Pediatrics (System-Integrated)

Pediatric type 1 diabetes: management and DKA prevention

Clinical Overview and When to Suspect Pediatric Type 1 Diabetes

— Highest incidence in non-Hispanic white children; rising ~3%/yr globally

— HLA-DR3/DR4-DQ8 confers strongest genetic risk; ~85% have no family history

— Associated autoimmune conditions: celiac disease, autoimmune thyroiditis, Addison disease, vitiligo

— Classic triad: polyuria, polydipsia, unintentional weight loss over days–weeks

— New-onset nocturnal enuresis in a previously toilet-trained child is a red flag

— Recurrent candidal vulvovaginitis or diaper dermatitis in a previously healthy child

— Fatigue, behavioral changes, declining school performance

— Vomiting/abdominal pain mistaken for gastroenteritis — always check a glucose

— Random glucose ≥200 mg/dL with symptoms

— Fasting glucose ≥126 mg/dL

— 2-hr OGTT glucose ≥200 mg/dL

— HbA1c ≥6.5% (less reliable in children; symptoms + glucose preferred)

Type 1 diabetes mellitus (T1DM) is autoimmune β-cell destruction → absolute insulin deficiency. Peak incidence bimodal: ages 4–6 and 10–14, but can occur in infancy through young adulthood.

Epidemiology and risk:

When to suspect in a pediatric office:

DKA at presentation: ~30–40% of US children present in DKA; rates higher in <5 yr olds and uninsured/minority groups. Younger children and lower SES = higher DKA risk at diagnosis.

Diagnostic thresholds (ADA, any one with symptoms):

Board pearl: In a child with "viral illness" who has Kussmaul breathing, fruity breath, or abdominal pain — check fingerstick glucose and venous blood gas before sending home. Missed DKA at first encounter is a recurring Step 3 vignette.

Step 3 management: Office discovery of glucose >200 mg/dL + ketonuria or ill appearance → direct admission to pediatric facility, not outpatient workup. Stable, well-appearing child with mild hyperglycemia and no ketosis → urgent same-day pediatric endocrinology evaluation, never delay >24h.

Presentation Patterns and Key History

— Polyuria (osmotic diuresis once glucose >180 mg/dL exceeds renal threshold)

— Polydipsia from intravascular volume depletion

— Polyphagia early, anorexia late (as ketosis develops)

— Weight loss despite eating (lipolysis, proteolysis, glycosuria)

— Blurred vision from osmotic lens changes

— Nausea, vomiting, diffuse abdominal pain (often mimics surgical abdomen)

— Kussmaul respirations (deep, sighing) — respiratory compensation for metabolic acidosis

— Fruity/acetone breath

— Altered mental status ranging from drowsy to comatose

— Dehydration signs: sunken eyes, dry mucosa, delayed capillary refill, tachycardia

— Duration of polyuria/polydipsia and weight trajectory

— Bedwetting in a previously dry child

— Recent viral illness, stress, or trauma as trigger

— Family history of T1DM, thyroid disease, celiac, Addison's

— Diet recall — distinguish from MODY (often AD inheritance) or T2DM (obesity, acanthosis)

— Medication exposures (glucocorticoids, atypical antipsychotics → secondary hyperglycemia)

Classic outpatient presentation (subacute, days to weeks):

DKA presentation (hours to days):

Key history questions (Step 3 vignette anchors):

Honeymoon phase awareness: After diagnosis and insulin initiation, residual β-cell function may transiently reduce insulin needs for weeks–months. Do not interpret as remission; parents must continue insulin and monitoring.

Key distinction: T1DM vs T2DM in the overweight adolescent — overlap exists. DKA at presentation, autoantibody positivity (GAD-65, IA-2, ZnT8, insulin), low C-peptide favor T1DM. Up to 25% of new pediatric T1DM are overweight; do not exclude based on BMI.

Board pearl: Recurrent yeast infections + nocturnal enuresis + weight loss in a 7-year-old = check glucose. The vignette rarely says "polyuria" outright.

Physical Exam Findings and Hemodynamic Assessment

— Ill-appearing, lethargic, or irritable in DKA; alert but thin in subacute presentation

— Weight loss documented against growth chart; growth velocity may have declined

— Tachycardia out of proportion to fever

— Hypotension is a late finding in children — they compensate then crash

— Tachypnea with Kussmaul pattern (deep, unlabored) — distinct from pneumonia's shallow tachypnea

— Hypothermia possible despite infection (mask of sepsis)

— Mild (3–5%): dry mucosa, mildly decreased turgor

— Moderate (5–7%): sunken eyes, delayed cap refill 2–3 sec, tachycardia

— Severe (>7–10%): cool extremities, cap refill >3 sec, weak pulses, oliguria, AMS

— Pediatric DKA fluid deficits typically estimated at 5–10%; avoid overestimating to reduce cerebral edema risk

— GCS, pupillary response, cranial nerves

— Headache, bradycardia + hypertension (Cushing's reflex), declining mental status during DKA therapy = cerebral edema until proven otherwise

General appearance:

Vital signs (DKA red flags):

Hydration assessment (critical for fluid plan):

HEENT: fruity breath, dry mucous membranes, sunken eyes; check thyroid (associated Hashimoto's), evaluate for Cushingoid features (rules out exogenous steroid hyperglycemia).

