肺部急症

肺部急症 署立桃園醫院胸腔內科李世偉醫師

前言 • 溺水(Near drowning) • 煙霧吸入嗆傷(Smoke inhalation) • 一氧化碳中毒(CO intoxication) • 張力性氣胸(Tension pneumothorax) • 大咳血(Massive hemoptysis) • 氣喘(Asthma) • 急性呼吸窘迫症候群(ARDS)

溺水(Near drowning) • 煙霧吸入嗆傷(Smoke inhalation) • 一氧化碳中毒(CO intoxication) • 張力性氣胸(Tension pneumothorax) • 大咳血(Massive hemoptysis) • 氣喘(Asthma) • 急性呼吸窘迫症候群(ARDS)

定義 • 溺死 ( drowning ):溺水後當場或24小時內死亡 • 溺水 ( near drowning ):溺水後存活超過24小時 • Submission:所有溺水者,不論預後好壞通稱之 • 濕溺 ( wet drowning ):溺水時,有明顯液體吸入 • 乾溺 ( dry drowning ):溺水時,約有10%的人因喉部反射使喉不緊閉,造成窒息,沒有吸入液體

病理生理學 • 缺氧 • 水分吸入:淡水及海水 • 淡水屬於低張力液體, 引起血容量增加,血液稀釋,電解質濃度減少,紅血球融解造成高血鉀症. • 海水屬於高張力液體, 引起血容量減少,血液濃縮,電解質濃度增加,導致肺水腫. • 喉部痙攣 • 繼發性溺水:約2-5%的溺水者,胸部X光可能為正常,但在24小時後會發生遲發性的肺水腫,引起呼吸窘迫症候群.

治療 • 心肺復甦術:越早做越好,要注意頸椎的保護. • 氧氣治療 • 人工呼吸器及PEEP • 預防性的抗生素及類固醇並不一定需要,但如有肺炎發生應給予抗生素治療.

預後 • 水溫 • 年齡 • 水的污染程度 • 心臟停止時間及開始心肺復甦術時間

Pathophysiology • Thermal injury • Chemical injury • Hypoxia

Bronchiolitis obliterans organizing pneumonia caused by inhalation of oxides of nitrogen in a silo filler.

Organizing pneumonia after sulfur dioxide intoxication.

Diffuse alveolar damage caused by anhydrous ammonia inhalation. An agricultural worker inhaled the gas when a hose broke during the transfer of this fertilizing agent.

Radiographic changes produced by diffuse alveolar damage. Chest radiograph of the same patient as in Figure 66-4 shows acute, diffuse alveolar and interstitial infiltrates.

Treatment • High concentration oxygen • Bronchodilator • Adequate fluid therapy • Intubation if upper airway obstruction • Ventilator with PEEP • Antibiotics • Prophylactic steroid is not necessary

一氧化碳中毒(CO intoxication)?

Carbon Monoxide • nonirritating, colorless, tasteless, and odorless gas • incomplete combustion of carbon-containing material • occurs in the setting of smoke inhalation, attempted suicide from automobile exhaust, and poorly ventilated burning charcoal or gas stoves

Pathophysiology • Carbonmonoxide binds to hemoglobin with an affinity that is 240 times greater than oxygen and decreases oxyhemoglobin saturation and blood oxygen-carrying capacity. • Its toxicity results from a combination of tissue hypoxia and direct inhibition of cellular respiration through cytochrome oxidase blockade.

Clinical Manifestation • The severity of carbon monoxide poisoning depends on the concentration of carbon monoxide, duration of exposure, and minute ventilation • Carboxyhemoglobin concentrations up to 5% may result in headache and mild dyspnea. • Carboxyhemoglobin concentrations between 10% and 30% cause headache, dizziness, weakness, dyspnea, irritability, nausea, and vomiting. • Carboxyhemoglobin concentrations > 50% result in coma, seizures, cardiovascular collapse, and death.

Diagnosis • high index of suspicion for carbon monoxide poisoning • Important historical clues can aid in the diagnosis. • Carboxyhemoglobin levels are determined by CO-oximetry. • Pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin at the wavelengths that are commonly generated by standard pulse oximeters.

Treatment • The most essential treatment for carbon monoxide poisoning is oxygen • Administration of 100% supplemental oxygen decreases the half-life of carboxyhemoglobin from 5 to 6 h on room air to 40 to 90 min. • Hyperbaric oxygen (2.8 atmospheres within 6 h of exposure) further decreases the half-life of carboxyhemoglobin to 15 to 30 min. • The role of hyperbaric oxygen in the management of carbon monoxide poisoning has been debated, and reviewed.

Prognosis • 10 to 30% of survivors acquire delayed neuropsychiatric sequelae (DNS). • DNS has been described to occur from 3 to 240 days after apparent recovery. • Its variable manifestations include persistent vegetative state, Parkinsonism, short-term memory loss, behavioral changes, hearing loss, incontinence, and psychosis. • At 1 year, 50 to 75% of patients with DNS experience a full recovery.

Bleb Bulla

Pneumothorax

PneumothoraxCharacteristics of pnx on supine film • Pnx easily missed on supine films (32%) • Features: • Increased radiolucency at lung bases • Sharp, elongated costophrenic/ cardiophrenic sulcus (deep sulcus) • Depression of hemidiaphragm • Flattening of heart border

When to Suspect PNX in Ventilated Patients • Clinical change in pt’s status • Sudden or progressive increase in PIP • Hypotension or cardiovascular collapse • Sudden onset of agitation and resp distress (fighting the ventilator) • CXR findings • General increase in volume or increase in relative radiolucency of hemithorax • Deep sulcus sign

Risk Factors for Alveolar Rupture During MV • Right main bronchus intubation • High peak inflation volume • Excessive tidal volume • Excessive PEEP • Auto-PEEP • Obstructive lung diseases (COPD, Asthma) • Heterogeneous lung disease • Nosocomial pneumonia • Late phase of ARDS

Steps to Reduce Alveolar Rupture During MV • Use small TV • Decrease TV as PEEP increases • Use PEEP cautiously in high risk pt • Avoid right main bronchus intubation • Monitor for auto-PEEP • High inspiratory flowrate with low I:E ratio • Bronchodilator if bronchospasm is present • Reduce minute ventilation

Chest decompression

Life-threatening hemoptysis According to Coss-Bu et al., major hemoptysis comprises large and massive bleeding, which correspond to blood expectoration of 150-400 mL per day and to more than 400 mL per day, respectively. Other definitions of massive hemoptysis range from 400 to 1000 mL per day Regardless of the exact amount of blood loss for each category of major hemoptysis, large and massive hemoptysis are both life-threatening.

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Bronchoscopy

Massive hemoptysis

Left, A: prominent areas of tissue enhancement are seen to be consistent with intense inflammation and hypervascularity (arrows) Swanson, K. L. et al. Chest 2002;121:789-795

Massive hemoptysis

肺部急症

肺部急症

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