Metabolic Glucose & Hormal Regulation - Diabetes Mellitus

Diabetes Mellitus

Metabolic disorders characterized by impaired glucose transport into cells.

Lack of insulin production OR Insulin resistance

↑ glucose accumulates in the bloodstream → systemic complications

Type 1 diabetes (juvenile diabetes)

Autoimmune-generated destruction of the pancreatic beta cells causes lack of insulin→ lifelong insulin replacement.

Children with type 1 diabetes present with

weight loss, polyuria, nocturia, polydipsia, irritability, and dehydration

Type 2 Diabetes

Cells insensitive to insulin; from genetic predisposition, and or lifestyle factors

Type 2 Diabetes requires

dietary modification, lifestyle modification, weight management, and sometimes the addition of medications

Type 1 Diabetes Risk factors

Genetics

Immune system dysfunction

Type 1 Diabetes Presents as

Hyperglycemia without acidosis

DKA

Type & Diabetes intial symptoms

Polydipsia

Polyuria

weight loss

Dehydration

Hyperglycemia

ketonemia (or ketonuria) - nausea, vomiting

Type 1 Diabetes New Dx-No acidosis:

Admit

SQ insulin begins

Hydration

Monitor labs: chemistries, check for other autoimmune diseases

Education begins

S&Ss of Diabetic Ketoacidosis (DKA)

Polyuria (frequent urination)

Polydipsia (excessive thirst)

Polyphagia (increased hunger)

Dehydration (dry mucous membranes, poor skin turgor, prolonged cap refill)

Kussmaul respirations (deep, rapid breathing)

Fruity/acetone breath odor

Nausea and vomiting

Abdominal pain

Fatigue, weakness

Confusion or decreased level of consciousness

Tachycardia

Hypotension

Signs of metabolic acidosis (low pH, low bicarbonate)

If DKA

Dx: ↑glucose, + ketones, weight loss, abdominal pain, N&V, Kussmaul breathing

Admit to PICU (depending on pH)

DKA nursing

Assess, GCS, IV access, labs, blood gas, u/a

Always a concern for cerebral edema!*

Fluids, fluids, insulin

ASSESS, ASSESS, ASSESS- GCS, VS, labs: Glucose, electrolytes, blood gas

S&Ss of cerebral edema

worsening headache, decreased level of consciousness, irritability, restlessness, vomiting, bradycardia, hypertension (Cushing's triad), seizures, and changes in pupil size or responsiveness.Although deaths from pediatric DM are relatively low...

Dehydration & Acidosis →

Poor cerebral perfusion

Rapid Treatment (fluids/insulin) →

drop in serum osmolality

Fluid Shifts into Brain Cells →

Swelling due to osmotic imbalance

Electrolyte Disruption →

sodium shifts

Inflammatory Mediators →

Disrupted blood-brain barrier → fluid leak

Children more susceptible to cerebral edema

Higher brain water content

Immature cerebral blood flow

Often more acidotic

Brain more sensitive to treatment shifts

Although deaths from pediatric DM are relatively low...

50-80 % DM related deaths in children are caused by cerebral injury

Management of DM with DKA Hourly

VS

Blood glucose

Neuro status/GCS - Cerebral edema concern

Management of DM with DKA Every 2 Hours

Electrolytes, BUN, creatinine, venous blood gas (VBG)

BOHB (Beta-Hydroxybutyrate (BHB) Blood Test)-to check the ketone level

Management of DM with DKA Fluid replacement

Initial bolus isotonic solution (NS or RL) 10 to 20 mL/kg

Maintenance rate after bolus

K+ added as needed

Management of DM with DKA

Continous ECG

Insulin drip - 0.1 unit/kg/hour

Patient/Family Education: Diabetes management plan

Start as soon as stable (out of ICU) - Family and patient together

Insulin

Carb counting/Healthy eating

Glucose monitoring

Sick day rules

How to recognize and manage hyperglycemia and hypoglycemia

Developmental, cultural, and psychosocial considerations

Emotional impact on patient/family

Coping, school-readiness, and peer-related concerns

Discharge planning and follow-up

Endocrine, school nurse, emergency contacts, resources

Hypoglycemia S&Ss

Lethargy

Hunger

Sweating

Pallor

Seizures

Coma

Hyperglycemia S&Ss

Sweet fruity-breath

Dehydration

Decreased sodium, potassium, bicarbonate, chloride, and phosphate levels

Vomiting

Abdominal pain

Coma

Diabetes Mellitus Teaching

Long-term management requires extensive patient and parent education.

