Increased hilar shadow
Introduction
Introduction Pulmonary edema was blurred and enlarged in the hilars during X-ray examination. Pulmonary edema (pulmonary edema) refers to the formation of imbalance and imbalance of reflux in the lungs for some reason, so that a large amount of tissue fluid can not be absorbed by the pulmonary lymph and pulmonary venous system in a short time, from the extravasation of the pulmonary capillaries, accumulate in the alveoli , pulmonary interstitial and small bronchi, resulting in severe ventilation and ventilation function, clinical manifestations of extreme dyspnea, sitting breathing, cyanosis, sweating, paroxysmal cough with a lot of white or pink foam Hey, the lungs are full of symmetrical wet squeaks, and the chest X-rays of the two lungs show blushing shadows of the two lungs, and shock or even death can occur in the late stage. Early arterial blood gas analysis may have low O2, low CO2 partial pressure, severe O2 deficiency, CO2 retention and mixed acidosis, which is one of the clinical critical illnesses.
Cause
Cause
(1) Causes of the disease
The etiology of pulmonary edema can be divided into two categories: cardiogenic and non-cardiac. The latter can be divided into several types depending on the pathogenesis.
Cardiogenic pulmonary edema
Under normal circumstances, the left and right heart discharges remain relatively balanced, but in some pathological conditions, such as the return of blood volume and right heart discharge increased sharply or the left heart discharge suddenly decreased severely, causing a large amount of blood to accumulate in the pulmonary circulation, The pulmonary capillary venous pressure is sharply increased. When it rises above the colloidal osmotic pressure of the pulmonary capillaries, on the one hand, the hemodynamics in the capillary changes, on the other hand, the pulmonary circulation is congested, the permeability of the pulmonary capillary wall is increased, and the liquid is filtered through the capillary wall to form the lung. Edema. Clinically, acute pulmonary edema caused by hypertensive heart disease, coronary heart disease and rheumatic valvular heart disease accounts for the vast majority of cardiogenic pulmonary edema. Myocarditis, cardiomyopathy, congenital heart disease, and severe tachyarrhythmia can also be caused.
2. Non-cardiogenic pulmonary edema
(1) Increased pulmonary capillary permeability:
1 Infectious pulmonary edema caused by infection of bacteria, viruses, fungi, mycoplasma, protozoa, etc. throughout the body and/or lungs.
2 Inhalation of harmful gases such as phosgene (COCl2), chlorine, ozone, carbon monoxide, nitrogen oxides, etc.
3 blood circulation toxins and vasoactive substances, such as alloxan, snake venom, organic phosphorus, histamine, serotonin and the like.
4 diffuse capillary leak syndrome, such as endotoxemia, the application of a large number of biological agents.
5 severe burns and disseminated intravascular coagulation.
6 allergic reactions, plus drug-specific reactions, allergic alveolitis and so on.
7 radiation pneumonitis, such as high-dose radiation therapy for chest malignant tumors can cause pulmonary edema.
8 uremia, such as uremic pneumonia is a manifestation of pulmonary edema.
9 drowning, fresh water and seawater drowning can cause pulmonary edema.
10 acute respiratory distress syndrome, is the most serious acute pulmonary interstitial edema caused by various reasons.
11 oxygen poisoning, long-term inhalation of high concentrations (>60%) of oxygen, can cause increased reactive oxygen free radicals, causing lung damage and pulmonary edema.
12 heat strokes.
(2) Increased pulmonary capillary pressure:
1 pulmonary vein occlusion or pulmonary vein stenosis.
2 Infusion overdose, infusion or transfusion too much too fast, so that the blood volume is excessive or too fast, resulting in pulmonary hydrocephalus increased hydrostatic pressure and pulmonary edema. Also known as venous congestion syndrome. Common in trauma, blood loss or shock patients with a large number of rapid intravenous rehydration support circulation function.
(3) Plasma colloid osmotic pressure reduction:
1 liver and kidney disease causes hypoproteinemia.
2 protein loss enteropathy.
3 dystrophic hypoproteinemia.
(4) Lymphatic dysfunction.
(5) Increase in tissue interval negative pressure:
1 After re-expansion of pulmonary edema, such as pneumothorax, pleural effusion or thoracic surgery lead to lung collapse, rapid venting, rapid re-expansion of the lungs after pumping, increased tissue interval negative pressure, acute pulmonary edema.
2 pulmonary edema after upper airway obstruction, upper airway obstruction caused by various causes, tracheal intubation, tracheotomy, etc., acute pulmonary edema that occurs rapidly after obstruction is relieved.
(6) Other composite factors:
1 high altitude pulmonary edema: pulmonary edema caused by high altitude and low oxygen environment is called high altitude pulmonary edema.
