Tear glucose level in diabetes mellitus
The main source of energy for body tissue is glucose. A fixed range of glucose
concentration in different body tissue is essential to maintain, a normal metabolism of the related tissue as a raised or low concentration either affects the normal metabolism of tissue or is pathognomonic of certain diseases like increase in blood glucose levels reflecting the deficiency of glucose utilisation resulting into diabetic mellitus which in turn affecting the metabolism of different organs of the body including the ocular tissues mainly as Rubeosis iridis, Iridocyclitis and Diabetic retinopathy. Average glucose in tears is 2.5 to 4.1 mg%. represents 40% of total reducing substance whereas it makes upto 80% of total reducing substance of the blood. Tear film is composed of three layers. Glucose is present in the middle layer which is secreted by lacrimal glands and accessory glands of Krause and Wolfring. This layer is 6.5 to 7.5 milli microns thick. It also contains inorganic salts, and urea as well as biopolymers, proteins and glycoproteins. Glucose plays a vital role in corneal nutrition and metabolism and also to maintain normal osmotic concentration of the tears. This osmotic concentration of tears is of prime importance since optical integrity of the cornea is significantly influence by the tonicity of the tears. The total osmotic pressure is proportional to the dissolved crystalloid mainly to glucose. The normal osmotic pressure of the tears is equivalent to 0.9%- 0.95% NaCI solution and the variation of osmotic pressure between 0.65% - 1.3% NaCI, equivalent appears to be well tolerated by the eye. But beyond this discomfort is experienced. In ophthalmic practice whether disease is involving anterior or posterior segment of the eye the estimation of blood glucose level is often required to exclude diabetes mellitus because the prognosis and management of many ocular conditions chiefly depend upon the control of blood sugar level. Increasing interest has been shown regarding the level of glucose in tears, in ocular inflammations as glucose, not only helps in metabolism of normal and inflammed tissue, but at the same time forms a good culture media for organisms to grow and also decreases the lysozyme level in tears, which is the main antibacterial enzyme of tears.
In 1958, Lewis JG and Stephen PJ in their series of 15 diabetic patients tried to find out semi-quantitative and quantitative correlation of tear glucose and blood glucose level. They reported 14 cases who have shown a positive clinistix reading where blood sugai varied from 106 mg% to 31O mg% and total reducing substance in tears varied 15 mg% to 150 mg%. In 1968 Antonio R Gasset, Lewis et al reported a definite correlation of tear glucose with blood sugar, particularly in hyperglycemic subjects by quantitative and semi-quantitative methods. Benjamin Milder, has reported that there is definite correlation between tear glucose and hyperglycemia. In 1982 MS Gaur, GK Sharma et al in their series estimated levels of blood and tear glucose, fasting and under glucose load in 50 uncontrolled diabetics, in 50 chemical diabetics and 50 controlled subjects. They found that tear glucose level bears statistically significant correlation with blood glucose level in all groups. In 1983 R.K.Mediratta and J.N.Rohatgi observed that the rise in glucose level in tears is much higher than in the blood glucose in decompensated diabetics. A study conducted by Rajan. Saxena (1985) to find out changes in tear glucose level diabetes mellitus Diabetic patients with no ocular manifestation were chosen for the study. The tear glucose levels were 7 mg% to 20 mg% and the blood glucose level were 123 rng% to 266 mg%. Thus the tear glucose level were 5.69'% to 8,45% of the blood glucose level. In the same study tear glucose levels in normal subjects were found to be 2.75 to 4.75 mg% and blood glucose levels 69 to 98 mg%. The tear glucose concentration was 3.61 to 4.89 % of blood glucose level. Thus there exists a definite correlation of tear glucose level with blood glucose level in hyperglycemia.
Thus the clinical implications of finding tear glucose level lies in the fact that it affects the
immune response of the ocular tissue to infections, affects the structural integrity and refractory i.e. physiologic integrity of cornea.
Ocular infections in diabetes mellitus
The normal response to infection is complex and it involves four major steps:
- chemotaxis in response in bacterial product
- adherence of poly morpho nuclear leucocytes (PMNL) to endothelium at the site of
invasion
- phagocytosis involving oposonins
- microbicidal activity
Chemotaxis and phagocytosis are both disturbed in diabetes mellitus and keto acidotic
patients. There is also impairment of microbicidal activity of PMNL in diabetics. The intrinsic properties of PMNL is altered and its physiological functions are impaired consistently when fasting blood sugar levels exceed 10 milli mol./Utre.
