CCS Integrated Cases

CCS case: DKA with severe acidosis

Clinical Overview and When to Suspect DKA with Severe Acidosis

— Severe DKA: pH <7.00, HCO₃ <10, anion gap >12, altered mental status, or hemodynamic instability — this is the CCS case profile.

— Known T1DM with missed insulin, pump failure, illness, or noncompliance.

— New-onset T1DM (children, lean young adults with polyuria/polydipsia/weight loss).

— T2DM under severe stress: sepsis, MI, stroke, pancreatitis, steroids, cocaine, SGLT2 inhibitors (euglycemic DKA — glucose may be <200).

— Pregnancy with hyperemesis, infection, or steroid use (can develop at lower glucose).

CCS pearl: On the CCS interface, the first three orders for a suspected severe DKA should be fingerstick glucose, IV access ×2 large bore, and continuous cardiac monitoring/pulse oximetry — then send labs and start fluids before insulin. Insulin before fluids in a hypovolemic patient worsens shock and can precipitate cerebral edema, especially in young patients. Always screen for the precipitant in parallel; treating DKA without identifying the trigger is an incomplete case and the simulator will dock you on the final score.

Definition triad (ADA): hyperglycemia (>250 mg/dL, though euglycemic DKA exists), anion-gap metabolic acidosis (pH <7.30, HCO₃ <18), and ketonemia/ketonuria (β-hydroxybutyrate ≥3 mmol/L).

Pathophysiology: absolute or relative insulin deficiency + counter-regulatory surge (glucagon, cortisol, catecholamines, GH) → lipolysis → free fatty acids → hepatic ketogenesis (acetoacetate, β-hydroxybutyrate) and unchecked gluconeogenesis.

When to suspect on CCS:

Common precipitants — the "5 I's": Infection (UTI, pneumonia — #1), Infarction (MI, CVA, mesenteric), Insulin noncompliance/insufficient dosing, Iatrogenic (steroids, atypical antipsychotics, SGLT2i), Intoxication (alcohol, cocaine).

Presenting CCS clock: patient arrives ED with Kussmaul breathing, fruity breath, dehydration, abdominal pain, vomiting — order initial workup within minutes, not hours.

Presentation Patterns and Key History

— Polyuria, polydipsia, polyphagia → progresses to anorexia, nausea, vomiting.

— Weight loss over days to weeks (especially new-onset T1DM).

— Diffuse abdominal pain in ~50% — mimics surgical abdomen; resolves with DKA correction. Do not rush to laparotomy until DKA treated and pain reassessed.

— Generalized weakness, fatigue, blurred vision.

— Altered sensorium: drowsiness → stupor → coma (correlates with serum osmolality, not just pH).

— Last insulin dose, type, and route (basal vs bolus); pump users — ask about site, occlusion, battery.

— Recent illness, fever, cough, dysuria, diarrhea, chest pain, focal weakness.

— Medications: corticosteroids, atypical antipsychotics (olanzapine, clozapine), thiazides, SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin).

— Substance use: alcohol binge, cocaine, methamphetamine.

— Pregnancy status in any reproductive-age female (pregnancy test is mandatory order).

— Prior DKA episodes (recurrent DKA flags psychosocial issues, eating disorders, insulin omission for weight control — "diabulimia").

Board pearl: Euglycemic DKA — glucose <200 mg/dL but anion-gap acidosis with ketonemia. Triggers: SGLT2 inhibitors (hold perioperatively ≥3 days; canagliflozin ≥4 days), pregnancy, prolonged fasting, alcohol use, gastroparesis. These patients are easily missed because the glucose doesn't scream DKA — always check a venous gas and β-hydroxybutyrate in a sick diabetic regardless of glucose level.

Key distinction: DKA evolves over hours (younger, T1DM, more acidosis, less hyperosmolar) vs HHS over days (older, T2DM, glucose often >600, osmolality >320, minimal ketosis, profound dehydration, higher mortality). Mixed pictures occur in ~30% — treat the dominant physiology but anticipate overlap.

Classic symptom evolution (hours to 1–2 days in T1DM; slower in T2DM):

Targeted history questions on CCS:

Pediatric/adolescent flag: new-onset T1DM presents in DKA in ~30% of cases; ask about enuresis, school performance decline, candidal infections.

Physical Exam Findings and Hemodynamic Assessment

— Tachycardia (compensatory for volume loss and acidemia).

— Hypotension or orthostasis — fluid deficit averages 6 L (~100 mL/kg) in severe DKA.

— Tachypnea with Kussmaul respirations — deep, sighing, labored (respiratory compensation; pCO₂ may drop to 10–15).

— Temperature: often normal or low even with infection (acidosis blunts febrile response) — absence of fever does not exclude sepsis.

— Hypothermia portends poor prognosis.

— Fruity/acetone breath (acetoacetate volatility).

— Dry mucous membranes, decreased skin turgor, sunken eyes, prolonged capillary refill.

— Altered mental status — quantify with GCS; correlates with osmolality >320 mOsm/kg.

— Clear lungs typically; rales suggest pneumonia (precipitant) or fluid overload (over-resuscitation).

— Listen for S3, friction rub (uremia from AKI), or murmurs (endocarditis as trigger).

