Hyperglycemic crisis -
In addition, new-onset type 1 diabetes or discontinuation of or inadequate insulin in established type 1 diabetes commonly leads to the development of DKA.
Elderly individuals with new-onset diabetes particularly residents of chronic care facilities or individuals with known diabetes who become hyperglycemic and are unaware of it or are unable to take fluids when necessary are at risk for HHS 6.
Drugs that affect carbohydrate metabolism, such as corticosteroids, thiazides, and sympathomimetic agents e. Factors that may lead to insulin omission in younger patients include fear of weight gain with improved metabolic control, fear of hypoglycemia, rebellion from authority, and stress of chronic disease 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.
Occasionally, the entire symptomatic presentation may evolve or develop more acutely, and the patient may present in DKA with no prior clues or symptoms. For both DKA and HHS, the classical clinical picture includes a history of polyuria, polydipsia, polyphagia, weight loss, vomiting, abdominal pain only in DKA , dehydration, weakness, clouding of sensoria, and finally coma.
Physical findings may include poor skin turgor, Kussmaul respirations in DKA , tachycardia, hypotension, alteration in mental status, shock, and ultimately coma more frequent in HHS. Endoscopy has related this finding to the presence of hemorrhagic gastritis. 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. Hypothermia, if present, is a poor prognostic sign Caution needs to be taken with patients who complain of abdominal pain on presentation, because the symptoms could be either a result or an indication of a precipitating cause particularly in younger patients of DKA.
Further evaluation is necessary if this complaint does not resolve with resolution of dehydration and metabolic acidosis. Bacterial cultures of urine, blood, and throat, etc.
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. A chest X-ray should also be obtained if indicated. Tables 1 and 2 depict typical laboratory findings in patients with DKA or HHS.
The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration. Serum sodium concentration is usually decreased because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia, and less commonly, serum sodium concentration may be falsely lowered by severe hypertriglyceridemia.
Serum potassium concentration may be elevated because of an extracellular shift of potassium caused by insulin deficiency, hypertonicity, and acidemia. 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.
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. Abdominal pain and elevation of serum amylase and liver enzymes are noted more commonly in DKA than in HHS. 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 which is more typically hyperchloremic acidosis rather than high-anion gap acidosis.
Clinical history of previous drug intoxications 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 14 — 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.
Guidelines for the management of patients with DKA and HHS follow and are summarized in Figs. Table 3 includes a summary of major recommendations and evidence gradings. Initial fluid therapy is directed toward expansion of the intravascular and extravascular volume and restoration of renal perfusion.
In the absence of cardiac compromise, isotonic saline 0. Subsequent choice for fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output.
In general, 0. 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 14 — 20 , Initial fluid therapy is directed toward expansion of the intravascular and extravascular volume and restoration of renal profusion.
The need for vascular volume expansion must be offset by the risk of cerebral edema associated with rapid fluid administration. The 1st hour of fluids should be isotonic saline 0.
Continued fluid therapy is calculated to replace the fluid deficit evenly over 48 h. Therapy should include monitoring mental status to rapidly identify changes that might indicate iatrogenic fluid overload, which can lead to symptomatic cerebral edema 23 — Unless the episode of DKA is mild Table 1 , regular insulin by continuous intravenous infusion is the treatment of choice.
An initial insulin bolus is not recommended in pediatric patients; a continuous insulin infusion of regular insulin at a dose of 0. 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 hyperosmolarity in HHS are resolved.
Ketonemia typically takes longer to clear than hyperglycemia. Direct measurement of β-OHB in the blood is the preferred method for monitoring DKA.
The nitroprusside method only measures acetoacetic acid and acetone. However, β-OHB, the strongest and most prevalent acid in DKA, is not measured by the nitroprusside method. During therapy, β-OHB is converted to acetoacetic acid, which may lead the clinician to believe that ketosis has worsened.
Therefore, assessments of urinary or serum ketone levels by the nitroprusside method should not be used as an indicator of response to therapy.
During therapy for DKA or HHS, blood should be drawn every 2—4 h for determination of serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH for DKA.
Generally, repeat arterial blood gases are unnecessary; venous pH which is usually 0. With mild DKA, regular insulin given either subcutaneously or intramuscularly every hour is as effective as intravenous administration in lowering blood glucose and ketone bodies Thereafter, 0.
Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h. When the patient is able to eat, a multiple-dose schedule should be started that uses a combination of short- or rapid-acting and intermediate- or long-acting insulin as needed to control plasma glucose.
Continue intravenous insulin infusion for 1—2 h after the split-mixed regimen is begun to ensure adequate plasma insulin levels. An abrupt discontinuation of intravenous insulin coupled with a delayed onset of a subcutaneous insulin regimen may lead to worsened control; therefore, some overlap should occur in intravenous insulin therapy and initiation of the subcutaneous insulin regimen.
Patients with known diabetes may be given insulin at the dose they were receiving before the onset of DKA or HHS and further adjusted as needed for control. Finally, some type 2 diabetes patients may be discharged on oral antihyperglycemic agents and dietary therapy. Despite total-body potassium depletion, mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises.
Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5.
Rarely, DKA patients may present with significant hypokalemia. Bicarbonate use in DKA remains controversial Prospective randomized studies have failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH between 6.
In patients with a pH of 6. Insulin, as well as bicarbonate therapy, lowers serum potassium; therefore, potassium supplementation should be maintained in intravenous fluid as described above and carefully monitored.
See Fig. Thereafter, venous pH should be assessed every 2 h until the pH rises to 7. See Kitabchi et al. Phosphate concentration decreases with insulin therapy. Prospective randomized studies have failed to show any beneficial effect of phosphate replacement on the clinical outcome in DKA 32 , and overzealous phosphate therapy can cause severe hypocalcemia with no evidence of tetany 17 , No studies are available on the use of phosphate in the treatment of HHS.
Continuous monitoring using a flowsheet Fig. Commonly, patients recovering from DKA develop hyperchloremia caused by the use of excessive saline for fluid and electrolyte replacement and transient non-anion gap metabolic acidosis as chloride from intravenous fluids replaces ketoanions lost as sodium and potassium salts during osmotic diuresis.
These biochemical abnormalities are transient and are not clinically significant except in cases of acute renal failure or extreme oliguria.
Cerebral edema is a rare but frequently fatal complication of DKA, occurring in 0. The efficacy of low-dose versus conventional therapy of insulin for treatment of diabetic ketoacidosis.
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Correspondence to Guillermo E. Division of Endocrinology, Diabetes and Metabolism, University and Hospital Trust of Verona, Verona, Italy. Diabetes Division, Diabetes Research Unit, University of Texas Health Science Center, San Antonio, TX, USA.
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Cite This Citation McCoy RG , Galindo RJ , Swarna KS, et al. Original Investigation. September 1, Rozalina G. McCoy, MD, MS 1,2 ; Rodolfo J. Galindo, MD 3 ; Kavya Sindhu Swarna, MPH 2 ; et al Holly K.
eTable Hyperglycemi. Crude and Adjusted Rates Hypreglycemic Hyperglycemic Crises Among Patients With Type Sugar replacement choices and Type 2 Diabetes, eTable 5. Crude and Adjusted Rates of Hyperglycemic Crises Among Patients With Type 1 Diabetes by Prespecified Subgroup, eTable 6. Michael Cellulite reduction exercises for belly, Hypeglycemic, is an assistant professor of medicine in Cellulite reduction exercises for belly Criisis of Diabetes, Endocrinology, and Metabolism, Vanderbilt Eskind Diabetes Clinic, Sports supplements guide Vanderbilt Gut health diet Medical Center Hypertlycemic Nashville, Tenn. He is an Hypdrglycemic editor of Clinical Crusis. Editor's crisiz This article Hyperglycdmic Cellulite reduction exercises for belly 9th in a part series reviewing the fundamentals of diabetes care for physicians in training. The patients never stop making water and the flow is incessant …. Life is short, unpleasant and painful, thirst unquenchable, drinking excessive …. If for a while they abstain from drinking, their mouths become parched and their bodies dry; the viscera seem scorched up: the patients are affected by nausea, restlessness and a burning thirst, and within a short time, they expire. Michael Fowler; Hyperglycemic Crisis in Adults: Pathophysiology, Presentation, Pitfalls, and Prevention.
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