呼吸困难的鉴别诊断

Step-by-step diagnostic approach of dyspnea.

Clinical history

Careful history-taking is the most useful first step in elucidating the aetiology of dyspnoea. Several factors need to be addressed in the clinical history when constructing the initial differential diagnosis.

Time course

?Acute dyspnoea appears suddenly or in a matter of minutes. It typically indicates acute and severe conditions that may be

life-threatening. Examples of conditions causing sudden-onset

dyspnoea include acute pulmonary embolism, myocardial infarction, acute heart valve insufficiency, pneumothorax, anaphylaxis,

foreign body aspiration, pulmonary oedema, or cardiac tamponade.

[16]

?Subacute dyspnoea develops over hours to days. Common causes include acute asthma, exacerbation of COPD, or pulmonary oedema.

Less common causes include myocarditis, superior vena cava syndrome, acute eosinophilic pneumonia, or cardiac tamponade.[16] [17] [18] ?Chronic dyspnoea develops over weeks to months. It is associated with chronic pathology, such as congestive heart failure, COPD,

cardiomyopathy, idiopathic pulmonary fibrosis, pulmonary vascular disease, pulmonary hypertension, valvular heart disease, or

anaemia. [19] Less common causes include muscular dystrophies,

kyphoscoliosis, amyotrophic lateral sclerosis, pulmonary alveolar proteinosis, chronic eosinophilic pneumonia, uraemia, or

constrictive pericarditis. [18] [20] [21] [22] [23] ?Recurrent dyspnoea may indicate paroxysmal tachycardias or intermittent complete heart block.

Severity

?There is no universally agreed measure of dyspnoea; several scales are available in both research and clinical practice. [24] ?Dyspnoea is highly subjective, and, for a given level of functional impairment, severity varies widely.

?Severe dyspnoea is typically accompanied by associated symptoms and is more likely to be life-threatening. It may be associated with acute asthma, tension pneumothorax, acute upper airway obstruction,

massive pulmonary embolism, or myocardial infarction. Mild

dyspnoea may be a sole symptom and may indicate a benign aetiology.

It may be caused by stable COPD, deconditioning, non-critical

airway obstruction, or normal ageing.

Associated symptoms

?Dyspnoea often occurs with other symptoms, and their co-existence may help to localise the origin of dyspnoea to the involved organ system and help to narrow the differential diagnosis.

?Fever manifests with dyspnoea in many infectious and inflammatory conditions, including pneumonia, bronchitis, laryngitis, viral

syndromes (e.g., Hantavirus pulmonary syndrome and severe acute

respiratory syndrome [SARS]), vasculitides, and sepsis.[25] [26] Dyspnoea plus fever and cough may indicate community-acquired

pneumonia or opportunistic infection in immunocompromised hosts.

A CXR is necessary to exclude pneumonia. Post-obstructive pneumonia

is possible in patients with foreign body aspiration or a chest

malignancy.

?Central chest pain may suggest coronary artery disease, pulmonary embolism, pneumothorax, pneumomediastinum, or foreign body

aspiration. [27] Pleuritic chest pain may indicate pneumonia,

pneumothorax, pulmonary embolism, a solitary fibrous tumour of the pleura, or pleuritis.[28] Pericardial constriction and effusions are characterised by typical pericardial pain that is referred to the scapular region, worsened by position and changes in

intrathoracic pressure, and relieved by leaning forwards.

?Palpitations may be present in paroxysmal tachyarrhythmias, pulmonary embolism, valvular heart disease, or anxiety attacks.

?Syncope may accompany dyspnoea associated with tachyarrhythmias or pulmonary embolism. [29]

?Wheezing may indicate asthma, COPD, pulmonary oedema, bronchiolitis, or aspiration of a foreign body. Cough may be present in bronchitis, acute infectious pneumonia, acute eosinophilic

pneumonia, interstitial lung disease, COPD, asthma, bronchiectasis, or chronic pneumonitis.[18] Chronic sputum production may indicate COPD or bronchiectasis, while large amounts of clear secretions may be present in bronchoalveolar carcinoma. [30]

?Change in the pitch of the voice may accompany dyspnoea associated with pneumomediastinum, gastro-oesophageal reflux,

retropharyngeal haematoma, aortic aneurysm, or lung cancer. [31] ?Haemoptysis may accompany dyspnoea in patients with bronchitis, exacerbation of bronchiectasis, chest malignancies, vasculitides, acute infectious pneumonia, cryptogenic organising pneumonia,

pulmonary embolism, cocaine toxicity, tuberculosis, or diffuse

alveolar haemorrhage. [32] [33] [34] [35] [36] [37] ?Dysphagia or odynophagia may be present in a dyspnoeic patient with granulomatous laryngitis, pneumomediastinum, foreign body

aspiration, tetanus, and epiglottitis. [38] [39] [40] In

epiglottitis, dyspnoea may be additionally accompanied by drooling.

Vomiting and diarrhoea may accompany dyspnoea in thyrotoxicosis or botulism.[41] [42] Heartburn may be present in gastro-oesophageal reflux with aspiration.

