Why it happens

1. Liver glycogen becomes depleted.
2. Insulin levels fall and glucagon rises.
3. Fat is broken down into free fatty acids.
4. The liver converts these into ketone bodies, mainly beta-hydroxybutyrate and acetoacetate.
5. Ketones are acids, so their accumulation lowers serum bicarbonate and pH.

Typical findings

• History: fasting, vomiting, eating disorder, severe food insecurity, prolonged illness, pregnancy with hyperemesis, or postoperative poor intake
• Nausea, vomiting, abdominal discomfort, weakness, dehydration, rapid deep breathing if significant acidosis
• Elevated serum ketones or beta-hydroxybutyrate
• Low bicarbonate and increased anion gap
• Blood glucose is often normal or low, unlike typical diabetic ketoacidosis
• Potassium, phosphate, and magnesium may be depleted

Important distinctions

• Diabetic ketoacidosis (DKA): usually marked hyperglycemia, though euglycemic DKA can occur, particularly with SGLT2-inhibitor drugs.
• Alcoholic ketoacidosis: associated with heavy alcohol use, recent cessation, vomiting, and poor nutrition.
• Lactic acidosis, renal failure, salicylate or toxic alcohol ingestion: other urgent causes of anion-gap acidosis that must be excluded.

Treatment principles

• Give oral or IV glucose/dextrose as appropriate.
• Correct dehydration.
• Monitor and replace potassium, phosphate, and magnesium.
• Give thiamine before or with carbohydrate if malnutrition or alcohol use is possible, to reduce risk of Wernicke encephalopathy and complications related to refeeding.
• Treat the cause of poor intake or vomiting.
• Assess carefully for DKA, pregnancy-related ketoacidosis, sepsis, toxic ingestion, or renal failure.

Core diagnostic pattern

• Reduced intake or prolonged fasting
• High-anion-gap metabolic acidosis
• Elevated beta-hydroxybutyrate / ketones
• Normal or low glucose, or only modest elevation
• No alternative major cause, such as DKA, alcoholic ketoacidosis, lactic acidosis, renal failure, or toxic ingestion

Treatment of starvation ketoacidosis

1. Assess urgently and exclude other causes
   • Check glucose, beta-hydroxybutyrate, electrolytes, blood gas, lactate, renal function, and anion gap.
   • Exclude DKA or euglycemic DKA, alcoholic ketoacidosis, sepsis/lactic acidosis, kidney failure, and toxic alcohol or salicylate ingestion.
2. Give fluids
   • If dehydrated or vomiting, IV isotonic fluid is commonly needed.
   • Adjust fluids for heart failure, kidney disease, pregnancy, and sodium abnormalities.
3. Give carbohydrate
   • Oral carbohydrate is appropriate only for mild illness when the person is alert, not vomiting, and can drink safely.
   • More significant cases usually require IV dextrose-containing fluid.
   • This corrects hypoglycemia if present and switches off ketogenesis. Emergency medicine guidance describes volume repletion plus supplemental dextrose and electrolyte correction for pathologic ketoacidosis.
4. Give thiamine when indicated
   • Give thiamine before or at the time carbohydrate is started when there is malnutrition, prolonged poor intake, vomiting, alcohol use, or risk of thiamine deficiency.
   • This is particularly important when alcoholic ketoacidosis could coexist.
5. Monitor and replace electrolytes
   • Repeat glucose, bicarbonate/anion gap, potassium, magnesium, and phosphate.
   • Potassium, phosphate, and magnesium can drop after glucose/nutrition begins because insulin shifts them into cells.
   • Replace deficits promptly, with cardiac monitoring if abnormalities are significant.
6. Prevent refeeding syndrome
   • In people who have had little or no nutrition for several days, especially with severe weight loss or chronic malnutrition, nutrition should be restarted cautiously with close electrolyte monitoring.
   • Hypophosphatemia is often an early sign and may occur in the first 24 to 72 hours. This case-based review describes the risk and need for thiamine, fluids, dietetic input, and electrolyte replacement.
7. Treat the cause
   • Control vomiting, restore adequate oral intake when safe, and address the trigger such as pregnancy hyperemesis, infection, eating disorder, postoperative obstruction, or inability to access food.

Usually not routine

• Insulin is usually not needed in pure starvation ketoacidosis because carbohydrate stimulates the person's own insulin secretion. It may be needed if DKA or substantial hyperglycemia is present.
• Sodium bicarbonate is not routinely used. It is considered only in exceptional, severe acidemia under clinician supervision after addressing the cause.

• pH 7.24: acidemia
• HCO₃⁻ 15.6 mmol/L: metabolic acidosis
• PaCO₂ 35 mmHg: compensation is slightly inadequate. By Winter's formula, expected PaCO₂ is about 31 ± 2 mmHg, so there may be a small concurrent respiratory acidosis or fatigue/hypoventilation.
• Cl⁻ 115 mmol/L: hyperchloremia, suggesting a normal-anion-gap component as well.
• Calculated anion gap is about 15.4. This is only mildly raised, so the ABG alone does not prove starvation ketoacidosis. It could be mixed ketoacidosis plus hyperchloremic acidosis, especially if the patient has had diarrhea, renal bicarbonate loss, or already received substantial normal saline.

