Diabetes mellitus (pediatrics): Clinical sciences

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Diabetes mellitus (pediatrics): Clinical sciences

Endocrine Midterm

Endocrine Midterm

Pituitary gland histology
Pituitary apoplexy
Pituitary adenoma
Hypopituitarism: Pathology review
Anatomy of the diencephalon
Sheehan syndrome
Hypopituitarism
Kallmann syndrome
Hypoprolactinemia
Hyperprolactinemia
Pituitary tumors: Pathology review
Thyroid and parathyroid gland histology
Parathyroid disorders and calcium imbalance: Pathology review
Anatomy of the thyroid and parathyroid glands
DiGeorge syndrome
Parathyroid hormone
Hypoparathyroidism
Thymic aplasia
Hyperparathyroidism
Hyperparathyroidism: Clinical sciences
Approach to hypocalcemia: Clinical sciences
Hyperphosphatemia
Hypercalcemia
Bone remodeling and repair
Hypomagnesemia
Approach to hypocalcemia (pediatrics): Clinical sciences
Thyroid nodules and thyroid cancer: Pathology review
Thyroid cancer
Thyroid nodules: Clinical sciences
Thyroid carcinoma: Clinical sciences
Thyroid hormones
Thyroid eye disease (NORD)
Thyroid storm
Hashimoto thyroiditis
Postpartum thyroiditis
Riedel thyroiditis
Hashimoto thyroiditis: Clinical sciences
Subacute granulomatous thyroiditis
Anatomy clinical correlates: Viscera of the neck
Approach to hypothyroidism: Clinical sciences
Approach to hyperthyroidism and thyrotoxicosis: Clinical sciences
Hyperthyroidism: Pathology review
Euthyroid sick syndrome
Hypothyroidism: Pathology review
Hypothyroidism
Graves disease: Clinical Sciences
Hyperthyroidism medications
Hypothyroidism medications
Thyroglossal duct cyst
Pancreas histology
Pancreatic cancer
Pancreatitis: Pathology review
Chronic pancreatitis
Approach to pancreatic masses: Clinical sciences
Acute pancreatitis
Pancreatic secretion
Insulins
Insulin
Hypoglycemics: Insulin secretagogues
Pancreatic neuroendocrine neoplasms
Approach to hypoglycemia: Clinical sciences
Diabetes mellitus: Pathology review
Growth hormone deficiency
Diabetes mellitus
Hypokalemia
Diabetes mellitus (Type 1): Clinical sciences
Diabetic ketoacidosis: Clinical sciences
Diabetes mellitus (pediatrics): Clinical sciences
Diabetes in pregnancy (GDM, T1DM, and T2DM): Clinical sciences
Approach to hyperkalemia: Clinical sciences
Diabetes mellitus (Type 2): Clinical sciences
Approach to hypoglycemia (pediatrics): Clinical sciences
Hunger and satiety
Approach to diabetes in pregnancy: Clinical sciences
Glucagon
Growth hormone and somatostatin
Somatostatin
Managing diabetes during the holidays: Information for patients and families
Diabetes insipidus and SIADH: Pathology review
Diabetic nephropathy
Gestational diabetes
Chronic kidney disease: Clinical sciences
Obesity and metabolic syndrome: Clinical sciences
Dyslipidemia: Clinical sciences
Miscellaneous hypoglycemics
Adrenal hormone synthesis inhibitors
Adrenal gland histology
Adrenal insufficiency: Pathology review
Congenital adrenal hyperplasia
Adrenal insufficiency: Clinical sciences
Adrenal masses: Pathology review
Primary adrenal insufficiency
Cushing syndrome
Pheochromocytoma: Clinical sciences
Glucocorticoids
Mineralocorticoids and mineralocorticoid antagonists
Cortisol
Cushing syndrome and Cushing disease: Clinical sciences
Endocrine system anatomy and physiology
Cushing syndrome and Cushing disease: Pathology review
Multiple endocrine neoplasia
Multiple endocrine neoplasia: Pathology review
Multiple endocrine neoplasia: Clinical sciences
Prolactinoma
Potassium sparing diuretics
Polycystic ovary syndrome (PCOS): Clinical sciences
Conn syndrome

Decision-Making Tree

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Diabetes mellitus, or DM, is a condition characterized by reduced insulin secretion or resistance to insulin, which eventually results in various issues with carbohydrate, protein, and fat metabolism.

Now, there are three main types of diabetes mellitus, including type 1 diabetes mellitus, type 2 diabetes mellitus, and monogenic diabetes, also called maturity-onset diabetes of the young.

