What’s behind diabetes re-hospitalisation?

CDC Reports Rise in DKA Hospitalizations in the United States – What’s behind this change?

What’s behind diabetes re-hospitalisation?


Latest statistics from the CDC show that rates of hospitalization from diabetic ketoacidosis (DKA) steadily increased from 2009 to 2014. Prior to this, rates had been on the decline. So what changed?

The Centers for Disease Control and Prevention (CDC) Morbidity and Mortality Weekly Report might not be part of your weekly reading list, but the March 30, 2018 publication is one to take a close look at.

First Up – What’s DKA?

Diabetic ketoacidosis (DKA) is a life-threatening but often preventable complication of diabetes. It occurs when the body is not receiving enough insulin to break down glucose, forcing the body to break down fat as fuel.

This releases ketones into the bloodstream, which can cause the blood to become acidic, resulting eventually in system failure and even death. Early symptoms include: elevated ketones in urine, high blood glucose levels, frequent urination and thirst.

More extreme warning signs include: fatigue, flushed skin, nausea, vomiting, shortness of breath, and fruity breath smell. Read more here on how to test for ketones and when to seek help.

Okay – back to the data

From 2009 to 2014 the rate of DKA hospitalizations increased a total of 54.9%, from 19.5 to 30.2 hospitalizations per 1,000 people with diabetes. Each year between 2009 and 2014, there was a more than 6% rise in DKA hospitalizations annually across all age groups, with highest rates among people under 45 years old.

But while the CDC report does break out DKA hospitalizations by age, that’s about as far as the data segmentation goes. What’s missing? Importantly, the differences between DKA hospitalization rates at diagnosis versus during management. And equally important: DKA hospitalization rates broken down by Type 1 diabetes versus Type 2 diabetes.

In their report, the CDC takes a stab at explaining the rising trend.

They offer that perhaps DKA hospitalization is on the rise because people are more aware of the dangerous and even deadly nature of DKA and are therefore more ly to seek hospital care.

If that’s true, it’s potentially good news – maybe awareness campaigns are working! Perhaps people experiencing DKA symptoms are recognizing them, testing for ketones, and seeking immediate medical care.

Unfortunately, this is not the only possible explanation for rising DKA hospitalizations. And without more descriptive data, it’s impossible to decisively conclude anything. The CDC report states that “DKA is more common among persons with type 1 diabetes, it also occurs among persons with type 2 diabetes” – but what do the numbers really look ?

The best study we could find looked at 226 patients admitted to the hospital for DKA, and found that 47% had known Type 1 diabetes, 26% had known Type 2 diabetes and 27% had newly diagnosed diabetes.

This represents a small data set taken over 20 years ago. But it’s clear that DKA hospitalizations happen in all three of these groups.

Effective prevention of DKA requires better information about who, exactly, is impacted – so we can better understand why.

Beyond Type 1 has called upon the CDC to segment data by diabetes type in the past. This is a perfect example of why segmented data matters. More detailed data allows us to take aim at a possible cause, hone a more effective prevention campaign. This data leaves us with more questions than answers.

If the primary driver of this rise is DKA at onset of diabetes, we have an awareness problem. 41% of people with Type 1 diabetes in the USA are in DKA at the time of diagnosis. This number could be growing. Or the number of diagnoses overall could be growing – overall rates of Type 1 diabetes are, in fact, on the rise.

If rates of DKA hospitalization are primarily rising among people with known Type 1 diabetes in the United States, we should indeed be alarmed. 

The very basis of diabetic ketoacidosis is not enough insulin in the body. List prices for popular fast-acting insulins Humalog and Novolog have both risen 290% over the past decade. People with Type 1 diabetes without health insurance (or with high-deductible health insurance) face monthly costs upwards of $600 – sometimes much more – simply for the insulin needed to stay alive.

Insulin pricing and access advocate Laura Marston was quick to point out this trend in the data. Put simply in a tweet: “when insulin prices skyrocket, so do DKA hospital admissions. Notice the similar upward trajectories beginning in 2009.”

Endocrinologists have spoken up in articles and penned op-eds, explaining the insulin access issues their patients face.

“I continually see patients who try to stretch their [insulin] prescription with the hope that it will last longer,” said Dr.

Joshua Miller, an assistant professor of medicine and endocrinology at Stony Brook University School of Medicine in an interview for NewsDay.