— Look for source of infection: cellulitis, foot ulcer, abscess, sacral decubitus.

— Acanthosis nigricans (T2DM clue), thyromegaly, lipohypertrophy at injection sites.

— Focal deficits → suspect stroke as precipitant or, in children/adolescents, herald of cerebral edema during treatment (headache, bradycardia, hypertension = Cushing response).

CCS pearl: Order continuous telemetry, automated BP q15min initially, urine output via Foley if obtunded or hemodynamically unstable, and strict I/Os. Reassess vitals and mental status at the bedside at 1 hour, 2 hours, then q2h. If a pediatric/adolescent patient develops headache or lethargy 4–12 hours into therapy, stop, give mannitol 0.5–1 g/kg or 3% saline, head CT, neuro consult — cerebral edema mortality is 20–40%.

Vitals on arrival (severe DKA pattern):

General:

Cardiopulmonary:

Abdomen: diffuse tenderness, decreased bowel sounds, possible voluntary guarding — re-examine after 4–6 hours of DKA therapy before surgical consult.

Skin/extremities:

Neuro:

Diagnostic Workup — Initial Labs

— Fingerstick glucose (POC).

— Venous blood gas (VBG) — pH, pCO₂, HCO₃ (VBG correlates well with ABG, avoids arterial stick unless respiratory failure).

— BMP/CMP: glucose, Na, K, Cl, HCO₃, BUN, Cr, calculated anion gap.

— Serum β-hydroxybutyrate (preferred; nitroprusside urine ketones detect acetoacetate only and underestimate severity).

— Serum osmolality (or calculate: 2×Na + glucose/18 + BUN/2.8).

— CBC with differential (leukocytosis up to 25k can occur from stress alone — do not assume infection).

— Phosphate, magnesium, calcium.

— Lactate (rule out concurrent lactic acidosis, especially in metformin users or shock).

— Urinalysis — glucose, ketones, nitrites/leuks (UTI screen), culture.

— Pregnancy test (β-hCG) in reproductive-age females.

— ECG — look for STEMI/NSTEMI as precipitant, and for hyperkalemia/hypokalemia changes (peaked T waves, U waves).

— Troponin if chest pain, age >40, or ECG changes.

— Blood cultures ×2 if any infection suspicion.

— Lipase (DKA can cause elevated amylase/lipase without pancreatitis — correlate clinically and with imaging).

— HbA1c (chronic control, helps distinguish acute vs chronic decompensation).

— Glucose 400–800; pH <7.00; HCO₃ <10; anion gap >20.

— Pseudohyponatremia: correct Na by adding 1.6 mEq/L per 100 mg/dL glucose above 100.

— Potassium paradox: serum K may be normal or high despite total body deficit of 3–5 mEq/kg (acidosis shifts K extracellularly).

— BUN/Cr elevated from prerenal AKI.

Step 3 management: If initial K <3.3 mEq/L, hold insulin and replete K (20–40 mEq/h) first — giving insulin drives K into cells and can precipitate fatal arrhythmia. This is one of the most tested DKA decision points on the exam.

Order immediately on arrival (CCS first 5 minutes):

Expected lab pattern in severe DKA:

Diagnostic Workup — Advanced and Precipitant Studies

— Chest X-ray in all severe DKA: pneumonia, pulmonary edema (post-resuscitation), aspiration.

— CT head if focal neuro findings, persistent altered mentation despite metabolic correction, or trauma — rule out stroke, hemorrhage, cerebral edema.

— CT abdomen/pelvis with contrast if abdominal pain persists after 6 hours of DKA correction or if surgical abdomen suspected — appendicitis, cholecystitis, mesenteric ischemia, pancreatitis.

— Right upper quadrant ultrasound if cholestatic LFTs or RUQ pain.

— Echocardiogram if new murmur, suspected endocarditis, or cardiogenic component to shock.

— Toxicology screen (urine drug screen, ethanol level, salicylate, methanol/ethylene glycol if osmolar gap is elevated disproportionately).

— TSH — thyroid storm can precipitate DKA.

— Cortisol/ACTH if hemodynamic instability persists despite adequate resuscitation (rule out adrenal crisis — can coexist as autoimmune polyendocrine syndrome).

— Glucose q1h via POC.

— BMP (electrolytes, anion gap, HCO₃) q2–4h until anion gap closed.

— VBG q2–4h until pH >7.30.

— Phosphate, Mg q4–6h.

— β-hydroxybutyrate q4h is the most direct marker of resolution (preferred over urine ketones, which lag).

— Glucose <200 mg/dL AND two of:

— pH >7.30

— HCO₃ ≥15

— Anion gap ≤12

CCS pearl: Do not rely on urine ketones to judge resolution — they may remain positive for 24–48h after DKA resolves because nitroprusside test detects acetoacetate, and β-hydroxybutyrate (the dominant ketone in DKA) is converted to acetoacetate as the patient recovers, paradoxically making urine ketones appear worse during clinical improvement.

Hunt the trigger — order based on clinical clues:

Follow-up trending labs (CCS clock — set these as recurring orders):

DKA resolution criteria (all required):

First-Line Management Logic — The Three-Pronged Approach

— 1. Fluids first — restore intravascular volume.

