00 : 00 / 05: 00 (Preview)

This discussion has ended. Watch the recording on Medflix app,

Diabetic Microvascular Complications

Mar 31 | 2:00 PM

Diabetes Mellitus (DM) is a metabolic condition marked by hyperglycemia and caused by abnormalities in insulin secretion, insulin action, or both. Chronic hyperglycemia causes long-term damage and failure of multiple organ systems, with the eyes, nerves, kidneys, and heart being the most affected. The micro-vascular disease leads to retinopathy, neuropathy, and nephropathy, which causes varying degrees of vision impairment, nerve damage including peripheral or autonomic manifestations, and kidney function to deteriorate, respectively. Join us live on Medflix to discuss the techniques of early detection and management of diabetes with Dr. Benny Negalur, an eminent physician and diabetologist!

[Music] good evening everyone uh i dr ucha welcome you all to this amazing session and i'm glad you all are here uh we have with us uh dr benny necklord uh she is a consultant physician and diabetologist uh practicing in mumbai currently uh welcome mom uh i am glad uh you could make it and thanks a lot for your valuable time uh so we will be discussing diabetic microvascular complications uh every one of us needs this even if we are in normal opd medicine operating surgical operating so we all see all of this complications so mom will be walking us through uh it in detail over to you thank you so much dr and a very good evening to all of you listeners out there in the audience and today we are going to discuss a very very kind of extensively exhausting huge topic of diabetic microvascular complications we know that the incidence and prevalence of diabetes is rising in india itself we have more than 75 million diabetes patients and we have an equal number of pre-diabetes in our country who are waiting and kind of to become diabetic so the burden of diabetes itself is so large with the discovery of insulin in 1921 by banking and best that error was a area error of survival patients used to die because there was no treatment but subsequently you know insulin was discovered and then we had a chain we had human insulin porcine insulin beef insulin then now we have insulin analogues and we have basal insulin we have long acting and very long acting basal insulins and we have short and very short rapid acting insulins and then we have the whole lot of ohs since 1930s onwards now we have a handful of drugs which we can treat diabetes with and therefore diabetes on the whole is kind of getting into control but not all the time and with the advance of statins and aspirin we the mortality cardiovascular mortality has come down but the microvascular complications have been on the rise increasing the morbidity of the patient and that disturbs the quality of life makes them absent from work and also sneezes kind of snatches away the happiness that they should that they rightly deserve so coming to the complications you know in diabetes there is a microvascular complication and microvascular complication microvascular complications are in the large blood vessels involving the coronatory disease cerebrovascular disease and peripheral artery disease and the microvascular complications where the occlusion of the arteries happens in the micro circulation very close to the tissue level and therefore it involves the major organs like the kidney causing nephropathy neuropathy the nervous involvement and retinopathy which is involvement of the eye and somewhere between the two there is a bridge causing erectile dysfunction and cardiac autonomic neuropathy microvascular complications are secretly of diabetes following uncontrolled chronic hyperglycemia and the time to develop microvascular calming for complications are faster than the microvascular complication easy to realize because the arterials are smaller the capillary circulation is smaller and therefore occlusion in those vessels is earlier this is the landmark trial done by um in india by dr sanjay karla from karnala he found at the end of one year microvascular complications were significantly higher in individuals from indian non-metropolitan cities than the metropolitan cities and among the microvascular complication neuropathy was the most common complication in both the groups and this was a presentation in 2021 the latest presentation so why does this happen there are predictors they in if the a if the age is advanced if the duration of diabetes is long and the severity of hyperglycemia is high then the complications especially the microvascular complications are higher and this was shown in the dcct trial which was done for type 1 diabetes as you can see the graph on the left hand side those who put on intensive therapy uh had lower complications of retinopathy nephropathy and neuropathy but in those who are on conventional treatment you can see here that as the a1c increases the risk of these microvascular complications increase so diabetic and those in the intensive group the diabetic disease was decreased by 76 percent by maintaining an hb a1c of 7. the advancements of progression of eye disease was decreased by 54 percent diabetic kidney disease was decreased by 50 percent and diabetic nerve disease was decreased by 60 telling us thereby that at the onset of diabetes itself if we maintain a good glycemic um a1c then it produces a legacy where the complications are minimum and that gives a good quality of life to our patients it was also seen in the uk pbs study this is a landmark trial for type 2 diabetes which shows that the risk reduction with just one percent decline in the annual mean a1c reduce the microvascular complications by 37 peripheral vascular disease by 43 and the remainder of the complications like mitral like myocardial infarct stroke heart failure and cataract extraction was reduced between 12 to 19 and that's a good sign again reiterating that a good glycemic control is important now the microvasculature which actually starts from the terminal arteriole and onwards into the capillary circulation and the tissues and the venules this micro circulation is highly susceptible to damage due to chronic hyperglycemia this is because when the the exchange of glucose happens in the capillary circulation and the tissues there which receive these glucose from the circulation are so overwhelmed with high glucose in the tissue itself that the cell cannot cope with this excess glucose the glycolytic pathway is overwhelmed where the excess glucose is now transferred to other pathways for the cell to survive but if this happens repeatedly and over a longer duration then there is apoptosis of these cells but it does these complications are not seen in everybody there is a genetic predisposition so if the father has say for example diabetes and kidney disease and the sun is most likely to have diabetes and also kidney disease so genes play a big role in microvascular complications and those who develop that they have a lot of disability