This paints an alarming picture – high out-of-pocket costs for insulin in the United States have left some with Type 1 diabetes rationing insulin in an attempt to save money and make ends meet. One dangerous side effect of limiting insulin intake? Hospitalization due to DKA.

The CDC report doesn’t give us strong enough data to make a decisive call on why DKA hospitalization rates are on the rise. But it’s certainly enough to know that we should be asking critically important questions.

It is not enough for the CDC to solely conclude that rates are rising because of “lower thresholds for hospitalization.

” We need to know – is this the result of insulin access challenges? Of an increase in diagnoses of Type 1 diabetes? Are more people with Type 2 diabetes transitioning to insulin dependency and landing in the hospital with DKA as a result?

Maybe the rise is a result of all of these issues. Maybe several. Maybe other variables entirely. Join us in calling on the CDC to segment DKA data by diabetes Type.

And in the absence of conclusive data, we must keep pushing on all fronts: raising awareness for DKA symptoms at diabetes onset, advocating for access to insulin for everyone living with diabetes, and demanding data that serves all diabetes communities.  

Learn more about Beyond Type 1’s DKA Awareness Campaign, sign the petition for CDC to segment diabetes data, and read more access coverage.

Advocacy, Community, Management

Source: https://beyondtype1.org/cdc-reports-rise-in-dka-hospitalizations-in-the-united-states-whats-behind-this-change/

Management of Diabetes and Hyperglycemia in Hospitalized Patients

What’s behind diabetes re-hospitalisation?

Diabetes is a prevalent metabolic disorder that affects more than 415 million people globally [1]. Globally, diabetes care has been estimated at $1.31trillion [2]. Further, according to the International Diabetes Federation, 1 in 10 adults will have diabetes by 2040 [1].

In the United States, data from the National Diabetes Statistics reported in 2012 that a total of 29.1 million Americans, or 9.3% of the population, had diabetes [3]. The percentage of the population with diagnosed diabetes is expected to rise, with one study projecting that as many as one in three U.S. adults will have diabetes by 2050 [4].

Patients with diabetes have a 3-fold greater chance of hospitalization compared to those without diabetes [5,6], and it is estimated that more than 20% of all adults discharged have diabetes, with 30% of them requiring 2 or more hospitalizations in any given year [5-7]. In 2012 in the U.S., there were over 7.

7 million hospital stays for patients with diabetes (i.e., diabetes as either a principal diagnosis for hospitalization or as a secondary diagnosis, coexisting condition) and in the UK the 2016 National Diabetes Inpatient Audit suggested that the prevalence of diabetes amongst inpatients had risen from 15% in 2010 to 17% in 2016 [8].

In addition, patients hospitalized with a diagnosis of diabetes stay in the hospital for longer than those without a diagnosis of diabetes admitted for the same condition [9].

Diabetes remains the 7th leading cause of death in the United States in 2014, with 76,488 death certificates listing it as the underlying cause of death, accouting for 24 deaths per 100,000 of the population [10].

The care of patients with diabetes imposes a substantial burden on the economy, with a total estimated cost of diagnosed diabetes in the United States in 2012 was $245 billion; including $176 billion in direct medical costs and $69 billion in reduced productivity [11].

The largest component of this medical expenditure is hospital inpatient care , accounting for 43% of the total medical cost [11].

Hyperglycemia is defined as a blood glucose greater than 140 mg/dl (7.8 mmol/l) [12,13]. It is reported in 22% to 46% of non-critically ill hospitalized patients [7,12].

Extensive observational and trial data indicate that inpatient hyperglycemia, in patients with or without a prior diagnosis of diabetes, is associated with an increased risk of complications and mortality, a longer hospital stay, a higher admission rate to the intensive care unit (ICU), and a higher need for transitional or nursing home care after hospital discharge [7].

Several studies and meta-analyses have shown that intensive insulin therapy is associated with increased risk of hypoglycemia [14-18], which has been associated with increased morbidity and mortality in hospitalized patients [12,15,19-22]. Thus, while insulin therapy is recommended for the management of hyperglycemia in hospitalized patients, the concern about hypoglycemia has led to revised glucose target recommendations from professional organizations [13,17,23-26].

