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PostSubject: DIABETIC KETOACIDOSIS   DIABETIC KETOACIDOSIS Icon_minitimeWed Feb 01, 2012 3:09 am

Diabetic ketoacidosis (DKA) is a state
of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia,dehydration, and acidosis-producing derangements in intermediary metabolism.
The most common causes are underlying infection, disruption of insulintreatment, and new onset of diabetes. DKA typically is characterized by
hyperglycemia over 300 mg/dL, low bicarbonate (<15 mEq/L), and acidosis (pH<7.30) with ketonemia and ketonuria.

Many of the underlying
pathophysiologic disturbances in DKA are directly measurable by the clinician and need to be followed throughout the course of treatment. Close attention to
clinical lab data allows the emergency physician not only to track the underlying acidosis and hyperglycemia but also to prevent common potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia.

The absence of insulin, theprimary anabolic hormone, means that tissues such as muscle, fat, and liver do
not take up glucose. Counterregulatory hormones, such as glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty
acids and gluconeogenesis, which is the main cause for the elevation in serum glucose in DKA. Beta-oxidation of these free fatty acids leads to increased
formation of ketone bodies. Overall, metabolism in DKA shifts from the normal fed state characterized by carbohydrate metabolism to a fasting state
characterized by fat metabolism.

Secondary consequences of the primary metabolic derangements in DKA include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced osmotic
diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose. Commonly, the total body water deficit is 10%, and the potassium
deficit is 5 mEq per kg of body weight. The total body potassium deficit may be
masked by the acidosis, which sustains an increased serum potassium level. The potassium level can drop precipitously once rehydration and insulin treatment start. Urinary loss of ketoanions with brisk diuresis and intact renal function also may lead to a component of hyperchloremic metabolic acidosis.


  • In the US: DKA is seen primarily in patients
    with type 1 (insulin-dependent) diabetes. The incidence is roughly 2/100
    patient years of diabetes, with about 3% of type 1 diabetic patients
    initially presenting with DKA. It can occur in type 2
    (non–insulin-dependent) diabetic patients as well.

Mortality/Morbidity: With modern fluid management, the mortality rate of DKA is about 2% per episode. Before the discovery of insulin
in 1922, the mortality rate was 100%.

Sex: No predilection exists.

DKA tends to occur in individuals
younger than 19 years, the more brittle type 1 diabetic patients, but may occur
in diabetic patients of any age.




  • Classic symptoms of hyperglycemia

    • Thirst

    • Polyuria, polydipsia

    • Nocturia

  • Other symptoms

    • Generalized weakness

    • Malaise/lethargy

    • Nausea/vomiting

    • Decreased perspiration

    • Fatigue

    • Anorexia or increased appetite

    • Confusion

  • Symptoms of associated infections and conditions

    • Fever

    • Dysuria

    • Chills

    • Chest pain

    • Abdominal pain

    • Shortness of breath


  • General signs

    • Ill appearance

    • Dry skin

    • Labored respirations

    • Dry mucous membranes

    • Decreased skin turgor

    • Decreased reflexes

  • Vital signs

    • Tachycardia

    • Hypotension

    • Tachypnea

    • Hypothermia

    • Fever, if infection

  • Specific signs

    • Ketotic breath (fruity, with acetone smell)

    • Confusion

    • Coma

    • Abdominal tenderness


  • The most common scenarios are underlying or
    concomitant infection (40%), missed insulin treatments (25%), and newly
    diagnosed, previously unknown diabetes (15%). Other associated causes make
    up roughly 20% in the various series.

  • Urinary tract infections (UTIs) are the single most
    common infection associated with DKA, but many other associated illnesses
    need to be considered as well.

  • Myocardial infarction

  • Cerebrovascular accident
  • Complicated pregnancy

  • Trauma

  • Stress

  • Surgery

  • Idiopahic (20-30%)



4 of 10

Alcoholic Ketoacidosis
Appendicitis, Acute
Hyperglycemic Nonketotic Coma
Lactic Acidosis
Metabolic Acidosis
Myocardial Infarction
Shock, Septic
Toxicity, Salicylate
Urinary Tract Infection,
Urinary Tract Infection,

Other Problems to be

Acute hypoglycemia coma



Lab Studies:

  • Glucose: Levels may be as low as 250 mg/dL. The
    clinician can do a fingerstick glucose while waiting for the serum
    chemistry panel.

