Adegbenga B. ADEMOLU1, MBBS,Abiola O. ADEMOLU2, MBBS Anthonia O OGBERA1,MBBS,MPH,MWACP,FMCP,FACE,FACP Olufemi A FASANMADE3,MBBS,FWACP,FEMSON,FACE.
- Department of Medicine, Lagos State University Teaching Hospital(LASUTH)
- Department of Paediatrics, Olabisi Onabanjo University Teaching Hospital (OOUTH)
- Department of Medicine, LAGOS UNIVERSITY TEACHING HOSPITAL ,LAGOS.(LUTH).
CORRESPONDENCE TO: Dr. Adegbenga B. ADEMOLU. Department of Medicine.
Lagos State University Teaching Hospital(LASUTH),Ikeja.
BACKGROUND/OBJECTIVE: Hypoglycaemia is a random blood sugar of 70mg/dl (3.9mmol/L) or less or a fasting blood sugar of 55mg/dl(3.1mmol/L).It was noticed that the rate of sudden collapse was on the increase in a rural community in ikorodu with some resulting in death, hypoglycaemia was entertained as one of the possible causes amongst others. This raises the question what is the frequency of hypoglycaemia in this community and what is the level of its severity if present? Does it occur among people living with diabetes or non-diabetics in this community? The aim of this study is to determine the frequency of hypoglycaemia in a rural community setting in ikorodu.
METHODOLOGY: The random blood sugar of 49 participants was checked using a brand new accu-chek glucometer which was coded with the code key. The glucometer was calibrated in mg/dl. The screening was done after obtaining consent from each participant through their opinion leader. The exercise lasted for about 3hours between 11.30 in the morning and 2.30 in the afternoon. None of the participants ate, smoked took alcohol or any medication at least 4hours before measurement of the blood sugar. The participants were randomly selected.
RESULT:A total number of 49 participants with age range 25-75years were recruited into the study. Only 2(4.08%)cases of hypoglycaemia was recorded.
DISCUSSION The frequency of hypoglycaemia in maya ikorodu is 4.08%.Of the two male hypoglycaemic participants, one was a 27years old youngman whose glucometer reading displayed low!(that is less than 10mg/dl!) and he was asymptomatic. CONCLUSION The frequency of hypoglycaemia in ikorodu is 4.08%.
KEYWORDS: Hypoglycaemia, Asymptomatic, Metabolism, Behaviour, Classification, Ademolus Phenomenon, Correlation.
Hypoglycaemia is a random blood sugar of 70mg/dl (3.9mmol/L) or less or a fasting blood sugar of 55mg/dl(3.1mmol/L).The geographical distribution of hypoglycaemia knows no boundary, It also has no ethnic, gender or age exception. It was noticed that the rate of sudden collapse was on the increase in a rural community in ikorodu with some resulting in death, hypoglycaemia was entertained as one of the possible causes amongst others since hypoglycaemia is a well-documented cause of sudden collapse in the public. This raises the question what is the frequency of hypoglycaemia in this community and what is the level of its severity if present? Does it occur among people living with diabetes or non-diabetics in this community? Many studies have been done on hypoglycaemia both locally and internationally. Recent studies have shown that rats and human small intestine is an insulin sensitive glucogenic organ, the glucose-6-phosphatase gene is expressed in the small intestine apart from in the liver and kidney, it has also been shown that it is induced in insulinopenic states such as fasting and diabetes(1).Evidence have shown that conjugated linoleic acid is able to normalize impaired glucose tolerance and improve hyperinsulinemia in the pre-diabetic zucker diabetic fatty fa/fa rat(2).It has been suggest also that pyridoxal phosphate protects neurons from glucose deprivation- induced damage by enhancing the formation of energy-yielding products and relieving extracellular load of glutamate. The observed phenomena further indicate that pyridoxal phosphate might be used prophylactically against neuronal death induced by metabolic disorders(3).