This chapter reviews the pathophysiology of hyperglycemia during illness, the mechanisms for increased complications and mortality due to hyperglycemia and hypoglycemia, and reviews the evidence on the different therapies available for the management of inpatient diabetes and hyperglycemia in the critical care and in the general medicine and surgical settings.

In subjects without diabetes during the fasted state, plasma glucose is maintained between 70-100 mg/dl (3.9 – 5.6 mmol/l) by a finely regulated balance between hepatic glucose production and glucose utilization in peripheral tissues.

Maintenance of normal glucose level is essential for central nervous system function as the brain can neither synthesize nor store glucose [35]. Systemic glucose balance is maintained by dynamic, minute-to-minute regulation of endogenous glucose production and of glucose utilization by peripheral tissues [36].

Glucose production is accomplished by gluconeogenesis or glycogenolysis primarily in the liver and in a lesser degree by the kidneys [37]. Gluconeogenesis results from conversion of non-carbohydrate precursors such as lactate, alanine, and glycerol to glucose in the liver [38].

Excess glucose is polymerized to glycogen, which is mainly stored in the liver and muscle. Hyperglycemia develops because of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues (Figure 1).

Pathogenesis of hyperglycemia. Hyperglycemia results from increased hepatic glucose production and impaired glucose utilization in peripheral tissues.

Reduced insulin and excess counterregulatory hormones (glucagon, cortisol, catecholamines and growth hormone) increase lipolysis and protein breakdown (proteolysis), and impair glucose utilization by peripheral tissues.

Hyperglycemia causes osmotic diuresis that leads to hypovolemia, decreased glomerular filtration rate, and worsening hyperglycemia. At the cellular level, increased blood glucose levels result in mitochondrial injury by generating reactive oxygen species, and endothelial dysfunction by inhibiting nitric oxide production.

Hyperglycemia increases levels of pro-inflammatory cytokines such as TNF-α and IL-6 leading to immune system dysfunction. These changes can eventually lead to increased risk of infection, impaired wound healing, multiple organ failure, prolonged hospital stay and death. Adapted from ref. [15].

From the quantitative standpoint, increased hepatic glucose production represents the major pathogenic disturbance.

Increased hepatic glucose production results from the high availability of gluconeogenic precursors including the amino acids alanine and glutamine, as a result of accelerated proteolysis and decreased protein synthesis; lactate as a result of increased muscle glycogenolysis; and glycerol as a result of increased lipolysis; and from the increased activity of gluconeogenic enzymes (phosphoenol pyruvate carboxykinase, fructose-1,6-bisphosphatase, and pyruvate carboxylase) [37,38].

Glucose metabolism is maintained by an interaction of glucoregulatory hormones – insulin and counterregulatory hormones (glucagon, cortisol, growth hormone and catecholamines). Insulin controls hepatic glucose production by suppressing hepatic gluconeogenesis and glycogenolysis.

In insulin-sensitive tissues such as muscle, insulin promotes protein anabolism, glucose uptake and glycogen synthesis, and inhibits glycogenolysis and protein breakdown [36,39,40].

In addition, insulin is a powerful inhibitor of lipolysis, free fatty acid oxidation, and ketogenesis [39,40].

Counterregulatory hormones (glucagon, cortisol, growth hormone and catecholamines) also play an important role in the regulation of glucose production and utilization. Glucagon is the most important glycogenolytic hormorne, therefore, regulates hepatic glucose production during normal state and in every state of hyperglycemia [37].

During stress, excess concentration of counterregulatory hormones result in altered carbohydrate metabolism by inducing insulin resistance, increasing hepatic glucose production, and reducing peripheral glucose utilization.

In addition, high epinephrine levels stimulates glucagon secretion and inhibits insulin release by pancreatic β-cells [41,42].

The development of hyperglycemia results in an inflammatory state characterized by an elevation of pro-inflammatory cytokines and increased oxidative stress markers [43-45].

Circulating levels of tumor necrosis factor-α, interleukin [IL]-6, IL1-ß, and IL-8, C-reactive protein are significantly increased two- to fourfold on admission in patients with severe hyperglycemia compared with control subjects, and levels returned to normal levels after insulin treatment and resolution of hyperglycemic crises [43].

TNF-α leads to insulin resistance by interaction at the level of the insulin receptor and through altered regulation of the insulin-signaling pathway. Increasing evidence indicates that during acute stressful states, increased concentrations of these inflammatory cytokines can increase insulin resistance by interfering with insulin signaling [44,46].

