symmetric purpura of limb with arthralgia of abdominalgia, hemuresis, is usually in anaphylactoid purpura.
General cutaneomucous purpura with ulemorrhsagia, nosebleed or hemafecia, hemuresis is common in primary thrombopenic purpura.
Purpura with jaundice is often seen in coagulation disorder of hepatic diseases.
Hemophilia and congenital platelet dysfunction should be considered when with excessive bleeding after microtrauma from a child, joint hemorrhage and having family history.
Chapter 5 Dyspnea
Dyspnea is defined as an awareness of difficulty in breathing. It is therefore a symptom, usually described by the patient as “shortness of breath,” whether the sensation is due to actual difficulty in breathing or is essentially an awareness of hyperventilation. If the symptom becomes striking, it always companies with dilatation of nares, cyanosis, use of accessory muscles of respiration and abnormalities of respiratory rate, depth or rhythm.
The most frequent causes of dyspnea are cardiorespiratory disease. It also can be initiated by the other factors. Such as toxic, neuropsychogenic, hematologic. In addition, the increase of abdominal pressure (massive ascites, pregnancy etc) can develop dyspnea too. Normal person may experience the physiologic dyspnea during heavy exercise.
Mechanism and clinical feature
Dyspnea can be classified according to the etiology as follows:
1. Respiratory dyspnea:
Respiratory dyspnea is caused by abnormal ventilation and gas exchange, reduction in ventilatory capacity, hypercapnia and hypoxemia resulting from respiratory disease.
Respiratory dyspnea can be divided into three clinical types.
(1) Inspiratory dyspnea
Inspiratory dyspnea tends to occur primarily when there is obstruction, such as inflammation, edma, tumor and foreigh body in larynx, trachea and major bronochi. It is characterized by the depression sigh, in which visible indrawing over the sternal notch, the supraclavioular spaces, the intercostal spaces and the epigastrium in the inspiration can be seen often this accompanied by a coarse, low pitched inspiratory wheezing and dry cough. It is commonly present in stenosis and obstruction of larynx, trachea, and bronchi.
(2) Expiratory dyspnea
Expiratory dyspnea is due to the decrease of lung elasticity and spasm narrowing of the bronchioles and smaller bronchi as in emphysema, bronchial asthma and asthmatic bronchitis, Expiration is prolonged and laboured with wheezing.
(3) Mixed dyspnea
Mixed dyspnea occurs with the extensive lung disease, such as severe pneumonia, pulmonary fibrosis, massive atelectasis, pleural effusion and pneumothorax, resulting in the decrease of ventilators and gas exchange capacity. Breathing is difficult during both inspiration and expiration.
2. Cardiac dyspnea
Cardiac dyspnea is usually attributable to pulmonary vascular congestion resulting from the left and/or right heart failure.
The dyspnea caused by right-sided heart failure is less severe than that one caused by left-sided. Left-sided heart failure leads to impaired gas exchange. Compliance is reduced, and therefore, ventilation is decreased to the edematous lung regions and vital capavity reduced. Alveoli are stiff and more work is needed to overcome elastic recoil, the high alveolar pressure will stimulate stretch receptor and initiate the inflation reflex resulting in early turning off of inspiration and an increase in respiratory rate.
Right-sided heart failure causes stasis systemic circulation. The mechanism includes (1) the pressure of right atrial and superior vena cava is the natural stimulus of respitatory center. (2) The decrease of oxygen content and the accumulation of the acid metabolites, such as lactic, stimulate respiratory center. (3) The restriction of the respiratory movement caused by enlargement of liver resulting from congestion, ascites and pleural effusion.
Symptoms of congestive heart failure can cause orthopnea and paroxysmal nocturnal dyspnea when elevated-filling pressure is present. Orthopnea is difficulty in breathing in the supine position, this may be relived by sitting up, which reduces the degree of pulmonary congestion by pooling blood in the lower extremities and lowering left ventricular filling pressures, improving the diaphragmatic movement, increasing vital capacity.
Paroxysma nocturnal dyspnea is a specific symptom. The patient awakes short of breath at night, but often obtain relief by sitting up for a period of time. It is belived in that assumption of supine posture for sleep result resorbtion of extracellar fluid into the intravascular space, causing arise in filling pressure. In the most advanced cases, the patients become acutely dyspneic, cyanotic and very frequently produce foany sputum tinged with blood. On physical examination, their are moist rales at the both lung bases, tachycardia, wheezing and bronchospasm. The markedly accentuated second heart sound in the pulmonic area. The paroxysmal dyspnea is termed as cardiac asthma, which can be seen in the hypertensive heart disease and coronary heart disease.
3. Toxic dyspnea.
In the metabolic acidosis (uremia and diabetic ketosis), the acid metabolites stimulate the respiratory center, causing deep and regular respiration with snoring.
The overdose of morphine and pentobarbital can depress respiratory center causing deep respiration or Cheyne-Stokess respiration.
4. Neuro-Psychogenic dyspnea.
Dyspnea may occur in the patients suffering from cerebro vascular diseases (intra cranial hemorrhage, elevated intracerebral pressure). The respiratory center loses the blood supply or is compressed. The respiration becomes deep, slow and irregular. In some cases the dyspnea may be psychogenic, which is characterized by repetitive deep, signing respiration with numbness of extremities or lips, cheiropedal spasm. These are also manifestations of acute hypocapnia and respiratory alkalosis.
5. Hematologic dyspnea
In severe anemia, sulfhemoglobinemia, methaemoglobinemia or carbon monoxide poisoning the decrease of oxygen-carrying capacity and oxygen content develop abnormal respiration and increased heart rate. The respiration rate also increases in shock which stimulates respiration center because of hypotension.