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AUTHORS: Irl B Hirsch, MDMichael Emmett, MD SECTION EDITOR: David M Nathan, MD DEPUTY EDITOR: Katya Rubinow, MD
Literature review current through: $literature-review-date$. | This topic last updated: Feb 11, 2026.
INTRODUCTION
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. DKA and HHS often occur together (mixed DKA/HHS). Ketoacidosis with mild hyperglycemia or even normal blood glucose ("normoglycemic" DKA) has become more common with the increased use of sodium-glucose cotransporter 2 [SGLT2] inhibitors.
The treatment of DKA in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of DKA and HHS are discussed separately, as is the treatment of HHS in adults. DKA in children is also reviewed separately.
DISTINGUISHING DKA FROM HHS
●(See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".)
●(See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".)
●(See "Hyperosmolar hyperglycemic state in adults: Treatment".)
●(See "Diabetic ketoacidosis in children: Clinical features and diagnosis".)
●(See "Diabetic ketoacidosis in children: Treatment and complications".)
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) differ clinically according to the presence of ketoacidosis and, usually, the degree of hyperglycemia (table 1) [1-3]. However, approximately one-third of patients have a mixed presentation of DKA and HHS.
The typical total body deficits of water and electrolytes in DKA and HHS are compared in the table (table 2). (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on 'Serum glucose' and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on 'Diagnostic criteria'.)
TREATMENT
Overview and protocols — The treatment of diabetic ketoacidosis (DKA) (algorithm 1 ) includes correcting the fluid and electrolyte abnormalities that are typically present (hyperosmolality, hypovolemia, metabolic acidosis, and potassium depletion) and administering insulin [ 7 ].
●In DKA, metabolic acidosis, ketonemia, and hyperglycemia are typically the major findings. The serum glucose concentration is generally below 800 mg/dL (44.4 mmol/L) and often in the 350 to 500 mg/dL (19.4 to 27.8 mmol/L) range [2-4]. However, serum glucose concentrations may exceed 900 mg/dL ( mmol/L) in patients with DKA, usually in association with coma [3,5], or may be normal or minimally elevated (<200 mg/dL [11.1 mmol/L]) in patients with normoglycemic DKA. Normoglycemic DKA occurs more often in patients with poor oral intake, those treated with insulin prior to arrival in the emergency department, pregnant women, those who use sodium-glucose cotransporter 2 [SGLT2] inhibitors, and insulin pump-treated patients in whom insulin delivery is interrupted due to catheter or pump failure.
●In HHS, ketoacid accumulation is mild or absent, the serum glucose concentration frequently exceeds 1000 mg/dL (56 mmol/L), the plasma osmolality may reach 380 mOsmol/kg, and neurologic abnormalities are frequently present (including coma in 25 to 50 percent of cases) [2,4,6].
●Determine the site of care – For the vast majority of patients, treatment of DKA should occur in the emergency room or inpatient setting where volume and electrolyte repletion and insulin therapy can be administered safely. Outpatient
Managing DKA requires frequent clinical and laboratory monitoring and the identification and treatment of any precipitating events, including infection [ 10 ]. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, which can precipitate DKA, should be discontinued. Permanent discontinuation of the SGLT2 inhibitor should be strongly considered. (See 'Monitoring' below and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on 'Precipitating factors'.)
Our approach outlined below is based upon clinical experience and is largely in agreement with consensus guidelines from the American Diabetes Association (ADA), Joint British Diabetes Societies for Inpatient Care (JBDS), American Association of Clinical Endocrinology (AACE), and Diabetes Technology Society (DTS) for the management of hyperglycemic crises (algorithm 1) [4,11,12].
Fluid replacement — In patients with DKA, we recommend IV electrolyte and fluid replacement to correct both hypovolemia and hyperosmolality.
Initial choice of fluid
with uncomplicated mild to moderate DKA. (See 'Insulin' below.)
●IV isotonic fluid – Isotonic saline (0.9 percent sodium chloride [NaCl]) or isotonic buffered crystalloid (eg, Lactated Ringer) should be used for volume repletion. Buffered crystalloid may reduce time to DKA resolution and reduces the degree of hyperchloremic, non-anion gap metabolic acidosis that often results from high volume isotone saline administration.
