was; & partly on co-management by an Optometrist.
Note that after seven(7) days post cataract extraction surgery the chances of developing endophthalmitis reduces exponentially. A stable refraction on a post cataract eye is partly dependent on prognosis following cataract extraction & partly dependent on time, in 3 weeks to 4 weeks after surgery refraction is usually stable. Management of comorbid conditions are managed appropiately after surgery wound has healed. Children less than 5 years are very difficult to implant IOLs, even if it becomes implanted, they still need to wear bifocals since IOL do not induce accomodation. Slit Lamp is very important during post cataract surgical care. Always ensure that IOP is measured in an eye following catarct surgery. Comorbid conditions like amblyopia, maculopathies, Retinopathies, Glaucomas, Uveitis etc should be managed after cataract extraction. 80-90 % of normal cataract eyes that undergo surgery have successful prognosis.
That said, Optometrists managing post cataract surgery patients should look out for:
a) Conjunctival hyperemia, subconjunctival injection, cilliary injections around the limbus.
b) Profuse discharge exceeding 7 days after surgery.
c) Continous ocular hypotension or persistant ocular hypertension.
d) Uveitis or Keratitis or Episcleritis or scleritis.
e) Associated photophobia exceeding 3 weeks to 1 month following surgery.
f) Chronic Epiphora following surgery.
g) Itching in the eye.
h) Visual acuity improvement following surgery.
i) Bleb healing.
j) Any complaint from the patient leading to reduced functional vision.
Finally, there are about 17 million persons with cataracts and unless a very good working relationship is built amongs the eye care experts (The Ophthalmologists & the Optometrists) we might not be able to reduce or eliminate the epidemic of functional blindness this disease would cause in the coming years! Shadow boxing is a mere waste of valuable time. Every day someone somewhere becomes blind. We might lose the fight if we do nothing. We can still plant a tree now, though we would have had a tree today if we had planted it 20 years ago! We still can.
Concluded...
Dr Ezebuiroh Okwudiri Victor.
Sunday, 29 January 2012
Can cerebrospinal fluid pressure influence optic nerve head neuropathy in glaucoma?2
Optom
In my last blog on this topic, I presented cerebrospinal fluid pressure as a factor of Normal Tension Glaucoma. This could explain the reason behind the seemingly 'low' to 'normal' IOP is this group of Open angle glaucoma types. But does it totally explain the optic nerve head neuropathy?
Optic nerve head neuropathy is a function of optic nerve fibre deaths otherwise known as optic nerve fibre apoptosis. What is responsible for optic nerve fibre apoptosis in NTG? It is true that the translaminar pressure gradient on the lamina cribosa skews it posteriorly, distorting it & oftentimes disrupting its normal physiological function. It could be theorized that @ this point the optic nerve fibres start degenerating, dying off & replaced by the neuropathy @ the disk head! Two types of gene mutations is said to be associated with glaucomatous optic nerve head neuropathy- Optoneurin mutation on gene OPTN & Myocilin/trabecular meshwork glucocorticoid inducible response mutation.
Optoneurin is a coiled protein that was first identified for its anti-apoptotic activity against a genetic strain of adenovirus protein (E3-14.7K). Tumour necrosis factor alpha (TNF-alpha) stimulates the activities of Optoneurin. Optoneurin protein plays a neuro-protective role in the eyes where it is found in the retina, the non-pigmentent cilliary epithelium, the optic nerve head, the lamina cribosa and in the trabecular meshwork. It is also known for its ability to interact with tranferrin via the transferrin receptors which influences the axiomatic flow of optic nerve fibres. Over-espression of optoneurin can induce the formation of a mutant type of optoneurin that has been shown to cause retinal ganglion cell apoptosis, the E50K.
E50K mutant is a variant of Optoneurin protein that is known to stimulate cell apoptosis using Tumour Necrosis Factor alpha (TNF-alpha) as a catalyst, just like in the normal optoneurin response. Hence instead of performing its intended anti-apoptotic function, E50K has been found to stimulate retinal ganglion cell degeneration in the retina & in the optic nerve head consistant with glaucomatous optic nerve neuropathy. Again, the secretion of TNF-alpha in the retinal area is achieved over-time by stimulated ischaemia of the optic nerve vessels & elevated hydrostatic (a.k.a. translaminar) pressure in return this causes the cellular 'insult' that will produce more mutant Optoneurin in a viscious cycle of retinal ganglion cell deaths beginning from the periphery to the optic nerve head. Also the mutant E50K often interferes with the 'normal' interaction of the Optoneurin with tranferrin which influences axiomatic flow in the optic nerve fibres. E50K "dumps" the tranferrin which consequently alters axiomatic flow & hence apoptosis of nerve cell fibres if the altered axiomatic flow is not 'repaired'. About 17% cases of Normal Tension Glaucoma (NTG) patients are reported to show increased presence of mutant Optoneurin, E50K.
Myocilin, Trabecular meshwork inducible glucocorticiod response (TIGR), is a protein which in human is encoded by the MYOC gene. The MYOC gene is known to have a signal sequence, albeit not functional, that directs proteins to the peroxisomes degradation. The actual function of Myocilin protein in the trabecular meshwork, in the retina, in the optic nerve head, in the lamina cribosa, in the cornea.. in almost all structures in of eye, is unknown. But it has been found to abound in about 36% of children suffering from Juvenile onset open angle glaucoma shows over-expression of MYOC/TIGR mutant gene. 4.6% of those with adult onset open angle glaucoma, with or without high IOP, had shown increased expression of the mutant MYOC. This mutant MYOC/TIGR is theorized to use its functional signaling sequence (in normal MYOC gene the signal sequence is not functional) to direct degradation of cell protein & hence subsequently cell degradation in the lamina cribosa & in the optic nerve fibres. Mutant MYOC/TIGR to cause neuropathy by cell protein degradation via peroxisome pathway.
Ishaemia of the optic nerve blood vessels, translaminar pressure of the eye, hereditory, prolonged use of topical dexmethasones, traumatic insults, inflamation of the optic nerve head etc are likely triggers that can cause mutations of both Optoneurin protein & the myocilin protein which are shown to be precursors to glaucomatous changes in the optic nerve head. I therefore agree that optic nerve head neuropathy in NTG is a physiological issue that manifests anatomically even in the absence of high intra-ocular pressure.
Thanks,
Dr Ezebuiroh Victor Okwudiri.
Note: There is no financial interest in this publication. thanks.
In my last blog on this topic, I presented cerebrospinal fluid pressure as a factor of Normal Tension Glaucoma. This could explain the reason behind the seemingly 'low' to 'normal' IOP is this group of Open angle glaucoma types. But does it totally explain the optic nerve head neuropathy?
Optic nerve head neuropathy is a function of optic nerve fibre deaths otherwise known as optic nerve fibre apoptosis. What is responsible for optic nerve fibre apoptosis in NTG? It is true that the translaminar pressure gradient on the lamina cribosa skews it posteriorly, distorting it & oftentimes disrupting its normal physiological function. It could be theorized that @ this point the optic nerve fibres start degenerating, dying off & replaced by the neuropathy @ the disk head! Two types of gene mutations is said to be associated with glaucomatous optic nerve head neuropathy- Optoneurin mutation on gene OPTN & Myocilin/trabecular meshwork glucocorticoid inducible response mutation.
