Eduovisual
Endocrine
Inpatient glycemic management and insulin dosing
— Hyperglycemia is defined in the hospital as any blood glucose (BG) >140 mg/dL; persistent BG >180 mg/dL warrants intervention
— Affects 30–40% of non-ICU and >80% of ICU patients; includes known diabetes, stress hyperglycemia, and newly diagnosed diabetes
— Independently associated with infection, delayed wound healing, longer LOS, and mortality across surgical, cardiac, stroke, and oncology populations
— Known diabetes (T1DM or T2DM): has home regimen, A1c usually available
— Stress hyperglycemia: no prior diagnosis, A1c <6.5%, BG normalizes with illness resolution — still treat in hospital
— Newly diagnosed diabetes: A1c ≥6.5% discovered during admission; needs discharge regimen and outpatient follow-up
— Random BG >140 mg/dL on admission in any patient → check A1c if not done in past 3 months
— Steroid initiation, TPN, enteral feeds, post-transplant, or pancreatitis admissions are highest-yield screening windows
— Recurrent infections (UTI, cellulitis, candidiasis), unexplained weight loss, or fatigue prompting admission
— Non-ICU: premeal 100–140 mg/dL, random <180 mg/dL
— ICU/critically ill: 140–180 mg/dL (avoid <110; NICE-SUGAR showed harm with tight 80–110 targets)
— More stringent (110–140) acceptable in select cardiac surgery patients without hypoglycemia risk
Board pearl: Every hospitalized patient with hyperglycemia needs an A1c if none in the last 3 months — this single test reclassifies "stress hyperglycemia" into newly diagnosed diabetes and changes discharge planning entirely.
Step 3 management: Order admission BG, A1c, and basal-bolus glucose monitoring schedule (AC + HS or q6h NPO) within the first 24 hours of any patient with diabetes risk factors.
— Glucocorticoids: prednisone, dexamethasone — peak BG in afternoon/evening with morning prednisone; predictable post-lunch spike
— Enteral/parenteral nutrition: continuous tube feeds produce sustained hyperglycemia; TPN especially with high dextrose load
— Surgical stress, sepsis, MI, stroke: catecholamine and cortisol surge
— Medications: tacrolimus, cyclosporine, antipsychotics (olanzapine, quetiapine), thiazides, octreotide, protease inhibitors, checkpoint inhibitors (can cause new T1DM)
— Type of diabetes (T1 vs T2) — critical because T1DM patients always require basal insulin even when NPO, or they develop DKA within hours
— Home regimen with doses, timing, last dose taken
— Recent A1c → guides whether home regimen is adequate or needs intensification
— Hypoglycemia history, awareness, frequency
— Diet at home, expected PO intake in hospital, NPO status for procedures
— Polyuria/polydipsia with N/V, abdominal pain, Kussmaul breathing → DKA workup
— Altered mentation with BG >600 → HHS
— Recurrent hypoglycemia, especially nocturnal — often missed; check 3 AM BG
— "When did you last take your insulin/oral agents?"
— "Have you been eating normally?"
— "Any sick-day adjustments?"
— "Do you have a CGM or insulin pump?" — pump management requires endocrine consult and clear orders
Key distinction: Stress hyperglycemia (A1c <6.5%) vs newly diagnosed diabetes (A1c ≥6.5%) — same inpatient management, completely different discharge planning. The first gets lifestyle counseling and outpatient repeat A1c; the second leaves on antihyperglycemic therapy with structured follow-up.
Board pearl: A T1DM patient made NPO who has basal insulin held will be in DKA before morning rounds — basal insulin is never fully held in T1DM, only reduced (typically to 80% of home dose).
