Eduovisual
Endocrine
Hyperosmolar hyperglycemic state: CCS-style management
— Relative (not absolute) insulin deficiency suppresses lipolysis enough to prevent ketogenesis, but not enough to control gluconeogenesis or peripheral glucose uptake.
— Massive osmotic diuresis → free-water loss (often 8–12 L, ~100–200 mL/kg) → hemoconcentration, prerenal AKI, hyperosmolarity, CNS depression.
— Older adult (often >60), type 2 diabetic or undiagnosed, brought in obtunded, severely dehydrated, glucose "HIGH" on fingerstick.
— Nursing home patient with poor PO intake, recent illness, or thiazide/steroid/atypical antipsychotic exposure.
— Precipitants (the "I's"): Infection (pneumonia, UTI – #1), Infarction (MI, stroke, mesenteric), Insulin noncompliance, Iatrogenic (steroids, TPN, atypicals, SGLT2 stopped abruptly), Intoxication.
Board pearl: A patient with glucose 900, pH 7.32, bicarb 20, small ketones, and confusion is HHS, not DKA — the dominant problem is water deficit and osmolarity, and the dominant intervention is fluids before insulin.
CCS pearl: On the CCS interface, your first three orders for suspected HHS should be: (1) 0.9% NS bolus 1 L IV stat, (2) fingerstick glucose, BMP, serum osmolality, β-hydroxybutyrate, VBG, lactate, CBC, UA, ECG, and (3) continuous cardiac monitor + pulse oximetry + 2 large-bore IVs. Hold insulin until potassium is back and fluids are running.
— Polyuria, polydipsia, weight loss for days, then decreased urine output as volume depletion worsens.
— Altered mental status: from drowsiness → focal deficits → seizures → coma. AMS correlates with osmolality — most patients with osmolality >320 are symptomatic; coma typically ≥340 mOsm/kg.
— Focal neurologic findings (hemiparesis, hemianopsia, focal seizures) are surprisingly common in HHS and reverse with correction — but you must rule out stroke first.
— Diabetes history: type, duration, A1c, regimen, adherence. ~30–40% present with newly diagnosed T2DM.
— Precipitant search: recent fevers, cough, dysuria, chest pain, abdominal pain, missed dialysis, new medications.
— Medications: glucocorticoids, thiazides, atypical antipsychotics (olanzapine, clozapine), phenytoin, sympathomimetics, recent SGLT2 inhibitor discontinuation or switching, TPN.
— Access to water: bedbound, dementia, post-stroke, restrained, or institutionalized patients can't self-correct early dehydration — classic HHS substrate.
— Social: caregiver capacity, baseline cognition, advance directives.
Key distinction: Abdominal pain dominates DKA (from ketoacidosis); in pure HHS, abdominal pain is uncommon — its presence should prompt a search for a precipitant (mesenteric ischemia, pancreatitis, appendicitis) or a mixed HHS-DKA picture.
Board pearl: Any obtunded elderly diabetic with a fingerstick over 600 has HHS until proven otherwise — but the stem nearly always hides a precipitant you must find and treat in parallel.
— Profoundly dehydrated: sunken eyes, dry mucous membranes, tenting skin, dry axillae (best bedside sign).
— No Kussmaul respirations (key DKA differentiator) — breathing pattern usually normal unless precipitant causes tachypnea.
— No fruity/acetone breath (minimal ketones).
— Tachycardia (compensatory), orthostatic or frank hypotension, narrow pulse pressure.
— Temperature: may be normal or low even with sepsis — hyperosmolarity blunts febrile response. Do not exclude infection based on absence of fever.
— Tachypnea suggests pneumonia, PE, or coexisting acidosis (mixed picture, lactic acidosis from hypoperfusion, or sepsis).
— Spectrum: lethargy → stupor → coma; GCS roughly tracks osmolality.
— Focal deficits (hemiparesis, aphasia, hemianopia), focal motor seizures (often epilepsia partialis continua) — can mimic stroke.
— Hyperreflexia or, late, areflexia.
— Lungs: crackles, consolidation → pneumonia.
— Skin/feet: cellulitis, diabetic foot ulcer, perineal/Fournier necrosis.
— Abdomen: RUQ pain (cholangitis), epigastric (pancreatitis), CVA tenderness (pyelo).
— Cardiac: new murmur, S3, irregular rhythm → MI, AF with rapid response.
— Lines/devices: infected catheters, prosthetic joints.
Step 3 management: Document a clear shock vs. non-shock determination on arrival. SBP <90 or signs of shock → resuscitate with NS 1–1.5 L/hr boluses until perfusion restored before switching to maintenance fluids. This single decision drives the first hour of CCS orders.