Optoneurin is a coiled protein that was first identified for its anti-apoptotic activity against a genetic strain of adenovirus protein (E3-14.7K). Tumour necrosis factor alpha (TNF-alpha) stimulates the activities of Optoneurin. Optoneurin protein plays a neuro-protective role in the eyes where it is found in the retina, the non-pigmentent cilliary epithelium, the optic nerve head, the lamina cribosa and in the trabecular meshwork. It is also known for its ability to interact with tranferrin via the transferrin receptors which influences the axiomatic flow of optic nerve fibres. Over-espression of optoneurin can induce the formation of a mutant type of optoneurin that has been shown to cause retinal ganglion cell apoptosis, the E50K.
E50K mutant is a variant of Optoneurin protein that is known to stimulate cell apoptosis using Tumour Necrosis Factor alpha (TNF-alpha) as a catalyst, just like in the normal optoneurin response. Hence instead of performing its intended anti-apoptotic function, E50K has been found to stimulate retinal ganglion cell degeneration in the retina & in the optic nerve head consistant with glaucomatous optic nerve neuropathy. Again, the secretion of TNF-alpha in the retinal area is achieved over-time by stimulated ischaemia of the optic nerve vessels & elevated hydrostatic (a.k.a. translaminar) pressure in return this causes the cellular 'insult' that will produce more mutant Optoneurin in a viscious cycle of retinal ganglion cell deaths beginning from the periphery to the optic nerve head. Also the mutant E50K often interferes with the 'normal' interaction of the Optoneurin with tranferrin which influences axiomatic flow in the optic nerve fibres. E50K "dumps" the tranferrin which consequently alters axiomatic flow & hence apoptosis of nerve cell fibres if the altered axiomatic flow is not 'repaired'. About 17% cases of Normal Tension Glaucoma (NTG) patients are reported to show increased presence of mutant Optoneurin, E50K.
Myocilin, Trabecular meshwork inducible glucocorticiod response (TIGR), is a protein which in human is encoded by the MYOC gene. The MYOC gene is known to have a signal sequence, albeit not functional, that directs proteins to the peroxisomes degradation. The actual function of Myocilin protein in the trabecular meshwork, in the retina, in the optic nerve head, in the lamina cribosa, in the cornea.. in almost all structures in of eye, is unknown. But it has been found to abound in about 36% of children suffering from Juvenile onset open angle glaucoma shows over-expression of MYOC/TIGR mutant gene. 4.6% of those with adult onset open angle glaucoma, with or without high IOP, had shown increased expression of the mutant MYOC. This mutant MYOC/TIGR is theorized to use its functional signaling sequence (in normal MYOC gene the signal sequence is not functional) to direct degradation of cell protein & hence subsequently cell degradation in the lamina cribosa & in the optic nerve fibres. Mutant MYOC/TIGR to cause neuropathy by cell protein degradation via peroxisome pathway.
Ishaemia of the optic nerve blood vessels, translaminar pressure of the eye, hereditory, prolonged use of topical dexmethasones, traumatic insults, inflamation of the optic nerve head etc are likely triggers that can cause mutations of both Optoneurin protein & the myocilin protein which are shown to be precursors to glaucomatous changes in the optic nerve head. I therefore agree that optic nerve head neuropathy in NTG is a physiological issue that manifests anatomically even in the absence of high intra-ocular pressure.
Thanks,
Dr Ezebuiroh Victor Okwudiri.
Note: There is no financial interest in this publication. thanks.
Thursday, 19 January 2012
Can Cerebrospinal fluid pressure influence Optic nerve head neuropathy in Normal Tension Glaucoma?
Optom
Normal Tension Glaucoma is a type of Glaucoma without the common classical sign of Glaucoma pathogenesis- increased intraocular pressure (IOP). Increase in the pressure within the eyeball is the single most important factor that could indicate Glaucoma but it often times not enough to predict all types of Glaucomas. In Normal Tension Glaucoma, Optic nerve head neuropathy is the single most important sign of a pathology. The intraocular pressure (IOP) looks 'normal' but other signs like the dilation of the pupil & its apparent inability to react to light or acccomodation can be appreciated, especially when the disease has stayed for sometime...
Then comes the almighty question, why does the pupil becomes fixed & dilated when there is no 'high' IOP which should have compressed the Edinger Welpher pathway? Or how does the lamina cribosa death and optic nerve fibre appoptosis becomes possible in the presence of what appears to be 'normal' pressure?
Lets take a tour! The Optic nerve head tranverses through the the Optic disk via the lamina cribosa & terminates at the Optic chiasm. The lamina cribosa is the weakest portion of the sclera located at the posterior pole of the eyeball and perforated by the many fibres of the optic nerve. The optic nerve fibres @ this point (Optic disk area) is loosely attached to each other because of the absence of the cells of Muller. The weakness of the lamina cribosa area and the absence of the Muller cells in this position makes the optic disk head very vulnerable to inflamation and changes in pressure through the optic and neural pathways! The IOP of the eye is actually the pressure difference between the cornea and the atmospheric pressure. It is known as the transcorneal pressure. On the other hand, the pressure in the cranium and in the spinal cord is known as intracranial pressure (ICP). The later is a pressure difference between the atmosphere and the cranial compartments- the cranium and the vertebra.
Aqueous humor and the cerebrospinal fluid both similar in origin (a filtration substance) determines the IOP and ICP respectively. IOP should always be slightly higher than the ICP hence giving the optic disk head its classical depression. There is a homostatic arrengement as felt on the lamina cribosa and it is known as translaminar pressure, a pressure difference between the eyeball and the cranium and the spinal cord. Translaminar pressure has been attributed as the single most important phenomenon that discribes the stetching and subsequent atrophy of the lamina cribosa.
Translaminar pressure as felt on the lamina cribosa is calculated as (IOP-ICP). If the ICP is higher than the IOP a pseudo-tumor celebri or papilloedema or papillitis results. On the other hand, a very high IOP & low ICP results in Glaucomatous changes. It is attributed that the so called 'normal' tension glaucoma is as a result of the cushioning effect of the ICP on the lamina cribosa. The apparently 'high' IOP is cushioned by a not-too-low ICP causing a strain on the lamina cribosa to the point of nerve fibre cell apoptosis.
The average IOP is 16mmHg while the average ICP is 12mmHg, hence giving us a 4mmHg difference on the lamina cribosa. This gives the optic disk head a depression equivalent to the tranlaminar pressure difference of 4mmHg.
Even though glaucoma is not fully understood, I believe that ICP plays a role in normal tension glaucoma. It therefore becomes important to put such in consideration in diagnosis and management of this single most important silent thief of sight!
Thanks,
Dr Victor Ezebuiroh.
N/B: This article draws no financial interest anywhere.
Normal Tension Glaucoma is a type of Glaucoma without the common classical sign of Glaucoma pathogenesis- increased intraocular pressure (IOP). Increase in the pressure within the eyeball is the single most important factor that could indicate Glaucoma but it often times not enough to predict all types of Glaucomas. In Normal Tension Glaucoma, Optic nerve head neuropathy is the single most important sign of a pathology. The intraocular pressure (IOP) looks 'normal' but other signs like the dilation of the pupil & its apparent inability to react to light or acccomodation can be appreciated, especially when the disease has stayed for sometime...
Then comes the almighty question, why does the pupil becomes fixed & dilated when there is no 'high' IOP which should have compressed the Edinger Welpher pathway? Or how does the lamina cribosa death and optic nerve fibre appoptosis becomes possible in the presence of what appears to be 'normal' pressure?
