Resuscitation of Adult Diabetic Ketoacidosis

June 21,2021 by Shahriar Lahouti


Basic physiology

The three essential fuels for cellular metabolism are glucose, fatty acids and amino acids. Insulin and counterregulatory hormones can alter the metabolic milieu of carbohydrate, protein and lipid metabolism. The prominent metabolic effect of insulin on glucose include1:

  • Decreased hepatic glucose production ( ↓glycogenolysis, ↓gluconeogenesis, ↑glycogen synthesis)
  • Increased glucose uptake in peripheral tissue e.g. fat, muscles etc  

The cardinal cellular fuel is glucose in most tissues. The availability of glucose for intracellular metabolism is dependent upon adequate serum glucose and sufficient amounts of insulin. When glucose is not available, the primary cellular fuel menu flips from glucose to ketone body consumption.

Ketone bodies are derived from metabolism of fat in the liver. This process is tightly regulated by a series of biochemical reactions and regulatory hormones. Summarized briefly, insulin deficiency and or resistance, glucagon excess and increased secretion of catecholamines, cortisol, and growth hormone (which oppose the actions of insulin), also contribute to the increases in glucose and ketoacid production (figure 1 below). 

Suppression of ketogenesis is more sensitive to insulin than the inhibition of de novo glucose production (gluconeogenesis). In other words, the critical insulin level which is required to prevent ketogenesis is lower than the level required to prevent gluconeogenesis. 

The deficiency in insulin is more severe in DKA compared with HHS. The residual insulin level in HHS is sufficient to minimize ketogenesis and development of ketoacidosis, but not adequate to control hyperglycemia.

The baseline insulin level in an individual patient is determined by interaction between following parameters:

  • Individual’s baseline pancreatic beta cell reserve
    • T1DM patients have poor pancreatic reserve
    • T2DM patients have residual pancreatic reserve
  • Severity of precipitating factors (whether there’s one or multiple of the following parameters)
    • States of increased insulin demand: In the presence of a catecholaminergic state, there’s more insulin demand to get back the metabolic profile to euglycemic state. It is worth mentioning here that some stressors are strong e.g. urosepsis whereas other stressors are relatively weak such as UTI.
    • Decreased pancreatic beta cell insulin secretion (i.e. pancreatic exhaustion): This happens following days-to-weeks of poor glycemic control during which pancreatic beta cells are overwhelmed with insulin hypersecretion and finally become exhausted and insulin secretion drops. 
    • Decreased providing insulin: patient may miss insulin dose

The old maxim that patients with T1DM are prone to develop DKA whereas T2DM are prone to develop HHS is not true! In fact, this depends on the baseline insulin level. If the baseline insulin drops below the level which is required to prevent ketogenesis, then metabolic profile shifts more toward DKA and if the insulin level is sufficient enough to prevent ketogenesis, then metabolic profile swings more toward HHS 2.

The hyperglycemic metabolic emergencies i.e. diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are not all or none; rather it is a spectrum of metabolic derangement 3. These represent extremes of the same continuum, with different levels of insulin deficiency, dehydration, ketosis, and metabolic acidosis (figure 1). Indeed, both entities may coexist in one third of the cases.

Ketone bodies: 

There are three different ketone bodies which are produced to variable amounts in ketogenic states, including: 

  1. Acetoacetate
  2. Beta Hydroxybutyrate (BHB)
  3. Acetone

Normally the ratio of BHB to acetoacetate is 1:1. This ratio is altered in DKA to 3:1 and in alcoholic ketoacidosis to 10:1 (see here).

Of note, acetone is a neutral ketone body and does not cause acidosis or elevated anion gap. In contrast, the two other ketone bodies (acetoacetate and BHB) are acidic and cause ketoacidosis with high anion gap 1. Ketone bodies can be detected via

    1. Nitroprusside test reagent which can be applied to urine or serum. However it’s a qualitative method and can only detect acetoacetate and acetone (BHB is not measurable by NTP)
    2. Direct measurement of serum BHB: in the presence of elevated serum glucose level (poor controlled diabetes), an elevated serum BHB > 3.0mM/L can be used to diagnose DKA 2

In the following table the rough correlation between severity of ketonuria (NPT regent) and severity of ketonemia (direct measurement of BHB) is shown.

Definition and diagnosis of DKA

According to the most recent guidelines there is no definitive criteria for diagnosis of DKA 5. Therefore it is of paramount importance to have a low threshold for considering the diagnosis in any diabetic patient who presents with hyperglycemia related signs and symptoms (figure below).

Most patients with DKA will have the triad of hyperglycemia, high anion gap metabolic acidosis and ketonemia, however there are important exceptions:  

  1. DKA patients can have a normal glucose (euglycemic DKA, more on this here )
  2. DKA patients can have a normal pH and a normal bicarbonate. This usually occurs due to a combination of ketoacidosis plus metabolic alkalosis from vomiting or triggering illness. Therefore patients with DKA can have a totally normal VBG!

In patients with high blood glucose, DKA can be diagnosed by high anion gap (>12) and significant elevation of BHB (>3 mM/L) 2

  • Anion gap (figure 2 below) is defined as unmeasured anions and calculated as: Na – Cl – HCO3
  • This can be calculated simply as above and does need correction for albumin, glucose or potassium. You do not need to correct measured sodium for hyperglycemia for calculation of anion gap as well.