However no defect has been found in the complement system or in opsonin production
arid function even in keto acidotic diabetics.
The basic pathogenetic mechanism underline the decreased PMNL activity is that the
diabetic granulocytes had diminished glycogen content and this may be critical in limiting maximal energy production. Another important factor favouring intractable ocular infection is decreased local immunity due to decrease in tear lysozyme level and an increase in tear glucose level which act as a good nutrient media for flourishing bacteria.
The important ocular infection in diabetes mellitus are:
- Blepharitis
- Recurrent styes or hordeolum externum
- Infective keratitis developing into a ring abscess
- Iritis which is a particularly most common.
Clinical implications of ocular infections in diabetic patients lies in the fact that there is
increase incidence of post operative haemorrhages and iritis.
Cataract In diabetes
Cataract is a known complication of diabetes 3 types of cataract are usually seen in
diabetes.
1. Snowflake cataract
2. Senile cataract
3. Complicated cataract.
1. Snowflake cataract : This is also known as Flocculent, snow storm or metabolic
cataract. This type of cataract is primarily seen in young diabetic patients with uncontrolled diabetes. A sudden myopia presumably associated with hyperglycemia and lens swelling is followed by rapidly developing sub capsular snow storm cataract affecting anterior and posterior cortexes of the lens. Pathophysiology which is responsible for occurrence of diabetic cataract is understood by studying the carbohydrate metabolism of the lens. Glucose in lens is metabolised through 4 pathways. The 3 major pathways are Glycolysis, Kreb's cycle and Pentose Mono Phosphate Shunt mediated through the enzyme hexokinase. In the fourth alternate pathway glucose is converted into Sorbitol by the enzyme Aldose Reductase which in turn is converted to fructose by Polyol Dehydrogenase. Sorbitol is an impermeable sugar alcohol.
Diabetes Mellitus
Poorly Controlled
Blood Glucose Level 200 mg%
Aqueous Glucose Level 200 mg%
Saturation of Enzyme Hexokinase
Shunting of Glucose through Sorbitol Pathway
Accumulation of Sorbitol and Fructose in Lens
Increased Intralenticular Osmolarity
Increased Water Absorption in Lens
Development of Water Vacoules and Clefts
Increased Permeability of Hydropic Lens Fibres
Rupture of Lens Fibres
Increased entry of Sodium in Lens
Exudation of Potassium Glutathione, Proteins
and Aminoacids outside the Lens.
Diabetic Cataract
The above hypothesis is supported by the fact that in Alloxan induced diabetic dogs the
minimum blood sugar for cataract formation was 225 mg%. It was also shown that local and oral administration of Aldose Reductase enzyme inhibitors delay the development of diabetic cataract. Prevalence of metabolic cataract among-patients with diabetes developing in childhood and observed after 10-20 years has varied widely from 2 to 47%. Lens opacities are more common in diabetic women than in men and women show a faster progression of cataract. The snowflake appearance starts in the subcapsular regions of lens. Opacification takes place rapidly and in some cases maturation of the lens leading to blindness occurs within days. Early signs includes change in the refraction of lens, with tendency towards myopia and weakness of accommodation. Prevention depends upon early diagnosis and treatment of diabetes with diet and insulin as hyperglycemia per se appears to be the primary factor related to changes in lens metabolism and structure producing the cataract. Histopathological studies have revealed that in early stages before the denaturation of lens proteins occur control of diabetes may halt further progress and even result in disappearance of opacities. With a dense cataract, it is always difficult to know whether diabetic retinopathy may have developed during its maturation. Retinopathy accounts for blindness after extraction in only 1/3 of cases from whom a lens is removed. Surgical treatment of diabetic cataract should be avoided when it is complicated by proliferative retinopathy One more hypothesis is being suggested for diabetic cataract According to which, excessive protein glycation of the lens fibres is responsible for cataract formation.
2) Senile cataract: This is the most common type of cataract found in diabetic individuals- The greater number of cataract extractions among diabetic patients appears to be related to a more rapid rate of progression of lens deterioration. Correlation of more rapid maturation of senile cataracts in the diabetics than in nondiabetics has recently gained considerable support from studies showing grossly poorer diabetic control among patients than in normal subjects. The diabetic thus have an appearance of normal lens about 15 years older. There is increased incidence of senile cataract in diabetes because it is reflection of rapid senescence. Sometimes the presence of senile cataract in diabetes has been attributed to the duration of diabetes.
