P-II-14. Respiratory disease, Case 1

呼吸器疾患症例1

Case I — 33-year-old female with dyspnea and fever (ARDS)

Medical history:

Patient has had fever, cough, symptoms of cold for 2 weeks, and shortness of breath and weakness for 3 days. At the Pulmonology Ward combined oral antibiotic treatment due to pneumonia, but after 2 days her condition deteriorates, radiology shows progression, chest X-ray indicates ARDS. PaO2 38 mmHg, upon 4 l/min O2 administration PaO2 is 42 mmHg, nasal O2 administration and “high flow nasal oxygen” (HFNO) treatment do not improve the hypoxemia, pO2/FiO2 = 180. PaCO2 was 27 mmHg. Admission to the ICU.

Signs and symptoms:

Dyspnea, cyanosis, cough, respiratory rate: 40/min, blood pressure: 100/60 mmHg, pulse 120/min.

Signs and symptoms (cont.):

neutrophilia: 11 G/l
Hb: 83 g/l
CRP: 158 mg/l
Procalcitonin: 0.32 ug/l (normal: <0.5 ug/l)
Na: 140 mmol/l
K: 4.2 mmol/l
pH: 7.49, pO2: 221 mmHg (FiO2: 80%), pCO2: 28 mmHg, BE: -1.5 mmol/l, lactate: 1.7 mmol/l (normal)
Horowitz index: pO2 (mmHg)/FiO2% (normal: 100/0.21 = 476); in this case: 221/0.8 = 276. (The Horowitz index indicates that without O2 administration the pO2 would be about 55 mmHg.)

Chest X-ray: taken before and after intensive treatment.

Assessment of right-to-left shunting (in intubated patient): Under healthy conditions, with 80% O2 concentration of inhaled air (FiO2) the PaO2 is over 550 mmHg. In this patient PaO2 was 221 mmHg — there was shunting of almost 20% of the pulmonary circulation.

Blood gas and acid-base balance after treatment:

Main elements of treatment: invasive, bilevel positive airway pressure ventilation (4 days); parenteral antibiotic therapy: imipenem-cilastatin + clarithromycin.

5 days later:

CRP: 12 mg/l
pH: 7.45, pO2: 97 mmHg with 2 l/min O2 administration (FiO2: 27%), pCO2: 36 mmHg, BE: 1.5 mmol/l, lactate: 0.4 mmol/l
Horowitz index: 97/0.27 = 359 (improved but not yet normal)

Key Quotes & What They Tell Us

Quote / Value	Interpretation
“chest X-ray indicates ARDS”; preceding pneumonia	Acute respiratory distress syndrome triggered by pneumonia (a direct lung insult)
“pO2/FiO2 = 180”; Horowitz 221/0.8 = 276	A low P/F ratio defines and grades ARDS (the lower the ratio, the more severe)
“HFNO … do not improve the hypoxemia”; PaO2 38→42 mmHg on O2	Refractory hypoxaemia — oxygen-resistant, characteristic of shunt physiology
“shunting of almost 20% of the pulmonary circulation”	Right-to-left intrapulmonary shunt (perfused but non-ventilated alveoli) → why O2 fails to correct it
RR 40/min; pH 7.49, pCO2 27–28 mmHg	Respiratory alkalosis from compensatory hyperventilation
Procalcitonin 0.32 (normal); CRP 158	Marked inflammation but low procalcitonin → possible viral/non-bacterial trigger
After ventilation + antibiotics: CRP 12, P/F 359	Recovery of gas exchange as alveolar injury/oedema resolves

Key Points

Diagnosis: Acute respiratory distress syndrome (ARDS) secondary to pneumonia.
Defining feature: Acute, severe hypoxaemia with a low PaO2/FiO2 ratio and bilateral infiltrates.
Pathophysiology: Diffuse alveolar damage → protein-rich oedema and collapse → perfused but unventilated alveoli → large right-to-left shunt → oxygen-refractory hypoxaemia.
Acid-base: Tachypnoea produces respiratory alkalosis (low pCO2).
Management shown: Invasive positive-pressure ventilation plus treatment of the underlying infection → gradual improvement in the P/F ratio.

一問一答

▶What is the diagnosis in a patient with pneumonia, bilateral infiltrates, and severe oxygen-refractory hypoxaemia with P/F 180?

Acute respiratory distress syndrome (ARDS).

▶What does the PaO2/FiO2 (Horowitz) ratio measure, and how does it grade ARDS?

It quantifies oxygenation efficiency; a lower P/F ratio indicates more severe ARDS (≤300 mild, ≤200 moderate, ≤100 severe).

▶Why is the hypoxaemia in ARDS refractory to supplemental oxygen?

Right-to-left intrapulmonary shunting means blood passes non-ventilated alveoli, so added O2 cannot reach it.

▶What is a right-to-left intrapulmonary shunt?

Perfusion of alveoli that are not ventilated (collapsed/fluid-filled), so blood bypasses gas exchange.

▶What is the underlying pathophysiology of ARDS?

Diffuse alveolar damage with protein-rich pulmonary oedema and alveolar collapse, impairing gas exchange.

▶Why does this patient have respiratory alkalosis (pH 7.49, pCO2 27–28)?

Hypoxaemia drives tachypnoea/hyperventilation, blowing off CO2.

▶Why is the pulmonary oedema of ARDS described as non-cardiogenic?

It results from increased alveolar-capillary permeability (inflammatory injury), not elevated cardiac filling pressures.

▶What ventilation strategy is used to limit further lung injury in ARDS?

Lung-protective ventilation: low tidal volumes with adequate PEEP to recruit alveoli.

▶How does PEEP improve oxygenation in ARDS?

It keeps collapsed alveoli open at end-expiration, reducing shunt and improving gas exchange.

▶What are common triggers of ARDS?

Direct lung insults (pneumonia, aspiration) and indirect insults (sepsis, severe trauma, pancreatitis).

▶What do the Berlin criteria require to diagnose ARDS?

Acute onset (≤7 days), bilateral infiltrates not fully explained by cardiac failure, and PaO2/FiO2 ≤300 with PEEP ≥5.

▶Why does a normal procalcitonin (0.32) with very high CRP (158) suggest a non-bacterial trigger?

Procalcitonin rises mainly in bacterial sepsis; its normal level points to a possible viral cause of the inflammation.

▶Why does decreased lung compliance occur in ARDS?

Alveolar oedema, collapse, and surfactant dysfunction make the lungs stiff and hard to inflate.

▶How does surfactant dysfunction contribute to ARDS?

Damage to type II pneumocytes reduces surfactant, increasing surface tension and promoting alveolar collapse.

▶Why does cyanosis appear in this patient?

Severe arterial hypoxaemia raises deoxygenated haemoglobin, causing bluish discoloration.

▶Why is treating the underlying cause essential in ARDS?

ARDS is a syndrome — resolving the trigger (e.g. infection) allows the alveolar injury to heal.

▶Why might rising P/F ratio and falling CRP indicate recovery here?

Improving oxygenation and declining inflammation show the alveolar injury and infection are resolving.

▶What long-term complication can follow severe ARDS?

Pulmonary fibrosis with persistent restrictive impairment of lung function.

▶Why does ARDS cause increased work of breathing and tachypnoea (RR 40/min)?

Stiff, oedematous lungs and hypoxaemia drive a rapid, laboured breathing pattern.

▶Why is a healthy person's PaO2 on 80% O2 (>550 mmHg) used to estimate shunt fraction?

A markedly lower-than-expected PaO2 despite high FiO2 reveals the proportion of cardiac output passing through shunt.