Abdomen: Diffuse tenderness common in DKA — resolves with treatment. Persistent focal pain after correction → re-evaluate for surgical pathology (appendicitis can co-occur and precipitate DKA).

Neuro exam baseline (must document):

Skin: Acanthosis nigricans suggests T2DM; necrobiosis lipoidica rare in pediatrics but associated with T1DM; vitiligo suggests polyglandular autoimmunity.

CCS pearl: On the CCS interface, in suspected pediatric DKA: order fingerstick glucose, VBG, BMP, β-hydroxybutyrate, urinalysis simultaneously with establishing IV access and continuous cardiac/neuro monitoring — clock starts immediately.

Diagnostic Workup — Initial Labs

— Fingerstick glucose (instant) — confirms hyperglycemia

— Venous blood gas (VBG) — pH and bicarb classify DKA severity

— Basic metabolic panel — Na, K, Cl, HCO3, BUN, Cr, glucose

— Serum or urine ketones — β-hydroxybutyrate preferred (urine acetoacetate lags)

— Urinalysis — glucosuria, ketonuria, rule out UTI as trigger

— CBC with diff — leukocytosis common in DKA without infection; left shift more concerning

— HbA1c — confirms chronicity (typically >9% at T1DM diagnosis)

— Phosphate, magnesium, calcium — depleted in DKA

— Hyperglycemia >200 mg/dL PLUS

— Venous pH <7.30 or bicarbonate <18 mEq/L PLUS

— Ketonemia (β-OHB ≥3 mmol/L) or moderate–large ketonuria

— Mild: pH 7.2–7.3, HCO3 10–18

— Moderate: pH 7.1–7.2, HCO3 5–10

— Severe: pH <7.1, HCO3 <5 → ICU

— Corrected sodium = measured Na + 1.6 × [(glucose − 100)/100]; pseudohyponatremia from hyperglycemia

— Potassium: total body depleted but serum often normal/high due to acidosis-driven extracellular shift — anticipate rapid drop with insulin

— Anion gap elevated (β-hydroxybutyrate)

At suspicion of new-onset T1DM or DKA, obtain simultaneously:

DKA diagnostic criteria (ISPAD/ADA pediatric):

DKA severity stratification:

Electrolyte interpretation pearls:

Trigger workup if DKA: UA/urine culture, blood culture if febrile, CXR if respiratory symptoms, lipase if persistent abdominal pain post-correction.

Board pearl: Initial K >5.5 → hold insulin briefly, start fluids. K 3.3–5.5 → start insulin with K in fluids. K <3.3 → hold insulin, replace K first — insulin without K replacement causes lethal hypokalemia.

Step 3 management: Order labs q1h initially (glucose) and q2–4h (BMP, VBG) during DKA therapy.

Diagnostic Workup — Confirmatory and Comorbidity Studies

— Islet autoantibodies (≥1 positive supports T1DM):

— GAD-65 (glutamic acid decarboxylase) — most common in older children

— IA-2 (insulinoma-associated)

— ZnT8 (zinc transporter 8)

— Insulin autoantibodies (IAA) — most common in young children, only valid before exogenous insulin given

— C-peptide: low/undetectable in T1DM (distinguishes from T2DM, MODY); draw with simultaneous glucose

— Fasting insulin: low in T1DM, high in T2DM/insulin resistance

— Strong AD family history across 3 generations

— Antibody-negative

— Detectable C-peptide >2 years after diagnosis

— Diagnosed <6 months → neonatal diabetes (KCNJ11, ABCC8 — may respond to sulfonylureas)

— TSH + free T4 + thyroid peroxidase antibodies — autoimmune thyroiditis in 20–30%

— Tissue transglutaminase IgA + total IgA — celiac disease in 5–10%

— Lipid panel once stable (after metabolic stabilization)

— Urine albumin-to-creatinine ratio — baseline (begin annual screening at age ≥10 yr with ≥5 yr duration, or at puberty)

— Thyroid: every 1–2 years

— Celiac: every 1–2 years for first 4 years, then every 2–5 years

— Lipids: every 3 years if normal; annually if abnormal

Type 1 confirmation (not always needed acutely, but board-relevant):

When to consider MODY testing:

Screen at diagnosis (ISPAD/ADA pediatric):

Periodic re-screening:

Adrenal insufficiency workup only if symptomatic (unexplained hypoglycemia, hyperpigmentation, fatigue, hyponatremia) — morning cortisol + ACTH.

Key distinction: Antibody-negative + obese + acanthosis + family history T2DM = type 2; consider OGTT and fasting insulin. However, presence of DKA does not rule out T2DM ("ketosis-prone T2DM") but is uncommon in children.

Board pearl: Recurrent hypoglycemia in a previously stable T1DM child → screen for Addison disease and celiac before adjusting insulin blindly.

Risk Stratification and First-Line Management Logic

— DKA (any severity) → admit; severe (pH <7.1, AMS, age <5) → PICU

— New-onset T1DM without DKA, stable, ketones small/negative → admit to pediatric ward for insulin initiation and education (US standard; some centers do outpatient with robust team)

— Known T1DM, mild hyperglycemia/ketosis, family competent → outpatient management with phone support

— Step 1: Fluids first — 10–20 mL/kg isotonic saline bolus over 30–60 min for shock; reassess. Avoid aggressive bolus (>40 mL/kg) — cerebral edema risk.