— 2. Potassium correction or repletion — before or alongside insulin.

— 3. Insulin infusion — only after K ≥3.3 and fluids initiated.

— 4. Identify and treat precipitant — concurrent.

— 0.9% NaCl 1–1.5 L IV bolus over first hour (15–20 mL/kg) — repeat if hemodynamically unstable.

— After initial bolus, reassess corrected Na:

— If corrected Na normal or high → switch to 0.45% NaCl at 250–500 mL/h.

— If corrected Na low → continue 0.9% NaCl at 250–500 mL/h.

— When glucose reaches 200 mg/dL, change fluid to D5 ½NS (or D5NS) at 150–250 mL/h to allow continued insulin without hypoglycemia and to slowly clear ketones.

— Balanced crystalloids (LR, Plasma-Lyte) are increasingly preferred — PLUS-DKA and SCOPE-DKA trials showed faster anion gap closure and less hyperchloremic acidosis. ADA 2024 guidance accepts either.

— K <3.3 → hold insulin; KCl 20–40 mEq/h until K ≥3.3.

— K 3.3–5.2 → add 20–30 mEq KCl to each liter of IVF; start insulin.

— K >5.2 → no K supplementation; start insulin; recheck K q2h.

Step 3 management: Sequence on the CCS timeline — (0 min) IV access, labs, monitors; (5 min) NS 1 L bolus; (15–30 min) insulin drip if K ≥3.3; (1 h) reassess vitals, glucose, K; (2 h) repeat BMP/VBG; (when glucose 200) transition to dextrose-containing fluid and continue insulin until anion gap closes — do not stop insulin just because glucose normalizes.

The DKA bundle (start within 30 min of arrival):

Fluid resuscitation (CCS order set):

Potassium algorithm (check K before insulin):

Bicarbonate: Only if pH <6.9 — 100 mEq NaHCO₃ in 400 mL sterile water + 20 mEq KCl over 2 hours; recheck pH q2h. Routine bicarb worsens cerebral edema risk, paradoxical CNS acidosis, and hypokalemia.

Pharmacotherapy — Insulin Regimen

— Optional bolus: 0.1 units/kg IV push (ADA notes bolus can be omitted if continuous infusion started promptly; bolus offers no benefit if infusion rate adequate).

— Continuous infusion: 0.1 units/kg/h (typical 5–10 units/h).

— Lower-dose protocol (0.14 units/kg/h without bolus) is equivalent.

— Target glucose decline: 50–75 mg/dL/h.

— If glucose does not drop by ≥10% in first hour → re-bolus 0.1 units/kg or double infusion rate; also check IV line integrity and fluid status.

— Reduce insulin infusion to 0.02–0.05 units/kg/h.

— Add dextrose to fluids (D5 ½NS).

— Maintain glucose 150–200 mg/dL until anion gap closes (this is the cardinal teaching point — insulin clears ketones, not just glucose).

— Criteria: glucose <200, anion gap ≤12, HCO₃ ≥15, pH >7.30, patient able to eat.

— Give basal SC insulin (glargine or detemir) at least 1–2 hours before stopping IV insulin — failure to overlap is the most common cause of DKA recurrence on the wards.

— Calculate total daily dose: 0.5–0.8 units/kg/day for known diabetics (use home dose if well-controlled), 0.5 units/kg/day for new-onset T1DM.

— Split: 50% basal (glargine qHS), 50% bolus (rapid-acting with meals, divided TID).

Board pearl: The #1 reason for DKA "rebound" within 24h of apparent recovery is stopping the insulin drip without overlapping subcutaneous basal insulin. Always overlap ≥1–2 hours. On CCS, write the basal SC insulin order, wait the clock forward, then discontinue the drip.

Regular insulin IV infusion (preferred for severe DKA):

When glucose reaches 200 mg/dL:

Transition to subcutaneous insulin (when DKA resolved):

Subcutaneous rapid-acting insulin protocols (lispro/aspart q1–2h) are an alternative for mild–moderate DKA only — not appropriate for severe DKA with pH <7.0, altered mentation, or hemodynamic instability.

Adjunctive Pharmacology and Treating the Precipitant

— Routine repletion not recommended.

— Replace if phosphate <1.0 mg/dL, or 1.0–2.0 with cardiac dysfunction, respiratory depression, hemolytic anemia, or rhabdomyolysis.

— Give potassium phosphate 20–30 mEq in IVF over 6 hours; monitor Ca (risk of hypocalcemia and metastatic calcification with overzealous repletion).

— Infection: empiric antibiotics if SIRS/sepsis features — e.g., ceftriaxone 1–2 g IV q24h for community pneumonia/UTI; piperacillin-tazobactam 4.5 g IV q6h ± vancomycin 15–20 mg/kg q8–12h for severe sepsis or healthcare-associated source. Tailor by culture.

— MI: dual antiplatelet, anticoagulation, cardiology consult, cath lab if STEMI — do not delay reperfusion for DKA correction.

— Stroke: non-contrast head CT, neuro consult; tPA window applies.

— Pancreatitis: supportive; verify with imaging (DKA itself can mildly elevate lipase).

— SGLT2-induced euglycemic DKA: stop the SGLT2 inhibitor immediately; do not restart until clearly indicated and after dietitian/endocrine counseling on sick-day rules.