No trials have directly compared saline with buffered crystalloid specifically in patients with DKA. In a subgroup analysis of two cluster-randomized trials evaluating choice of isotonic fluid in an emergency or critical care setting, adults with DKA who received buffered crystalloids (n = 94) had a shorter time to DKA resolution compared with those who received saline (n = 78; median 13 versus 16.9 hours, respectively) [ 13 ]. A subsequent cohort study and meta- analysis both reached similar conclusions [14,15].
●Adding dextrose to IV fluids – For patients who present with an initial serum glucose <250 mg/dL [13.9 mmol/L]), dextrose is added to IV fluids at the initiation of therapy. Such patients require both insulin and glucose to treat the ketoacidosis and prevent hypoglycemia, respectively.
Initial rate of fluid administration — The optimal rate of initial isotonic saline infusion depends on the volume status of the patient:
The goal is to correct estimated deficits within the first 24 to 48 hours. Osmolality should not be reduced too rapidly, because this may precipitate cerebral edema. Adequacy of fluid replacement is judged by frequent hemodynamic and laboratory monitoring. (See 'Monitoring' below and 'Cerebral edema' below.)
Subsequent fluid management
●In patients with hypovolemic shock, isotonic fluid should initially be infused as quickly as possible. (See "Treatment of severe hypovolemia or hypovolemic shock in adults".)
●In hypovolemic patients without shock or heart or kidney failure, isotonic fluid is infused at a rate of 15 to 20 mL/kg lean body weight per hour (approximately 1000 mL/hour in an average-sized person) for the first few hours, with a maximum of <50 mL/kg in the first four hours (algorithm 1) [ 1 ].
●In patients with mild hypovolemia or euvolemia, isotonic fluid is infused at a lower rate, guided by clinical assessment.
●Switching to hypotonic fluid – After the second or third hour of fluid administration, optimal fluid replacement depends upon the volume and hydration status, serum electrolyte levels, and urine output. The most appropriate IV fluid composition is determined by the sodium concentration "corrected" for the degree of hyperglycemia. The "corrected" sodium concentration can be approximated by adding 2 mEq/L to the plasma sodium concentration for each 100 mg/dL (5.5 mmol/L) increase above 100 mg/dL (5. mmol/L) (calculator 1).
If the "corrected" serum sodium concentration is [ 1 ]:
- <135 mEq/L, isotonic fluid infusion should be continued at a rate of approximately 250 to 500 mL/hour
- ≥135 mEq/L, isotonic fluid infusion is generally switched to one-half isotonic saline at a rate of 250 to 500 mL/hour to provide electrolyte-free water
●Adding dextrose to IV fluids – For patients who present with hyperglycemic DKA, we add dextrose (5 to 10 percent) to the saline solution when the serum glucose declines to <250 mg/dL (13.9 mmol/L) (algorithm 1).
Careful monitoring of serum potassium is critical in all patients with DKA. Insulin administration rapidly shifts potassium into cells, which can result in a dramatic fall in the serum potassium concentration even with potassium replacement [18,19]. However, potassium replacement must be performed carefully, particularly in patients with impaired kidney function or urine output is less than 50 mL/hour. (See 'Monitoring' below and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis", section on 'Potassium depletion'.)
Osmotic effect of potassium salts — Potassium salts added to IV fluids have the same osmotic effect as sodium salts, and this should be considered when determining the potential impact of IV fluid infusion on osmolality. As an example, 40 mEq of KCl added to 1 L of fluid generates 80 mOsmol/L of electrolyte osmolarity. The addition of 40 mEq of potassium to 1 L of one-half isotonic saline creates a solution with an osmolarity of 234 mOsmol/L (77 mEq NaCl and 40 mEq KCl), which is osmotically equal to three-quarters isotonic saline. (The osmolarity of isotonic saline is 308 mOsmol/L.) If 40 mEq of KCl is added to isotonic saline, the final osmolarity will be approximately 388 mOsmol/L. However, KCl will not have the same extracellular fluid (ECF) expansion effect as NaCl, because most of
peripheral veins. Such high infusion rates also require cardiac rhythm monitoring.
●Initial serum potassium 3.5 to 5.0 mEq/L (normal):
- Add IV potassium chloride (10 to 20 mEq) to each liter of IV fluid.
- Start IV insulin immediately.
- Adjust potassium replacement to maintain the serum potassium concentration in the range of 4 to 5 mEq/L.