— DKA: Kussmaul respirations, fruity (acetone) breath, dry mucous membranes, tachycardia, abdominal tenderness (especially in children), altered mentation late
— HHS: profound dehydration, hypotension, tachycardia, focal neuro deficits, seizures, coma — mentation correlates with osmolality
— Volume status: orthostatics, JVP, skin turgor (less reliable in elderly), capillary refill, urine output trend
— Acanthosis nigricans (neck, axillae) — insulin resistance marker
— Necrobiosis lipoidica, diabetic dermopathy, eruptive xanthomas (severe hypertriglyceridemia)
— Candida intertrigo, balanitis, vulvovaginitis
— Peripheral neuropathy on monofilament/vibration, absent ankle reflexes
— Diminished pedal pulses, hair loss, dependent rubor — PAD
— Retinopathy on funduscopy (rarely diagnostic inpatient)
— Inspect interdigital spaces, heels, pressure points for ulcers
— Probe-to-bone test on any ulcer → osteomyelitis until proven otherwise
— Document monofilament sensation in 10 sites
— Heel offloading orders in any bed-bound diabetic to prevent pressure injury
— Diaphoresis, tremor, tachycardia, confusion → hypoglycemia until BG checked
— Sympathetic symptoms blunted in patients on beta-blockers and those with hypoglycemia unawareness from frequent lows
— Always check BG before treating altered mentation in any diabetic — Dextrose 50% 25 g IV if symptomatic and BG <70
CCS pearl: On any diabetic admission, your standing orders should include: fingerstick BG q6h or AC+HS, hypoglycemia protocol (D50 if BG <70 with symptoms or <54 regardless), and a daily foot inspection nursing order. These three orders prevent the most common inpatient diabetes errors and appear repeatedly in CCS scoring rubrics for diabetic patients.
— BMP (Na, K, Cl, HCO3, BUN, Cr, glucose) — calculate anion gap
— A1c if none in past 3 months
— Beta-hydroxybutyrate or urine ketones if BG >250 or symptomatic
— VBG/ABG if AG elevated or HCO3 <18
— Serum osmolality if BG >400 or altered mentation
— Phosphate, magnesium — depleted in DKA, important during refeeding and insulin therapy
— Lipid panel and urine albumin/Cr ratio if newly diagnosed (baseline)
— Na corrected = measured Na + 1.6 × [(glucose − 100)/100]
— Pseudohyponatremia from hyperglycemia resolves with glucose correction; true hyponatremia after correction signals additional pathology
— Eating patient: fingerstick AC (before each meal) + HS (bedtime) = 4×/day
— NPO or continuous tube feeds: q4–6h
— IV insulin infusion: q1h until stable, then q2h
— CGM: increasingly used inpatient but confirm with fingerstick before treating hypoglycemia or dosing decisions
— Reflects 2–3 month average; unaffected by acute illness
— Unreliable in hemolysis, recent transfusion, hemoglobinopathies, CKD with EPO use, iron deficiency
— Use fructosamine if A1c unreliable and chronic control assessment needed
— Daily BMP while on IV insulin or with AKI
— Anion gap closure (not BG normalization) defines DKA resolution
— Bicarbonate trend, K trend with insulin
Board pearl: In DKA, anion gap closure — not glucose normalization — defines resolution. Glucose will fall first (often by hour 4–6); the gap takes 12–24 hours. Stopping the insulin drip when BG hits 200 without overlapping subcutaneous insulin precipitates recurrent DKA — a classic Step 3 error.
Step 3 management: Order A1c reflexively on any admission BG >140 in a patient without diabetes — this single decision identifies new diabetes diagnoses missed in primary care.
— Increasing recognition that ~10% of "T2DM" in adults is actually LADA (latent autoimmune diabetes of adults)
— Suspect T1/LADA when: lean body habitus, rapid progression to insulin requirement, DKA at presentation, personal/family history of autoimmunity, age <30
— Antibody panel: GAD-65 (most sensitive in adults), IA-2, ZnT8, insulin autoantibodies
— C-peptide: low or undetectable in T1DM; normal/elevated in T2DM and insulin resistance — interpret only with simultaneous glucose
— Cushing syndrome: 24h urinary free cortisol, late-night salivary cortisol, low-dose dexamethasone suppression
— Acromegaly: IGF-1
— Hemochromatosis: ferritin, transferrin saturation (bronze diabetes)
— Chronic pancreatitis or pancreatic cancer: especially new diabetes >50 with weight loss → consider abdominal imaging
— Medication-induced: glucocorticoids, antipsychotics, immune checkpoint inhibitors (can cause fulminant T1DM)
— Urine albumin-to-creatinine ratio (microalbuminuria)
— Dilated retinal exam within 1 year (T2DM) or 5 years post-diagnosis (T1DM)
— Lipid panel, BP assessment
— Foot exam with monofilament and vibration
— TSH (autoimmune cluster with T1DM)
— DKA: BG ≥250, pH <7.3, HCO3 <18, ketones positive, AG >10–12
— HHS: BG ≥600, osmolality >320, minimal ketones, pH >7.3, HCO3 >18, altered mentation
— Mixed pictures common — treat the dominant abnormality
Key distinction: A lean adult with "new T2DM" who goes into DKA on a sulfonylurea is LADA until proven otherwise — order GAD-65 and C-peptide before assuming oral agent failure. Missing this delays appropriate insulin therapy and increases DKA recurrence risk.