  • Sodium: The osmotic effect of hyperglycemia moves
    extravascular water to the intravascular space. For each 100 mg/dL of
    glucose over 100 mg/dL, the serum sodium is lowered by approximately 1.6
    mEq/L. When glucose levels fall, the serum sodium will rise by a
    corresponding amount.

  • Potassium: This needs to be checked frequently, as
    values drop very rapidly with treatment. An ECG may be used to assess the
    cardiac effects of extremes in potassium levels.

  • Bicarbonate: Use in conjunction with the anion gap
    to assess degree of acidosis.

  • Complete blood count (CBC): High WBC counts (>15
    x 109/L) or marked left shift suggest underlying bacterial

  • Arterial blood gases (ABG): pH is often <7.3.
    Venous pH may be used for repeat pH measurements.

  • Ketones: The Acetest and Ketostix products measure
    blood and urine acetone and acetoacetic acid. They do not measure the more
    common ketone body, beta-hydroxybutyrate, so the patient may have
    paradoxical worsening as the latter is converted into the former during
    treatment. Specific testing for beta-hydroxybutyrate can be performed by
    many laboratories.

  • Urinalysis (UA): Look for glycosuria and urine
    ketosis. Use to detect underlying UTI.

  • Osmolality: Measured as 2(Na+) (mEq/L) +
    glucose (mg/dL)/18 + BUN(mg/dL)/2.8. Patients with DKA who are in a coma
    typically have osmolalities >330 mOsm/kg H20. If the
    osmolality is less than this in a comatose patient, search for another
    cause of obtundation.

  • Phosphorous: If the patient is at risk for
    hypophosphatemia (eg, poor nutritional status, chronic alcoholism), then
    serum phosphorous should be determined.

  • Hyperamylasemia may be seen even in the absence of

  • BUN is increased.

  • Anion gap is higher than normal.

  • Repeat labs are critical. Potassium needs to be
    checked every 1-2 hours during initial treatment. Glucose and other
    electrolytes should be checked every 2 hours or so during initial
    aggressive volume, glucose, and electrolyte management. If the initial
    phosphorous was low, it should be monitored every 4 hours during therapy.

  • Be aware that high serum glucose levels may lead to
    dilutional hyponatremia; high triglyceride levels may lead to factitious
    low glucose; and high levels of ketone bodies may lead to factitious
    elevation of creatinine.

Imaging Studies:

  • Chest x-ray (CXR): Rule out pulmonary infection.

  • CT scan: The threshold should be low for obtaining a
    head CT scan in children with DKA who have altered mental status, as this
    may be caused by cerebral edema.

  • Telemetry: Consider telemetry to monitor for
    ischemia and hypokalemia effects.

Other Tests:

  • Electrocardiogram (ECG): DKA may be precipitated by
    a cardiac event, and the physiological disturbances of DKA may cause
    cardiac complications


  • Intubation and airway management should be
    considered for coma (especially if the patient is hypoventilating or
    unable to protect the airway) or for cerebral edema.

  • Nasogastric tube should be considered to prevent
    aspiration if the patient is comatose.



Prehospital Care: Isotonic saline solution should be
given as a bolus up to 1 L, depending on the patient's vital signs and other
indicators of hypovolemia.

Emergency Department
extreme vigilance for any concomitant process such as infection,
cerebrovascular accident (CVA), MI, sepsis, or deep venous thrombosis (DVT).

  • Fluid resuscitation is a critical part of treating
    DKA. Intravenous (IV) solutions replace extravascular and intravascular
    fluids and electrolyte losses. They also dilute both the glucose level and
    the levels of circulating counterregulatory hormones. Insulin is needed to
    help switch from a catabolic to an anabolic state, with uptake of glucose
    in tissues and the reduction of gluconeogenesis as well as free fatty acid
    and ketone production.

    • Administer 1 L of isotonic
      saline (or more if needed for significant hypovolemia) in the first hour.
      Further isotonic saline should be administered at a rate appropriate to
      maintain adequate blood pressure and pulse, urinary output, and mental
      status. If a patient is severely dehydrated and significant fluid
      resuscitation is needed, switching to a balanced electrolyte solution
      (such as Normosol-R, in which some of the chloride in isotonic saline is
      replaced with acetate) may help to avoid the development of a hyperchloremic

    • After initial stabilization with
      isotonic saline, switch to half-normal saline at 200-1000 mL/h
      (half-normal saline matches losses due to osmotic diuresis).