CCS pearl: Order strict I/Os, hourly urine output via Foley if obtunded, and serial neuro checks q1h — these are the parameters the case grades you on, not just lab trends.
— Fingerstick glucose (will read "HIGH" >500).
— 12-lead ECG — silent MI is a top precipitant in elderly; also screens for hyperkalemia/hypokalemia changes.
— Pulse oximetry, continuous telemetry.
— BMP/CMP: glucose, measured Na, K, Cl, HCO3, BUN, creatinine, calcium, magnesium, phosphate.
— Serum osmolality (measured) — diagnostic anchor.
— β-hydroxybutyrate (preferred over urine ketones) — must be <3 mmol/L for pure HHS.
— VBG (ABG only if respiratory compromise) — pH >7.30, HCO3 >18.
— Lactate — elevated suggests hypoperfusion or sepsis.
— CBC with differential — leukocytosis common from stress; left shift or bands → infection.
— UA + urine culture, blood cultures ×2 if any infectious suspicion.
— Troponin — broad threshold to order in elderly diabetics.
— Lipase if abdominal pain.
— HbA1c — for chronicity and discharge planning.
— Effective osmolality = 2(Na) + glucose/18. Diagnostic if ≥320 mOsm/kg. (Do not include BUN — urea is an ineffective osmole.)
— Corrected sodium: add 1.6 mEq/L to measured Na for every 100 mg/dL glucose above 100 (some use 2.4 for glucose >400). Pseudohyponatremia is the rule; corrected Na guides fluid choice.
— Anion gap — usually mildly elevated; large gap → mixed picture, lactic acidosis, or alternative diagnosis.
— CXR — pneumonia screen.
— CT head — if focal deficits, seizure, persistent AMS after osmolar correction, or anticoagulated/falls history.
— CT abdomen if abdominal pain or unexplained leukocytosis.
Board pearl: Measured Na may look "normal" or low in HHS because hyperglycemia pulls water into the vascular space — always correct it. A corrected Na >145 mandates switching to 0.45% NS after initial resuscitation.
CCS pearl: Order labs q2–4h during active management: glucose q1h initially, BMP/Mg/Phos q2–4h, osmolality q4h until trending down appropriately.
— Plasma glucose ≥600 mg/dL
— Effective serum osmolality ≥320 mOsm/kg
— Arterial/venous pH >7.30
— Serum bicarbonate >18 mEq/L
— Minimal ketonuria/ketonemia (β-OHB <3 mmol/L)
— Altered sensorium or coma
— Glucose ≥600 + osmolality ≥320 + pH <7.30 or HCO3 <18 + significant ketosis.
— Manage with the DKA insulin protocol but with the fluid aggressiveness of HHS.
— Troponin trend + serial ECGs — NSTEMI is common, often atypical/silent.
— CT head non-contrast for stroke mimic vs. true stroke; MRI if persistent focal deficit after osmolar correction.
— CT chest/abdomen/pelvis for occult infection or mesenteric ischemia (especially if lactate elevated and atrial fibrillation).
— TSH if precipitant unclear (myxedema can coexist).
— Procalcitonin can help risk-stratify infection but does not replace cultures.
— DVT/PE workup: HHS is a prothrombotic state; have a low threshold for CTPA if tachycardic/hypoxic disproportionate to volume status.
— Phosphate and magnesium — both deplete during insulin therapy.
— C-peptide and GAD-65/IA-2 antibodies — defer to outpatient; useful if new diabetes diagnosis to distinguish T1 vs. T2 (especially in younger or lean patients).
— Cortisol/ACTH if hypotension persists despite fluids → consider adrenal insufficiency.
— Clearly state "HHS" with osmolality, precipitating diagnosis, and any AKI/electrolyte derangements as separate problems — drives DRG and quality metrics.
Key distinction: β-hydroxybutyrate is the preferred ketone assay; nitroprusside-based urine ketone strips miss β-OHB and can falsely reassure in early presentation or when β-OHB predominates over acetoacetate.
Step 3 management: If the patient does not clinically improve as osmolality corrects, escalate the precipitant search — repeat imaging, cultures, troponin, and lactate. HHS that "won't fix" almost always has an untreated trigger.
— 1) Fluids → 2) Potassium repletion gate → 3) Insulin → 4) Treat the precipitant → 5) Transition to subcutaneous insulin.
— Hour 0–1: Establish 2 large-bore IVs, draw all labs, start 0.9% NS at 15–20 mL/kg (1–1.5 L) in the first hour. Place Foley if obtunded. ECG, telemetry, fingerstick q1h. Begin precipitant workup.
— Hour 1–4: Reassess volume and corrected Na.
— Corrected Na normal or high → switch to 0.45% NS at 250–500 mL/hr.
— Corrected Na low → continue 0.9% NS at 250–500 mL/hr.
