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Authors: Robert Daum,Jason Canel

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(B) sodium bicarbonate drip
(C) bolus of IV insulin
(D) bolus of IV sodium bicarbonate
(E) a subcutaneous dose of insulin

8.
What would the most appropriate initial management be if her serum blood sugar was 250 mg/dL, serum ketones small, pH 7.38, and she appeared well hydrated?

(A) a subcutaneous dose of insulin
(B) bolus of IV insulin
(C) start an oral hypoglycemic medication
(D) watch and repeat serum glucose in 6-24 hours
(E) bolus of normal saline

9.
What would the most appropriate initial management be if her serum blood sugar was 180 mg/dL, ketones negative, pH 7.38, and she has had an illness with a fever for the last week?

(A) a subcutaneous dose of insulin
(B) bolus of IV insulin
(C) start an oral hypoglycemic medication
(D) watch and repeat serum glucose in 6 hours
(E) none of the above

10.
Her mother, maternal aunt, maternal grandmother, and maternal great-grandmother all have a history of diabetes. This family history would worry you most about what type of diabetes?

(A) type 1 diabetes
(B) type 2 diabetes
(C) atypical diabetes
(D) gestational diabetes
(E) maturity-onset diabetes of youth

11.
In a child in DKA, when would you worry most about the development of cerebral edema?

(A) before any treatment
(B) immediately after the initial bolus of normal saline
(C) with the start of insulin therapy
(D) several hours after the institution of therapy
(E) once the ketosis clears

12.
Which of the following is not a manifestation of cerebral edema?

(A) tachycardia
(B) papilledema
(C) widened pulse pressure
(D) headache
(E) coma

13.
Which of the following would not be an appropriate initial treatment for cerebral edema associated with DKA?

(A) decrease IV fluids
(B) stop insulin therapy
(C) hyperventilation
(D) mannitol
(E) all of the above are appropriate treatments

14.
You diagnose your patient with type 1 diabetes and start her on subcutaneous insulin. Several months later the mother calls you to inform you that her daughter is ill and has vomited 4 times in the last 2 hours. She has not been eating well, and her mother is unsure of what to do. You would advise she do which of the following first?

(A) hold the insulin since she is not eating
(B) check urine ketones
(C) come directly to the emergency department
(D) push fluids and call you back in 4 hours
(E) administer glucose tablets

15.
Several months later you get a page at 6 am from the child’s mother because the child is having a seizure. You would advise the mother to do which of the following first?

(A) administer glucose tablets
(B) administer glucose gel
(C) give orange juice
(D) hold the insulin dose
(E) administer glucagon

16.
On a routine follow-up 2 years later, your patient reports that she checks her blood sugar 4 times daily (they range from 80 to 120), and she follows her meal plan consistently. She does all of her own care. You note on examination that she has lost 10 lb in the past 3 months and is now below the 5th percentile for weight. Her hemoglobin A1c is elevated at 12%. What should be your main concern at this time?

(A) anorexia
(B) poor compliance
(C) insulin resistance
(D) celiac disease
(E) hyperthyroidism

17.
On your initial examination, you notice that the patient is obese and has acanthosis nigricans. This can be a marker for which of the following?

(A) hyperglycemia
(B) type 1 diabetes
(C) autoimmunity
(D) hyperandrogenism
(E) hyperinsulinism

18.
On hospital follow-up in 3 months, your patient has gained 10 kg and now has a body mass index (BMI) of 36. Which of the following would be most helpful with distinguishing between type 1 and type 2 diabetes in your patient?

(A) reported blood glucose
(B) required insulin dosage
(C) hemoglobin A1c level
(D) C-peptide
(E) family history

ANSWERS

 

1.
(D)
Diabetes mellitus. Typical clinical symptoms of diabetes mellitus include polyuria, polydipsia, and polyphagia. Vomiting is often seen in DKA associated with ketosis. Abdominal pain is also present in many cases and may mimic appendicitis or pancreatitis. The abdominal pain usually resolves within a few hours of fluid and insulin therapy. Cerebral obtundation can be present and is usually related to the degree of hyperosmolarity. Kussmaul respirations (deep, sighing, and rapid) are often seen with profound acidosis.

2.
(E)
Urinalysis. A urinalysis is an important first step to detect glucosuria. A serum amylase and abdominal ultrasound would only be required if the patient’s abdominal pain did not subside after several hours of fluid resuscitation and improvement of the patient’s metabolic state. A hemoglobin A1c is important to confirm the presence of hyperglycemia over the last several months and is important in long-term follow-up of the patient, but it does not usually help in the acute management of the patient.