— Step 2: Calculate maintenance + deficit over 48 hours (not 24) — slower correction reduces cerebral edema

— Step 3: Insulin infusion 0.05–0.1 units/kg/hr IV starting 1–2 hours after fluids begin — never bolus insulin in pediatric DKA

— Step 4: Add dextrose to fluids when glucose reaches 250–300 mg/dL (transition to D5 then D10) — continue insulin to clear ketones

— Step 5: Potassium replacement in fluids (20–40 mEq/L) once K <5.5 and urinating

— Step 6: Avoid bicarbonate unless pH <6.9 with cardiovascular compromise — bicarb associated with cerebral edema

— pH >7.30, HCO3 >18, anion gap closed, β-OHB <1 mmol/L

— Then transition to SC insulin, overlapping IV insulin for 15–30 min before discontinuing

Disposition triage at diagnosis:

DKA management framework (ISPAD 2022, ADA-aligned):

Resolution of DKA criteria:

Step 3 management: Two-bag system (one bag normal saline, one D10 normal saline, both with K) allows rapid titration of dextrose without changing insulin rate. Boards love this.

CCS pearl: Never stop the insulin drip when glucose drops — add dextrose. Stopping insulin reopens ketogenesis and prolongs DKA.

Pharmacotherapy — Insulin Regimens for Maintenance

— Prepubertal: 0.5–0.75 units/kg/day

— Pubertal: 0.75–1.0 units/kg/day (insulin resistance peaks)

— Honeymoon phase: may need <0.5 units/kg/day

— Post-DKA initiation: often 0.7–1.0 units/kg/day

— 50% basal: glargine, detemir, degludec (ultra-long, less hypoglycemia) once daily

— 50% bolus: rapid-acting (lispro, aspart, glulisine) before each meal

— Use insulin-to-carb ratio (ICR): starting ~1 unit per 15 g carbs (varies by age)

— Correction factor (sensitivity): ~1800/TDD (rapid-acting) for mg/dL drop per unit

— Target premeal glucose: 80–130 mg/dL; bedtime 90–150; A1c <7.0% (ADA pediatric 2023)

— Rapid-acting only; programmable basal rates + meal boluses

— Advantages: tighter control, fewer injections, dose flexibility

— Risk: pump failure → rapid DKA (no basal depot) — must have backup pen insulin

— Pramlintide rarely used in pediatrics

— Metformin off-label only if obesity + insulin resistance ("double diabetes") in adolescents

— SGLT2 inhibitors are NOT approved for pediatric T1DM — DKA risk

Total daily dose (TDD) starting estimate:

Basal-bolus regimen (preferred, MDI):

Continuous subcutaneous insulin infusion (CSII / pump):

Automated insulin delivery (AID/hybrid closed-loop): preferred when available — CGM-driven basal adjustment; improves time-in-range, reduces hypoglycemia. Strongly recommended by ADA for youth.

NPH/regular split-mix regimens are outdated but still tested — rigid meal timing, more hypoglycemia.

Adjuncts:

Board pearl: Dawn phenomenon (early-morning hyperglycemia from GH/cortisol surge) → increase basal or shift basal to evening. Somogyi effect (rebound from nocturnal hypoglycemia) → check 3 AM glucose; reduce evening basal.

Step 3 management: Sick-day rules — never omit basal insulin; check ketones q4h if glucose >250; give correction doses; hydrate; seek care if vomiting or ketones rising.

Glucose Monitoring, CGM, and Technology Integration

— ADA 2023 recommends CGM for all youth with T1DM, regardless of insulin delivery method

— Devices: Dexcom G6/G7, FreeStyle Libre 2/3, Medtronic Guardian

— Provides time-in-range (TIR) 70–180 mg/dL as primary metric; goal >70% for youth

— Time below range (<70 mg/dL): goal <4%; <54 mg/dL: <1%

— Alarms for hypo/hyperglycemia improve safety, especially nocturnally

— If no CGM: ≥4 checks/day (pre-meals, bedtime, occasional 3 AM)

— Even with CGM: confirm with fingerstick if symptoms don't match CGM, during rapid changes, or for calibration

— Tandem Control-IQ, Medtronic 780G, Omnipod 5 (approved down to age 2–6 depending on device)

— CGM informs pump to adjust basal and deliver correction boluses

— Reduces nocturnal hypoglycemia and DKA episodes; improves A1c without weight gain

— <7.0% for most youth with access to technology and without significant hypoglycemia

— <7.5% if limited resources or hypoglycemia unawareness

— Individualize — avoid hypoglycemia in <6 yr olds (neurocognitive risk)

— Section 504 plan in US schools — accommodations for glucose checks, insulin, snacks, field trips

— Diabetes Medical Management Plan (DMMP) signed by provider

— Glucagon must be available at school; staff trained

— Check glucose before exercise; if <100 mg/dL, give 15 g carbs

— Reduce basal/bolus or increase carbs around activity

— Delayed post-exercise hypoglycemia can occur up to 12 hours later — check overnight

Continuous glucose monitoring (CGM) — standard of care:

Fingerstick monitoring:

Hybrid closed-loop systems (AID):

A1c targets (ADA 2023 pediatric):

School integration (Step 3 systems issue):

Exercise considerations:

CCS pearl: When transitioning patient from IV insulin drip to subcutaneous, give the first SC long-acting dose 2 hours before stopping the drip; rapid-acting given at meal 15 min before stopping. Otherwise rebound hyperglycemia/DKA.