Immediate hospital approach

1. Urgent senior/physician review and monitored setting
   • Check BP, pulse, respiratory effort, urine output, mental state, temperature, and capillary glucose.
   • ECG and cardiac monitoring if electrolyte abnormalities, severe illness, or IV electrolyte replacement is required.
2. Confirm the cause before labeling it starvation ketoacidosis Send urgently:
   • Capillary and laboratory glucose
   • Serum beta-hydroxybutyrate
   • Repeat electrolytes, urea/creatinine, magnesium and phosphate
   • Serum lactate
   • Albumin, to interpret/correct anion gap
   • CBC, LFTs, urinalysis
   • Consider serum osmolality/osmolar gap, salicylate level, ethanol level, and toxic alcohol evaluation if history is uncertain
   • HbA1c, diabetes history, and medication review, particularly SGLT2 inhibitors
   Do not miss euglycemic DKA, which can present with normal or only moderately elevated glucose.
3. Fluids
   • If hypovolemic or vomiting, give IV crystalloid and reassess perfusion, urine output, sodium, chloride, and acid-base status.
   • Because chloride is already 115 mmol/L, avoid excessive 0.9% saline if alternatives are appropriate locally. A balanced crystalloid is often preferable to limit worsening hyperchloremic acidosis.
   • Individualize for heart failure or renal impairment.
4. Carbohydrate therapy, if starvation ketosis is confirmed or strongly likely
   • After drawing glucose and ketone samples, provide a dextrose-containing IV fluid if oral intake is not safe or reliable.
   • This is the key treatment: carbohydrate raises endogenous insulin and suppresses ketone formation.
   • A clinical review of starvation ketoacidosis describes IV dextrose with close electrolyte monitoring and replacement.
5. Thiamine
   • If malnourished, prolonged fasting, vomiting, or alcohol use is possible, give IV thiamine before or together with dextrose, according to local protocol.
6. Electrolyte surveillance and replacement
   • Potassium is 4.16 mmol/L now, but it can fall promptly after dextrose/nutrition.
   • Recheck K⁺, Mg²⁺, phosphate, glucose, bicarbonate/anion gap, and beta-hydroxybutyrate frequently.
   • Replace potassium, magnesium, and phosphate as required. Watch closely for refeeding syndrome, particularly over the first 24 to 72 hours.
7. Do not routinely give insulin or bicarbonate
   • Insulin is generally not required for confirmed pure starvation ketoacidosis, but is required if DKA/euglycemic DKA is diagnosed.
   • With pH 7.24, bicarbonate is not routine. Treat the underlying ketogenesis, volume depletion, and electrolyte abnormalities. Consider bicarbonate only for exceptional severe acidemia with clinician/specialist oversight.
8. Repeat testing
   • Repeat VBG/ABG and metabolic panel after initial resuscitation and during treatment.
   • Escalate if pH falls, bicarbonate declines, PaCO₂ rises, mental status changes, hypotension develops, or acidosis fails to improve.

Interpretation in this post-CABG patient

• pH 7.24, HCO₃⁻ 15.6, base excess -12.4: moderate metabolic acidosis.
• Chloride 115 mmol/L with anion gap 15.9: most consistent initially with a prominent hyperchloremic metabolic acidosis, often after cardiopulmonary bypass and chloride-rich fluid administration.
• PaCO₂ is 35 mmHg. Expected PaCO₂ for HCO₃ 15.6 is about 31 ± 2 mmHg, so compensation may be mildly inadequate. Check for residual sedation, opioid effect, atelectasis, fatigue, or ventilatory limitation.
• Oxygenation on this ABG is acceptable, but it does not rule out low cardiac output or tissue hypoperfusion.