— Check K+ before insulin: K <3.3 → hold insulin, replete K at 20–30 mEq/hr; K 3.3–5.2 → start insulin and add 20–30 mEq KCl/L; K >5.2 → start insulin, no K, recheck q2h.
— Hour 2 onward: Start regular insulin 0.1 U/kg/hr infusion (most guidelines now recommend skipping the bolus). Target glucose fall of 50–100 mg/dL/hr.
— When glucose ~250–300 mg/dL: add D5 to fluids and reduce insulin to 0.02–0.05 U/kg/hr to maintain glucose 250–300 until osmolality <315 and mental status normalizes. Do not normalize glucose too fast — risks cerebral edema and hypoglycemia.
— Correct half the water deficit in the first 12h, remainder over next 12–24h.
— Drop osmolality by no more than 3 mOsm/kg/hr.
— Drop corrected Na by <10 mEq/L/24h.
CCS pearl: Order "insulin drip — regular insulin per institutional HHS protocol" only after you have confirmed K ≥3.3. If you order insulin before checking K, the case penalizes you and the patient can arrest from hypokalemia.
Board pearl: The single highest-yield concept on HHS questions: fluids fix more of HHS than insulin does. Glucose will fall by 80–200 mg/dL with the first 2 L of saline alone.
— Initial bolus: 0.9% NS 15–20 mL/kg in hour 1 (typically 1–1.5 L). Repeat if hypotensive.
— Maintenance: 0.45% NS at 250–500 mL/hr if corrected Na ≥135; 0.9% NS if corrected Na <135 or persistent hypotension.
— Add D5 when glucose reaches 250–300 mg/dL: D5 ½ NS at 150–250 mL/hr.
— Total deficit: ~9 L — aim to replace ~50% in first 12h, balance over 12–24h.
— Regular insulin IV infusion 0.1 U/kg/hr, no bolus required.
— If glucose does not fall ≥50 mg/dL in the first hour and volume is adequate, double the rate.
— When glucose ~250–300 mg/dL → drop to 0.02–0.05 U/kg/hr + dextrose-containing fluids.
— Continue infusion until: osmolality <315, mental status normal, anion gap closed (if mixed), AND patient eating.
— Overlap subcutaneous basal insulin (glargine 0.2–0.3 U/kg) 2 hours before stopping the drip — failure to overlap is a classic CCS pitfall causing rebound hyperglycemia.
— Replete to keep K 4–5 mEq/L. Add 20–30 mEq KCl per liter of maintenance fluid once K <5.2 and urine output adequate.
— K <3.3 → hold insulin, give 10–20 mEq/hr until K ≥3.3.
— Routine repletion not recommended. Replace only if PO4 <1.0 mg/dL or symptomatic (respiratory weakness, hemolysis, cardiac dysfunction): K-phos 20–30 mEq over 6h, monitoring Ca.
— Replete if <1.8 or refractory hypokalemia — 2–4 g MgSO4 IV.
Step 3 management: Order glucose q1h, BMP q2–4h, Mg/Phos q4–6h, osmolality q4h, neuro checks q1–2h, strict I/Os as the standing monitoring set on CCS.
— Two large-bore peripheral IVs (16–18 G) suffice for most patients.
— Central venous access indicated for: refractory hypotension requiring vasopressors, inability to obtain peripheral access, need for concentrated K+ (>40 mEq/L) infusion, or prolonged ICU stay.
— Arterial line if requiring vasopressors or frequent ABGs.
— Most HHS patients improve mentally with osmolar correction and do not require intubation.
— Intubate for: GCS <8 with inability to protect airway, aspiration, refractory shock, or respiratory failure from pneumonia/sepsis.
— Beware: rapid sequence induction in hypovolemic HHS can cause profound hypotension — fluid-resuscitate first; consider etomidate/ketamine.
— Place for all obtunded or hemodynamically unstable patients to monitor urine output (target ≥0.5 mL/kg/hr) — the single best bedside marker of adequate resuscitation.
— Consider if persistent vomiting or ileus, especially in mixed HHS-DKA with gastroparesis.
— PCI if STEMI precipitant — coordinate with cardiology; HHS does not delay primary PCI.
— Source control for sepsis: drain abscesses, debride necrotizing soft tissue infections, remove infected lines.
— Hemodialysis: rarely needed for hyperosmolarity itself; consider for refractory hyperkalemia, severe AKI with uremia, or volume overload in ESRD patients who develop HHS.
— Subcutaneous rapid-acting insulin (lispro/aspart) protocols (0.2 U/kg load, then 0.1 U/kg q1–2h) are validated for uncomplicated DKA but NOT first-line for HHS given altered absorption with peripheral vasoconstriction.
