What does elevated beta-hydroxybutyrate (BHB) with normal pH indicate in a patient with right lower quadrant abdominal pain?

Elevated Beta-Hydroxybutyrate with Normal pH

An elevated beta-hydroxybutyrate (BHB) level of 10 mmol/L with normal pH indicates significant ketosis without metabolic acidosis, which in the context of right lower quadrant pain requires immediate contrast-enhanced CT imaging to rule out surgical emergencies like appendicitis while simultaneously investigating the underlying cause of ketosis.

Clinical Significance of This Laboratory Pattern

• BHB elevation with preserved pH represents a compensated ketotic state that can occur in several distinct clinical scenarios, none of which should be dismissed in a patient presenting with acute abdominal pain 1.

• The dissociation between elevated ketones and normal pH distinguishes this from diabetic ketoacidosis (DKA), where severe metabolic acidosis (pH <7.3) typically accompanies BHB levels above 3 mmol/L 2, 1.

• A BHB level of 10 mmol/L is markedly elevated (normal <0.5 mmol/L) and demands investigation, as this degree of ketosis can occur with starvation, alcoholic ketosis, or early/compensated diabetic crisis 2.

Immediate Diagnostic Approach for RLQ Pain

Obtain contrast-enhanced CT of the abdomen and pelvis immediately to evaluate for appendicitis and other surgical emergencies, as recommended by the American College of Radiology for patients with RLQ pain 3, 4.

• CT with IV contrast achieves sensitivity of 85.7-100% and specificity of 94.8-100% for appendicitis, and can identify alternative diagnoses including pancreatitis, bowel obstruction, mesenteric ischemia, and gynecologic pathology 3, 4.

• The presence of ketosis does not exclude surgical pathology—in fact, acute pancreatitis can trigger severe ketosis and even progress to full DKA 2.

• Do not delay imaging based on laboratory abnormalities alone, as up to 46% of patients with DKA present with abdominal pain that may mask or mimic surgical conditions 1.

Differential Diagnosis for Ketosis with Normal pH

Starvation Ketosis

• Prolonged fasting (>12-24 hours) or severe caloric restriction produces BHB levels typically 1-8 mmol/L, though levels of 10 mmol/L can occur with extended fasting 5.
• The body maintains normal pH through respiratory compensation and renal bicarbonate retention.
• Assess dietary intake over the preceding 24-48 hours and evaluate for eating disorders or inability to eat due to pain/nausea.

Alcoholic Ketosis

• Heavy alcohol consumption with poor oral intake produces marked ketosis (BHB often 5-15 mmol/L) with initially preserved or minimally decreased pH 1.
• Patients with DKA and abdominal pain have significantly higher rates of alcohol abuse (51%) compared to those without pain (24%) 1.
• Check blood alcohol level, obtain detailed alcohol history, and assess for signs of chronic liver disease.

Early or Compensated Diabetic Crisis

• Prediabetes or undiagnosed diabetes can deteriorate directly into ketotic states, particularly when triggered by acute illness like pancreatitis 2.
• A patient with prediabetes (HbA1c 6.4%) developed severe DKA (BHB 28 mmol/L) triggered by acute pancreatitis, illustrating the "chicken and egg" paradigm where pancreatitis triggers ketosis and ketosis causes abdominal pain 2.
• Check blood glucose, HbA1c, and assess for polyuria, polydipsia, and recent weight loss.

Ketogenic Diet or Exogenous Ketone Supplementation

• Therapeutic ketogenic diets or oral BHB supplementation can elevate BHB to 1-6 mmol/L, though 10 mmol/L would be unusually high from diet alone 5, 6.
• Exogenous BHB supplementation is safe and well-tolerated, with minimal acid-base effects in healthy individuals 5.

Critical Pitfalls to Avoid

Do not attribute abdominal pain solely to ketosis without imaging, as this can result in missed surgical emergencies 4, 1.

• In DKA patients, abdominal pain correlates strongly with severity of acidosis (86% with bicarbonate <5 mmol/L vs. 13% with bicarbonate 15-18 mmol/L), but your patient has normal pH, making ketosis an unlikely primary cause of pain 1.

• Five of 189 DKA patients with abdominal pain required surgical intervention for conditions including cholecystitis, appendicitis, and abscess 1.

Do not assume normal pH excludes evolving diabetic crisis, as compensatory mechanisms can temporarily maintain pH while ketosis progresses 2.

• Monitor serial pH, bicarbonate, anion gap, and glucose every 2-4 hours if diabetic crisis is suspected.
• Prediabetes can directly deteriorate into severe ketoacidosis when triggered by acute illness 2.

Do not delay treatment of underlying surgical pathology while managing metabolic abnormalities, as treating the trigger is equally important as correcting metabolic derangements 2.

Management Algorithm

Step 1: Immediate Imaging

• Obtain CT abdomen/pelvis with IV contrast to evaluate for appendicitis, pancreatitis, bowel obstruction, or other surgical emergencies 3, 4.

Step 2: Assess Ketosis Etiology

• Check blood glucose, HbA1c, comprehensive metabolic panel, blood alcohol level, and pregnancy test (if applicable).
• Obtain detailed history of oral intake, alcohol use, medication use (including SGLT2 inhibitors), and dietary patterns.
• If glucose >250 mg/dL or HbA1c >6.5%, consider evolving diabetic crisis and monitor closely for acidosis development 2.

Step 3: Treat Based on CT Findings

• If appendicitis identified: Proceed to surgical consultation for appendectomy, as preoperative CT reduces negative appendectomy rates from 16.7% to 8.7% 4.
• If pancreatitis identified: Stratify severity, monitor for organ failure, and manage hyperglycemia aggressively as this promotes recovery 4, 2.
• If no surgical pathology: Address underlying cause of ketosis (refeeding for starvation, IV dextrose and thiamine for alcoholic ketosis, insulin for diabetic crisis).

Step 4: Serial Monitoring

• Recheck BHB, pH, bicarbonate, and anion gap every 2-4 hours until ketosis resolves and pH remains stable.
• If pain persists after metabolic correction or if acidosis develops, repeat imaging to reassess for evolving pathology 1.