it accelerates mortality and finally fails to avail work on regular basis due to the illness now which are the cells that are involved in microvascular complications so in the retina it is the endothelial cells the pericytes the muller cells and the ganglion cells we have to remember that retina has 10 layers the ganglion and the nerve cells are more posterior whereas choroid and all the other cells parasites etc more anterior and the renal glomerulus it is the messaging cells and the podocytes that are involved whereas in the peripheral nerve the schwann cells and the endothelial cells and the parasites are involved in the peripheral nerve as i told you the classical pathway for glucose oxidation is the end in mia pathway i'm sure all of us know this we have learned this in medical school but in chronic hyperglycemia this pathway is overwhelmed there is excess of glucose and then it opens up other pathways these are the four major pathways that are opened up which are otherwise dormant in normal people whenever there is excess glucose entering the cell so you have the polyol pathway the polyol pathway the glucose gets converted into fructose and then sorbitol and sorbitol once it enters the cell it remains there it's very difficult for sorbitol to get out it swells the cell swells with osmosis and causes death of the cell and causes death then you have the age or the advanced glycated end product pathway where there is glycation between the proteins in the cell and the excess glucose giving rise to destruction of tissue and then the protein kinase pathway that actually produces a new vessel formation increase permeability of the blood vessels and produces oxidants to pass through into cells causing its destruction and finally we have the hexosamine pathway the hexosaming pathway converts the glucose into urine phosphate and finally it produces um it interferes with the dna and the proteins in proteins inside the cell giving rise to epigenetic changes in the dna and subsequently producing destruction of cells so all these excess pathways are are opened up and these are the pathways which are not normal that can give rise to uh cell dysfunction and complications we'll see now diabetic kidney disease it is characterized by protein urea and a declining egfr it doesn't require both these to produce diabetic kidney disease may not because if i tell you in simple words there is a cliff here and the cliff is end stage renal disease and there is a train that is advancing towards the cliff and that train is the gfr now it depends how far from the cliff is this trains so if it is far away from the cliff it means that the gfr is normal as it comes closer to the cliff then the gfr decreases slowly over time finally taking it to the end of the cliff giving rise to end stage renal disease now does protein area come in protein urea is kind of the speed of the drain the ex the more the protein era the more is the speed of the train and so the advancement towards the clip will be faster if the speed of the train is fast that means if there's a declining glr gfr and in addition there is advancing protein urea then it hastens the hastens the kidney damage towards end stage renal disease now this occurs in 30 percent of type 1 patients and 40 percent of type 2 patients it is more common in african americans asians and native americans and associated with cardiovascular disease this is a good diagram to show you what is normal on the left hand side that's the glomerular capillary basement membrane and you can see the podocytes there the podocytes are on the side of the bowman's capsule and there's a and there's a basement membrane which actually acts as a filter and then on the other side you see the endothelial cells so the endothelial cells or the capillary network is in close contact with the basement membrane and the bowman's capsule these foot processes as they are known as on the end of the bowmen's capsule are actually so tightly packed that anything that is filtered and like albumin that is for macromolecules that are filtered are not allowed to go into the bowmen's capsule then what happens in diabetes you will see on the right hand side there is glycation of proteins there is excess deposition of collagen there is excess deposition of basement membrane material which causes the basement membrane to get thickened not only thickened but because of the cross linking of these proteins this basement membrane trips off kind of breaks in various parts very well depicted in this figure it's just like a filter when you're filtering t and there is t powder there on one side if the filter is good the tea powder remains on one side and the tea is filtered but if there are fenestrations or holes in that filter you will see that the powder also gets into the tea exactly the same thing happens here so you see there are fenestrations in this basement membrane which thickening causes separation of the food processes which are partially destroyed because of glycation and also the capillaries on the other side are separated allowing the macromolecules like albumin to pass through the basement membrane and get filtered into the bowels capsule and into the tubules giving rise to albumin urea this is the starting point of diabetic kidney disease and you can see on the right hand side very well depicted is a capillary lumen along with the basement membrane very well shown and in the center is the mesengium the mesangium is the one that holds the capillaries if the mesangium was not there the entire a tuft of capillaries would have collapsed so it keeps the capillaries separated and then you go to the next stage where you can see the glomerulus showing diffuse basement membrane thickening here with nodular glomerular changes and these changes actually destroy the glomeruli and and it goes into a glomerular sclerosis and you can see the red staining fibrin can be seen in the wall of the afferent arteriole as well this is the classical nodular glomerular sclerosis the glomerulus shows marked increase in the mesangium the glomerular sclerosis and the messenger expansion along with the thickening of the basement membrane is the high mark of diabetic kidney disease and at the periphery of the nodules you can see a small flake of red staining fibrin at one point of the bowman's capsule and this is complete hyalinization of the glomerulus it is advanced stability nephropathy the glomerulus here is completely replaced by acellular hyline and the glomerus has been totally dysfunctional and destroyed and the tubular and interstitial changes of chronic pylon nephritis are also seen in this picture there is hyalinization of also the arterioles the both the efferent and the afferent arteriole suggesting that it is a totally dysfunctional kidney and fibrin as you can see is again present in the walls of the arteries now having said this let's see what are the clinical stages of diabetic nephropathy i said that you have to have two types the gfr decreases in diabetic