●Initial serum potassium >5.0 mEq/L (high):
- Do not start potassium replacement initially.
- Begin IV insulin immediately to treat ketoacidosis and lower serum potassium by shifting it intracellularly.
- Once serum potassium level is ≤5.0 mEq/L, add IV potassium chloride (10 to 20 mEq) to each liter of IV fluid.
the potassium will shift into cells very rapidly. (See "Maintenance and replacement fluid therapy in adults", section on 'Choice of replacement fluid'.)
Insulin
Initiating insulin treatment
Moderate to severe DKA
Intravenous insulin — In moderate to severe DKA, treatment can be initiated with a fixed-rate continuous infusion of regular insulin of 0.1 units/kg per hour (equivalent to 7 units/hour in a 70-kg patient) (algorithm 1) [22,24-27]. Alternatively, a variable
●Timing of insulin initiation:
- Serum potassium ≥3.5 mEq/L (normal or high) – Begin IV insulin immediately in all patients with DKA who have a serum potassium ≥3.5 mEq/L. Early insulin administration is essential to reverse ketoacidosis and prevent life-threatening complications of DKA.
- Serum potassium <3.5 mEq/L (low) – Delay insulin therapy if the initial serum potassium level is <3.5 mEq/L. Insulin drives potassium into cells, which can worsen hypokalemia and precipitate cardiac arrhythmias and respiratory muscle weakness [1,18,19]. (See 'Fluid replacement' above and 'Potassium replacement' above.)
- Patients with an initial low serum potassium <3.5 mEq/L should receive IV fluids and potassium replacement prior to treatment with insulin.
- Insulin therapy should be withheld until the serum potassium is corrected to ≥3.5 mEq/L to avoid complications of hypokalemia.
●Effects on glucose and ketoacidemia – Insulin therapy lowers the serum glucose concentration (primarily by decreasing hepatic glucose production and also by enhancing peripheral utilization [ 21 ]), diminishes ketone production (by reducing both lipolysis and glucagon secretion), and may augment ketone utilization. Inhibition of lipolysis and ketogenesis requires a much lower level of insulin than that required to reduce the serum glucose concentration. Therefore, if the administered dose of insulin is reducing the glucose concentration, it should be sufficient to stop ketone generation [21-23]. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis", section on 'Pathogenesis'.)
Insulin titration and dextrose administration — When the serum glucose is < mg/dL (13.9 mmol/L), add 5 to 10 percent dextrose to the IV fluid, and decrease the insulin infusion rate to 0.05 units/kg per hour (or according to the variable rate protocol) [7,9,24]. If possible, do not allow the serum glucose to fall rapidly to below 200 mg/dL (11.1 mmol/L), because this may promote the development of cerebral edema. (See 'Cerebral edema' below and "Diabetic ketoacidosis in children: Cerebral injury (cerebral edema)".)
Serum glucose should be maintained between 150 and 200 mg/dL (8.3 and 11. mmol/L) until resolution of DKA. (See 'Resolution criteria' below.)
Uncomplicated mild to moderate DKA
Subcutaneous insulin — Patients with uncomplicated, mild to moderate DKA (table 1 ) can be safely treated with subcutaneous, rapid-acting insulin analogs on a general medical floor or in the emergency department, provided adequate staffing is available to carefully monitor the patient and check capillary blood glucose with a reliable glucose meter, typically every hour. We do not recommend the use of continuous glucose monitoring (CGM) in this setting due to a lack of supporting evidence.
In patients with uncomplicated DKA, IM, subcutaneous, and IV insulin therapy show similar efficacy and safety [30-34]. Subcutaneous administration is less painful than IM, and trial data support the safety of rapid-acting insulin analogs (eg, insulin lispro, aspart) given every one or two hours (algorithm 1) [30,31]. In patients with mild DKA, intermediate- or long-acting insulin can be administered at the initiation of treatment, along with rapid-acting insulin.
from improved kidney perfusion, and a reduction in stress hormone levels [26,29].
●Insulin bolus – An initial bolus of rapid-acting insulin 0.1 units/kg body weight should be administered.
