shtf how much insulin to give as emergency treatment for hyperglycemia -hospital

How is hyperglycemia treated in the emergency department (ED)?

Treatment of inpatient hyperglycemia beginning in the emergency department: a randomized trial using insulins aspart and detemir compared with usual care An aspart insulin protocol safely lowers BG levels in the ED without prolonging LOS.

How is hyperglycemia treated in patients treated with insulin?

Patients treated with insulin may have knowledge of an adjustment algorithm for management of hyperglycemia. In insulin-sensitive patients, BG levels may fall 100 mg/dL (or more) with each 1 unit of rapid-acting insulin used. For example 2 extra units of rapid-acting insulin would be predicted to lower the glucose from 350 mg/dL to 150 mg/dL.

How much insulin do you give a diabetic patient at urgent care?

If an urgent care provider is uncertain about the degree of a patient’s insulin resistance, a correction dose of 0.1 to 0.15 units/kg of rapid-acting insulin given SQ should be sufficient to return the glucose to a more acceptable range. Management of children is another special case.

When should rapid acting insulin be given to patients with hyperglycaemia?

○ If short acting GCs are used, then an increase of rapid-acting insulin at the time point of GC intake might be sufficient. A correctional rapid-acting insulin dose can be administered in case of persistent hyperglycaemia after 3–4 h when the rapid-acting insulin action has tapered off.

How much insulin is in an emergency?

Critically ill patients may be given insulin, with a loading dose of regular insulin (0.1 units/kg body weight to a maximum of 10 units), followed by an infusion of regular insulin (0.1 units/kg body weight/hour, to a maximum of 10 units/hour)15,16.

How much does 10 unit of insulin bring down blood sugar?

Theoretically, to reduce 400 mg/dL blood sugar to about 100 mg/dL, you would need at least 10 units of insulin.

How much does 1 unit of insulin bring down glucose?

Generally, to correct a high blood sugar, one unit of insulin is needed to drop the blood glucose by 50 mg/dl. This drop in blood sugar can range from 30-100 mg/dl or more, depending on individual insulin sensitivities, and other circumstances.

What is the emergency treatment for hyperglycemia?

Emergency treatment for severe hyperglycemia Treatment usually includes: Fluid replacement. You'll receive fluids — usually through a vein (intravenously) — until you're rehydrated. The fluids replace those you've lost through excessive urination, as well as help dilute the excess sugar in your blood.

How do I calculate how much insulin I need?

Add up all the carbohydrates in your meal. Divide the total carbohydrates by the insulin to carbohydrate ratio. The result is the amount of insulin units needed.

What is the 1800 rule for diabetics?

For short-acting insulin, use the “1800 rule.” This tells you how much your blood sugar will drop for each unit of short-acting insulin. For example, if you take 30 units of short-acting insulin daily, divide 1800 by 30. This equals 60.

Is 10 units of insulin a lot?

Long-acting (basal) insulin. Each has its own dosage. Depending on the type, you might start with 10 units a day. Or your doctor may base the first dose on your weight, based on about 0.2 units for every 2.2 pounds. This may be less than you need, but it's a good starting point.

What is the maximum units of insulin you can take?

Available insulin syringes can deliver a maximum of 100 units, and insulin pen devices can deliver only 60–80 units per injection.

What is the 500 rule in diabetes?

2. Use the 500 Rule to estimate insulin-to-carb ratio: 500/TDD = number of carb grams covered by a unit of insulin. Example: 500/50=10; 1unit of insulin will cover about 10 grams of carbohydrate.

What insulin is used in an emergency?

Short-acting (regular insulin) and Rapid-acting Insulins One brand of regular insulin (e.g., Humulin R, Novolin R) may be substituted for another brand of regular insulin and for rapid-acting insulins (e.g., Humalog, NovoLog, Apidra), and vice versa, on a unit-per-unit basis in emergency conditions.

Do you give insulin for hyperglycemia?

Insulin, given either intravenously or subcutaneously, is the preferred regimen for effectively treating hyperglycemia in the hospital.

How can I lower my blood sugar instantly in an emergency?

When your blood sugar level gets too high — known as hyperglycemia or high blood glucose — the quickest way to reduce it is to take fast-acting insulin. Exercising is another fast, effective way to lower blood sugar. In some cases, you should go to the hospital instead of handling it at home.