— U-500 insulin, GLP-1 agonists, SGLT2 inhibitors — held during acute HHS; SGLT2s can precipitate euglycemic DKA and should be stopped 3–4 days preoperatively in known diabetics.
CCS pearl: Always order DVT prophylaxis, stress ulcer prophylaxis (if intubated/coagulopathic), and a diabetes educator consult before the case clock advances to discharge planning — these are graded items often missed.
— Highest mortality demographic. Mean age ~60–70; >70% have comorbid CAD, CKD, or dementia.
— Blunted thirst response and limited water access drive presentation; once volume-depleted, they cannot compensate.
— Fluid resuscitation caveats: monitor for pulmonary edema in those with HFrEF, severe valvular disease, or CKD. Use smaller boluses (250–500 mL), assess after each, consider point-of-care ultrasound (IVC, B-lines) to titrate.
— Goal MAP ≥65 but avoid overshooting in chronic HTN — accept slightly higher BP targets if baseline elevated.
— Delirium screening: persistent AMS after osmolar correction → consider stroke, sepsis, ICU delirium, drug effect.
— Polypharmacy review: discontinue offending agents (thiazides, steroids, atypicals) when feasible; document reason and follow-up plan.
— Baseline reduced GFR means HHS develops at lower glucose levels (sometimes <600) because the renal glucose threshold is lost — diagnose by osmolality and clinical picture, not glucose alone.
— ESRD patients on HD: anuric, so the protective osmotic diuresis is absent → severe hyperkalemia and volume overload risk with aggressive fluids. Limit boluses, early nephrology/dialysis consult, often need emergent HD for correction.
— Insulin requirements fall in advanced CKD (reduced renal clearance); use lower infusion rates and watch for hypoglycemia.
— Cirrhotics have impaired gluconeogenesis but also altered insulin metabolism; HHS less common but mixed lactic acidosis more likely. Lactate >4 in HHS with cirrhosis → broaden to sepsis and hepatic decompensation workup.
— Avoid hypotonic overload in cirrhotics with ascites — prefer 0.9% NS with careful K monitoring.
Step 3 management: In any elderly HHS patient, before discharge, obtain a functional/cognitive assessment, medication reconciliation with deprescribing, and a caregiver-capable plan for insulin administration. These are CCS-graded social orders.
Key distinction: Elderly HHS with mild glucose elevation but osmolality >320 and AMS is still HHS — do not be falsely reassured by "only" 450 mg/dL glucose in a CKD patient.
— Increasingly recognized in obese adolescents with newly diagnosed T2DM, particularly African American and Hispanic males.
— Mortality higher than adult HHS — up to 30% in some series — driven by malignant hyperthermia–like rhabdomyolysis, cerebral edema, and circulatory collapse.
— Diagnostic criteria same as adult: glucose ≥600, osmolality ≥320, minimal ketosis, AMS.
— Mixed HHS-DKA is common in this group; treat with fluid-first strategy but lower initial bolus (10–20 mL/kg over 1h), then continue at 1.5× maintenance.
— Watch for rhabdomyolysis (CK >1000), malignant hyperthermia, and venous thromboembolism — get CK on admission and consider prophylactic anticoagulation in adolescents per institutional pediatric endocrine protocols.
— Cerebral edema risk: monitor neuro status closely; mannitol 0.5–1 g/kg or 3% saline if cerebral edema suspected.
— HHS is rare in pregnancy; DKA at lower glucose levels (euglycemic DKA) is more typical, especially in T1DM third trimester.
— Management mirrors non-pregnant: fluids, insulin, K+, but involve OB and MFM early, monitor fetus with continuous toco/FHR if viable gestation.
— Left lateral decubitus positioning, avoid hypotension which compromises uteroplacental perfusion.
— Postpartum: insulin requirements fall sharply — re-titrate.
— 30–40% of HHS cases are first presentations of T2DM.
— Obtain HbA1c, C-peptide, GAD-65 antibodies to classify and direct outpatient regimen.
— Adolescents: consider MODY if atypical phenotype, family history, lean.
— Insulin cost and rationing is a documented HHS precipitant in the US — screen for affordability and connect with social work/manufacturer assistance.
Board pearl: An obese 14-year-old African American boy with glucose 950, osmolality 360, mild ketosis, and obtundation → adolescent HHS with possible rhabdo — order CK, careful fluid resuscitation, and pediatric ICU.
Step 3 management: Always order social work consult for newly diagnosed HHS to address insulin access, food security, and follow-up.
— Hypoglycemia: from failing to add dextrose when glucose hits 250–300, or from continuing insulin after the gap closes. Check fingerstick q1h on drip.
— Hypokalemia: insulin shifts K intracellularly; can precipitate fatal arrhythmias. Always K-replete before/with insulin.