3.
(A)
Hyperkalemia. Measured serum potassium is usually normal to high; however, patients are usually depleted of total body potassium for the following reasons: insulin deficiency causes decreased Na/K adenosine triphosphatase (ATPase) activity, and decreased Na/K exchange leading to increased extracellular K, acidosis causes exchange of K from intracellular to extracellular compartment in exchange for H+ ions, which move into the cell along a concentration gradient, and K+ is then lost in part via osmotic diuresis and vomiting, and in part via the actions of aldosterone, which is elevated secondary to volume depletion. Blood glucose in DKA is typically greater than 300 mg/dL. However, the blood glucose can be less than 300 mg/dL in known diabetics because of vomiting with decreased carbohydrate intake and continued insulin administration. The primary mode of ketoacid production in DKA is from free fatty acid. The ketoacids relative to DKA are betahydroxybutyric acid and acetoacetic acid. Acetone has no effect on blood pH but is clinically important because of its characteristic odor. Most laboratories measure acetoacetate in blood and urine. However, the ratio of acetoacetate to beta-hydroxybutyrate is 1:3 in the fasted state and 1:7-1:15 in DKA. Thus the degree of ketosis in DKA is typically underestimated. Acidosis is defined as a blood pH less than 7.3 or serum bicarbonate less than 15 mEq/L. In DKA, acidosis is predominantly because of the accumulation of ketoacids, and thus patients have an increased anion gap. Other mechanisms contributing to acidosis include lactic acidosis from tissue hypoperfusion and hyperchloremic acidosis during fluid replacement. In general, the degree of acidosis in DKA bears no relation to the degree of hyperglycemia.

4.
(D)
Prolactin. The cardinal hormonal alterations seen in diabetic ketoacidosis include an absolute or relative insulin deficiency, with an excess of the stress hormones epinephrine, cortisol, and growth hormone (GH). Epinephrine activates glycogenolysis, gluconeogenesis, and lipolysis, and it inhibits insulin release by the pancreas. Cortisol decreases glucose use in muscle and stimulates gluconeogenesis. GH increases lipolysis and impairs insulin action on muscle. The catabolic and metabolic effects of each of the stress hormones are accentuated during insulin deficiency. Prolactin plays no known role in DKA.

5.
(D)
She should have additional potassium in the IV fluids. The serum sodium is usually factitiously low because of the hyperglycemia. For every 100 mg/dL glucose increment over 100 mg/dL, there is a decrease of 1.6 mEq/L sodium. Thus this patient’s true sodium is closer to 139 mEq/L. Measured serum potassium is usually normal or high, but patients are usually depleted of total body potassium (see answer to question 3). It is therefore important to treat with 30-40 mEq/L K+ once the child urinates because correction of acidosis, restoration of intravascular volume, insulin, and improvement of renal function tend to decrease extracellular K+. Approximately a fourth to a half of K+ administered during fluid replacement is lost in the urine. Hypokalemia is one of the avoidable causes of fatality in DKA. It is also important to monitor and replace phosphate because these patients can have a total body depletion of phosphate as a result of extracellular shifting and subsequent loss in the urine because of the catabolic state. Furthermore, with insulin treatment and fluid replacement, phosphate shifts back into the intracellular compartment, and a hypophosphatemic state occurs if phosphate is not replaced. Hypophosphatemia impairs insulin action and results in a decrease in synthesis of adenosine triphosphate (ATP) and other energy intermediates. Sodium bicarbonate should only be used if the serum pH is less than 7.1 and if the patient is unstable. Sodium bicarbonate should never be administered as a bolus. Serum blood glucose should be lowered slowly to avoid osmotic shifts.

6.
(E)
Rise in CSF pH. The use of sodium bicarbonate in DKA may increase the risk of cerebral edema because of osmotic shifts. Other drawbacks include hypokalemia, impaired tissue oxygenation with left shift of the oxyhemoglobin dissociation curve, rebound alkalosis, sodium overload, and the potential for a paradoxical fall in CSF pH while correcting peripheral acidosis.

7.
(A)
Bolus of normal saline. Dehydration is virtually universal in patients with DKA, and if unrecognized or mismanaged, it contributes significantly to the morbidity and mortality of DKA. The degree of dehydration varies from patient to patient, and the extent of the losses is unpredictable in any given patient. In DKA, there is an osmotically driven shift of water from intracellular to extracellular compartments. This results in underestimation of the extent of dehydration and is responsible for the unusual laboratory finding of hyponatremia despite dehydration and hyperosmolarity. The three main mechanisms of water and electrolyte loss in DKA include osmotic diuresis secondary to hyperglycemia, losses via the respiratory tract secondary to hyperventilation from metabolic acidosis, and losses from the gastrointestinal (GI) tract from vomiting. Serum blood sugar typically decreases with a normal saline bolus. To avoid rapid shifts in osmolality, the serum glucose should be lowered by 100 mg/dL per hour. Thus a continuous insulin drip is preferred to a bolus of either IV or subcutaneous insulin because it allows titration of the insulin based on the blood glucose response. Sodium bicarbonate should be avoided as discussed in the answer to question 6.

8.
(A)
A subcutaneous dose of insulin. In this situation, the patient is not in DKA with the lack of acidosis and will respond to subcutaneous insulin.

9.
(D)
Watch and repeat serum glucose in 6 hours. In this situation, the child may have stress-induced hyperglycemia rather than diabetes mellitus, which warrants close following and treatment if worsening hyperglycemia or ketosis develops. There are no current data to suggest that children with stressinduced diabetes in the absence of islet cell and GAD-65 autoimmunity are a greater risk of developing diabetes in the future.

BOOK: Pediatric Examination and Board Review
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