Diabetic Ketoacidosis (Case 8)

 A family reports that their 5-year-old son has been increasingly confused over the last several hours. His emergency department vital signs show a heart rate of 180 beats/min, a blood pressure of 80/50 mm Hg, a tem-perature of 36.1°C (97°F), and slow, deep respirations. His capillary refill is 5 seconds, and he has skin tenting as well as altered mental sta-tus. His mother reports that he has had a several pounds of weight loss over the last few weeks, has been increasingly tired for several days, and that she has been concerned about his 2- or 3-day history of thirst, fre-quent daytime urination, and new onset of nocturnal enuresis. 

What is the most likely diagnosis?

What is the best therapy?

Summary: A 5-year-old with weight loss, polydipsia, and polyuria who pres-ents with dehydration and Kussmaul breathing.

Most likely diagnosis: Diabetic ketoacidosis (DKA).

Best therapy: Fluid rehydration, insulin, and close monitoring of serum glu-cose level and acidemia.



1. Understand the presentation of patients in DKA.

2. Appreciate the initial treatment strategies in the management of DKA.

3. Become familiar with pitfalls in the treatment of DKA.


This patient is in extremis. He is tachycardic, hypotensive, hypothermic, and has delayed capillary refill with tenting of the skin. The ABCs of medicine apply. He is confused but not obtunded; he probably requires neither his air-way controlled nor his breathing regulated. His examination suggests at least 10% dehydration; his circulatory status is marginal and requires rapid volume restoration. His history and physical examination suggest diabetes; a finger-stick glucose test confirms the diagnosis. The therapy for DKA rests on (1) aggressive volume repletion, (2) glucose control with insulin, and (3) correction of metabolic abnormalities.


Diabetic Ketoacidosis


KETOACIDOSIS: A condition resulting from deficient insulin availability, leading to lipid oxidation and metabolism rather than glucose metabolism. The insulin absence results in free fatty acid (FFA) released from adipose tis-sue and in unregulated hepatic FFA oxidation and ketogenesis.

TYPE I DIABETES: Known by a variety of names, it is caused by a severe endogenous insulin deficiency and a requirement for exogenous insulin to prevent ketoacidosis.

TYPE II DIABETES: Known by a variety of names, it usually consists of tissue-level insulin resistance (although exogenous insulin is often required) and rarely leads to ketoacidosis.

KUSSMAUL BREATHING: Deep, rapid respirations associated with acidosis. 


Patients with DKA represent a medical emergency. Such patients may require intubation, but usually this is seen later in the disease course. Children more commonly present with signs and symptoms of severe dehydration and acidosis. The history often is positive for polyuria, nausea, vomiting, and abdominal complaints. Hypothermia, hypotension, Kussmaul respirations, and acetone on the breath are common. As these signs and symptoms may be nonspecific, especially in younger children, a high index of suspicion is required to make the diagnosis.

Laboratory data demonstrate an elevated glucose level (often 400-800 mg/dL), metabolic acidosis (with anion gap, ie, excess endogenous anion production such as from lactic acid), and hyperketonemia. Serum electrolyte levels usually show hyponatremia and normal or slightly elevated potassium (despite intracellular potassium depletion). Elevated blood urea nitrogen and creatinine levels are com-monly seen, reflecting the dehydration. White blood cell counts (WCBs) often are elevated, especially if a bacterial infection is exacerbating the condition.

Treating DKA includes initial vascular volume expansion (often with normal saline) and then correction of the hyperglycemia and hyperketone-mia. Intravenous (IV) fluid boluses sufficient to stabilize the heart rate and blood pressure are sometimes required, and then a slower IV rate (usually a saline solution with or without some glucose) to replace fluid losses and to ensure adequate urine flow is initiated. Potassium is added to IV fluids after urine output is established to counteract the patient’s total body potassium depletion (treatment of the hyperglycemia and acidosis drives potassium intracellularly; hypokalemia is an avoidable complication). A continuous insulin infusion at a rate of approximately 0.1 U/kg/h is also started (a bolus of 0.1 U/kg is often given initially), with the IV rate adjusted based on the results of hourly glucose measurements. Glucose is added to IV fluids when the serum glucose level drops to approximately 250 or 300 mg/dL, and addi-tional insulin rates adjustments are made based on serum glucose levels. The low plasma pH and elevated serum ketone levels will correct significantly in the first 8 to 10 hours; the serum bicarbonate level may remain low for approximately 24 hours or more. Improvement is characterized by a decrease in IV insulin rates and resolution of the ketonuria; then, the patient can take oral feedings, and insulin is converted from the IV to subcutaneous route.

Several pitfalls should be avoided during the treatment of DKA. IV fluids with insulin and improvement in acidosis levels often are associated with a fall in serum potassium levels; addition of potassium to the IV fluids usually is indicated to prevent serious hypokalemia. Bicarbonate infusion usually is avoided except in extreme situations, because it may (1) precipitate hypokalemia, (2) shift the oxygen dissociation curve to the left, worsening organ oxygen delivery, (3) overcorrect the acidosis, and (4) result in worsen-ing cerebral acidosis while the plasma pH is being corrected (transfer into the cerebrum of CO2 formed when the bicarbonate is infused in an acid serum). Cerebral edema (etiology unknown) sometimes occurs, manifesting as headache, personality changes, vomiting, and decreased reflexes. Treatment of cerebral edema consists of reduction in IV fluid, administration of IV man-nitol, and hyperventilation. Episodes of DKA (especially in the known dia-betic) can be precipitated by bacterial infection. An evaluation for infection sources with institution of antibiotics (if appropriate) is required.