3) Complicated cataract: The incidence of complicated cataract in diabetics is no more than the normal subjects. This type of cataract usually is a sequelae to another pre-existing ocular condition due to diabetes like iritis, iridocyclitis, high myopia, secondary to hyperglycemia, vitreous haemorrhage, traction detachment of retina, retinopathy, rubeosis etc.
Refractive and accommodative errors in diabetes
The incidence of transitory refractive errors in diabetic patients ranges from 5 -50%
according to whether patients are examined during a period of good diabetic control or are from newly treated or uncontrolled group. Essential features of this condition are that the changes of refraction come on suddenly and bilaterally and that a myopic change is with a rise and hypermetropia with a fall in sugar concentration of the blood and that the hypermetropia changes seems not to occur as a initial phenomenon but to follow a myopic change. The alteration in refraction is frequently associated with astigmatic changes also. It commonly involves an alteration of 2 to 3 diopters, but changes upto -6 D to +9D in highest meridian have been recorded and in terminal stages of ketoacidotic coma a much higher myopia may develop. There is an interesting fact that most of these refractive changes are characteristically seen, more commonly in age group over 50 years. In any diabetic patient with or without lens opacities, the rapid rise in blood glucose level may induce a marked myopia and a rapid reduction in of blood glucose level to normal may induce marked hypermetropia and a return to normal refractive ability of eye may require several weeks. Diabetic mellitus is the most common systemic cause of transient myopia, often this is the presenting sign of an undiagnosed diabetic patient. The osmotic hypothesis is most accepted explanation for the refractory errors. Myopic change is recorded when the control of diabetes is lost and it is corrected within 3 weeks after diabetes is controlled. Hypermetropia develops suddenly after the institution of insulin therapy in a newly discovered diabetic but passes within a period of 4 to 6 weeks. A spectacle should not therefore be prescribed until diabetes is stable for 4 to 6 weeks.
Diabetes Mellitus
Hyperglycemia
Hydration of Cortical Layers of Lens
Increased Osmolarity of Cortical Lens
Increased Curvature of Lens Increased Refractive Index
Surface of nucleus in relation
to cortex
Combined Myopigenic Effect
Transient Myopia
Rational Control of Rapid Aberrant Control
Hyperglycemia of Hyperglycemia
Reversal of Myopia Hypoglycemia
Emmetropia Hypermetropia
Accommodative changes in diabetic mellitus
Diabetes is often characterised by an insufficiency of accommodation sometimes
amounting to a deficiency of 3-4D, It usually occurs 4% of diabetic population.
Light Near Dissociation : Diabetes Mellitus is the most common cause of light near
dissociation. The aetiology which is suggested for this is a selective neuropathy that involves pupilomotor parasympathetic fibres. It may be due to the consequence of aberrant regeneration of third nerve. Third nerve fibres originally destined for the medial rectus muscle terminate instead on pupillary sphincter. Thus when a patient is asked to look at something close, the eyes converge impulses to the pupils result in pupillary constriction. Aberrant regeneration of third nerve is almost never seen in diabetes mellitus and this differentiates it from light near dissociation due to tumour and syphillis.
Diabetes and glaucoma
Glaucoma is characterised by an increase in intraocular pressure. Diabetic patients are
also prone to development of glaucoma. Diabetics are more prone to glaucomatous changes in the eye, but in contrast, diabetic ketoacidotic, may cause profound hypotony of eye. Two types of glaucoma are commonly seen in patients of diabetes mellitus.
1) Primary open angle glaucoma
2) Secondary angle closure glaucoma
1) Primary open angle glaucoma : The incidence of open angle glaucoma is found to be 6.6 % in diabetic patients. In the randomly selected diabetic group, primary glaucoma was observed to be three times as high as in control group. Adult diabetic patients have shown to have a much greater prevalence of elevated intraocular pressure after corticosteroid testing than in nondiabetics. Diabetes mellitus is the second most important factor linked with primary open angle glaucoma. A very curious, unexplained relationship exists between the two. Diabetes mellitus patients have an increased incidence of primary open angle glaucoma and vice versa. It is still in research phase whether these two conditions complement each other or a single confounding factor is responsible for the occurrence of the two. Thus patients of diabetes mellitus should have a glaucoma evaluation and patients of primary open angle glaucoma should have an oral GTT.