What is the best treatment for severe hyperglycemia?

Severe and symptomatic hyperglycemia – administer insulin (both a low dose of regular or rapid-acting insulin and long-acting insulin) – consult endocrine or internal medicine.

Where should hyperglycemia be monitored?

Patients with newly identified severe/symptomatic hyperglycemia should be monitored in an observation unit (or admitted).

What is the treatment for DKA and HHS?

Treatment of DKA and HHS is focused on fluid resuscitation, addressing potassium imbalances, correcting ketoacidosis (in DKA), normalizing glucose and other electrolyte levels, addressing the underlying precipitant, and preventing complications.

How to prevent relapse of IV insulin?

Avoid abruptly stopping IV insulin. Ensure appropriate transition of insulin therapies to prevent relapse (i.e. sufficient overlap of IV and SC).

Why should a serum osmolality rate of fall be avoided?

Serum osmolality – a rate of fall ≥3mmol/kg/h should be avoided due to risk of cerebral edema.

What is stress induced hyperglycemia?

Stress-induced hyperglycemia is a transient response that may be present in acutely ill patients (e.g., sepsis, trauma, burns).

How often should you check your response to insulin?

At least every 2 hours, the response to therapy should be assessed through vitals and level of consciousness, volume status and intake/output, insulin dosage, and repeat labs (glucose, electrolytes, bicarbonate, pH, anion gap, osmolality).

How much insulin should I take for hyperglycemia?

A suggested protocol for marked hyperglycemia (above 400 mg/dL) in patients without known insulin-deficient DM such as type 2 DM is to provide a SQ bolus of rapid-acting insulin, starting with 0.1 to 0.15 units/kg. The precise dose selected can be modified based on the possible predicted degree of underlying insulin sensitivity or possibly based on a history of the patient’s insulin doses or response to insulin, if he or she is already on an insulin regimen. Factors requiring consideration of lower insulin dosing include low body weight, known insulin sensitivity, and underlying renal and liver disease. Factors suggesting a need for higher insulin dosing than the starting protocol would be high body mass index (BMI > 35), features of insulin resistance (acanthosis nigricans on skin examination, known PCOS, steroid treatment, significant stress). A follow-up BG level should be done 2 to 4 hours after the bolus. If needed, the insulin can be rebolused, with or without dose adjustment based on the response. If repeated insulin boluses are used, insulin need may be decreased as glucose toxicity is reversed and there may be “stacking” or the residual effects of the prior insulin administrations, depending on the dosing insulin and individual insulin clearance. An urgent care provider should always be encouraged to add his or her own clinical judgment and experience to the insulin protocol being used. We recommend a treatment goal of 150 mg/dL (120-180 mg/dL).

How should elevated blood glucose levels be treated acutely if treatment is provided?

How should elevated blood glucose levels be treated acutely if treatment is provided? Insulin is the logical choice for acute management. Rapid-acting insulin analogs (glulisine [Apidra, Sanofi-Aventis U.S. LLCJ]), insulin aspart (NovoLog, Novo Nordisk Pharmaceuticals Inc.) and insulin lispro (Humalog, Eli Lilly and Co.) have superior insulin kinestics to regular insulin. Regular insulin, when given SQ, requires at least 30 minutes for onset of action, therefore, use of rapid-acting analogs may be preferable. The available rapid-acting insulin agents are sufficiently similar that all are reasonable choices. Each facility will presumably decide based on economic or other practical considerations (Table 1). Use of long-acting insulin such as NPH, detemir (Levimir, Novo, Nordisk), glargine (Lantus, Sanofi) will likely be done les soften and selectively. Long-acting insulin preparations are used by patients with type 1 and insulin-deficient type 2 DM to provide a low level of background insulin to suppress hepatic gluconeogenesis and prevent hyperglycemia due to excess endogenous glucose production. These insulin preparations wil likely have a limited role in management of acute hyperglycemia but may be needed in cases of newly diagnosed DM where glucose toxicity is present.

How long does it take for insulin to cause hypoglycemia?

