Acute Differential Diagnosis and Management
This patient requires immediate evaluation for diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS), both of which can present with altered mental status and neurological deficits in the setting of poorly controlled diabetes.
Immediate Diagnostic Workup
Priority Laboratory Studies
Obtain stat capillary or venous blood glucose, venous blood gas with pH, serum bicarbonate, calculated anion gap, serum electrolytes (especially potassium), BUN, creatinine, and direct serum β-hydroxybutyrate measurement to distinguish between DKA (glucose >250 mg/dL, pH <7.3, bicarbonate <15 mEq/L, positive ketones) and HHS (glucose ≥600 mg/dL, pH >7.3, bicarbonate >15 mEq/L, minimal ketones) 1, 2, 3.
Check serum osmolality using the formula: 2×[Na] + [glucose]/18 + [BUN]/2.8; HHS typically presents with effective osmolality ≥320 mOsm/kg, which directly correlates with altered mental status 3.
Obtain complete blood count with differential, urinalysis with culture, blood cultures, and chest X-ray to identify infection as the most common precipitating cause of hyperglycemic crises 1, 2.
Perform electrocardiogram to monitor for arrhythmias related to electrolyte abnormalities, particularly hypokalemia 2.
Critical Neuroimaging Considerations
The existing CT showing chronic encephalomalacia does not exclude acute stroke or diabetic striatopathy; hyperglycemia can both mimic stroke (through HHS) and accentuate symptoms of minor infarcts 4.
Consider urgent MRI brain with diffusion-weighted imaging (DWI) and CT angiography if the patient is appropriate for acute stroke intervention, particularly since HHS can present with focal neurological deficits that fully resolve with glucose normalization 4.
Be aware that diabetic striatopathy can present with involuntary movements and striatal hyperintensity on T1-weighted MRI that mimics hemorrhage, but this typically occurs with extreme hyperglycemia and resolves over months with glucose control 5.
Most Likely Acute Diagnoses
1. Diabetic Ketoacidosis or Hyperosmolar Hyperglycemic State
Given the HbA1c of 12% (indicating chronic severe hyperglycemia), one-week behavioral changes, and acute neurological deterioration, this patient most likely has either DKA or HHS.
DKA presents with glucose >250 mg/dL, pH <7.3, bicarbonate <15 mEq/L, and moderate-to-large ketonemia/ketonuria**, while **HHS presents with glucose ≥600 mg/dL, pH >7.3, bicarbonate >15 mEq/L, and minimal ketones 3.
Mental status changes correlate with severity: DKA patients may be alert to stuporous, whereas HHS patients are typically stuporous or comatose due to severe hyperosmolality (≥320 mOsm/kg) 3.
Both conditions require immediate hospital admission with continuous cardiac monitoring and frequent laboratory assessment 2.
2. Acute Stroke (Ischemic or Hemorrhagic)
Diabetes increases stroke risk 2-6 fold, and this patient has multiple vascular risk factors including hypertension, prior stroke, and poorly controlled diabetes 6, 7.
Hyperglycemia during acute ischemic stroke is associated with higher risk of hemorrhagic transformation and poor functional outcome, necessitating early glucose management 7.
However, HHS can mimic acute stroke with focal deficits that completely resolve with glucose normalization, making it essential to exclude hyperglycemic crisis before attributing symptoms solely to stroke 4.
3. Infection-Precipitated Metabolic Decompensation
Infection is the most common precipitant of DKA and HHS, and the patient's parental history of pulmonary tuberculosis 20 years ago raises concern for reactivation or other opportunistic infections in the setting of uncontrolled diabetes 2.
Urinary tract infection is particularly common given the mild right hydronephrosis on ultrasound, which could represent obstruction or infection 2.
Immediate Management Algorithm
Step 1: Assess Airway and Hemodynamic Stability
If Glasgow Coma Scale <8, pH <7.15 with respiratory acidosis, or severe respiratory distress, proceed with endotracheal intubation to protect the airway 1.
Measure blood pressure in both arms and lower limb to detect aortic dissection, though this is less likely given the clinical presentation 8.
Step 2: Initiate Fluid Resuscitation
Begin aggressive isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour to restore circulatory volume; the typical total body water deficit in DKA/HHS is 6-9 liters 1, 2.
