DKA management -
High levels of ketones can poison the body. When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2.
Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly. DKA usually develops slowly. But when vomiting occurs, this life-threatening condition can develop in a few hours.
Early symptoms include the following:. DKA is dangerous and serious. You can detect ketones with a simple urine test using a test strip, similar to a blood testing strip. Ask your health care provider when and how you should test for ketones.
When you are ill when you have a cold or the flu, for example , check for ketones every four to six hours. If your health care provider has not told you what levels of ketones are dangerous, then call when you find moderate amounts after more than one test.
Often, your health care provider can tell you what to do over the phone. Do NOT exercise when your urine tests show ketones and your blood glucose is high. High levels of ketones and high blood glucose levels can mean your diabetes is out of control.
Check with your health care provider about how to handle this situation. Diabetes Complications. Know the warning signs of DKA and check urine for ketones, especially when you're sick.
What are the warning signs of DKA? Early symptoms include the following: Thirst or a very dry mouth Frequent urination High blood glucose blood sugar levels High levels of ketones in the urine Then, other symptoms appear: Constantly feeling tired Dry or flushed skin Nausea, vomiting, or abdominal pain.
Vomiting can be caused by many illnesses, not just ketoacidosis. If vomiting continues for more than two hours, contact your health care provider. In most cases, the trigger is an infection, new-onset diabetes, or lack of compliance with treatment.
This activity highlights the role of the interprofessional team in evaluating and managing patients suffering from this disorder in order to achieve the best outcomes. Objectives: Review the etiology of diabetic ketoacidosis. Describe the management of a patient with diabetic ketoacidosis.
Summarize the abnormal laboratory parameters in a patient with diabetic ketoacidosis. Explain the importance of improving care coordination among an interprofessional team to improve outcomes for patients affected by diabetic ketoacidosis. Access free multiple choice questions on this topic.
Diabetic ketoacidosis DKA is characterized by hyperglycemia, acidosis, and ketonemia. It is a life-threatening complication of diabetes and typically seen in patients with type-1 diabetes mellitus, though it may also occur in patients with type-2 diabetes mellitus.
In most cases, the trigger is new-onset diabetes, an infection, or a lack of compliance with treatment. Diabetic ketoacidosis more commonly occurs in patients with type 1 diabetes, though it can also occur in patients with type 2 diabetes.
Patients with type 2 diabetes are also at risk. In both populations, catabolic stress of acute illness or injuries such as trauma, surgery, or infections may be a trigger. Common precipitating factors for DKA are non-compliance, new-onset diabetes, and other acute medical illness. The most common types of infections are pneumonia and urinary tract infections.
Other conditions like alcohol abuse, trauma, pulmonary embolism, and myocardial infarction can also precipitate DKA. Drugs that affect carbohydrate metabolisms, such as corticosteroids, thiazides, sympathomimetic agents, and pentamidine, may precipitate DKA.
Conventional, as well as atypical antipsychotic drugs, may also cause hyperglycemia and rarely DKA. SGLT2 inhibitors can predispose to diabetic ketoacidosis via multiple mechanisms.
When SGLT2 inhibitors are used together with insulin, insulin doses are often decreased to avoid hypoglycemia. A lower dose of insulin may not be sufficient to suppress lipolysis and ketogenesis.
SGLT2 is also expressed in pancreatic α-cells. SGLT2 inhibitors promote glucagon secretion and may decrease urinary excretion of ketone bodies, leading to an increase in plasma ketone body levels as well as hyperglycemia and DKA. SGLT-2 inhibitors may precipitate euglycemic DKA. One of the major causes of recurrent DKA in the inner-city population in the United States is non-compliance with insulin.
Socioeconomic and educational factors play a significant role in poor adhesion to medications, including insulin. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Diabetic ketoacidosis incidence ranges from 0 to 56 per person-years, shown in different studies from different geographic areas.
