Eduovisual
Endocrine
Diabetic ketoacidosis: CCS-style management
— Hyperglycemia: glucose >250 mg/dL (euglycemic DKA possible if <250, especially with SGLT2 inhibitors, pregnancy, or prolonged fasting)
— Anion gap metabolic acidosis: pH <7.30, bicarbonate <18 mEq/L, anion gap >12
— Ketonemia/ketonuria: beta-hydroxybutyrate ≥3 mmol/L is the most sensitive marker
— Infection (pneumonia, UTI most common — check even without fever)
— Infarction (MI, stroke, mesenteric ischemia)
— Insulin nonadherence (most common cause in known T1DM, especially adolescents and those with cost/access barriers)
— Iatrogenic (steroids, atypical antipsychotics, SGLT2 inhibitors, thiazides)
— Initial presentation of T1DM (25% of new T1DM presents in DKA)
— Any T1DM with vomiting, abdominal pain, polyuria, polydipsia, altered mental status, or Kussmaul respirations
— Hyperglycemia + tachypnea in any diabetic
— Unexplained anion gap acidosis in a patient on SGLT2 inhibitor — check ketones even if glucose normal
— Pediatric: any child with vomiting + dehydration + hyperglycemia
— Mild: pH 7.25–7.30, HCO3 15–18, alert
— Moderate: pH 7.00–7.24, HCO3 10–15, drowsy
— Severe: pH <7.00, HCO3 <10, stupor/coma → ICU
CCS pearl: On the CCS case, when DKA is suspected, your first three orders should be fingerstick glucose, BMP (for anion gap and K+), and venous blood gas — not arterial. Advance the clock only after fluids and insulin are running. Order "continuous cardiac monitoring" and "IV access, 2 large bore" early; these are easy CCS points.
— Polyuria, polydipsia, polyphagia → weight loss → nausea, vomiting → abdominal pain → tachypnea (Kussmaul) → lethargy → coma
— Symptom evolution faster in T1DM (24–48 h) than in HHS (days to weeks)
— Present in 40–75% of DKA cases, especially in children and severe acidosis (pH <7.0)
— Key distinction: DKA-related abdominal pain resolves with correction of acidosis. Persistent pain after pH normalization → search for a surgical abdomen, pancreatitis, or mesenteric ischemia as the precipitant
— Order lipase but interpret cautiously — lipase can be mildly elevated in DKA without true pancreatitis
— Last insulin dose, regimen, pump status (pump failure is a classic precipitant)
— Fever, dysuria, cough, diarrhea (infection screen)
— Chest pain, dyspnea (silent MI in diabetics)
— Medication list: SGLT2 inhibitors (canagliflozin, empagliflozin, dapagliflozin) → euglycemic DKA; recent steroid burst; new atypical antipsychotic
— Pregnancy in any reproductive-age female (lower threshold for DKA, can occur at glucose <200)
— Substance use: cocaine, alcohol (alcoholic ketoacidosis mimic), missed meals
— New-onset T1DM often misdiagnosed as gastroenteritis or viral illness
— Bedwetting in a previously continent child
— Weight loss + fatigue + fruity breath
— Pump occlusion, infusion set failure, or site infection can cause DKA within 4–6 hours
— Patients on pumps have no long-acting insulin reservoir — DKA develops faster than on basal-bolus regimens
Board pearl: A young woman on an SGLT2 inhibitor presenting with nausea, tachypnea, and glucose of 180 is a classic euglycemic DKA stem — check beta-hydroxybutyrate and a VBG. Do not be falsely reassured by a normal glucose.
— Tachycardia (volume depletion + acidosis-driven catecholamines)
— Tachypnea with Kussmaul respirations — deep, sighing, regular breaths compensating for metabolic acidosis (respiratory rate often 25–40)
— Hypotension is a late and ominous finding — adults typically lose 6 L of fluid and 300–500 mEq sodium
— Temperature: usually normal or low even with infection (acidosis blunts fever response) — do not exclude sepsis based on afebrile status
— Dry mucous membranes, decreased skin turgor, sunken eyes
— Capillary refill >3 seconds, cool extremities
— Orthostatic vitals if patient can stand
— Estimate deficit: ~10% of body weight in severe DKA (7 L in 70-kg adult)
— Mild DKA: alert and oriented
— Moderate: drowsy, slowed cognition
— Severe (pH <7.0 or osmolality >320): stupor, coma → secure airway
— Key distinction: Mental status correlates more tightly with serum osmolality than with pH or glucose. If a DKA patient is comatose but osmolality is normal, look for another cause (stroke, intoxication, meningitis)
— Fruity (acetone) breath odor
— Warm, dry skin in early DKA shifts to cold and clammy with shock
— Capillary refill, mucous membranes more reliable than orthostatics
— Watch for headache, irritability, bradycardia, hypertension, papilledema — heralds of cerebral edema, the leading cause of pediatric DKA death
— Lung auscultation (pneumonia), CVA tenderness (pyelo), foot exam (diabetic foot infection — often missed), pelvic/skin exam, line/port sites
CCS pearl: On CCS, order a full physical exam as one of your first actions in DKA cases. Hidden foot ulcer or perirectal abscess as the precipitant is a common testing trick — finding and treating it gets you scoring credit beyond just correcting the metabolic derangement.