Review the meal plan and teach how to adjust when engaged in extra activity.

Insulin administration.

Blood glucose monitoring.

Oral antidiabetic therapy.

Signs and symptoms of hypo/hyperglycemia and actions to take for each.

Basal Insulin

Glargine/Lantus: peak-less

Given once daily. Lasts 20-24 hours

Bolus Insulin

Humalog/Lispro: onset 15-20 min, peak 1-3 hours

To cover blood sugar/carb count prn

Insulin Pump: 1 year after diagnosis

Fewer injections

Better glucose control

Education on Use of Insulin

Select correct pen (insulin type)

Prime with each new pen (2 units)

Clean site & top of pen

Attach clean needle to pen

Dial appropriate dose on pen

Apply pen at 90-degree angle to selected & cleaned site

Push pen top button to dispense insulin

Count to 10 or wait for no clicks (depends on pen manufacturer)

Remove pen

Dispose of needle safely

Using an Insulin Pump

Only rapid-acting insulins are used in insulin pumps to mimic the body's natural insulin release

Pumps generally changed every 2-3 days

2 Types:

Traditional - with tubing

No tubing-Patch pump

Basal rate generally every 10 min

Bolus insulin as needed

Better glucose control + improved quality of life for child/family

Counting Carbs and Insulin to Carb Ratio

Patients/families taught to read labels or use an app to determine carb count.

Carb correction factor will be determined by the diabetes team.

It essentially tells how many grams of carbohydrates one unit of insulin will effectively "cover".

Sick Day Management

Monitor blood glucose every 1-2 hours (can increase to 2-4 hours if stable)

Monitor urine ketones every void

Maintain hydration

Adjust insulin doses based on blood glucose

Call provider if:

Age <5 years

Vomiting > 2 hours

Confusion/lethargy

Hyperventilating

Abdominal pain

Blood glucose < 70 or rising despite added insulin doses

Urine ketones remain large after added insulin & hydration

Hypoglycemia

Blood Sugar: < 60mg/dl

Ketones negative

Urine Output: normal

Mood: irritable, anxious

Mental Status: difficulty concentrating

Skin: pale, sweating

Resp.: shallow, normal

Pulse: tachycardia

Breath: normal

Hyperglycemia

Blood Sugar: > 150-200 mg/dl (depends on age)

Ketones large

Urine Output: early polyuria->oliguria, enuresis, nocturia, incontinence

Mood: lethargic

Mental Status: confused

Skin: dry

Resp: deep, rapid (Kussmaul)

Pulse: weak

Breath: fruity, acetone

Type 2 Diabetes Mellitus: Insulin Resistance

Key factors: Hyperglycemia and insulin resistance

Type 2 Diabetes Mellitus Risk Factors

Obesity

Genetics

Ethnicity

Symptoms of Type 2 DM

Polyuria, polydipsia

Blood glucose >200

A1C > 6.5

Acanthosis Nigricans

Type 2 DM Screen for Comorbidities

Metabolic syndrome

Non-alcoholic fatty liver disease (NAFLD)

Polycystic ovary syndrome (PCOS)

Sleep apnea

Depression

Type 2 DM Goals: Self-management

Glycemic control (blood glucose testing, goals)

Treat/manage comorbidities

Prevent vascular complications

Type 2 DM Non-Pharmacological Therapy

Nutrition therapy

Exercise/activity (regularly)

Psychosocial therapy/guidance

Type 2 DM Pharmacological Therapy

Oral hypoglycemic agents

Metformin (1st line therapy)

Insulin (if needed)

GLP-1 Agonists

SGLT2 (reduces glucose in urine)

SGLT2 (Sodium-Glucose Cotransporter 2) inhibitors

are a class of oral medications for type 2 diabetes that lower blood sugar by forcing the kidneys to remove excess glucose through urine.

Glucagon-like peptide-1 (GLP-1) receptor agonists

are a class of medications that mimic the natural GLP-1 hormone to treat Type 2 diabetes and obesity by stimulating insulin release, reducing glucagon secretion, and slowing gastric emptying. They promote weight loss by increasing satiety and reducing hunger.

Poor glycemic control, obesity, and elevated LDL levels

put a child at risk for developing cardiovascular disease