Hypoglycaemia can occur in persons with or without diabetes. In diabetic it occurs as complication of insulin or oral hypoglycaemic agent therapy. In non-diabetics, it occurs with lesser frequency. It can occur in the fasting state, it can occur in non-diabetics post prandial(reactive hypoglycaemia) occurring within 4 hours of high carbohydrate intake due to excessive endogeneous insulin release. It can occur after binge alcohol intake. It can be asymptomatic or symptomatic,mild or severe. Hypoglycemia occurs from a relative excess of insulin in the blood and results in low blood glucose levels. The level of glucose that produces symptoms of hypoglycemia varies from person to person and varies for the same person under different circumstances. Symptoms of hypoglycemia can be divided into adrenergic (rapidly falling and changing glucose levels) and neuroglycopenic (low central nervous system [CNS] glucose).The adrenergic symptoms are inversely correlated to the developing rate of hypoglycemia, being most pronounced with acute onsets. Adrenergic features, when present, precede neurobehavioral features, thus functioning as an early warning system. (4)
Hypoglycaemia can occur in different settings, in the community, at work, in hospital setting, in intensive care unit and so on. The aim of this study is to determine the frequency of hypoglycaemia in a rural community setting in ikorodu. Hypoglycaemia constitutes a medical emergency; however, most individuals recover completely. In the Diabetes Control and Complications Trial (DCCT), there were > 1,000 episodes of loss of consciousness associated with hypoglycaemia. However, there were no deaths, myocardial infarctions, or strokes definitively attributed to hypoglycaemia, and to date there is no evidence of brain damage resulting from any of these episodes.(4) Although no deaths occurred in the individuals participating in the DCCT, hypoglycaemia that is not reversed can progress from lethargy to coma and ultimately to death. Even with treatment, there are reported cases of long-lasting severe hypoglycaemia leading to transient and even permanent cerebral damage.(4)
In a joint statement from American Diabetic Association(ADA) and American Association of Clinical Endocrinologist(AACE)on the National Institute of Clinical Excellence(NICE) NICE-SUGAR study on intensive versus conventional glucose control in critically ill patients, it was noted that more recent study have identified severe hypoglycaemia(low blood sugar)as a significant risk of intensive glucose control. The NICE-SUGAR trial, a very large multicentre, multinational study, showed severe hypoglycaemia(blood glucose below 40mg/dl)occurred in approximately 6.8% of intensively treated patients compared to 0.5% of conventionally treated patients.(5).
The random blood sugar of 49 participants was checked using a brand new accu-chek glucometer which was coded with the code key. The glucometer was calibrated in mg/dl. The glucometer strip was then inserted to the glucometer till the glucometer is ready for use by showing a blinking drop of blood on the screen, then a participant had a finger prick using a sterile needle after cleaning the thumb with a spirit swab, the oozing blood is then applied to the orange area(the demarcated spot on the strip meant for a drop of blood) of the glucometer strip. The reading was then taken after which the strip was removed and discarded and reading was recorded. The procedure was repeated with each participants taking turns. The exercise lasted about three hours between 11.30 in the morning and 2.30 in the afternoon. The limit of detection of the glucometer(lower display limit) is 10mg/dl(0.6mmol/L).The method is linear within the range from 10 to 600mg/dl(0.6-33.3mmol/L).The screening was done after obtaining consent from each participant through their opinion leader. The exercise lasted for about 3hours.None of the participants ate, smoked took alcohol or any medication at least 4hours before measurement of the blood sugar. The participants were randomly selected. The study location was in ikorodu, in a community called maya in ikorodu north local council development area.
A total number of 49 participants with age range 25-75years were recruited into the study, of these 26(53.06%)were male while 23(46.94%)were female. Only 2(4.08%)cases of hypoglycaemia was recorded and both were male. In the study population 2(4.08%)were known diabetics one male, one female but none were hypoglycaemic.
The frequency of hypoglycaemia in maya ikorodu is 4.08%.Of the two male hypoglycaemic participants, one was a 27years old young man whose glucometer reading displayed low!(that is less than 10mg/dl!), and he was asymptomatic. The second was a 63year old man with a glucometer reading of 65mg/dl. Both were asymptomatic. At the onset of this research it was not known that a glucometer reading of less than 10mg/dl will be encountered on the research field and when it was incidentally encountered, fluoride oxalate bottle was not readily available for blood sample to be taken for laboratory analysis as the research was done with the aid of a glucometer, however it should be noted that a brand new glucometer bought purposefully for the study was used and that the use of glucometer to diagnose hypoglycaemia is approved by the endocrine society.
The 27year old participant was immediately advised to go and take a glucose drink as his blood sugar level is dangerously low. Since a random blood sugar of less than 10mg/dl without neuroglycopenic symptoms or any other hypoglycaemic symptoms is not found in literature, l hereby propose that this phenomenon of asymptomatic hypoglycaemia at random blood sugar of less than 10mg/dl be called ADEMOLUS PHENOMENON. For the clinical practice of endocrinology to be more objective as far as hypoglycaemia is concerned l hereby propose ADEMOLUS CLASSIFICATION OF HYPOGLYCAEMIA (see table 1).