In addition, TNF-α by preventing insulin-mediated activation of phosphatidylinositol 3-kinase reduces insulin- stimulated glucose uptake in peripheral tissues [44,46,47].

A recent prospective randomized study of intensive insulin therapy in cardiac surgery patients measured longitudinal changes in inflammatory response and differences between patients with and without diabetes and perioperative complications [45].

The authors observed significant elevations in acute inflammatory response markers after the 3rd and 5th day of surgery, which returned to baseline levels after 1 month of follow-up. Patients with surgical complications had higher levels of inflammatory and oxidative stress markers without significant differences in the inflammatory response in subjects with or without diabetes treated with intensive (target BG: 100-140 mg/dl [5.6 – 7.8 mmol/l]) or conservative (BG: 141-180 mg/dl [7.9-10.0 mmol/l]) insulin regimens [45].

A large body of literature including observational and prospective randomized clinical trials, in patients with and without diabetes, as well as in critically ill and non-critically ill patients has shown a strong association between hyperglycemia and poor clinical outcomes, such as mortality, infections and hospital complications [5,48-57]. This association correlates with severity of hyperglycemia on admission as well as during the hospital stay [55,58,59]. Of interest, increasing evidence indicates an increased risk of complications and mortality in patients without a history of diabetes (stress induced) compared to patients with known diagnosis of diabetes [7,52,58,60,61]. It is not clear if stress hyperglycemia is the direct cause of poor outcomes or it is a general marker of severity of illness.

The mechanisms implicated on the detrimental effects of hyperglycemia during acute illnesses are not completely understood.

Current evidence indicates that severe hyperglycemia results in impaired neutrophil granulocyte function, high circulating free fatty acids, and overproduction of pro-inflammatory cytokines and reactive oxygen species (ROS) that can result in direct cellular damage, and vascular and immune dysfunction [62].

The majority of evidence linking hyperglycemia and poor outcomes comes from studies in the ICU. Falciglia et al in a retrospective study of over 250,000 veterans admitted to various ICUs reported that hyperglycemia is an independent risk factor for mortality and complications [58].

In a nonrandomized, prospective study, Furnary followed 3,554 patients with diabetes that underwent coronary artery bypass graft. Patients treated with subcutaneous insulin (SCI) who had an average blood glucose of 214 mg/dl (11.9 mmol/l) and patients treated with continuous insulin infusion (CII) with an average blood glucose of 177 mg/dl (9.

8 mmol/l) had significantly more deep sternal wound infections [56] and a 50% higher risk-adjusted mortality [63]. In a different ICU study, patients with blood glucose levels >200 mg/dl (>11.1 mmol/l ) were shown to have higher mortality compared to those with blood glucose levels 11.

0 mmol/l) had a greater risk of mortality and complications than those with glucose < 198 mg/dl (162 mg/dl (9.0 mmol/l) compared to patients with a blood glucose of 108 mg/dl (6.0 mmol/l) [64].

General surgery patients with hyperglycemia during the perioperative period are also at increased risk for adverse outcomes. In a case-control study, elevated preoperative glucose levels increased the risk of postoperative mortality in patients undergoing elective non-cardiac non-vascular surgery [65].

Patients with glucose levels of 110-200 mg/dl (5.6-11.1 mmol/l) and those with glucose levels of >200 mg/dl (11.1 mmol/l) had, respectively, 1.7-fold and 2.1-fold increased mortality compared to those with glucose levels < 5.6 mmol/l ( 220 mg/dl (>12.

2 mmol/l ) on the first postoperative day had a rate of infection 2.7 times higher than those who had serum glucose levels 10.0 mmol/l ) or 180 mg/dl [10 mmol/l]) Treatment goal: For most patients, target a glucose level between 140-180 mg/dl.

More stringent goals (110-140 mg/dl) may be appropriate for selected patients, if achievable without significant risk for hypoglycemia

No specific guidelines If treated with insulin, pre-meal glucose targets should generally be

Source: https://www.ncbi.nlm.nih.gov/books/NBK279093/

The relationship between diabetes mellitus and 30-day readmission rates

What’s behind diabetes re-hospitalisation?

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9 Symptoms of Type 1 & Type 2 Diabetes: Complications, Causes & Diet

What’s behind diabetes re-hospitalisation?

These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication).

Eye Complications

The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina.

Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization).

Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.

To treat diabetic retinopathy, a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels.

Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% retinopathy after 15 years of the disease.

Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes.

Cataracts and glaucoma are also more common among diabetics. It is also important to note that since the lens of the eye lets water through, if blood sugar concentrations vary a lot, the lens of the eye will shrink and swell with fluid accordingly.

As a result, blurry vision is very common in poorly controlled diabetes. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled.

This allows for a more accurate assessment of what kind of glasses prescription is required.

Kidney damage

Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine.

Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood.

In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.

The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in patients with diabetes.

Nerve damage

Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia).

Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them.

Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal.

Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.

Diabetic nerve damage can affect the nerves that are important for penile erection, causing erectile dysfunction (ED, impotence). Erectile dysfunction can also be caused by poor blood flow to the penis from diabetic blood vessel disease.

Diabetic neuropathy can also affect nerves to the stomach and intestines, causing nausea, weight loss, diarrhea, and other symptoms of gastroparesis (delayed emptying of food contents from the stomach into the intestines, due to ineffective contraction of the stomach muscles).

The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders.

Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression.

While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly.

The pain of diabetic nerve damage may also improve with better blood sugar control, though unfortunately blood glucose control and the course of neuropathy do not always go hand in hand. Newer medications for nerve pain include Pregabalin (Lyrica) and duloxetine (Cymbalta).

Source: https://www.medicinenet.com/diabetes_mellitus/article.htm

Hyperglycemia in the Hospital

What’s behind diabetes re-hospitalisation?

Hyperglycemia is the medical term for blood glucose (sugar) that is too high. High blood glucose (HBG) is a common problem for people with diabetes. Blood glucose can also rise too high for patients in the hospital, even if they do not have diabetes. This patient guide explains why some patients develop HBG when they are hospitalized and how their HBG is treated.

Until recent years, doctors thought that HBG in hospitalized patients was not harmful as long as the blood glucose levels stayed at or below 200 milligrams per deciliter (mg/dL). Recent research studies show that HBG above 180 increases the risk of complications in hospital patients. Keeping blood sugar below this level with insulin treatment lowers the risk for these problems.

Most doctors agree that controlling blood sugar so it stays below 180 mg/dl but not below 140 mg/dl is best for very ill patients in intensive care units (ICU). Less clear is what the best target blood sugar should be for inpatients who are admitted for general surgery or non-critical medical conditions.

In some patients, some non-insulin therapies as well as insulin treatment can cause low blood sugar, called hypoglycemia. Just blood sugar levels that are too high, blood sugars that are too low are not safe and should be avoided.

This patient guide for glucose control in the hospital is The Endocrine Society’s practice guideline for health care providers on preventing and treating HBG. This guide applies just to patients on a regular hospital floor, not those who are in an ICU.

Many conditions can cause or worsen HBG in hospital patients. These include:

  • Physical stress of illness, trauma, or surgery
  • Decrease in physical activity
  • Steroids prednisone and some other medicines
  • Skipping diabetes medicines
  • Liquid food given through a feeding tube or nutrition given intravenously
  • Certain medical conditions such as Cushing disease or syndrome

Patients with HBG have more problems in the hospital, including:

  • Longer hospital stay
  • Slower wound healing
  • More infections
  • More disability after discharge from the hospital
  • Higher risk of death
  • Increased risk for getting readmitted to the hospital

How is HBG found?

Health care providers find HBG by doing a simple blood test. Blood sugar is usually measured by pricking the finger and testing a drop of blood with a glucose meter. The glucose meters used in hospitals are calibrated on a regular basis leading to more reliability and accuracy of results.

Your blood sugar should be measured either by fingerstick testing or testing blood from your veins when you are admitted to the hospital. You may need this test more than once if you are at high risk for HBG.

For example, you have a higher risk for HBG if you have diabetes, are treated with medications that increase your blood sugar, or are receiving tube feeding or intravenous (IV) feeding.

In-hospital HBG is defined as a pre-meal blood sugar above 140 mg/dL. After finding HBG, your care providers will check your blood sugar before meals and at bedtime.

You may need more testing in some cases. This includes if you are not eating, are receiving intravenous (IV) insulin, have a medication change that could affect blood sugar, or have frequent bouts of low blood sugar (hypoglycemia).

What are the blood sugar targets in the hospital?

