Pathophysiology
P-I-6. Obesity–Diabetes, Case 2
肥満・糖尿病 症例2
A 15-year-old girl was admitted to the ICU because of sudden vomiting, dizziness, disorientation and immobilization. The mother claims the girl was fatigued, lost 3 kg despite having a good appetite and in the last 24 hrs she had no appetite at all.
- Height: 172 cm
- Weight on admission: 55 kg
- Blood pressure: 111/79 Hgmm
- Pulse: 110/min
- Respiratory rate: 38/min (normal: 18-22/min)
Laboratory results on admission:
- Blood sugar: 28.5 mmol/l
- Na⁺: 132 mmol/l
- K⁺: 5.6 mmol/l
- Cl⁻: 92 mmol/l
- HCO₃⁻: 11 mmol/l
- blood pH: 7.1
- pCO₂: 18 mm Hg
- BUN: 8.2 mmol/l
- creatinine: 140 μmol/l
- ASAT: 28 U/L
- ALAT: 35 U/L
- ALP: 48 U/L
- T. bilirubin: 19 μmol/l
- D. bilirubin: 3.1 μmol/l
Urinalysis:
- Sugar: strongly positive
- Ketone bodies: positive
- Protein: negative
- Specific gravity: 1009 kg/L
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “fatigued, lost 3 kg despite having a good appetite” | Catabolic state of insulin deficiency — typical of new-onset type 1 diabetes |
| Blood sugar 28.5 mmol/L; urine sugar strongly positive | Severe hyperglycaemia with glucosuria |
| Urine ketones positive; blood pH 7.1; HCO₃⁻ 11 mmol/L | High anion-gap metabolic acidosis from ketone bodies → diabetic ketoacidosis (DKA) |
| pCO₂ 18 mmHg; respiratory rate 38/min | Kussmaul breathing — respiratory compensation blowing off CO₂ for the metabolic acidosis |
| K⁺ 5.6 mmol/L (high) | Acidosis shifts potassium out of cells; total-body potassium is actually depleted |
| Na⁺ 132 mmol/L (low) | Pseudohyponatraemia from osmotic shift due to hyperglycaemia |
| Creatinine 140 µmol/L, BUN 8.2 mmol/L; “vomiting … immobilization” | Pre-renal impairment from dehydration; reduced consciousness from severe acidosis/dehydration |
Key Points
- Diagnosis: New-onset Type 1 diabetes mellitus presenting as diabetic ketoacidosis (DKA).
- Pathophysiology: Absolute insulin deficiency → hyperglycaemia + unrestrained lipolysis → ketone production → metabolic acidosis.
- Compensation: Deep, rapid (Kussmaul) breathing lowers pCO₂ to partly offset the acidosis.
- Electrolyte traps: Hyperkalaemia despite total-body potassium depletion; pseudohyponatraemia from hyperglycaemia.
- Emergency management: IV fluids, insulin, and careful electrolyte (especially potassium) correction.
一問一答
▶What is the diagnosis in a 15-year-old with vomiting, hyperglycaemia (28.5 mmol/L), ketonuria, and pH 7.1?
New-onset type 1 diabetes mellitus presenting as diabetic ketoacidosis (DKA).
▶What is the pathophysiology of diabetic ketoacidosis?
Absolute insulin deficiency → hyperglycaemia plus unrestrained lipolysis → ketone production → metabolic acidosis.
▶Why did the girl lose weight despite a good appetite before admission?
Insulin deficiency causes a catabolic state with fat and protein breakdown, typical of new-onset type 1 diabetes.
▶What is Kussmaul breathing and why does it occur in DKA?
Deep, rapid breathing (here RR 38, pCO₂ 18) that blows off CO₂ to provide respiratory compensation for the metabolic acidosis.
▶What type of acid-base disturbance occurs in DKA?
High anion-gap metabolic acidosis from ketone bodies.
▶Why is serum potassium high (5.6 mmol/L) in DKA despite total-body depletion?
Acidosis and insulin deficiency shift K⁺ out of cells, raising serum K⁺ even though total-body potassium is depleted.
▶Why is sodium low (132 mmol/L) in DKA?
Pseudohyponatraemia — high glucose draws water into the extracellular space, diluting measured sodium.
▶Why are creatinine and BUN elevated in this DKA patient?
Pre-renal impairment from dehydration caused by osmotic diuresis and vomiting.
▶Why does the patient have disorientation and reduced consciousness?
Severe acidosis, dehydration, and hyperosmolality impair cerebral function.
▶What is the emergency management of DKA?
IV fluids, insulin, and careful electrolyte (especially potassium) correction.
▶Why must potassium be monitored and replaced carefully during DKA treatment?
Insulin and acidosis correction drive K⁺ back into cells, unmasking the true depletion and risking dangerous hypokalaemia.
▶Why does insulin deficiency lead to ketone production?
Without insulin, lipolysis is unrestrained; free fatty acids are converted by the liver into ketone bodies.
▶How does the low pCO₂ (18 mmHg) relate to the acidosis in DKA?
It is the expected respiratory compensation — hyperventilation lowers CO₂ to partly correct the metabolic acidosis.
▶Why is glucosuria strongly positive in this DKA patient?
Severe hyperglycaemia (28.5 mmol/L) far exceeds the renal glucose threshold.
▶Why does DKA cause dehydration?
Hyperglycaemia drives an osmotic diuresis, and vomiting adds further fluid loss.
▶Why does type 1 diabetes typically present acutely with DKA, unlike type 2?
Type 1 is autoimmune β-cell destruction causing absolute insulin deficiency, which rapidly leads to ketoacidosis.
▶How does giving insulin reverse the metabolic acidosis in DKA?
Insulin stops lipolysis/ketogenesis and promotes glucose uptake, halting acid production and allowing pH to normalize.
▶Why is the patient tachycardic (pulse 110) on admission?
Dehydration and hypovolaemia trigger a compensatory increase in heart rate.
▶Why is IV fluid the first priority in DKA management?
It restores intravascular volume and renal perfusion, dilutes glucose, and improves tissue perfusion before/with insulin.
▶What is the anion-gap concept that explains the acidosis in DKA?
Accumulating ketoacids add unmeasured anions, widening the anion gap and lowering bicarbonate.