— Fingerstick glucose (q1h after treatment starts)
— BMP/CMP: glucose, anion gap, K+, bicarbonate, BUN/Cr, calculated osmolality
— Venous blood gas (VBG): pH and pCO2 — venous is adequate, no need to traumatize an artery
— Beta-hydroxybutyrate (preferred over urine ketones — urine measures acetoacetate, which underestimates severity early and overestimates during recovery)
— CBC with differential (leukocytosis up to 25,000 is common in DKA without infection — stress demargination; left shift with bands suggests true infection)
— Urinalysis (ketones, glucose, signs of UTI)
— Phosphorus, magnesium, calcium
— Lactate (concurrent lactic acidosis worsens prognosis)
— ECG (look for ischemia as precipitant; K+ effects)
— Troponin if any chest symptoms or age >40
— HbA1c (establishes chronicity and adherence)
— Lipase, LFTs (pancreatitis screen)
— Blood and urine cultures, CXR if any infection suspicion
— Pregnancy test in reproductive-age females
— AG = Na − (Cl + HCO3); normal 8–12
— Corrected sodium = measured Na + 1.6 × (glucose − 100)/100 — important because pseudohyponatremia from hyperglycemia is common
— Total body K+ is always depleted (3–5 mEq/kg deficit) regardless of serum value
— Serum K+ is shifted out of cells by insulin deficiency and acidosis, so it often appears normal or high
— K+ <3.3 → hold insulin, give KCl first (insulin will drop K+ further and cause arrhythmia)
— K+ 3.3–5.2 → start insulin AND add 20–30 mEq KCl per liter of IVF
— K+ >5.2 → start insulin, recheck K+ q2h, hold KCl
Board pearl: The single most dangerous early move in DKA is giving insulin to a hypokalemic patient. Always have the K+ before insulin flows.
— Calculated effective osmolality = 2(Na) + glucose/18; >320 mOsm/kg suggests HHS overlap
— Mixed acid-base disorders: use delta-delta ratio (ΔAG/ΔHCO3); ratio ~1 = pure AG acidosis; <1 = concurrent non-AG (hyperchloremic) acidosis from prior NS resuscitation; >2 = concurrent metabolic alkalosis (vomiting)
— Winter's formula for respiratory compensation: expected pCO2 = 1.5(HCO3) + 8 ± 2
— Beta-hydroxybutyrate (β-OHB) is the dominant ketone in severe DKA
— Nitroprusside-based urine ketone tests detect acetoacetate but NOT β-OHB → can be falsely low early
— Key distinction: As DKA improves, β-OHB converts to acetoacetate, so urine ketones may paradoxically rise during successful treatment. Do not panic — follow the anion gap and serum β-OHB
— Lipase >3× ULN with imaging confirmation for true pancreatitis (mild lipase elevation alone is nonspecific in DKA)
— Troponin and ECG for MI screening, especially in older patients or those with chest discomfort
— CT head for any DKA patient with focal neuro signs, persistent altered mental status after metabolic correction, or headache (rule out stroke, cerebral edema)
— Lumbar puncture if meningitis suspected (after CT)
— CT abdomen for persistent abdominal pain after pH correction
— HHS: glucose >600, osmolality >320, pH >7.30, minimal ketones, profound dehydration, altered mental status
— DKA: glucose >250 (often 400–800), pH <7.30, significant ketones, less mental status change
— Overlap syndrome occurs in ~30% — manage as DKA
— Serum bicarbonate baseline is lower (18–22) due to physiologic respiratory alkalosis
— DKA can occur at glucose <200; lower threshold to check β-OHB and VBG
CCS pearl: Order β-hydroxybutyrate, not just urine ketones, on the initial CCS workup. Recheck the anion gap (not glucose) to track resolution — the AG closes before glucose normalizes.