One potential downside to treatment of acute hyperglycemia with insulin is the possibility of causing hypoglycemia 2 to 4 hours after the dose is given (duration of action of rapid-acting insulin is 4 hours). The risk should be minimized by using a suitable protocol with BG monitoring (using meters appropriate for the urgent care setting). The authors propose aiming for a glucose target between 120 and 180 mg/dL. There is currently no evidence-based literature to guide the goal of treatment, once undertaken. However, the authors proposed this target range to minimize the risk of hypoglycemia (< 70 mg/dL) while being clinically effective. Another potential side effect of treatment may be the intracellular shift of potassium from insulin and resultant hypokalemia. It may be prudent to check electrolyte levels in patients treated with insulin prior to discharge.

What is IV hydration?

IV hydration is required for all patients with a glucose levels > 600 with symptoms, signs or laboratory features of significant dehydration. For more marked hyperglycemia and if IV access is being used, IV boluses of insulin (regular insulin or rapid-acting analog insulin) can be considered or used.

Why do diabetics check their BG?

For all patients with a history of DM, it is logical and reasonable to check aBG level to detect significant hypoglycemia or hyperglycemia. In diabetic patients who provide a history of having stopped their prescribed DM medications for beyond a few days, states of metabolic decompensation, such as diabetic ketoacidosis and hyperosmolar non-ketotic syndrome, should be identified if present. Random BG levels are also appropriate if the medical history raises a suspicion of new-onset or undiagnosed DM (classic symptoms such as polyuria, polydipsia, rapid weight loss, blurred vision, suspicious infections (significant skin yeast infections, abscess, anaerobic infections, foot infections, hidradenitis suppurativa), and patients present with severe illness (increased likelihood of at least stress-induced hyperglycemia and may be a marker of worse outcomes).

What is stress induced hyperglycemia?

Stress-induced hyperglycemia can result from an acute process, such as infection, pain, trauma, or vascular accident, or can be associated with pre-existing diabetes mellitus (DM) or previously unknown DM (new onset or undiagnosed). DM affects 25.8 million people in the United States, more than 7 million of whom are undiagnosed. 1.

What is acute hyperglycemia?

Urgent message: Acute hyperglycemia is a common and potentially challenging problem in urgent care that deserves to be managed appropriately based on the best available evidence and suitable consideration of the associated complexities.

What are the two most serious hyperglycemic emergencies?

Diabetes mellitus, if uncontrolled, may lead to serious hyperglycemic emergencies. The two most serious hyperglycemic emergencies are diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). (Hyperglycemic hyperosmolar state is synonymous with hyperosmolar syndrome and hyperglycemic hyperosmolar nonketotic state which are both older names.) DKA most commonly occurs in patients with Type 1 diabetes mellitus or pancreatic disease, while HHS occurs more frequently with Type 2 diabetes. The presentation of the two syndromes can be distinguished by several factors. Both DKA and HHS patients present with hyperglycemia, but DKA is characterized by ketonemia, ketonuria, and metabolic acidosis while HHS involves dehydration without significant ketoacidosis. It is also possible that a patient presents with a mixture of DKA and HHS.1

What happens when insulin is not present in a diabetic patient?

When these patients are in a fuel deprived state, there is a lack of insulin and a high amount of counter-regulatory hormones present. This causes the system to spiral out of control and leads to hyperglycemia, dehydration, ketoacidosis, and ketonuria.

How to treat DKA and HHS?

Insulin treatment for both DKA and HHS is the same. All patients should be given 10-20U regular insulin IV push. After that, they should be given 0.1 U/kg/hr continuous IV infusion of regular insulin. Anion gap, pH, and hyperglycemia should be monitored. If no improvement is seen within 2 hours, the dose should be doubled each hour until the desired results are seen. It is important to note that insulin should not be given without concomitant fluid infusions which will help expand the intravascular space. Otherwise, vascular collapse may occur as the osmolarity decreases and fluid flows out of the intravascular space back into the intracellular compartments. Also, while insulin therapy is being given, a transient rise in urinary ketones may be seen. However, this is simply a complication of the method used for measuring urine ketones and is not a true elevation.

How does insulin affect K+?

In other words, at a higher pH, more H+ is being pumped out of the cells while the K+ is being moved back inside the cells. In addition to this, the presence of insulin promotes the uptake of K+ into the cells. Therefore, in DKA, if serum K+ is less than 3.5 mEq/L and pH is <7.3, the first liter of IV fluids should have 20-40 mEq of KCl added to it. Cardiac monitoring should also be initiated in these patients. If this is not the case, the KCl should be added to the second liter of IV fluids. Once the patient is able to tolerate oral fluids, they may be switched to oral K+ replacement. Serum K+ should be monitored every 1-2 hours. If the patient is urinating and the K+ remains less than 5.5 mEq/L, K+ should continue to be added to the IV fluids.