●Initial insulin regimen – Following the initial bolus, either of the following rapid-acting insulin regimens may be used:
- 0.1 units/kg given every hour
or
- 0.2 units/kg given every two hours
Insulin titration and dextrose administration — When the serum glucose is < mg/dL (13.9 mmol/L), do both of the following:
Normoglycemic DKA (glucose <200 mg/dL [11.1 mmol/L]) — For patients who present with normoglycemic DKA, initial treatment is similar to that for patients with mild to moderate DKA. However, our approach differs as follows:
If normoglycemic DKA is associated with SGLT2 inhibitor use, the SGLT2 inhibitor should be stopped immediately. For people who develop DKA during SGLT inhibitor treatment, restarting the agent after DKA resolution is not recommended [ 4 ].
Method of glucose measurement — Serum glucose measurements should be done with hospital-approved bedside devices or in the chemistry laboratory and not with CGM devices. CGM devices measure interstitial rather than circulating glucose concentrations. As a result, if glucose is rapidly changing, changes in CGM-derived values may have a 10- to 15-minute delay relative to venous glucose levels. Further, CGM may be less accurate in the setting of severe hyper- or hypoglycemia, volume depletion, large volume shifts, and/or acidosis. (See "Glucose monitoring in the ambulatory management of nonpregnant adults with diabetes mellitus", section on 'CGM systems'.)
Bicarbonate and metabolic acidosis
Indications for bicarbonate (rarely administered) — Although the indications for sodium bicarbonate therapy are controversial [ 35 ], selected patients may benefit from cautious alkali therapy. They include:
●Reduce the insulin dose to 0.05 units/kg every hour or 0.1 units/kg every two hours.
●Add 5 to 10 percent dextrose to the IV fluid. For patients who initially present with serum glucose <250 mg/dL, dextrose should be added immediately to IV fluids and initiated concurrently with insulin therapy.
●Dextrose (5 to 10 percent) should be added immediately to IV fluids and initiated concurrently with insulin therapy.
●We do not administer a rapid-acting insulin bolus.
●The initial insulin dose is 0.05 units/kg every hour or 0.1 units/kg every two hours.
Phosphate repletion (rarely needed) — We do not recommend the routine use of phosphate replacement in the treatment of DKA.
However, if severe hypophosphatemia occurs (serum phosphate concentration < mg/dL or 0.32 mmol/L), phosphate replacement should be administered, especially if cardiac dysfunction, hemolytic anemia, and/or respiratory depression develop [45-49]. When needed, potassium or sodium phosphate 20 to 30 mEq can be added to 1 L of IV fluid.
Although whole-body phosphate depletion is common in uncontrolled diabetes mellitus, the serum phosphate concentration may initially be normal or elevated due to movement of phosphate out of the cells [46,50]. Like potassium, phosphate depletion and hypophosphatemia may be rapidly unmasked following the institution of insulin therapy and IV volume expansion. This frequently leads to asymptomatic hypophosphatemia, which gradually resolves. (See "Hypophosphatemia: Clinical manifestations of phosphate depletion".)
Prospective, randomized trials of patients with DKA have failed to show a beneficial effect of phosphate replacement on the duration of ketoacidosis, dose of insulin required, or the rate of morbidity or mortality [51-53]. In addition, phosphate replacement may have adverse effects, such as hypocalcemia and hypomagnesemia [51,54-56].
MONITORING
Monitoring schedule — A flow sheet of laboratory values and clinical parameters allows better visualization and evaluation of the clinical picture throughout
ketosis [ 43 ]. Animal studies indicate that bicarbonate infusion can accelerate ketogenesis. This may be due to a "braking effect" of acidemia on organic acid generation that is attenuated by any intervention that increases systemic pH [ 39 ].
●Alkali administration can lead to post-treatment metabolic alkalosis. Insulin accelerates the metabolism of ketoacid anions and consequently generates bicarbonate; thus, insulin alone is usually sufficient to correct the metabolic acidosis. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis", section on 'Anion gap metabolic acidosis'.)
treatment of diabetic ketoacidosis (DKA) (form 1).
●Hyperglycemia and metabolic acidosis – The serum glucose should initially be measured every hour until stable, while serum electrolytes, blood urea nitrogen (BUN), phosphorus, creatinine, and venous pH should be measured every two to four hours, depending upon disease severity and the clinical response [1,7]. Serum glucose measurement should be done with hospital-approved bedside devices or in the chemistry laboratory and not with continuous glucose monitoring (CGM) devices, which may not reflect rapidly changing levels and may be less accurate in the setting of volume depletion. (See 'Method of glucose measurement' above.)