— Critically ill / ICU / DKA / HHS / post-op cardiac: IV insulin infusion
— Non-ICU eating patient: subcutaneous basal-bolus-correction regimen
— Non-ICU NPO or continuous tube feeds: basal + correction (no nutritional bolus) or basal + scheduled q6h regular insulin
— Reactive, not proactive — chases highs rather than preventing them
— Associated with wider glycemic excursions, more hyperglycemia AND hypoglycemia
— Acceptable only as correction component layered onto basal-bolus, or for very brief admissions in mild hyperglycemia with low insulin needs (<20 units/day)
— Insulin-naive: 0.3–0.5 units/kg/day total
— Use lower end (0.2–0.3) if: elderly, AKI/CKD eGFR <45, low BMI, frail, hypoglycemia history
— Use higher end (0.5–0.6) if: obese, on glucocorticoids, severe hyperglycemia, insulin resistance
— Already on insulin: continue 75–80% of home TDD initially (illness alters needs); titrate up
— 50% basal (glargine, detemir, degludec once daily; or NPH BID)
— 50% bolus divided across three meals as rapid-acting (lispro, aspart, glulisine)
— Add correction scale matched to insulin sensitivity (typical: 1 unit per 50 mg/dL above 150 for sensitive; 1 unit per 25 above 150 for resistant)
— Hold nutritional bolus if patient not eating that meal (>50% of tray)
— Never hold basal in T1DM
— Reduce basal by 20% if hypoglycemia overnight
Step 3 management: Convert "sliding scale only" orders to basal-bolus on hospital day 2 if BG remains >180 — this is among the most-tested inpatient diabetes management decisions. Document insulin-naive TDD calculation and rationale.
— Glargine U-100 (Lantus): once daily, peakless ~24h
— Glargine U-300 (Toujeo): flatter, longer; less hypoglycemia
— Detemir: 12–24h, often BID
— Degludec: 42h half-life, very flat, forgiving of timing errors
— NPH: BID, peak at 4–8h — causes lunch/early morning hypoglycemia; useful as steroid-matched basal (see below)
— Rapid-acting (lispro, aspart, glulisine): onset 10–15 min, peak 1–2h, give 0–15 min before meal
— Ultra-rapid (Fiasp, Lyumjev): can give at start of meal or up to 20 min after — useful when PO intake uncertain
— Regular insulin: 30 min before meals; preferred for IV infusion and for continuous tube feeds (longer duration matches feeding)
— Morning prednisone causes afternoon/evening peaks → NPH in the morning matched to prednisone dose covers the peak (typical: 0.1 unit/kg NPH per 10 mg prednisone, max ~0.4 units/kg)
— Dexamethasone (24h action) requires basal coverage with glargine
— Anticipate need to taper insulin as steroids taper — 20% reduction per 50% steroid reduction
— TPN: add regular insulin directly to TPN bag; start 0.1 unit per gram of dextrose, titrate based on BG
— Continuous tube feeds: NPH or glargine q12h + correction regular q6h; if feeds interrupted, give D10 at same rate until next insulin dose
— Bolus tube feeds: treat like meals — rapid-acting with each bolus
— Calculate 24h IV insulin requirement when stable
— Give 80% of that as subcutaneous TDD, split basal/bolus
— Overlap: give basal SC 2 hours before stopping drip to prevent rebound hyperglycemia/DKA recurrence
Board pearl: Stopping an insulin drip without 2-hour overlap of subcutaneous basal is the single most common cause of DKA recurrence on the floor — and the most commonly tested transition error on Step 3.
— Generally held on admission for acutely ill patients; insulin is preferred for titratability and safety
— Metformin: hold if AKI, sepsis, contrast exposure, hemodynamic instability (lactic acidosis risk); resume when Cr stable and eGFR >30
— SGLT2 inhibitors: hold 3–4 days preoperatively and during acute illness — euglycemic DKA risk (BG often <250, normal anion gap workup misses it)
— Sulfonylureas: hold — prolonged hypoglycemia risk, especially with AKI
— GLP-1 agonists: hold if NPO, ileus, gastroparesis, pancreatitis; held 1 week preop per recent ASA guidance (aspiration risk from delayed gastric emptying)
— DPP-4 inhibitors (sitagliptin, linagliptin): weight-neutral, low hypoglycemia risk; can be continued or used as adjunct in mild hyperglycemia non-ICU patients
— Pioglitazone: hold in HF, fluid overload
— Triggered by surgery, fasting, infection, alcohol
— BG often 150–250 with significant ketosis and AG acidosis
— Treat as standard DKA: IV fluids, IV insulin, dextrose added early to allow continued insulin while ketosis clears
— Do not restart SGLT2i during admission
— Continue pump if patient is competent and not critically ill; document pump settings
— Convert to basal-bolus SC or IV if ICU, altered mentation, MRI, surgery >2h, DKA
— CGM accuracy reduced with vasopressors, hypothermia, acetaminophen (some sensors), severe acidosis — confirm with fingerstick
— Hold short-acting insulin morning of surgery; give 50–80% basal
— Target intraop BG 140–180; IV insulin for prolonged or cardiac cases
— Resume home regimen when eating reliably
CCS pearl: When admitting a patient on an SGLT2 inhibitor with vomiting or planned surgery, discontinue the SGLT2i immediately and check beta-hydroxybutyrate even if glucose looks "fine" — euglycemic DKA is a high-yield CCS trap.