As such, DKA can be defined purely on the basis of blood chemistry (basic metabolic profile), urine ketones and serum BHB measurement (if necessary). VBG is not necessarily required for diagnosis of DKA (more on this here).

Severity of DKA

DKA severity can be classified based on certain clinical features and laboratory findings (table 1 below).


Differential diagnosis

DKA consists of the biochemical triad of hyperglycemia, ketonemia and anion gap metabolic acidosis, each of these components can be seen in other metabolic conditions 6.

👉The differential diagnosis of hyperglycemia include

  • Poor controlled diabetes: 
  • Stress hyperglycemia
  • DKA
  • HHS: In the following table, the key differences between DKA and HHS are summarized.

The core features of pure HHS are profound hyperglycemia and  altered mental status in the context of elevated serum osmolality. HHS can be defined as:

  • Profound hyperglycemia (e.g. >> 600 mg/dL) should always raise concerns for HHS.
  • Absence of substantial ketoacidosis (serum BHB < 3 mM or anion gap < 15mM)
  • Altered mental status  
  • High serum osmolality > 320 mOsm (as explained below)

Osmolality is a measurement of the number of particles in a solution. The serum osmolality is determined by concentration of uncharged solute in plasma. In physiologic state, the primary circulating uncharged solutes are sodium salt (mainly sodium chloride and sodium bicarbonate), glucose and urea. If other solutes are present in serum at high concentration (>5 mmol/L) such as ethanol and toxic alcohols; they will also account for determination of serum osmolarity. 

  • Osmolality can be directly measured in the laboratory (based on freezing point depression). 
  • Alternatively it can be calculated (use MDCalc). For diagnosis of HHS, serum osmolarity can be calculated and in this setting it  is > 320 mOsm.

Tonicity (aka. effective serum osmolality) is a measure of the osmotic pressure gradient between two solutions across the semipermeable membrane (i.e. referring to how much the particles in a solution pull water across a semipermeable membrane). This depends on the number of effective osmoles in the solution.

👉Tonicity is more clinically important than osmolality because tonicity is what actually determines whether cells swell or shrink. In physiologic state, effective serum osmolality depends on:

  • Sodium: is an effective osmole, because it cannot cross the semipermeable membrane.  Therefore, sodium will tend to pull water across the membrane.
  • Glucose: is sometimes an effective osmole, but sometimes it’s not!
    • When a patient first presents with HHS, low insulin causes glucose to stay outside the cells.  This causes glucose to function as an effective osmole.
    • During treatment with insulin, glucose enters the cells. At this point, glucose is an ineffective osmole.

Ineffective osmoles: These can diffuse freely into the cells; hence do not cause pressure gradient across the cells. Examples include urea and ethanol

The key principle to avoid cerebral edema is to avoid rapid change in sodium or glucose concentration (more on this below) especially in younger patients and those whose medical condition has been established chronically.

👉The differential diagnosis of high anion gap metabolic acidosis include 7

  • Ketoacidosis: diabetic and alcoholic ketoacidosis
  • Renal failure (uremia)
  • Exogenous poisoning: Methanol, ethylene glycol, salicylate, isoniazid intoxication
  • Lactic acidosis such as sepsis, cardiac arrest, liver failure, intoxication with iron, metformin, cyanide etc. 

👉The differential diagnosis of ketoacidosis include

  • DKA
  • Alcoholic ketoacidosis: Blood glucose is low or normal. lIn the presence of low or normal glucose levels, it is less likely that it is DKA (more on this below).
  • DKA-HHS overlap (see below)

Step 1: Investigations

Precipitating cause

The goal of initial investigation is to diagnose the metabolic hyperglycemic emergencies (see above) and the possible triggering events. A precipitating event can usually be identified in patients with DKA or HHS, though DKA occasionally is the first presentation of diabetes. Conditions and factors associated with DKA and HHS include:

  • Poor compliance with the insulin regimen, inadequate dosing, or insulin pump failure
  • Acute major illnesses such as myocardial infarction, cerebrovascular accident, bowel ischemia, sepsis, or pancreatitis.
  • Infection: gastroenteritis, appendicitis, pneumonia, urinary tract infection, diabetic foot infection etc.
  • Pregnancy
  • Trauma, surgery, any other source of physiologic stress
  • Substance abuse (e.g. cocaine8)  or alcoholism
  • Medications (e.g. steroid 9, atypical antipsychotics 10, lithium 11 , sympathomimetics e.g. dobutamine, terbutaline; SGLT-2 inhibitors 12, anti-calcineurin immunosuppressives 13,HIV protease inhibitors 14).

Evaluation for the cause of DKA 

Primary neurologic problem: patients with mild-moderate DKA are often alert and awake. Altered mental status can be seen in patients with severe DKA and it is commonly seen in patients with HHS (due to elevated serum osmolarity). As a rule of thumb, serum osmolarity above 320 mOsm/kg can cause altered mental status. If the calculated serum osmolarity is < 320 mOsm/kg and the patient is altered, other etiologies for altered consciousness should be considered such as

  • Ischemic CVA, intracranial hemorrhage, cerebral vein thrombosis
  • Meningitis
  • Respiratory failure causing hypercapnic encephalopathy
  • Cerebral edema (as a complication of treatment) when the altered mentation does not improve with the treatment and so the clinical course is deteriorating. 