Why is serum K+ increased in DKA?

Additionally, serum K+ is increased due to a deficit of insulin which normally promotes K+ uptake into cells. In DKA, since the body is in an acidotic state, serum K+ is increased by a 3rd mechanism which involves pH related exchange of vascular H+ and cellular K+. Therefore, K+ must be corrected in DKA (but not in HHS) in the following way:

How much water is lost in DKA?

Patients with DKA and HHS present with significant fluid loss. About 100ml/kg of water is lost in DKA while 100-200 ml/kg of water is lost in HHS. Interestingly, because glucose osmotically pulls water out of the intracellular compartments, patients with DKA and HHS rarely experience cardiovascular collapse even though the fluid deficits exceed the normal intravascular volume. Therefore, health professionals who are assessing these patients must be careful not to underestimate the level of dehydration in these patients since the clinical picture may look better than expected.

How is glucose regulated in the body?

Glucose is regulated by one of two mechanisms in the body, depending on the type of tissue involved. In insulin-insensitive tissues, such as the brain, glucose is not regulated by insulin and is therefore available in both fasting and fed states. This is essential for survival since glucose is the primary fuel source for the brain. Insulin-sensitive tissues, in contrast, only use glucose in the fed state. Once in the fasting state, these tissues obtain their fuel from sources other than glucose. Specifically, adipose tissues will undergo lipolysis while liver and muscle tissue will alter their intermediary metabolism to fat metabolism. These changes occur in the fuel deprived fasting state due to a decrease in insulin and an increase in the counter-regulatory hormones catecholamines, glucagon, and cortisol. Counter-regulatory hormones are also responsible for the increased glucose production, decreased peripheral utilization of glucose, and the production of ketones from fatty acids in the liver that takes place during the fasting state. As a net result of these hormonal changes, the body is in a state of hyperglycemia and ketones are present in the bloodstream. Normally, the presence of excess glucose and ketones in the fasting state acts as a counter-regulatory signal which promotes the production of insulin. This response is crucial because the production of insulin allows for normoglycemia to be restored in this stressful metabolic state.

Importance of Tight Glucose Control

The use of tight glucose control contributes to decreased morbidity and mortality in hospitalized patients. 3 Hyperglycemia leads to various complications, such as increased risk of infections, kidney damage, adrenal failure, and organ failure.

Epidemiology

The prevalence of hyperglycemia in critically ill patients is difficult to ascertain because of the different thresholds used to determine abnormal glucose concentrations. However, trauma patients in the emergency department tend to have much higher mortality rates because of poorer glucose control due to lack of management.

Etiology and Pathophysiology

The etiology of hyperglycemia in critically ill patients has been shown to be multifactorial. Whether diabetic or nondiabetic, patients can develop stress-induced hyperglycemia because of the body’s response to the disruption in homeostasis. This may occur as an endocrine, metabolic, and/or immune response to a critical illness.

Evidence for Glucose Control

The 2001 Leuven Surgical Trial was a single-center, nonblinded, randomized, controlled study that assessed ICU mortality between different serum glucose ranges in the SICU in 1,548 patients undergoing intensive versus lenient glucose control.

Glycemic Management

The American College of Physicians’ 2011 clinical practice guideline for the use of intensive insulin therapy for the management of glycemic control in hospitalized patients recommends a blood glucose target of 140 mg/dL to 200 mg/dL in critically ill adult patients once insulin is started.

Conclusion

Hyperglycemia in critically ill patients has been shown to be a significant cause of morbidity and mortality in patients admitted to the ICU. Although patients are managed based on hospital-specific glucose ranges, no standard range has been found to have the highest rate of survivability in the ICU patient population.

What is the target glucose level for SIHG?