Health care providers want most ICU patients to have a blood sugar between 140 and 180 mg/dl. Outside the ICU, most providers aim to keep blood sugar between 100 and 140 mg/dl before meals and below 180 mg/dl at other times.

What is the treatment of HBG?

Insulin is the currently identified as the most reliable treatment for HBG in the hospital. This is true even if you do not have diabetes or if you do not use insulin at home. Insulin injection is the most effective way to control blood sugar.

  Some non-insulin therapies that are used in the outpatient setting for diabetes treatment can cause low blood sugar or other health problems while you are sick. For these reasons, you may have to stop taking your non-insulin diabetes medicines during your hospital stay.

Hospital patients with HBG should receive insulin shots under the skin (subcutaneous injections). You should get basal (long- or intermediate-acting) insulin once or twice a day to keep blood sugar levels steady.

The effect of these injections tends to be over 24 hours and should not be skipped if you do not eat, although doses may need to be adjusted if you are not eating. Before meals, getting bolus (rapid-acting) insulin helps prevent blood sugar levels from going too high after eating.

Besides mealtime insulin, some patients with HBG may need additional insulin injections. This scheduled insulin treatment prevents HBG or, in some patients, a dangerous health problem called diabetic ketoacidosis (when acids and substances called ketones build up in the blood due to lack of insulin).

Intravenous insulin is another way that HBG is treated in the hospital. This is used when the blood sugar is extremely high or unstable or not responding to subcutaneous injections. This is a temporary way of treating HBG and is usually replaced by subcutaneous insulin when there is improvement in blood glucose levels or hospital discharge is anticipated.

For people who are on insulin pumps, your health care provider may decide to keep you on the pump during the hospital stay if you are admitted to a hospital that has a policy for this in place. Please inform your nurse and physician that you use an insulin pump so they can work with you to manage your blood sugar in the hospital.

You will be fully responsible for the mechanics of managing the insulin pump. If you think you are unable to do so, let your team know. If you wear a continuous glucose monitor (CGM), check with your team if you are allowed to wear it in the hospital. You will have to remove pump and CGM devices for radiographic testing such as X-rays, CT scans or MRI scans.

There are situations when your health care team may decide to stop pumps or CGM devices. In this case, you will be started on standard subcutaneous insulin injections. For all patients with HBG, good nutrition is important to help control blood sugar. A dietitian should work with you to plan your meals.

The point is to make sure you get enough calories and eat the right amount and types of sugars or carbohydrates. These include whole grains, fruits, vegetables, and low-fat milk. Some hospitals may base your premeal insulin the amount of carbohydrates you will consume.

How should patients with diabetes who are having surgery be treated?Before surgery, patients who take insulin should continue to receive insulin. If you do not take insulin, your care providers usually will sometimes stop or adjust non-insulin medicines and advise you to receive insulin if you develop HBG while in the hospital. Before and after surgery, all patients with type 1 diabetes and most patients with type 2 diabetes should receive insulin especially basal insulin to prevent HBG. Insulin can be given through an IV or by multiple injections under the skin. When you can eat again, you should get mealtime (bolus or rapid-acting) insulin before meals.

Is there a risk for low blood sugar?

Low blood sugar (defined as a blood sugar below 70 mg/dL) can occur with insulin treatment, if you are not eating, or after a sudden stop to tube or IV feedings.

If you receive insulin or other diabetes medicines, your care providers will check your blood sugar often to make sure it does not drop too low. They may need to change the dose or timing of your insulin to prevent low blood sugar.

Low blood sugar is treated with juice or glucose gels or tablets if you are able to take food by mouth. If not, you might get injections of glucose or glucagon if needed

What can you do to help with your hospital care?

If you have diabetes, let your nurse and doctor know this information when you go into the hospital. Ask your doctor to make sure this information goes into your patient chart.

You will need to have your blood sugar checked at least four times a day (before each meal and at bedtime if you are eating regular meals or every six hours if you are not eating). So that your care providers know your usual blood sugar control, you should have a hemoglobin A1c test (blood test that shows your average blood sugar over the past three months).

If you do not have diabetes but your blood sugar is above 140 mg/dL, you will need to have this test to determine if you have previously undiagnosed diabetes or are at risk for this in the future.

If your hospital provider diagnoses you with diabetes, you will need to learn how to do home glucose testing and how to recognize and treat high and low blood glucose levels. In some cases, you may also need to learn how to inject insulin.