— Relax targets: premeal 100–150, random <200 acceptable; avoid <100 in frail elderly
— Hypoglycemia causes falls, MI, arrhythmia, cognitive decline — far more harmful than mild hyperglycemia in this group
— Lower starting TDD: 0.2–0.3 units/kg/day
— Simplify regimens: prefer once-daily basal + correction over complex basal-bolus when possible
— Avoid sulfonylureas (especially glyburide — long-acting metabolites cause prolonged hypoglycemia)
— Screen for cognitive impairment that affects self-administration at discharge
— Insulin is renally cleared — dose reduction with declining GFR
— eGFR 10–50: reduce TDD by 25%
— eGFR <10 or dialysis: reduce TDD by 50%
— Hemodialysis days: anticipate post-dialysis hypoglycemia; some patients need basal reduction on HD days
— Metformin: contraindicated if eGFR <30; reduce dose if 30–45; hold during AKI
— SGLT2i: initiate down to eGFR 20 for CV/renal benefit (empagliflozin, dapagliflozin) but hold in acute illness
— GLP-1 RAs: safe in CKD; semaglutide and dulaglutide have CV/renal benefit
— Reduced gluconeogenesis → prolonged hypoglycemia risk
— Lower insulin doses, more frequent monitoring
— Avoid pioglitazone (hepatotoxicity), sulfonylureas
— Metformin generally avoided in advanced cirrhosis (lactic acidosis risk)
— Falsely low in CKD with EPO therapy, hemolysis, recent transfusion, advanced cirrhosis
— Falsely high in iron deficiency, splenectomy, uremia (with some assays)
— Use fructosamine or CGM-derived glucose management indicator as alternative
Step 3 management: For any patient >70 or with eGFR <45, start with TDD 0.2–0.3 units/kg, choose glargine over NPH (less nocturnal hypoglycemia), avoid glyburide, and document hypoglycemia awareness assessment in your daily note.
— Targets: fasting <95, 1h postprandial <140, 2h postprandial <120, A1c <6%
— Insulin is first-line; only metformin and glyburide have any acceptable use, and insulin is preferred (glyburide crosses placenta, metformin crosses)
— Insulin requirements increase ~50% from second to third trimester, then drop precipitously postpartum — adjust to 70% of pre-pregnancy dose immediately after delivery
— Hold ACE/ARB, statins, SGLT2i, GLP-1 RAs (teratogenic or insufficient safety data)
— Inpatient labor management: IV insulin infusion + D5 to maintain BG 70–110
— T1DM predominates; new-onset often presents in DKA
— Insulin pumps common; involve pediatric endocrinology
— Lower TDD: 0.5–1 unit/kg/day depending on pubertal status
— Cerebral edema is the feared DKA complication — avoid rapid fluid resuscitation and rapid BG correction (>100 mg/dL/h)
— Anticipate 50–100% increase in insulin requirements
— Match insulin profile to steroid profile (NPH AM for prednisone AM; glargine for dexamethasone)
— Taper insulin in parallel with steroid taper
— Counsel patients on home glucose monitoring during outpatient steroid courses
— IV insulin infusion with target 140–180 (NICE-SUGAR)
— Hourly BG until stable, then q2h
— Account for vasopressor-induced inaccuracy of fingersticks (use arterial samples if available)
— Transition to SC when stable, eating, off pressors
— Tacrolimus, steroids drive new-onset diabetes after transplant (NODAT) — 10–30% incidence
— Screen with fasting glucose and A1c at 1, 3, 6, 12 months post-transplant
Board pearl: Postpartum insulin requirements drop by 50% within hours of placental delivery — failing to halve the dose causes immediate severe hypoglycemia. This abrupt change is uniquely tested for diabetic pregnancy management.