kidney disease at the same time they could be increasing albumin urea so the hyperfiltration is the first stage or the hypertrophy of the kidney then it goes into stage two where the albumin urea is normal subsequently going into microalbuminuria and then overt proteinuria and finally end stage renal disease and if you see the structural changes starting from stage one initially there's a glomerular hypertrophy then there's a thickening of the glomerular basement membrane and still further thickening giving rise later on to clear abnormalities there is an expansion of the messenger matrix and the cell and finally the globular closure as i showed you in my previous slides so the gfr can be increased initially in stage one and slowly declining o's two and three and finally into state four and five the gfr decreases markedly at the same time we do the urinary albumin excretion which which slowly uh kind of decreases and you see here somewhere around stage three four and five you see uh albuminuria we know that the normal albumin is less than 30 and between 30 and 300 you call that micro albuminuria although this terminology actually is not used nowadays so you actually look at the urinary albumin excretion and going from stage 3 to five you see the albumin keeps on increasing the blood pressure is not is also to be noticed mind you as the kidney goes on deteriorating the blood pressure keeps on increasing and and when we need to treat diabetic kidney disease we not only have to look at the kidney itself but also at the blood pressure if the blood pressure is not treated adequately that give me further deteriorates in function so you can see from stage 1 to stage 5 somewhere after stage 3 the blood pressure increases and hypertension persists beyond that but when we see a patient clinically we normally look at the gfr we need to calculate the gfr and now we have calculators here the ndrp formula can be estimated from the calculator in your mobile phone you can calculate the egfr you need to know the serum creatinine age race etc you fill in and finally you get the egfr so if if um at stage 1 the gfr is more than 90 stage 2 the gfr keeps on declining over the other stages between 60 and 89 is stage 2. between 30 and 59 is stage 3 between 15 and 29 is stage 4 and less than 15 is stage 5 which is kidney failure now this is what we know one want to know in practice because we have to modulate the drugs we have to take off some anti-diabetic regimens we have to put this patient on insulin at the same time we also need to take care of the other co-morbidities of kidney disease itself which i will subsequently tell you this is a very good diagram now uh recently in 2021 put in diabetes care which is uh by the american diabetes association microvascular complications and this is the standards of medical care and you will see on one side on the right hand side is the increasing albumin urea and on the left hand side you can see the decrease in gfr and both if they are present you can get one and not the other or you can get one early and the other late so you have beautifully shown in this diagram the various colors of uh of the two types of kidney disease the advancing albuminuria the decrease in gfr both put together to give you advancing kidney disease and you can see that from green color which is normal it is going into the yellow the orange and finally the red color which is severe kidney damage now when you come to severe kidney damage uh starting from the stage to 3 a and 3b and finally it is mandatory that we send this patient to the nephrologist for good kidney care so this uh this is what i was talking about these are the co-morbidities of renal disease itself we not only look at the gfr and the albumen you look at the greenhouse pentagon as its holes as a whole and we know that as the kidney function decreases the a1c starts getting control this is one indicator that kidney function is deteriorating in otherwise uncontrolled patients patients of renal disease diabetic renal disease have marked variability in their blood sugars on a daily basis you can see a patient within with a blood sugar of say 250 in the morning and somewhere in the afternoon at 4 o'clock it goes to 40 and then increases to 300 at night so these fluctuations of blood sugars on a daily basis and fluctuation of a1c is a phenomenon that is almost characteristic of diabetic kidney disease and that is what we should watch for watch for we have to see that they do not go into hypoglycemia at any time because that can be detrimental and we need to correct the hyperglycemia besides that you look at the other parameters the blood pressure the lipids look at the iron status the iron also goes down the hemoglobin anemia is a feature of chronic kidney disease you look at the bone mineral the calcium the phosphates look at the electrolytes normally as the kidney function deteriorates the potassium goes up and also monitor the gfr and the albumin we should remember that these patients are the one who get frequent urinary tract infections and therefore it is it is necessary that we look for these from time to time especially if there's a rapid deteriorating kidney function or there is a marked fluctuation in the a1c when the patient remains uncontrolled so based on the presence of albuminuria and reduced gfr in the absence of signs and symptoms of other primary causes of kidney damage is a diagnosis of diabetic kidney disease but if there's an active urinary sediment or there is rapidly increasing albuminuria or nephrotic syndrome or rapidly decreasing egfr or the absence of rich nopathy then it suggests an alternative or additional cases of diabetic kidney disease remember that if kidney disease occurs in a diabetic patient we tend to focus only on the sugar we tend to say that okay you have diabetic kidney disease but we should remember that there are other kidney problems as well that can co-exist with diabetes for example in a male you can get obstructive uropathy secondary to prostate enlargement or you can get say a women chronic pyelonephritis or chronic ascending urinary infection that can actually speed up or deteriorate an already existing kidney disease so we need to look at all these factors as well and and refer to the nephrologist on time so that he can um so that he can look as a kidney in a better way than a diabetologist or a physician the american diabetes association has also given shortcuts for screening this is a palm size meter driven by two batteries and you can see that it gives you various profiles glucose protein bilirubin neurobilinogen etc ph of the urine etc it is not the great test to have but it can be used as a screening test where you can you know get kind of a reading on the spot and further work up with the serum creatine and estimate the gfr in in your patients so the screening recommendations by the ada standard of medical care and diabetes says that we need to do a urine urinary albumin and egfr as an annual assessment