— Fluids first
— Potassium before/with insulin
— Insulin to shut off ketogenesis
— Initial bolus: 0.9% NS 15–20 mL/kg over the first hour (~1–1.5 L in adults)
— After first hour, reassess corrected Na+ and volume status:
· Corrected Na+ normal/high → switch to 0.45% NS at 250–500 mL/h
· Corrected Na+ low → continue 0.9% NS at 250–500 mL/h
— When glucose reaches 200 mg/dL → switch fluids to D5 1/2NS at 150–250 mL/h to allow continued insulin infusion without hypoglycemia
— Pediatric exception: more cautious fluid resuscitation (10 mL/kg bolus, then deficit replacement over 24–48 h) to reduce cerebral edema risk
— K+ <3.3 → 20–40 mEq KCl/h, hold insulin until K+ >3.3
— K+ 3.3–5.2 → 20–30 mEq KCl per liter IVF
— K+ >5.2 → no KCl, recheck q2h
— Goal: maintain K+ 4–5 mEq/L throughout treatment
— Regular insulin IV: 0.1 U/kg bolus, then 0.1 U/kg/h infusion (or skip bolus and start at 0.14 U/kg/h)
— Target glucose decline 50–75 mg/dL/h; if <50 mg/dL/h drop in first hour, double the rate
— Once glucose <200 → reduce insulin to 0.02–0.05 U/kg/h AND add dextrose-containing fluids
— Do not stop insulin when glucose normalizes — continue until anion gap closes and β-OHB <1
— Only consider if pH <6.9: 100 mEq NaHCO3 in 400 mL sterile water + 20 mEq KCl over 2 hours
— Routine bicarb is harmful — worsens cerebral edema risk, paradoxical CNS acidosis, hypokalemia
Step 3 management: Resolution criteria — glucose <200 AND two of: HCO3 ≥15, venous pH >7.30, anion gap ≤12. Glucose normalization alone is not resolution.
— Bolus 0.1 U/kg IV push (optional; can omit if starting at 0.14 U/kg/h)
— Continuous infusion 0.1 U/kg/h (e.g., 7 U/h in 70-kg adult)
— Titration: increase rate by 1 U/h if glucose falls <50 mg/dL/h; halve rate if dropping >75 mg/dL/h
— Once glucose reaches 200 mg/dL: decrease to 0.02–0.05 U/kg/h AND start D5 1/2NS
— Lispro or aspart 0.2 U/kg SC bolus, then 0.1 U/kg q1h, OR 0.3 U/kg initial then 0.2 U/kg q2h
— Equivalent efficacy to IV regular insulin in mild DKA, cheaper, no ICU required
— Contraindicated in severe DKA, shock, or anasarca (unreliable absorption)
— Only transition when all resolution criteria met AND patient able to eat
— Give SC long-acting basal insulin (glargine or detemir) 1–2 hours BEFORE stopping IV infusion to prevent rebound DKA
— Key distinction: Stopping IV insulin without overlapping SC basal insulin is a top cause of recurrent DKA on the floor and a common CCS pitfall
— For insulin-naive patients: total daily dose 0.5–0.7 U/kg/day, split 50% basal / 50% prandial
— For known diabetics: resume prior outpatient regimen if it was effective
— Phosphate replacement only if PO4 <1.0 mg/dL with cardiac/respiratory/skeletal muscle weakness — give K-phos 20–30 mEq/L
— Magnesium replacement if Mg <1.8 (especially in setting of hypokalemia)
— Antiemetics (ondansetron) for vomiting
— Empiric antibiotics if infection suspected — do not delay for cultures in septic-appearing patients
— Routine bicarbonate (only pH <6.9)
— Excessive normal saline (causes hyperchloremic non-AG acidosis that prolongs apparent recovery — consider balanced crystalloids like LR or Plasma-Lyte after initial resuscitation)
Board pearl: "Patient improved, anion gap closed, IV insulin stopped — 4 hours later DKA returns." The missing step was overlapping subcutaneous glargine before discontinuing the drip.
— Two large-bore peripheral IVs minimum
— Central line if: shock, need for vasopressors, no peripheral access — femoral or subclavian acceptable
— Arterial line not routinely needed; VBG suffices for serial monitoring
— Foley catheter if obtunded or strict I/O needed; not routine
— Continuous cardiac monitoring for arrhythmia surveillance during K+ shifts
— Intubation rarely needed and is dangerous in DKA — paralysis abolishes Kussmaul respirations and causes precipitous pCO2 rise → catastrophic acidosis
— If intubation required: match pre-intubation minute ventilation aggressively (RR 25–30, low PEEP), avoid permissive hypercapnia
— Stop pump on admission, document basal rates for later resumption
— Restart pump only after full resolution and patient demonstrates understanding of site/troubleshooting
— Consult diabetes educator and endocrinology before discharge
— Stop the SGLT2 inhibitor immediately and document as adverse drug reaction
— Treat with insulin + dextrose-containing fluids from the start (glucose is already normal)
— Target β-OHB <1 and AG closure rather than glucose targets
— Hold SGLT2i for 3 days before any surgery in diabetic patients (FDA warning)
— Glucose q1h
— BMP, VBG, β-OHB q2–4h until AG closed
— Mental status checks q1h (especially in pediatric patients — cerebral edema)
— Strict I/O hourly
— UTI: empiric ceftriaxone pending cultures
— Pneumonia: ceftriaxone + azithromycin
— MI: standard ACS pathway (aspirin, heparin, cath if STEMI) — DKA is not a contraindication to PCI
— Pump failure: replace site, switch to MDI temporarily
CCS pearl: When the CCS clock advances and labs reveal AG closed + glucose 180 + patient eating → order "insulin glargine SC," wait 2 hours on the clock, then "discontinue insulin drip." This sequence is worth scoring points.