?Muscle weakness or myalgias associated with dyspnoea may indicate deconditioning, adverse effects of medications, muscular

dystrophies, amyotrophic lateral sclerosis, acute polio or

post-polio syndrome, Guillain-Barre syndrome, West Nile and other viral infections, leptospirosis, Cushing's myopathy, or botulism.

[20] [26] [43] [44] [45] [46] [47] [48] [41] Visual disturbances

may occur with dyspnoea in myasthenia and tetanus, and headache may be present in carbon monoxide poisoning. [39] [49] [50] ?Bone pain may be associated with acute chest syndrome due to sickle cell anaemia or fat embolism associated with long-bone fractures.

[51]

?Anxiety may be a reaction to dyspnoea of any aetiology but may also cause dyspnoea in acute panic or anxiety attacks. [52] Dyspnoea

associated with stress may indicate anxiety, hyperventilation, or takotsubo cardiomyopathy. [53]

Positionality

?Orthopnoea is the presence of dyspnoea while supine, with an improvement in the upright position. It is characteristically

linked with congestive heart failure but may also be present in

asthma, COPD, inflammatory and degenerative neurological diseases, gastro-oesophageal reflux, pericardial effusion, or bilateral

diaphragmatic paralysis. [20] [54] [55] [56]

?Platypnoea is the worsening of dyspnoea on assuming an upright position, with alleviation while supine. It is typical of patent foramen ovale, abdominal muscle deficiency, or hepatopulmonary

syndrome. [57] [58]

?Trepopnoea is an infrequent finding in which dyspnoea is present only in the lateral decubitus position. It is associated with

congestive heart failure, sinus of Valsalva aneurysms, or status post-pneumonectomy. [59] [60]

?Variable positional changes in dyspnoea may also be seen in primary and metastatic cardiac tumours. [61] [62]

Pattern of dyspnoea

?Dyspnoea that appears during the working week and resolves over periods off work may be related to occupational exposure and

suggests occupational asthma.[63] Occupational exposure may also be implicated in cases of asbestos-related lung disease and

hypersensitivity pneumonitis. [64] A history of occupational or leisure exposure to aerosolised solvents, fumes, organic dust,

moulds, and animals should be elicited and may be implicated in interstitial lung disease. Dyspnoea developing in indoor hockey players may reflect nitrogen dioxide or carbon monoxide toxicity from faulty ice resurfacing equipment. [65]

?Seasonal dyspnoea or shortness of breath related to cold, pets, exercise, or non-specific irritants may suggest asthma or reactive airway disease. [66]

Past medical history

?Dyspnoea may be associated with obesity or occur during a normal pregnancy. In pregnant patients it may also indicate the presence of a previously undiagnosed medical condition, such as valvular heart disease, pulmonary hypertension, alpha-1 protease inhibitor deficiency, pulmonary embolism, spontaneous pneumothorax or

pneumomediastinum, progression of a pulmonary arteriovenous

malformation, or deterioration of myasthenia. [67] [68] [69] [70]

[71] [72] [73]

?In a patient who is or recently was in labour, dyspnoea may indicate pulmonary embolism, septic or toxic shock, amniotic fluid or

trophoblastic embolism, pneumothorax, or pneumomediastinum. [9]

[74]

?Dyspnoea in the post-operative period may indicate pulmonary embolism, an acute coronary event, or pulmonary oedema related to fluid resuscitation. Less frequently a pneumothorax or previously unrecognised muscular dystrophy may be implicated. [75] Specific surgical interventions may be followed by dyspnoea due to fat

embolism (liposuction, long-bone surgery), talc-induced acute lung injury (pleurodesis), or pulmonary vein stenosis (mitral valve

surgery). [10] [76] [77] A history of previous venothromboembolic disease, inadequate anticoagulation, immobilisation, admission to hospital, long-distance travel, vascular access, or leg injury may indicate pulmonary embolism as the cause of dyspnoea.

?The presence of a known autoimmune or rheumatological disease predisposes the patient to dyspnoea resulting from pulmonary

embolism, pulmonary hypertension, interstitial lung disease,

pleural effusion, or pulmonary haemorrhage.[78] Known malignancy may cause dyspnoea through airway obstruction by the primary or

metastatic tumour, malignant effusion, post-obstructive pneumonia, pulmonary tumour embolism, lymphangitic spread into the lung, or pericardial or endocardial involvement. [79] [80] History of

rheumatological diseases, uncorrected obstructive sleep apnoea,

and obesity may indicate pulmonary hypertension. Recurrent

pneumonia may indicate gastro-oesophageal reflux with aspiration,

a retained foreign body, benign or malignant tumours, or a vascular

ring. [81] [82] [83] Pleural effusions can accompany pneumonia,

heart failure, pleural tuberculosis, malignancy, rheumatological diseases, or mesothelioma.

? A history of thoracic radiation for malignancy should be elicited.

Dyspnoea due to radiation pneumonitis typically appears 1 to 6

months after the radiation treatments. [84]

Drug history

?Medications may cause dyspnoea or contribute to it through a variety of mechanisms, including several forms of pulmonary toxicity

(interstitial disease, pulmonary oedema, pulmonary haemorrhage,

airways disease, pleural effusion, pulmonary vascular changes),

induction of metabolic acidosis (nucleoside reverse-transcriptase inhibitors, topiramate), or induction of bradycardia and

chronotropic insufficiency (digoxin, calcium-channel blockers,

beta-blockers). [The drug-induced lung diseases] [85] [86] ?Beta-blockers may worsen airway obstruction in COPD and asthma.

