What is the most likely diagnosis for a 56‑year‑old female presenting with polyuria, polydipsia, dry mucous membranes, poor skin turgor, orthostatic hypotension, tachycardia, weight loss, blurred vision, fasting glucose 298 mg/dL, random glucose 342 mg/dL, hemoglobin A1c 10.2 %, positive urine glucose and ketones, and elevated serum osmolality?

Suspected Diagnosis: Hyperosmolar Hyperglycemic State (HHS) with Possible Mixed DKA/HHS

This patient most likely has Hyperosmolar Hyperglycemic State (HHS), though the presence of urine ketones raises concern for a mixed DKA/HHS presentation that requires immediate emergency department evaluation and intensive care unit admission. 1, 2

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CJMM Phase 1: Recognize Cues

Four Abnormal Assessment Findings:

• Hypotension (96/60 mm Hg) with tachycardia (104 bpm) indicating significant volume depletion from osmotic diuresis 1, 2
• Poor skin turgor and dry mucous membranes reflecting severe dehydration with estimated fluid deficit of 100-220 mL/kg (approximately 9 liters in adults) 2, 3
• Unintentional weight loss of 12 lb in 2 months suggesting prolonged insulin deficiency and catabolic state 1
• Blurred vision resulting from osmotic changes in the lens due to severe hyperglycemia 1

Two Abnormal Laboratory Values:

• Random blood glucose 342 mg/dL (markedly elevated, though HHS typically presents ≥600 mg/dL; this may represent early HHS or mixed presentation) 2, 3
• Hemoglobin A1C 10.2% indicating chronic poor glycemic control over the preceding 2-3 months 1

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CJMM Phase 2: Analyze Cues

How Hyperglycemia Contributes to Polyuria and Dehydration:

Severe hyperglycemia exceeds the renal threshold for glucose reabsorption (approximately 180 mg/dL), causing glucose to spill into urine and create an osmotic gradient that prevents water reabsorption in the renal tubules. 1 This osmotic diuresis leads to massive fluid losses (100-220 mL/kg in HHS), with concurrent loss of sodium, potassium, and other electrolytes. 2 The resulting hyperosmolality (calculated as 2[Na+] + glucose/18) draws water from intracellular to extracellular compartments, worsening cellular dehydration despite initial preservation of intravascular volume. 1, 2

Relationship Between Insulin Deficiency/Resistance and Weight Loss:

Insulin deficiency or severe resistance prevents glucose utilization by peripheral tissues, forcing the body into a catabolic state where it breaks down muscle protein and adipose tissue for alternative energy sources. 1 The combination of increased hepatic and renal glucose production with impaired peripheral glucose utilization results in persistent hyperglycemia despite tissue starvation. 1 Additionally, the osmotic diuresis causes loss of calories through urinary glucose excretion (glycosuria), further contributing to weight loss. 1

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CJMM Phase 3: Prioritize Hypotheses

Most Likely Health Problem:

Hyperosmolar Hyperglycemic State (HHS), potentially with mixed DKA features given the presence of urine ketones. 1, 2 The clinical presentation of polyuria, polydipsia, weight loss developing over weeks, severe dehydration, and marked hyperglycemia with A1C 10.2% is classic for HHS in a middle-aged adult with type 2 diabetes. 1, 2 However, the presence of urine ketones requires urgent assessment of serum ketones (β-hydroxybutyrate preferred), arterial pH, and bicarbonate to rule out concurrent DKA, as up to one-third of patients present with mixed features. 4, 5

One Acute Complication at Risk:

Vascular thrombotic events (deep vein thrombosis, pulmonary embolism, stroke, myocardial infarction) due to severe hyperosmolality and hyperviscosity from profound dehydration. 2, 3 HHS carries mortality rates up to 15%, significantly higher than DKA, with thrombotic complications being a major contributor. 2, 6

Priority Concern at This Time:

Hemodynamic instability from severe volume depletion evidenced by hypotension (96/60 mm Hg), tachycardia (104 bpm), and clinical signs of dehydration. 1, 2 This requires immediate aggressive fluid resuscitation to restore circulating volume and prevent cardiovascular collapse, acute kidney injury, and thrombotic events. 2, 3

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CJMM Phase 4: Generate Solutions

Two Priority Nursing Interventions:

1. Establish large-bore IV access immediately and initiate rapid isotonic saline (0.9% NaCl) infusion at 15-20 mL/kg/hour (approximately 1-1.5 L in first hour for this patient). 2, 3 Fluid resuscitation is the cornerstone of HHS management and takes priority over insulin administration. 4

2. Obtain STAT laboratory studies including: serum electrolytes with calculated anion gap, arterial or venous blood gas for pH and bicarbonate, serum β-hydroxybutyrate (preferred over urine ketones), serum osmolality, BUN, creatinine, complete blood count, and ECG. 1, 2 These are essential to confirm HHS diagnosis (osmolality ≥320 mOsm/kg, pH ≥7.30, bicarbonate ≥15 mEq/L, ketones ≤3.0 mmol/L), differentiate from DKA, and guide electrolyte replacement. 2, 3

