---

DKA and Starvation Ketosis: Patient Management Perspective

---

DIABETIC KETOACIDOSIS (DKA)

Clinical Features

• Nausea and vomiting in any diabetic patient warrant lab evaluation for DKA.
• Cerebral edema is the most serious complication, seen most often in children.
• Signs of infection should be sought even in the absence of fever.

---

Severity Classification

---

Laboratory Profile (Table 416-7)

• Beta-hydroxybutyrate is synthesized at 3x the rate of acetoacetate but is NOT detected by nitroprusside - measure serum beta-OHB directly.
• Serum potassium may be elevated at presentation despite total-body deficit (due to acidosis and volume depletion).
• Leukocytosis does not necessarily mean infection in DKA.
• Hyperamylasemia is usually of salivary origin; if pancreatitis suspected, check serum lipase.
• Corrected sodium: add 1.6 meq/L for each 100 mg/dL rise in glucose. A normal sodium in DKA signals a more profound water deficit.

---

Management of DKA (Table 416-9)

• Elevated serum glucose + elevated serum beta-hydroxybutyrate + metabolic acidosis.

• Severe DKA: ICU.
• Mild-moderate: step-down unit with close nursing and lab monitoring.
• Insert NGT if vomiting or altered mental status (aspiration prevention).
• Start a comprehensive flow sheet recording vitals, fluid I/O, labs, and insulin.

• Serum electrolytes: K+, Na+, Mg2+, Cl-, bicarbonate, phosphate.
• Acid-base: pH, HCO3-, pCO2, beta-hydroxybutyrate.
• Renal function: creatinine, urine output.
• Identify and treat precipitating cause aggressively.

• Initial (first 1-3 h): 2-3 L of 0.9% normal saline OR lactated Ringer's at 10-20 mL/kg/h.
  • Lactated Ringer's is associated with more rapid DKA resolution and less hyperchloremia.
• Subsequently: 0.45% saline at 250-500 mL/h.
• When glucose reaches 250 mg/dL (13.9 mmol/L): Switch to 5-10% dextrose + 0.45% saline (or LR) at 150-250 mL/h.
• Total fluid deficit is often 3-5 L and is replaced over 24 hours.
• Avoid volume overexpansion with isotonic saline - can cause volume overload or hyperchloremic acidosis.

• IV route (preferred): Bolus 0.1 units/kg regular insulin, then infusion at 0.1 units/kg/h.
  • If no response by 2-4 hours, increase 2-3 fold.
• SC route (mild-moderate DKA alternative): 0.1 units/kg rapid-acting insulin analogue, then 0.1 units/kg every 1 hour OR 0.2 units/kg every 2 hours.
• Critical rule: If initial serum K+ is <3.3 mmol/L, do NOT start insulin until potassium is corrected first.
• Expected glucose fall: 50-100 mg/dL per hour (first 1-2 h decline may be faster, mostly from volume expansion).
• Ketoacidosis resolves more slowly than hyperglycemia - anion gap normalizes before bicarbonate.
• As DKA resolves, insulin infusion can be reduced to 0.02-0.1 units/kg/h.

• Start long-acting insulin as soon as the patient is eating.
• Allow a 2-4 hour overlap between IV infusion and SC long-acting insulin injection to prevent rebound ketosis.

• Routine bicarbonate is NOT recommended and has not been shown to improve outcomes.
• Use only for arterial pH <7.0: give 50 mmol NaHCO3 in 200 mL sterile water with 10 meq/L KCl over 1 hour, until pH >7.0.
• Risk: cerebral edema (give only limited amounts).

• Hypophosphatemia and hypomagnesemia may develop during therapy; supplement if severe.

• Blood glucose every 1-2 hours.
• Electrolytes, bicarbonate, phosphate, anion gap every 4 hours for the first 24 hours.
• Vitals, mental status, fluid I/O every 1-4 hours.

• Patient stable, glucose goal 150-200 mg/dL (8.3-11.1 mmol/L).
• Plasma ketones normal, pH normal, bicarbonate ≥18 mmol/L.
• Note: a hyperchloremic acidosis (bicarb 15-18 meq/L) often follows successful treatment and resolves gradually as kidneys regenerate bicarbonate.

---

Prognosis and Follow-up

• Mortality is <1% with appropriate treatment, mostly tied to the precipitating event (e.g., sepsis, MI).
• Even a single DKA episode carries a greatly increased 1-year mortality.
• Patient education on DKA symptoms, precipitating factors, and sick-day insulin rules is essential after recovery.
• Recurrent DKA may indicate underlying mental health issues or structural barriers (insulin cost, social determinants of health).

---

STARVATION KETOSIS

Pathophysiology and Key Distinctions from DKA

Euglycemic DKA vs. Starvation Ketosis

• eGFR context (SGLT-2 inhibitor history)
• Degree of ketonemia (much higher in eDKA, beta-OHB >3.0 mmol/L)
• Severity of acidosis

Management of Starvation Ketosis

1. Carbohydrate refeeding - the primary treatment. Oral carbohydrate intake restores the insulin-to-glucagon ratio, suppresses lipolysis, and halts ketogenesis.
2. IV glucose if the patient cannot take oral feeds (e.g., protracted vomiting).
3. No insulin is required (glucose is normal; insulin would cause hypoglycemia).
4. Monitor electrolytes - refeeding can cause phosphate shifts; check and replace as needed.
5. Identify the underlying cause - eating disorder, malignancy, hyperemesis gravidarum, iatrogenic fasting.
6. Acid-base disturbance is typically minimal and corrects with refeeding; bicarbonate supplementation is not needed.

---

Quick Comparison Table: DKA vs. Starvation Ketosis vs. AKA

• Harrison's Principles of Internal Medicine 22E, Chapter 416 (pp. 3260-3262)
• Harrison's Principles of Internal Medicine 22E, Chapter 55 (Acid-Base Disorders, p. [block6])