Hyperglycemic crisis and metabolic acidosis -
Patients with underlying cardiac and renal disease may require lower initial fluid resuscitation rates and more frequent monitoring of clinical status to avoid fluid overload. Insulin therapy for DKA and HHS is typically administered intravenously, although uncomplicated mild to moderate DKA may be managed with subcutaneous insulin therapy.
Typically, in the absence of hypokalemia, patients receive a bolus of intravenous regular insulin at 0. Doses may be titrated based on clinical response, which will vary based on the degree of insulin resistance.
For example, patients with type 2 diabetes who present in DKA will typically require a higher dose of insulin than those with type 1 diabetes because of higher insulin resistance. If subcutaneous insulin is to be used to treat uncomplicated DKA, patients typically receive an initial dose of 0.
Such approaches may be associated with a lower cost of hospitalization by avoiding intensive care unit placement. Electrolytes, glucose, blood urea nitrogen, osmolality, creatinine, and pH arterial or venous should be drawn every hours to monitor patients' responses to therapy and to allow titration of insulin and fluids.
It is important to note that hyperglycemia typically resolves before ketosis; therefore, dextrose should be added to fluids as glucose declines as described above.
Ketosis should be measured via β-hydroxybutyric acid whenever possible because that is the prevalent ketone body produced in DKA. The nitroprusside reaction, which is still used in many laboratories to detect ketone formation, does not detect β-hyrdoxybutyric acid and therefore may yield false-negative results.
Most patients presenting in DKA exhibit hyperkalemia as a result of insulin deficiency and acidosis despite total body potassium depletion. Treatment with insulin, restoration of normal circulatory volume, and resolution of acidosis allow total body potassium depletion to manifest itself as hypokalemia during treatment of DKA.
Including mEq of potassium in each liter of fluid is usually sufficient to maintain a potassium concentration within normal limits. This will help to avoid cardiac arrhythmia and skeletal muscle dysfunction because insulin initiation can cause an acute decline in serum potassium concentration.
Use of bicarbonate to raise pH is controversial. Patients also frequently exhibit hypophosphatemia at presentation in DKA, but phosphate repletion has not demonstrated a beneficial effect on clinical outcomes in DKA. Patients receiving phosphate therapy should be monitored closely for hypocalcemia, which can result from phosphate administration.
Patients should resume rapid-acting insulin at meals and intermediate- or long-acting insulin when they are able to eat substantial carbohydrate. It is important to continue intravenous insulin for several hours after resumption of subcutaneous insulin to avoid recurrent hyperglycemia and a possible return to ketosis.
The most common complications that occur when treating adults with ketoacidosis are hypokalemia and hypoglycemia. Potassium depletion is the most life-threatening electrolyte abnormality in the treatment of DKA.
As previously described, total body potassium at presentation in DKA is low despite hyperkalemia because of metabolic acidosis. Delayed potassium supplementation can lead to considerable hypokalemia as the serum potassium concentration drops precipitously in the presence of insulin and resolution of ketoacidosis.
In the setting of normal renal function, patients should receive potassium supplementation in their fluids when the potassium level approaches normal values.
Hypoglycemia is also a potential complication of DKA. The threat of hypokalemia and hypoglycemia both also illustrate the importance of frequent reassessment of patients treated for DKA. Care must also be taken in intravenous fluid administration. Patients with underlying medical conditions such as renal insufficiency or congestive heart failure are susceptible to fluid overload.
Patients should be assessed for such disorders before initiation of fluid resuscitation. Cerebral edema is yet another potential complication of DKA and HHS.
It occurs more frequently in pediatric patients than in adults. Signs of cerebral edema include mental status changes, vomiting, headache, lethargy, elevated diastolic blood pressure, decorticate or decerebrate posturing, cranial nerve palsies, or Cheyne-Stokes respiration.
Treatment options include use of mannitol or hypertonic saline to decrease cerebral edema, although there have been no large controlled trials clearly demonstrating benefit.
Hyperchloremic nonanion gap metabolic acidosis is a very frequent finding after resolution of DKA. It may occur because of the loss of ketoanions during DKA and is exacerbated by supplementation with supraphysiological levels of chloride in normal saline.
The extent of hyperchloremic metabolic acidosis may be lessened by limiting the amount of chloride administered during treatment, but it is important to note that this finding is self-limiting and not associated with adverse clinical outcomes.
Prevention of DKA and HHS is targeted toward treatable precipitating factors. Because infection is a frequent cause of DKA and HHS, patients should be instructed to monitor glucose closely should they develop early symptoms of infection such as cough, fever, nausea, or wounds. Patients should also be educated regarding foot care, especially in the setting of peripheral sensory neuropathy, which may predispose to infection.