— Definitions: Level 1 <70, Level 2 <54, Level 3 = severe (requires assistance)
— Causes: missed meal after bolus given, renal failure, basal-bolus overlap with sliding scale, sulfonylurea, hepatic failure, sepsis resolution, octreotide, beta-blocker masking
— Symptoms: tremor, diaphoresis, palpitations, confusion, seizure, coma; blunted in elderly, beta-blocked, frequent-hypoglycemia patients
— Treatment algorithm:
— Conscious + PO: 15 g fast carbs (4 oz juice, glucose tabs), recheck in 15 min
— NPO or altered: D50 25 g IV (50 mL of 50% dextrose)
— No IV access: glucagon 1 mg IM/SC
— Always identify and address the cause — recurrent hypoglycemia in one shift requires regimen change, not just rechecks
— Triggers: insulin omission (#1 inpatient cause), infection, MI, surgery, SGLT2i
— Pitfalls: stopping drip too early, inadequate K replacement (K must be >3.3 before insulin), missing cerebral edema in children
— Mortality up to 20%; older patients
— Slow correction of Na and osmolality (avoid >3 mOsm/kg/h drop) to prevent cerebral edema
— Aggressive volume replacement is the cornerstone
— Surgical site infection (especially cardiac, orthopedic)
— Pneumonia, UTI, candidiasis
— Delayed wound healing, anastomotic leak
— AKI, electrolyte derangements
— Prolonged LOS and 30-day readmission
— Wrong concentration (U-100 vs U-500), wrong type (long-acting given as bolus), wrong timing (basal at bedtime in NPO patient)
— Verbal orders for insulin should be avoided
Key distinction: Hypoglycemia in a hospitalized diabetic should trigger a regimen change, not just glucose treatment — repeat events within 24 hours are a sentinel event in most hospitals and the most common preventable diabetes harm.
— DKA with pH <7.0, HCO3 <5, altered mentation, hemodynamic instability, or refractory electrolyte abnormalities
— HHS with osmolality >330 or coma
— Persistent hyperglycemia >400 despite escalating SC insulin
— Recurrent severe hypoglycemia
— Need for IV insulin infusion in a unit without floor capability
— Insulin pump or hybrid closed-loop user requiring inpatient pump management
— Recurrent DKA or brittle diabetes
— Steroid-induced hyperglycemia not controlled on standard basal-bolus
— TPN with persistent hyperglycemia despite >0.2 unit/g dextrose
— Newly diagnosed T1DM requiring education before discharge
— Suspected secondary cause (Cushing, acromegaly, pheochromocytoma)
— Pregnancy with diabetes
— Insulin requirements >2 units/kg/day (insulin resistance workup)
— Diabetes educator/CDE: every newly diagnosed patient; insulin initiation; pump training
— Nutrition: carbohydrate counting, sick-day rules, renal/cardiac diet integration
— Podiatry: any active foot ulcer, Charcot suspicion, ingrown toenail in diabetic
— Wound care/vascular surgery: non-healing ulcer, suspected PAD
— Ophthalmology: symptomatic vision changes; baseline dilated exam for newly diagnosed
— Nephrology: rapidly rising Cr, proteinuria >1 g/day, eGFR <30
— Social work/case management: insulin affordability, home glucose monitoring access
— Two consecutive BG >300 → reassess regimen, don't just add correction
— Any BG <54 → notify provider, reassess regimen, consider basal reduction
— Failure to close anion gap by hour 12 on IV insulin → re-examine drip rate, dextrose addition, missed sepsis
CCS pearl: A diabetic foot ulcer with exposed bone or positive probe-to-bone test mandates immediate MRI, vascular surgery + podiatry consult, IV antibiotics covering MRSA + GNR + anaerobes, and glycemic optimization — order all four simultaneously on the CCS clock.