Monitoring with arterial blood gases is unnecessary during the treatment of DKA; venous pH, which is approximately 0.03 units lower than arterial pH [ 57 ], is adequate to assess the response to therapy and avoids the pain and potential complications associated with repeated arterial punctures. If blood chemistry results are promptly available, an alternative to monitoring venous pH is to monitor the serum bicarbonate concentration (to assess correction of the metabolic acidosis).
●Ketonemia
- Blood or serum beta-hydroxybutyrate (preferred when available) – Blood or serum beta-hydroxybutyrate should be measured every two hours. Where available, bedside ketone meters that measure capillary blood beta- hydroxybutyrate are an alternative to measuring serum beta-hydroxybutyrate [4,58]. These devices are increasingly available, reliable, and convenient.
- Serum anion gap – When bedside meters and serum beta-hydroxybutyrate measurement are not available, monitoring venous pH and/or the venous bicarbonate with a calculated serum anion gap is sufficient. Accumulation of ketoacid anions (the sum of beta-hydroxybutyrate and acetoacetate) increases the anion gap above its baseline, and the increment reflects the sum of their concentrations in serum. The anion gap is calculated by subtracting the major measured anions (chloride and bicarbonate) from the major measured cation (sodium). The sodium concentration used for this calculation is the concentration reported by the laboratory, not the "corrected" sodium concentration.
Timing of initial dose — The IV insulin infusion should be continued for one to two hours after initiating subcutaneous rapid-acting insulin. The first dose of basal
intravenous (IV) insulin requirements are significantly higher than their usual insulin requirements, it is reasonable to increase the basal rate temporarily. For those using partially automated insulin delivery (hybrid closed-loop) systems, it is also reasonable to stay in "manual mode" for the first 24 to 48 hours while insulin requirements return to baseline. If automated insulin delivery is immediately resumed, blood glucose levels likely will be higher for the first few days.
●New-onset diabetes
- Total daily dose – In patients with new-onset type 1 diabetes who presented with DKA, an initial total daily dose (TDD) of 0.5 to 0.6 units/kg of insulin per day is reasonable, until an optimal dose is established. In patients at increased risk of hypoglycemia, an initial TDD of 0.3 units/kg may be used. (See "Management of blood glucose in adults with type 1 diabetes mellitus" and "General principles of insulin therapy in diabetes mellitus".)
- Basal insulin – Approximately 40 to 60 percent of the TDD should be given as basal insulin, either as once- or twice-daily U-100 glargine or detemir (to be discontinued in the United States in 2024), or as twice-daily intermediate-acting insulin (neutral protamine Hagedorn [NPH]). The long-acting insulin can be given either at bedtime or in the morning; the NPH is usually given as approximately two-thirds of the dose in the morning and one-third at bedtime. In this setting, we do not use degludec or ultra long-acting U-300 insulin glargine, as these require at least three to four days to reach steady state due to their long half-life [ 61 ].
- Prandial insulin – The remainder of the TDD is given as short-acting or rapid- acting insulin, divided before meals. If NPH is the basal insulin used, a mid-day (pre-lunch) rapid-acting insulin may not be necessary. Frequent glucose monitoring or preferably continuous glucose monitoring (CGM) and comprehensive diabetes education are vital after initiating a new insulin regimen in treatment-naïve patients. (See "General principles of insulin therapy in diabetes mellitus" and "Management of blood glucose in adults with type 1 diabetes mellitus", section on 'Designing an MDI insulin regimen' and "Insulin therapy in type 2 diabetes mellitus".)
insulin also should be administered before IV insulin is discontinued. If short- or long-acting insulin is initiated without rapid-acting insulin, the IV insulin infusion should be continued for two to four hours after subcutaneous insulin administration. Abrupt discontinuation of IV insulin acutely reduces insulin levels and may result in recurrence of hyperglycemia and/or ketoacidosis.
Basal insulin (eg, NPH, U-100 glargine, or detemir) can be administered either at the same time as the first injection of rapid-acting insulin (eg, in the morning before breakfast) or at bedtime the previous night.
COMPLICATIONS
Hypoglycemia and hypokalemia are the most common complications of diabetic ketoacidosis (DKA) treatment. These complications have become much less common since low-dose intravenous (IV) insulin treatment and careful monitoring of serum potassium have been implemented [ 62 ]. Hyperglycemia may recur from interruption or discontinuation of IV insulin without adequate overlap coverage with subcutaneous insulin.