In hospitalized patients a target glucose range of 7.8–10.0 mmol/L (140–180 mg/dL) is recommended for the majority of critically and non-critically ill patients. More stringent goals such as 6.1–7.8 mmol/L (110–140 mg/dL) may be appropriate for selected patients, if this goal can be achieved without relevant hypoglycaemia [30]. However, when aiming to achieve lower target glucose levels it has to be considered that people with SIHG often suffer from severe underlying disease (e.g., cancer), are in the perioperative care setting (e.g., recently transplanted patients or those requiring steroids as supportive therapy [31]), receive concomitant complex therapies (chemotherapy, immunosuppressants, antimicrobial therapy, etc.) and thus, might be prone to larger glucose fluctuations. In the course of treatment, GCs need frequent dose adaptions that result in altered requirements of glucose lowering therapies. As a consequence, the risk for hypoglycaemia is increased when stringent glucose targets were chosen. Therefore, in specific patient populations (incurable disease with short life expectancy, advanced age and comorbidities, susceptibility for hypoglycaemia and impaired awareness of hypoglycaemia) the major aim will be the avoidance of hypoglycaemia and hyperglycaemic symptoms [29,32,33].

How to adjust insulin dose?

In a pragmatic approach, insulin dose can be adjusted by half the percentage of the GC dose change. For example, when GCs are increased or tapered by 50%, insulin dose is suggested to be increased or reduced by 25%, respectively. In patients with pre-existing DM a deterioration of glycaemic control secondary to GC therapy can be expected. In this regard, type of GC agent as well as time point and interval of GC application have to be taken into account.

What is SIHG in diabetes?

SIHG is defined as abnormally elevated blood glucose associated with the use of GCs in patients with or without pre-existing DM. The diagnostic criteria for SIHG do not differ from other types of diabetes and include a confirmed fasting blood glucose ≥7 mmol/L (≥126 mg/dL), a glucose level of ≥11.1 mmol/L (≥200 mg/dL) at 2 h following ingestion of 75 g glucose in an oral glucose tolerance test (OGTT), an HbA1c ≥6.5% (≥48 mmol/mol) or a random blood glucose ≥11.1 mmol/L (≥200 mg/dL) [26]. However, in patients with SIHG, diagnosis can be more challenging: fasting blood glucose might be normal especially when short- or intermediate-acting GCs are administered in single morning doses. Apart from its difficulties in implementation of oGTT in hospitalized patients, hyperglycaemia might be absent after glucose exposure in an oGTT, especially when it is performed in the morning when the diabetogenic effect of the GCs is not yet present. HbA1c might be inconspicuous especially in those with new-onset GC therapy as it reflects the glycaemic situation in the weeks prior to the time point of measurement. In addition, several conditions such as chronic kidney disease or hemoglobinopathies, that are frequently present in people requiring steroids, affect the reliability of HbA1c measurements. Nevertheless, determination of HbA1c can be useful to evaluate glycaemic control in patients who are on long-term GC therapy or to distinguish between new-onset diabetes and pre-existing DM in a situation of hyperglycaemia after GC initiation. Due to the mentioned limitations of the usual diagnostic approach to detect SIHG, it is recommended to perform frequent (capillary) glucose monitoring in those who receive high doses of GCs (defined as >20 mg prednisolone or equivalent). This approach is particularly recommended in people with a high risk to develop SIHG (e.g., advanced age, higher BMI, previously present impaired glucose tolerance, prediabetes or family history of diabetes). Then, a random glucose value ≥11.1 mmol/L (≥200 mg/dL) can be utilized to establish the diagnosis of SIHG [27].

What is the prevalence of SIHG?

The prevalence of SIHG is dependent on the dose, indication and setting of use. Individual conditions such as age, baseline body mass index (BMI) and family history of diabetes are known to impact the risk of SIHG development. Older observational data indicate that 2% of incident diabetes cases in a primary care population are associated with GC therapy and the odds ratios for presenting with new-onset diabetes after introduction of GCs in various studies has been described to range from 1.36–2.31 [6]. Patients without history of diabetes developed in-hospital hyperglycaemia (≥10 mmol/L; ≥180 mg/dL) in 70% when relevant doses of GCs were administered [7]. A meta-analysis summarized studies in which patients without pre-existing diabetes who received systemic GCs and showed a rate of SIHG development in 32.3% and in further 18.6% diabetes was sustainable during the follow up [8]. In patients who received solid organ transplantation and GC therapy the prevalence was described to be between 17% and 32% [9,10] and in a high-risk population of people who received high dose systemic therapy for acute Graft-versus-Host disease, two thirds of the cohort showed median glucose readings in the hyperglycaemic range (defined as fasting glucose ≥7 mmol/L or ≥126 mg/dL) [11]. As SIHG is suggested to be a transient problem resolving after the discontinuation of GCs, data indicate that diabetes can persist and GCs just unmasked a pre-existing glucose metabolism disorder [12,13]. While mainly systemic steroids were identified to expose the patient to an increased risk for hyperglycaemia, recently, topically used GCs were also shown to be associated with an elevated risk of diabetes [14].