— Cerebral edema: rare in adults, more common in pediatric HHS; from overly rapid osmolar correction. Target Na fall <10 mEq/L/24h and osmolality drop <3 mOsm/kg/hr.
— Volume overload/pulmonary edema: especially in elderly, HFrEF, CKD. Reassess after each liter.
— Hyperchloremic non-anion-gap metabolic acidosis: from large-volume NS resuscitation. Self-resolves; consider balanced crystalloids (LR, Plasma-Lyte) if pronounced.
— Venous thromboembolism: hyperosmolar/hypercoagulable state — DVT, PE, stroke (arterial), mesenteric ischemia. Start prophylactic LMWH unless contraindicated.
— Acute kidney injury: prerenal from dehydration; usually resolves with fluids but can become intrinsic (ATN) if prolonged.
— Rhabdomyolysis: check CK on admission; immobility + hyperosmolarity is the substrate.
— Stroke and MI: both as precipitants and complications — maintain low threshold for repeat imaging/troponins.
— Acute pancreatitis: can precipitate or complicate HHS; hypertriglyceridemia common.
— ARDS: uncommon but described.
— Aspiration pneumonia in obtunded patients — elevate HOB, NPO until alert.
— Pressure ulcers, line infections in prolonged ICU stays.
— Delirium and functional decline — early mobilization once stable.
— Cognitive decline persists in 25% of survivors.
— 30-day readmission rate ~20% — high-touch transitions critical.
— 1-year mortality in elderly HHS survivors approaches 40%, mostly from underlying comorbidities.
Key distinction: Persistent AMS after osmolality normalizes (<315) is no longer HHS — order CT/MRI head, EEG, infection workup, and toxic-metabolic panel to find the alternative cause.
Board pearl: A drop in serum K from 4.2 to 2.8 four hours into insulin therapy is the classic vignette of insulin-induced hypokalemia — preventable with proactive K+ in the IV fluids.
— GCS <12, hemodynamic instability, severe electrolyte derangements, requirement for insulin infusion, osmolality >320, or any organ failure.
— Most institutions admit all HHS to ICU or step-down for the first 24h because of monitoring intensity (q1h glucose, q2–4h labs, q1h neuro checks).
— Mental status returned to baseline.
— Osmolality <315, glucose <250 on dextrose-containing fluids with low-rate insulin.
— Hemodynamically stable, urine output ≥0.5 mL/kg/hr.
— K, Mg, Phos stable.
— Precipitant identified and treated.
— Endocrinology: all HHS — for protocol adherence and discharge regimen.
— Diabetes educator/CDE: all patients before discharge.
— Nutrition: carbohydrate counting, meal planning.
— Cardiology: if MI precipitant or new-onset arrhythmia.
— Nephrology: AKI not improving, ESRD patient, refractory electrolyte issues.
— Neurology/stroke: focal deficits persisting >24h after correction.
— Infectious disease: complicated infection (necrotizing fasciitis, endocarditis, fungal in immunocompromised).
— Social work and case management: insulin access, home health, SNF placement.
— Pharmacy: medication reconciliation and adherence support.
— Discharge to home only if patient/caregiver can demonstrate insulin administration, glucose monitoring, hypoglycemia recognition, and sick-day rules.
— Otherwise → SNF, home health with skilled nursing, or caregiver training extension.
— Schedule PCP follow-up within 1–2 weeks; endocrinology within 4 weeks.
— Send discharge summary to PCP same-day, including precipitant, A1c, regimen changes, and pending labs.
Step 3 management: Document a read-back, teach-back insulin training session with caregiver before discharge — a known patient-safety best practice and frequent test point.
CCS pearl: Never close an HHS case on the simulator without ordering: discharge insulin regimen, glucometer with strips, glucagon kit (if on insulin), ketone strips, follow-up appointments, MedicAlert ID counsel, and diabetic foot/eye exam referrals.
— Younger, T1DM typically (but T2DM increasingly), rapid onset hours to a day.
— Glucose often 300–800 (lower than HHS); pH <7.30, HCO3 <18, anion gap >12, β-OHB ≥3 mmol/L.
— Kussmaul respirations, fruity breath, abdominal pain, vomiting.
— Management: fluids + insulin together, bicarb only if pH <6.9, treat hypokalemia first.
— Key distinction: AMS in DKA tracks with acidosis severity; AMS in HHS tracks with osmolality.
— Meets criteria for both. Treat with DKA insulin/bicarb thresholds but HHS-volume aggressiveness.
— Recognize: glucose >600, osmolality >320, AND pH <7.30 with significant ketones.
— Glucose often <250 but anion gap acidosis with ketonemia.
— Triggers: SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin), pregnancy, prolonged fasting, alcohol use, bariatric surgery.
