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[ Home ](https://mdster.com) 2. [ Blog ](https://mdster.com/blog) 3. [ Case Discussion ](https://mdster.com/blog?category=case-discussion) 4. Hyperosmolar Hyperglycemic State Revealing Silent NSTEMI [ Case Discussion ](https://mdster.com/blog?category=case-discussion) Hyperosmolar Hyperglycemic State Revealing Silent NSTEMI ========================================================== A board-focused case discussion on distinguishing HHS from DKA, correcting sodium, and managing concurrent acute coronary syndrome. [ MDster Editorial Team ](https://mdster.com/about) · Mar 08, 2026 · 5 min read · 104 [ Reviewed by Dr. Ali Ragab, MBBCH, MSc, MCAI ](https://mdster.com/medical-reviewers/dr-ali-ragab) [Editorial Policy](https://mdster.com/editorial-policy) | [Corrections Policy](https://mdster.com/corrections) [ Board Review ](https://mdster.com/blog?tag=board-review) [ Internal Medicine ](https://mdster.com/blog?tag=internal-medicine) [ NSTEMI ](https://mdster.com/blog?tag=nstemi) [ Hyperosmolar Hyperglycemic State ](https://mdster.com/blog?tag=hyperosmolar-hyperglycemic-state) [ Diabetic Emergencies ](https://mdster.com/blog?tag=diabetic-emergencies) Share this article Share this post A 78-year-old woman arrives obtunded, profoundly dehydrated, and hypotensive, with glucose **850 mg/dL** and osmolality **345 mOsm/kg**. Her pH is **7.38**, bicarbonate **24 mmol/L**, ketones are negative, and the ECG shows inferolateral ischemic change with a positive troponin. The metabolic diagnosis is **HHS**, but the teaching point is broader: when an older patient with diabetes presents with delirium, you must diagnose the hyperglycemic emergency and the precipitant in parallel. In this case, the precipitant is likely a **silent NSTEMI**. This discussion reflects the 2024 international hyperglycemic-crises consensus report, ADA 2026 Standards, and the 2025 ACC/AHA ACS guideline. [\[1\]](#cite-1 "Reference [1]") Why this is HHS, not DKA ------------------------ The distinction that matters at the bedside is not semantic; it determines the tempo of therapy. Current adult criteria define **HHS** by severe hyperglycemia, hyperosmolality, absent or mild ketonemia, and absent significant acidosis, whereas **DKA** requires hyperglycemia/diabetes plus ketonemia and metabolic acidosis. Clinical overlap is common, so mixed DKA/HHS should always remain in the differential. [\[1\]](#cite-1 "Reference [1]") FeatureThis caseBoard implicationGlucose850 mg/dLFavors HHSpH / HCO37.38 / 24 mmol/LAgainst DKAKetonesNegativeAgainst DKAOsmolality345 mOsm/kgDiagnostic for HHSMental statusObtundedFits hyperosmolar encephalopathy What often traps trainees is the mental model that DKA is the “sicker” presentation. In older adults, **HHS can look quieter biochemically but be more dangerous hemodynamically and neurologically** because the water deficit is larger and the precipitating illness is often major. Acute myocardial infarction is a recognized trigger of HHS. [\[1\]](#cite-1 "Reference [1]") Corrected sodium is the next useful calculation. Using the classic board-style correction of **+1.6 mEq/L** for each 100 mg/dL glucose above 100, her corrected sodium is about **144 mEq/L**. That supports severe free-water loss rather than true hyponatremia. The nuance is that different references use different correction factors in marked hyperglycemia; JBDS uses **2.4 mEq/L** in this range, which is why serial **osmolality** is more informative than obsessing over one corrected sodium value. A rising measured sodium during treatment is often expected as glucose falls and is not, by itself, a reason to reflexively switch to hypotonic fluid. [\[1\]](#cite-1 "Reference [1]") > **Clinical Pearl:** In HHS, the target is not simply a lower glucose. The real safety variable is a controlled fall in **osmolality**. [\[1\]](#cite-1 "Reference [1]") The precipitant you cannot miss ------------------------------- Her daughter reports only “flu-like” symptoms and weakness, but the ECG and troponin change the case immediately. In diabetes, **cardiovascular autonomic neuropathy** can blunt ischemic pain perception; reduced autonomic function is strongly associated with **silent myocardial ischemia**. Consequently, confusion, weakness, nausea, or dyspnea may be the only clue to ACS in a patient whose chart never contains the words “chest pain.” [\[2\]](#cite-2 "Reference [2]") This is why the best frame is not “HHS versus MI,” but **HHS because of MI until proven otherwise**. Infection, stroke, and medication effects remain alternative precipitants, and her ongoing delirium should not be attributed to hyperosmolality forever. If mentation fails to improve as osmolality falls, reassess for stroke, sepsis, drug effect, cerebral edema, or persistent hypoperfusion rather than congratulating yourself on a better glucose. [\[1\]](#cite-1 "Reference [1]") Management in the first hours ----------------------------- ### Fluids come first In HHS, initial treatment is **isotonic crystalloid**. The consensus report recommends **0.9% saline or a balanced crystalloid at 500–1,000 mL/h for the first 2–4 hours** in adults without major cardiac or renal limitation; JBDS still emphasizes **0.9% saline** as the principal initial fluid. In this patient, hypotension and tachycardia argue for immediate volume expansion, but age and myocardial ischemia argue for frequent reassessment after each bolus with lung exam, urine output, bedside ultrasound, and hemodynamics. Clinical judgment dictates a more cautious rhythm if pulmonary edema begins to emerge. [\[1\]](#cite-1 "Reference [1]") ### Insulin is necessary, but not immediately Pure HHS is not DKA with a bigger glucose. Because some endogenous insulin activity is preserved, the