Diabetes Mellitus
Excessive Deposition of Glycoprotein in
Trabecular Mesh Work
Obstruction at Angle of
Anterior Chamber
Impaired Outflow of Aqueous
Increased in Intraocular Tension
Primary Glaucoma
2) Secondary angle closure glaucoma : (Rubeosis iridis, neovascular glaucoma, haemorrhagic glaucoma). Rubeosis iridis is a neovascular response of the iris vessels mainly attributable to three principle factors a) hypoxia; b) venous-stasis and c) tissue viability. The etiopathogenesis of secondary angle closure glaucoma is demonstrated in the following flow chart.
Diabetes Mellitus
Microangiopathy Affecting Iris Vessels Iris Ischemia
Extension
of Iris Ischemia
Membrane
on Limbus Iris Hypoxia
Stimulation of Angiogenesis
Formation
of Complete
Anterior
Syndrome Proliferation of Mesenchymal Cells
And Minute Vessels on Surface of Iris
Formation of Fibrovascular Membrane
usually in Peri-pupillary Area
Obstruction
to Outflow Bleeding
of Aqueous Progressive Extension of from fraglile
Membrane towards periphery neovascular
tissue
Encroachment on Angle Structures
Retraction of Membrane Recurrent
Hyphaema
Pulling of Peripheral iris up against
Angle Structures
Deposition
Complete Obstruction of Anterior of Blood
Chamber Angle Clots in
Trabecular
Secondary Angle Closure Glaucoma Mesh Work
Neuro-ophthahnologic manifestations of diabetes mellitus
There is a large spectrum of neuroocular manifestations of diabetes mellitus. The various
presentations associated with diabetes are:
1. Optic neuropathy
2. Ophthaimoplegia
3. Argyll-Robertson-Pupil (ARP)
4. Tonic accommodation
5. Tonohaptic reaction
6. Insufficiency and paralysis of accommodation
7. Amblyopic pupillary paralysis
8. A rare variety of toxic ptosis
9. Nystagmus
1. Optic Neuropathy
Optic neuropathy is rarely seen in patients of diabetes. However it is sometimes followed
by optic atrophy which is usually due to other toxic influences such as tobacco which have an additive effect with existing diabetes mellitus. Existence of primary optic atrophy represents a grave situation.
2. Ophthaimoplegia
Cranial nerve palsies are associated with diabetes mellitus. It involves all cranial nerves
with sparing of first and eleventh cranial nerves. Etiological factor linked to occurrence of ocular palsies is ascribed to hyperglycemia, thrombotic and haemorrhagic lesion involving the nerves. Involvement of 3rd, 4th and 6th nerve is usually early. Prevalence of ocular motor palsies is 5% and may be the first symptom of the disease. Isolated cranial nerve palsies are more common in 3rd or 4th cranial nerves, but combination may also be seen. Recently, 3rd cranial nerve palsy is found to be the most common nerves involved, but patient may present with a recurrent facial nerve palsy. The first symptom is diplopia which is associated with ipsilateral headache, forehead pain and painful eye. The onset of symptom is acute and complete recovery occurs over weeks to months. In 3rd nerve palsy due to diabetes mellitus pupils are spared. Preservation of pupillary reactivity to light in diabetic neuropathy is presumably related to involvement of the inner fibres of the nerve and sparing of the outer fibre which are responsible for pupiloconstrictor function. The peripheral location of pupilary fibre allows them to be nourished by the venous blood where the nerve lies free in the cavernous sinus. This point is very diagnostic in differentiating 3rd nerve palsy due to aneurysm tumour and extrinsic compression of 3rd nerve in which case pupils are involved.
Salient features of diabetic ophthalmoplegia are
(a) Generally the patient is an adult who has had diabetes for a long time and in whom the
disease has been diagnosed relatively late in its course or is poorly controlled.
(b) When third nerve is involved, the pupil usually is not dilated and reacts to light.
(c) Recovery usually occurs in 1-9 months.
(d) Aberrant regeneration of third nerve does not occur.
(e) Other diabetic complications are usually present.
The most probable etiology suspected for changes is ischemia resulting from
microangiopathy, other suggested etiology are' microhaemorrhages, infarction of nuclear complex in mid brain and metabolic neuropathy.
3. Argyll Robertson Pupil (ARP)
Sluggish reaction to light, excessive miosis and even loss of light reflecx is reported in 9 to
25 % of diabetics. This abnormality of pupillary function is mainly attributed to autonomic neuropathy. Abnormal pupillary reaction are mainly seen in persons with long duration or maturity onset diabetes. The prolonged latency of pupillary reaction is caused by peripheral neuropathy affecting pupillary fibres.