Should symptoms develop, patients should monitor glucose closely and take extra precautions such as administering correction doses of insulin and maintaining adequate hydration in the setting of hyperglycemia-induced diuresis.
Sickday education should also include instructions to avoid prolonged fasting and to never discontinue insulin therapy. If patients do not administer their own insulin or medications, their caregivers should receive similar instructions as to proper treatment of hyperglycemia and infection.
In addition to infection, DKA and HHS are also frequently associated with incorrect use of or omission of insulin. Careful education regarding the proper use and dosing of insulin at routine visits may help reduce the recurrence of DKA.
Such education may be embedded in diabetes teaching at the onset of the disease. Patients who experience recurrent DKA may also omit insulin or administer incorrect amounts of insulin because of socioeconomic factors, lack of knowledge regarding insulin dosing, or behavioral reasons.
DKA and HHS are both life-threatening disorders that carry significant risk of morbidity and mortality. Physicians caring for diabetic patients in the inpatient setting or working in emergent care will likely treat significant numbers of patients with DKA and HHS.
Fortunately, most patients recover uneventfully. Careful attention to proper treatment and early identification of the underlying causes of hyperglycemia will allow for the most rapid patient recovery and lowest risk of morbidity and mortality. Detailed patient education and instruction regarding outpatient care may help prevent initial occurrences or the recurrence of DKA or HHS.
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Adults should have an ECG to screen for acute myocardial infarction and to help determine the significance of abnormalities in serum potassium. Common causes include diuretic use, diarrhea, heart failure Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.
As acidosis is corrected, serum potassium drops. An initial potassium level 4. read more which may be present in patients with alcoholic ketoacidosis Alcoholic Ketoacidosis Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia.
read more and in those with coexisting hypertriglyceridemia. Buse JB, Wexler DJ, Tsapas A, et al : Update to: Management of Hyperglycemia in Type 2 Diabetes, A Consensus Report by the American Diabetes Association ADA and the European Association for the Study of Diabetes EASD.
Diabetes Care 43 2 —, doi: Garber AJ, Handelsman Y, Grunberger G, et al : Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm executive summary.
Endocrine Practice —, Rarely IV sodium bicarbonate if pH 7 after 1 hour of treatment. The most urgent goals for treating diabetic ketoacidosis are rapid intravascular volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia 1, 2 Treatment references Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis.
Identification of precipitating factors is also important. Treatment should occur in intensive care settings because clinical and laboratory assessments are initially needed every hour or every other hour with appropriate adjustments in treatment.
Intravascular volume should be restored rapidly to raise blood pressure and ensure glomerular perfusion; once intravascular volume is restored, remaining total body water deficits are corrected more slowly, typically over about 24 hours. Initial volume repletion in adults is typically achieved with rapid IV infusion of 1 to 1.
Additional boluses or a faster rate of infusion may be needed to raise the blood pressure. Slower rates of infusion may be needed in patients with heart failure or in those at risk for volume overload.
If the serum sodium level is normal or high, the normal saline is replaced by 0. Pediatric maintenance fluids Maintenance requirements Dehydration is significant depletion of body water and, to varying degrees, electrolytes.
Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree read more for ongoing losses must also be provided. Initial fluid therapy should be 0. Hyperglycemia is corrected by giving regular insulin 0. Insulin adsorption onto IV tubing can lead to inconsistent effects, which can be minimized by preflushing the IV tubing with insulin solution.
Children should be given a continuous IV insulin infusion of 0. Ketones should begin to clear within hours if insulin is given in sufficient doses. Serum pH and bicarbonate levels should also quickly improve, but restoration of a normal serum bicarbonate level may take 24 hours.
Bicarbonate should not be given routinely because it can lead to development of acute cerebral edema primarily in children. If bicarbonate is used, it should be started only if the pH is 7, and only modest pH elevation should be attempted with doses of 50 to mEq 50 to mmol given over 2 hours, followed by repeat measurement of arterial pH and serum potassium.
A longer duration of treatment with insulin and dextrose may be required in DKA associated with SGLT-2 inhibitor use. When the patient is stable and able to eat, a typical basal-bolus insulin regimen Insulin regimens for type 1 diabetes General treatment of diabetes mellitus for all patients involves lifestyle changes, including diet and exercise.