Social history

? A smoking history with documentation of the number of pack-years smoked is essential. Several smoking-related conditions, including COPD, lung cancer, and certain forms of interstitial lung disease, may produce dyspnoea.

Dyspnoea scales

?Although dyspnoea is by its nature a subjective complaint, attempts have been made to grade it. Several dyspnoea scales exist, although their use in everyday practice is limited.

?The Veterans Specific Activity Questionnaire (VSAQ) assesses the functional capability of the patient and estimates the aerobic

capacity in metres. [87] The degree of impairment can then be

inferred. The approach and testing for a 25-year-old with trouble running an 8-minute mile is different from that of an 80-year-old with trouble climbing a 12-step staircase. The VSAQ establishes the

baseline function and provides an objective measure for

longitudinal assessment of progress or the lack thereof.

?Other classification schemes are the New York Heart Association functional classification and the Medical Research Council

dyspnoea scale. [88] [89]

Physical exam

Careful physical exam helps to narrow the differential and rule in or out life-threatening conditions. Generally, dyspnoea with the presence of signs of acute distress ("dyspnoea that a doctor can see") fares worse than dyspnoea reported by a patient with a normal or near-normal physical exam.

Vital signs

?Hypotension, tachycardia, and tachypnoea may indicate acute myocardial infarction, pulmonary embolism, aortic dissection,

acute valvular insufficiency, cardiac tamponade, or an acute

infectious process with sepsis. [90]

?Hypertension in a dyspnoeic patient may point to

hypertension-related diastolic heart failure with pulmonary oedema, hyperthyroidism, or phaeochromocytoma. [91]

?Pulsus paradoxus may be a sign of asthma, COPD, or cardiac tamponade.

[16]

General exam

?Mental status change may be present with dyspnoea in some conditions, including stroke, hypoxaemic or hypercarbic respiratory failure

related to congestive heart failure, pulmonary oedema, asthma, COPD, pneumonia, sepsis, or CNS infections. [92]

?Frequent sighing may accompany hyperventilation and anxiety states.

[93]

?Cyanosis may indicate acute respiratory failure caused by exacerbated COPD, pulmonary embolism, acute airway obstruction,

acute drug toxicity, congenital cyanotic valvular disease,

mechanical valve malfunction, cardiac tamponade, pulmonary

arteriovenous malformations, aspiration, or methaemoglobinaemia.

[90] [94] [95] [96] [97]

?Jaundice may accompany dyspnoea in liver failure or leptospirosis.

[47]

?Facial oedema may be present in dyspnoeic patients with superior vena cava syndrome or anaphylaxis.

? A goitre may accompany retrosternal goitre causing airway obstruction or may be the sign of Graves' disease with

thyrotoxicosis. [98] [99]

?Laryngeal height of 4 cm or more is associated with a diagnosis of COPD. [100]

?Kyphoscoliosis, either idiopathic or resulting from a neuromuscular process, may cause restriction of chest movement and subsequent dyspnoea. [21]

?Clubbing may be present in lung cancer, interstitial lung disease, portopulmonary hypertension, or pulmonary arteriovenous fistulas.

[101] [102] [103] [104]

?Increased abdominal girth may indicate congestive heart failure, hepatic cirrhosis with ascites and pleural effusions, or

constrictive pericarditis. [105]

?Urticarial rash may accompany dyspnoea in systemic anaphylaxis.

[106] Purpura may indicate thrombotic thrombocytopenic purpura,

meningococcaemia, or vasculitis. [107]

Cardiovascular exam

?Neck vein engorgement may present in dyspnoeic patients with congestive heart failure, COPD, pneumothorax, or cardiac tamponade.

Elevated neck veins, extra heart sound (S3 gallop rhythm), and fluid retention indicate congestive heart failure. Chronic dyspnoea

resulting from pericardial constriction and effusions may be

accompanied by elevated neck veins, pulsus paradoxus, a pericardial knock, pericardial rub, and the Kussmaul's sign. [108] ?An irregular or fast heart beat may lead to a diagnosis of a tachyarrhythmia or atrial fibrillation. A loud S2 may be associated with pulmonary hypertension and cor pulmonale. A systolic heart

murmur may indicate acute valvular insufficiency, mechanical valve malfunction, or congenital or rheumatic valvular disease. [95] ?Lower extremity oedema may indicate congestive heart failure with pulmonary oedema, volume overload, pulmonary thromboembolism,

myocardial infarction, arrhythmias, constrictive pericarditis,

pulmonary hypertension, inferior vena cava thrombosis,

hypothyroidism, or cardiac tumours. [105] [109]

Respiratory exam

?Pursed lip breathing may be present in a patient with COPD.