Lets take a tour! The Optic nerve head tranverses through the the Optic disk via the lamina cribosa & terminates at the Optic chiasm. The lamina cribosa is the weakest portion of the sclera located at the posterior pole of the eyeball and perforated by the many fibres of the optic nerve. The optic nerve fibres @ this point (Optic disk area) is loosely attached to each other because of the absence of the cells of Muller. The weakness of the lamina cribosa area and the absence of the Muller cells in this position makes the optic disk head very vulnerable to inflamation and changes in pressure through the optic and neural pathways! The IOP of the eye is actually the pressure difference between the cornea and the atmospheric pressure. It is known as the transcorneal pressure. On the other hand, the pressure in the cranium and in the spinal cord is known as intracranial pressure (ICP). The later is a pressure difference between the atmosphere and the cranial compartments- the cranium and the vertebra.
Aqueous humor and the cerebrospinal fluid both similar in origin (a filtration substance) determines the IOP and ICP respectively. IOP should always be slightly higher than the ICP hence giving the optic disk head its classical depression. There is a homostatic arrengement as felt on the lamina cribosa and it is known as translaminar pressure, a pressure difference between the eyeball and the cranium and the spinal cord. Translaminar pressure has been attributed as the single most important phenomenon that discribes the stetching and subsequent atrophy of the lamina cribosa.
Translaminar pressure as felt on the lamina cribosa is calculated as (IOP-ICP). If the ICP is higher than the IOP a pseudo-tumor celebri or papilloedema or papillitis results. On the other hand, a very high IOP & low ICP results in Glaucomatous changes. It is attributed that the so called 'normal' tension glaucoma is as a result of the cushioning effect of the ICP on the lamina cribosa. The apparently 'high' IOP is cushioned by a not-too-low ICP causing a strain on the lamina cribosa to the point of nerve fibre cell apoptosis.
The average IOP is 16mmHg while the average ICP is 12mmHg, hence giving us a 4mmHg difference on the lamina cribosa. This gives the optic disk head a depression equivalent to the tranlaminar pressure difference of 4mmHg.
Even though glaucoma is not fully understood, I believe that ICP plays a role in normal tension glaucoma. It therefore becomes important to put such in consideration in diagnosis and management of this single most important silent thief of sight!
Thanks,
Dr Victor Ezebuiroh.
N/B: This article draws no financial interest anywhere.
Monday, 16 January 2012
Cataract, its treatment and the role of Optometry in Nigeria 3
Optom
Continuing, it is important to know the impact of cataract to the general population. Cataract functionally causes blindness in its final stages. About 17 million persons are blind from cataract only.
In its early stage, especially when it affects one eye alone, the individual is almost symptomless. After sometime, depending on the causal agent and/or inducing agents, symptoms like photophobia, anisometropias, diplopia, secondary redness of the ipsilateral eyes, epiphora, itching, increased glare sensitivity etc could make the patient seek for medical attention. Most Optometrists in Nigeria become the first healthcare expert consulted. In later stages, other symptoms that are sight threatening starts showing up. Like secondary closed angle glaucoma, reduced vision on the ipsilateral eye with implications such as amblyopia in children etc; uveitis as the cataract intaracts with the iris and ciliary bodies etc. The last stage of such cataract, as I reinterated before, is functional and/or absolute blindness depending on the presence of conditions like induced glaucomas, secondary uveitis and bad surgery and/or followup.
Cataract becomes a bigger burden when it is bilateral. The symptoms show earlier and visual handicap is more obvious. It tends to affect activities of daily living among patients and renders individuals vulnerable. The most important symptom in this form of cataract is reduced bilateral vision especially at far. The use of glass correction is desirable at this early stage. Patients become sensitive to glare, and contrast sensitivty is said to be affected too. This patient is worried and wants to remove the source of discomforts in the eyes which includes itching, epiphora, sandy sansation etc. Bilateral cataract is very common in malnourished children, in Diabetics or in individuals taking very high doses of steroids for a long time or people exposed to very high radiations absorbed by the crystalline lens.
Visual challenges posed by bilateral cataract is severe and sudden, not to mention the effect of colour vision challenges and seeing haloes around light that accompanies cataract development! Medical care is seeked earlier than in the case of monocular cataract.What does the Optometrist do? Since this individual had variously visited the chemist drugstores and/or the unorthodox medicine practitioner without any lasting solution, we can imagine what such individual's expectations would be. It becomes imparative for the Optometrist to run an extensive eye examination. First, do monocular and binocular visual acuity examination at far and at near. This should be followed by objective refraction using either a Retinoscope or using an auto-refractor. After the refraction, patients are expected to be subjected to subjective refraction to ascertain whether glasses can reduce the induced blur. Then a suitable tonometer is used to check for induced increased intraocular pressure in the eye(s) with the cataract. Unless in eyes with associated Glaucoma, Optometric practioners are adviced to dilate the cataractous eyes with a dilating agent to access the extent of the cataract development.
One thing should remain obvious to the primary eye care practitioner- the patient's expectations! It is therefore important to have an open communication with your patient. Discuss surgery as the last option. Use glasses and drugs to try reduce blur, especially in its early stages. Use tints or photochromic lenses to manage glare, photophobia and effect of illumination. Reduce or remove symptoms like epiphora, itching and diplopia while encouraging patient to be coming for check-ups till cataract becomes ready for extraction. Meanwhile, the Optometrist should initiate a contact with a cataract surgeon as it regards this patient. The patient's medical records should be reviewed by the surgeon and an appointment is sheduled when appropiate. If the cataract is either drug induced or pathology related, a general practitioner or the personal Doctor of the patient is expected to play a significant role in managing such patients. Medical reports from the various healthcare practitioners should be made available and documented, as much as possible!
It is the role of the practitioner to know how desireous of surgery the patient is or should be. The rule of the thumb is that eyecare practitioner should never push a patient for surgery, except in children under 9 years or in traumatic cataract or the very hyper-mature cataract whose complications far outweighs post-surgical complications!
Drugs like N-Acetyl carnosine is reported all over the internet health world to be able to disolve cataract, others like Pirenoxine (Catalin), Potassium & Sodium Iodide combination (Vitrolent) are used to manage early cataract. It becomes imparative for the Optometrist to know which of the ophthalmic agents will be good for the patient and use it!
I will discuss Cataract surgery in my subsequent blog... Meanwhile, Happy new year readers!
Dr Okwudiri Victor Ezebuiroh
Note: This blog does not have any financial interest anywhere!
Continuing, it is important to know the impact of cataract to the general population. Cataract functionally causes blindness in its final stages. About 17 million persons are blind from cataract only.
In its early stage, especially when it affects one eye alone, the individual is almost symptomless. After sometime, depending on the causal agent and/or inducing agents, symptoms like photophobia, anisometropias, diplopia, secondary redness of the ipsilateral eyes, epiphora, itching, increased glare sensitivity etc could make the patient seek for medical attention. Most Optometrists in Nigeria become the first healthcare expert consulted. In later stages, other symptoms that are sight threatening starts showing up. Like secondary closed angle glaucoma, reduced vision on the ipsilateral eye with implications such as amblyopia in children etc; uveitis as the cataract intaracts with the iris and ciliary bodies etc. The last stage of such cataract, as I reinterated before, is functional and/or absolute blindness depending on the presence of conditions like induced glaucomas, secondary uveitis and bad surgery and/or followup.
Cataract becomes a bigger burden when it is bilateral. The symptoms show earlier and visual handicap is more obvious. It tends to affect activities of daily living among patients and renders individuals vulnerable. The most important symptom in this form of cataract is reduced bilateral vision especially at far. The use of glass correction is desirable at this early stage. Patients become sensitive to glare, and contrast sensitivty is said to be affected too. This patient is worried and wants to remove the source of discomforts in the eyes which includes itching, epiphora, sandy sansation etc. Bilateral cataract is very common in malnourished children, in Diabetics or in individuals taking very high doses of steroids for a long time or people exposed to very high radiations absorbed by the crystalline lens.