Grade 1(mild) is random blood sugar (RBS) between 55-70mg/dl, Grade 2(moderate) is RBS between 40-54.9mg/dl. Grade 3(severe) is RBS between 10-39.9mg/dl. Grade 4(very severe) is RBS less than 10mg/dl. It should be noted that symptomatic hypoglycaemia above 70mg/dl is a subset of Grade 1,and asymptomatic Grade 4 is ADEMOLUS PHENOMENON. The advantages of this classification are many(see table 2).
Generally, it will help endocrinologist to prognosticate better in hypoglycaemic patients. The comparison between hypoglycaemia-inducing agents like sulphonyureas in particular, alcohol, quinine will be more objective worldwide with respect to gender, race, ethnicity and decades of life. The blood swing between hypoglycaemia and hyperglycaemia seen in diabetics on fluoroquinolones will be better characterised with the advantage of comparing the grade(s) of hypoglycaemic events(6).The severity of hypoglycaemia in disease conditions will be better defined for instance in insulinoma it will be more objective to state that the usual grade of presentation of hypoglycaemia in insulinoma is ? ? rather than saying 85% of patients with insulinoma presents with symptoms of hypoglycaemia(7) which is a vague statement, the grading will help to monitor progression or deterioration of symptom as tumour size increases. In legislation on driving with respect to hypoglycaemia, while grade 1 hypoglycaemic patients may correct the hypoglycaemia by taking glucose drink and waiting for say 30 minutes to ensure normoglycaemia before driving, grade 3, if still couscious, may wait for longer period or may be forbidden by law to drive until reviewed and certified fit by an endocrinologist. Furthermore, easy flow charts or protocol of management for different grades in different settings e.g. intensive care unit, general hospital wards, etc can be drawn. Recently researchers said diabetics develops hypoglycemia at all glycosylated haemoglobin (HbAlc) levels(8),but l will like to ask them what grades of hypoglycaemia do they develop at HbA1c <6.5% and at HbA1c >6.5%?
Whipples triad consist of hypoglycaemia symptoms, low plasma glucose measured at time of symptoms and relief of symptoms when the glucose is raised to normal. With this classification the rate of recovery of patients with the time frame with different grades of hypoglycaemia can be better characterised using whipples triad. we will then be able to say objectively that ? grade of hypoglycaemia recover faster than ? grade using whipples triad. Has anyone tried to study why the time of recovery from hypoglycaemia differs from one patient to the other? lt may be related to grade of hypoglycaemia ab initio before resurcitation. It will also help to grade gestational hypoglycaemia and will assist in predicting sequelae in both mother and fetus more accurately, it will also help to understand somogyl phenomenon better ,it will help to grade gastric bypass surgery induced hypoglycaemia and monitors its progress. The grade(s) of hypoglycaemia commonly associated with rebound hypoglycaemia following treatment will also be better characterised for better management and monitoring purposes. There are many more application of this ADEMOLUS CLASSIFICATION OF HYPOGLYCAEMIA worldwide that goes beyond the boundaries of endocrinology as a subspecialty. When fully accepted worldwide, it can be a landmark study that can change the science world for the better!
The ADA/Endocrine society: Classification of hypoglycaemia in persons with diabetes(see table 3) is ambiguous in that it classify hypoglycaemia only in diabetics(see table 4),if we are to follow it wholly and only then we will need another classification of hypoglycaemia in insulinoma, drug induced hypoglycaemia, paraneoplastic syndrome, gastric by-pass surgery and another in every disease condition associated with hypoglycaemia, without the advantage or ability to compare the severity of the hypoglycaemia across board whether diabetic or non diabetic, from this it is obvious that the classification is vague, deficient, inappropriate and superceded by ADEMOLUS CLASSIFICATION which put persons living with diabetes and others into consideration. To correlate the two classifications then: pseudohypoglycaemia is a subset of grade one .Probable symptomatic hypoglycaemia can be any of grade 1to 4.Asymptomatic hypoglycaemia is commonly grade 1 and can be in other grades especially now that asymptomatic hypoglycaemia is being described in grade 4 that is ADEMOLUS PHENOMENON . Documented symptomatic hypoglycaemia can be either grade1 to 4 ,the demerit(see table 4) of this part of ADA/Endocrine society classification is that it does not recognise progression from mild through moderate to severe hypoglycaemia but lumps virtually all recorded symptomatic cases together as documented symptomatic hypoglycaemia, now this is very dangerous both for the patients well-being and for the safety of the endocrinologist who should avoid litigation.