— Often present with HHS or mixed DKA-HHS rather than pure DKA
— Higher mortality (up to 20% vs <5% in younger adults)
— More likely to have silent MI or stroke as precipitant — order ECG and troponin routinely
— Cognitive impairment may delay symptom recognition; check medication adherence with family
— Fluid resuscitation more cautious: 250–500 mL/h after initial bolus; monitor for CHF
— Lower insulin infusion rates (0.05 U/kg/h) acceptable to avoid hypoglycemia
— Higher risk of hospital-acquired complications: delirium, falls, pressure injury, DVT — order DVT prophylaxis (heparin SC) on admission
— Baseline acidosis from CKD complicates AG interpretation; trust β-OHB
— Reduced insulin clearance → may need lower infusion rates and longer transition overlap with SC basal
— Volume status assessment harder; consider POCUS IVC or bedside echo
— Avoid LR if K+ already elevated (LR contains 4 mEq/L K+)
— Discontinue metformin (lactic acidosis risk) and SGLT2 inhibitor; reassess at discharge
— Patients are anuric — fluid resuscitation must be far more conservative (500 mL boluses, reassess)
— May require urgent dialysis for volume overload or refractory hyperkalemia
— Insulin still required despite oliguria — ketogenesis is the driver, not glucose excretion
— Key distinction: In ESRD, glucose levels may be misleadingly elevated because there is no glucosuria. Trust ketones and AG over glucose
— Cirrhotics can develop DKA with concurrent lactic acidosis or alcoholic ketoacidosis
— Lower glycogen reserves → higher hypoglycemia risk during treatment — start dextrose earlier (glucose <250 rather than <200)
— Albumin-corrected AG more useful: corrected AG = measured AG + 2.5 × (4 − albumin)
Step 3 management: In ESRD patients with DKA, treat with insulin and minimal fluids; if hyperkalemia is refractory or volume status precludes safe resuscitation, call nephrology for urgent hemodialysis rather than escalating crystalloid.
— Occurs in 1–3% of pregnancies complicated by T1DM; can occur in gestational diabetes
— Euglycemic DKA threshold: can develop at glucose 180–200 due to fetal glucose sink and physiologic insulin resistance
— Maternal mortality <1% with prompt treatment; fetal mortality 9–35% — call OB and MFM immediately
— Common precipitants: hyperemesis gravidarum, beta-mimetic tocolytics (terbutaline), antenatal steroids (betamethasone), UTI
— Management: same fluid/insulin/K+ algorithm but with continuous fetal monitoring after 24 weeks gestation
— Left lateral decubitus positioning to optimize uterine perfusion
— Do not deliver for fetal distress until maternal metabolic correction is underway — fetal tracing often improves dramatically as acidosis resolves; premature delivery in unstable maternal DKA worsens both outcomes
— Bicarbonate buffer is lower in pregnancy (18–22), so threshold for diagnosis is more permissive
— Cerebral edema incidence 0.5–1% but accounts for 60–90% of DKA deaths in children
— Risk factors: age <5, new-onset T1DM, severe acidosis (pH <7.1), elevated BUN, low pCO2, rapid fluid administration, bicarbonate use
— Warning signs (recheck mental status q1h): headache, altered mental status, bradycardia + hypertension (Cushing reflex), incontinence, cranial nerve palsies, papilledema
— Treatment: elevate head of bed, mannitol 0.5–1 g/kg IV or 3% hypertonic saline 5 mL/kg, intubate with hyperventilation, urgent CT head, neurosurgery consult
— Prevention: avoid bicarbonate, limit fluid rate to 1.5–2× maintenance, gradual rehydration over 24–48 h
— Initial bolus 10 mL/kg NS (not 20)
— Calculate deficit (5–10% body weight) and replace over 24–48 h
— Insulin infusion 0.05–0.1 U/kg/h — never bolus insulin in pediatric DKA
Board pearl: A pediatric DKA patient develops new headache and bradycardia 6 hours into treatment — next step is mannitol or hypertonic saline immediately, then CT head. Do not delay osmotherapy for imaging.