Anticipated Medications or Treatments:

• IV 0.9% sodium chloride for aggressive volume repletion with goal to correct estimated 9-liter deficit within 24 hours, monitoring for fluid overload especially given age >50 years 2, 3
• Delay insulin therapy until glucose stops falling with IV fluids alone (unless significant ketonemia is present), then initiate IV regular insulin at 0.1 units/kg/hour without bolus 2, 3
• Potassium replacement at 20-30 mEq/L (2/3 KCl, 1/3 KPO₄) once renal function confirmed and serum K+ known; hold insulin if K+ <3.3 mEq/L until corrected 2
• Dextrose 5% or 10% added to 0.45% saline when glucose reaches 250-300 mg/dL to prevent overly rapid glucose decline while maintaining insulin infusion at reduced rate (0.05-0.1 units/kg/hour) 2

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CJMM Phase 5: Take Action

Immediate Nursing Actions Required:

1. Transfer patient to emergency department immediately for ICU-level care, as HHS requires intensive monitoring with mortality rates up to 15% and risk of life-threatening complications. 2, 3, 6

2. Establish continuous cardiac monitoring and hourly vital signs to detect arrhythmias from electrolyte shifts and monitor hemodynamic response to fluid resuscitation. 2

3. Insert Foley catheter for strict intake/output monitoring with goal urine output ≥0.5 mL/kg/hour as marker of adequate renal perfusion. 3

4. Draw blood every 2-4 hours to monitor glucose, electrolytes, osmolality, and venous pH to guide therapy adjustments and ensure osmolality reduction does not exceed 3-8 mOsm/kg/hour (critical to prevent cerebral edema and central pontine myelinolysis). 2

5. Calculate corrected sodium by adding 1.6 mEq/L for each 100 mg/dL glucose elevation above 100 mg/dL, and calculate effective osmolality as 2[Na+] + glucose/18 to accurately track treatment response. 2

6. Initiate VTE prophylaxis given extreme hypercoagulability from hyperosmolality and dehydration. 3

Patient Education to Begin Today:

• Explain that this is a life-threatening diabetic emergency requiring hospitalization and that she likely has type 2 diabetes (given age, presentation, and A1C 10.2%). 1, 2

• Teach recognition of warning signs: excessive thirst, frequent urination, unexplained weight loss, weakness, and blurred vision require immediate medical attention before progression to crisis. 1

• Emphasize that infection is the most common trigger for HHS; any fever, cough, urinary symptoms, or wounds must prompt immediate glucose monitoring and medical evaluation. 1, 2

• Stress the importance of maintaining hydration during illness and never stopping diabetes medications without medical guidance. 1

• Discuss that certain medications (corticosteroids, thiazide diuretics, SGLT2 inhibitors) can precipitate hyperglycemic crises and require close monitoring. 2

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CJMM Phase 6: Evaluate Outcomes

Findings Indicating Improvement:

• Effective serum osmolality decreasing at 3-8 mOsm/kg/hour toward goal <300 mOsm/kg without exceeding maximum safe reduction rate 2, 3
• Blood pressure normalizing (systolic >100 mm Hg) with heart rate <100 bpm indicating restored circulating volume 2
• Urine output ≥0.5 mL/kg/hour demonstrating adequate renal perfusion 3
• Mental status returning to baseline alertness as hyperosmolality resolves 2, 3
• Blood glucose declining at 50-75 mg/dL/hour toward target of 250-300 mg/dL in first 24 hours 2
• Resolution criteria met: osmolality <300 mOsm/kg, hypovolemia corrected, cognitive status at pre-morbid baseline, glucose <270 mg/dL 2, 3

Findings Requiring Urgent Reevaluation:

• Osmolality decreasing >8 mOsm/kg/hour indicating excessive correction rate with risk of cerebral edema or central pontine myelinolysis (70% mortality once clinical symptoms develop) 2
• Worsening mental status, new headache, or seizures suggesting cerebral edema from overly rapid osmolality correction 2
• Serum potassium <3.3 mEq/L requiring immediate insulin hold and aggressive potassium replacement to prevent life-threatening arrhythmias 2
• Glucose falling >75 mg/dL/hour or dropping below 250 mg/dL before osmolality corrected necessitating dextrose addition and insulin rate reduction 2
• Development of pulmonary rales or respiratory distress indicating fluid overload, particularly concerning in patients >50 years 2
• Persistent hypotension despite 2-3 liters fluid resuscitation suggesting septic shock, myocardial infarction, or other precipitating acute illness requiring additional workup 1, 2
• Anion gap >12 mEq/L with pH <7.30 or bicarbonate <15 mEq/L confirming mixed DKA/HHS requiring modified treatment approach with earlier insulin initiation 1, 4