?Stridor in a dyspnoeic patient is usually caused by upper airway obstruction with a foreign body, infectious or inflammatory oedema

(e.g., diphtheria, tetanus, epiglottitis, angio-oedema),[39] [40]

[110] [111] dysfunction of the upper airway structures (vocal cord

dysfunction, tetany),[112] [113] tumours of the airway wall (base of the tongue, larynx, oesophagus, trachea, and airway

papillomatosis), or airway limitation by its extrinsic compression (retrosternal goitre, thyroid cancer, lymphoma).[98] [114] [115] Associated fever and difficulty in swallowing may indicate

epiglottitis, while a characteristic cough in a child with an upper respiratory tract infection may indicate croup. Hoarseness may

accompany dyspnoea in laryngitis, laryngeal tumours, relapsing

polychondritis, [38] [116] or unilateral idiopathic and benign

(aortic aneurysm, Ortner's syndrome) or malignant vocal cord

paralysis. [117]

? A barrel chest (increased anteroposterior diameter) is seen in emphysema and cystic fibrosis.

?The trachea may deviate away from the lesion in tension pneumothorax or a large pleural effusion.

?Unilateral dullness to percussion may be due to pleural effusion, atelectasis, foreign body aspiration, pleural tumours, or

pneumonia. [118] Hyper-resonance may indicate pneumothorax or

severe emphysema. Subcutaneous emphysema may indicate the presence of pneumomediastinum. [27]

?Unilateral decreased or absent breath sounds may be due to pleural effusion, atelectasis, foreign body aspiration, or pneumothorax.

Pulmonary hypertension is suggested by a loud P2 on auscultation.

Distant breath sounds suggest a pleural effusion. [119] Wheezing accompanies dyspnoea in asthma, COPD, anaphylaxis, vocal cord

dysfunction, pulmonary congestion and oedema, cystic fibrosis, or pulmonary embolism. In COPD, wheeze is associated with acute

dyspnoea and a laryngeal descent of at least 4 cm. [19] Pulmonary rales may indicate pulmonary congestion (fine, bibasal) or oedema, acute or chronic pneumonia, or some interstitial lung diseases, including sarcoidosis, hypersensitivity pneumonitis, or

idiopathic pneumonitides. Velcro crackles should alert the

clinician to the possibility of interstitial lung disease. A

prolonged expiratory phase may be observed in asthma, COPD, cystic fibrosis, bronchiectasis, or bronchiolitis.

Neurological exam

?Cranial nerve palsies may accompany dyspnoea in botulism. [41] ?Ptosis may be present in myasthenia gravis, myotonic dystrophy, or botulism. [41] [49] [75]

Investigations

Results of preliminary laboratory testing and radiographic investigations help to narrow the diagnosis and focus on only some of the numerous differential diagnoses of dyspnoea. Initial investigations for dyspnoea include pulse oximetry and ABG; an FBC; D-dimer, B-type natriuretic peptide (BNP), and TSH levels; a 12-lead ECG and CXR; and spirometry (including carbon monoxide diffusing capacity [DLCO]) and cardiopulmonary exercise testing. [120] [121] [122] The choice of investigations is dictated by the clinical history and physical exam findings.

?Pulse oximetry: this allows detection and ongoing monitoring of hypoxaemia with initiation of oxygen supplementation as necessary, while undertaking diagnostic work-up for its cause.

?ABG: not all patients with dyspnoea display abnormal findings on ABG, and not all abnormal ABG results manifest with dyspnoea.

However, the ABG results may help in constructing a differential diagnosis and, along with exertional oximetry, may be indicated to evaluate gas exchange abnormalities in conditions associated with hypoxaemia. Hypercapnia (PaCO2 >45 mmHg) may accompany dyspnoea in exacerbation of COPD, neuromuscular disease, stroke, upper airway obstruction, or obesity-hypoventilation syndrome. Hypocapnia may be present in anxiety states and accompany any process that presents with hyperventilation, such as pulmonary embolism. Hypoxaemia

(PaO2 <70 mmHg at sea level) has a broader differential, including conditions causing shunting (acute respiratory distress syndrome, pneumonia, pulmonary oedema, cyanotic valvular disease), V/Q

mismatching (COPD, asthma, pulmonary embolism), diffusion

impairment (interstitial lung disease), or hypoventilation (COPD exacerbation, neuromuscular disease, stroke, upper airway

obstruction, or obesity-hypoventilation syndrome). The dyspnoea differentiation index, which combines the PaO2 with the PEFR ([PEFR x PaO2]/1000), has a reported diagnostic accuracy of 79% in

differentiating cardiac from pulmonary causes of dyspnoea. [123] Acidosis (pH <7.36) is a potent stimulus of breathing and may

accompany dyspnoea in the late phases of almost any process

presenting with dyspnoea, including sepsis, pulmonary oedema,

exacerbation of COPD, and cyanide toxicity. [124] It may also be present in idiopathic or medication-induced renal tubular acidosis and thiamine deficiency. [125] Acidosis may result from using

medications such as nucleoside reverse-transcriptase inhibitors and topiramate.[85] [86] Alkalosis may be a consequence of anxiety, panic attacks, dehydration, pulmonary embolism, ovarian

hyperstimulation syndrome, or pulmonary leukostasis. [126] [14]