Primary abdominal problem

DKA can cause abdominal pain by itself, however the provider needs to sort out whether the pain is secondary to DKA or it is due to a primary underlying abdominal problem (e.g. pancreatitis, cholangitis, appendicitis etc.). This can be accomplished by considering the following concepts:

  • Severe abdominal pain out of proportion to severity of DKA (i.e. mild DKA) argues against DKA-induced abdominal pain 15.
  • Abdominal pain due to DKA should resolve following resolution of ketoacidosis by appropriate treatment 16. If serial abdominal examination is still revealing pain, then one must consider appropriate investigation such as abdominal CT with IV contrast.

Primary infectious trigger

DKA itself may cause leukocytosis which is proportional to the degree of ketonemia, so the presence of an elevated WBC count is nonspecific. Infection is suggested by fever, bandemia (>10%), marked left-shift, or severe leukocytosis (>20,000 – 25,000) 17.

Primary hemodynamic derangement

Patients with HHS usually have severe volume depletion with low MAP, while patients with DKA often have low-normal MAP (patients with severe DKA may present with low MAP secondary to severe acidosis).However, BP easily normalizes following initial resuscitation in patients with DKA. If MAP does not normalize following intravascular volume repletion, one may consider other etiologies of primary hemodynamic derangement such as sepsis, GI bleeding and profound acidemia.

Initial evaluation panel

CBC, extended electrolytes, creatinine, BUN, as well as consideration for:

  • If diagnosis of DKA is unclear:  beta-hydroxybutyrate level & lactate
  • If an infectious trigger is suspected: Cultures, urine analysis etc.
  • Only if history or EKG suggest myocardial ischemia, then troponin is requested.
  • If pregnancy is suspected, BHCG is requested (pregnancy may be a trigger for DKA)
  • If significant abdominal pain/tenderness:  
    • Lipase (note that DKA itself can increase lipase substantially)18
    • Additional investigation including abdominal CT scan may be deemed necessary in appropriate clinical settings. 
  • Additional workup as clinically appropriate (e.g. toxicology evaluation, CT scan to evaluate for septic focus).

Step 2: Initial resuscitation

Goal: The initial goals of treatment in patients with DKA include:

  • Correction of fluid deficits
  • Replacement of potassium
  • Stopping ketone production by closing the anion gap with insulin
  • Treating underlying precipitant

The fundamental concept in appropriate treatment of patients with DKA is that the issue with diabetes ketoacidosis is not hyperglycemia by itself, rather is an excess ketone body production due to low level of circulating insulin. Therefore the cornerstone of treatment is reducing ketone production via insulin and not the correction of hyperglycemia.


IV Access:

Most DKA patients can be treated with peripheral IV access, but for the sickest patients central access may be needed.

Fluid resuscitation

Osmotic diuresis from hyperglycemia, vomiting and reduced oral intake make patients with DKA profoundly volume depleted. The hypovolemia triggers stress hormone release which causes insulin resistance and makes hyperglycemia more difficult to treat.  

Fluid resuscitation restores intravascular volume, improves organ perfusion and renal function and decreases insulin resistance at the tissue level.

Most patients require 2-4L of crystalloid upfront. Both NS or RL can be used (RL is the preferred choice). Start with 1000-1500mL of RL over 1 hr and then adjust to the patient’s hemodynamic and electrolytes status.

  • For young DKA patients with normal cardiorenal function, if the HR is >100 bpm then they probably need more fluid.
  • Ultrasound-guided fluid resuscitation is useful for patients with heart failure or patients on hemodialysis.


Patients with DKA and HHS have a large total body potassium deficit (roughly 300-600 mEq/L) largely due to osmotic diuresis induced by hyperglycemia. However the initial potassium reading can be normal or even high (in 25% of patients) due to the following mechanisms:

  1. Intracellular fluid (ICF) shrinkage makes ICF more concentrated. K will shift passively through the potassium channels.
  2. Solvent drag phenomenon: refers to passive shift of water out of the cell. This will drag K drag potassium ions too. 
  3. Insulin deficiency: Insulin promotes uptake of potassium. Insulin deficiency contributes to outward shift of potassium out of the cells. 

👉Remember that transient hyperkalemia is not due to acidosis. It’s true that acidosis can shift K outward, but this can happen for inorganic acids. In case of organic acidosis {ketoacidosis and lactic acidosis}, the role of acidemia is minimal. That’s why ↑K could be seen in HHS as well (in HHS there’s minimal to no acidosis).

Pearls: The ticket to start insulin is presence of serum K >3.5 mmol/L.

Keep in mind that DKA treatment will cause the potassium to drop rapidly. The potassium replacement can be followed as following (depending on initial serum K): 

  • If the initial serum potassium > 5.3 mmol/L: Do not add potassium into the IV fluid. Start Insulin and check serum potassium every 2h 5.
    • IV calcium is considered for patients with critical hyperkalemia {K> 5.5 mmol/L with any EKG signs of hyperkalemia or K>6.5mmol/L even in the absence of EKG changes}. Remember that following resuscitation for DKA, the hyperkalemia will resolve promptly.
  • If the initial serum potassium is 3.5 to 5.3 mmol/L: Start potassium repletion and then start insulin for treatment of ketoacidosis. 
    • Initial potassium 4.0 – 5.3 mmol/L: Add 10 mEq/L KCL per hour to IV fluid.
    • Initial potassium 3.5 – 4.0 mmol/L: Add 20 mEq/L KCL per hour to IV fluid. Remember that you can stay on core IV Fluid (NS or RL) if no more than 20mEq/L/h KCL is going to be given.
  • If the initial serum potassium is below 3.5 mmol/L: HOLD insulin. Add KCL 20 – 40 mEq/L/h to IV fluid 19 20. Place on continuous cardiac monitoring. 
    • Remember that for giving KCL at > 40 mEq/L you need to change core IV fluid to half saline.
    • You can administer 40mEq/L KCL through 2 peripheral lines (20mEq/L/h via each peripheral line) or alternatively you can give 40mEq/L/h KCL through the central line.
    • Check serum K every 1hr. 
    • Insulin can be started when serum K stays above 3.5 mmol/L.
    • Continue to aggressive K repletion and shoot for a potassium >5.3 mM (targeting a high potassium prevents you from falling behind).