Cerebral edema — Cerebral edema in uncontrolled diabetes mellitus is primarily a disease of children, and almost all affected patients are younger than 20 years old [ 63 ]. Symptoms typically emerge within 12 to 24 hours of the initiation of treatment for DKA but may exist prior to the onset of therapy. Issues related to cerebral edema in DKA, including pathogenesis, are discussed in detail separately but will be briefly reviewed here. (See "Diabetic ketoacidosis in children: Cerebral injury (cerebral edema)".)
●Clinical features — DKA-associated cerebral edema has a mortality rate of approximately 30 percent [ 4 ]. Thus, careful monitoring for changes in mental or neurologic status that would permit early identification and therapy of cerebral edema is essential. Headache is the earliest clinical manifestation, followed by lethargy and decreased arousal. Neurologic deterioration may be rapid. Seizures, incontinence, pupillary changes, bradycardia, and respiratory arrest can develop. Symptoms progress if brainstem herniation occurs, and the rate of progression may be so rapid that clinically recognizable papilledema does not develop.
●Preventive measures – The following preventive measures may reduce the risk of cerebral edema in high-risk patients:
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hyperglycemic emergencies".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain
language, at the 5th^ to 6th^ grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th^ to 12th^ grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
SUMMARY AND RECOMMENDATIONS
●Basics topics (see "Patient education: Diabetic ketoacidosis (The Basics)" and "Patient education: Diabetic ketoacidosis – Discharge instructions (The Basics)" and "Patient education: Hyperosmolar hyperglycemic state (The Basics)")
●General principles – The treatment of diabetic ketoacidosis (DKA) involves correcting of the fluid and electrolyte abnormalities that are typically present, including hyperosmolality, hypovolemia, metabolic acidosis, and potassium depletion, and administering insulin (algorithm 1 and table 1 and table 4). Frequent monitoring is essential, and underlying precipitating events should be identified and corrected. (See 'Overview and protocols' above.)
●Fluid replacement – Individuals with DKA require intravenous (IV) fluid replacement to correct both hypovolemia and hyperosmolality. Isotonic saline and isotonic buffered crystalloid (eg, Lactated Ringer) are both reasonable options. The optimal rate is guided by clinical assessment.
For patients who present with an initial serum glucose <250 mg/dL [13. mmol/L]), dextrose (5 to 10 percent) is added to IV fluids at the initiation of therapy.
- Initial rate of administration – Fluid replacement should correct estimated volume deficits within the first 24 to 48 hours, with care to avoid an overly rapid reduction in the serum osmolality. (See 'Fluid replacement' above.)
- Hypovolemia with shock – Isotonic fluid (0.9 percent saline or buffered crystalloid) should be infused as quickly as possible in patients with hypovolemic shock. (See "Treatment of severe hypovolemia or hypovolemic shock in adults", section on 'Nonhemorrhagic shock'.)
- Hypovolemia without shock – In hypovolemic patients without shock or heart failure, we suggest isotonic fluid infused at a rate of 15 to 20 mL/kg per hour (approximately 1000 mL/hour in an average-sized person) for the first few hours (Grade 2C).
- Mild hypovolemia or euvolemia – Isotonic fluid is infused at a lower rate than in hypovolemic patients without shock, guided by clinical assessment.
- Subsequent fluid management – After the fluid deficit is corrected, one-half isotonic (0.45 percent) saline is administered at a rate of approximately 250 to 500 mL/hour if the serum sodium (corrected for hyperglycemia) is normal or elevated; isotonic saline is continued at a rate of approximately 250 to 500 mL/hour if the serum sodium (corrected for hyperglycemia) is low. (See 'Subsequent fluid management' above.)
●Potassium replacement – Most patients with DKA require IV potassium replacement. The dose depends on the initial serum potassium level (algorithm 1 ). For patients with high potassium (>5.0 mEq/L) and/or low urine output (eg, <50 mL/hour or 0.5 mL/kg/hour), potassium replacement should not begin until treatment with IV insulin and IV fluids yields a serum potassium ≤5.0 mEq/L and urine output ≥50 mL/hour. Typically, treatment with IV insulin results in a