?PEFR: this simple bedside test may help to differentiate between pulmonary and cardiac causes of dyspnoea. Low peak flow rates are associated with obstructive lung disease such as asthma, COPD, and cystic fibrosis. [123]

?FBC: leukocytosis may accompany dyspnoea in any infectious process involving the respiratory system, as well as in sepsis, autoimmune disease, parasitic infections, and leukemia. [14] [127]

Eosinophilia may be present in a dyspnoeic patient with parasitic disease, certain vasculitides (e.g., Churg-Strauss syndrome), asthma, eosinophilic pneumonia, or cocaine use. [127] [128] [129] [130] Anaemia may be the primary reason for dyspnoea or may

accompany it in drug-related lung injury, hereditary haemorrhagic telangiectasia, acute chest syndrome of sickle cell disease, pulmonary alveolar haemorrhage, or widespread infectious processes.

[131] [132] Thrombocytopenia may be present with dyspnoea in viral infections, including influenza, SARS, and Hantavirus pulmonary syndrome. [25] [26] It may also be due to adverse drug reactions, especially with chemotherapy.

?Electrolytes: hyponatraemia may accompany dyspnoea in congestive heart failure, chronic kidney disease, liver failure, or

hypothyroidism.

?Liver function tests: bilirubin may be elevated in dyspnoeic patients with liver failure, congestive heart failure,

leptospirosis, and thoracic amoebiasis. [47] [133] [134]

Transaminases may be elevated in liver failure, acute myocardial infarction, atypical pneumonia (especially Legionella pneumonia), and viral infections such as SARS and Hantavirus pulmonary syndrome.

[25] [26]

?Kidney function tests: dyspnoea accompanied by laboratory evidence of renal insufficiency may be due to uraemic pleurisy, long-term volume overload with pleural effusions, pneumonia, and several types of acute vasculitis. [135] [136] [137] [138]

?Cardiac enzymes: elevated troponin I/T, myoglobin, and CK-MB may accompany acute myocardial infarction, myocarditis, takotsubo cardiomyopathy, or hypothyroidism. [53] [139] It may also reflect chronic coronary artery disease with superimposed physiological stress (e.g., sepsis).

?BNP: elevated B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) have been associated with congestive heart failure, but also sepsis, coronary artery disease, pulmonary embolism, COPD with cor pulmonale, renal failure, liver cirrhosis, and hyperthyroidism.[140] [141] [142] A low normal BNP level (<100 nanograms/L [<100 picograms/mL]) is helpful in excluding

congestive heart failure.

?CXR: this is important to exclude spontaneous or secondary pneumothorax. Pulmonary venous congestion and an enlarged heart suggest congestive heart failure. An enlarged cardiac silhouette may also indicate valvular heart disease, a pericardial cyst, or cardiac tamponade.[16] [143] Dyspnoea accompanied by parenchymal infiltrates may be present in infectious pneumonia, pulmonary oedema, eosinophilic pneumonitis, radiation pneumonitis, [144] some interstitial lung diseases (sarcoidosis, usual interstitial pneumonitis, non-specific interstitial pneumonitis, cryptogenic interstitial pneumonitis, lymphoid interstitial pneumonitis, acute interstitial pneumonitis), [145] [146] [147] [148] [149] pneumoconioses (silicosis, asbestosis, berylliosis), drug-related lung disease, autoimmune disease-related lung disease (lupus, rheumatoid arthritis, scleroderma, polymyositis, vasculitis), or metastatic lung disease. Pleural effusion may accompany congestive heart failure, liver failure, uraemia, nephrotic syndrome,

malignancy, pneumonia, pulmonary embolism, or pleuritis. Pleural thickening and nodularity may be seen in pleural tumours.[28] Lung hyperinflation may be present in COPD, exacerbation of asthma, or foreign body aspiration. Elevation of the hemidiaphragm may

indicate its paralysis. Unilateral lucidity may indicate

pneumothorax or a diaphragmatic hernia. [150] Prominent hilar vessels may be apparent in pulmonary hypertension.

?ECG: this helps to diagnose acute coronary syndromes as the cause of dyspnoea with ST-T-segment changes. It also identifies complete heart block, bradycardias, and tachyarrhythmias, and detects changes suggestive of pericarditis, cardiac tamponade (low

voltage), and pulmonary embolism. Changes in the p-wave morphology may help diagnose right atrial enlargement (typical of a chronic pulmonary process) or left atrial enlargement (typical of valvular heart disease). Change in the QRS axis may indicate right (COPD, pulmonary hypertension) or left (hypertension, valvular heart disease) ventricular enlargement or hypertrophy.

?Echocardiogram: this can detect pericardial disease and pulmonary hypertension. It can also be used to delineate valvular heart disease, measure diastolic dysfunction, and differentiate between systolic and diastolic failure. The diagnosis of constrictive and restrictive heart diseases with heart failure requires

echocardiographic study.

?Holter monitoring: continuous monitoring of the heart rate over a period of days or weeks allows for the detection of intermittent arrhythmias.