Insulin Therapy

Remember that the primary problem in DKA is ketoacidosis but not hyperglycemia. The goal of treatment is to titrate insulin to eliminate ketoacidosis and close the anion gap. 

Since glucose measurement is more feasible than serum ketones, therefore blood glucose is used as a surrogate measurement of the efficacy of insulin therapy. Supplemental glucose should be provided as glucose approaches normal to allow for continued insulin therapy to resolve the ketoacidosis while avoiding hypoglycemia.

Unless the patient is hypokalemic, insulin infusion should be started immediately (see above).

  • Start short acting IV insulin at a fixed weight-based dosing of 0.1 U/kg/hr (up to maximum of 15 units/hour in morbid obesity) 5.
    • Patients with severe acidosis (e.g. pH< 6.9 or bicarbonate <5mM ) or those with high daily insulin requirement may require higher doses of insulin e.g. 0.2-0.3 U/kg/h.
    • Insulin bolus is not required 5 except in a few situations such as severe acidosis (pH < 6.9, HCO3 <5mM) or critical hyperkalemia or peri-arrest state; where a bolus of rapid acting insulin at 10U is given intravenously before initiation of insulin drip. If setting up the insulin infusion will take > 30 minutes, then one may consider insulin bolus (10 units IV) as well.
  • Target blood glucose of 210-250 mg/dL 5.
  • The insulin infusion should be up-titrated as needed (e.g. double the initial dose) to drop the glucose by 50-70 mg/dL per hour.
  • When serum glucose reaches 200-250 mg/dL, reduce the rapid acting insulin infusion (but not lower than 0.05 U/Kg/h) 5.
  • When blood glucose < 250 mg/dL, add dextrose dextrose infusion to prevent hypoglycemia while continuing insulin infusion.
  • If glucose falls < 70mg/dL, do not stop insulin infusion, but decrease by 50% (no less than 0.05U/kg/hr), provide 1 amp of D50 and switch dextrose infusion from D5 to D10.
  • Patients should also be allowed to eat if it is deemed safe to do so. There is no evidence to support keeping the patient NPO.

For patients with “Mild” DKA, one may consider administration of rapid acting insulin via subcutaneous route (SC) as 21:

  • Initially give short acting insulin SC at 0.3U/Kg.
  • Second dose of rapid acting insulin SC at 0.2U/Kg is given 1h later.
  • Repeat 0.2U/Kg rapid acting insulin every 2 hrs.

Management of severe acidosis

The most effective strategy to manage patients with severe acidosis (e.g. pH< 6.9 or bicarbonate < 5mM) is to increase the insulin dose (usually along with administration of additional glucose and potassium).

  • Don’t wait for the insulin to arrive from the pharmacy: bolus 10 units regular insulin IV immediately. 
  • Consider starting at 0.2 U/kg/hr in the sickest patients.  

Role of bicarbonate in treatment of severe DKA

Current evidence does not support replacing bicarbonate in patients with DKA 22 23 24 .There is evidence of transient worsening of ketosis and an increased need for potassium supplementation in patients who received bicarbonate 25 26. Therefore routine use of bicarbonate for treatment of DKA is not recommended. The decision to give bicarbonate should be made on an individual basis depending upon hemodynamic and acid-base status. Experts recommend considering giving some bicarbonate prior to intubation if the bicarbonate level is <10 mEq/L as it may help transiently buffer the pH against the rise in CO2 that occurs during induction +/- paralysis.

Step 3: Closing the anion gap


During initial phase of treatment (first 6hrs), one should follow up as:

  • Glucose every 1hr.
  • Extended electrolyte (including Phos & Mg) every 2 hrs.
  • Urine output. Glucose >250 mg/dL  functions as a diuretic, so patients should produce lots of urine. Poor urine output raises concerns about shock or renal failure

Long acting insulin

Start long acting insulin in the ED early in the treatment course. It has been shown that early initiation of long acting insulin facilitates transitioning off the insulin infusion, reduces the incidence of hyperglycemia, and may decrease hospital length of stay1. Glargine (Lantus) has a delayed onset compared to some older forms of insulin (e.g. NPH), so the traditional two-hour overlap may not work well with glargine 27.

Patients can generally be treated with their home insulin regimen (ideally a single daily dose of glargine). For a patient naive to insulin, a starting dose of 0.25 units/kg daily of Lantus may be given.

Maintenance fluid infusion

Once moderate-severe hypovolemia is corrected, start a maintenance fluid infusion at 250-500cc/h. The type of given fluid depends on corrected serum sodium and blood glucose.

Keep in mind  that in both DKA and HHS the high blood glucose causes dilutional hyponatremia i.e. the measured serum sodium is falsely lower than actual values. The sodium correction for hyperglycemia can be calculated (use MDCalc) for appropriate fluid management (e.g. time to switch from NS to half-saline). 