in patients with type 2 diabetes irrespective of treatment and in patients of diabetes if the urine albumin is more than 300 milligrams per gram of creatine and or the gfr is between 30 and 60 ml then they have to be monitored twice a year so the management depends on the overall cardiovascular risk reduction blood pressure control the glycemic control and the inhibition of the renin angiotensin system so we have now protective drugs for kidney in our armamentarium of anti-diabetic care the ace and the arbs as seen in several trials in the past the renal trial the indt trial for acenometers and the benedict style for arbs have clearly shown that they protect the kidney from protein urea and albumin urea so it is mandatory that we put the patient on ace or arvs in a diabetic patient who has hypertension because it not only protects the kidney from albumin urea but it also decreases the blood pressure how do they act they act on the efferent blood vessel as we know in diabetes the efferent blood vessel arteriole is actually narrowed because of decrease of insulin ah so when you give an as asynrb air b it dilates that if the different arterials thereby reducing the barotrauma in the kidney reducing the pressure in the glomerulus and thereby decreasing the albumin area of protein urea we need to do their serum creatinine and gfr monitoring continuously in patients who are rapidly going into advanced renal failure and in early stages as we recommended by the american diabetes association maybe once or twice a year optimize the blood pressure we tend to forget this we need to target a blood pressure of 140 by 90 if you have a blood pressure 130 by 80 without other co-morbidities you can make that will be good for the patient optimize the blood sugar maintain an a1c of less than seven for most of the patients if they have comorbidities you can maintain them at seven to seven point five or maybe also eight in some patients nephrology referral referral is usually done when the gfr goes below thirty but if there is an uncertain diagnosis or it's difficult to manage this patient or as a rapid progression or the albuminuria increases then you need to refer to a nephrologist pretty early we now have another group of drugs the sglt2 inhibitors we know that the sglt2 inhibitors are anti-diabetic drugs which push out the glucose in the urine and thereby control the blood sugars they are used pretty early in diabetic kidney disease along with ace and arvs because they are known as kidney protectors and therefore help in the prevention of progression of diabetic kidney disease so we have now two drugs on the on board to prevent the acceleration of diabetic kidney disease what about our anti-diabetic therapy bicones as you know metformin is contraindicated if the egfr goes below 30 and between 30 and 45 gfr you need to reduce the metformin you can but you also need at the same time to monitor monitor the patient and call them for frequent follow-ups we know our indian patients you call them after one month or two months or even three months sometimes uh you know they are okay with the treatment they look at their sugars but they don't bother to see their gm part and you have already put them on metformin because they are between 30 and 45 and they might come to you after six months with a rising create need so if it is at that time you need to uh monitor them very frequently and this has to be addressed to the patient and discussed sulfonylureas are best avoided because they are long-acting drugs and they can push the patient into a prolonged hypoglycemia but you can use shorter acting sulfonylureas like glyphicide and glycoside which may be used in mild to moderate renal insufficiency we normally put these patients of moderate and severe insufficiency on insulin sometimes you need to combine sulfate in urease with insulin or give another oha along with insulin to stabilize the glucose variability that happens in the day reperglanide is safe in kidney failure it can be given three times a day 0.5 or 1 milligram or even 2 milligrams that can be given glitter zones and a carbos are best avoided in patients of kidney disease but all the glypton ceta wilder can be given with a dose adjustment half the dose has to be given but if the patient is on leaner glypton then it can be used without those adjustment insulin is the treatment of choice we need to give regular basal boneless therapy in these patients remember it is always nice to give regular rapid acting insulin if the patients are not getting control with a basal insulin at night sometimes you need to give the rapid insulin even four times a day depending on how many times the patient eats when the kidney disease advances of course insulin is required but maybe you can put them also on glp rna and refer them to the nephrologist so that's a diabetic nephropathy we go on to the next microvascular complication that's diabetic retinopathy retinopathy is a highly specific vascular complication of both type 1 and type 2. remember that retinal blood vessels are the only blood vessels in the body that you can see with the with the fundoscope you cannot see any other blood vessels so it gives you a good picture of what the complication vascular complications of diabetes are and that is why in most of the trials they use retinopathy as the outcome end point because that's what you can see very easily and also count the arteries than in the various quadrants that are involved the prevalence is strongly related to both again the duration of diabetes and the level of glycemic control most common causes of new case of blindness among adults is diabetic retinopathy i remember when i was a student at two days to say vitamin a deficiency was the most common cause of blindness but now the picture has totally changed um diabetes is the cause of most common cause of blindness but you can also get glaucoma and cataracts and other disorders of the eye it's classified between uh into a non-proliferative diabetic retinopathy or and a proliferative diabetic retinopathy advance occurs from non-proliferative early mild to moderate and then severe and finally going to kind of end stage proliferative diabetic retinopathy which can be very detrimental and and can cause loss of vision so that is the proposed disease severity level and that's and on the right hand side you can find the findings on a dilated ophthalmoscopy so when there's no retinopathy there are no abnormalities and as you progress into proliferative retinopathy you will see the appearance of micro aneurysms these micro aneurysms become increase in number and if you have any one of the following that is more than 20 intra-retinal hemorrhages in each of four quadrants or a definite venus bleeding in more than two quadrants or you have a prominent intra-retinal microvascular abnormality in just one quadrant these are signs of severe nonproliferative diabetic retinopathy and then finally advancement into proliferative retinopathy will be either newest