? A negative D-dimer by ELISA has a negative predictive ratio of 0.1 for the presence of venothromboembolism, similar to that of a lower

extremity duplex ultrasound scan, and a normal to near-normal V/Q lung scan. [13]

?CT angiography of the chest: this is the best investigation for diagnosing and excluding pulmonary embolism and may be indicated if the D-dimer is abnormal. CT of the chest can also detect and help define the extent of pulmonary parenchymal disease (infectious and non-infectious infiltrates), suggest the presence of pulmonary oedema, define airway (benign stenoses, foreign body, malignancy) and vascular (congenital and acquired stenoses of the intrathoracic blood vessels, aneurysms) abnormalities, confirm the presence of pleural effusion, or evaluate other intrathoracic (thymus,

retrosternal goitre) structures.

?High resolution CT chest: this imaging study is necessary in evaluating interstitial lung disease, which is not excluded by a normal CXR. [151]

?Ventilation-perfusion (V/Q) scan: unmatched perfusion defects on V/Q scan suggest pulmonary embolism in an appropriate clinical setting. Three-dimensional single-photon emission CT (SPECT) technology improves sensitivity and specificity of the V/Q scan.

[152]

?Lateral X-ray of the neck may show an enlarged epiglottis, the “thumb sign”, which in an appropriate clinical scenario is suggestive of epiglottitis.

?Lung biopsy: a thoracoscopic lung biopsy is the mainstay of diagnosis for many interstitial lung diseases. It may also be used in diagnosing autoimmune or vascular diseases of the lung.

Transthoracic needle aspiration may be useful in confirming the malignant aetiology of intrathoracic nodules.

?Spirometry: this simple clinic-based test allows the detection of an obstructive deficit, which is revealed by a disproportionate reduction in the FEV1 in relation to the FVC. Obstructive deficits are characteristic of asthma, emphysema, or chronic bronchitis.

More symmetrical reduction in FEV1 and FVC may suggest restriction and warrants full pulmonary function testing, with measurement of lung volumes and carbon monoxide diffusing capacity (DLCO). [153] ?Pulmonary function testing: this involves spirometry, measuring lung volumes, and evaluating DLCO. The 2 most common patterns of ventilatory defect are an obstructive deficit (low FEV1/FVC ratio, increased residual volume, increased total lung capacity), seen in asthma, bronchitis, and emphysema, and a restrictive deficit (symmetrical reduction of FEV1 and FVC, high FEV1/FVC ratio, low total lung capacity), seen in interstitial lung disease. Less common patterns include a fixed or variable extrathoracic flow limitation in vocal cord obstruction and tumours, an isolated

reduction of the DLCO in pulmonary hypertension and interstitial lung disease, and a low maximal voluntary ventilation in

neuromuscular diseases.

?Cardiopulmonary exercise testing: this involves a detailed analysis of the cardiorespiratory response to exercise and allows the evaluation of cardiac function, pulmonary gas exchange, and ventilation, and the detection of cardiac ischaemia,

exercise-related obstructive lung disease, and deconditioning.

[122]

?Nocturnal oximetry: continuous nocturnal non-invasive measurement of oxygen saturation by pulse oximetry allows the detection of hypoventilation, sleep apnoea, or neuromuscular disease.

?Polysomnography: comprehensive monitoring of several physiological variables allows the detection of sleep apnoea, hypoventilation, nocturnal arrhythmias, and seizures, and the observation of findings suggestive of congestive heart failure or neuromuscular weakness.