Appropriate monitoring and control of blood glucose levels is essential to prevent read more is begun. IV insulin should be continued for 2 hours after the initial dose of basal subcutaneous insulin is given. Children should continue to receive 0. If serum potassium is 3. Initially normal or elevated serum potassium measurements may reflect shifts from intracellular stores in response to acidemia and belie the true potassium deficits that almost all patients with DKA have.
Insulin replacement rapidly shifts potassium into cells, so levels should be checked hourly or every other hour in the initial stages of treatment. Causes include alcohol use disorder, burns, starvation, and diuretic use.
Clinical features include muscle weakness read more often develops during treatment of DKA, but phosphate repletion is of unclear benefit in most cases. If potassium phosphate is given, the serum calcium level usually decreases and should be monitored.
Treatment of suspected cerebral edema is hyperventilation, corticosteroids, and mannitol , but these measures are often ineffective after the onset of respiratory arrest.
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Diabetic meabolic DKA is an acute metabolic Importance of gut health ajd diabetes characterized by hyperglycemia, andd, and metabolic acidosis. Hyperglycemia causes an mtabolic diuresis with significant fluid and electrolyte Stay cool and energized with hydrating fluids. DKA occurs mostly in type Supercharge thermogenic process diabetes mellitus. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. See also Diabetes Mellitus Diabetes Mellitus DM Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia. Official websites use. Importance of gut health A. gov website belongs to Huperglycemic official government organization in the United States. gov website. Share sensitive information only on official, secure websites. Metabolic acidosis develops when too much acid is produced in the body.Abbas E. KitabchiGuillermo E. UmpierrezMary Beth ZndRobert A. Kreisberg; Hyperglycemic Crises in Crksis Patients With Diabetes : A consensus statement from the Netabolic Diabetes Association. Diabetes Care 1 December ; 29 12 : managing blood sugar levels effectively Diabetic ketoacidosis DKA and hyperosmolar hyperglycemic state HHS are acidodis two most serious acute metabolic complications of diabetes.
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Crlsis two Fast weight loss pills common precipitating factors in the development of DKA or HHS are Gluten-free dairy-free or inappropriate insulin therapy or ahd 148 — Other precipitating factors include mteabolic, myocardial infarction, cerebrovascular accident, and drugs.
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Beforethe use of continuous subcutaneous insulin infusion devices had also been associated with an increased frequency of DKA 22but with improvement in technology and better education of patients, the incidence of DKA appears to have reduced in pump users. However, additional prospective studies are needed to document reduction of DKA incidence with the use of continuous subcutaneous insulin infusion devices During the past decade, an increasing number of DKA cases without precipitating cause have been reported in children, adolescents, and adult subjects with type 2 diabetes.
Observational and prospective studies indicate that over half of newly diagnosed adult African-American and Hispanic subjects with unprovoked DKA have type 2 diabetes 24 — In such patients, clinical and metabolic features of type 2 diabetes include a high rate of obesity, a strong family history of diabetes, a measurable pancreatic insulin reserve, low prevalence of autoimmune markers of β-cell destruction, and the ability to discontinue insulin therapy during follow-up 28 This variant of type 2 diabetes has been referred to in the literature as idiopathic type 1 diabetes, atypical diabetes, Flatbush diabetes, type 1.
At presentation, they have markedly impaired insulin secretion and insulin action 252629but aggressive management with insulin significantly improves β-cell function, allowing discontinuation of insulin therapy within a few months of follow-up 25 — Furthermore, a novel genetic mechanism related to the high prevalence of glucosephosphate dehydrogenase deficiency has been linked with ketosis-prone diabetes The process of HHS usually evolves over several days to weeks, whereas the evolution of the acute DKA episode in type 1 diabetes or even in type 2 diabetes tends to be much shorter.
The classic clinical picture of patients with DKA includes a history of polyuria, polydipsia, weight loss, vomiting, abdominal pain, dehydration, weakness, mental status change, and coma. Physical findings may include poor skin turgor, Kussmaul respirations, tachycardia, hypotension, alteration in mental status, shock, and ultimately coma.
Mental status can vary from full alertness to profound lethargy or coma, with the latter more frequent in HHS. Although infection is a common precipitating factor for both DKA and HHS, patients can be normothermic or even hypothermic primarily because of peripheral vasodilation Severe hypothermia, if present, is a poor prognostic sign.
The abdominal pain usually resolves with correction of hyperglycemia and metabolic acidosis. The most common clinical presentation in patients with HHS is altered sensorium 4811 Physical examination reveals signs of dehydration with loss of skin turgor, weakness, tachycardia, and hypotension.
Fever due to underlying infection is common, and signs of acidosis Kussmaul breathing, acetone breath are usually absent. In some patients, focal neurologic signs hemiparesis, hemianopsia and seizures partial motor seizures more common than generalized may be the dominant clinical features 1468.