CCS pearl: On the CCS, after stabilization, add these standing orders before advancing the clock: finger-stick glucose q1h, BMP q2h until AG closed then q6h, VBG q4h, Mg/Phos q6h, strict I/Os, head of bed 30°, DVT prophylaxis, NPO until mentation clears, and document the suspected precipitant in your problem list — the simulator scores you on systematic, complete order sets.

Phosphate:

Magnesium: replete if <1.8 mg/dL — MgSO₄ 1–2 g IV; needed for K repletion to be effective.

VTE prophylaxis: DKA is prothrombotic; once acutely stabilized, enoxaparin 40 mg SC daily (or heparin 5000 SC q8h if CrCl <30) unless contraindicated.

Treating precipitants (don't forget the trigger):

Glucocorticoid-induced: continue steroids only if essential; adjust insulin upward to compensate.

Special Populations — Elderly and Renal/Hepatic Impairment

— Often present with HHS or mixed DKA-HHS picture rather than pure DKA — glucose >600, osmolality >320, mental status changes predominant.

— Higher mortality (5–20% vs <1% in young DKA) — driven by precipitant (MI, stroke, sepsis), not the DKA itself.

— More cautious fluid resuscitation: assess CHF, baseline renal function. Use smaller boluses (500 mL) with frequent reassessment for pulmonary edema, JVD, S3, and oxygen requirement.

— Watch for occult MI — order serial troponins and ECG; chest pain may be absent (diabetic autonomic neuropathy).

— Cognitive baseline may be hard to establish — document with family/SNF report; persistent confusion after metabolic correction warrants delirium workup and possibly CT head.

— Glucose readings may be unreliable on peritoneal dialysate exposure.

— Anion gap interpretation: baseline uremic acidosis may raise AG; trend the gap rather than absolute value.

— Fluid management: more conservative; consider central venous monitoring or POCUS IVC assessment in oligo-anuric patients.

— K management: monitor q1–2h initially; dialysis may be needed for refractory hyperkalemia or volume overload.

— Insulin clearance reduced — anticipate need for lower infusion rates after initial correction; SC basal dosing on discharge often reduced 25–50%.

— Avoid metformin — DKA is a contraindication; lactic acidosis risk especially with AKI.

— Reduced gluconeogenesis can paradoxically lead to hypoglycemia during recovery — increase glucose-monitoring frequency.

— Coagulopathy increases bleeding risk with central lines and heparin prophylaxis — dose-adjust or use mechanical prophylaxis.

Step 3 management: In an elderly DKA patient with CHF, fluid-resuscitate in 250–500 mL aliquots with reassessment after each, target SBP >100 and urine output >0.5 mL/kg/h. Get a stat ECG and troponin — silent MI is the precipitant in up to 15% of elderly DKA presentations, and missing it is a high-frequency board distractor.

Elderly (>65 years):

Chronic kidney disease / AKI:

Hepatic impairment:

Special Populations — Pregnancy, Pediatrics, and Adolescents

— DKA can occur at glucose levels as low as 150–200 mg/dL (euglycemic DKA of pregnancy) due to increased insulin resistance, accelerated starvation ketogenesis, and respiratory alkalosis lowering buffering reserve.

— Most common in 2nd/3rd trimester; precipitated by infection, hyperemesis, steroid use for fetal lung maturity (betamethasone), β-agonists for tocolysis.

— Fetal mortality 10–25% even with treatment — continuous fetal monitoring (FHR, contractions) is mandatory; obstetrics consult immediately.

— Position in left lateral decubitus to maximize uterine perfusion.

— Lower threshold to initiate dextrose-containing fluids (when glucose ~250 vs 200 in non-pregnant).

— Avoid bicarbonate (worsens fetal acidosis paradoxically).

— Do not deliver during active DKA unless fetal distress is refractory — maternal correction usually resolves fetal heart rate abnormalities.

— Cerebral edema occurs in 0.5–1%, mortality 20–40%, accounts for most pediatric DKA deaths.

— Risk factors: age <5, new-onset T1DM, severe acidosis, high BUN, low pCO₂, bicarbonate use, rapid fluid administration, rapid Na drop.

— Slower fluid resuscitation: 10–20 mL/kg NS bolus over 1 hour, then maintenance + deficit replaced over 24–48h.

— Insulin: 0.05–0.1 units/kg/h, no bolus (bolus contraindicated in children).

— Monitor for headache, bradycardia, hypertension, altered mentation, papilledema — give mannitol 0.5–1 g/kg IV or 3% saline 5–10 mL/kg immediately; head CT after stabilization.

Board pearl: Sudden headache and bradycardia 4–12 hours into pediatric DKA treatment = cerebral edema until proven otherwise. Treat empirically with hypertonic saline or mannitol before imaging.

Pregnancy:

Pediatric DKA (highest cerebral edema risk):

Adolescents: ask about insulin omission for weight loss ("diabulimia") — pattern of recurrent DKA with normal A1c trajectory ruined by binges of skipped doses; refer to mental health and diabetes educator.

Complications and Adverse Outcomes

— Mostly pediatric; 0.5–1% incidence, 20–40% mortality, 25% survivors with neuro sequelae.