呼吸困难诊断与处理的专家共识

呼吸困难诊断评估与处理的专家共识 呼吸困难（dyspnea）是一种常见的临床表现。国外文献报道，9%~13%社区成人有轻至中度的呼吸困难症状，＞40岁者中15%~18%、≥70岁者中25%~37%有呼吸困难症状。美国每年因呼吸困难急诊就诊达300万~400万人次。研究显示，呼吸困难为心肺疾病住院和死亡的原因之一，在某些疾病中与5年生存率密切相关，而且与心脏疾病死亡关系更明显。 呼吸困难的病因涉及呼吸、循环、消化、神经、血液、精神等多个系统，进行鉴别诊断需要系统和科学的临床思维方法，因其在临床诊治中常发生误诊，故提高呼吸困难诊断与处理水平十分重要。1999年和2012年美国胸科协会（ATS）发表了关于呼吸困难的专家共识。 目前我国在呼吸困难诊断与处理方面的研究尚有不足，尤其对呼吸困难的定义、语言表述及评估和诊断流程等方面尚无统一认识。因此，中国医师协会北京医师分会组织有关专家，参照ATS相关文件及近年发表的有关呼吸困难的重要文献，经认真讨论撰写了本共识，希望在呼吸困难的定义、描述、评估及处理等方面进一步统一认识，提高呼吸困难诊断与处理水平。 ―、呼吸困难的定义 目前我国通用的教科书中对呼吸困难的定义为"呼吸困难是指患者主观上感到空气不足、呼吸费力，客观上表现为呼吸费力，严重时可出现张口呼吸、鼻翼扇动、端坐呼吸、甚至发绀、呼吸肌辅助参与呼吸运动，并可有呼吸频率、深度与节律的改变"。2012年ATS呼吸困难共识中的定义为"呼吸困难是某种包括不同强度、不同性质的呼吸不适感的主观体验"。 ATS的定义是狭义呼吸困难的定义，仅将呼吸困难作为患者主诉，从而将呼吸困难定义为患者的一种主观感受。我国的呼吸困难定义则为广义呼吸困难的定义，既包括了患者主观症状感受，也包括了患者的客观体征表现。但我国呼吸困难的定义未指出患者主观感受与客观感受间的关系，易使人误解为呼吸困难必须同时伴有客观呼吸费力的表现。 本共识认为，呼吸困难的界定是深入研究呼吸困难的基础。呼吸困难既可以是患者表述的一种症状，又可以作为医生判断病情的依据。虽然呼吸困难是一种患者的主观感受，但医生还应关注呼吸困难的客观表现，因此对广义呼吸困难的定义，不仅应含有患者主观感受及体征描述（如端坐呼吸，发绀等），还应包括对患者主观感受之外的附加客观表现的描述（如呼吸费力等）。 因此本共识将呼吸困难定义为：呼吸困难指患者的某种不同强度、不同性质的空气不足、呼吸不畅、呼吸费力及窒息等呼吸不适感的主观体验，伴或不伴呼吸费力表现，如张口呼吸、鼻翼扇动、呼吸肌辅助参与呼吸运动等，也可伴有呼吸频率、深度与节律的改变，患者的精神状况、生活环境、文化水平、心理因素及疾病性质等对其呼吸困难的描述具有一定的影响。 对呼吸困难性质的分类有多种，按病程分为急性呼吸困难与慢性呼吸困难；急性呼吸困难是指病程3周以内的呼吸困难，慢性呼吸困难是指持续3周以上的呼吸困难。按病因可分为肺源性呼吸困难、心源性呼吸困难、中毒性呼吸困难、血源性呼吸困难和神经精神性呼吸困难，其中肺源性呼吸困难又分为呼气性、吸气性和混合性呼吸困难。

诊断复习题呼吸困难

呼吸困难 一、填空题 1.呼吸困难的病因主要是和疾病。 2.呼吸系统疾病引起的呼吸困难包括：①、②、③、④、⑤。 3.从发生机制及症状表现，呼吸困难分为：、、 、。 4.发作性呼吸困难伴有哮鸣音者，见于、。 5.呼吸困难伴有大量浆液性泡沫样痰，见于和。 6.呼吸困难伴昏迷，可见于、、、、 、等。 7.呼吸困难伴血性泡沫样痰见于。 8.骤然发生的严重呼吸困难见于、、、等。 9.呼吸困难伴一侧胸痛见于、、、、 、等。 10.呼吸困难伴发热可见于、、、、 等。 11.呼吸困难伴咳嗽、咳脓痰者见于、、 、、等。 12.呼吸困难伴咳脓痰较多者可见于、等。 13.癔病患者由于或的影响可有呼吸困难，其特点是呼吸频率可达60～100次/分，常因通气过度可发生。严重时可有。 14.叹息样呼吸实际上是一种。 二、判断题

1.判断呼吸困难客观表现应注意呼吸频率、节律和深度的异常变化。（） 2.呼吸困难者不一定有发绀表现。（） 3.出现呼吸困难的主要疾病是呼吸系统和心血管系统疾病。（） 4.肺源性呼吸困难是由于通气、换气功能障碍，导致缺氧和（或）二氧化碳潴留引起。（） 5.吸气性呼吸困难严重者可出现“三凹征”（three depression sign）（） 6.呼气性呼吸困难常伴有干啰音。（） 7.心源性呼吸困难主要是由于左心和（或）右心衰竭引起，两者发生机制相同。（） 8.急性左心衰竭的呼吸困难又称“心源性哮喘”（Cardiac asthma）（） 9.右心衰竭时呼吸困难的原因主要是体循环淤血所致。（） 10.出现深长规则的呼吸，可伴有鼾声，称为酸中毒大呼吸（Kussmael）呼吸。（） 11.呼吸中枢受抑制，致呼吸缓慢、变浅，且常有呼吸节律异常，如Cheyne-Stokes或Biots呼吸。（） 12.癔病患者出现的呼吸困难是由于精神或心理因素的影响所致。（） 三、名词解释 1.呼吸困难 2.心源性哮喘 四、选择题 A型题： 1.引起呼吸困难的病因最多见的是：（） A.呼吸系统疾病 B.心血管疾病 C.中毒 D.血液病 E.神经精神因素 2.在呼吸系统疾病中，突发呼吸困难（吸气或呼气）或和哮鸣音，下列哪种情况最多见：（） A.隔肌运动受限 B.神经肌肉疾病 C.胸廓疾病 D.肺疾病 E.气道阻塞 B型题： 问题（3-7） A.气道阻塞 B.心力衰竭 C.尿毒症 D.重度贫血 E.脑出血