  • Potassium replacement

    • Add 20-40 mEq/L of KCl to each
      liter of fluid once K+ is under 5.5 mEq/L.

    • Can give potassium as follows:
      two thirds as KCl, one third as KPO4.

  • Bicarbonate typically is not replaced, although some
    physicians do so when pH <7. Administration of bicarbonate has been
    correlated with cerebral edema in children.

  • Phosphate and magnesium replacements typically are
    not needed, since levels correct when patient resumes eating.

  • Use data flow sheets to monitor timing of labs and

Consultations: Intensivist



Treatment of ketoacidosis
should aim at correcting dehydration, reversing the acidosis and ketosis,
reducing plasma glucose concentration to normal, replenishing electrolyte and
volume losses, and identifying the underlying cause.
Please see specific chapters for dosing regimens.

Category: Antihyperglycemic
These agents lower plasma glucose and ketone levels.

Drug Name

(Humulin, Humalog, and Novolin) -- In addition to lowering glucose levels and
preventing further ketone production, insulin stimulates cellular uptake of
potassium within 20-30 min. Glucose should be administered along with insulin
to prevent hypoglycemia once glucose levels are lowered to 200 mg/dL. Monitor
blood glucose levels frequently.
Regular insulin is used to reduce blood glucose levels in DKA.

Adult Dose

dose: 0.1-0.15 U/kg IV bolus (note that some consider this optional)
Maintenance ED doses: 0.1 U/kg/h IV infusion, typically 5-7 U/h

Pediatric Dose

as in adults


hypersensitivity, hypoglycemia; profound hypokalemia


a clinical concern in the treatment of DKA in the ED


- Usually safe but benefits must outweigh the risks.


glucose and institute D5 isotonic saline with 3-7 U/h insulin IV/IM/SC once
serum glucose reaches 200 mg/dL to prevent iatrogenic hypoglycemia

Category: Mineral solutions
-- These solutions
replenish mineral deficiencies.

Drug Name

chloride -- Potassium deficits are high in DKA even with paradoxically high K+
due to acidotic state, which shifts H+ into cells and K+
out of cells into blood. Monitor potassium q1-2 h initially. Repletion with
potassium phosphate often thought unnecessary, although some recommend giving
potassium phosphate to replete both of these electrolytes.

Adult Dose

mEq/L of KCl to each liter of fluid once K+ is <5.5 mEq/L; give
two thirds as KCl and one third as KPO4+

Pediatric Dose

as in adults


renal failure, conditions associated with potassium retention, oliguria or
azotemia, crush syndrome, severe hemolytic reactions, anuria, and
adrenocortical insufficiency


ACE inhibitors may elevate serum potassium concentrations; potassium-sparing
diuretics and potassium-containing salt substitutes can produce severe
hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin
toxicity; caution if discontinuing potassium administration in patients
maintained on digoxin


- Safe in pregnancy


patients with elevated potassium initially, hold until K+ <5.5
mEq/L—should happen rapidly with saline/insulin treatment; can check ECG to
assess effects of elevated potassium if in doubt, but mildly elevated
potassium levels may not produce ECG changes



Further Inpatient

  • Admit to ICU or floors depending on clinical status.
    Patients undergoing continuous insulin require frequent monitoring, which
    is best done in the ICU.

  • Ocsionally, patients with mild acidosis and
    fluid/electrolyte deficits can be stabilized adequately in the ED if very
    close follow-up can be arranged.

Further Outpatient

  • Typically, patients with DKA are admitted.

  • Complications of associated illnesses, including
    sepsis and diffuse ischemic processes, are possible.

  • The leading cause of DKA mortality in children is
    cerebral edema, which occurs 4-12 hours into treatment. Recent research by
    Glaser et al indicated that cerebral edema occurs in 1% of children with
    DKA, with a mortality rate of 21% and neurologic sequelae in another 21%
    of patients.