priority is restoring perfusion first. If there is no significant ketonemia or acidosis, start a fixed-rate IV insulin infusion at **0.05 units/kg/h** only after fluids are underway and potassium is acceptable. If the patient has mixed DKA/HHS physiology, the infusion should be **0.1 units/kg/h**. An upfront bolus is generally unnecessary and risks an excessive fall in tonicity. [\[1\]](#cite-1 "Reference [1]") ### Monitor what can hurt the brain and the myocardium Capillary glucose should be checked every **1–2 hours** and electrolytes/renal function/osmolality about every **4 hours** in HHS. Fluid alone often lowers glucose substantially; once insulin is added, the aim is to avoid a glucose fall faster than about **90–120 mg/dL/h** and an osmolality decline faster than **3–8 mOsm/kg/h**. If potassium is **<3.5 mmol/L**, insulin should be delayed while potassium is replaced. [\[1\]](#cite-1 "Reference [1]") ### Thrombosis prevention and ACS treatment must run in parallel HHS is prothrombotic enough that JBDS recommends **prophylactic LMWH for the full admission** unless contraindicated. However, this patient already has probable **NSTE-ACS**, so prophylaxis alone is not enough; antithrombotic therapy should follow ACS pathways. The 2025 ACC/AHA guideline recommends an **invasive approach during hospitalization** for intermediate- or high-risk NSTE-ACS and supports aspirin-based antiplatelet therapy, anticoagulation, and high-intensity statin therapy as the default framework, modified by bleeding risk and the revascularization plan. [\[3\]](#cite-3 "Reference [3]") Clinical Application -------------------- The exam-relevant subtlety is that two common errors pull in opposite directions: **undertreating shock** because the sodium looks “low,” and **overcorrecting osmolality** because the glucose looks frightening. The first hour is therefore a resuscitation problem, not a glucose problem. After that, it becomes a monitoring problem. If sodium rises while osmolality falls appropriately, stay calm. If glucose falls but osmolality is dropping too fast, slow down. If mentation does not improve, broaden the differential instead of escalating insulin reflexively. [\[1\]](#cite-1 "Reference [1]") There is also an ethics point hidden in this scenario. A delirious patient cannot give meaningful informed consent for urgent catheterization. The physician should **document impaired decision-making capacity**, identify the appropriate surrogate, and ask the surrogate to use **substituted judgment** when the patient’s preferences are known, or the **best-interest standard** when they are not. If no surrogate is available and delay would threaten the patient, emergency treatment may proceed without prior consent. [\[4\]](#cite-4 "Reference [4]") Key Points for Board Exams -------------------------- - **HHS** is defined by marked hyperglycemia, hyperosmolality, minimal ketonemia, and no significant acidosis; mixed **DKA/HHS** is common. [\[1\]](#cite-1 "Reference [1]") - In this case, corrected sodium is about **144 mEq/L** by the classic 1.6 correction factor; serial osmolality is more useful than a single sodium value. [\[1\]](#cite-1 "Reference [1]") - In pure HHS, give **fluids before insulin**; start IV insulin at **0.05 units/kg/h** once circulation is improving and potassium is safe. [\[1\]](#cite-1 "Reference [1]") - Safe correction matters: glucose should not fall faster than about **90–120 mg/dL/h** and osmolality should fall **3–8 mOsm/kg/h**. [\[1\]](#cite-1 "Reference [1]") - In diabetes, **silent MI** may reflect autonomic neuropathy; never let absent chest pain talk you out of ACS. [\[2\]](#cite-2 "Reference [2]") Conclusion ---------- The memorable lesson from this case is not just how to separate **HHS from DKA**, but how to resist anchoring on the metabolic emergency alone. HHS in an older patient is often a marker of a second disaster—here, likely **silent NSTEMI**. The best clinicians resuscitate volume, correct tonicity deliberately, and chase the precipitant with equal urgency. References (9) ------------------ 1. 1. [ pmc.ncbi.nlm.nih.gov/articles/PMC11272983 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC11272983) [↩](#cite-ref-1-1 "Back to text") 2. 2. [ pubmed.ncbi.nlm.nih.gov/12716821 ](https://pubmed.ncbi.nlm.nih.gov/12716821/) [↩](#cite-ref-2-1 "Back to text") 3. 3. [ pmc.ncbi.nlm.nih.gov/articles/PMC10107355 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC10107355/) [↩](#cite-ref-3-1 "Back to text") 4. 4. [ code-medical-ethics.ama-assn.org/ethics-opinions/informed-consent ](https://code-medical-ethics.ama-assn.org/ethics-opinions/informed-consent) [↩](#cite-ref-4-1 "Back to text") 5. 5. American Diabetes Association; European Association for the Study of Diabetes; Joint British Diabetes Societies for Inpatient Care; American Association of Clinical Endocrinology; Diabetes Technology Society. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report. Diabetes Care. 2024;47(8):1257-1275. 6. 6. American Diabetes Association Professional Practice Committee. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes—2026. Diabetes Care. 2026;49(Suppl 1):S132-S149. doi:10.2337/dc26-S006. 7. 7. Mustafa OG, Haq M, Dashora U, et al; Joint British Diabetes Societies for Inpatient Care Group. Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults: An updated guideline from the Joint British Diabetes Societies (JBDS) for Inpatient Care Group. Diabet Med. 2023;40:e15005. doi:10.1111/dme.15005. 8. 8. American Heart Association. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Published February 27, 2025. 9. 9. AMA Code of Medical Ethics Opinion 2.1.1, Informed Consent; Opinion 2.1.2, Decisions for Adult Patients Who Lack Capacity. 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