Special Considerations — Renal, Hepatic, and Comorbidity Adjustments

— Rare at diagnosis but emerges with diabetic nephropathy over years

— Screen annually with urine albumin-to-creatinine ratio (UACR) starting age ≥10 yr with ≥5 yr duration (some guidelines say at puberty regardless of duration)

— Confirmed albuminuria (UACR >30 mg/g on 2 of 3 samples) → ACE inhibitor or ARB, optimize glycemia, BP control

— As GFR declines: insulin clearance falls → reduce insulin doses to prevent hypoglycemia

— Glycogenic hepatopathy (Mauriac syndrome) in chronically poorly controlled T1DM: hepatomegaly, transaminitis, growth delay, cushingoid features — reversible with glycemic control

— Distinguish from NAFLD (more common with T2DM/obesity)

— Hypothyroidism: subtle growth slowing, fatigue, weight gain, unexplained low insulin needs

— Hyperthyroidism (Graves): weight loss despite eating, worsening glycemia, tremor

— Treat thyroid → glycemic needs change; reassess insulin doses

— Screen with TTG-IgA + total IgA at diagnosis and periodically

— Symptomatic or biopsy-confirmed → gluten-free diet

— Untreated celiac causes erratic glycemia (variable absorption), short stature, anemia

— Adolescent girls particularly at risk: omitting insulin for weight loss

— Recurrent DKA, A1c >10%, weight concerns → screen

— Multidisciplinary team: endocrinology, mental health, nutrition

— Suspect if recurrent unexplained hypoglycemia, hyperpigmentation, hyponatremia

— Stress-dose hydrocortisone required during illness

Renal impairment in pediatric T1DM:

Hepatic considerations:

Thyroid disease (20–30% comorbidity):

Celiac disease (5–10% comorbidity):

Eating disorders ("diabulimia"):

Adrenal insufficiency (Addison, autoimmune polyglandular syndrome type 2):

Board pearl: Unexplained drop in insulin requirements + fatigue + hyperpigmentation = Addison disease in T1DM patient. Check morning cortisol and ACTH before just lowering insulin.

Special Populations — Toddlers, Adolescents, and Transition of Care

— Diluted insulin (U-10, U-25) for tiny doses; insulin pumps preferred for precision

— Erratic eating → post-meal rapid-acting bolusing based on actual intake is acceptable

— Higher cerebral edema risk in DKA; very strict avoidance of severe hypoglycemia (neurocognitive impact)

— A1c target individualized, often <7.5%

— Consider neonatal diabetes (KCNJ11/ABCC8) if <6 months — genetic testing; may transition to sulfonylurea with dramatic improvement

— Establish school 504 plan, glucagon at school, trained personnel

— Encourage self-monitoring with adult supervision; gradual independence

— Camp participation: diabetes camps build self-management skills

— Puberty-induced insulin resistance → TDD often 1.0–1.5 units/kg/day

— Risk-taking, depression, eating disorders, alcohol — alcohol blunts hepatic glucose output → delayed hypoglycemia

— Driving safety: glucose ≥90 mg/dL before driving; recheck every 2 hours; carbs in car

— Contraception: pregnancy in poorly controlled T1DM = congenital anomalies risk; preconception counseling at every adolescent visit

— Begin transition planning at age 12–14; structured transfer by 18–21

— Use a transition checklist (Got Transition framework): self-advocacy, medication knowledge, insurance, appointment scheduling

— Loss to follow-up during transition → DKA hospitalizations spike; warm handoff to adult endocrinologist

— Preconception A1c <6.5% reduces anomaly risk

— Multidisciplinary team; insulin needs change every trimester

— Stop ACE/ARBs (teratogenic); switch to labetalol/nifedipine if needed

Infants and toddlers (<5 years):

School-age children:

Adolescents:

Transition to adult care (key Step 3 systems item):

Pregnancy in adolescents with T1DM:

Step 3 management: At every adolescent visit — screen for depression (PHQ-9), eating disorders, substance use, sexual activity, contraception — these directly affect glycemic stability and DKA recurrence.