Visual challenges posed by bilateral cataract is severe and sudden, not to mention the effect of colour vision challenges and seeing haloes around light that accompanies cataract development! Medical care is seeked earlier than in the case of monocular cataract.What does the Optometrist do? Since this individual had variously visited the chemist drugstores and/or the unorthodox medicine practitioner without any lasting solution, we can imagine what such individual's expectations would be. It becomes imparative for the Optometrist to run an extensive eye examination. First, do monocular and binocular visual acuity examination at far and at near. This should be followed by objective refraction using either a Retinoscope or using an auto-refractor. After the refraction, patients are expected to be subjected to subjective refraction to ascertain whether glasses can reduce the induced blur. Then a suitable tonometer is used to check for induced increased intraocular pressure in the eye(s) with the cataract. Unless in eyes with associated Glaucoma, Optometric practioners are adviced to dilate the cataractous eyes with a dilating agent to access the extent of the cataract development.
One thing should remain obvious to the primary eye care practitioner- the patient's expectations! It is therefore important to have an open communication with your patient. Discuss surgery as the last option. Use glasses and drugs to try reduce blur, especially in its early stages. Use tints or photochromic lenses to manage glare, photophobia and effect of illumination. Reduce or remove symptoms like epiphora, itching and diplopia while encouraging patient to be coming for check-ups till cataract becomes ready for extraction. Meanwhile, the Optometrist should initiate a contact with a cataract surgeon as it regards this patient. The patient's medical records should be reviewed by the surgeon and an appointment is sheduled when appropiate. If the cataract is either drug induced or pathology related, a general practitioner or the personal Doctor of the patient is expected to play a significant role in managing such patients. Medical reports from the various healthcare practitioners should be made available and documented, as much as possible!
It is the role of the practitioner to know how desireous of surgery the patient is or should be. The rule of the thumb is that eyecare practitioner should never push a patient for surgery, except in children under 9 years or in traumatic cataract or the very hyper-mature cataract whose complications far outweighs post-surgical complications!
Drugs like N-Acetyl carnosine is reported all over the internet health world to be able to disolve cataract, others like Pirenoxine (Catalin), Potassium & Sodium Iodide combination (Vitrolent) are used to manage early cataract. It becomes imparative for the Optometrist to know which of the ophthalmic agents will be good for the patient and use it!
I will discuss Cataract surgery in my subsequent blog... Meanwhile, Happy new year readers!
Dr Okwudiri Victor Ezebuiroh
Note: This blog does not have any financial interest anywhere!
Tuesday, 27 December 2011
Cataract, its treatment and the role of Optometry in Nigeria 2
Optom
We discussed the crystalline lens extensively in a previous blog. It is important to discuss how cataract is developed in this avascular structure.
As I said earlier, Cataract is a clouding of the crystalline lens with a resultant reduction in subjective visual output! This clouding phenomenon undermines the transparent mechanism of the crystalline lens. Such factors ensure lens transparency and they include a) Avascularity of the lens materials, b) Tightly packed lens cell fibres, 3) The structural arrengements of lens cell proteins, 4) Semi-permeable nature of the lens cell capsule, 5) Active transport mechanism of the lens cell fibres, 5)Auto-oxidation and high concentration of reduced gluthatione in lens cells and, 6) coluration of the crystalline lens including other factors.
To fully understand pathogenesis of cataract formation, it becomes important to shed light on some factors that disrupts lens transparency.
For instance the primary reson the crystalline lens is avascular is to enable the structure transmit light without shadows or haloes that vascularity of structures often promote. Again, it is histologically documented that lens cell fibres are arrenged in a lattice three-dimensional way to reduce any interferance with light refraction though this medium. Also it should be noted that the tightly packed lens cell fibres especially as we approach the lens nucleus is apparently meant to reduce hydration of the lens cell fibres. Any disruption in this state of homeostasis triggers an apparent denaturing of lens protein, consequent upon which lens clouding ensues. What could disrupt this homeostasis relationship? Injury could. Aging is another factor. Let us not forget diseases like Diabetes, also the effect of radiation like the infra-red ray wich is absorbed in the crystalline lens (this is a protective function of the crystalline lens which in turn filters the kind of light reaching the very sensitive retina!) etc.
Metabolism of the lens fibre uses osmotic differentials to keep hydration in check, while using active transport to maintain sodium, potassium and calcium levels in the crystalline lens. Gluthatione, in its reduced form. Active transport mechanism helps allow selected materials into the crystalline lens and push out others into the surrounding areas while maintaining a threshood 'tension' that regulates dehydration of the lens fibre cells. Diseases, trauma, age and genetic disruptions have reportedly altered the metabolic activities of the crystalline lens hence the formation of cataract.
It should be noted that as the lens grow old it does not shed its old materials, it rather pushes them to the middle and associated wear and tear phenomenon of the lens makes the lens change from transparent to a graying shift. The later, including disruption in protein synthesis with age in some persons, is generally responsible for geriatric kind of cataract!
Commonly among the children is congenitial or genetic-induced cataract. Diseases among the parents prior to delivery could cause this. It could also be a result of food habit amongs the pregnant women. Exposure harmful rays in pregnant women or the use of drugs among these group has been implicated in the formation of congenital cataract!
There are about 17 million persons living with cataract all over the world and 75% are in Asia and Africa!
The most common type of cataract is geriatric cataract. Other types of cataract are not uncommon. In the youths and children the most common cause of cataract is genetic disruptions and trauma. Among a large swath of outdoor workers, radiation cataract is very common either through synthetic toxic materials or as a result of unhindered absorption of infra-red rich light common in hot regions.
Thanks... To be continued!
Dr Okwudiri Ezebuiroh.
This blog does not draw any financial interest anywhere. Thanks.
We discussed the crystalline lens extensively in a previous blog. It is important to discuss how cataract is developed in this avascular structure.
As I said earlier, Cataract is a clouding of the crystalline lens with a resultant reduction in subjective visual output! This clouding phenomenon undermines the transparent mechanism of the crystalline lens. Such factors ensure lens transparency and they include a) Avascularity of the lens materials, b) Tightly packed lens cell fibres, 3) The structural arrengements of lens cell proteins, 4) Semi-permeable nature of the lens cell capsule, 5) Active transport mechanism of the lens cell fibres, 5)Auto-oxidation and high concentration of reduced gluthatione in lens cells and, 6) coluration of the crystalline lens including other factors.
To fully understand pathogenesis of cataract formation, it becomes important to shed light on some factors that disrupts lens transparency.
For instance the primary reson the crystalline lens is avascular is to enable the structure transmit light without shadows or haloes that vascularity of structures often promote. Again, it is histologically documented that lens cell fibres are arrenged in a lattice three-dimensional way to reduce any interferance with light refraction though this medium. Also it should be noted that the tightly packed lens cell fibres especially as we approach the lens nucleus is apparently meant to reduce hydration of the lens cell fibres. Any disruption in this state of homeostasis triggers an apparent denaturing of lens protein, consequent upon which lens clouding ensues. What could disrupt this homeostasis relationship? Injury could. Aging is another factor. Let us not forget diseases like Diabetes, also the effect of radiation like the infra-red ray wich is absorbed in the crystalline lens (this is a protective function of the crystalline lens which in turn filters the kind of light reaching the very sensitive retina!) etc.
Metabolism of the lens fibre uses osmotic differentials to keep hydration in check, while using active transport to maintain sodium, potassium and calcium levels in the crystalline lens. Gluthatione, in its reduced form. Active transport mechanism helps allow selected materials into the crystalline lens and push out others into the surrounding areas while maintaining a threshood 'tension' that regulates dehydration of the lens fibre cells. Diseases, trauma, age and genetic disruptions have reportedly altered the metabolic activities of the crystalline lens hence the formation of cataract.