— Onset 4–12h into therapy, occasionally before treatment.

— Mechanism: osmotic shifts, idiogenic osmoles, possible ischemia-reperfusion.

— Prevention: avoid overly rapid fluid administration, avoid bicarbonate, allow gradual fall in glucose and Na.

Key distinction: Most "DKA deaths" are actually deaths from the precipitating illness. If your patient is decompensating despite correcting metabolic parameters, the trigger is undertreated — re-image, re-culture, re-examine.

Cerebral edema:

Hypoglycemia: failure to add dextrose when glucose hits 200; rebound symptoms with adrenergic surge. Treat with D50 25 g IV and adjust drip.

Hypokalemia: can precipitate ventricular arrhythmias, respiratory muscle weakness, ileus. Most common iatrogenic complication — proactive monitoring and repletion prevent it.

Hyperchloremic non-anion-gap metabolic acidosis: from large-volume NS resuscitation; usually self-limited, resolves over 24–48h; balanced crystalloids reduce incidence.

Acute kidney injury: prerenal from dehydration; usually reverses with fluids. Watch for ATN if hypotension was prolonged.

VTE — DVT/PE: hypercoagulability from dehydration, hyperosmolality, inflammation; central lines compound risk. Prophylactic anticoagulation indicated.

ARDS: rare; from aggressive fluid resuscitation or aspiration.

Aspiration pneumonitis: obtunded patients; gastroparesis common in DKA. NPO and consider NG decompression if persistent vomiting.

Rhabdomyolysis: from immobility and electrolyte derangements; check CK if persistent AKI or muscle pain.

Mucormycosis (rhino-orbital-cerebral): rare but classic association with poorly controlled DM and acidosis — facial pain, black eschar on palate/nasal turbinates, vision change, cranial neuropathies. Emergent ENT consult, liposomal amphotericin B 5–10 mg/kg/day IV, surgical debridement; mortality >50%.

Death: overall DKA mortality <1% in young adults, 5–20% in elderly — usually from precipitant (sepsis, MI), not DKA itself.

When to Escalate — ICU, Consult, and Disposition

— pH <7.00 or HCO₃ <10.

— Altered mental status, GCS <14.

— Hemodynamic instability requiring vasopressors.

— Severe electrolyte derangement (K <3.0 or >6.0, Na <120 or >160).

— Osmolality >320 mOsm/kg.

— Age <5 or >65 with severe physiology.

— Pregnancy.

— Need for continuous insulin infusion (some institutions allow step-down/IMC; many require ICU).

— Concurrent critical illness — MI, sepsis, stroke, pancreatitis.

— Endocrinology — diabetes management, insulin regimen optimization, education.

— Critical care — for ICU admission.

— Diabetes educator / CDE — pre-discharge teaching is non-negotiable.

— Social work — insulin access, insurance, supply costs (insulin-rationing is a documented driver of recurrent DKA).

— Psychiatry / behavioral health — if eating disorder, depression, or substance use suspected.

— OB — any pregnant patient, regardless of trimester.

— Pediatric ICU — all pediatric severe DKA.

— ID — refractory or unusual infection sources, mucormycosis suspicion.

— Nephrology — refractory acidosis, AKI requiring dialysis.

— Anion gap closed.

— Tolerating PO.

— On SC insulin regimen for ≥4–6 hours without recurrence.

— Hemodynamically stable, mentation at baseline.

CCS pearl: Don't forget to "change location" on the CCS interface when transferring from ED → ICU → floor — the simulator tracks appropriate level-of-care decisions. Discharging directly from the ICU is a red flag and will dock points; route through a med-surg or step-down stay for 24h of stable SC insulin before discharge.

ICU admission criteria (severe DKA — most CCS cases of this topic):

Step-down/telemetry: mild–moderate DKA with reliable monitoring, intact mentation, glucose-trending capability.

Consults to place on CCS:

Floor transfer criteria:

Key Differentials — Same-Category (Anion-Gap Acidoses and Diabetic Emergencies)

— Older T2DM, glucose >600, osmolality >320, pH >7.30, HCO₃ >18, minimal ketosis.

— Mental status changes dominant; mortality 10–20%.

— Treatment similar but more fluid (deficit 9 L), less insulin, slower correction of Na/osmolality.

— Recent binge with subsequent food/alcohol cessation, vomiting.

— Glucose usually normal or low; β-hydroxybutyrate elevated.

— Treat with D5NS + thiamine 100 mg IV before glucose to prevent Wernicke's; insulin not needed.

— Anion gap closes with carbohydrate provision.

— Type A (hypoxic): shock, sepsis, ischemia.

— Type B: metformin, linezolid, NRTIs, malignancy, thiamine deficiency.

— Lactate >4; treat underlying cause; D-lactic acidosis in short bowel syndrome can cause encephalopathy with normal L-lactate.

— Methanol — visual changes, retinal edema, formic acid metabolite.

— Ethylene glycol — calcium oxalate crystals in urine, AKI.

— Elevated osmolar gap early, anion gap later.

— Treat: fomepizole 15 mg/kg IV load, hemodialysis if severe.

Board pearl: Use MUDPILES (Methanol, Uremia, DKA, Propylene glycol/Paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates) and check the osmolar gap when DKA "doesn't fit" — disproportionate gap suggests toxic alcohol co-ingestion.