Complications and Adverse Outcomes

— DKA — recurrence common with insulin omission, illness, pump failure; mortality 0.15–0.30% per episode in children

— Cerebral edema — 0.5–1% of pediatric DKA episodes; mortality 20–25%, morbidity in survivors high

— Risk factors: age <5, new-onset DKA, severe acidosis, high BUN, bicarbonate use, rapid Na correction, fluid overload

— Signs: headache, vomiting, bradycardia, hypertension, AMS, posturing

— Treatment: IV mannitol 0.5–1 g/kg OR hypertonic 3% saline 5 mL/kg, intubation, head elevation; do NOT delay for imaging

— Hypoglycemia: tremor, sweating, confusion, seizures; severe hypoglycemia in young children → cognitive impairment

— Treatment: 15 g fast carbs if conscious; glucagon 0.5 mg (<25 kg) or 1 mg (≥25 kg) IM/SC if unconscious; nasal glucagon (Baqsimi) 3 mg available

— Hyperglycemic hyperosmolar state: rare in pediatric T1DM, more T2DM

— Retinopathy — screen with dilated exam at puberty or 3–5 years after diagnosis, then annually

— Nephropathy — annual UACR; ACEi/ARB if albuminuria

— Neuropathy — annual foot exam, monofilament testing starting puberty

— Accelerated atherosclerosis; lipid screening every 3 years (more often if abnormal)

— Statin if LDL >160 (or >130 with risk factors) in children ≥10 yr

— BP target <90th percentile for age/sex/height

— Depression 2–3× more common; anxiety, diabetes distress, burnout

— Family stress, parental burnout

— Poor control → growth delay, delayed puberty (Mauriac syndrome in extreme)

— Repeated hypoglycemia blunts counter-regulatory response

— Treatment: strict avoidance of hypoglycemia for 2–3 weeks restores awareness

Acute complications:

Chronic microvascular complications:

Macrovascular complications:

Psychosocial:

Growth and puberty:

Hypoglycemia unawareness:

Board pearl: Sudden death in young T1DM ("dead-in-bed syndrome") — nocturnal hypoglycemia → cardiac arrhythmia (QT prolongation). CGM with alarms is protective.

When to Escalate — ICU, Consults, and Inpatient Triage

— Age <5 years (cerebral edema risk)

— Severe acidosis: pH <7.1 or HCO3 <5

— Altered mental status (GCS <14) or any neurologic concern

— Hemodynamic instability, shock

— Severe electrolyte derangement (K <3.0, Na <125 corrected)

— Need for hourly neuro checks and frequent labs beyond ward capacity

— Mild–moderate DKA with normal mentation

— New-onset T1DM without DKA — for education and insulin initiation

— Recurrent DKA in known T1DM for stabilization and root-cause analysis (pump failure, omission, infection, eating disorder)

— Pediatric endocrinology — mandatory at diagnosis and for all admissions; longitudinal care

— Diabetes educator, dietitian — initial and ongoing

— Social work — insurance, school plan, food security

— Mental health — at diagnosis and screen annually; urgent referral for diabulimia, depression

— Ophthalmology — at puberty or 3–5 yr post-diagnosis

— Genetics — suspected MODY or neonatal diabetes

— Headache during therapy → stop and reassess for cerebral edema

— Bradycardia + hypertension (Cushing reflex)

— Declining GCS, posturing, cranial nerve palsy

— Sudden hypoxia (could indicate aspiration or pulmonary edema)

— Persistent acidosis despite therapy → check for sepsis, missed pump site infection

— Resolution of DKA (pH >7.30, HCO3 >18, AG closed)

— Tolerating PO, transitioned to SC insulin successfully

— Stable mental status and hemodynamics

PICU admission criteria for pediatric DKA:

General ward admission:

Consultations:

Signs requiring urgent escalation during DKA treatment:

Transfer-out criteria from PICU to ward:

CCS pearl: If GCS drops or headache emerges during DKA management on the CCS interface, immediately order mannitol or 3% saline, elevate head of bed, intubate if obtunded — don't wait for CT. CT is for after stabilization.

Step 3 management: Document calculated fluid rate, insulin rate, lab trends q1-2h clearly — handoff failures are a common patient safety theme on Step 3.

Key Differentials — Other Causes of Hyperglycemia/Polyuria in Children

— Obesity, acanthosis nigricans, family history, minority ethnicity

— Insidious onset; DKA less common but possible ("ketosis-prone")

— Antibody-negative, high C-peptide, hyperinsulinemia

— Treat with metformin ± insulin; lifestyle

— Autosomal dominant; 3-generation family history

— Antibody-negative, detectable C-peptide

— Most common subtypes:

— HNF1A (MODY 3): highly sulfonylurea-responsive

— GCK (MODY 2): mild stable fasting hyperglycemia, usually no treatment needed

— HNF4A (MODY 1): macrosomia at birth, neonatal hypoglycemia

— Genetic testing diagnostic

— KCNJ11, ABCC8 mutations → respond to sulfonylureas, not insulin long-term

— Always genetically test diabetes presenting under 6 months

— Glucocorticoid exposure (asthma, IBD, nephrotic syndrome treatment)

— Resolves with steroid taper

— Critical illness, sepsis, trauma

— Self-limited; not diabetes if antibody-negative and resolves

— Adolescents with CF; screen with annual OGTT from age 10

— Insulin treatment; avoid carbohydrate restriction (CF nutrition needs)

— Atypical antipsychotics (olanzapine, risperidone)

— Tacrolimus, cyclosporine (post-transplant diabetes)

— L-asparaginase (oncology)

— Cushing syndrome, acromegaly (rare), pheochromocytoma — distinct exam findings

Type 2 diabetes mellitus:

Maturity-onset diabetes of the young (MODY):

Neonatal diabetes (<6 months age):

Steroid-induced hyperglycemia:

Stress hyperglycemia:

Cystic fibrosis-related diabetes (CFRD):

Drug-induced:

Endocrinopathies:

Key distinction: DKA + obesity + acanthosis + no antibodies in adolescent = ketosis-prone T2DM. Initial management = insulin; transition to metformin ± GLP-1 when stable; many can come off insulin.