— Hypoglycemia — most common complication; prevent by adding D5 when glucose reaches 200, halving insulin rate, q1h glucose checks
— Hypokalemia — most dangerous; can cause fatal arrhythmia. Always check K+ before starting insulin
— Hyperchloremic non-AG metabolic acidosis — from large-volume NS; self-resolves but prolongs apparent recovery. Consider balanced crystalloids (LR, Plasma-Lyte) after initial resuscitation
— Cerebral edema — pediatric > adult; mortality 20–50%
— Pulmonary edema/ARDS — from over-resuscitation, especially in elderly or CKD
— Volume overload — monitor with daily weights, lung exam, oxygen requirement
— Acute kidney injury — pre-renal from dehydration; usually resolves with fluids. Persistent AKI → consider contrast nephropathy, rhabdomyolysis, or sepsis
— Venous thromboembolism — DKA is a hypercoagulable state; give prophylactic SC heparin or enoxaparin to all admitted DKA patients
— Aspiration pneumonia — from vomiting + altered mental status; elevate head of bed
— Rhabdomyolysis — check CK if prolonged immobility or severe acidosis
— Mucormycosis (rhino-orbital-cerebral) — rare but classic DKA complication. Suspect with facial pain, periorbital swelling, black eschar on nasal mucosa, cranial nerve deficits. Treatment: emergent surgical debridement + IV amphotericin B (liposomal)
— Acute pancreatitis — true (not just lipase elevation) in 10–15%; usually mild
— Age >65, severe acidosis (pH <7.0), HHS overlap, comorbid sepsis or MI, delayed presentation
— Overall DKA mortality <1% in young adults, 5% in adults overall, up to 20% in elderly with HHS overlap
— ~20% recurrence rate within 1 year, mostly from insulin nonadherence
— Address root causes: cost (insulin assistance programs), mental health, substance use, social support
Key distinction: Hyperchloremic acidosis post-resuscitation has a normal AG and elevated chloride; it's not treatment failure. Track AG closure and β-OHB, not just bicarbonate, to confirm true DKA resolution.
— pH <7.0 or HCO3 <10 (severe acidosis)
— Altered mental status (GCS <12)
— Hemodynamic instability requiring vasopressors
— Need for mechanical ventilation
— Severe electrolyte derangements (K+ <2.5 or >6.5)
— Concurrent critical illness: sepsis, MI, GI bleed, stroke
— Pregnancy with DKA after 20 weeks
— All pediatric DKA <5 years or severe pediatric DKA (PICU)
— pH 7.0–7.25, hemodynamically stable, alert
— Requires q1h glucose, q2–4h labs — most floors cannot provide this cadence
— pH >7.25, HCO3 >15, alert, hemodynamically stable
— Suitable for SC rapid-acting insulin protocol
— Most patients can be managed here if labs follow expected trajectory
— Mild DKA can occasionally be reversed and discharged after 12–24h observation with endocrinology follow-up arranged — but uncommon and requires reliable patient, social support, and confirmed resolution
— Endocrinology — all DKA admissions, especially new-onset T1DM, recurrent DKA, pump patients
— Critical care — severe DKA, shock, intubated patients
— Obstetrics/MFM — all pregnant DKA patients
— Nephrology — ESRD, refractory hyperkalemia, severe AKI
— Infectious disease — atypical infections (mucormycosis, emphysematous pyelonephritis, necrotizing fasciitis)
— Cardiology — DKA precipitated by MI or with ECG changes
— Diabetes educator and dietitian — all admissions before discharge
— Social work / case management — adherence barriers, insulin cost, food insecurity, substance use
— Psychiatry — eating disorders (insulin omission as a weight-loss behavior, "diabulimia"), depression, suicidality
— Pediatric DKA at adult facility → transfer to pediatric center after stabilization if cerebral edema risk
— Pregnant patient → tertiary center with MFM and NICU
CCS pearl: Order DVT prophylaxis, head-of-bed elevation, and finger-stick glucose protocol in your standing admission orders. These get scored even though they aren't disease-specific.
— Glycols (ethylene glycol, propylene glycol)
— Oxoproline (chronic acetaminophen, especially malnourished women)
— L-lactate (sepsis, ischemia, metformin, shock)
— D-lactate (short bowel syndrome with bacterial overgrowth)
— Methanol
— Aspirin (salicylate toxicity)
— Renal failure (uremia)
— Ketoacidosis (DKA, AKA, starvation)
— History: chronic alcohol use, recent binge, abrupt cessation, poor PO intake, vomiting
— Glucose usually normal or low (<250); β-OHB markedly elevated
— Treatment: D5NS + thiamine (give thiamine FIRST to prevent Wernicke encephalopathy), correct electrolytes; insulin NOT needed
— Resolves in 12–24 hours with glucose and thiamine
— Prolonged fasting (>3 days), pregnancy with hyperemesis, eating disorders
— Mild acidosis (HCO3 >18), mild ketosis; glucose normal or low
— Treatment: refeeding with carbohydrates
— Mixed disorder: respiratory alkalosis (direct CNS stimulation) + anion gap metabolic acidosis
— Tinnitus, hyperthermia, altered mental status, hyperventilation
— Diagnosis: serum salicylate level; treat with alkalinization (NaHCO3 to urine pH >7.5), consider hemodialysis if level >100 mg/dL
— High osmolar gap (>10) in addition to AG acidosis
— Methanol: visual disturbance, blindness ("snow field" vision)
— Ethylene glycol: calcium oxalate crystals in urine, hypocalcemia, AKI
— Treatment: fomepizole (first-line) or ethanol, hemodialysis
— Type A (hypoxic): sepsis, shock, ischemia
— Type B (non-hypoxic): metformin, linezolid, HIV antiretrovirals, malignancy
Key distinction: A diabetic with vomiting and acidosis but glucose 90 isn't DKA — think AKA, starvation ketosis, or toxic ingestion. Calculate the osmolar gap before anchoring.