It should be noted that as the lens grow old it does not shed its old materials, it rather pushes them to the middle and associated wear and tear phenomenon of the lens makes the lens change from transparent to a graying shift. The later, including disruption in protein synthesis with age in some persons, is generally responsible for geriatric kind of cataract!
Commonly among the children is congenitial or genetic-induced cataract. Diseases among the parents prior to delivery could cause this. It could also be a result of food habit amongs the pregnant women. Exposure harmful rays in pregnant women or the use of drugs among these group has been implicated in the formation of congenital cataract!
There are about 17 million persons living with cataract all over the world and 75% are in Asia and Africa!
The most common type of cataract is geriatric cataract. Other types of cataract are not uncommon. In the youths and children the most common cause of cataract is genetic disruptions and trauma. Among a large swath of outdoor workers, radiation cataract is very common either through synthetic toxic materials or as a result of unhindered absorption of infra-red rich light common in hot regions.
Thanks... To be continued!
A catactous eye as seen under biomicroscope view courtesy of Karl
Dr Okwudiri Ezebuiroh.
This blog does not draw any financial interest anywhere. Thanks.
Monday, 12 December 2011
Cataract, its treatment and the role of Optometry in Nigeria 1
Optom
Cataract is a condition of the crystalline lens which leads to its (crystaline len's) opacification. The crystalline lense is an avascular and transparent structure which consists of the lens capsule, the lens epithelium, the lens fibre- the nucleus and the peripheral cortex. The crystalline lens is situated behind the iris but lies anterior to the vitreous chamber and the retina.
The lens capsule is the thin, transparent hyaline membrane that surrounds the crystalline lens. It is rich in elastins and collagen. It also contains phospholipids in the form of glycosaminoglycans, a substance the provides connective tissue-like reinforcement to the lens capsule. The cilliary body attaches zonules projecting from the lens capsule known as suspensory ligaments.
The lens epithelium is a basal membrane that is situated in the anterior portion of the lens. It is made up of single layer of cubiodal cells with active mitosis taking place throughout life. The older lens fibre produced are pushed to the middle where it forms the nucleus and the outer surface forms the peripheral cortex. The lens fibre, it should be noted, consists of the main mass of the lens material. The fibres are formed by the multiplication and differentiation of the lens epithelial cells. The posterior portion of the lens has no epithelium.
The crystalline lens is composed of chiefly of crystallins. Crystallins are transparent proteins that gives the crystallines its transparency including the parallel arrengement of lens cell materials. Crystallins commonly found in the human is alpha-, beta- & gamma-crystallins and it composes of about 90% of the total lens protein. The crystalline lens is bathed anteriorly by the more active aqueous humor, while the less active vitreous humor bathes posterior aspect of the crystalline lens. Any loss of transperency of the lens results to cataract.
Cataract causes functional blindness to the individual.
To be continued...
Fig 1. An African Woman with OD mature cataract.
Dr Ezebuiroh Victor Okwudiri.
Cataract is a condition of the crystalline lens which leads to its (crystaline len's) opacification. The crystalline lense is an avascular and transparent structure which consists of the lens capsule, the lens epithelium, the lens fibre- the nucleus and the peripheral cortex. The crystalline lens is situated behind the iris but lies anterior to the vitreous chamber and the retina.
The lens capsule is the thin, transparent hyaline membrane that surrounds the crystalline lens. It is rich in elastins and collagen. It also contains phospholipids in the form of glycosaminoglycans, a substance the provides connective tissue-like reinforcement to the lens capsule. The cilliary body attaches zonules projecting from the lens capsule known as suspensory ligaments.
The lens epithelium is a basal membrane that is situated in the anterior portion of the lens. It is made up of single layer of cubiodal cells with active mitosis taking place throughout life. The older lens fibre produced are pushed to the middle where it forms the nucleus and the outer surface forms the peripheral cortex. The lens fibre, it should be noted, consists of the main mass of the lens material. The fibres are formed by the multiplication and differentiation of the lens epithelial cells. The posterior portion of the lens has no epithelium.
The crystalline lens is composed of chiefly of crystallins. Crystallins are transparent proteins that gives the crystallines its transparency including the parallel arrengement of lens cell materials. Crystallins commonly found in the human is alpha-, beta- & gamma-crystallins and it composes of about 90% of the total lens protein. The crystalline lens is bathed anteriorly by the more active aqueous humor, while the less active vitreous humor bathes posterior aspect of the crystalline lens. Any loss of transperency of the lens results to cataract.
Cataract causes functional blindness to the individual.
To be continued...
Dr Ezebuiroh Victor Okwudiri.
Tuesday, 22 November 2011
Allergic conjunctivities in Clinical Optometry!
Optom
Wow its been long time folks and friends. Sorry for the long absense. Thanks goodness, the world is a little bit better with such persons like Ghaddaffi, Sadam Hussain, Osama bin Laden etc gone... It is also heart warming to know that the referendum for South Sudan became a reality! The Arab spring is still spewing out more loosers e.g. in Yemen but life still goes on.
Without dwelling much on frivolities lets get blogging...
As the name implies, Allergic conjunctivities is a group of allergic conditions of the conjunctiva that is triggered when mast cells laden with IgE comes in contact with an allergen (antigen) and an antibody/antigen complex reaction is formed. Mast cell contains unreleased histmine. When a mast cell laden with IgE cross-links an antigen after been primed by Beta-chemokines (a type of cytokines that actively involves in chemotaxis!) they (the mast cells) release histamine and a host other active intermediaries. These intermediaries are prostalglandin-G, Serotonin, leukotrienes, platlet activating factor and cytokines that further lead to priminig of more mast cells to repeat the circle. The T cells too play a role in the activation and degranulation process of mast cells. T cells contributes the specific IgE for a given mast cell. The release of these substances results in ocular itching, conjunctval and lid edema, formation of mucus (the string-like type of mucus common in allergic conjunctivitis).
In situations where the allergen becomes perennial, the cytokines in the viscious circle of mast cell degranulations will also attract Basophils and recruit tissue damaging body immune substances like T cells, macrophages, neutrophils & eosinopils. These immune substances form a complex pathway to the resulting tissue damage and deeper allergic reactions like papillae formations on the conjunctiva,sinusitis, rhinitis, tinitus etc
Apart from an allergen or injury causing degranulation of mast cells, it has been reported that a particular amount of stress can activate the mast cells even in the absense of IgE , especially those in the cerebrum! The complex mechanism, it is said, leads to mast cell reactions even in the absense of an allergen! (Theoharis C.T., David E.C. [2003]). Hypothetically it could explain why some refractive or binocular difficulties in the eye can trigger ocular itching!
From the foregoing discussion, it can be understood that allergic conjunctivitis is an immuno- sensitization degenerative condition of the outer 1/6 of the eye. It is very difficult to manage and usually it is self-limiting after a period of time. Lets discuss some ways to manage this condition.
First this condition causes vasodilation of conjunctival blood vessels. Histamine is responsible for this dilation of conjuntival blood vessels. One method to arrest this sign is by using steroids as vasoconstrictors. It is used as a short-term remedy. In the long run, it is important to combine it with an anti-histamine like gutt: spercellerg and/or tablets like tab: chlorophetamine while tappering the steroids. Anti-histamines tend to influence the effect of the elaborated histamines from the degranulated mast cells. Other class of drugs that could play an active role in combating this allergy includes Sodium cromoglycates, lodoxamide, nedocromil are known as mast cell stabilizers. They function by inhibiting the calcium ions that triggers the elaboration of histamine onto the tissue. They are the most effective therapy for this allergic condition. Other non medical mesures includes using cold compresses, wearing shades when outdoors and proper ventillation.