— Hold SGLT2, give D5-containing fluids + insulin simultaneously — the dextrose enables continued insulin without hypoglycemia to shut off ketogenesis.
— Hospitalized patients (sepsis, post-op, steroids) with glucose 180–400, no acidosis, no significant osmolar shift, often non-diabetic.
— Manage with basal-bolus or sliding-scale insulin; does not require HHS protocol.
— Polyuria + hypernatremia + hyperosmolality, but glucose normal and urine osmolality inappropriately low.
— Treat with DDAVP (central DI) or thiazide/low-Na diet (nephrogenic DI) and free water replacement.
Board pearl: In a T2DM patient on empagliflozin with vomiting, glucose 220, pH 7.15, HCO3 12, large ketones → euglycemic DKA — the glucose number does not exclude the diagnosis, and dextrose-containing fluids must run alongside insulin from the start.
Step 3 management: When diagnostic criteria sit on the boundary, treat as the more severe overlap (e.g., mixed HHS-DKA) and document the rationale.
— Hypoglycemia: always check fingerstick first — easy reversal.
— Hyponatremia/hypernatremia: independently cause AMS; HHS has both pseudohyponatremia and true hypernatremia after correction.
— Uremic encephalopathy: BUN >100, asterixis — overlap with diabetic ESRD.
— Hepatic encephalopathy: asterixis, fetor hepaticus, elevated ammonia.
— Thyroid emergencies: myxedema coma (hypothermia, bradycardia, hypoglycemia) or thyroid storm (tachycardia, fever).
— Adrenal crisis: hypotension refractory to fluids, hyperkalemia, hyponatremia, hypoglycemia.
— Alcohol/drug intoxication or withdrawal: check tox screen, ethanol level.
— Ischemic stroke: focal deficits — but remember HHS can produce stroke-like focal deficits that reverse with osmolar correction. Get CT first if focal.
— Intracranial hemorrhage: anticoagulated, hypertensive patients.
— Status epilepticus (especially non-convulsive): consider EEG if AMS persists.
— Meningitis/encephalitis: fever, meningismus, headache — LP if suspected.
— MI with cardiogenic shock → ECG, troponin.
— Septic shock: hyperglycemia is common stress response — don't anchor on HHS if lactate is high and clinical picture is sepsis.
— Hyperthyroidism with hyperglycemia + AMS — looks like HHS but TSH suppressed, T4 high.
— Pheochromocytoma crisis — paroxysmal hypertension, sweating, hyperglycemia.
Key distinction: Glucose >600 + osmolality ≥320 is the gate — without both, look harder for alternative explanations. Conversely, an elderly diabetic with glucose 280 and AMS is not HHS by definition; pursue sepsis, stroke, or other causes.
Board pearl: When the vignette describes an obtunded diabetic with fever, hypotension, and glucose 350, the diagnosis is septic shock with stress hyperglycemia, not HHS — resuscitation, antibiotics, and lactate-guided care take priority.
— Basal-bolus is standard post-HHS: weight-based total daily dose (TDD) 0.4–0.6 U/kg/day, split 50% basal (glargine/detemir/degludec at bedtime) and 50% prandial (lispro/aspart/glulisine before meals).
— Insulin-naïve T2DM with newly diagnosed HHS: typically 0.3–0.5 U/kg/day TDD.
— Reconcile with pre-admission regimen; reduce basal by 20% if A1c was at-goal pre-HHS to avoid post-discharge hypoglycemia.
— Metformin: restart once eating, eGFR ≥30, no contrast within 48h, no AKI.
— GLP-1 agonists (semaglutide, liraglutide): continue or initiate — strong cardiovascular and renal benefit.
— SGLT2 inhibitors: restart cautiously after full recovery; counsel on sick-day rules and DKA risk.
— Sulfonylureas: avoid in elderly (hypoglycemia risk); deprescribe if possible.
— Pioglitazone: avoid in HFrEF, osteoporosis, bladder cancer history.
— Statin (moderate or high-intensity) — all diabetics 40–75; high-intensity if ASCVD or 10-yr risk ≥20%.
— ACEi or ARB if HTN, albuminuria, or ASCVD.
— Aspirin if established ASCVD.
— BP target <130/80; A1c target 7.0% (individualize: <6.5% in young/healthy, 7.5–8% in frail elderly).
— Influenza (annual), pneumococcal (PCV20 or PCV15+PPSV23), COVID-19, Tdap, hepatitis B (if <60 and unvaccinated), shingles (≥50).
— Medical nutrition therapy referral.
— 150 min/week moderate exercise.
— Smoking cessation, alcohol limits.
— Sick-day rules: check glucose q2–4h, check ketones, hydrate, do not stop insulin, call provider when glucose >250 with ketones or unable to keep fluids down.