A subset of hypoglycaemia can be very severe with possible irreversible brain damage. The ADA/Endocrine society classification which is majorly a clinical classification did not recognise this.
Hypoglycaemia can cause brain dysfunction, brain injury and death. It has been demonstrated that brain extracellular glucose concentration parallel those of serum during hypoglycaemia and hyperglycaemia and are similar to whole brain glucose concentrations. This suggests that no major gradients for glucose exist across brain cell membranes. The cats have high resistance to brain injury from hypoglycaemia. In a study that studied three groups of cats exposed to fasting and insulin-induced hypoglycaemia, euglycaemic respiratory depression and combined hypoglycaemia respiratory depression with the hypoglycaemia maintained at <1.5mmol(mean 1 mmol)serum glucose concentration for 2 to 6.6hours.It was suggested that additional influences such as respiratory depression might play a facilitating role in developing brain injury due to hypoglycaemia, This experimental hypoglycaemia models contribution lies in recognizing additional factors that critically define the occurrence of hypoglycaemic brain injury(9).This 27year old asymptomatic hypoglycaemic at RBS less than 10mg/dl possibly did not have additional medical condition or factors that could have made him develop brain injury from the low glucose level.
Iatrogenic hypoglycemia causes recurrent morbidity in most people with type 1 diabetes and many with type 2 diabetes, and it is sometimes fatal. The barrier of hypoglycemia generally precludes maintenance of euglycemia over a lifetime of diabetes and thus precludes full realization of euglycemia’s long-term benefits. While the clinical presentation is often characteristic, particularly for the experienced individual with diabetes, the neurogenic and neuroglycopenic symptoms of hypoglycemia are nonspecific and relatively insensitive; therefore, many episodes are not recognized. Hypoglycemia can result from exogenous or endogenous insulin excess alone. However, iatrogenic hypoglycemia is typically the result of the interplay of absolute or relative insulin excess and compromised glucose counter-regulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counter-regulatory factors that normally prevent or rapidly correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counter-regulation. Reduced sympathoadrenal responses cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure in diabetes posits that recent antecedent hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. Thus, short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients In a patient with hypoglycemia unawareness (which implies recurrent hypoglycemia) a two- to three-week period of scrupulous avoidance of hypoglycemia is advisable. Pending the prevention and cure of diabetes or the development of methods that provide glucose-regulated insulin replacement or secretion, we need to learn to replace insulin in a much more physiological fashion, to prevent, correct, or compensate for compromised glucose counterregulation, or both if we are to achieve near-euglycemia safely in most people with diabetes.(10)
Neuroglycopenic signs occur when the brain’s dependence on glucose, coupled with its limited glycogen stores, results in rapid CNS dysfunction.(11) If warning signs are absent or ignored and the blood glucose level continues to fall, more severe hypoglycemia may lead to alteration of mental function that proceeds to headache, malaise, impaired concentration, confusion, disorientation, irritability, lethargy, slurred speech, and irrational or uncontrolled behaviour, which may be confused with dementia.(12) Notable CNS dysfunction, including focal seizures, hemiplegia, paroxysmal choreoathetosis, and patchy brain stem and cerebellar involvement mimicking basilar artery thrombosis, has also been reported. The medullary phase of hypoglycemia, characterized by deep coma, pupillary dilatation, shallow breathing, bradycardia, and hypotonicity, occurs at a blood glucose level of ∼ 10 mg/dl.(13). Most individuals with diabetes never suffer such severe hypoglycemia. (4)
The counter-regulatory response to hypoglycaemia is a complex and well-coordinated process. As blood glucose concentration declines, peripheral and central glucose sensors relays this information to central integrative centers to coordinate neuroendocrine, autonomic, and behavioural responses and avert the progression of hypoglycaemia. Diabetes, both type 1 and 2 can perturb these counter-regulatory responses. Moreover, defective counter-regulation in the setting of diabetes can progress to hypoglycaemia unawareness. While the mechanisms that underlie the development of hypoglycaemia unawareness are not completely known, possible causes include altered sensing of hypoglycaemia by the brain and/or impaired coordination of responses to hypoglycaemia.(14).