polarization or vitreous hemorrhage or pre-retinal hemorrhage as you can see in this picture this is non-proliferative diabetic retinopathy on the starting from the left hand side you can see a few exudates here but you can see a new results you can see dilated veins again you can see in the middle beading looping of the veins and also a large number of hemorrhages and few exudates and on the right hand side you can see a large number of hemorrhages in the lower panel beading dilatation of the retinal veins with bleeding and the last picture will show you an ischemic lesion there looks like cotton wool but that ischemic lesion is secondary to occlusion of the micro blood vessels in the layers of the optic nerve which line the retina posteriorly that can get obstructive and give rise to new vessel formation so this is the kind of a forerunner of new vessel formation these are the pictures of proliferative retinopathy proliferative retinopathy is easy to understand there's proliferation that means there is new vessel formation and as shown in the arrow here on the left hand the first two picture you can see small blood vessels will grow anyhow do not follow the pattern of the retinal blood vessels they are like weeds kind of hanging in the water and these are very susceptible to hemorrhage and you can see a picture of a hemorrhage on the right in the upper panel a large hemorrhage in the lower panel and in the middle picture you can see uh the retinal detachment because of traction of um the healing of a retinal hemorrhage that had occurred in the past now all these can give rise to a pure and the acute blindness so proliferative retinopathy is a dangerous situation the last picture is proliferation of the blood vessels in the iris and this is also a edematous maculopathy anything that happens in the macula as we know the macula is the area of the finest vision there are maximum rods and cones there so you can that is gives you the acuity of vision and anything happening in the macula whether it's edema whether it's deposition of exudates or there's a bleeding there it can give rise to sudden blindness on the right hand side you see an optical tomography here oct it is known as uh where the layers of the retina are actually separated by filling up by fluid which is edema actually in the layers of the retina giving rise to lifting of the layers of the retina and that can decrease the vision markedly in a patient of diabetic eye disease so screening it is vital that we do the screening for every patient we don't want our patients to go into the late stage of frictionapathy we don't want a patient to have low vision and blindness so type one patient annually you have to start up to the age of ten or after five years post diagnosis and type 2 patients you start do it annually shortly after diagnosis at the time of diagnosis i do it in my patients i get an eye examination from the of the knowledges so we know where we are consider less frequent if one or no normal examinations are done retinopathy now in 2020 screening is recommended because it was revised to include the consideration of a retinal photograph now we have in our consulting room itself a small instrument which is there in the next slide with a remote reading and this reading can be shown to your doctor or to the ophthalmologist and then it it and then you you might be advised to see the after knowledges or not to see the octal model which is uh accordingly it is a validated assessment tool as a way to improve the screening excess and you can see here this is the fundus remedies with ai it's a new design and it can be hand-held handheld fundoscopy is done normally done at various scans some of the doctors also keep it in the consulting room to have an idea of what the state of the fundus is so this is the step care individuals with type 2 diabetes should have an initial dilated and comprehensive eye examination by ophthalmologist at the time of diagnosis and if there is no evidence of retinopathy for one or more annual exam screening is recommended every one or two years but women with pre-existing type 2 diabetes should be counseled on the risk of development or progression of diabetic retinopathy when they get pregnant and therefore before pregnancy or in the preconception stage itself and ophthalmic examination has to be done and repeatedly in the first second and third trimester they have to be monitored we know that pregnancy is a time which can the retinopathy can suddenly progress and we need to take care of that so what is the treatment laser photocoagulation is the treatment of choice for proliferative rich napati they might choose to do a rational photocopulation or a grid photocalculation or maybe a pandatana photography depending on the advice of the ophthalmologist or the retinal surgeon vitrectomy is done in hemorrhage of the vitreous humor or the posterior bands which actually produce retinal detachment and now we have vascular endothelial growth factors is known as anti-vegf so they are intravitreal injections and you can see a microgen roof and others now the new ones that have come these are injected into the into the in into the fluid of the eye and that can prevent the new blood vessels from forming because they inhibit the growth factors and now we come to the third part of our section the diabetic neuropathy as we know that that neuropathy is a diagnosis of exclusion more than 50 may be symptomatic or not but we need to recognize this pretty early and autonomic neuropathy can be a severe disabling factor which can disturb the quality of life immensely so there are various kind the focal neuropathies are these are the neuropathies that are common in diabetes as you can see the third nerve six now seventh now are the intercostal nerves of the lateral popliteal and the medial nerve and these single nerves which cause mono neuropathy are usually secondary to the infection of the blood vessels that supply that now very beautifully seen on the right hand side and this is the example of mono neuropathies starting on the left hand side you see this man with the third now policy in the center you see a six now policy inability to turn to the right hand side and giving rise to diplopia or vision and then the commonly seen seventh now policy in that lady and in the lower panel you can get a medium of pulsing which causes atrophy of the thinner eminence and the lateral popliteal nerve pulsey that can give rise to a foot drop these are the common mono neuropathies but the most common 90 of the patient have a diffuse neuropathy which is bilateral symmetrical sensory motor starting from the toes and ascending upward giving rise to symptoms first in the feet and then and then maybe rising up and then going to the hands somewhere where the symptoms come up to mid leg now that it as we know there are large and small fibers here large fibers supply the proprioception or the or in the patient if they are disturbed you might see imbalance of gait and the