Immediate ICU plan

1. Assess perfusion and cardiac output
   • MAP and vasopressor requirement
   • Heart rate/rhythm, ECG
   • Urine output hourly
   • Peripheral temperature, capillary refill, mental state
   • Chest drain output and hemoglobin: exclude bleeding/hypovolemia
   • Bedside echo: LV/RV function, tamponade, regional dysfunction, preload, significant valvular issue
   • Check cardiac index or ScvO₂/SvO₂ if monitoring is available
2. Send or repeat urgently
   • Serial lactate and repeat ABG/VBG
   • Serum electrolytes, urea/creatinine, magnesium, phosphate
   • Laboratory bicarbonate and albumin
   • Blood glucose and serum beta-hydroxybutyrate
   • CBC, coagulation profile, ionized calcium
   • Review all IV fluids, bypass prime/cardioplegia, diuretics, insulin, inotropes, and medications.
   • Specifically confirm whether the patient used an SGLT2 inhibitor such as dapagliflozin or empagliflozin preoperatively. These drugs can cause postoperative euglycemic ketoacidosis even when glucose is not high.
3. Fluids
   • If bleeding, hypovolemia, or low filling is present, resuscitate based on hemodynamics and echo.
   • With chloride already 115 mmol/L, avoid further large-volume 0.9% saline unless there is a specific reason.
   • Use a balanced crystalloid if additional crystalloid is clinically needed and compatible with the local cardiac-surgery protocol.
4. If lactate is elevated or rising
   • Treat as possible low oxygen delivery/low-cardiac-output syndrome until proven otherwise.
   • Correct hypoxemia, anemia/bleeding, inadequate preload, poor cardiac function, arrhythmia, tamponade, graft-related ischemia, sepsis, or excessive vasoconstriction, according to the ICU cardiac-surgery pathway.
5. If beta-hydroxybutyrate is raised
   • If glucose is normal or low and the patient has prolonged fasting: give dextrose-containing fluid, thiamine if malnourished or alcohol use is possible, and monitor K, Mg, and phosphate.
   • If diabetic, recently on SGLT2 inhibitors, or ketones are substantially raised: treat as possible euglycemic DKA with the cardiac ICU/endocrine protocol. This may require insulin plus dextrose, not dextrose alone.
6. Ventilation
   • Review ventilator settings and sedation. PaCO₂ of 35 is a little higher than expected for this bicarbonate level.
   • Do not hyperventilate aggressively without addressing the metabolic cause, but avoid hypoventilation while acidemic.
7. Bicarbonate
   • Do not give bicarbonate solely because the pH is 7.24.
   • It is not standard treatment for saline-related acidosis or presumed starvation ketosis. Consider only if acidosis becomes severe or causes hemodynamic compromise, after the team identifies and treats the cause.

Bottom line

1. Lactic acidosis from low cardiac output or hypoperfusion
2. Bleeding, tamponade, graft ischemia, or RV/LV dysfunction
3. Acute kidney injury
4. Euglycemic DKA, especially if taking an SGLT2 inhibitor
5. True starvation ketoacidosis

• Pulse 101/min: mild tachycardia
• BP 110/64 mmHg: MAP about 79 mmHg
• RR 15/min
• SpO₂ 100%

Practical plan now

1. Do not give routine sodium bicarbonate
   • pH 7.24 is acidemic but, with stable BP and oxygenation, focus on identifying and correcting the cause rather than correcting the number.
   • Reassess if pH falls below about 7.15 to 7.20, hypotension develops, hyperkalemia occurs, or there is ventricular dysfunction/arrhythmia.
2. Check these urgently
   • Serial lactate now and in 2-4 hours
   • Serum glucose and beta-hydroxybutyrate
   • Urea, creatinine, Na, K, Cl, bicarbonate, Mg, phosphate, ionized Ca
   • Hemoglobin, chest-drain output, hourly urine output
   • Albumin, since low albumin may conceal a clinically meaningful raised anion gap
   • Preoperative diabetes medicines, especially dapagliflozin/empagliflozin/canagliflozin or another SGLT2 inhibitor
3. Review fluids and stop chloride loading
   • Review intraoperative and postoperative volume of 0.9% saline, bypass prime, cardioplegia, and blood products.
   • Avoid further large saline volumes if not specifically required.
   • If fluid is clinically indicated, discuss using a balanced crystalloid with the cardiac ICU team.
   • Saline administration during surgery can produce hyperchloremic metabolic acidemia, as described in Barash, Cullen, and Stoelting's Clinical Anesthesia. A study of post-cardiac surgery patients found this pattern was often transient, but it should not distract from checking lactate and perfusion in each individual patient, as explained in this cardiac-surgery review.
4. Assess ventilation
   • With HCO₃⁻ 15.6, expected PaCO₂ by Winter's formula is about 31 ± 2 mmHg; actual PaCO₂ is 35.
   • RR 15 may be insufficient compensation if the patient is sedated, in pain, splinting, fatigued, or hypoventilating.
   • Review sedation/opioids, chest expansion, analgesia, CXR for atelectasis/effusion, and ventilator settings if intubated. Avoid over-sedation.
5. If ketones are elevated
   • If beta-hydroxybutyrate is high and glucose is normal/low after fasting: give thiamine if malnourished or alcohol risk exists, then start carbohydrate with a dextrose-containing fluid, while closely monitoring potassium, magnesium, and phosphate.
   • If the patient has diabetes or recent SGLT2-inhibitor exposure: manage as possible euglycemic DKA, with cardiac ICU/endocrinology input. This needs insulin plus dextrose, not dextrose alone.
6. Trend, do not treat one ABG in isolation
   • Repeat ABG and electrolytes after fluid strategy changes and within a few hours.
   • Follow lactate clearance, urine output, mental status, chest-drain loss, ECG/rhythm, and bedside echocardiography if any concern.

Escalate immediately if

• Lactate rises or is markedly elevated
• MAP falls, urine output declines, or inotrope requirement rises
• Increasing chest drain output or hemoglobin drops
• New ischemic ECG changes, arrhythmia, poor peripheral perfusion, or altered consciousness
• pH decreases, PaCO₂ rises, or bicarbonate continues to fall