DKA has a higher prevalence rate among women and non-Whites. Incidence is higher among patients using injectable insulin compared to the subcutaneous insulin infusion pumps. Rates of DKA among children varies widely from country to country. The lowest incidence was found in Nigeria 2.
The highest incidence rate was found in Sweden and Finland, with Increased mortality was associated with nursing home residence among patients with DKA. Death in these conditions is rarely because of the metabolic complications of hyperglycemia or ketoacidosis alone.
The prognosis substantially worsens at the extremes of age in the presence of coma, hypotension, and severe comorbidities. Substance abuse is a major contributing factor for non-adherence to therapies.
Obesity is common in Blacks with DKA; it is found in more than half of those with newly diagnosed diabetes mellitus. Enhanced patient education and better access to medical care help in reducing the development of these hyperglycemic emergencies.
Diabetic ketoacidosis DKA is one of the life-threatening but preventable complications of diabetes. CDC's United States Diabetes Surveillance System USDSS indicated an increase in hospitalization rates for DKA from to , most notably in persons aged less than 45 years.
Scope for further improvement remains, especially to further reduce death rates among Black men and to prevent deaths occurring at home. The geriatric population is at particular risk for developing hyperglycemic crises with the development of diabetes.
Some of the causes are increased insulin resistance and a decrease in the thirst mechanism. The elderly are particularly vulnerable to hyperglycemia and dehydration, the critical components of hyperglycemic emergencies.
With increased diabetes surveillance and aggressive early treatment of hyperglycemia and its complications, morbidity, and mortality from acute diabetic crises in the geriatric population can be significantly reduced. Diabetes mellitus is characterized by insulin deficiency and increased plasma glucagon levels, which can be normalized by insulin replacement.
Insulin decreases hepatic glucose production by inhibiting glycogenolysis and gluconeogenesis. Glucose uptake by skeletal muscle and adipose tissue is increased by insulin.
Both of these mechanisms result in the reduction of blood sugar. In diabetic ketoacidosis, insulin deficiency and increased counter-regulatory hormones can lead to increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization.
This will ultimately cause worsening hyperglycemia. Insulin deficiency and increased counterregulatory hormones also lead to the release of free fatty acids into circulation from adipose tissue lipolysis , which undergo hepatic fatty acid oxidation to ketone bodies beta-hydroxybutyrate and acetoacetate , resulting in ketonemia and metabolic acidosis.
Diuresis induced by hyperglycemia, dehydration, hyperosmolarity, and electrolyte imbalance results in a decrease of glomerular filtration. Potassium utilization by skeletal muscle is also impaired by hyperosmolality and impaired insulin function.
This results in intracellular potassium depletion. Osmotic diuresis also leads to loss of potassium resulting in low total body potassium. The potassium level in patients with DKA varies, and a patient's normal plasma potassium level might indicate low total body potassium.
New data suggests that hyperglycemia leads to a severe inflammatory state and an increase in proinflammatory cytokines tumor necrosis factor-alpha and interleukin-beta, -6, and -8 , C-reactive protein, lipid peroxidation, and reactive oxygen species, as well as cardiovascular risk factors, plasminogen activator inhibitor-1 and free fatty acids in the absence of apparent infection or cardiovascular pathology.
After insulin therapy and IV fluid hydration, the pro-inflammatory cytokines return to normal values within 24 hours. The patient with diabetic ketoacidosis may present with a myriad of symptoms and physical exam findings.
Patients may have symptoms of hyperglycemia like polyphagia, polyuria, or polydipsia. As patients become more volume-depleted, they may experience decreased urine output, dry mouth, or decreased sweating indicative of dehydration.
They may complain of many other symptoms, including anorexia, nausea, vomiting, abdominal pain, and weight loss. If there is a superimposed infection that triggered the episode of DKA, the patient may have other infectious symptoms like fever, cough, or other urinary symptoms.
In patients who may be developing cerebral edema, headache, or confusion may be present. Medication history should also be elicited, including what medications the patient is prescribed and how the patient has been using them. Substance use drug and alcohol should be ascertained.
