Pathophysiology
P-II-19. Acid-base disorder, Case 2
酸塩基平衡障害 症例2
Case Presentation
A 55-year-old man with diabetes presents at the clinic accompanied by his wife. According to his wife, he has become increasingly indifferent and tired in recent days.
Physical examination: Obese male, looks older than his age.
Vital signs:
- Blood pressure 160/98 mmHg
- Pulse 76/min
- Respiratory rate 20/min
- No fever
Examination findings:
- Heart/lung: no abnormalities
- No cyanosis or edema
Laboratory Values
Arterial blood gas:
- pH 7.30
- PCO₂ 22 mmHg
- PO₂ 108 mmHg
- Bicarbonate 10 mmol/l
Chemistry (value / normal range):
- Sodium 142 (135–146 mmol/l)
- Potassium 4.4 (3.5–5.1 mmol/l)
- Chloride 105 (98–107 mmol/l)
- Calcium 2.35 (2.2–2.65 mmol/l)
- BUN 7 (2.8–7.2 mmol/l)
- Creatinine 75 (45–84 µmol/l)
- Glucose 12.5 (3.9–5.8 mmol/l)
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| pH 7.30; HCO₃ 10 mmol/l (very low) | Acidaemia with markedly low bicarbonate → metabolic acidosis |
| PCO₂ 22 mmHg (low) | Marked respiratory compensation (Kussmaul-type hyperventilation) |
| Anion gap = 142 − (105 + 10) = 27 (high) | High anion gap metabolic acidosis → accumulation of unmeasured acids |
| Diabetes; glucose 12.5 mmol/l (high) | Hyperglycaemia in a diabetic → ketoacids are the likely unmeasured anions (ketoacidosis) |
| “increasingly indifferent and tired” | Reduced consciousness from acidosis/metabolic decompensation |
| Chloride 105 (normal) | Normochloraemic — fits a high-anion-gap (not hyperchloraemic) acidosis |
Key Points
- Diagnosis: High anion gap metabolic acidosis due to diabetic ketoacidosis (DKA).
- Compensation: Very low PCO2 reflects deep compensatory hyperventilation.
- Mechanism: Insulin deficiency → lipolysis and ketone-body (acid) production → consumption of bicarbonate and a widened anion gap.
- Clinical clue: Hyperglycaemia plus obtundation in a known diabetic.
- Contrast: Differs from diarrhoeal acidosis (normal gap) — here unmeasured ketoacids raise the anion gap.
一問一答
▶What is the acid-base diagnosis in a diabetic with pH 7.30, HCO3 10, and an anion gap of 27?
High anion gap metabolic acidosis due to diabetic ketoacidosis.
▶How is the anion gap calculated here, and why is it high?
AG = Na − (Cl + HCO3) = 142 − (105 + 10) = 27; the high value reflects unmeasured ketoacids.
▶What is the mechanism of acidosis in diabetic ketoacidosis?
Insulin deficiency drives lipolysis and hepatic ketone (acid) production, consuming bicarbonate.
▶What does a very low PCO2 (22 mmHg) represent in DKA?
Deep compensatory hyperventilation (Kussmaul breathing) to offset the acidosis.
▶What is Kussmaul breathing?
Deep, rapid breathing that compensates for severe metabolic acidosis by blowing off CO2.
▶Which ketone bodies accumulate in diabetic ketoacidosis?
Beta-hydroxybutyrate and acetoacetate (with acetone).
▶Why is this patient increasingly indifferent and tired?
Acidosis and metabolic decompensation reduce consciousness/mentation.
▶Why is the chloride normal (105) in this high-gap acidosis?
Unmeasured ketoacid anions, not chloride, account for the lost bicarbonate, so it is normochloraemic.
▶What is the cornerstone of DKA treatment?
IV fluids, insulin, and careful potassium replacement (plus treating the trigger).
▶What are the common causes of a high anion gap metabolic acidosis (MUDPILES/GOLDMARK)?
Ketoacidosis, lactic acidosis, renal failure (uraemia), and toxins (methanol, ethylene glycol, salicylates).
▶Why must potassium be monitored and replaced during DKA treatment?
Insulin drives potassium into cells; total-body potassium is depleted, so therapy can cause dangerous hypokalaemia.
▶Why does hyperglycaemia cause osmotic diuresis and dehydration in DKA?
Glucose exceeding the renal threshold drags water and electrolytes into the urine, causing polyuria and volume loss.
▶How does DKA differ from a hyperosmolar hyperglycaemic state (HHS)?
DKA (often type 1) has marked ketosis/acidosis; HHS (often type 2) has very high glucose and osmolality with little or no ketosis.
▶What commonly precipitates an episode of DKA?
Infection, missed insulin doses, or new-onset diabetes.
▶Why might this patient's glucose (12.5) seem only moderately raised despite DKA?
Ketoacidosis severity depends on ketone production, not glucose level; significant acidosis can occur with modest hyperglycaemia (e.g. euglycaemic DKA).
▶Why does insulin reverse ketogenesis in DKA?
Insulin suppresses lipolysis and hepatic ketone production while promoting glucose uptake.
▶Why is bicarbonate therapy usually avoided in DKA?
Correcting the underlying ketosis with insulin/fluids restores bicarbonate; bicarbonate can cause harm and is reserved for severe acidaemia.
▶Why does a 'fruity' breath odour occur in DKA?
Exhaled acetone (a volatile ketone) produces the characteristic sweet/fruity smell.
▶What is the delta ratio / delta gap used for in acid-base analysis?
It checks whether the change in anion gap matches the change in bicarbonate, revealing a coexisting normal-gap acidosis or metabolic alkalosis.
▶Why does the metabolic acidosis in DKA stimulate central and peripheral chemoreceptors?
A fall in pH stimulates chemoreceptors to increase ventilation, lowering CO2 to compensate.