Comprehension Questions

8.1    A 14-year-old adolescent female from another state was followed for 7 years for a history of insulin-dependent diabetes mellitus. At your clinic her hemoglobin A1C is 14.9%. This laboratory test indicates which of the following?

A. Her glucose control is poor.

B. She does not have insulin-dependent diabetes.

C. She has entered the “honeymoon phase” of her diabetes.

D. She has an underlying infection.

E. She is demonstrating the Somogyi phenomenon.

8.2    Six months after being diagnosed with what appears to be insulin-dependent diabetes, the 5-year-old in the case presentation has a sig-nificant decrease in his insulin requirement. Which of the following is the most likely explanation?

A. His diagnosis of insulin-dependent diabetes was incorrect.

B. He had a chronic infection that is now under control.

C. He has followed his diabetes diet so well that he requires less insulin.

D. He is demonstrating the Somogyi phenomenon.

E. He has entered the “honeymoon phase” of his diabetes.

8.3    A 15-year-old adolescent female has experienced abdominal pain, vomiting, and lethargy for 3 days. Her chest and throat examinations are clear, but her abdominal examination is significant for right lower quadrant pain. Rectal examination is equivocal for pain, and her pelvic examination is remarkable for pain upon movement of her cervix. Laboratory data include a white blood cell count of 18,000/mm3, serum glucose level of 145 mg/dL, and serum bicarbonate level of 21 mEq/dL. Her urinalysis is remarkable for 1+ white blood cells, 1+ glucose, and 1+ ketones. Which of the following is the most likely diagnosis?

A. Appendicitis

B. Diabetic ketoacidosis (DKA)

C. Gastroenteritis

D. Pelvic inflammatory disease (PID)

E. Right lower lobe pneumonia

8.4    A 16-year-old obese adolescent female has enuresis, frequent urination, a white vaginal discharge, and a dark rash around her neck. Her serum glu-cose level is 250 mg/dL, and her urinalysis is positive for 2+ glucose but is otherwise negative. Which of the following is the most likely diagnosis?

A. Chemical vaginitis

B. Chlamydia cervicitis

C. Psoriasis

D. Type II diabetes

E. Urinary tract infection (UTI)


8.1    A. The patient likely has poor diabetes control. The hemoglobin A1C, commonly used to follow glucose control, measures the average glu-cose levels over the previous 2 or 3 months. The hemoglobin A1C goal for most diabetics is 6% to 9%. Levels greater than 12% suggest poor control, and levels 9% to 12% represent fair control. In the Somogyi phenomenon, a patient has nocturnal hypoglycemic episodes mani-fested as night terrors, headaches, or early morning sweating and then presents a few hours later with hyperglycemia, ketonuria, and gluco-suria. Counter-regulatory hormones, in response to the hypoglycemia, cause the hyperglycemia.

8.2    E. Up to 75% of newly diagnosed diabetics have a progressive decrease in the daily insulin requirement in the months after their diabetes diagnosis; a few patients temporarily require no insulin. This “honey-moon” period usually lasts a few months, and then an insulin require-ment returns. Patients are told that the “honeymoon” period is not a cure and that they should expect a return to insulin requirement.

8.3    D. The patient likely has PID; glucosuria is a stress response to the infection and does not represent glucose metabolism problems. All of the options in the question can cause abdominal pain. Although dia-betes mellitus is in the differential, DKA more likely presents with ketoacidosis (significantly decreased serum bicarbonate levels) and high serum glucose levels.

8.4    D. The description is of an obese adolescent female with candida vaginitis (the vaginal discharge) and acanthosis nigricans (the nuchal dark rash) consistent with type II diabetes. This condition is far more common in overweight children, especially those with a family history of the condition.

Clinical Pearls

Diabetic ketoacidosis (DKA) is a medical emergency that can present with nonspecific signs of dehydration, polyuria, nausea, vomiting, and abdomi-nal complaints.Hypothermia, hypotension, Kussmaul respirations, and ace-tone on the breath are also seen. A high index of suspicion is required to make the diagnosis, especially in the younger child.

Cerebral edema is a potentially life-threatening complication in diabetic ketoacidosis treatment presenting as headache, personality changes, vom-iting, and decreased reflexes.

Electrolyte disturbances are common in diabetic ketoacidosis.Hypokalemia can occur during treatment if adequate sources are not provided. Bicarbonate administration usually is avoided except in extreme situations for a variety of physiologic reasons.


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Stanton BF, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, PA: WB Saunders;


Cooke DW. Type 2 diabetes mellitus. In: McMillan JA, Feigin RD, DeAngelis CD,

Jones MD, eds. Oski’s Pediatrics: Principles and Practice. 4th ed. Philadelphia, PA:

Lippincott Williams & Wilkins; 2006:2115-2122.

Gitelman SE. Diabetes mellitus. In: Rudolph CD, Rudolph AM, Hostetter MK, Lister G,

Siegel NJ, eds. Rudolph’s Pediatrics. 21st ed. New York, NY: McGraw-Hill; 2003:


Plotnick LP. Type 1 (insulin-dependent) diabetes mellitus. In: McMillan JA, Feigin

RD, DeAngelis CD, Jones MD, eds. Oski’s Pediatrics: Principles and Practice. 4th ed.

Philadelphia, PA: Lippincott Williams & Wilkins; 2006:2103-2115.

A 2-month-old child you have followed since birth arrives for his routine

“baby shots.” His mother’s pregnancy was uncomplicated, and he

has been healthy without significant problems.

➤ What is the next step in the care of this patient?

Diabetic Ketoacidosis (Case 8) Diabetic Ketoacidosis (Case 8) Reviewed by WebofPediatric on December 15, 2021 Rating: 5

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