CCS pearl: Order diabetic eye exam (within 1 month), diabetic foot exam, and microalbumin/UACR at follow-up — these are graded preventive items and the annual ADA standard.
Board pearl: The single most effective prevention strategy for recurrent HHS is structured diabetes self-management education plus sick-day rules — proven to reduce readmission.
— PCP visit within 1–2 weeks of discharge — medication reconciliation, hypoglycemia screen, social/financial barriers.
— Endocrinology within 4 weeks, especially newly diagnosed or insulin-requiring patients.
— Diabetes educator within 1 week for insulin technique, glucometer, sick-day rules.
— Ophthalmology within 1 month for dilated retinal exam (annual thereafter).
— Podiatry annually or sooner for foot ulcer history.
— Dental every 6 months.
— HbA1c every 3 months until stable at goal, then every 6 months.
— Fingerstick glucose 4×/day initially (fasting + premeal + bedtime); transition to CGM if available — CGM is reimbursed for any insulin user.
— BMP, lipid panel, UACR (urine albumin/creatinine ratio), eGFR annually — earlier if AKI during admission.
— LFTs if on statin and any baseline elevation.
— TSH annually in T1DM, every 1–2 years T2DM.
— B12 annually if on metformin long-term.
— Hypoglycemia recognition and treatment (15-15 rule: 15 g carbs, recheck in 15 min); prescribe glucagon nasal spray or auto-injector for insulin users.
— Sick-day management — written plan.
— Driving safety — check glucose before driving, treat if <90, do not drive if <70.
— Insulin storage and pen technique — teach-back required.
— MedicAlert bracelet/ID.
— Mental health screening (PHQ-2/9) — diabetes distress and depression are common precipitants of nonadherence.
— Annual lipid panel, BP at every visit, ASCVD risk score every 4–6 years.
— Consider coronary calcium scoring in selected intermediate-risk patients.
Step 3 management: Schedule a post-discharge telephone call within 48–72 hours by a nurse or pharmacist — high-yield intervention shown to reduce 30-day readmissions in HHS survivors.
Key distinction: A1c can be falsely low in CKD, hemolysis, recent transfusion, or pregnancy — use fructosamine or CGM-derived GMI as alternatives when A1c is unreliable.
— HHS patients are frequently decisionally incapacitated on arrival. Treatment proceeds under emergency doctrine (implied consent) until capacity returns.
— Once oriented, obtain consent for invasive procedures (central line, intubation) if not already placed.
— For chronic care decisions (long-term insulin, dialysis), reassess capacity formally and identify surrogate decision-maker per state hierarchy (spouse → adult child → parent → sibling).
— Document capacity assessment using a structured tool (e.g., MacArthur, Aid to Capacity Evaluation).
— Many HHS patients are elderly with multiple comorbidities and high in-hospital and 1-year mortality.
— Address goals of care, code status, POLST/MOLST early in the admission — ideally within 24–48 hours of stabilization.
— Palliative care consult appropriate for recurrent HHS in frailty or dementia.
— Suspected elder abuse or neglect (caregiver withholding insulin/food) → mandated reporting to Adult Protective Services.
— Driving: providers in some states (CA, OR, PA, NV, NJ, DE) must report severe hypoglycemia or AMS that affects driving safety; in others, counsel and document.
— Self-neglect: social work consult; mental health/capacity evaluation.
— Medication reconciliation errors are the leading source of post-discharge harm in HHS survivors. Use two-source verification (patient/caregiver + pharmacy).
— Read-back/teach-back insulin instructions documented in discharge summary.
— Same-day discharge summary to PCP; closed-loop communication with outpatient endocrinology.
— Insulin access: verify pharmacy fill, copay, and insurance coverage before discharge — undisclosed cost barriers drive recurrent HHS.
— Black, Hispanic, and uninsured patients have higher HHS incidence and mortality. Screen for food insecurity (Hunger Vital Sign), housing, transportation at discharge.
— If iatrogenic hypoglycemia, hypokalemic arrest, or cerebral edema occurs, disclose openly, document, and file incident report per institutional and Joint Commission standards.
Step 3 management: Always order social work, pharmacy med-rec, and a documented teach-back session before discharge — the trifecta of transition safety on the CCS.
Board pearl: A discharge without verified insulin access in an uninsured patient is predictable readmission — escalate to social work and manufacturer assistance before signing the paperwork.
— Glucose ≥600 mg/dL, osmolality ≥320 mOsm/kg, pH >7.30, HCO3 >18, β-OHB <3 mmol/L, AMS.
— Effective osmolality = 2(Na) + glucose/18 (no BUN).
— Corrected Na = measured Na + 1.6 × [(glucose – 100)/100].