— Glucose >600 mg/dL, osmolality >320 mOsm/kg, pH >7.30, minimal ketones, profound dehydration (often 9–10 L deficit)
— Typical patient: elderly T2DM, dementia, nursing home, recent infection or stroke
— Mortality 5–20% (higher than DKA)
— Management: more aggressive fluid resuscitation than DKA (deficit replacement over 24h), lower insulin rates (0.05 U/kg/h), prolonged hospital course
— Mixed DKA-HHS in 30% — manage as DKA
— Glucose 200–400 in a critically ill non-diabetic; absent or minimal ketones; lactic acidosis dominates
— Treat underlying sepsis; manage glucose with sliding scale insulin (target 140–180); do not run DKA protocol
— Glucocorticoids, atypical antipsychotics (olanzapine, clozapine), tacrolimus, thiazides, beta-blockers
— Usually no ketosis or AG acidosis — straightforward hyperglycemia
— T1DM: younger, leaner, autoantibodies positive (GAD-65, IA-2, ZnT8, insulin antibodies), low C-peptide
— Ketosis-prone T2DM (formerly "Flatbush diabetes"): African American or Hispanic adults, obese, present in DKA but subsequently controlled on oral agents; autoantibody-negative, preserved C-peptide
— Order autoantibodies and C-peptide before discharge to clarify type and guide long-term therapy
— Child with vomiting, abdominal pain, dehydration → always check fingerstick glucose
— New-onset T1DM frequently dismissed as "stomach bug" → returns in florid DKA
— Glucose elevated but ketones minimal, AG mild
— Treat infection; insulin sliding scale; not full DKA protocol
— Can both cause and result from DKA
— Confirm with imaging if lipase persistently elevated after pH correction
Board pearl: "Elderly nursing home patient, glucose 900, sodium 155, pH 7.32, minimal ketones, obtunded" — that's HHS, not DKA. Fluids are the priority; insulin is secondary.
— Established T1DM: resume prior regimen if it was effective and adherence is feasible
— New T1DM: total daily dose 0.4–0.6 U/kg/day, split 50% basal (glargine or degludec) + 50% prandial (lispro/aspart with meals)
— Ketosis-prone T2DM: discharge on basal-bolus initially; can often transition to oral agents within 3–6 months under endocrinology guidance
— Last IV insulin dose must overlap with first SC basal dose by 1–2 hours
— Glucometer, test strips, lancets
— Insulin pens or vials + syringes
— Glucagon emergency kit (especially for T1DM)
— Ketone meter (β-OHB strips) — critical for home monitoring
— Sick-day rules: never stop insulin, check glucose q2–4h, check ketones q4h if glucose >250, hydrate, contact provider if vomiting >2h or ketones moderate/large
— Insulin storage, injection technique, rotation of sites
— Adherence: explore cost (340B clinics, manufacturer assistance, GoodRx, $35 insulin cap for Medicare), transportation, mental health
— Infection: complete antibiotic course
— Pump dysfunction: replace, retrain, or transition to MDI
— SGLT2 inhibitor-related: discontinue permanently in T1DM (not approved); in T2DM, weigh CV/renal benefits against recurrence risk and counsel on sick-day rules (hold during illness, surgery, fasting)
— HbA1c at discharge; target individualized (<7% for most non-pregnant adults)
— Statin: moderate or high intensity for all diabetics 40–75 years
— ACEi/ARB if albuminuria, hypertension, or CKD
— Aspirin only if established ASCVD (not for primary prevention in most diabetics per ADA)
— Annual eye, foot, urine albumin-creatinine ratio, lipid panel
— Vaccines: influenza yearly, pneumococcal (PCV20 or PCV15+PPSV23), hepatitis B if <60, COVID, RSV if eligible
Step 3 management: Before discharge, schedule endocrinology follow-up within 1–2 weeks and primary care within 1 week. Provide a written sick-day action plan and confirm patient can demonstrate insulin administration.