— T1DM: absolute insulin deficiency; lean, antibody-positive, prone to DKA; requires basal insulin always
— T2DM: insulin resistance + relative deficiency; obesity, family history, acanthosis
— LADA: autoimmune diabetes in adults, often misdiagnosed as T2DM, fails oral agents within years
— MODY: monogenic, young, non-obese, strong family history, often well-controlled on sulfonylurea
— Ketosis-prone diabetes (Flatbush diabetes): presents with DKA but later behaves like T2DM; common in African-American and Hispanic populations
— Cystic fibrosis-related diabetes: screen annually with OGTT from age 10; insulin-only treatment
— Post-pancreatectomy / pancreatogenic (Type 3c): brittle, low glucagon response, hypoglycemia-prone; need insulin and pancreatic enzymes
— Transient, illness-driven, A1c <6.5%
— Resolves with illness resolution
— Still treat in hospital; outpatient repeat A1c at 3 months
— Higher risk of developing overt diabetes within 1–5 years — counsel on lifestyle
— Glucocorticoids, antipsychotics (especially olanzapine, clozapine), tacrolimus, cyclosporine, thiazides, beta-blockers, statins (modest), niacin, protease inhibitors, immune checkpoint inhibitors (can cause fulminant T1DM)
— Document drug-related onset; some reversible after withdrawal
— TPN overfeeding (>4 mg/kg/min dextrose)
— Continuous high-carb tube feeds
— Sugary IV fluids (D5 maintenance in unrecognized hyperglycemia)
Key distinction: New-onset DKA in a previously healthy adult on a checkpoint inhibitor (pembrolizumab, nivolumab) is autoimmune fulminant T1DM until proven otherwise — discontinue the agent, start insulin, and check antibodies and C-peptide. This is increasingly tested as immunotherapy expands.
— Cushing syndrome: central obesity, striae, proximal weakness, hypertension, hypokalemia; suspect with refractory hyperglycemia on steroids or pituitary findings
— Acromegaly: coarse features, ring/shoe size change, headaches, sleep apnea; IGF-1 elevated
— Pheochromocytoma: episodic hypertension, palpitations, diaphoresis; plasma/urine metanephrines
— Glucagonoma: necrolytic migratory erythema, weight loss, mild diabetes
— Hyperthyroidism: worsens glycemic control, increases insulin clearance
— Chronic pancreatitis with exocrine + endocrine failure
— Pancreatic adenocarcinoma: new diabetes after age 50 with weight loss is a red flag — consider CT pancreas
— Hereditary hemochromatosis: bronze diabetes, hepatomegaly, arthralgias
— Severe sepsis, burns, trauma — stress response
— Acute MI, stroke — catecholamine surge
— Pancreatitis — transient hyperglycemia from inflammation
— Pheochromocytoma crisis
— Adrenal insufficiency: hyponatremia, hyperkalemia, hypotension, hypoglycemia in fasting
— Hypopituitarism
— Insulinoma: Whipple's triad with documented endogenous insulin (high C-peptide with hypoglycemia)
— Factitious: high insulin with suppressed C-peptide; check sulfonylurea screen
— Severe malnutrition, sepsis, hepatic failure, post-bariatric dumping
— Beta-blocker overdose, alcohol-induced (impaired gluconeogenesis)
— Fingerstick falsely high: maltose-containing IV products (icodextrin), pressors, hypoperfusion
— Fingerstick falsely low: anemia, very high hematocrit affects differently
— Confirm with central lab in any decision-critical reading
Board pearl: "New diabetes + unintentional weight loss in a patient over 50" should prompt CT pancreas — pancreatic cancer presents as new-onset diabetes in 1–2% of cases and is among the highest-yield "don't miss" diagnoses in the differential.
— A1c <7%, well-controlled on home regimen: resume home regimen; reinforce education
— A1c 7–9%, T2DM on orals: intensify — add second agent (GLP-1 RA or SGLT2i preferred for CV/renal benefit; consider basal insulin if symptomatic)
— A1c >9% or symptomatic: discharge on basal insulin (start 0.1–0.2 units/kg or 10 units), continue/start metformin if eGFR adequate, add GLP-1 RA if no contraindication
— A1c >10% with weight loss/ketosis or T1DM: full basal-bolus regimen with structured education
— Newly diagnosed T2DM: metformin + lifestyle if mild; add GLP-1 RA or insulin if more severe
— ASCVD or high CV risk: GLP-1 RA (semaglutide, dulaglutide, liraglutide) or SGLT2i (empagliflozin, canagliflozin)
— HFrEF or HFpEF: SGLT2i regardless of diabetes status
— CKD with albuminuria: SGLT2i (renal protective down to eGFR 20); finerenone if albuminuria persists
— Weight loss priority: GLP-1 RA, especially semaglutide or tirzepatide
— Moderate-intensity statin for any DM age 40–75 (high-intensity if ASCVD); reassess at discharge
— BP target <130/80 in most diabetics; ACEi/ARB first-line if albuminuria
— Aspirin: secondary prevention only (no longer routinely for primary prevention)
— Insulin injection technique, site rotation, storage
— Glucose meter use, target ranges, when to call
— Hypoglycemia recognition and treatment, glucagon prescription if on insulin
— Sick-day rules: never stop insulin, increase monitoring, hydrate, check ketones
— Foot care, dental care, smoking cessation
Step 3 management: Every diabetic discharge order set should include: home glucose meter and strips, glucagon kit if on insulin or sulfonylurea, statin, ACEi/ARB if indicated, scheduled PCP follow-up within 1–2 weeks, and a written sick-day plan.