Board pearl: Diabetes diagnosed <6 months old is never type 1 — pursue genetic testing for monogenic neonatal diabetes; some children come off insulin entirely with sulfonylureas.

Key Differentials — Non-Diabetic Causes of the Presentation

— Diabetes insipidus (central or nephrogenic): dilute urine, hypernatremia, normal glucose; water deprivation test, desmopressin trial

— Primary polydipsia (psychogenic): dilute urine but normal-to-low sodium; behavioral

— Hypercalcemia (Williams syndrome, hyperparathyroidism)

— Hypokalemia

— Hyperthyroidism (Graves) — tachycardia, tremor, goiter

— Inflammatory bowel disease — diarrhea, abdominal pain, growth failure

— Celiac disease — bloating, steatorrhea

— Malignancy (leukemia, lymphoma) — fatigue, lymphadenopathy, bruising

— Eating disorders — body image concerns, restrictive intake

— Chronic infection (TB, HIV)

— Salicylate poisoning — mixed metabolic acidosis + respiratory alkalosis, tinnitus

— Sepsis with lactic acidosis — toxic appearance, infection source

— Inborn errors of metabolism in infants — organic acidemias, MMA, PA

— Toxic alcohol ingestion (methanol, ethylene glycol) — adolescents

— Uremia (advanced renal failure)

— Appendicitis, gastroenteritis, pancreatitis (can co-occur with DKA), UTI

— DKA abdominal pain resolves with metabolic correction; persistent pain after correction warrants imaging

— Meningitis, encephalitis, intracranial hemorrhage, toxic ingestion, seizure (postictal), hypoglycemia

— Always check glucose in any child with AMS

— Hyperthyroidism, malabsorption, parasitic infection

Polyuria/polydipsia without hyperglycemia:

Weight loss differentials in pediatrics:

Kussmaul respirations / metabolic acidosis differentials:

Abdominal pain mimics:

Altered mental status differentials:

Polyphagia:

Key distinction: Polyuria + polydipsia + normal glucose + dilute urine = diabetes insipidus, not diabetes mellitus. Step 3 may test this contrast directly.

Board pearl: In the febrile vomiting toddler — always check glucose. Missed pediatric DKA presenting as "gastroenteritis" is a recurring sentinel event vignette and tort case.

Long-Term Plan, Secondary Prevention, and Discharge Planning

— Family demonstrates insulin injection technique (pen and/or syringe)

— Glucose meter and CGM use mastered

— Carbohydrate counting competency

— Glucagon emergency kit prescription + administration training

— Sick-day rules written and verbalized

— Hypoglycemia recognition and treatment

— Ketone testing (urine or blood β-OHB meter)

— Follow-up appointment scheduled within 1–2 weeks

— 24/7 endocrinology contact phone number

— Basal insulin (glargine/degludec)

— Rapid-acting insulin (lispro/aspart)

— Glucose meter + strips + lancets

— CGM if available

— Glucagon (injectable or nasal)

— Ketone strips (urine) or β-OHB meter

— Medical alert ID recommended

— A1c every 3 months; target <7.0% (individualized)

— Annual: lipids (every 3 yr if normal), UACR (from age ≥10 with ≥5 yr duration), TSH, celiac panel periodically, dilated eye exam (from puberty/5 yr), foot exam, dental exam

— BP at every visit; target <90th percentile

— Immunizations: annual influenza, pneumococcal, COVID-19, HPV, routine peds schedule

— Statin: LDL >160, or >130 with additional risk factors, age ≥10

— ACEi/ARB: confirmed albuminuria or hypertension

— Never stop insulin even if not eating

— Sick-day rules: check glucose q2–4h, ketones if glucose >250 or ill, hydrate

— Pump users: backup pen insulin available; suspect pump failure if unexplained hyperglycemia + ketones

— Address eating disorders, depression, family conflict

— Insurance/financial access to insulin and supplies (US insulin cost crisis)

Discharge from initial T1DM diagnosis admission requires:

Prescriptions at discharge:

Secondary prevention pillars (longitudinal):

DKA prevention strategies (high yield):

Step 3 management: Recurrent DKA = systems failure, not patient failure. Investigate insulin access, mental health, family dynamics, school support — root-cause approach.