You may receive education while you are in the hospital and will ly need to arrange for additional diabetes education through your primary care provider following discharge.

When you leave the hospital, you will receive a written care plan for home diabetes management. It is important to fill the medications prescribed at time of your discharge.

Please check back with your team if you have difficulty in filling medications at your pharmacy or if you have questions about the diabetes plan you were given.  If you had HBG or low blood sugar in the hospital, your care plan should include how to control your blood sugar and when to see your doctor next. It also should explain how and when to take your diabetes medications. By following this advice, you will have the best chance of a good recovery after your hospital stay.

Developed for patients Management of Hyperglycemia in Hospitalized Patients in Non-Critical Care Setting, an Endocrine Society Clinical Practice Guideline

Editor(s): Mary Korytkowski, M.D., Guillermo Umpierrez, M.D., Marie McDonnell, M.D.

Last Updated: May 2019

Source: https://www.hormone.org/diseases-and-conditions/diabetes/hyperglycemia-in-the-hospital

Diabetes and heart failure are linked; treatment should be too

What’s behind diabetes re-hospitalisation?
(Maskot, Getty Images)

Having Type 2 diabetes or heart failure independently increases the risk for getting the other, and both often occur together, further worsening a patient's health, quality of life and care costs, a new report says.

Many of the risk factors and mechanisms behind Type 2 diabetes and heart failure are similar, yet there's a lack of guidance on how to care for people with both conditions, according to a scientific statement from the American Heart Association and the Heart Failure Society of America published Thursday in the journal Circulation.

Recent studies have found new treatments for diabetes may also improve heart failure outcomes, showing the interplay between the two conditions, the report says.

The statement summarizes what's known about the inner workings of diabetes and heart failure and the best ways to treat the conditions when they occur simultaneously.

But it also encourages clinicians to coordinate the care and treatment of patients who have both conditions in “a thoughtful and cohesive way,” said Dr. Shannon Dunlay, who co-chaired the report's writing committee.

It's not uncommon for a patient to see a cardiologist for heart failure and then visit a primary care doctor or endocrinologist for help managing diabetes, she said. But physicians need to be aware of how medications used for one condition affect the outcome of another.

“There's so much new data coming out all the time. We want to bring attention to the fact that diabetes and heart failure have substantial overlap, and it's important to stay up to date on new information,” said Dunlay, a heart failure cardiologist at the Mayo Clinic in Rochester, Minnesota.

Ideally, all the patient's care teams would be aligned.

“It's easy to focus on the main problem you are treating, such as heart failure. But it's important to think about other medical conditions patients have when prescribing new therapies,” she said.

People who have Type 2 diabetes, characterized by elevated blood sugar levels, are two to four times more ly to develop heart failure than someone without diabetes. But heart failure, a condition in which the heart fails to efficiently pump oxygenated blood through the body, also is a risk factor for diabetes.

Both disorders are characterized by insulin resistance and high levels of inflammation, said Dr. Rozalina McCoy, another member of the statement's writing committee.

“People who have both these conditions have a much higher risk of worse health outcomes – more hospitalizations, more emergency department visits, earlier death, and worse health overall than people who have just one of these conditions,” said McCoy, an endocrinologist and internal medicine physician at Mayo Clinic.

Since people who have either condition are at increased risk for developing the other, they should take proactive steps to improve their health, she said.

It's important to get regular exercise, maintain a healthy weight and eat a well-balanced diet. People with diabetes also need to keep their blood sugar levels under control.

The statement describes in detail a new class of medications called SGLT-2 inhibitors that lower blood sugar in adults with diabetes.

But research shows these drugs also are effective in reducing the risk of developing heart failure and helping manage the condition in those who already have it, preventing heart failure-related hospitalizations and deaths.

It's important that people with either or both conditions touch base regularly with their doctors, Dunlay said.

“There's still a lot that we don't know about how best to manage patients with diabetes and heart failure, but a number of ongoing studies will help to elucidate things further,” she said. “This is an exciting area in medicine and science right now, and we're going to find a lot of opportunities to improve patient management and outcomes.”

If you have questions or comments about this story, please email editor@heart.org.

Source: https://www.heart.org/en/news/2019/06/06/diabetes-and-heart-failure-are-linked-treatment-should-be-too