The initial laboratory evaluation of patients with suspected DKA or HHS should include determination of plasma glucose, blood urea nitrogen, creatinine, serum ketones, electrolytes with calculated anion gaposmolality, urinalysis, urine ketones by dipstick, as well as initial arterial blood gases and complete blood count with differential.
An electrocardiogram, chest X-ray, and urine, sputum, or blood cultures should also be obtained, if clinically indicated. HbA 1c may be useful in determining whether this acute episode is the culmination of an evolutionary process in previously undiagnosed or poorly controlled diabetes or a truly acute episode in an otherwise well-controlled patient.
The diagnostic criteria for DKA and HHS are shown in Table 1. DKA consists of the biochemical triad of hyperglycemia, ketonemia, and metabolic acidosis.
Accumulation of ketoacids results in an increased anion gap metabolic acidosis. The severity of DKA is classified as mild, moderate, or severe based on the severity of metabolic acidosis blood pH, bicarbonate, ketones and the presence of altered mental status 1.
Significant overlap between DKA and HHS has been reported in more than one-third of patients 12 The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration 2 The admission serum sodium is usually low because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia.
An increase in serum sodium concentration in the presence of hyperglycemia indicates a rather profound degree of water loss. Unless the plasma is cleared of chylomicrons, pseudonormoglycemia and pseudohyponatremia may occur in DKA 37 Serum potassium concentration may be elevated because of an extracellular shift of potassium caused by insulin deficiency, hypertonicity, and acidemia 310 Patients with low normal or low serum potassium concentration on admission have severe total-body potassium deficiency and require very careful cardiac monitoring and more vigorous potassium replacement, because treatment lowers potassium further and can provoke cardiac dysrhythmia.
The classic work of Atchley et al. Studies on serum osmolality and mental alteration have established a positive linear relationship between osmolality and mental obtundation Amylase levels are elevated in the majority of patients with DKA, but this may be due to nonpancreatic sources, such as the parotid gland A serum lipase determination may be beneficial in the differential diagnosis of pancreatitis; however, lipase could also be elevated in DKA.
Finally, abnormal acetoacetate levels may falsely elevate serum creatinine if the clinical laboratory uses a colorometric method for the creatinine assay Not all patients with ketoacidosis have DKA. DKA must also be distinguished from other causes of high anion gap metabolic acidosis, including lactic acidosis; ingestion of drugs such as salicylate, methanol, ethylene glycol, and paraldehyde; and chronic renal failure.
A clinical history of previous drug abuse or metformin use should be sought. Measurement of blood lactate, serum salicylate, and blood methanol level can be helpful in these situations.
Ethylene glycol antifreeze is suggested by the presence of calcium oxalate and hippurate crystals in the urine. Paraldehyde ingestion is indicated by its characteristic strong odor on the breath. Because these intoxicants are low—molecular-weight organic compounds, they can produce an osmolar gap in addition to the anion gap acidosis 10 A recent report 44 suggested a relationship between low carbohydrate dietary intake and metabolic acidosis.
Finally, four case reports have shown that patients with undiagnosed acromegaly may present with DKA as the primary manifestation of their disease 45 — Successful treatment of DKA and HHS requires correction of dehydration, hyperglycemia, and electrolyte imbalances; identification of comorbid precipitating events; and above all, frequent patient monitoring.
Protocols for the management of patients with DKA and HHS are summarized in Figs. Initial fluid therapy is directed toward expansion of the intravascular and extra vascular volume and restoration of renal perfusion.
In the absence of cardiac compromise, isotonic saline 0. The subsequent choice for fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output. In general, 0.
Successful progress with fluid replacement is judged by hemodynamic monitoring improvement in blood pressuremeasurement of fluid input and output, laboratory values, and clinical examination. Fluid replacement should correct estimated deficits within the first 24 h. In patients with renal or cardiac compromise, monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid overload 134101216 Adequate rehydration with subsequent correction of the hyperosmolar state has been shown to result in a more robust response to low-dose insulin therapy If plasma glucose does not decrease by 50—75 mg from the initial value in the first hour, the insulin infusion may be doubled every hour until a steady glucose decline is achieved.
Thereafter, the rate of insulin administration or the concentration of dextrose may need to be adjusted to maintain the above-glucose values until acidosis in DKA or mental obtundation and hyperosmolality in HHS are resolved. Prospective and randomized studies have reported on the efficacy and cost effectiveness of subcutaneous rapid-acting insulin analogs in the management of patients with uncomplicated DKA.