Follow-Up, Monitoring, and Counseling

— Quarterly endocrinology visits (every 3 months) — A1c, growth, BP, exam, insulin regimen review, technology download review

— More frequent in first 6 months post-diagnosis, during puberty, after DKA, regimen changes

— Telehealth visits supplement in-person; CGM downloads enable remote management

— A1c trend and time-in-range (CGM data)

— Hypoglycemia frequency and severity

— Injection sites (rotate to avoid lipohypertrophy)

— Insulin dosing adjustments based on logs

— Growth (height, weight, BMI on growth charts) and pubertal stage (Tanner)

— BP and exam (thyroid, skin, foot)

— Psychosocial: school, mood, sleep, family

— Adherence to monitoring and injections

— Sick-day rule recall

— UACR (from age ≥10 with ≥5 yr duration)

— Lipid panel (every 3 yr if normal)

— Dilated retinal exam (puberty or 3–5 yr post-dx)

— Foot exam with monofilament (puberty)

— TSH, free T4

— Celiac panel periodically (TTG-IgA, total IgA)

— Dental exam every 6 months

— Young child: parent-led, school 504 plan, glucagon training

— Pre-teen: gradual self-management, camp, peer support

— Adolescent: driving safety, alcohol, sexuality, contraception, mental health, transition planning

— Pregnancy preconception (any sexually active adolescent female): A1c <6.5%, folate, stop teratogens

— Reinforce sick-day rules every visit (recurrent testing item)

— Carbohydrate counting reinforcement, label reading

— Exercise adjustments

— Travel planning (insulin storage, time zones, supplies)

Visit cadence:

At each visit, review:

Annual screenings (consolidated):

Counseling topics by age:

Family and patient education themes:

Board pearl: Lipohypertrophy from non-rotated injection sites causes erratic absorption and unexplained glycemic variability. Examine and palpate injection sites at every visit.

Step 3 management: A1c rising without clear cause → review injection technique, sites, insulin storage (heat-degraded), expired insulin, missed doses, depression screening before escalating doses.

Ethical, Legal, and Patient Safety Considerations

— Pediatric assent + parental consent; emancipated minors and mature minor doctrine vary by state

— Adolescents should be involved in their care decisions developmentally

— Insulin pump and CGM initiation — discuss risks/benefits with both patient and parent

— Mental health, sexual activity, substance use discussions may be confidential per state law

— Eating disorder ("diabulimia") — balance confidentiality with safety; involve parents when imminent harm

— Suspected medical neglect — caregivers withholding insulin, missing critical appointments, recurrent DKA without medical reason → child protective services report required in most US states

— Document specific concerns, repeated education, missed appointments before reporting

— Insulin affordability — US insulin cost crisis; $35/month cap for Medicare and many states for commercial plans; manufacturer patient assistance programs

— Food insecurity affects glycemic control; screen with 2-question Hunger Vital Sign

— Disparities: minority and low-SES youth have higher DKA, lower CGM/pump access, higher A1c — actively address with social work, navigation

— Section 504 plan and Diabetes Medical Management Plan; staff trained in glucagon

— Discrimination in school activities (field trips, sports) is illegal — advocate

— Pediatric → adult endocrinology gap doubles DKA rate

— Use structured transition tools, warm handoff, copy records, share contact between teams

— Cybersecurity (FDA recalls for pump vulnerabilities)

— Device failure backup plan must be in writing

— Hypoglycemia while driving = liability and harm; states may require physician reporting of severe hypoglycemia (varies)

— Pediatric assent for trials (e.g., teplizumab to delay T1DM onset in at-risk relatives — FDA-approved 2022 for stage 2 T1DM)

Informed consent for adolescents:

Confidentiality in adolescents:

Mandatory reporting:

Health equity and access:

School safety:

Transition-of-care safety (Step 3 high yield):

Pump and CGM safety:

Driving safety:

Research and trials:

Board pearl: Recurrent DKA in a teen with restrictive eating, secret insulin omission, and weight preoccupation = diabulimia — refer urgently to eating disorder team; ethical duty to involve family despite confidentiality concerns when safety at stake.

High-Yield Associations and Rapid-Fire Facts

— HLA-DR3, DR4, DQ8 → highest T1DM risk

— HLA-DR2 → protective

— First antibody often IAA in young children, GAD-65 in older

— Identical twin concordance ~30–50%

— Stage 1: ≥2 islet autoantibodies, normoglycemia

— Stage 2: ≥2 antibodies + dysglycemia, asymptomatic

— Stage 3: clinical diabetes with symptoms

— Teplizumab (anti-CD3) delays progression from stage 2 to stage 3 by ~2 years

— "FIG-PICK": Fluids first, Insulin (not bolus), Glucose monitoring, Potassium, Identify trigger, Continuous monitoring, Ketone resolution

— "FLAT" for cerebral edema risk: Fluids excessive, Low age, Acidosis severe, Treatment with bicarb

— Mannitol 0.5–1 g/kg IV over 10–15 min, OR

— 3% hypertonic saline 5 mL/kg over 10–15 min

— Lispro/aspart/glulisine: onset 15 min, peak 1 hr, duration 3–5 hr

— Regular: onset 30 min, peak 2–4 hr, duration 6–8 hr

— NPH: peak 4–10 hr, duration 12–18 hr

— Glargine: peakless, 24 hr

— Detemir: 12–24 hr

— Degludec: >42 hr (most flexible timing)

— <25 kg or <6 yr: 0.5 mg IM/SC; ≥25 kg: 1 mg

— Nasal glucagon: 3 mg intranasal, ≥4 yr

Genetic and immune:

Stages of T1DM (JDRF/ADA):

DKA management mnemonics:

Cerebral edema treatment doses:

Insulin pharmacokinetic pearls:

Glucagon dosing:

DKA fluid rule: maintenance + deficit over 48 hours; no >40 mL/kg in first 4 hr in young child

Honeymoon phase: weeks to 2 years post-diagnosis; continue low-dose insulin even if needs minimal

Acanthosis nigricans = insulin resistance marker, favors T2DM

Mauriac syndrome = hepatomegaly + growth failure + cushingoid in chronically uncontrolled T1DM

Step 3 management: Recurrent DKA with no clear trigger → screen for eating disorder, mental health, family dysfunction, and insulin access/cost before assuming nonadherence.