On examination, vital signs typically reveal tachycardia and tachypnea. Due to the possibility of an infectious trigger for DKA, the patient may be febrile or hypothermic.
Blood pressure may also vary, though hypotension is possible and indicative of a more severe disease process. Patients are often ill-appearing. Kussmaul breathing, which is labored, deep, and tachypneic, may occur.
Some providers may appreciate a fruity scent to the patient's breath, indicative of the presence of acetone. Patients may have signs of dehydration, including poor capillary refill, skin turgor, and dry mucous membranes.
Abdominal tenderness is possible. In the most severe cases, altered mental status, general drowsiness, and focal neurologic deficits can be appreciated and are signs of cerebral edema. If found, this needs to be treated immediately. Typical examples are vomiting or diuretic use. The majority of patients with DKA who present to the hospital are found to have leukocytosis.
Serum sodium in the lab report is falsely low in DKA and can be corrected by adding 1. Serum potassium is usually elevated because of a shift of potassium from the intracellular to the extracellular space caused by acidosis and insulin deficiency.
However, total body potassium may be depleted or may quickly become depleted with insulin administration. Magnesium is often low and requires repletion as well.
The serum phosphate level in DKA may be elevated despite total-body phosphate depletion. Other tests like cultures of urine, sputum, and blood, serum lipase, and chest radiograph may need to be performed depending upon the case.
Pneumonia and urinary tract infections are the most common infections precipitating DKA. Measurement of glycated hemoglobin A1C provides information about glucose trends over months.
In acute DKA, the ketone body ratio 3-beta-hydroxybutyrate:acetoacetate rises from normal to as high as In response to insulin therapy, 3-beta-hydroxybutyrate 3-HB levels commonly decrease long before acetoacetate AcAc levels.
The frequently employed nitroprusside test only detects acetoacetate in blood and urine. This test provides only a semiquantitative assessment of ketone levels and is associated with false-positive results. Recently, inexpensive quantitative tests of 3-HB levels have become available for common use, and these tests offer options for monitoring and treating diabetes and other states characterized by the abnormal metabolism of ketone bodies.
The serum level of pancreatic enzymes is elevated in DKA due to disorder in carbohydrate metabolism. Lipid derangement is commonly seen in patients with DKA.
An ECG will help detect ischemic changes or signs of hypokalemia or hyperkalemia. Peaked T waves can signal hyperkalemia, and low T waves with U wave indicating hypokalemia.
Imaging: A chest X-ray may be done to rule out consolidation. MRI, and to some degree, CT imaging of the head can detect cerebral edema, but imaging should not delay treatment if cerebral edema is suspected.
Fluid resuscitation and maintenance, insulin therapy, electrolyte replacement, and supportive care are the mainstays of management in diabetic ketoacidosis. Hydration improves glycemic control independent of insulin. Isotonic fluids have been well established for more than 50 years as preferred fluids.
Colloids vs. crystalloids were compared for critically ill patients, in a meta-analysis, and crystalloid was found to be non-inferior.
There has been a concern that normal saline may contribute to hyperchloremia and hyperchloremic metabolic acidosis; however, this typically occurs when it is used for large volumes.
There have been small studies comparing normal saline with other solutions like Ringer lactate. These studies did not show differences in clinical outcomes. Infusion of ml per Kg body weight in the first 1 hour is typically appropriate. Slower hydration was found to be equally effective.
There has been extensive debate regarding the risk of cerebral edema in patients with aggressive early volume resuscitation. There are studies that have demonstrated rates of increased cerebral edema with aggressive volume, particularly in the pediatric population.
Yet other studies show no difference in outcome and theorize that patients at greatest risk from cerebral edema present at a later stage and are the most severe volume depleted.
The subsequent choice for fluid replacement depends on hemodynamics, the state of hydration, serum electrolyte levels, and urinary output. Intravenous insulin by continuous infusion is the standard of care. Previous treatment protocols have recommended the administration of an initial bolus of 0.