— Mortality 10–20%; ~10× higher than DKA.
— Infection (#1, ~40% — pneumonia, UTI, skin), Infarction (MI/CVA), Insulin nonadherence/access, Iatrogenic (steroids, thiazides, atypicals, TPN, SGLT2 cessation), Intoxication (alcohol, cocaine), Inadequate water access (institutionalized).
— Water deficit 100–200 mL/kg (~9 L in a 70-kg adult). Replace 50% in 12h, rest over 12–24h.
— Drop Na <10 mEq/L/24h and osmolality <3 mOsm/kg/hr.
— Start 0.1 U/kg/hr regular insulin IV after K ≥3.3.
— Drop to 0.02–0.05 U/kg/hr with D5 fluids when glucose hits 250–300.
— Overlap subcutaneous basal 2 hours before stopping drip.
— Total body K is depleted even when serum K is normal/high.
— Hold insulin if K <3.3; replete first.
— Phosphate replacement only if <1.0 or symptomatic.
— Elderly, T2DM, institutionalized, Black/Hispanic, lower socioeconomic status.
— Adolescents with severe obesity and new T2DM — rising incidence.
— Atypical antipsychotics: olanzapine, clozapine, quetiapine.
— Thiazides, loop diuretics, β-blockers (mask hypoglycemia), glucocorticoids.
— Phenytoin, pentamidine, didanosine, protease inhibitors, calcineurin inhibitors.
— Focal seizures reversing with osmolar correction — classic HHS.
— Rhabdomyolysis — especially in adolescents.
— Hypercoagulability → DVT/PE/stroke — prophylactic LMWH.
— 30-day readmission ~20%; 1-year mortality in elderly survivors ~40%.
Board pearl: "Osmolality drives mental status; pH drives DKA breath; potassium drives the order in which you give insulin." Three sentences = most HHS questions answered.
— 78-year-old from SNF with 5 days of decreased PO intake, glucose 880, Na 148 (measured), K 4.5, HCO3 22, pH 7.34, β-OHB 1.2, osmolality 358, GCS 10.
— Answer: Start 0.9% NS 1 L bolus, check K (already 4.5 — OK), start insulin infusion at 0.1 U/kg/hr after first liter. Do NOT give bicarb.
— Same patient, but K is 3.1. The trap answer is "start insulin." The right answer: hold insulin, give KCl 20–30 mEq/hr, recheck K, then start insulin when K ≥3.3.
— On hour 4, glucose is 270 mg/dL, osmolality 332, mental status improving but not normal. What next?
— Answer: Add D5 to 0.45% NS and decrease insulin to 0.02–0.05 U/kg/hr. Continue until osmolality <315 and mentation normal.
— T2DM on empagliflozin with vomiting, glucose 240, pH 7.12, anion gap 24, ketones positive.
— Answer: Euglycemic DKA from SGLT2; hold SGLT2, D5-containing fluids + insulin simultaneously.
— Right hemiparesis with glucose 1100, osmolality 365. CT head negative.
— Answer: Likely HHS-related focal deficit; treat HHS, repeat neuro exam after osmolality normalizes; MRI if deficit persists.
— 15-year-old obese male with glucose 1000, osmolality 360, CK 5000, AMS.
— Answer: Adolescent HHS with rhabdomyolysis; cautious fluids (10–20 mL/kg bolus then 1.5× maintenance), PICU, monitor for cerebral edema.
— HHS resolving, on drip, blood sugars 180s. PO tolerating. Next step?
— Answer: Give subcutaneous basal insulin 2 hours before discontinuing drip, transition to basal-bolus, arrange diabetes educator and PCP follow-up within 1–2 weeks.
Step 3 management: When a question asks "what's the next best step" in HHS, the answer ladder is almost always: fluids → K check → insulin → dextrose addition → SC overlap → discharge planning.
Board pearl: If the stem highlights abdominal pain in an HHS-criteria patient, look for a precipitant (pancreatitis, mesenteric ischemia, appendicitis) or mixed HHS-DKA — pure HHS rarely causes abdominal pain.
Hyperosmolar hyperglycemic state is a profound water-deficit emergency of older type 2 diabetics defined by glucose ≥600, effective osmolality ≥320, minimal ketosis, and altered mental status — managed in a strict CCS sequence of aggressive fluids first, potassium gating before insulin, low-dose insulin infusion with dextrose added at glucose 250–300, parallel hunt for the precipitating "I" (infection, infarction, insulin nonadherence, iatrogenic drug, intoxication, inadequate water access), and a discharge bundle of basal-bolus insulin, diabetes education, follow-up, and social support to prevent recurrence.
Board pearl: Fluids fix more of HHS than insulin does — and the precipitant kills more often than the glucose number.