Board Question Stem Patterns

— "5-year-old with 3 days of vomiting, Kussmaul breathing, glucose 480, pH 7.05, bicarb 6, K 5.8."

— Answer: Isotonic fluids first (10 mL/kg over 1 hr), then insulin infusion 0.05–0.1 U/kg/hr after 1–2 hr, replace fluid deficit over 48 hr, add K when <5.5, add dextrose when glucose 250–300. PICU. Do NOT give insulin bolus. Do NOT give bicarb.

— "8-year-old in DKA, 6 hours into therapy, develops headache, vomiting, bradycardia, declining GCS."

— Answer: 3% saline 5 mL/kg or mannitol 0.5–1 g/kg IV immediately, elevate head, intubate if needed, then CT after stabilization

— Obese adolescent with DKA, acanthosis, positive family history T2DM, negative antibodies, high C-peptide.

— Answer: Ketosis-prone T2DM — initial insulin, transition to metformin

— Lean adolescent, mild fasting hyperglycemia, 3-generation family history, antibody-negative, detectable C-peptide.

— Answer: Genetic testing for HNF1A → sulfonylurea; or GCK → no treatment

— Adolescent T1DM with recurrent severe hypoglycemia, fatigue, hyperpigmentation, low Na.

— Answer: Addison disease — check morning cortisol, ACTH; stress-dose hydrocortisone for illness

— "Mother stopped insulin because child not eating during gastroenteritis; now in DKA."

— Answer: Counseling — never omit basal insulin; check ketones; hydrate

— Adolescent on pump develops hyperglycemia + ketones overnight after activity.

— Answer: Pump site/infusion failure; give SC rapid-acting injection, change site, check ketones

— 19-year-old with T1DM presents in DKA after losing pediatric endocrinologist contact.

— Answer: System failure; warm handoff, structured transition protocols

— 15-year-old female, recurrent DKA, weight concerns, omits insulin.

— Answer: Multidisciplinary eating disorder care; mental health referral

Pattern 1: New-onset DKA in young child

Pattern 2: Cerebral edema during DKA treatment

Pattern 3: Distinguishing T1 from T2

Pattern 4: MODY

Pattern 5: Hypoglycemia mechanism

Pattern 6: Sick-day mistake

Pattern 7: Pump failure

Pattern 8: Transition-of-care

Pattern 9: Diabulimia

Board pearl: When pH <6.9 in DKA, bicarbonate is still controversial and not routinely recommended in pediatrics — focus on fluids and insulin.

One-Line Recap

Pediatric type 1 diabetes is autoimmune absolute insulin deficiency managed with lifelong basal-bolus insulin (or pump/AID), CGM-guided fine-tuning, vigilant DKA prevention through sick-day rules and continuous insulin, multidisciplinary support, and proactive screening for autoimmune and microvascular comorbidities — with DKA treatment in children defined by slow fluid correction over 48 hours, delayed insulin (no bolus), and obsessive vigilance for cerebral edema.

— DKA treatment sequence: Fluids first (cautious, 10–20 mL/kg bolus only if shock), insulin infusion 0.05–0.1 U/kg/hr started 1–2 hr after fluids (never bolus), correct deficit over 48 hours, add K when serum K <5.5 and urinating, add dextrose when glucose hits 250–300, avoid bicarbonate unless pH <6.9 with cardiovascular compromise

— Cerebral edema is the leading cause of DKA mortality in children — risk highest in age <5, severe acidosis, high BUN, rapid Na correction; treat empirically with mannitol 0.5–1 g/kg or 3% saline 5 mL/kg at first sign (headache, bradycardia, declining GCS) — do not wait for imaging

— Maintenance regimen: basal-bolus insulin with glargine/degludec + lispro/aspart; TDD ~0.5–1.0 U/kg/day; pump or hybrid closed-loop preferred; A1c target <7.0%, time-in-range >70%, time below range <4%

— DKA prevention: never omit basal insulin, sick-day rules (check glucose and ketones q2–4h when ill), backup pen for pump users, address eating disorders/mental health/insulin access; recurrent DKA = systems failure requiring root-cause analysis, not blame

— Always screen at diagnosis and longitudinally: thyroid (TSH, TPO Ab), celiac (TTG-IgA + total IgA), lipid panel, UACR (age ≥10 with ≥5 yr duration), retinal exam (puberty/5 yr), foot exam, BP, growth, mental health

— Transition to adult care at 18–21 with structured handoff prevents DKA spike; teplizumab now delays stage 2 → stage 3 progression in at-risk relatives

High-yield recap bullets:

Board pearl: If you remember nothing else: fluids before insulin, never bolus insulin in pediatric DKA, watch for cerebral edema, never stop basal insulin even when sick, and recurrent DKA is a systems and psychosocial diagnosis until proven otherwise.