  • In patients with low corrected serum sodium (e.g. <135 mEq/L), either RL or NS can be used for replacement of volume deficit.
  • Patients with a normal or high corrected sodium concentration can be switched to 0.45% sodium chloride after the first hour of fluid replacement
  • Once BS drops below 250 mg/dL, dextrose should be added to the IV fluid to allow continued insulin infusion at a rate sufficient to resolve DKA while avoiding hypoglycemia. 
    • Drop and split method: Cut the running fluid in half e.g. from 200ml/h to 100ml/h. Add D10W infusion at equal rate e.g. 100ml/h.The advantage of giving the components separately is that it provides you more control with regards to adjusting the amount of sodium you are giving versus the amount of dextrose. For example, if you want to give additional D% you can up-tirate the D10W infusion (without giving the patient more sodium and causing volume overload).
    • Alternatively you may switch to D5-1/2NS at 200-250cc/h.

Repletion of the electrolytes


Keep potassium repletion as explained above. In patients with renal failure be more conservative with K repletion. If the patient can tolerate oral potassium replacement, it is preferred over the IV route as it is thought to have better systemic absorption.


Phosphate will drop during treatment, especially in patients with severe DKA. Follow the phosphate and replete if severe hypophosphatemia occurs (<1 mg/dL).


Maintaining a high-normal magnesium level may tend to protect against hypokalemia-induced arrhythmia if the potassium falls too low (isolated hypokalemia is usually well tolerated, whereas the combination of hypokalemia plus hypomagnesemia is more dangerous).

Make sure the anion gap is closing

If the anion gap is not closing, consider the following possibilities:

  • Inadequate fluid resuscitation
  • Inadequately low insulin dose
  • Malfunction of insulin infusion
  • Underlying diagnosis contributing to anion gap that has not been addressed

Interventions if the anion gap is not closing:

  • Evaluate fluid status (e.g. with ultrasonography), provide additional crystalloid if necessary
  • Consider increasing the insulin infusion rate
  • Re-evaluate for a missed underlying diagnosis
  • Consider checking beta-hydroxybutyrate and lactate levels, to exclude an occult/worsening lactic acidosis

Treat the non-anion gap metabolic acidosis (NAGMA) with IV bicarbonate

Following resolution of ketoacidosis, some patients may develop NAGMA caused by two factors:

✓Resuscitation with NS or half-normal saline

✓Excretion of keto acids in urine. 

  • Kidney avidly excrete keto acid salts unless renal function is impaired or renal blood flow is reduced due to severe volume depletion. 
  • Remember that administration of IV fluid promotes normalization of intravascular volume and renal blood flow, hence promoting excretion of keto acid salt in urine. In contrast, the institution of insulin for DKA enhances intracellular metabolism of keto acids and regeneration of bicarbonate.

Development of NAGMA is revealed as closing or near-closing anion gap (AG <12-18 mEq/L) despite that bicarbonate is remaining low (e.g. < 18 mEq/L).

The clinical significance of the NAGMA relies on the fact that in the presence of acidosis, there is still insulin resistance at the level of tissue. So stopping off the insulin drip while the patient is still acidotic may lead to recurrent DKA.

This will justify treatment of NAGMA with IV bicarbonate before discontinuing insulin drip (more on this here). The treatment goal is to achieve serum bicarbonate level of 18-20 mEq/L before discontinuing the insulin infusion. Oftentimes 100-150 mEq of bicarbonate is adequate.

  • If the patient is hyponatremic, then two or three ampules of hypertonic bicarbonate can be used (each ampule contains 50 mEq sodium bicarbonate in 50 ml water).

If the patient’s sodium is normal or elevated, then isotonic bicarbonate may be used (e.g. one liter of D5W with three ampules of bicarbonate, to generate a 150 mEq/L bicarbonate solution, infused over 3-4 hours).  

Step 4: Stopping the drip


👉Resolution of ketoacidosis evidenced by serum anion gap < 10-12mEq/L and or serum BHB <0.6mM.

  • An exception here is a patient with end-stage renal disease, who may chronically have an elevated anion gap due to uremia which never normalizes.  In this situation, normalization of the BHB level (<0.6 mM) is a more useful way to determine that ketoacidosis has resolved.

👉Glucose is reasonably well controlled (e.g. < 250 mg/dL)

👉There should be at least >2 hrs of overlap of insulin drip and long acting insulin (if Lantus has not been given yet)

👉The patient should be hungry (indicating that ketoacidosis has been resolved) and tolerate “PO” 

  • If the insulin infusion is stopped and the patient doesn’t eat anything or receive any IV glucose, this increases the risk of recurrent DKA.
  • An exception can be made for patients with gastroenteritis or diabetic gastroparesis, who may not be hungry for a while. In this situation, the insulin infusion can be stopped, but patients should remain on low-dose intravenous glucose (e.g. D5W at 75 ml/hr). If the patient’s glucose level increases, they should be treated with PRN short-acting insulin. Ongoing administration of carbohydrate plus PRN insulin will help keep the anion gap closed.

👉The patient isn’t significantly acidotic (bicarbonate > 18-20 mEq/L).  If the patient has developed NAGMA then treat with IV bicarbonate as described above

Start meal-associated & sliding scale insulin

✓Start meal-associated and sliding-scale insulin.

  • If the patient isn’t already on a prescribed regimen of meal-associated insulin, a dose of ≈ 0.08 U/kg rapid-acting insulin per meal is reasonable. Follow glucose and titrate to effect.