small fibers supply the paint and temperature which gives rise to kind of loss of pencil sensation and that can be detrimental and subject to patient's feet for amputation so again saying that small fibers are usually affected first compared to the larger fibers these patients with predominant small fibers can have burning pain lacinating pain paresthesias cutaneous loss of pain and temperature and fertilisers whereas those who have predominant large fibers can have imbalance of gait and they can show atrophy of the intrinsic muscles of the feet and hand giving rise to intrinsic minus feet and intrinsic minus hand decreasing mobility of the patient and decreasing the power of the muscles a classical case of small fiber neuropathy both this is a predominant small fiber neuropathy normally both of them uh are affected so this you see the patient presents with drying of the feet with constant calluses and these calluses are normally present at the head of the metatarsals of the food that are susceptible to the pressure of the weight of the patient and that can give rise to ulcerations and these ulcerations are bottle of entry of infection they can give rise to infection of the feet and cellulitis making them susceptible to amputation in the future so that should not happen and therefore we need to screen these patients at every visit so 20 percent of type 1 diabetes they get neuropathy up to 20 years 10 to 15 percent are of new onset type 2 diabetes and 50 of them get 10 years after 10 years of type 2 diabetes remember that that at the time of diagnose itself when the patient comes for the first time please look for neuropathy just like we are doing for retinopathy and nephropathy the initial presentation could be just tingling the sensory science come earlier than the motor science um but when you examine you might find nothing so if the patient just says burning tingling you can do the vibration perception threshold and then that can give you an early diagnosis and immediate corrective foot care can be given to the patient so that it doesn't progress neuropathy as we know contributes to amputations both long fiber neuropathy which can make the patients susceptible to falls and fractures and therefore amputation and small fiber neuropathy which can give rise to ulcerations and then amputations fifty percent of these patients are asymptomatic this is a very classical a myotrophy normally when we talk neuropathy we are talking of sensory systems but this is one neuropathy that affects the proximal muscles not the distal which i just talked about so you see they have uh acute wasting of the guests of the um of the quarter cells muscle and also of the gluteal muscle where the patient has difficulty in getting up from the sitting position it usually happens unilaterally but can extend to both and involve the lumbar girdle so the patient has difficulty in movement and lifting up the legs so walking is also difficult but this is a kind of autoimmune disorder it's brunt garland syndrome where the if diagnosed correctly they can give ivig to the patient and recovery is seen pretty early if diagnosed late then it recovers spontaneously but it takes more than a year for recovery so it's necessary to screen for neuropathy all patients should be assessed for diabetic peripheral neuropathy starting at time of diagnosis and annually thereafter for diagnosing you have to take a careful history assessment of temperature pinprick and vibration sensation using a hertz tuning for a 10 gram monofilament testing to identify the fetal transparceration and prevention of amputation made is necessary every time but now as the ada has given shortcuts for screening this is a neurotype small handheld meter that actually by bluetooth on testing the sensations of the feed gives it to an app on the mobile phone and from there it's gone it goes on a cloud-based and the doctor the practitioner gets it and prints it downloads and prints it and that's the print out of the patient where the patient has taken his vibration perception threshold at home so all this can be done nowadays with technology it has revolutionized the pace of diabetic management and finally the diabetic autonomic neuropathy which is a very very vast topic but i'll just touch on what happens in autonomic neuropathy so subclinical abnormalities can be seen esophageal dysfunction cardiovascular reflexes become abnormal and also the you have difficulty in recognizing hypoglycemia because of blunted counter regulatory responses and increased periphery blood flow giving ties to edema of the feet and then there are symptomatic grossly symptomatic autonomic neuropathies like gustatory swelling the patient just puts a muscle of food in the mouth and starts sweating profusely and doesn't understand why he's not even taking spicy food and there is postural hypotension gastroparesis is a big problem especially in indian patients we are always complaining about the abdomen you see 90 percent of the patient will say i'm having this abdominal gas gas gas is a famous word that they use and they are continuously taking proton pump inhibitors on their own over the counter so we have to remember that gastroparesis diabetic diarrhea can happen neurogenic bladder can happen where the patient in the long run has to self catheterize erectile dysfunction is common now in youngsters as well and shaco osteoarthropathy which is a which is an autonomic neuropathy of the feet giving rise to alterations or of the architecture of the foot can be present which is kind of a pre-amputation problem so management is to optimize glucose control to slow the progression of neuropathy essence and treat the patient related to diabetic peripheral neuropathy and symptoms of autonomic neuropathy to improve quality of life pre-gabilan duloxetine and gabapentin are recommended as initial pharmacological treatments take care of the diabetic food explain explain the food care that they have to take see that the footwear is worn all the time the nails are cut straight and not and not circular you need to keep a mirror down because it's difficult for the patient to bend down and see the sole of the foot but the sole of the foot has to be seen every day in patients of neuropathy because they can get an ulceration if they walk barefoot or something in the footwear itself can can actually bite them and they can get an ulcer and they will have no knowledge of it and subsequently they have an ulcer then it has to be attended to and off loading has to be done offloading is is the correct treatment to do to prevent further ulceration but early recognition is is vital to prevent the mortality and mobility mobility of the diabetic foot a comprehensive foot evaluation has to be done annually patients with evidence of sensory loss of prior ulceration of our amputation have should get their feet inspected at every visit and ask for the history of all these in your patient current symptoms of neuropathy and vascular disease have to be attended