4. Tonohaptic reaction
Pupillary reaction characterised by an extremely long latent period preceding both
contraction to light and redilatation followed in each instance by a short but prompt movement. In the phase of contraction, the terminal sympathetic component which normally completes the reaction are absent.
Miscellaneous ocular conditions associated with diabetes mellitus
a) Xanthelasma and xanthoma of eye lid
b) Asteroid Hyalitis - Asteroid bodies in aqueous humor was initially thought to be pathognomonic of diabetes mellitus and/or hypercholesterolemia but recent studies have shown that prevalence of AH in diabetic and non-diabetic population is about same (0.5%). These are golden coloured bodies floating in front of eyes.
c) Punctate Epithelial Dystrophy - These are small fiery fluorescein stainable dystropic areas on cornea usually epithelial and prevalent in lower half of the cornea. It is more common in diabetic females and it is shown in upto 62% of diabetics.
These lesions usually precede retinopathy in all most all cases thus may be considered to
be diagnostic harbinger lesion to retinal involvement. They are sometimes considered to be earliest lesion occurring in diabetics.
(d) Interstitial lipoid keratitis - This condition is usually present in association with lipemia retinalis and is due to precipitation of lipids in corneal interstitium due to its low temperature. They present as multitude of fine granulation arranged in radial bands.
(e) Lipemia Retinalis - This is a rare ophthalmic manifestation of acutely uncontrolled diabetes mellitus. The fundus changes are pathognomonic. The retinal vessels appear pink salmon, waxy or white in colour as if filled with cream. There is poor or more often absent light reflex. Visual acuity is at times affected during acute phase, but returns to normal after clearing of the phenomenon. This condition arises when total plasma lipid rise above 3.5 gm %. The hyper lip oprotenemia associated with diabetes is characterised by a striking elevation of pre beta lipoprotein and chylomicron fraction. Clinical manifestations which accompany Lipemia Retinalis include interstitial lipoid keratitis, xanthomas and a tender hepatosplenomegaly. The response of LR and associated symptoms to proper diet and insulin therapy is dramatic and may occur in disappearance to significant degree within 1-3 days.
Diabetic retinopathy
Diabetic retinopathy is the most dreaded complication of ocular manifestations of
diabetes. Prevalence of diabetic retinopathy is higher in 1DDM (40%) than in NIDDM (20%). The prevalence of diabetic retinopathy in the whole diabetic population was found to be 25%. Clinically three main types of retinopathy are classified (i) Background (ii) Preproliferative (iii) Proliferative.
Most significant risk factor for development of diabetic retinopathy is the duration. It is
extremely rare for diabetic retinopathy to develop within 5 years of onset of diabetes mellitus, but 5% of NIDDM have background diabetic retinopathy at presentation. The following data supports the above statement:
In one study, the prevalence of diabetic retinopathy was found to be 7% in patients with
diabetes for less than 10 years, 26% in patients with diabetes for 10 to 14 years and 63% in patients with diabetes for 15 or more years.
The etiopathogenesis of diabetic retinopathy is
(a) Abnormalities of platelet function - Platelet aggregation in vitro normally proceeds in two stages. The first stage occurs spontaneously and the second stage induced by the addition of ADR Normally platelets following ADP induced aggregation tend to disaggregate spontaneously. Platelet samples from patients with diabetic retinopathy show an abnormally increased tendency to aggregate at low concentration of ADP. Patients with diabetic retinopathy also show a decreased rate of disaggregation, i.e. platelet aggregates are more stable. An abnormal plasma factor whose biochemical nature has not been elucidated also enhances ADP induced platelet aggregation.
(b) Defective fibrinolytic system - Patients with proliferative retinopathy have a decreased spontaneous fibrinolytic activity and a higher propensity to develop retinal arteriolar and venular obstruction.