A more recent prospective randomized trial demonstrated that a bolus is not necessary if patients are given hourly insulin infusion at 0. Treatment of adult patients who have uncomplicated, mild diabetic ketoacidosis can be treated with subcutaneous insulin lispro hourly in a non-intensive care setting may be safe and cost-effective as opposed to treatment with intravenous regular insulin in the intensive care setting as shown in many studies.
Then insulin dose was decreased to 0. Patients with DKA should be treated with insulin until resolution. Patients can be transitioned to subcutaneously administered insulin when DKA has resolved, and they are able to eat. Those previously treated with insulin might be recommended on their home dose if they had been well controlled.
Insulin-naive patients should receive a multi-dose insulin regimen beginning at a dose of 0. To prevent the recurrence of ketoacidosis in the transition period, insulin infusion should be continued for 2 hrs after the starting of subcutaneous insulin and check blood sugar and complete metabolic profile again before stopping the insulin drip.
If the patient cannot tolerate oral intake, intravenous insulin, and fluids may be continued. The use of long-acting insulin analogs during the initial management of DKA may facilitate the transition from intravenous to subcutaneous insulin therapy. Patients with DKA are often found to initially have mild to moderate hyperkalemia, despite a total body deficit of potassium.
The initiation of insulin causes an intracellular shift of potassium and lowers the potassium concentration, potentially resulting in severe hypokalemia.
The administration of 20 to 30 mEq of potassium per liter of fluids is sufficient for most patients; however, lower doses are required for patients with acute or chronic renal failure.
Hypokalemia is commonly associated with hypomagnesemia. Repletion of both potassium and magnesium may need to be done, and it may be difficult to improve potassium levels until magnesium levels are repleted.
Bicarbonate replacement does not appear to be beneficial. In one study, the difference in time to resolution of acidosis 8 hours vs. However, it may be used in patients with severe acidemia.
The most recent ADA guidelines do recommend the use of sodium bicarbonate therapy in patients with pH less than 7. The role of phosphate replacement in DKA has been looked at in different studies. In one randomized study with 44 patients, phosphate therapy did not alter the duration of DKA, insulin dosage required to correct the acidosis, abnormal muscle enzyme levels, glucose disappearance, or morbidity and mortality.
Although theoretically appealing, phosphate therapy is not an essential part of the treatment for DKA in most patients, an unusual case of severe hypophosphatemia 1.
There are multiple risks associated with intubation in patients with DKA. Intubation should be avoided if at all possible.
Treating as above with a focus on administering fluids and insulin will almost always lead to an improvement in acidosis and overall clinical presentation. Patients attempt to compensate for severe acidosis by creating a compensatory respiratory alkalosis that manifests via tachypnea and Kussmaul breathing.
If patients are no longer able to generate respiratory alkalosis due to comatose state or severe fatigue, intubation should be considered.
If a patient is intubated and placed on a ventilator, it is essential to attempt to match the patient's minute ventilation such that respiratory alkalosis is created to compensate for the metabolic acidosis of DKA. If not, there will be worsening acidosis, which can ultimately lead to cardiac arrest.
However, care should be taken that auto-PEEP is not occurring due to the rapid respiratory rate. Mental status and neurologic exam should be monitored in all patients with DKA.
In any patient who is severely obtunded or comatose or who has declining mental status despite treatment or focal neurologic deficits, there should be a very low threshold to treat for cerebral edema.
Infection is a very common trigger for DKA in patients who have new-onset diabetes and previously established diabetes. If there is any suspicion of infection, antibiotics should be administered promptly.
As discussed, there can be other events that trigger DKA as well. Treating both DKA and any other underlying etiologies should be done. Diabetic ketoacidosis has a diverse presentation, and this is why several other common pathologies may mimic this diagnosis.