— Primary care: 1 week post-discharge for medication reconciliation, vital signs, glucose log review
— Endocrinology: 1–2 weeks (new T1DM, recurrent DKA, pump patient) or 4 weeks (established patient)
— Diabetes educator: within 2 weeks
— Behavioral health if mental health/adherence factors identified
— Ophthalmology: within 3–6 months if not seen in past year
— HbA1c every 3 months until at goal, then every 6 months
— Fingerstick glucose log review (or CGM data download)
— Urine albumin-creatinine ratio annually
— Lipid panel annually
— Comprehensive foot exam annually (more often if neuropathy or prior ulcer)
— Dilated eye exam annually
— TSH yearly in T1DM (autoimmune association)
— Celiac screening (TTG-IgA) if symptoms — also autoimmune association
— Strongly recommended for all T1DM and T2DM on intensive insulin
— Covered by Medicare for patients on insulin (any insulin regimen as of 2023)
— Targets: time in range (70–180 mg/dL) >70%, time below range (<70) <4%, time below <54 <1%
— Reduce DKA recurrence when used reliably
— Require strong patient engagement; not appropriate during acute mental health crisis
— Sick-day management — review at every visit
— Recognition of DKA symptoms (polyuria, nausea, abdominal pain, fruity breath)
— When to come to ED: vomiting >2 h, persistent ketones, glucose >300 with symptoms
— Glucagon training for household members
— Hypoglycemia management (rule of 15: 15 g carbs, recheck in 15 min)
— PHQ-9 for depression annually
— Screen for diabetes distress (validated DDS-17 scale)
— Eating disorder screening, especially in young women with T1DM and recurrent DKA — "diabulimia" (insulin restriction for weight loss) is a high-mortality syndrome
CCS pearl: On the CCS post-discharge phase, order "diabetes education referral, endocrinology follow-up, HbA1c in 3 months, urine albumin-to-creatinine ratio, lipid panel, statin therapy, and influenza vaccine" — comprehensive secondary prevention earns scoring points.
— DKA patients with severe acidosis or osmolality >320 are not decision-capable
— Provide emergency treatment under implied consent doctrine; document mental status and why consent could not be obtained
— As mentation clears, reassess capacity and obtain consent for ongoing interventions
— Surrogate decision-maker (spouse > adult child > parent > sibling in most state hierarchies) for non-emergency decisions
— Mature minors may have confidentiality rights regarding pregnancy, sexual health, substance use, mental health
— Diabetes management generally falls under parental purview, but discuss confidentially with adolescent about adherence barriers (eating disorder, substance use, depression)
— Mandatory reporting if child neglect suspected (parent withholding insulin or failing to obtain refills) — call CPS
— Insulin restriction for weight loss is a recognized eating disorder behavior in T1DM
— Carries 3× mortality compared to T1DM without ED
— Screen for, treat under combined endocrine + psychiatric care, consider involuntary hold if imminent danger
— Insulin rationing due to cost is a leading cause of recurrent DKA in the US
— Medicare $35/month cap (2023), state-level caps, manufacturer patient assistance programs, community health center 340B pricing
— Social work consult mandatory for any patient citing cost as adherence barrier
— Insulin is the #1 high-alert medication implicated in inpatient adverse events
— Double-check rates, pump programming, and overlap with SC basal at every transition (ED→floor→discharge)
— Medication reconciliation at discharge — confirm insulin type, dose, timing, supply, and follow-up
— Read-back orders for insulin verbal orders
— Continuous cardiac monitoring during K+ replacement
— Frequent neurologic checks in pediatric DKA
— DVT prophylaxis on all DKA admissions
— In patients with advanced illness (metastatic cancer, end-stage dementia), discuss whether aggressive DKA treatment aligns with goals of care
— Comfort-focused approach may be appropriate; ethics consult if disagreement
Board pearl: A teenager with recurrent DKA and unexplained weight loss may have diabulimia — refer to a multidisciplinary eating disorder program; treat as both an endocrine and psychiatric emergency.
— Diagnostic criteria: glucose >250, pH <7.30, HCO3 <18, AG >12, β-OHB ≥3
— Initial fluid: 15–20 mL/kg NS in first hour
— Insulin: 0.1 U/kg/h IV
— K+ thresholds: <3.3 hold insulin; 3.3–5.2 give 20–30 mEq/L; >5.2 no K
— Switch to D5 1/2NS when glucose <200
— Bicarbonate only if pH <6.9
— Resolution: glucose <200 + 2 of (HCO3 ≥15, pH >7.30, AG ≤12)
— Fruity breath = acetone exhalation
— Kussmaul respirations = compensatory hyperventilation for metabolic acidosis
— Pseudohyponatremia → correct sodium 1.6 mEq/L for every 100 mg/dL glucose above 100
— Pseudonormokalemia → total body K+ depleted despite normal serum value
— Leukocytosis up to 25k without infection (stress demargination)
— Lipase elevation without true pancreatitis common
— Mucormycosis = uncontrolled diabetes pathognomonic association
— Cerebral edema = pediatric DKA mortality driver
— Diabulimia = T1DM + eating disorder + recurrent DKA
— SGLT2 inhibitors → euglycemic DKA (canagliflozin, empagliflozin, dapagliflozin, ertugliflozin)
— Atypical antipsychotics → new-onset DKA (olanzapine, clozapine highest)
— Glucocorticoids → precipitate DKA in diabetics
— Thiazides, tacrolimus, pentamidine → drug-induced diabetes
— Terbutaline (tocolytic) → DKA in pregnancy
— Glucagon:insulin ratio drives ketogenesis
— β-hydroxybutyrate:acetoacetate ratio is ~3:1 in severe DKA, normalizes to 1:1 during recovery
— Hyperchloremic acidosis post-NS resuscitation prolongs apparent HCO3 normalization
— Adults: <1% young, 5% overall, 20% elderly with HHS overlap
— Pediatric: 0.15–0.30% — cerebral edema causes 60–90% of deaths
Key distinction: β-hydroxybutyrate is the best ketone to follow; urine ketones (acetoacetate) paradoxically rise during recovery as β-OHB converts. Don't be fooled.