The main objective of treatment is the removal of the allergen which could be dust, smoke,pollen grains from flower, chemicals, paints, lots of exogenous substances that might come in contact with the eye. It should be put in mind to remove any form of refractive stress or binocular stress that might accompany the eye. Please ensure you discuss ocular hygiene with your patient.
Different types of allergic conjunctivitis will be discussed subsequently and specific measures to contain them will be enumerated. Thanks
Dr Ezebuiroh Victor Okwudiri.
Wow its been long time folks and friends. Sorry for the long absense. Thanks goodness, the world is a little bit better with such persons like Ghaddaffi, Sadam Hussain, Osama bin Laden etc gone... It is also heart warming to know that the referendum for South Sudan became a reality! The Arab spring is still spewing out more loosers e.g. in Yemen but life still goes on.
Without dwelling much on frivolities lets get blogging...
As the name implies, Allergic conjunctivities is a group of allergic conditions of the conjunctiva that is triggered when mast cells laden with IgE comes in contact with an allergen (antigen) and an antibody/antigen complex reaction is formed. Mast cell contains unreleased histmine. When a mast cell laden with IgE cross-links an antigen after been primed by Beta-chemokines (a type of cytokines that actively involves in chemotaxis!) they (the mast cells) release histamine and a host other active intermediaries. These intermediaries are prostalglandin-G, Serotonin, leukotrienes, platlet activating factor and cytokines that further lead to priminig of more mast cells to repeat the circle. The T cells too play a role in the activation and degranulation process of mast cells. T cells contributes the specific IgE for a given mast cell. The release of these substances results in ocular itching, conjunctval and lid edema, formation of mucus (the string-like type of mucus common in allergic conjunctivitis).
In situations where the allergen becomes perennial, the cytokines in the viscious circle of mast cell degranulations will also attract Basophils and recruit tissue damaging body immune substances like T cells, macrophages, neutrophils & eosinopils. These immune substances form a complex pathway to the resulting tissue damage and deeper allergic reactions like papillae formations on the conjunctiva,sinusitis, rhinitis, tinitus etc
Apart from an allergen or injury causing degranulation of mast cells, it has been reported that a particular amount of stress can activate the mast cells even in the absense of IgE , especially those in the cerebrum! The complex mechanism, it is said, leads to mast cell reactions even in the absense of an allergen! (Theoharis C.T., David E.C. [2003]). Hypothetically it could explain why some refractive or binocular difficulties in the eye can trigger ocular itching!
From the foregoing discussion, it can be understood that allergic conjunctivitis is an immuno- sensitization degenerative condition of the outer 1/6 of the eye. It is very difficult to manage and usually it is self-limiting after a period of time. Lets discuss some ways to manage this condition.
First this condition causes vasodilation of conjunctival blood vessels. Histamine is responsible for this dilation of conjuntival blood vessels. One method to arrest this sign is by using steroids as vasoconstrictors. It is used as a short-term remedy. In the long run, it is important to combine it with an anti-histamine like gutt: spercellerg and/or tablets like tab: chlorophetamine while tappering the steroids. Anti-histamines tend to influence the effect of the elaborated histamines from the degranulated mast cells. Other class of drugs that could play an active role in combating this allergy includes Sodium cromoglycates, lodoxamide, nedocromil are known as mast cell stabilizers. They function by inhibiting the calcium ions that triggers the elaboration of histamine onto the tissue. They are the most effective therapy for this allergic condition. Other non medical mesures includes using cold compresses, wearing shades when outdoors and proper ventillation.
The main objective of treatment is the removal of the allergen which could be dust, smoke,pollen grains from flower, chemicals, paints, lots of exogenous substances that might come in contact with the eye. It should be put in mind to remove any form of refractive stress or binocular stress that might accompany the eye. Please ensure you discuss ocular hygiene with your patient.
Different types of allergic conjunctivitis will be discussed subsequently and specific measures to contain them will be enumerated. Thanks
Dr Ezebuiroh Victor Okwudiri.
Thursday, 23 June 2011
Vitamin A Deficiency & Childhood blindness
Optom
Vitamin A Deficiency in children is the lack of Vitamin A in their body to a point of creating functional changes & creating disease conditions in their human system.
Vitamin A deficiency, though it can affect adults, results in horrific ocular & immunologic consequences especially in children. It is both a precursor to measles & aggrevated by measles! It causes corneal blindness in children, especially those in developing countries like Africa & Asia.
Other ocular implications include Xerophthalmia (secondary to reduced presence & influence of meibomian gland & other secretory apparatus in the eyes), then chronic corneal ulceration followed by Keratomalasia & subsequent anterior Staphyloma. Night blindness, or Nyctalopia is usually the first implication of this condition. In Vitamin A deficiency, it involves the inability of the Rhodopsin to be ibe formed because Vitamin A which is the primary source of retinal (a Vitamin A precursor for Rhodopsin formation with the contributions of light sensitive opsin proteins! Nyctalopia can also be caused by a genetic condition known as Retinitis Pigmentosa, or could be attributed to genetic deficiency of the rods to function beyond threshhold but does not progress like the Retinitis Pigmentosa. This later condition is known as X-link congenital Stationary Night blindness.
Vitamin A deficiency (VAD) in children and pregnant women causes a weakness of the human immune system and has hence become implicated in low body defence response to diseases like measles & also to other bacterial infections, not common in healthy individuals! VAD affects 1 in every 3 children as at 2008! It is reported that between 250,000-500,000 children become blind annually as a result of VAD and half of these children die within 1 year of becoming blind. With the combined help of World Health Organization, United States Agency for International Development, Canadian International Developmental Agency and Micronutrient initiative under the umbrella of Vitamin A Global Initiative has been able to avert about 1.25 million deaths in about 40 countries since 1998! The year 2010 was put forward as the year VAD should be eliminated in the general population, but we are yet to see the end of this child-killer disease!
In Nigeria, Xerophthalmia was estimated to be 1.1 % prevalent in the children population and 7% have VAD (Ajayeoba A.I., 2001). Xerophthalmia describes the ocular manifestations of VAD. It is estimated, by projection, that about 1 million children are affected by VAD and about 100,000 could have an eye involvement (Xerophthalmia) and 50,000 may go blind while 25,000 children are estimated to die annually (Sommers, 1995). This condition is more prevalent in the northwest but least prevalent in the southeast! I think dietary differences play a role here and such findings should be varified by Optometric study nationally!
Treating VAD is done using Vitamin A supplementation therapy and managing the systemic effect like Diarrhea, Measles etc. If there is any ocular effect, it is most appropiate to manage the Xerophthalmia in its early stages when the cornea is not affected! It is best treated with Ocular lubricants, while such conditions like corneal ulceration is best managed with non steroidal anti inflamatory agents like Diclofenac Sodium, others includes topical antibiotic agents like Ciprofloxacin and chloramphenicol ointment! Look out for any corneal involvement in any reported case VAD! It could save that child's sight! It is very appropiate to educate pregnant women and lactating mothers on the need to avoid getting VAD. In these group of people, bilateral blindness could result! Treat them in conjunction with their Gynacologists/Obestricians. Their kind of blindness is retinal in nature!
VAD is a public health issue and Optometrists are adviced to contribute to eliminating this condition! Lets make the future of our children stress free because they are the leaders of tommorrow! Lets make vision 2020 a reality. I know we can. Happy December and Christmas in advance!