(c) Hyper viscosity and abnormal erythrocyte - Aggregation. There is significant elevation of serum viscosity in diabetic patients compared to non-diabetic controls. Diabetic with microangiopathic sequele i.e. retinopathy had a higher value than those without these sequele. Viscosity = shear stress/shear rate. In the vascular system, relatively low shear rate occur in the capillaries and venules. Therefore abnormality in RBC aggregation might be most important at the microvascular level where the velocity of blood flow and the shear rate dimmish. The viscosity of whole blood was found to be 20% higher in long term nonacidotic diabetics than in normal controls. A study shows that blood viscosity was not increased in short term diabetics who had no evidence of retinopathy or neuropathy. This suggested that high blood viscosity is a later phenomenon that may exacerbate established retinopathy, but may not be important in the formation of the very early retinal lesion. The elevated whole blood viscosity is being attributed to increase in a 2 globulin and b globulin. These proteins coat the RBC thus enhancing their tendency to rouleaux formation. In an invitro study it was found that rouleaux formation was greater in diabetic than in normal controls. An increase incidence of abnormal intravascular RBC aggregation has been found in diabetic patients in vivo by examining the conjunctival vessels.
There was a positive correlation between the incidence and degree of RBC aggregation in the conjunctiva and degree of retinopathy.
(d) Basement membrane (BM) thickening : BM thickening is a histopathologic hallmark of diabetes mellitus. BM thickening in skeletal muscle capillaries has been a controversial subject. Siperstein et al found BM thickening in the capillaries of skeletal muscles in diabetics and even in normoglyceinic children who were off springs of two diabetic parents known as prediabetics. Thus BM thickening is sometimes considered to be a genetic marker of diabetes rather than a result of overt hyperglycemia. There is positive correlation between duration of diabetes and thickening of BM and it is greater in diabetics with retinopathy than in those without retinopathy. Progressive BM thickening in retinal precapillary arterioles might lead to gradual closure of these vessels and to non perfusion of the capillary they supply
(e) Capillary endothelial cell damage and proliferation
(f) Changes in RBC leading to defective oxygen 'transport
Diabetic status control and retinopathy
Good control of metabolic aspect of diabetes delay the onset and decrease the severity of progression of retinopathy. Retrospective studies have shown that patients who achieve better control of their diabetes have a lower incidence and lesser severity of retinopathy. A prospective study of metabolic control was conducted on two groups of Alloxan induced diabetic dogs. In one randomly chosen group careful metabolic control was attempted by treatment twice daily with insulin. These dogs were free of glucosuria for 25-50% of time. The other group was poorly controlled only enough insulin was injected to prevent severe hyperglycemia and glucosuria. After 5 years of diabetes, retinal vessel changes indistinguishable from non-proliferative diabetic retinopathy in human were found in each animal of poorly controlled group and drastic reduction in incidence and severity of retinopathy was found in well controlled group. The above study proves that diabetic microangiopathy is not a genetic disorder that is inherited with, but is a manifestation of metabolic abnormality of diabetes and the good control of diabetes is always justified.
Diabetic retinopathy and other diabetic complications
There is a good evidence that more severe the retinal disease, the greater the likelihood of
serious associative disorder especially if proliferative diabetic retinopathy is present. The incidence, frequency and severity of clinical renal disease increases with severity of retinopathy. The frequency of proteinuria increases from 15% in patients with no retinopathy to 23-36% with mild form of retinopathy and to 73% in severe proliferative retinopathy. The major cause is that in patients of severe proliferative retinopathy there is either advanced renal disease or coronary artery disease. In a series of patients with proliferative disease, renal biopsies were performed and all patients had histologic evidence of glomerular disease while a significantly smaller frequency of renal disease was found in groups with milder or no retinopathy. Thus the clinician should be alert to detect proliferative disease because it is an alarming sign for onset of renal disease. Certain medical problems pose significant risk for the onset and progression of diabetic retinopathy. These are pregnancy, hypertension, chronic persistent hyperglycemia, renal disease, hyper lip id emia and presence of neuropathy and joint contracture.
Diabetic retinopathy and pregnancy
Many diabetic women go through pregnancy without adverse effects on the retina or on
vision. Others experience a worsening of theii retinopathy during pregnancy resulting sometimes in serious loss of vision. The highest risk of developing serious deterioration of retinopathy and vision during pregnancy exists among patients with proliferative diabetic retinopathy, the risk among patients without retinopathy or with nonproliferative diabetic retinopathy is relatively low. The risk of blindness is mainly attributed to rapid growth of proliferative lesion and development of massive vitreous haemorrhage. The risk is maximum during the first trimester. Although the rate of progression of proliferative retinopathy during-pregnancy may be alarmingly rapid, the role of pregnancy in producing this excerbation is still uncertain. The course of many eyes with proliferative retinopathy that deteriorates during pregnancy show a slowing or an actual regression after the termination of the pregnancy. This provides circumstantial evidence that pregnancy has adverse effects and therapeutic abortion may be considere