— PCP/endocrine visit within 1–2 weeks of discharge for any insulin change or newly diagnosed diabetes
— A1c every 3 months until at goal, then every 6 months
— Annual: dilated retinal exam, monofilament foot exam, urine albumin-to-Cr ratio, lipid panel, dental exam
— BMP every 3–6 months on metformin, SGLT2i, ACEi/ARB
— Annual influenza
— Pneumococcal: PCV15 + PPSV23 or PCV20 alone per current ACIP for adults with diabetes
— Hepatitis B series for adults 19–59 with diabetes (and 60+ at risk)
— COVID-19 per current guidance
— Tdap, shingles (≥50)
— Diabetes self-management education and support (DSMES) program — covered by Medicare at diagnosis, change in regimen, complication development, transitions
— Medical nutrition therapy with registered dietitian
— Mental health screening — depression doubled in diabetes; treat to improve adherence
— Covered by Medicare for any insulin-requiring patient
— Improves A1c and reduces hypoglycemia
— Counsel on alarm settings, calibration, sensor wear
— Smoking cessation: most impactful single intervention for CV risk reduction
— Weight loss: 5–10% reduces A1c, BP, lipids
— Physical activity: 150 min/week moderate aerobic + 2 sessions resistance training
— Alcohol moderation; counsel on hypoglycemia risk with insulin/sulfonylurea
— Sleep apnea screening — high prevalence in T2DM
— Ophthalmology annually
— Podiatry annually (more often with neuropathy or prior ulcer)
— Cardiology if ASCVD or symptoms
— Nephrology if eGFR <30 or rapidly declining
Board pearl: A diabetic discharged on new basal insulin who isn't seen by a provider within 2 weeks has a markedly higher 30-day readmission rate — structured early follow-up is the single most effective transition-of-care intervention for diabetes admissions and is heavily tested as a quality measure.
— ISMP designates insulin as one of the highest-risk inpatient medications
— Never use trailing zeros (write "10 units" not "10.0 units" — read as 100)
— Avoid "u" abbreviation (mistaken for "0") — write out "units"
— U-500 insulin requires special labeling and double verification — wrong concentration is a sentinel event
— Independent double-check for IV insulin infusions and pediatric dosing
— Wrong-dose insulin at discharge is among the top causes of 30-day readmission and ED visits
— Reconcile home regimen vs hospital regimen vs discharge regimen — document the rationale for any change
— Confirm patient can afford and access insulin (insulin pricing — Medicare $35/month cap helps but commercial varies)
— Provide written instructions in patient's preferred language at appropriate health-literacy level
— Teach-back method for injection technique
— Hypoglycemic patient with altered mentation cannot consent — treat hypoglycemia first; reassess capacity after correction
— DKA with severe acidosis and altered sensorium: emergency exception applies for life-saving treatment; involve surrogate when possible
— Insulin pump in a competent patient who wishes to self-manage: document shared decision-making, set safety parameters
— Severe hypoglycemia with loss of consciousness while driving: most states require physician reporting or patient self-reporting to DMV — counsel and document
— Occupational implications (commercial driver, pilot, heavy machinery): inform patient of regulatory requirements
— Insulin rationing due to cost is a recognized cause of DKA admissions — screen for affordability and refer to patient assistance programs
— Food insecurity worsens glycemic control — screen and refer
— Language and literacy barriers double medication error rates
— Indication, type, concentration, dose, route, frequency for every insulin order
— Hypoglycemia events with cause and regimen change
Step 3 management: Before any insulin-treated patient discharges, verify affordability, ability to self-administer, glucagon prescription, and follow-up appointment date — these four checks prevent the most common preventable readmissions and adverse events.