A few cases of symptomatic hypoglycaemia are reported in literature. A 62years old man a non-diabetic with rheumatoid arthritis developed hypoglycaemia(random blood sugar 10mg/dl)while on hydroxylchloroquine therapy. There is also the report of a diabetic rheumatoid arthritis patient who developed hypoglycaemia while on hydroxylchloroquine. (15,16,17,18).
In the 27years old young man that l described with asymptomatic hypoglycaemia at random blood sugar less than 10mg/dl(that is with ADEMOLUS PHENOMENON),l postulate that the protective effect of pyridoxal phosphate in preventing glucose-deprivation induced neuronal damage at low brain sugar level is probably the mechanism that explain his stable state in the presence of a dangerously low blood sugar level.
Most episodes of severe hypoglycemia are treated effectively at home or at work by friends, relatives, or colleagues and do not require the assistance of the emergency medical services (19). Cases treated in the hospital accident and emergency department are recognized to represent the “tip of the iceberg” (20), and the annual frequency of all emergency-treated episodes is uncertain because of incomplete ascertainment.
A common error is to over treat hypoglycemia with an excess of carbohydrate. This, in combination with the counter-regulatory hormone response to hypoglycemia, facilitates subsequent hyperglycemia. After treatment of any hypoglycemic episode, frequent bedside glucose monitoring should be continued until a stable glucose level is achieved. Depending on the time of day and insulin peak times, a balanced snack with carbohydrate, protein, and fat (i.e., peanut butter and crackers, or milk) can prolong treatment effectiveness. After treating a hypoglycemic event, search for the cause, correct the problem, and, if indicated, alter insulin or medication dose. This includes giving consideration to age-specific hypoglycemia concerns for pediatric and geriatric patients. Before discharge, patients should receive education in the form of verbal instructions, written materials, and referral for outpatient follow-up to avoid further events.
The frequency of hypoglycaemia in ikorodu is 4.08%. There is a need to have a generally acceptable classification of hypoglycaemia for objective management. The possible biochemical and clinical correlate of ADEMOLUS CLASSIFICATION OF HYPOGLYCAEMIA is that grade 1 has predominantly adrenergic features, grade 2 has adrenergic features with neuroglycopenic feature overlap, grade 3 has predominantly neuroglycopenic features that are majorly reversible while grade 4 has predominantly neuroglycopenic features with majorly irreversible brain damage. Hence ADEMOLUS CLASSIFICATION OF HYPOGLYCAEMIA is biochemically and clinically relevant.
ACKNOWLEDGEMENT: I want to thank all the recruited participants in the study who voluntarily accepted to be involved in this study which was done for the benefit of mankind. I likewise thank my teachers who taught me endocrinology and I appreciate my wife and children for being life companion.
- Croset M, Rajas F, Zitoun C, Hurot JM, Montano S, Mithieux G. Rat small intestine is an insulin-sensitive gluconeogenic organ. Diabetes 2001 Apr;50(4):740-6.
- Houseknecht KL, Vanden Heuvel JP, Moya-Camarena SY, Portocarrero CP, Peck LW, Nickel KP,et al. Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat. Biochem Biophys Res Commun 1998 Jun 29;247(3):911.
- Geng M.-Y.; Saito H.; Nishiyama N. Dr. N. Nishiyama, Protective effects of pyridoxal phosphate against glucosedeprivation- induced damage in cultured hippocampal neurons. Journal of Neurochemistry (USA), 1997, 68/6 (2500-2506).
- Donna Tomky, Detection, Prevention, and Treatment of Hypoglycemia in the Hospital.Diabetes Spectrum;January 2005, Vol. 18 Issue 1, p39-44.
- Alexandria, VA and Jacksonville, FL. Joint Statement from ADA and AACE on the NICE-SUGAR Study on Intensive Versus Conventional Glucose Control In Critically Ill Patients. Diabetes Pro. March – 25 – 2009.
- Michael Smith,Robert Jasmer,Dorothy Caputo.Fluoroquinolones Linked to Hypo-,Hyperglycemia.Medpage Today.2013.August 15.
- Zonera Ashraf Al,Jwles E. Harris,Pradyumna D. Phadak et al.Insulinoma.Medscape.2011 Nov.23.
- Cole Petrochko,Zalman S. Agus,Dorothy Caputo.Hypoglycaemia Happens at all HbA1c levels.Medpage Today.2013 August 8.