Now, if your pediatric patient is presenting with a chief concern suggesting Diabetes Mellitus, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, begin IV fluids, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Once you initiate acute management, obtain a focused history and physical examination, and obtain labs, including serum blood glucose, BMP, serum beta-hydroxybutyrate concentration, urinalysis, and arterial blood gas. Your patient or their caregiver often reports polyuria, polydipsia, and polyphagia, as well as vomiting, abdominal pain, or confusion. The physical examination may reveal somnolence often in combination with tachycardia, hypotension, and Kussmaul respirations, which refer to a consistently rapid, deep pattern of breathing. Other important findings include fruity breath and dry mucous membranes!

At this point, suspect Diabetic Ketoacidosis or DKA and assess the criteria for biochemical diagnosis. These include a blood glucose level greater than 200 milligrams per deciliter; arterial pH less than 7.3 OR serum bicarbonate level less than 15 milliequivalents per liter; a beta-hydroxybutyrate concentration of 3 millimoles per liter or higher, and moderate to severe ketonuria.

If your patient meets the criteria, diagnose DKA. Now, keep in mind that up to 25% of children with new-onset DM first present with DKA, and many report a precipitating event, such as an infection or acute illness. However, DKA can also occur in patients with previously diagnosed DM as a result of disrupted insulin treatment.

Once you diagnose DKA, begin IV fluid resuscitation to correct dehydration and hyperosmolality, and start an IV insulin drip. Additionally, begin electrolyte repletion, and monitor sodium and potassium levels. However, be cautious because aggressive correction of hyperglycemia can lead to rapid fluctuations in serum osmolality, resulting in cerebral edema and subsequent complications, like seizures. If you suspect cerebral edema, give intravenous mannitol. Finally, don’t forget to treat any underlying cause!

Now, here’s a clinical pearl to keep in mind! Another important complication of diabetes mellitus is hyperosmolar hyperglycemic syndrome. If labs reveal glucose levels above 600 mg/dL; pH above 7.3; bicarbonate levels greater than 18 with variable anion gap; serum osmolality above 320 mOsm/kg; with minimal to none serum and urine ketones, diagnose hyperosmolar hyperglycemic syndrome. Keep in mind that this condition is typically seen in older patients with type 2 diabetes mellitus!

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients. First, obtain a focused history and physical exam. Patients or their caregivers typically report 3 P’s, which include polydipsia, polyphagia, and polyuria. Moreover, previously toilet-trained children may even develop secondary enuresis. Some patients might report weight loss as well as a family history of DM or other autoimmune conditions, such as thyroid or celiac disease. Physical exam findings are often unremarkable but may include oral or perineal thrush as well as dry mucous membranes.

At this point, suspect diabetes mellitus, so order labs, including hemoglobin A1c, fasting and random blood glucose, and consider obtaining an oral glucose tolerance test. Next, assess findings using the diagnostic criteria for diabetes mellitus. These include hemoglobin A1C of 6.5 percent or greater; fasting blood glucose of 126 milligrams per deciliter or greater; a random blood glucose 200 milligrams per deciliter or greater; or a blood glucose during a 2-hour OGTT that is 200 milligrams per deciliter or greater. However, remember, these criteria are only useful if your patient is presenting with symptoms of DM. If asymptomatic, you might need to repeat testing to confirm diabetes.

Now, if your patient meets the criteria, diagnose Diabetes Mellitus, and order additional labs to identify the type. Start by obtaining C-peptide levels and islet cell autoantibodies, such as glutamic acid decarboxylase, or GAD65.

Now, here’s a clinical pearl to keep in mind! C-peptide is a portion of the proinsulin molecule that’s removed during insulin production. Even though C-peptide and insulin are secreted into the blood in similar amounts, insulin is metabolized more rapidly, so C-peptide levels provide a better estimate of insulin secretion.

Sources

  1. "Children and Adolescents: Standards of Care in Diabetes-2023" Diabetes Care (2023)
  2. "Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2018" Diabetes Care (2018)
  3. "Type 1 Diabetes in Children and Adolescents: A Position Statement by the American Diabetes Association" Diabetes Care (2018)
  4. "Diabetic Ketoacidosis" Pediatr Rev (2019)
  5. "Type 1 diabetes mellitus" Pediatr Rev (2013)
  6. "Management of Type 1 Diabetes in Children in the Outpatient Setting" Pediatr Rev (2022)
  7. "Type 2 Diabetes Mellitus in Childhood and Adolescence" Pediatr Rev (2021)
  8. "Nelson Essentials of Pediatrics, 8th ed." Elsevier (2023)
  9. "American Academy of Pediatrics Textbook of Pediatric Care, 2nd ed." American Academy of Pediatrics (2017)