Vitamin A Deficiency in children is the lack of Vitamin A in their body to a point of creating functional changes & creating disease conditions in their human system.
Vitamin A deficiency, though it can affect adults, results in horrific ocular & immunologic consequences especially in children. It is both a precursor to measles & aggrevated by measles! It causes corneal blindness in children, especially those in developing countries like Africa & Asia.
Other ocular implications include Xerophthalmia (secondary to reduced presence & influence of meibomian gland & other secretory apparatus in the eyes), then chronic corneal ulceration followed by Keratomalasia & subsequent anterior Staphyloma. Night blindness, or Nyctalopia is usually the first implication of this condition. In Vitamin A deficiency, it involves the inability of the Rhodopsin to be ibe formed because Vitamin A which is the primary source of retinal (a Vitamin A precursor for Rhodopsin formation with the contributions of light sensitive opsin proteins! Nyctalopia can also be caused by a genetic condition known as Retinitis Pigmentosa, or could be attributed to genetic deficiency of the rods to function beyond threshhold but does not progress like the Retinitis Pigmentosa. This later condition is known as X-link congenital Stationary Night blindness.
Vitamin A deficiency (VAD) in children and pregnant women causes a weakness of the human immune system and has hence become implicated in low body defence response to diseases like measles & also to other bacterial infections, not common in healthy individuals! VAD affects 1 in every 3 children as at 2008! It is reported that between 250,000-500,000 children become blind annually as a result of VAD and half of these children die within 1 year of becoming blind. With the combined help of World Health Organization, United States Agency for International Development, Canadian International Developmental Agency and Micronutrient initiative under the umbrella of Vitamin A Global Initiative has been able to avert about 1.25 million deaths in about 40 countries since 1998! The year 2010 was put forward as the year VAD should be eliminated in the general population, but we are yet to see the end of this child-killer disease!
In Nigeria, Xerophthalmia was estimated to be 1.1 % prevalent in the children population and 7% have VAD (Ajayeoba A.I., 2001). Xerophthalmia describes the ocular manifestations of VAD. It is estimated, by projection, that about 1 million children are affected by VAD and about 100,000 could have an eye involvement (Xerophthalmia) and 50,000 may go blind while 25,000 children are estimated to die annually (Sommers, 1995). This condition is more prevalent in the northwest but least prevalent in the southeast! I think dietary differences play a role here and such findings should be varified by Optometric study nationally!
Treating VAD is done using Vitamin A supplementation therapy and managing the systemic effect like Diarrhea, Measles etc. If there is any ocular effect, it is most appropiate to manage the Xerophthalmia in its early stages when the cornea is not affected! It is best treated with Ocular lubricants, while such conditions like corneal ulceration is best managed with non steroidal anti inflamatory agents like Diclofenac Sodium, others includes topical antibiotic agents like Ciprofloxacin and chloramphenicol ointment! Look out for any corneal involvement in any reported case VAD! It could save that child's sight! It is very appropiate to educate pregnant women and lactating mothers on the need to avoid getting VAD. In these group of people, bilateral blindness could result! Treat them in conjunction with their Gynacologists/Obestricians. Their kind of blindness is retinal in nature!
VAD is a public health issue and Optometrists are adviced to contribute to eliminating this condition! Lets make the future of our children stress free because they are the leaders of tommorrow! Lets make vision 2020 a reality. I know we can. Happy December and Christmas in advance!
Thursday, 16 June 2011
Ophthalmia Neonatorum and childhood blindness!
Optom
In our quest to fight against childhood blindness, I decided to start discussing some common causes of childhood blindness. Ophthalmia Neonatorum refers to any bilateral infection of the eyes of a child of less than one month old! Inshort, if your kid/ward of less than one week tears profusely, suspect ophthalmia neonatorum! Also suspect it when the child's eyeslids are swollen, shut and often smeared with mucous discharge especially produced by Neisseria Gonorrhoae as the infecting agent.
Other organisms too can cause Ophthalmia neonatorum. They include other bacterias like Staphylococcus aureus, streptococcus Pneumonia, Streptococcus haemolyticus; Serotypes D & K of Chlamydia Trachomatis; Chemicals used as prophylasis, Herpes Simplex virus etc But the Gonorraoeae type is the most complicating!
The eventual complication of Ophthalmia neonatorum is a form of corneal blindness that starts with corneal ulcer which then progresses to anterior staphyloma secondary to the opacification that the corneal ulcer precipitated.
This condition is often arrested by using a prophylasis like Silver Nitrate 1% in Crede's Method or the use of antibiotics like Erythromycin 0.5% or Tetracycline 1% drops one or two hours after birth of especially @ risk children. It should be noted that a pregnant woman an STD infection stands a very high chance of giving birth to a child with Ophthalmia neonatorum. Again, if there was injury to the child in the his or her eyes during delivery. The child could be infected in the womb or during delivery or after delivery! The most common infection comes during delivery. While Gonorrrhoeae type of the infection is reducing drastically globally, its a very common cause of Ophthalmia neonatorum in African children; while the Chlamydia type is the most common cause of this disease in children in developed economies! The onset of infection varies from infecting organisms from a matter of hours to days! But the end result, if not treated on time, is corneal blindness in these children. So beware.
While the best way to manage this disease is by either prevention, where the @risk mother is treated of any STDs and/or the child is treated prophylactically; some situations where the infection has become clinical requires a vigorous use of anti-biotics to manage after a microbial swab test has isolated the infecting organism (it should be noted that cemical induced Ophthalmia neonatorum is a self limiting condition, but do not relent to seek medical advice. It could save the eye of that child!).
An intensive use of broad spectrum antibiotic ophthalmic solution and ointment is very important. Check for any keratitis and manage it immediatly (The corneal involvement is usually very dangerous, blindness could occur in a matter of days!). Ocassionally systemic injections or tablets of broad spectrum antibiotics has proven to help in management of this condition!
In Vision 2020-right to sight, Ophthalmia neonatorum is a major issue in childhood blindness which has recieved an international attention. We ask Optometrists to be in the fore-front of tackling this menancing condition especially in Africa. We ask for a program that'll involve us educating mid-wives and gynacologists on the need for prophylasis in the new born child. We should also remind traditional mid-wives on the need for this eye-saving prophylasis! Vitamin A deficiency, Ophthalmia neonatorum and Measles in children are the main cause of corneal blindness and especially in developing countries like ours. This type of blindness in irreversible, but could be tackled after going through this article! We can give this children a sense of belonging by saving them from a live time of blindness and poverty! I will discuss Vitamin A deficiency as a cause of corneal blindness in my next article!
Great Optometry!
Great!
To be continued...
Dr Ezebuiroh Victor Okwudiri.
In our quest to fight against childhood blindness, I decided to start discussing some common causes of childhood blindness. Ophthalmia Neonatorum refers to any bilateral infection of the eyes of a child of less than one month old! Inshort, if your kid/ward of less than one week tears profusely, suspect ophthalmia neonatorum! Also suspect it when the child's eyeslids are swollen, shut and often smeared with mucous discharge especially produced by Neisseria Gonorrhoae as the infecting agent.
Other organisms too can cause Ophthalmia neonatorum. They include other bacterias like Staphylococcus aureus, streptococcus Pneumonia, Streptococcus haemolyticus; Serotypes D & K of Chlamydia Trachomatis; Chemicals used as prophylasis, Herpes Simplex virus etc But the Gonorraoeae type is the most complicating!
The eventual complication of Ophthalmia neonatorum is a form of corneal blindness that starts with corneal ulcer which then progresses to anterior staphyloma secondary to the opacification that the corneal ulcer precipitated.