Patients treated with subcutaneous rapid-acting insulin received an initial injection of 0. There were no differences in length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or number of hypoglycemic events among treatment groups.
In addition, the use of insulin analogs allowed treatment of DKA in general wards or in the emergency department, avoiding admission to an intensive care unit. Ketonemia typically takes longer to clear than hyperglycemia. Direct measurement of β-OHB in the blood is the preferred method for monitoring DKA and has become more convenient with the recent development of bedside meters capable of measuring whole-blood β-OHB The nitroprusside method, which is used in clinical chemistry laboratories, measures acetoacetic acid and acetone; however, β-OHB, the strongest and most prevalent acid in DKA, is not measured by the nitroprusside method.
: Hyperglycemic crisis and metabolic acidosis| Updates in the Management of Hyperglycemic Crisis | Google Scholar Ennis ED, Stahl EJVB, Kreisberg RA. Risperidone-associated transient diabetic ketoacidosis and diabetes mellitus type 1 in a patient treated with valproate and lithium. Adrogue HJ, Lederer ED, Suki WN, Eknoyan G. Winter RJ, Harris CJ, Phillips LS, Green OC. DKA occurs mostly in type 1 diabetes mellitus. van der Hoeven. |
| Buying options | org ADA Professional Books Clinical Compendia Clinical Compendia Home News Latest News DiabetesPro SmartBrief. At this timepoint, we analyzed his acid-base disturbance again see Table 1 for used laboratory findings. Lastly, the simplified Fencl-Stewart approach integrated the standard base excess and the Stewart analysis and usesfour variables: the standard base excess SBE , as measured by a bloodgas machine , and calculates the base excess effects of sodium-chloride, albumin and unmeasured ions[12,22]. Current American Diabetes Association guidelines continue to recommend bicarbonate replacement in persons with a pH lower than 6. At the other extreme, HHS without ketoacidosis typically occurs with lesser degrees of insulin deficiency, as seen in type 2 diabetes. |
| REVIEW article | Clin Case Acidossis Rev Stay cool and energized with hydrating fluids doi: Article PubMed Google Scholar Cahill Scidosis Jr. Maldonado MR, Otiniano ME, Lee R, Rodriguez L, Balasubramanyam A. In general, 0. Division of Endocrinology, Diabetes and Metabolism, University and Hospital Trust of Verona, Verona, Italy. |
| Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State | SpringerLink | Metabolic acidosis is a condition in which there is too much acid in the body fluids. There are several types of metabolic acidosis: Diabetic acidosis also called diabetic ketoacidosis and DKA develops when substances called ketone bodies which are acidic build up during uncontrolled diabetes usually type 1 diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Kidney disease uremia, distal renal tubular acidosis or proximal renal tubular acidosis. Lactic acidosis. Poisoning by aspirin, ethylene glycol found in antifreeze , or methanol. Severe dehydration. It can be caused by: Cancer Carbon monoxide poisoning Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar hypoglycemia Medicines, such as salicylates, metformin, anti-retrovirals MELAS a very rare genetic mitochondrial disorder that affects energy production Prolonged lack of oxygen from shock , heart failure , or severe anemia Seizures. Exams and Tests. Tests may include: Arterial or venous blood gas Basic metabolic panel, a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and functions Blood ketones Lactic acid test Urine ketones Urine pH Other tests may be needed to determine the cause of the acidosis. Outlook Prognosis. The outlook will depend on the underlying disease causing the condition. Possible Complications. Very severe metabolic acidosis can lead to shock or death. When to Contact a Medical Professional. Seek medical help if you have symptoms of any disease that can cause metabolic acidosis. Alternative Names. Insulin production and diabetes. Learn how to cite this page. Related MedlinePlus Health Topics. Kitabchi AE, Umpierrez GE, Murphy MB: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. In International Textbook of Diabetes Mellitus. Wachtel TJ, Silliman RA, Lamberton P: Prognostic factors in the diabetic hyperosmolar state. Wachtel TJ: The diabetic hyperosmolar state. Clin Geriatr Med. Gerich JE, Martin MM, Recant L: Clinical and metabolic characteristics of hyperosmolar nonketotic coma. Kitabchi AE, Fisher JN: Insulin therapy of diabetic ketoacidosis: physiologic versus pharmacologic doses of insulin and their routes of administration. In Handbook of Diabetes Mellitus. Chupin M. Charbonnel B, Chupin F: C-peptide blood levels in ketoacidosis and in hyperosmolar non-ketotic diabetic coma. ACTA Diabetol. 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