Why would a patient with diabetic ketoacidosis (DKA) and on a Clinical Institute Withdrawal Assessment (CIWA) protocol for alcohol withdrawal have a low blood urea nitrogen (BUN) level?

Low Blood Urea Nitrogen in DKA with Concurrent Alcohol Withdrawal

In a patient with DKA on CIWA protocol, low BUN most likely reflects alcoholic ketoacidosis (AKA) overlapping with DKA, chronic liver disease from alcohol use, or severe malnutrition—all common in patients requiring CIWA management.

Primary Mechanisms for Low BUN in This Clinical Context

Alcoholic Ketoacidosis Overlap

• Patients with chronic alcohol use presenting with ketoacidosis frequently have normal, low, or only mildly elevated glucose (rarely >250 mg/dL), distinguishing AKA from pure DKA 1, 2
• AKA results from poor glycogen stores, malnutrition, and metabolic derangements that lead to decreased urea production despite ketoacidosis 2
• The combination of DKA and AKA can occur simultaneously in diabetic patients with alcohol use disorder, creating a mixed picture where BUN may be paradoxically low despite volume depletion 1, 2

Chronic Liver Disease

• Patients requiring CIWA protocol have significant alcohol use disorder, placing them at high risk for alcohol-related liver disease with impaired hepatic urea synthesis 3
• Hepatic dysfunction reduces the liver's capacity to convert ammonia to urea, resulting in low BUN even in the presence of dehydration 3
• Short and intermediate-acting benzodiazepines (lorazepam, oxazepam) are specifically recommended for patients with hepatic dysfunction on CIWA protocol, suggesting liver disease is common in this population 3

Severe Malnutrition and Poor Protein Intake

• Patients with alcohol use disorder severe enough to require CIWA protocol typically have poor oral intake, malnutrition, and depleted protein stores 2
• Decreased dietary protein intake directly reduces substrate availability for urea production, lowering BUN 2
• The pathophysiology of AKA specifically involves poor glycogen stores from malnutrition, which extends to overall protein-calorie malnutrition 2

Expected vs. Paradoxical Findings

Why This Is Counterintuitive

• DKA typically causes significant volume depletion with BUN elevation due to prerenal azotemia 3, 4
• The typical total body water deficit in DKA is approximately 6 liters (100 ml/kg), which should elevate BUN 3
• BUN is routinely assessed in DKA to evaluate renal function and hydration status, with elevation being the expected finding 4

The Competing Pathophysiology

• When hepatic synthetic dysfunction or severe malnutrition coexists with volume depletion, the low urea production can mask or override the concentrating effect of dehydration
• This creates a "falsely reassuring" BUN that underestimates the degree of volume depletion 3

Critical Clinical Implications

Diagnostic Considerations

• Measure serum ketones (β-hydroxybutyrate preferred) to distinguish pure DKA from mixed DKA/AKA 4, 1
• Standard nitroprusside ketone tests may underestimate ketosis severity in AKA because they detect acetoacetate and acetone but NOT β-hydroxybutyrate, which predominates in AKA 1
• Check liver function tests and albumin to assess for chronic liver disease 3
• Calculate corrected sodium (add 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL) to accurately assess volume status 4

Management Pitfalls to Avoid

• Do not underestimate volume depletion based on low BUN alone—use clinical assessment, vital signs, and other markers like creatinine and hematocrit 3, 4
• Thiamine (100-300 mg/day) must be administered to all patients with alcohol withdrawal syndrome and maintained for 2-3 months, as thiamine deficiency is common and can worsen metabolic derangements 3
• If initial potassium is <3.3 mEq/L, delay insulin and aggressively replace potassium first to prevent fatal arrhythmias—this is particularly important as alcohol use disorder patients often have baseline electrolyte abnormalities 4
• Use lorazepam rather than long-acting benzodiazepines if liver dysfunction is suspected, as it is safer in hepatic impairment 3

Monitoring Strategy

• Monitor creatinine in addition to BUN, as the BUN/creatinine ratio may be abnormally low in liver disease
• Continue β-hydroxybutyrate monitoring until normalized, even after urine ketones clear, as urine ketones are unreliable during treatment 4
• Psychiatric consultation is recommended for evaluation, treatment, and long-term planning of alcohol abstinence in patients requiring CIWA protocol 3