✓Encourage patients to eat. Carbohydrate intake (along with meal-associated and sliding-scale insulin) is important at this step to prevent recurrent DKA.

Monitor for recurrence of DKA

Check glucose level q2hrs and electrolytes ≈  6 hrs following discontinuation of insulin drip.

Development of a progressively severe hyperglycemia may be an early sign of recurrent DKA and may pre-date the development of a widening anion gap by a few hours. If there is any concern regarding recurrence of DKA, consider electrolyte check to assess widening anion gap.

Recurrent DKA

Causes of recurrent DKA (widening anion gap after stopping drip)

  • Insulin drip was stopped despite not meeting all above five criteria
  • Inadequate long-acting insulin dose
  • Patient isn’t eating enough (which causes insufficient meal-associated & PRN insulin doses)
  • Ongoing systemic inflammation (e.g. DKA caused by infection, with persistent infection)


  • Restart the insulin infusion
  • Continue long-acting insulin (consider up-titrating the dose)
  • Address any reversible causes of DKA
  • Treat NAGMA to get the serum bicarbonate >20 mEq/L (this will improve insulin sensitivity).
  • Severely ill patients on admission may just need a bit longer on the insulin infusion

Complications and special situations

Avoiding intubation

Patients with DKA rarely have oxygenation problems, rather they may develop respiratory fatigue due to increased work of breathing. 

High-flow nasal cannula (HFNC) is a safe way to support the patient’s breathing. By facilitating CO2 elimination, HFNC can help the patient compensate for their metabolic acidosis.

BiPAP is not recommended for patients with DKA since there is increased risk of aspiration and emesis as they often concurrently have gastroparesis.

Intubation of DKA patients is challenging for several reason and possibly should be avoided:

  1. Increased risk of ventilator associated lung injury: The respiratory dynamics of hyperpnea to correct their underlying metabolic acidosis means the ventilator must equally match their large tidal volume and respiratory rate. This intrinsically puts the patient at risk for ventilator induced lung injury and subsequent development of ARDS
  2. Decompensation of acidosis and peri-intubation collapse: Most patients have severe metabolic acidosis with a compensatory respiratory alkalosis.  Paralysis takes away their respiratory compensation, potentially leading to profound acidosis.
  3. Hemodynamic collapse:  If hypovolemia isn’t corrected prior to intubation.
  4. Vomiting/aspiration:  Patients with DKA often have gastroparesis and ileus which put them at high risk of vomiting and aspiration.

For the above reasons unnecessary intubation👇 should be avoided as possible.

  • If you are intubating a patient with DKA for altered mental status, you should reconsider that mental status must improve within several hours of treatment and therefore close observation would be the best approach.

Indications for intubation may include:

  1. Respiratory arrest or impending to arrest 
  2. Clinically obvious signs of inability to protect airway (e.g. gurgling, inability to control secretions).
  3. Intubation before a warranted surgical procedure (e.g. patient with DKA and perforated viscus) 

If you must intubate:

    1. Mitigate the risk of hemodynamic collapse: resuscitate before you intubate 
      • Protect the MAP before intubation: Fluid resuscitation, consider to start vasopressor infusion (or push dose pressors) to keep MAP above 75 mmHg
      • Use hemodynamically stable induction (e.g. ketamine) 
    2. Avoid the risk of decompensation of acidosis
      • Give bicarbonate prior to intubation if the bicarbonate level is <10 mEq/L. For example, slowly push 2-3 ampules (100-150 mEq) of bicarbonate over 10-15 minutes, at least ~10 minutes prior to intubation. Bicarbonate contains dissolved CO2, which the patient must blow off. In order to benefit from the bicarbonate, the patient should have enough time to blow off additional CO2 prior to intubation
      • Use HFNC before induction (the high flow rate reduces the dead space and provides a more efficient ventilation and CO2 elimination). 
    3. Mitigate the risk of regurgitation and aspiration:
      • Perform gastric ultrasound and if distended, consider NG drainage before the intubation
      • Consider an antiemetic
    4. Meet the patient’s metabolic demand on mechanical ventilator
      • Use a relatively large ETT (e.g. ≧7.5mm ETT) to minimize airway resistance. This improves exhalation and prevents breath stacking while applying high respiratory rate on mechanical ventilation
      • As soon as the ETT is secured, increase tidal volume & respiratory rate to hyperventilate the patient (thus restoring respiratory compensation).
      • Set the tidal volume at 8 cc/kg.
      • Crank the respiratory rate as high as possible without causing autoPEEP (will often end up around ~24-28 breaths/minute).
      • Shoot for a very high minute ventilation (e.g. 12-18 liters/minute).

Avoid cerebral edema

Risk factor for developing cerebral edema include:

  • Younger (<25 yo) patients
  • Patients with elevated baseline serum osmolarity (e.g. > 330 mOsm)

Clinical presentation: 

Altered mental status associated with headache, seizure, recurrent vomiting and/or signs of brain herniation. DKA-related cerebral edema occurs most commonly after several hours of DKA treatment with insulin and intravenous fluids, but can also occur at the time of presentation to the ED, before treatment is administered.