    • Cerebral edema begins with mental
      status changes and is believed to be due partially to "idiogenic
      osmoles," which have stabilized brain cells from shrinking while the
      DKA was developing. The risk of cerebral edema is related to the severity
      and duration of DKA. It is often associated with ongoing hyponatremia.
      Cerebral edema is correlated with the administration of bicarbonate.
      Concerns about the role of overaggressive or overly hypotonic fluid
      resuscitation as a cause of the edema have been raised in the past.

    • Cerebral edema is a complication
      that affects primarily children.

  • Hypokalemia is a complication that is precipitated
    by failing to rapidly address the total body potassium deficit brought out
    by rehydration and insulin treatment, which not only reduce acidosis but
    directly facilitate potassium reentry into the cell

  • Hypoglycemia may result from inadequate monitoring
    of glucose levels during insulin therapy.

  • Acute pulmonary edema potentially is related to
    aggressive or excessive fluid therapy.

  • Other complications

    • CVT
    • MI
    • Acute gastric dilatation

    • Erosive gastritis
    • Late hypoglycemia

    • Respiratory distress
    • Infection

    • Hypophosphatemia
    • Mucormycosis


  • DKA accounts for 14% of all hospital admissions of
    patients with diabetes and 16% of all diabetes-related fatalities.

  • The overall mortality rate is 2% or less currently.

  • In children younger than 10 years, DKA causes 70% of
    diabetes-related fatalities.

Patient Education:

  • Control blood glucose carefully.

  • Monitor glucose particularly closely during
    infection, trauma, and other periods of stress.




  • Failure to consider other coexisting illnesses, such
    as pelvic or rectal abscess, pneumonia, and silent MI

  • Failure to evaluate for other causes of coma if
    osmolality is relatively normal

Special Concerns:

  • Pregnant patients

    • A fetal mortality rate as high
      as 30% is associated with DKA. The rate is as high as 60% in DKA with

    • Fetal death typically occurs in
      women with overt diabetes, but it may occur with gestational diabetes.

  • Children: Be alert to headache and altered mental
    status (eg, decreased alertness) since these are signs of impending
    cerebral edema.



  • Bell DS, Alele J: Diabetic ketoacidosis: Why early
    detection and aggressive treatment are crucial. Postgraduate Medicine
    1997; 101: 193-8, 203-4[Medline].

  • Brandenburg MA, Dire DJ: Comparison of arterial and
    venous blood gas values in the initial emergency department evaluation of
    patients with diabetic ketoacidosis. Ann Emerg Med 1998; 31(4):

  • Glaser N, Barnett P, McCaslin I: Risk Factors for
    Cerebral Edema in Children with Diabetic Ketoacidosis. NEJM 2001; 344:

  • Green SM, Rothrock SG, Ho JD, et al: Failure of
    adjunctive bicarbonate to improve outcome in severe pediatric diabetic
    ketoacidosis. Ann Emerg Med 1998; 31: 41-8[Medline].

  • Grimberg A, Cerri RW, Satin-Smith M: The "two
    bag system" for variable intravenous dextrose and fluid
    administration: benefits in diabetic ketoacidosis management. J Pediatr
    1999 Mar; 134(3): 376-8[Medline].

  • Kitabchi AE, Wall BM: Diabetic ketoacidosis. Med
    Clin North Am 1995 Jan; 79(1): 9-37[Medline].

  • Klekamp J, Churchwell KB: Diabetic ketoacidosis in
    children: initial clinical assessment and treatment. Pediatr Ann 1996 Jul;
    25(7): 387-93[Medline].

  • Marinac JS, Mesa L: Using a severity of illness
    scoring system to assess intensive care unit admissions for diabetic
    ketoacidosis. Crit Care Med 2000 Jul; 28(7): 2238-41[Medline].

  • Umpierrez GE, Khajavi M, Kitabchi AE: Review:
    Diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic syndrome.
    Am J Med Sci 1996; 311: 225-33[Medline].

  • Warner EA, Greene GS, Buchsbaum MS: Diabetic
    ketoacidosis associated with cocaine use. Arch Intern Med 1998; 158 (16):

  • Westphal SA: The occurrence of diabetic ketoacidosis
    in non-insulin-dependent diabetes and newly diagnosed diabetic adults. Am
    J Med 1996; 101: 19-24[Medline].

  • Whiteman VE, Homko CJ, Reece EA: Management of
    hypoglycemia and diabetic ketoacidosis in pregnancy. Obstet Gynecol Clin
    North Am 1996; 23: 87-107[Medline].


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