It is imperative for the providers to consider the following differential diagnoses when the diagnosis of DKA is suspected:. Diabetic ketoacidosis still carries a mortality rate of 0.
Patients who present in a comatose state, hypothermia, and oliguria tend to have the worst outcomes. For most patients treated promptly, the outcomes are good, especially if the trigger is not an infection. Elderly patients with concurrent illnesses such as myocardial infarction, pneumonia, or sepsis tend to have long hospital stays and high mortality.
The most important cause of mortality is cerebral edema, usually seen in younger patients. The cerebral edema is primarily due to the intracellular shifts.
Another important cause of morbidity is renal dysfunction. A recent study has noted that among patients with type-2 diabetes mellitus who develop DKA, there is a high risk of stroke within the first six months after the event. Hourly blood sugar monitoring is needed in the acute phase of treatment.
Hypokalemia is common. Severe hypokalemia can cause muscle weakness, cardiac arrhythmias, and cardiac arrest. Cerebral edema is less common in adults than in children.
Risk factors include younger age, new-onset diabetes, longer duration of symptoms, the lower partial pressure of carbon dioxide, severe acidosis, low initial bicarbonate level, low sodium level, high glucose level at presentation, rapid hydration, and retained fluid in the stomach.
Rhabdomyolysis may occur in patients with DKA though it occurs more commonly with HHS. It may result in acute kidney failure. Severe hypophosphatemia in relation to DKA can also cause rhabdomyolysis. Acute respiratory failure could be associated with DKA.
Causes could be pneumonia, ARDS, or pulmonary edema. Two varieties of pulmonary edema in DKA have been recognized, secondary to elevated pulmonary venous pressure, and because of increased pulmonary capillary permeability.
Education on the disease process of diabetes, including short and long term complications, should be given to all patients. Patients should be taught how and when to check their glucose. Dietitians, nurses, and multi-disciplinary home health can be important members of the team in assisting with this education.
Diabetic ketoacidosis is a life-threatening complication of diabetes, and any delay in treatment can lead to death. The disorder can present with varied signs and symptoms and affects many organs; thus, it is best managed by an interprofessional team dedicated to the management of patients with diabetes mellitus.
The majority of patients first present to the emergency department, and it is here that the treatment usually starts. The triage nurse has to be familiar with the signs and symptoms of DKA and immediately admit the patient and notify the emergency department physician.
While the patient is being resuscitated, placed on a monitor, and having blood drawn, the intensivist and an endocrinologist should be consulted. Immediate blood work is necessary to determine the state of ketoacidosis, and imaging may be necessary to rule out pneumonia.
If the mental status is altered, a CT scan may be required, and thus the radiologist must be notified about the patient's hemodynamic status. No patient with DKA should go unmonitored to a radiology suite.
The infectious disease expert and cardiologist should be consulted if there is suspicion of infection or MI as the trigger. The pharmacist and nurses should determine if the patient was compliant with insulin treatment. Following discharge, the social workers should be involved in the care since recurrent DKA admissions are common, especially in inner-city hospitals.
Socioeconomic status, education status, access to insulin, the presence of health care coverage, and the presence of mental illness, etc. play a big role in these patients. An interprofessional team, including social workers, are often needed to address these particular situations.
Meticulous discharge planning, involving social workers for patients with socioeconomic needs, and hospital initiated follow up clinics for discharged patients are some of the factors important to reduce the recurrences of DKA in the same individual.
Finally, patient education is highly recommended, as in many cases, the cause of DKA is failing to comply with treatment.
In developed countries, the morbidity and mortality rates are low chiefly because of a streamlined interprofessional approach to the management of these patients.
However, in developing countries, mortality rates of 0. The major cause of death in most young patients is cerebral edema. Disclosure: Jenna Lizzo declares no relevant financial relationships with ineligible companies. Disclosure: Amandeep Goyal declares no relevant financial relationships with ineligible companies.
Disclosure: Vikas Gupta declares no relevant financial relationships with ineligible companies. This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.
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