Hyperosmolar Hyperglycemic State (HHS):

Mixed DKA-HHS: ~30% of presentations; treat both physiologies — fluids generous, insulin titrated, watch K closely.

Alcoholic ketoacidosis (AKA):

Starvation ketosis: prolonged fasting; mild ketosis, pH usually >7.30, HCO₃ >18; resolves with feeding.

Lactic acidosis:

Toxic alcohols:

Salicylate toxicity: mixed respiratory alkalosis + anion-gap metabolic acidosis; tinnitus, hyperthermia; treat with urinary alkalinization, hemodialysis if level >100 or severe.

Uremic acidosis: chronic, modest AG; consider in advanced CKD.

Key Differentials — Other-Category Mimics

— Lactic acidosis, altered mentation, fever, hemodynamic instability — overlaps clinically with severe DKA.

— A diabetic with sepsis often has DKA as the metabolic stress response; treat both.

— Distinguish: lactate prominent vs ketones prominent; procalcitonin elevated supports infection.

— Diabetic neuropathy → painless MI presenting as nausea, weakness, hyperglycemia.

— ECG and troponins on every severe DKA patient over 40 or with cardiovascular risk.

— Altered mentation in DKA can mimic CVA; conversely, CVA can precipitate DKA.

— Persistent focal deficits after metabolic correction = imaging.

— Severe abdominal pain, vomiting, elevated lipase.

— DKA can mildly elevate lipase without true pancreatitis; CT differentiates.

— Pancreatitis can also cause DKA (β-cell injury).

— DKA abdominal pain usually resolves within 4–6h of treatment.

— Persistent pain → cross-sectional imaging.

— Hyponatremia, hyperkalemia, hypotension refractory to fluids, hypoglycemia.

— Often co-exists in T1DM as autoimmune polyglandular syndrome type II (Schmidt syndrome).

— Check cortisol, ACTH; treat with hydrocortisone 100 mg IV if suspected.

Key distinction: Persistent altered mental status after metabolic parameters normalize is a red flag — pursue non-contrast head CT for cerebral edema (especially pediatric), stroke, or ICH. Don't anchor on the DKA diagnosis once the labs are correcting.

Sepsis with shock:

Acute myocardial infarction:

Stroke / intracranial process:

Pancreatitis:

Acute abdomen (appendicitis, cholecystitis, perforation, mesenteric ischemia):

Adrenal insufficiency:

Thyroid storm: tachycardia, hyperthermia, agitation, AF, can precipitate DKA. Check TSH/free T4.

Pheochromocytoma crisis: episodic HTN, headache, sweating, hyperglycemia.

Psychogenic polydipsia / DI: polyuria and polydipsia without hyperglycemia — distinguished by glucose and osmolality.

Secondary Prevention and Discharge Medications

— Known T1DM: resume or optimize home regimen; total daily dose 0.5–1.0 units/kg.

— New-onset T1DM: start 0.5 units/kg/day; 50% basal, 50% prandial.

— Long-acting basal: glargine, detemir, degludec SC qHS or qAM.

— Rapid-acting prandial: lispro, aspart, glulisine before meals.

— Consider insulin pump or CGM referral for selected patients (recurrent DKA, hypoglycemia unawareness).

— Never stop basal insulin, even if not eating.

— Check glucose q2–4h during illness.

— Check urine or blood ketones when glucose >250 or feeling ill.

— Maintain hydration: sugar-free fluids if glucose high, sugar-containing if low.

— Give correction doses of rapid-acting insulin q2–4h based on glucose and ketones.

— Call provider or seek ER for: persistent vomiting, ketones moderate/large, glucose >300 not responding to correction, altered mentation.

— Hold for at least 3 days (canagliflozin 4 days) before any planned surgery, fasting, or low-carb diet.

— Recognize euglycemic DKA — symptoms with normal glucose are still emergent.

— Vaccination: influenza annually, COVID-19, pneumococcal (PCV20 or PCV15+PPSV23), Tdap, RSV ≥60.

— Smoking cessation counseling.

— Cardiovascular risk reduction: statin if indicated (most diabetics ≥40 qualify), ACEi/ARB if albuminuria or HTN, aspirin only if established ASCVD.

— Screen for depression (PHQ-9), eating disorder, substance use.

— Confirm insulin affordability — connect to manufacturer assistance, generic biosimilars, or 340B pharmacy.

Step 3 management: Document all four buckets before discharge: (1) insulin regimen and supplies, (2) sick-day rules written and verbalized, (3) follow-up appointments, (4) social/financial barriers addressed. Skipping any one of these predicts 30-day readmission.

Insulin regimen at discharge:

Sick-day rules — teach before discharge (must-do CCS counseling order):

SGLT2 inhibitor counseling (if discontinuation):

Address precipitant:

Mental health and social determinants:

Follow-Up, Monitoring Parameters, and Counseling

— Primary care: within 1–2 weeks of discharge.

— Endocrinology: within 2–4 weeks; sooner for new-onset T1DM or recurrent DKA.

— Certified Diabetes Care and Education Specialist (CDCES): within 1–2 weeks; ongoing education.