小儿常见病鉴别诊断

鉴别诊断： 1.流行性感冒：由流感病毒、副流感病毒引起，有明显的流行史、局部症状较轻，全身症状较重，常有高热、头痛、四肢肌肉酸痛，病程较长。该患儿发热1天，无上述症状，可除外。 2、急性传染病早期：上感常为各种传染病的前驱症状，应结合流行病史、临床表现及实验室资料等综合分析，并观察病情演变加以鉴别。 3. 上呼吸道感染为各种病原引起的上呼吸道炎症，为小儿最常见疾病，年长儿症状较轻，婴幼儿较重。患儿局部症状主要表现为鼻塞、流涕、干咳、咽部不适。全身症状为发热、烦躁不安、头痛、乏力等。体检可见咽部充血、扁桃体肿大。浅表淋巴结可触及肿大，肺部听诊一般正常。 4. 支气管肺炎是小儿时期最常见的肺炎，2岁以内儿童多发，最常见细菌和病毒感染，也可由病毒、细菌混合感染。起病多数较急，主要临床表现为发热、咳嗽、气促、呼吸困难及肺部固定中细湿罗音。胸片有助于诊断。 5. 过敏性紫癜：为小血管炎为主要病变，临床特点为血小板不减少性紫癜，多见四肢及紫癜，对称出现，以伸侧较多，初起为紫红色斑丘疹，高出皮面，压之不褪色，数日后转为暗紫色，最终呈棕褐色而消退，常伴关节肿痛，腹痛、血便和蛋白尿。辅助检查协助诊断。 6．水痘：本病为水痘-带状疱疹病毒引起的具有传染性极强的儿童期出疹性疾病，临床上以发热、全身不适、食欲不振，初起于躯干部，继而扩展至面部及四肢，四肢末端稀少，呈向心性分布，开始为红色斑丘疹或斑疹，数小时后变成椭圆形水滴样小水泡，周围红晕为特征，该患儿无上诉症状，皮疹特点与之不符，可除外。 7. 过敏性皮炎：为接触某种过敏物质或无明显诱因引起患儿全身皮肤红肿，瘙痒，严重者可出现心慌、气短、呼吸困难、腹痛、便血等，查体全身皮肤红肿，有时可见斑丘疹，肺部听诊可闻及喘鸣音。 8. 母乳性黄疸：可能与母乳中的β-葡萄糖醛酸进入患儿肠内，使肠道内未结合胆红素生成增加有关，可分早发性及晚发性，早发性黄疸出现时间出生后3-4天，晚发性则出生后6-8天，血胆红素以未结合胆红素为主，无论早发性或晚发性一旦停母乳或改配方奶48-72小时，黄疸即可明显消退。 9. 婴儿肝炎综合征：常是病理性黄疸延长，超过二十八天，多种原因所致，血中以结合胆红素增高为主，转氨酶异常，肝、脾可肿大，该患儿母乳喂养，谷丙转氨酶、谷草转氨酶均正常，目前可排除此病，需进一步确诊。 10.梗阻性黄疸：多由先天性胆道畸形引起，出生后1—2周或是3—4周出现黄疸逐渐加深，大便变为白陶土色，尿色变深黄，肝大质地硬，直胆高，肝功异常，出现营养和发育降低。

小儿常见病鉴别诊断(精)

鉴别诊断: 1.流行性感冒:由流感病毒、副流感病毒引起,有明显的流行史、局部症状较轻,全身症状较重,常有高热、头痛、四肢肌肉酸痛,病程较长。该患儿发热1天,无上述症状,可除外。 2、急性传染病早期:上感常为各种传染病的前驱症状,应结合流行病史、临床表现及实验室资料等综合分析,并观察病情演变加以鉴别。 3. 上呼吸道感染为各种病原引起的上呼吸道炎症,为小儿最常见疾病,年长儿症状较轻,婴幼儿较重。患儿局部症状主要表现为鼻塞、流涕、干咳、咽部不适。全身症状为发热、烦躁不安、头痛、乏力等。体检可见咽部充血、扁桃体肿大。浅表淋巴结可触及肿大,肺部听诊一般正常。 4. 支气管肺炎是小儿时期最常见的肺炎,2岁以内儿童多发,最常见细菌和病毒感染,也可由病毒、细菌混合感染。起病多数较急,主要临床表现为发热、咳嗽、气促、呼吸困难及肺部固定中细湿罗音。胸片有助于诊断。 5. 过敏性紫癜:为小血管炎为主要病变,临床特点为血小板不减少性紫癜,多见四肢及紫癜,对称出现,以伸侧较多,初起为紫红色斑丘疹,高出皮面,压之不褪色,数日后转为暗紫色,最终呈棕褐色而消退,常伴关节肿痛,腹痛、血便和蛋白尿。辅助检查协助诊断。 6.水痘:本病为水痘-带状疱疹病毒引起的具有传染性极强的儿童期出疹性疾病,临床上以发热、全身不适、食欲不振,初起于躯干部,继而扩展至面部及四肢,四肢末端稀少,呈向心性分布,开始为红色斑丘疹或斑疹,数小时后变成椭圆形水滴样小水泡,周围红晕为特征,该患儿无上诉症状,皮疹特点与之不符,可除外。 7. 过敏性皮炎:为接触某种过敏物质或无明显诱因引起患儿全身皮肤红肿,瘙痒,严重者可出现心慌、气短、呼吸困难、腹痛、便血等,查体全身皮肤红肿,有时可见斑丘疹,肺部听诊可闻及喘鸣音。