When should basal insulin be up titrated?

When basal insulin therapy was already initiated, up-titration by 10–20% should be performed in case of sustained hyperglycaemia (fasting glucose exceeding 11.1 mmol/L [200 mg/dL]) on 2–3 subsequent days [17,33]. Alternatively, adjustments can be performed in 2 IU increments (conservative approach) to reach the individual glucose target; however, a steady dose adjustment must be warranted. Persisting hyperglycaemia despite basal insulin titration with predominantly postprandial hyperglycaemia requires additional rapid-acting insulin administrations either as rapid-acting insulin injection or incorporated in premixed insulins.

How much PE increases TDD?

PE of 20 mg → 10% increase in TDD

How often are glucocorticoids given?

Schematic illustration of different glucocorticoids and their potential effect on glycaemia. Long-acting agents are usually administered only once daily. These examples are presuming people with normal glucose homeostasis prior to start of glucocorticoid therapy. X-axis: time of the day; y-axis: potential influence on glucose.

Why is hyperglycaemic emergency important?

Hyperglycaemic emergencies require urgent assessment and management to reduce preventable morbidity and mortality. Hyperglycaemic emergencies may occur as the first presentation of diabetes (undiagnosed), as well as an acute metabolic decompensation in those already diagnosed with diabetes. Identification of at-risk patients, together ...

Is DKA an emergency?

Suspected DKA is an emergency; transfer to an appropriate treating facility/hospital should not be delayed. • Euglycaemic ketoacidosis refers to ketosis and acidosis in the presence of normal blood glucose levels (or minor elevations of blood glucose levels) in symptomatic patients.

Is HHS more common in type 2 diabetes?

HHS is more common in type 2 diabetes in the presence of acute sepsis (eg urinary tract infection, pneumonia), after a cardiovascular event (myocardial ischaemia or stroke) or in people with renal dysfunction. HHS usually affects older people.

Do people with diabetes have a sick day plan?

Some people with known type 1 diabetes in particular may have a pre-existing sick day management plan (a written document provided by their treating specialist, healthcare professional or team). If clinical conditions do not require a rapid transfer to hospital, a pre-existing sick day plan may be put into place.

Can HHS be caused by DKA?

While metabolic acidosis present in a person with HHS will usually be due to a lactic acidosis related to the precipitant and to any renal impairment, HHS may sometimes occur with DKA in a mixed clinical picture of ketoacidosis and a hyperosmolar state. Box 2.

Subjects, Materials, and Methods

We conducted a qualitative study using constructivist grounded theory (CGT) methodology to explore our research questions. Because CGT probes how and why participants act and construct meanings in specific situations ( 12 ), it was well suited to explain why our participants chose to come to the ED with their hyperglycemia concerns.

Results

Twenty-two patients consented to be interviewed. Baseline characteristics of the participants, including age, sex, type of diabetes, ED disposition, and frequency of ED utilization, are summarized in Table 1. The interview length averaged 35 minutes (range 25–50 minutes).

Discussion

Our study explored patients’ choice to present to the ED for their concerns about hyperglycemia and found five reasons affecting their decision: urgency, expectation of acute interventions, advice from others, fear of complications, and convenience.

Article Information

This study was supported by a Canadian Association of Emergency Physicians’ Junior Investigator Grant. The funding source had no role in any part of the study conduct.

Importance of Tight Glucose Control

• The use of tight glucose control contributes to decreased morbidity and mortality in hospitalized patients.3 Hyperglycemia leads to various complications, such as increased risk of infections, kidney damage, adrenal failure, and organ failure. In a 2006 study of 767 critically ill patients who were in the ICU for more than 3 days, there was a 10% r...

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Epidemiology

Etiology and Pathophysiology

Evidence For Glucose Control

Glycemic Management

Conclusion