— 22-year-old T1DM, glucose 480, pH 7.15, K+ 3.0, started on NS bolus. Next step? → Hold insulin, give 40 mEq KCl IV, recheck K+ in 1 hour, then start insulin when K+ >3.3
— DKA patient 4 hours into treatment, glucose dropped from 600 to 220, AG still 18. Next step? → Change fluids to D5 1/2NS, continue insulin infusion (do not stop). Stopping insulin while AG is open is the wrong answer
— 28-year-old T2DM on empagliflozin, nausea/vomiting after fasting for procedure, glucose 165, pH 7.20, β-OHB 4.5. Diagnosis? → Euglycemic DKA; stop SGLT2i, treat with insulin + dextrose fluids
— 8-year-old in DKA, 6 hours into treatment, new headache, HR drops from 130 to 70, BP rises. Next step? → Mannitol 0.5–1 g/kg IV (or 3% saline), then CT head
— 26-year-old at 32 weeks GA with T1DM, hyperemesis, glucose 190, pH 7.18, β-OHB 5. Fetal heart rate showing late decelerations. Next step? → Treat maternal DKA (fluids, insulin, K+), continuous fetal monitoring, left lateral decubitus; do not deliver until maternal stabilization underway
— DKA resolved (AG 10, HCO3 17, glucose 180, eating). On insulin drip. Next step? → Give SC glargine, wait 1–2 hours, then stop IV insulin infusion. Stopping the drip without overlap is wrong
— 45-year-old with chronic alcohol use, vomiting, glucose 70, pH 7.20, ketones positive. Treatment? → Thiamine first, then D5NS, electrolyte repletion; insulin not indicated
— 78-year-old nursing home resident, glucose 950, Na 155, pH 7.31, minimal ketones, lethargic. Diagnosis and management? → HHS; aggressive fluid resuscitation (deficit over 24h), lower insulin rate (0.05 U/kg/h)
— Poorly controlled diabetic with facial pain, periorbital swelling, black eschar on palate. Next step? → Emergent surgical debridement + IV liposomal amphotericin B
— 19-year-old female T1DM, third DKA admission in 6 months, BMI 18, denies adherence problems but admits insulin omission for weight control. Diagnosis? → Diabulimia; refer to combined endocrine + eating disorder team
Board pearl: When the stem gives you potassium first, the answer involves potassium. When it gives you glucose <200, the answer involves dextrose. When it gives you eating + closed gap, the answer involves SC overlap.
DKA is the triad of hyperglycemia (>250, or normoglycemic with SGLT2i), anion gap metabolic acidosis (pH <7.30, HCO3 <18), and ketonemia (β-OHB ≥3), managed with the simultaneous trio of aggressive isotonic fluid resuscitation, potassium-aware IV insulin infusion, and identification/treatment of the precipitant, with transition to subcutaneous basal insulin only after the anion gap closes and overlapping with the IV drip by 1–2 hours.
— K+ <3.3 → hold insulin, give K+ first
— Glucose <200 → add D5, do NOT stop insulin
— AG closed + eating → SC glargine, overlap, then stop drip
— pH <6.9 → consider bicarbonate (otherwise never)
— Infection (UTI, pneumonia, foot ulcer, perirectal abscess)
— MI (silent in diabetics — ECG and troponin)
— SGLT2 inhibitor (euglycemic DKA at any glucose)
— Insulin nonadherence (cost, mental health, diabulimia)
— Pediatric cerebral edema → mannitol or 3% saline at first headache or bradycardia
— Hypokalemia-induced arrhythmia → telemetry + frequent K+ checks
— Pulmonary edema in elderly/CKD → judicious fluid rate
— Mucormycosis → emergent surgery + amphotericin B for facial necrosis
— Overlap SC basal before stopping IV insulin
— Diabetes education + sick-day rules + ketone meter
— Endocrinology follow-up in 1–2 weeks, primary care in 1 week
— Address root cause: cost, mental health, pump troubleshooting, infection completion
Step 3 management: DKA is not just a metabolic correction — it is a longitudinal disease event requiring precipitant identification, safe transition off IV insulin, comprehensive secondary prevention, and psychosocial assessment to prevent the 20% one-year recurrence rate.