— Ophthalmology: dilated exam within 1 year of diabetes diagnosis (T1DM ≥5 years post-diagnosis or at puberty; T2DM at diagnosis), then annually or per findings.

— Podiatry: annual comprehensive foot exam; sooner if neuropathy or prior ulcer.

— Dental: every 6 months.

— Behavioral health: within 2 weeks if eating disorder, depression, or substance use identified.

— HbA1c every 3 months until at goal, then q6 months (goal <7% for most; <6.5% if achievable without hypoglycemia; <8% in elderly/limited life expectancy).

— Lipid panel annually.

— Urine albumin-to-creatinine ratio (UACR) and eGFR annually (KDIGO; start ACEi/ARB if UACR ≥30 mg/g or HTN).

— TSH annually in T1DM (autoimmune comorbidity).

— Celiac screen (tTG-IgA) in T1DM at diagnosis and as symptoms arise.

— B12 annually if on metformin.

— Fingerstick glucose 4–6×/day, or CGM (preferred — Medicare-covered for T1DM and insulin-dependent T2DM since 2023).

— Time-in-range goal: >70% of readings between 70–180 mg/dL.

— Ketone-testing strips at home (blood β-hydroxybutyrate meter preferred).

— Hypoglycemia recognition; glucagon emergency kit (Baqsimi nasal or injectable).

— Driving safety — check glucose before driving.

— Pregnancy planning — preconception A1c <6.5%.

— Exercise — insulin/carb adjustment.

— Mental health — diabetes distress is real and screenable.

CCS pearl: On the final CCS screen, write orders for follow-up appointments (primary care 1–2 weeks, endocrine 2–4 weeks, diabetes educator), outpatient labs (HbA1c, UACR), and counseling (sick-day rules, hypoglycemia, smoking cessation if applicable). Missing the discharge bundle is a frequent score-killer.

Outpatient handoff cadence:

Monitoring labs:

Self-monitoring:

Counseling topics:

Ethical, Legal, and Patient Safety Considerations

— Insulin rationing is a documented cause of recurrent DKA in the US — 1 in 4 diabetics report skipping doses for cost.

— Ethical obligation to screen for affordability before discharging on a regimen the patient cannot fill. Connect to social work, manufacturer assistance, $35 cap programs, biosimilar/generic options.

— Inquire non-judgmentally; document barriers.

— Insulin omission for weight loss is an eating disorder behavior.

— Confidentiality with adolescents has limits — disclosure to guardians is appropriate when life-threatening (recurrent DKA qualifies).

— Mandatory reporting if neglect of a minor with T1DM is suspected (untreated diabetes in a child).

— DKA patients with altered mentation lack capacity during acute illness; deferring against-medical-advice (AMA) requests until metabolic correction is medically and legally appropriate.

— Document mental status assessment, treatment refusal discussions, and risks explained in plain language.

— Failure to overlap basal SC insulin with insulin drip → DKA recurrence within 24h.

— Failure to communicate discharge regimen to outpatient provider within 48h.

— Failure to ensure patient has insulin/supplies in hand before leaving.

— Use a discharge checklist with teach-back: patient demonstrates injection technique, glucose checking, and verbalizes sick-day rules.

— Impaired driving with recurrent hypoglycemia — state-specific (CA, OR, NV, NJ, PA require physician reporting; others rely on patient self-reporting).

— Document discussion and patient's responsibility.

— Insulin is a high-alert medication — double-check dosing, units (never abbreviate "U"), and route. Tall-man lettering (HumaLOG vs HumuLIN). IV insulin always pump-controlled.

Step 3 management: A teenager with recurrent DKA on third admission this year — investigate diabulimia, depression, family conflict, insulin access, and pump malfunction before labeling "noncompliant." Engage adolescent medicine, behavioral health, and social work. Punitive language in the chart harms future care.

Insulin access and affordability:

Adolescent autonomy and "diabulimia":

Capacity and AMA discharges:

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

Mandatory reporting:

Medical errors:

Informed consent for central lines, dialysis catheters, or intubation must be obtained from patient (if capable) or surrogate; document.

High-Yield Associations and Rapid-Fire Facts

— Water: 100 mL/kg (~6 L).

— Na: 7–10 mEq/kg.

— K: 3–5 mEq/kg.

— Phos: 1 mmol/kg.

Board pearl: If glucose drops appropriately but anion gap stays open, the patient is still in DKA — do not stop insulin; instead, add dextrose to fluids and continue insulin until ketones clear. This is the most tested DKA management nuance.

Most common precipitant: infection (UTI, pneumonia) — ~30–40%.

#1 cause in known diabetics: insulin nonadherence.

β-hydroxybutyrate : acetoacetate ratio: elevated in DKA (3:1 or higher); shifts to 1:1 with recovery — explains why urine ketone test can appear worse during improvement.

Pseudohyponatremia correction: add 1.6 mEq/L Na per 100 mg/dL glucose above 100 (some use 2.4 for glucose >400).

Total body deficits in severe DKA:

Insulin drip stops only when: anion gap closed AND SC basal insulin given 1–2h prior AND patient eating.

Bicarbonate threshold for use: pH <6.9 only.

Cerebral edema: pediatric, 4–12h into treatment, mortality 20–40%.