This condition is often arrested by using a prophylasis like Silver Nitrate 1% in Crede's Method or the use of antibiotics like Erythromycin 0.5% or Tetracycline 1% drops one or two hours after birth of especially @ risk children. It should be noted that a pregnant woman an STD infection stands a very high chance of giving birth to a child with Ophthalmia neonatorum. Again, if there was injury to the child in the his or her eyes during delivery. The child could be infected in the womb or during delivery or after delivery! The most common infection comes during delivery. While Gonorrrhoeae type of the infection is reducing drastically globally, its a very common cause of Ophthalmia neonatorum in African children; while the Chlamydia type is the most common cause of this disease in children in developed economies! The onset of infection varies from infecting organisms from a matter of hours to days! But the end result, if not treated on time, is corneal blindness in these children. So beware.
While the best way to manage this disease is by either prevention, where the @risk mother is treated of any STDs and/or the child is treated prophylactically; some situations where the infection has become clinical requires a vigorous use of anti-biotics to manage after a microbial swab test has isolated the infecting organism (it should be noted that cemical induced Ophthalmia neonatorum is a self limiting condition, but do not relent to seek medical advice. It could save the eye of that child!).
An intensive use of broad spectrum antibiotic ophthalmic solution and ointment is very important. Check for any keratitis and manage it immediatly (The corneal involvement is usually very dangerous, blindness could occur in a matter of days!). Ocassionally systemic injections or tablets of broad spectrum antibiotics has proven to help in management of this condition!
In Vision 2020-right to sight, Ophthalmia neonatorum is a major issue in childhood blindness which has recieved an international attention. We ask Optometrists to be in the fore-front of tackling this menancing condition especially in Africa. We ask for a program that'll involve us educating mid-wives and gynacologists on the need for prophylasis in the new born child. We should also remind traditional mid-wives on the need for this eye-saving prophylasis! Vitamin A deficiency, Ophthalmia neonatorum and Measles in children are the main cause of corneal blindness and especially in developing countries like ours. This type of blindness in irreversible, but could be tackled after going through this article! We can give this children a sense of belonging by saving them from a live time of blindness and poverty! I will discuss Vitamin A deficiency as a cause of corneal blindness in my next article!
Great Optometry!
Great!
To be continued...
Dr Ezebuiroh Victor Okwudiri.
Thursday, 9 June 2011
The month of May, Childhood blindness and the role of the Optometrist!
OptomWow! Its just like yesterday, the month of May, the month just gone by filled with intrigues, drama, war, stagnated 'peace processes', the Arab spring, increased Taliban insurgency, the killing of Osama bin Laden, the Memorial day in the United States of America and our own Children's Day (May 27th!); the pomp that accompanied that day all over the country, the joy on the faces of the children who matched, the pride of seeing our children march, salute and the stone-like expression on the faces of our executives who mounted the podium to observe the gallant leaders of tomorrow doing what they know best! In these children I saw our future. In these kids I saw the hope of continuity. They're the best stage of humanity. I thank God for these children. God bless Nigeria.But who is a child?UNICEF defined a child as anyone who is 16 years or less. These children are the most precious resource of families. They represent the family's future and their hopes. It should be noted that a blind child is a tragedy for his family and the society @ large. A child whose blindness could have been prevented or cured is even a great disaster.Childhood blindness is a collections of diseases or other factors like genetics and environmental influence that can definitively lead to blindness of the child. On its own, blindness is a visual acuity of less than 3/60 on the better seeing eye.While we watched our children march on May 27th, Children's Day, it might interest you to know that there are estimated 500,000 new cases of childhood blindness per year and approximately 50% of these children die between 1-2 years of life! Definitely childhood blindness increases the mortality rates of children of under 5 years. This is worth giving serious attention because, 57% of all childhood blindness is unavoidable (i.e. cannot be cured!). 47% of childhood blindness could either be preventable (about 28%) through improved primary health care services, especially prenatal care for women. While the remaining 15% could be treated through improved Primary eye care services (the Primary eye care Optometrists etc) and specialized surgical eye care and low vision services.
Curiously, childhood blindness is reportedly the second largest cause of blind person years after cataract! It contributes approximately 70 million blind person years globally! This means that a child who is either born blind or someone who becomes blind @ childhood is expected to live 50 years approximately blind and hence contributing a very huge burden to the family, the society and to the individual too! I believe this calls for urgency in tackling childhood blindness by the Optometrists and other eye health professionals!
Economically, blindness in general has been documented to cost communities billionns of dollars in lost productivity, in caring for the blind person, in rehabilitation of the blind person & for special education. Childhood blindness is believed to gulp 1/3 of the total economic cost! For instance, in Africa & Asia that accommodates about 75 percent of blindness & approximately same percentage of blind children, 0.5 percent GDP is lost to blindness in general population with childhood blindness taking 0.16 percent of GDP approximately! This is very baffling & calls for serious looking into!
1.4 million children are said to be blind globally, Africa & Asia accommodates about 75 percent of these children! The prevalence of blindness in developed economies (childhood blindness is said to correlate with economic status of any given region!) is 0.3/1000 persons, while in under-developed economies is as high as 1.5/1000 persons! It should interest us to know that for every blind child, three children have serious vision impairments and 13 children needs glasses!
Finally, the following have been pencilled down as the most common causes of childhood blindness & will require more elaboration in subsequent blogs-
1) Corneal scarring secondary to measles & Vit A deficiencies
2) Ophthalmia neonatorum
3) Retinal diseases
4) Central nervous system lesions
5)Hereditory & Genetic diseases etc
I will be discussing each conditions in details subsequently! Thanks for your readership! Your comments will be highly appreciated! Sorry ones again for the delay in releasing this piece, I found myself in an unusual tarrain but thank goodness that I was able to meander through it!
To be continued...
Dr Victor Okwudiri Ezebuiroh.
Curiously, childhood blindness is reportedly the second largest cause of blind person years after cataract! It contributes approximately 70 million blind person years globally! This means that a child who is either born blind or someone who becomes blind @ childhood is expected to live 50 years approximately blind and hence contributing a very huge burden to the family, the society and to the individual too! I believe this calls for urgency in tackling childhood blindness by the Optometrists and other eye health professionals!
Economically, blindness in general has been documented to cost communities billionns of dollars in lost productivity, in caring for the blind person, in rehabilitation of the blind person & for special education. Childhood blindness is believed to gulp 1/3 of the total economic cost! For instance, in Africa & Asia that accommodates about 75 percent of blindness & approximately same percentage of blind children, 0.5 percent GDP is lost to blindness in general population with childhood blindness taking 0.16 percent of GDP approximately! This is very baffling & calls for serious looking into!
1.4 million children are said to be blind globally, Africa & Asia accommodates about 75 percent of these children! The prevalence of blindness in developed economies (childhood blindness is said to correlate with economic status of any given region!) is 0.3/1000 persons, while in under-developed economies is as high as 1.5/1000 persons! It should interest us to know that for every blind child, three children have serious vision impairments and 13 children needs glasses!
Finally, the following have been pencilled down as the most common causes of childhood blindness & will require more elaboration in subsequent blogs-
1) Corneal scarring secondary to measles & Vit A deficiencies
2) Ophthalmia neonatorum
3) Retinal diseases
4) Central nervous system lesions
5)Hereditory & Genetic diseases etc
I will be discussing each conditions in details subsequently! Thanks for your readership! Your comments will be highly appreciated! Sorry ones again for the delay in releasing this piece, I found myself in an unusual tarrain but thank goodness that I was able to meander through it!
To be continued...
Dr Victor Okwudiri Ezebuiroh.
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