Best practice to avoid cerebral edema

  • Avoid over-aggressive fluid administration.
  • Don’t drop the glucose too fast. Avoid reducing the glucose below <200 mg/dL 
  • Replace fluid gradually. Avoid large volumes of hypotonic fluid.
    • Try to use only isotonic fluids (e.g. D5 LR can be used as a source of glucose-containing IV fluid, rather than hypotonic fluids such as D10W or D5 1/2 NS).
    • Avoid dropping the serum osmolality by more than 3 mMol/kg/hour or decreasing sodium by >10 mmol/24 hours
  • Note that the sodium will often initially increase during resuscitation due to glucose entering the cells. This doesn’t reflect an increase in serum osmolality, and doesn’t require treatment with free water. The key parameter to track is measured or calculated serum osmolarity (but not the sodium).
  • Avoid unnecessary bicarbonate during treatment 28 

Prevent venous thromboembolism 

Patients with DKA are at relatively higher risk of VTE relative to other critically ill patients29. Provide prophylaxis against DVT unless it is contraindicated.


DKA-HHS overlap patient

As discussed earlier 25% of patients with hyperglycemia metabolic emergencies present with DKA-HHS overlap. These patients have a combination of:

  • Significant ketoacidosis (serum BHB > 3 mM and substantial anion gap elevation)
  • Profound hyperglycemia (e.g. blood glucose > 1000 mg/dL) with elevated serum osmolality to >> 320 mOsm.

Essential concepts which should be reviewed here are:

  • First: In patients with pure HHS, the disease has been established over days to weeks (this is in contrast to DKA patients whose problems have been developed more acutely). As a rule of thumb,if an abnormal state develops gradually then it may be treated gradually. This is in contrast to pure DKA patients which often require more urgent treatment to correct their metabolic problems.
  • Second: remember that younger patients (< 40 yo) with DKA or HHS and those with profoundly high serum osmolality (>>320 mOsm) are at high risk for development of cerebral edema if their osmolality is rapidly decreased. 

By enlarge the principles of management of DKA-HHS overlap patients is the same as for DKA.The only difference is that if the patient is < 40 years old, there may be an increased risk of cerebral edema if the osmolality is decreased too rapidly. Thus, osmolality and sodium levels should be closely monitored 30

DKA in hemodialysis patient

Fundamental physiologic differences

  • Insulin clearance is reduced in patients with ESRD, therefore insulin requirement may be lower than other patients.
  • Osmotic diuresis secondary to hyperglycemia will not develop in ESRD patients who are anuric therefore severe volume depletion or hypokalemia is less likely to develop in these patients. In fact in some patients, hyperglycemia may osmotically pull water into the vasculature leading to hypervolemia. This can lead to volume overload with pulmonary edema, which may resolve following insulin administration (since the insulin causes a shift of glucose and water out of the vasculature and into the tissues). 
    • If you give excessive fluid or potassium, this will create a persistent problem that requires dialysis.

Principles of management 31

  1. Avoid aggressive volume resuscitation 
  2. Avoid aggressive potassium administration
  3. Insulin and dextrose administration
    • Be conservative with insulin administration, as it may be cleared slowly.  For patients who aren’t severely acidotic, it may be wise to start the insulin at a slower rate than usual (e.g. 0.05 units/kg/hour).
    • For euvolemic patients, D10W may be superior to D5W to avoid causing hyponatremia. If central access happens to be available, then higher concentrations could be used (e.g. D20W).
  4. Oftentimes patients just need insulin but not hemodialysis
    • Hemodialysis will remove keto acids and replace bicarbonate, therefore fix the problem. However it is not usually required since insulin alone is often adequate to improve acidosis and hyperkalemia. Hemodialysis is associated with risk of rapid osmotic shift especially in patients with increased serum osmolality > 330mOm/kg ,it might be associated with risk of cerebral edema.
    • Even if hemodialysis fixes everything, the patient still needs insulin to prevent slipping back into DKA.
  5. Remember that anion gap never normalizes in uremic patients
    • Patients on dialysis will always have an elevated anion gap, due to uremia.
    • If beta-hydroxybutyrate is available, this is the best way to determine the severity of the ketoacidosis.  DKA resolution may correlate with a beta-hydroxybutyrate level which is below 1 mM.
    • If beta-hydroxybutyrate is not available, look at the patient’s prior anion gap values to determine a sense of the patient’s baseline (often around 12-16 mM).  If the patient’s anion gap falls to within this range and remains stable over time despite insulin administration, then the ketoacidosis has likely resolved.

DKA in heart failure patient

Fundamental differences

  • Heart failure patients may be hypervolemic prior to developing DKA. Furthermore they may respond less strongly to the diuretic effect of hyperglycemia. Overall, the patient may not be severely hypovolemic at baseline.
  • If excessive fluid is administered, heart failure patients will tend to retain this fluid (unlike young DKA patients, who will eliminate any excess fluid via urination)

Principles of management

  • Serial assessment of volume status is needed (e.g. with ultrasonography).
  • Standard DKA protocols may not work. Specifically, these protocols will recommend excessive fluid administration 32

Euglycemic DKA

Definition and diagnosis:

  • Definition: Euglycemic DKA is defined as DKA with a glucose < 250 mg/dL33
  • Diagnosis: consider the possibility of DKA whenever the anion gap is elevated or ketones are present in the urine (even if the glucose is normal) in diabetic patients taking an SGLT-2 inhibitor who present with nausea, vomiting or shortness of breath.
    • DDx: Both EDKA and alcoholic ketoacidosis have low-normal blood glucose and elevated serum anion gap. However history provide useful clue to differentiate these two. Binge alcohol drinking suggests diagnosis of alcoholic ketoacidosis, while taking SGLT-2 inhibitors in patients with diabetes is in favor of diagnosis of EDKA.


  • SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin)34 35
  • Anything that exhausts the liver’s ability to synthesize glucose:
    • Starvation, prolonged nausea/vomiting
    • Pregnancy
    • Hepatic failure
  • Partial treatment with insulin before admission (either intentionally or unintentionally via an insulin pump)


In the following figure, the pathogenesis of EDKA in patients taking SGLT-2 inhibitor is shown.


  • By enlarge similar to usual treatment described for DKA.
  • However IV glucose will need to be started immediately (e.g. D10W or D5LR  infusion). These patients will require a combination of both IV glucose plus IV insulin to resolve their ketoacidosis.

Alcoholic ketoacidosis

Alcoholic ketoacidosis usually occurs in malnourished patients with chronic alcoholism who have a history of binge alcohol ingestion. Active drinking has often stopped because of the development of abdominal pain, nausea, and vomiting. After one to two days, the patient presents to the hospital. Blood ethanol levels at this time may be low or not detectable.

Pathogenesis: the metabolism of ethanol is shown in the following figure. 

Following ethanol withdrawal the increased catecholamine and cortisol level amplify the hormonal response to fasting (low insulin levels, high glucagon), causing a marked increase in lipolysis which is required for the brisk development of ketogenesis. The oxidation of ethanol to acetaldehyde and then to acetic acid each converts NAD+ to NADH. This redox shift of the NAD+/NADH ratio toward NADH has the following effects:

  • It suppresses gluconeogenesis and may result in hypoglycemia.
  • It increases the ratio of BHB/ acetoacetic acid. The shift from acetoacetic acid to BHB has no effect on the degree of bicarbonate reduction or anion gap elevation, since both acids have an identical effect on these parameters. However, it imposes diagnostic challenge when the nitroprusside test is used.
  • It favors the conversion of pyruvate to lactate. This effect is usually not important clinically, and a significant lactic acidosis in a patient with alcoholic ketoacidosis should prompt a search for other, more common disorders that are causes of a marked reduction in tissue perfusion, such as hypovolemia, heart failure, or sepsis

Diagnostic criteria for alcoholic ketoacidosis:

  • Binge drinking resulting in nausea, vomiting and decreased intake
  • Low, normal or slightly elevated serum glucose
  • Wide anion gap metabolic acidosis (without alternate explanation)
  • Positive serum ketones

Treatment of alcoholic ketoacidosis:

  • Give %5 dextrose in normal saline for rehydration. Then change to %5 dextrose in half normal saline as maintenance until oral uptake resumes.
  • Replace potassium and magnesium as needed.
  • Optional: consider 50-100 mg thiamine and 1mg folate IV concurrent with or after glucose administration.
  • Consider other causes of anion gap acidosis if the anion gap is < 20 mEq/L or fail to close with ongoing treatment.


  • Not all patients with profound hyperglycemia have DKA or HHS. Diagnosis should be made in appropriate clinical context and laboratory data.
  • Avoid ruling out DKA based on a normal or near normal VBG/bicarb or glucose. Calculate the anion gap please! 
  • In clinical practice almost 25% of patients have DKA-HHS overlap. 
  • The core features of DKA are  high anion gap and serum BHB > 3mOm
  • The main clinical features of HHS are profound hyperglycemia and elevated serum osmolality plus being unwell, especially altered mental status.
  • Do not miss the underlying cause of DKA e.g. sepsis, myocardial infarction. The most common cause of death among admitted DKA patients is not DKA, rather its associated condition.
  • DKA can cause abdominal pain by itself. However severe abdominal pain associated with mild DKA or persistence of pain despite improvement of ketoacidosis following treatment is worrisome. Make sure you perform appropriate investigations for possible underlying pathologies like pancreatitis, intra-abdominal vascular catastrophes like mesenteric vein thrombosis or intra-abdominal infection etc. 
  • Hyperglycemia rarely causes mental status changes unless the serum osmolality is >320 mOsm.  Thus, if the serum osmolality is <320 mOsm and mental status is significantly abnormal, look for an alternative explanation.
  • If mental status is progressively worsening with initial resuscitation, consider cerebral edema especially in a susceptible group of patients.
  • Profound hypotension despite initial fluid resuscitation in DKA patients should make you consider possible underlying causes like septic shock, ongoing bleeding e.g. GI bleeding etc.
  • The main goal of DKA treatment is closing the gap, not normalizing the glucose.
  • Fluid administration should precede insulin therapy in order to restore intravascular volume and tonicity.
  • The ticket for starting insulin is serum potassium above 3.5 mEq/L. Hold insulin therapy if serum K is < 3.5.
  • Start potassium replacement promptly with fluid resuscitation, if the initial potassium is < 5.3 mEq/L.
  • Patients with DKA have severe potassium deficit, though serum potassium may read high superficially in some patients. This transient hyperkalemia will rapidly respond to DKA treatment. 
  • Do not stop the insulin infusion when glucose falls below the normal range. Patients should meet all five criteria mentioned previously before insulin infusion is stopped. 
  • Avoid intubation of DKA patients if possible.  If you must intubate, proceed with extreme caution and preparation.

Going further:



Expand to view the reference list

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Shahriar Lahouti

Founder, Chief Editor
I am Shahriar Lahouti and RECAP EM is my primary FOAMed project. The philosophy of RECAP EM is to promote critical thinking and enlightening the mindsets with most rational, current evidence towards a safer practice.

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