Euglycemic DKA causes (mnemonic SPACE): SGLT2 inhibitors, Pregnancy, Alcohol, Chronic liver disease/Cirrhosis, Eating disorders/starvation.

DKA in T2DM is real: ketosis-prone T2DM ("Flatbush diabetes") — disproportionately affects African American and Hispanic adults; insulin can sometimes be weaned after recovery.

Mucormycosis triad: uncontrolled DM + acidosis + immunocompromise — facial pain, black eschar, cranial nerve deficits.

HHS osmolality threshold: >320 mOsm/kg.

DKA diagnostic cutoffs (ADA): glucose >250, pH <7.30, HCO₃ <18, AG >10, ketones positive.

Mortality: <1% young adults, 5–20% elderly — driven by precipitant.

ADA recommended HbA1c goal: <7% for most adults; individualize.

PLUS-DKA, SCOPE-DKA trials: balanced crystalloids reduce time to AG closure vs NS.

Most missed precipitant on Step 3 stems: silent MI in elderly diabetic.

Board Question Stem Patterns

— 19yo T1DM, pH 6.95, glucose 620, K 3.1. Most likely option: start IV fluids + KCl, hold insulin until K ≥3.3. Distractor: "start insulin drip immediately."

— 55yo T2DM on empagliflozin presents 5 days post-op with nausea, glucose 180, pH 7.18, AG 22, ketones positive. Answer: stop SGLT2, IV fluids, insulin drip, dextrose despite "normal" glucose.

— 8yo, 6 hours into DKA treatment, develops headache and bradycardia. Next step: IV mannitol 0.5–1 g/kg or 3% saline, then head CT.

— Anion gap closed, insulin drip stopped, breakfast given. Six hours later, glucose 380, AG 18. Why? Basal SC insulin not given before stopping drip.

— Severe DKA with pH 7.05, HCO₃ 8. Should bicarbonate be given? No — threshold is pH <6.9.

— Elderly diabetic, "no chest pain," but new T-wave inversions on ECG. Diagnosis: silent MI as DKA precipitant. Order serial troponins, ECG, cardiology.

— 28wks pregnant, glucose 220, pH 7.22, ketones positive. Next: left lateral decubitus, IV fluids, insulin drip, continuous fetal monitoring, OB consult, dextrose earlier (at 250).

— Poorly controlled DM, DKA, black eschar on palate, periorbital pain. Answer: liposomal amphotericin B + emergent ENT surgical debridement.

— Normal-weight 17yo, fourth DKA in 18 months, A1c 12%. Investigate: insulin omission for weight control (diabulimia); refer behavioral health.

— Glucose 165, AG 10, HCO₃ 18, tolerating PO, on SC insulin ×6h. Disposition: discharge home with sick-day rules, endocrine follow-up 2 weeks, diabetes educator.

Key distinction: When the stem mentions an SGLT2 inhibitor with a "normal" or only mildly elevated glucose in a vomiting/post-op/fasting patient — your reflex must be euglycemic DKA, not gastroenteritis.

Pattern 1 — "What's the next step?" potassium edition:

Pattern 2 — Euglycemic DKA / SGLT2:

Pattern 3 — Pediatric cerebral edema:

Pattern 4 — Transition failure:

Pattern 5 — Bicarbonate question:

Pattern 6 — Precipitant hunt:

Pattern 7 — Pregnant patient:

Pattern 8 — Mucormycosis:

Pattern 9 — Recurrent DKA in adolescent female:

Pattern 10 — Discharge readiness:

One-Line Recap

Severe DKA is a metabolic emergency defined by hyperglycemia (or euglycemia with SGLT2/pregnancy), anion-gap acidosis, and ketonemia, managed by a strict sequence of fluids first, potassium check before insulin, insulin infusion continued until the anion gap closes (not just until glucose normalizes), with concurrent identification and treatment of the precipitant — followed by overlapped transition to subcutaneous basal insulin and a structured discharge bundle.

Board pearl: Every recurrent-DKA stem on Step 3 has a fixable upstream cause — insulin access, pump failure, eating disorder, depression, or pump-site infection — find it, name it, and treat it; the simulator and the boards reward the physician who treats the patient, not just the gap.

The non-negotiable sequence: IVF bolus → check K → if K ≥3.3 start insulin drip at 0.1 u/kg/h → add dextrose when glucose hits 200 → continue insulin until AG closes → overlap SC basal insulin 1–2h before stopping drip.

Three lethal pitfalls: (1) starting insulin with K <3.3 (arrhythmia), (2) stopping insulin when glucose normalizes but AG still open (DKA persists), (3) failing to overlap basal SC insulin (rebound DKA within 24h).

Always hunt the trigger: infection (#1), MI (especially silent in elderly), insulin nonadherence, SGLT2 inhibitors (euglycemic DKA), pregnancy, steroids, substance use — treating DKA without the precipitant guarantees recurrence and is incomplete on the CCS.

Discharge bundle (Step 3 obsession): insulin regimen with patient demonstrating technique, sick-day rules verbalized, glucagon kit and CGM/glucometer in hand, follow-up scheduled (primary care 1–2 wk, endocrine 2–4 wk, diabetes educator 1–2 wk), affordability and mental health barriers addressed.