Monitor closely for fluid overload given the bilateral increased renal cortical echogenicity suggesting chronic kidney disease 1.
Step 3: Potassium Management BEFORE Insulin
This is the most critical pitfall to avoid: never start insulin if serum potassium is <3.3 mEq/L without first repleting potassium, as insulin drives potassium intracellularly and can precipitate fatal arrhythmias 1, 2.
- If K+ <3.3 mEq/L: delay insulin and give aggressive potassium replacement 1.
- If K+ 3.3-5.5 mEq/L: add 20-30 mEq/L potassium to IV fluids (approximately 2/3 KCl and 1/3 KPO4) 1.
- If K+ >5.5 mEq/L: hold potassium supplementation and recheck frequently 1.
Step 4: Insulin Therapy
Once serum potassium is ≥3.3 mEq/L, initiate continuous IV regular insulin infusion at 0.1 units/kg/hour without an initial bolus for critically ill patients with altered mental status 1, 2.
If blood glucose does not fall by ≥50 mg/dL in the first hour, double the insulin rate hourly until a steady decline of 50-75 mg/dL per hour is achieved 1.
When blood glucose falls to 200-250 mg/dL, add 5-10% dextrose to IV fluids while continuing insulin infusion to ensure ketoacidosis resolves before glucose normalizes 1, 2.
Step 5: Monitor for Cerebral Edema
- Avoid overly aggressive fluid resuscitation and continuously assess mental status to detect early signs of cerebral edema, a rare but serious complication 1.
Step 6: Identify and Treat Precipitating Causes
Start broad-spectrum antibiotics immediately after obtaining cultures if infection is suspected 2.
Review medications, particularly if the patient is on SGLT2 inhibitors (which should be stopped immediately) or sulfonylureas 2.
Assess for myocardial infarction with troponin and ECG, as acute coronary syndrome can precipitate hyperglycemic crises 2.
Monitoring During Treatment
Draw blood every 2-4 hours to measure glucose, electrolytes (Na+, K+, Cl-), BUN, creatinine, venous pH, bicarbonate, and anion gap 1, 2.
Use direct blood β-hydroxybutyrate measurements rather than urine ketones, as nitroprusside-based tests miss β-hydroxybutyrate (the predominant ketone in DKA) and can falsely suggest worsening ketosis during treatment 1, 2.
Venous pH is sufficient for monitoring after initial diagnosis; arterial blood gases are not required, as venous pH is typically 0.03 units lower than arterial pH in hemodynamically stable patients 1.
Resolution Criteria
DKA/HHS is considered resolved only when ALL of the following are met:
Transition to Subcutaneous Insulin
Do not stop IV insulin without giving basal subcutaneous insulin 2-4 hours prior, or ketoacidosis will recur 1, 2.
Administer basal insulin (NPH, detemir, glargine, or degludec) 2-4 hours before discontinuing IV insulin to prevent rebound hyperglycemia 1, 2.
Estimate the required basal dose by averaging the IV insulin rate over the preceding 12 hours 1.
Critical Pitfalls to Avoid
Do not rely on urine ketones or nitroprusside tests for diagnosis or monitoring, as they miss β-hydroxybutyrate and can be misleading 1, 2.
Do not discontinue IV insulin when glucose normalizes; ketoacidosis resolves more slowly than hyperglycemia 1, 2.
Do not use bicarbonate therapy routinely; it provides no benefit in DKA resolution and should be reserved only for pH <6.9 1, 2.
Do not overlook euglycemic DKA, particularly if the patient is on SGLT2 inhibitors—ketoacidosis can occur with glucose <250 mg/dL 2.
Do not attribute all neurological symptoms to old stroke without excluding acute metabolic decompensation, as HHS can mimic or accentuate stroke symptoms 4.
Disposition
Admit to intensive care unit for continuous cardiac monitoring and frequent laboratory assessment 2.
Continue treatment until all resolution criteria are met, then transition to subcutaneous insulin regimen 1, 2.
Provide structured diabetes self-management education focusing on sick-day rules, recognition of DKA/HHS symptoms, and prevention of infections before discharge 2.
Schedule outpatient follow-up within 1-2 weeks to optimize glycemic control and prevent recurrence 2.