— Lispro/aspart/glulisine: onset 10–15 min, peak 1h, duration 3–4h
— Regular: onset 30 min, peak 2–3h, duration 5–8h
— NPH: onset 1–2h, peak 4–8h, duration 10–16h
— Glargine/detemir: onset 1–2h, peakless, duration 20–24h
— Degludec: duration >42h
— U-500 regular: behaves like NPH; for severe insulin resistance
— IV to SC: 80% of 24h IV dose as total daily SC, split 50/50 basal/bolus
— Glargine BID to once daily: same total dose
— NPH to glargine: reduce by 20%
— Insulin to U-500: 1:1 unit conversion but different volumes — pharmacy verification
— Insulin sensitivity factor (correction): 1800 ÷ TDD (rapid-acting) or 1500 ÷ TDD (regular) = mg/dL drop per unit
— Carb ratio: 500 ÷ TDD = grams of carb covered per unit
— Corrected Na = measured + 1.6 × (glucose − 100)/100
— Anion gap = Na − (Cl + HCO3); normal 8–12
— DKA + abdominal pain in adult diabetic without obvious cause → check lipase (gallstone/alcohol pancreatitis can trigger DKA)
— Recurrent DKA in young patient → insulin omission (psychosocial), pump malfunction, or eating disorder
— New diabetes + necrolytic migratory erythema → glucagonoma
— Diabetes + hyperpigmentation + arthralgia → hemochromatosis
— Diabetes + steatorrhea + weight loss → chronic pancreatitis or pancreatic cancer
— Bullous lesions on feet/hands in diabetic → bullosis diabeticorum (benign)
— Erectile dysfunction often the first sign of autonomic neuropathy
— Tight ICU control (80–110) increased mortality (NICE-SUGAR) — use 140–180
— DCCT/UKPDS: tight outpatient control reduces microvascular complications; legacy effect for macrovascular
— SGLT2i and GLP-1 RA reduce CV mortality independent of glucose effect
Key distinction: "Tight glycemic control" benefits microvascular endpoints (retinopathy, nephropathy, neuropathy) far more than macrovascular in the short term — and tight ICU control causes harm. Step 3 frequently tests the contrast between outpatient A1c targets and inpatient BG targets.
— Hospital day 2, patient on sliding scale only, BGs 220, 280, 310. Next step? → Initiate basal-bolus regimen with TDD 0.4 units/kg, split 50/50. Do not simply increase the correction scale.
— DKA patient: BG now 200, AG still 18. Next step? → Continue insulin drip, add D5 to maintenance fluids, target BG 150–200 until AG closes. Do not stop insulin.
— DKA resolved, ready to transition. Next step? → Give SC basal 2 hours before stopping IV drip. Calculate SC TDD as 80% of last 24h IV requirement.
— Patient on prednisone 40 mg AM with afternoon BGs 280–340, fasting BG normal. Next step? → Add NPH in the morning matched to steroid dose; taper insulin as steroid tapers.
— Patient on empagliflozin presents post-op with N/V, BG 220, AG 22, pH 7.25, ketones positive. Diagnosis? → Euglycemic DKA. Treat as DKA with early dextrose, hold SGLT2i permanently during admission.
— T1DM patient NPO for procedure tomorrow. Orders? → Continue 80% of basal, hold short-acting boluses, start D5 maintenance, fingerstick q4–6h.
— 62-year-old with new diabetes, A1c 9.5%, 15-lb weight loss, mild back pain. Next step? → CT abdomen/pancreas to evaluate for pancreatic cancer.
— Diabetic with CKD on glyburide develops severe hypoglycemia. Next step? → Discontinue glyburide, admit for observation (long-acting metabolites), monitor 24–48h; switch to DPP-4i or insulin.
— A1c 5.8% but mean CGM glucose 180 in CKD patient on EPO. → A1c falsely low; use fructosamine or CGM-derived management indicator.
— T1DM patient just delivered; what to do with insulin? → Reduce to 50–70% of pre-pregnancy dose immediately; monitor closely.
Board pearl: When the stem mentions an SGLT2 inhibitor + acute illness/surgery/vomiting + acidosis, the answer is always euglycemic DKA regardless of glucose level — recognize the pattern, hold the drug, treat with insulin and dextrose.
Inpatient glycemic management requires individualized basal-bolus-correction insulin dosing targeting BG 140–180 mg/dL, with IV insulin for the critically ill, careful transitions, and structured discharge planning that integrates A1c-driven regimen selection, complication screening, and early follow-up.
Board pearl: The three highest-yield Step 3 errors to avoid in any diabetic admission are (1) sliding scale only, (2) stopping IV insulin without SC overlap, and (3) discharging on a new insulin regimen without verifying affordability, technique, and early follow-up — recognizing and correcting these three patterns answers a disproportionate share of inpatient diabetes questions and reflects the actual quality measures used in US hospitals.