- de Courten-Myers GM, Xi G, Hwang JH, Dunn RS, Mills AS, Holland SK et al. Hypoglycemic brain injury: potentiation from respiratory depression and injury aggravation from hyperglycemic treatment overshoots. J Cereb Blood Flow Metab. 2000 Jan;20(1):82-92.
- Philip E. Cryer,Stephen N. Davis, and Harry Shamoon. Hypoglycemia in Diabetes . Diabetes Care June 2003 vol. 26 no. 6 1902-1912 .
- Goetz CG: Textbook of Clinical Neurology. 2nd ed. Philadelphia, Pa., Elsevier 2003, p.822–823.
- Metchich LN, Petit WA, Inzucchi SE: The most common type of hypoglycemia is insulin-induced hypoglycemia in diabetes. Am J Med113 : 317–323,2002.
- Nolawit Tesfaye, and Elizabeth R. Seaquist. Neuroendocrine Responses to Hypoglycemia. Ann N Y Acad Sci. 2010 November; 1212: 12–28.
- Andreas Holstein, Olaf M. Patzer,Kathrin Machalke,Judith D. Holstein, Michael Stumvoll,and Peter Kovacs. Substantial Increase in Incidence of Severe Hypoglycemia Between 1997–2000 and 2007–2010. Diabetes Care. 2012 May;35(5):972-5.
- CynoberL, AusselC, VaubourdolleM, AgnerayJ, EkindjianOG. Modulation of insulin action on 2-deoxyglucose uptake by chloroquine in chick embryo fibroblasts. Diabetes 1987;36:27-32.
- AsamoahKA, RobbDA, FurmanBL. Chronic chloroquine treatment enhances insulin release in rats. Diabetes Res Clin Pract 1990;9:273-8.
- EmamiJ, PasuttoFM, MercerJR, JamaliF.Inhibition of insulin metabolism by hydroxychloroquine and its enantiomers in cytosolic fraction of liver homogenates from healthy and diabetic rats. Life Sci 1999;64:325-35.
- EmamiJ,GersteinHC,PasuttoFM,JamaliF.Insulin sparing effect of hydroxychloroquine in diabetic rats is concentration dependent. Can J Physiol Pharmacol 1999;77:118-23.
- Frier BM: Hypoglycaemia in the diabetic adult. Baillieres Clin Endocrinol Metab 7:567–623, 1993.
- Potter J, Clarke P, Gale EAM, Dave SH, Tattersall RB: Insulin-inducaed hypoglycaemia in an accident and emergency department: the tip of an iceberg? BMJ 285:1180–1182, 1982.
TABLE 1 TABLE 2
|HIGHLIGHT S OF APPLICATION OF ADEMOLUS CLASSIFICATION OF HYPOGLYCAEMIA|
|1. it will help endocrinologist to prognosticate better in hypoglycaemic patients whether diabetic or not;||7.With this classification the rate of recovery of patients with the time frame with different grades of hypoglycaemia can be better characterised using whipples triad.|
|2. help compare the severity of hypoglycaemia in hypoglycaemia inducing agents like oral hypoglycaemic agents(sulphonyureas in particular),quinine,alcohol etc ,||8. help to grade gestational hypoglycaemia and will assist in predicting sequelae in both mother and fetus more accurately.|
|3.help define more objectively the severity of hypoglycaemia in disease conditions e,g.insulinoma||9. help to understand somogyl phenomenon better|
|4. help define and compare the grade of hypoglycaemia seen as paraneoplastic syndrome in and among disease conditions.||10. help to grade gastric by pass surgery induced hypoglycaemia and monitors its progress|
|5. may also help in legislation on driving with respect to hypoglycaemia||11. the grade(s) of hypoglycaemia commonly associated with rebound hypoglycaemia following treatment will also be better characterised for better management and monitoring purposes.|
|6. will also assist easy flow chart or protocol of management for different grades in different settings to be drawn||12. There are many more application within and outside the practice of endocrinology.|
TABLE 3 TABLE 4 SOME HIGHLIGHTS OF DEMERITS OF ADA/ENDOCRINE SOCIETY CLASSIFICATION OF HYPOGLYCAEMIA IN DIABETICS.
|1. Application is restricted to diabetes|
|2.Gives no room for comparism among aetiological factors,agents/disease conditions|
|3.Does not recognise progression from mild through moderate to severe|
|4.Lumps virtually all recorded symptomatic cases together as documented symptomatic hypoglycaemia|
|5.Did not recognise a subset of hypoglycaemia can be very severe with possible irreversible brain damage.|