to inspect the skin assess the food deformities and do a neurological examination so the ada recommends a multi-disciplinary approach you need the diabetes you need the educator you need the surgeon you need the radiologist and you also need the foot care specialist so all these are required to just treat one patient with a neuropathy refer to food specialist for ongoing preventive care and general preventive self-care has to be given and specialized footwear see that the patients do not walk barefoot at any time inside the house and outside maintain their nutrition see that help them to do the exercise but in patients of neuropathy etc we need to count the steps you need to count the steps see that they don't walk too long because if they walk too long they're not able to feel the sensations and they can get fractures so counting the steps is important in severe neuropathy so we tell them to walk short distances at a time stop smoking give intensive gluco glycemic therapy and also control their lipids and nutritional optimization now this is the end of my talk i'll just take one case for you to understand the whole topic well so gita gita is a 58 year old lady she's got type 2 diabetes for 11 years she's got dyslipidemia hypertension albuminuria non-painful peripheral neuropathy she's obese she has never she has history of myocardial infarction three years ago then she has so many things she is on metformin one thousand milligram one straight lipid ten milligram five liters of 30 milligram listener pill 20 milligrams metoprolol 25 a total starting 80 and aspirin 75. on physical examination she has a non-proliferative retinopathy a normal heart lung sounds she's obese she has decreased vibratory and filament sensation in otherwise healthy appearing feet so the concerns would be in this patient she has many blood sugars in the 200 and 300 rage but occasionally it has gone down to 70 so she has high percent hypo she's 40 she has fatigue difficulty in losing weight and urinary frequency and lab shows she has an a1c of 10. the lipid sign target range is on high intensity statin as i told you in the history creatinine point nine hepatic function shows mild rise of triamines and the albumin is hundred and ten so in short in these two slides what did i say that this patient has microvascular disease atherosclerotic cardiovascular disease and she has microvascular disease as well she has early ckd she has neuropathy and she has early retinopathy so let us go back to the standards of k we know that if you see the guidelines and sglt2 inhibitor or a glp icon is in this patient uh can be given because they have stab she has stabilized cardiovascular disease and also an sglt2 inhibitor in the patient with chronic kidney disease with appropriate gfr is beneficial for preventing the progression and out of the patient's main complaint is difficulty in losing weight both of these drug classes are weight neutral or can promote weight loss basal insulin could also be considered here a1c is greater than 10 which symptoms so what can you do could do any of the following in this patient with established cardiovascular disease add a drug class glp a1 acornis or you add drug class sglt2 inhibitor or you use both of these for maximal weight loss you could do any of the following with established kidney disease preferentially add drug class sglt2 inhibitor gfr is satisfactory will definitely continue medforming because renal function is okay for this refer to diabetes educator and dietitian for interprofessional pain care nutrition etc assess the well-being of the patient and look at lifestyle factors we'll definitely consider to stop the glipizide to stop the biogluta zone and as we have more appropriate medications for this patients individually that is i think my last slide i have taught you about microvascular complications and how to take care and and a case which actually uh connects and tells you all about these complications the last slide we often forget that the skin is also involved in micro vascular complications and we wonder why they have kind of pigmentation over the lower limbs it's because of diabetes dermopathy again secondary to affection of the small blood vessels in the skin even the changes in the nails very commonly seen candid infection and you see carbuncles also very common where you need to incise and drain and pigmented areas over the feet or hands remember that diabetic dermapathy is also common microvascular complications so my is my last life complications can be avoided or minimized with good glucose control appropriate guideline based screening is important for early detection and we should know when to make appropriate reference so thank you very much i i have finished my talk and i'm open to questions now yeah man thanks a lot this was wonderful talk uh i have actually explained all the complications starting from neuropathy retinopathy and explained in very very detail uh everyone just loved it i could see a lot of appreciating comments uh dr ramashankar says it's excellent presentation doctor kulkarni sees amazing presentation so thanks a lot mom it was really uh wonderful i'll just take few questions uh so mom there is one question from uh doctor what is the key takeaway in delaying the progression of kidney damage yeah okay basically anytime the patient comes to you first time with diabetes please assess not only for sugar control but also for the complications so normally we do a blood test isn't it for every patient we don't do the blood sugar only we do the hva1c we do serum creatinine we do sgot pt so we assess the various organs of the body and this kidney function is seen by the serum creatinine and the gfr now if you feel that both these are altered and the urine also is normal then we have to look into the kidney disease in a special way so you do the urinary albumin excretion frequently treat the infections that might produce acute and chronic kidney disease and also look for albuminuria and the gfr if i want to say in just one word assess the gfr because we tend to do the creatinine all the time and we feel okay the creatinine is just 1.4 the gfr can be low even if the creatinine is 1.4 so please calculate the gfr and assess the function the key takeaway would be screen the patients at the onset of type 2 diabetes and also when you see a type 1 at the first instant we need to do the test and subsequently all the time so screening is the key and if they have any change in the gfr you need to call them for follow-up take care of the anti-diabetic drugs that we are giving especially metformin we don't know what stage they come in and ideally put them on renew friendly drugs now we have you know protective drugs like ac and these and sglt2 inhibitors and we have one in the horizon which i didn't mention phenerenone is the new drug that will come i think in a month or two and that will be the third reno protective drug that we have so we have a lot of uh thing in our kitty to prevent progression of kidney disease and destruction you know productive drugs is the addition uh that has been recently made right yeah uh so man for diabetic patients uh who are uh who also have ckd uh addressed interlinked child just take this first uh and that patient has a low uh hemoglobin level so what is the recommended line of management diabetics so first of all i have to assess what is really anemia due to always remember most of our patients also have iron deficiency anemia so you need to look at their hemoglobin serum parenting iron binding capacity and also their transparent saturation to lupine deficiency anemia and they also have b12 deficiency remember especially those who are long-standing metformin have additional b12 deficiency so we have to look at that and third is due to renal disease itself uh it can give rise to erythropoietin deficiency and therefore anemia and fourth is remember the diabetes is also associated with many of our patients with thyroid disease so hypothyroid can also give rise to anemia so assess all this and accordingly if it's iron deficiency component you can give iron to the patient b12 has to be given to the patient and patients of chronic kidney disease require erythropoietin injections subcutaneously from time to time for the correction of anemia and of course a good nutrition good nutrition registered dietitian that's also yeah but very important part so overall holistic approach is very important for the treatment uh thank you mom uh so what role of b12 and folic acid supplement for uh diabetic neuropathy how long should one uh give those supplements uh is the question yeah actually b12 deficiency is present in our population it's almost 100 percent in our population above the age of 30. and in patients of diabetes they are already on metformin so metformin will increase the b12 deficiency ideally one would do the b12 levels every year annually but in a non-affording patient it would be worthwhile to give b12 say for one or two months give a gap of five months and then again give for one or two months in non-affordable patient because the test itself is expensive but see that b12 is given to the patient not in two large doses but but frequently and patients who are taking larger doses of metformin you can give every three months for a month now we should remember that these patients of diabetes may have also intrinsic factor deficiency i have seen patients where i give b12 to the patient orally and then i re-estimate in those affording patients and the b12 is still low especially in older patients in those patients you need to give injectable bdd b12 so that is given um you know initially once a week for four weeks and then you give once a month for the subsequent months throughout life so intrinsic factor deficiency is generally forgotten and that has to be kept in mind my district thank you mom i hope doctor this answers your question dr pallavi uh so mom doctor ashok is asking how many anti-diabetic drugs are you can use to target diffranzo's omnious octet in patients not willing to take insulin uh so sometimes we use su's uh metformin glynides agis or dpp4 in given patient so what's the right approach for this the right approach to see a new whether the patient is a new onset diabetes or long-standing diabetes that is one which decides on the treatment the second is the level of glycemia if a patient comes to you with say just an hba1c of 7.5 and you've already given lifestyle changes good nutritional advice and advise them um exercise and they have already done it for a month or two and yet hba1c is high you can give just a combination of glypton and net form in just one tablet a day remember the compliance increases when you decrease the drug metformin is the first line of treatment but sometimes metformin when you give three times a day the patients are not compliant they go to work as you say they take the tablet in the morning and they forget to take in the afternoon and might take now in these patients who are not compliant because of pill burden these patients you can give just one tablet with uh one just one metformin is not enough so you can combine it with the glypton as the initial therapy if the hba1c is more than eight then you need to give them dual therapy or maybe even triple therapy along with lifestyle changes and if the hp a1c is more than 9 and 9.5 maybe you can give a short course of insulin get them to normal glycemia and later on take off the insulin and keep them on oha it's it's customized to the patient we cannot really uh if you give me a given patient i will tell you how to treat but these are the general guidelines in it you need to be aggressive enough you need to be aggressive in your patient uh if the hba1 c is high please don't start a step therapy pattern so you give one drug then wait for the hp1c to be controlled then start the second one then again wait and third one that that should not be the case you need to give aggressive therapy and you can even start at the triple dose therapy at the initial onset itself and then go down to dual therapy and then maybe the patient will require just one drug because now they are more compliant with exercise and also their diet they have to make a lifestyle change and that is lifelong remember life long is more important in these patients where you advise them yeah very insightful mom thank you uh it was a very generic advice for that particular category but definitely uh works uh so thanks a lot uh and so dr ponny marie says excellent and wonderful presentation and mom we have already covered all the questions we have actually covered in detail about each and every complication thank you so much for being part of it we would really love to have you again with us for some other session and i'm sure our users loved it uh today thank you thank you so much you are also our woman of substance because in this video you you also are tough so uh we all joined together and the women on top yeah yeah thank you so much i mean for the first time i saw all these hearts and you know claps and 100 and this going up and i realized i i i suppose that is supposed to be a good talk so i'm giving it to you it's wonderful really jake and i would like to come for your netflix sessions again maybe sometime in future so thank you so much and i thank you fatima also and the netflix team for um having uh got me here thank you so much thanks a lot

BEING ATTENDED BY

Dr. Murtuza Zozwala & 1052 others

SPEAKERS

dr. Benny Negalur

Dr. Benny Negalur

Consultant Physician & Diabetologist, Mumbai

+ Details
dr. Benny Negalur

Dr. Benny Negalur

Consultant Physician & Diabetologist, Mumbai

+ Details

About Medflix

Medflix is a new platform by PlexusMD, India's most active and trusted doctor community. On Medflix, you can discover live surgeries, discussions, conferences and courses from some of the top doctors and institutions across the world. Join clubs in your areas of interest and access hundreds of amazing live discussions everyday.