2 drug-induced pulmonary edema: such as aspirin, heroin, lidocaine, furantanidine, chlordiazepoxide, terbutaline, methadone and so on. In addition to some drugs related to allergic factors, some drugs mainly cause direct lung damage or direct effects on the central nervous system and acute pulmonary edema.
3 neurogenic pulmonary edema: acute pulmonary edema caused by increased intracranial pressure caused by craniocerebral trauma, surgery, subarachnoid hemorrhage, cerebral embolism and intracranial tumor.
(two) pathogenesis
The lungs can be structurally divided into four compartments, some filled with liquid, some quite dry, and moved and exchanged with each other.
1. Pulmonary vascular cavity: Pulmonary capillaries, venules, and small arteries have the characteristics of liquid permeability, small vacuoles in endothelial cells, one side discharges the liquid in the bubble, and the other side occupies the extracellular liquid.
2. Alveolar: The connection between epithelial cells is very tight, water is not easy to penetrate; surfactant can reduce surface tension and facilitate alveolar expansion.
3. Interstitial cavity: the thick interstitial cavity of the alveolar septum, which can regulate the storage of liquid.
4. Lymphatic lumen: It can continuously drain the fluid in the interstitial and absorb protein.
The liquid between the chambers maintains a dynamic balance, which is mainly determined by the colloid osmotic pressure and the hydrostatic pressure and the permeability of the alveolar capillary membrane.
Plasma colloid osmotic pressure is a major factor in preventing extravasation of intravascular fluids. When the total plasma protein is 70 g/L and the ratio of albumin to globulin is normal, the colloid osmotic pressure is 3.33 to 4.0 kPa. The plasma colloid osmotic pressure is too low, allowing intravascular fluid to penetrate into the pulmonary interstitial and alveolar. The hydrostatic pressure of the pulmonary capillaries averaged 1.07 to 1.33 kPa. The hydrostatic pressure of the pulmonary capillaries increases, and when the corresponding plasma colloid osmotic pressure is exceeded, the fluid in the pulmonary capillaries can be filtered out. The hydrostatic pressure of the pulmonary interstitial is caused by the negative pressure in the chest caused by respiratory exercise, which is about 1.33~2.27kPa; the colloid osmotic pressure of the interstitial lung is about 1.6~2.67kPa, and the changes of the two will also promote the liquid from The pulmonary capillaries are filtered out. The hydrostatic pressure of the lymphatic vessels is negative, and together with the colloidal osmotic pressure of the lymph fluid, causes the fluid to enter the lymphatics from the interstitium. The centripetal force generated by the surface tension of the alveoli reduces the pressure in the interstitial lungs, allowing fluid to be filtered out of the pulmonary capillaries. The gas pressure in the alveoli changes with the breathing movement, but has no significant effect on the liquid flow. The above relationship of liquid dynamics can be summarized by the starling formula: Qf=kf[(pv-pi)-(v-i) where Qf is the flow of water inside and outside the blood vessel, kf is the permeability coefficient of the blood vessel wall, and is back Absorption coefficient, p is hydrostatic pressure; is colloid osmotic pressure, v refers to the lumen of the blood vessel; i refers to the interstitial cavity.
The combined effect of the above kinetics, under normal circumstances, the liquid is continuously filtered out from the pulmonary capillaries into the interstitial lung, and the liquid is continuously drained from the interstitial through the lymphatic system, so that the liquid movement in the lung maintains a dynamic balance. Any pathological factors cause imbalance of fluid movement in the lungs, and when the filtered liquid is more than recovered, pulmonary edema is formed.
Pulmonary edema due to increased permeability of the pulmonary capillary wall is called osmotic pulmonary edema. The tight junctions between the pulmonary capillary endothelial cells allow water, small ions and metabolites to pass, while large molecular weight proteins cannot pass. Many factors, such as hypoxia, inflammation, toxic stimulation and the action of vasoactive substances, can cause damage and reaction of pulmonary capillary endothelial cells, resulting in increased permeability of the blood vessel wall, increased filtrate entering the interstitial, and large molecular weight proteins. It can also be filtered out to cause the osmotic pressure of the interstitial cavity colloid to rise, which promotes the formation of pulmonary edema.
When the lymphatic function is normal, the remission ability is large, and the lymphatic drainage can be increased to more than 10 times of the normal level. Pulmonary edema can only be formed when the amount of fluid filtered out of the pulmonary capillaries exceeds the compensatory capacity of lymphatic drainage, or the drainage is reduced due to pathological conditions leading to lymphatic dysfunction, or lymphatic function cannot exert compensatory capacity.
The intrapulmonary edema fluid initially accumulates in the interstitial space between the alveolar capillaries, and then flows to the loose interstitial space above the alveolar duct, including the small pulmonary vessels and the small airway and the interlobular septa, which is called "interstitial pulmonary edema". . If there is too much liquid in the interstitial, the tension will increase, which can cause the liquid to enter the alveoli and form "alveolar pulmonary edema."
Pathology: The surface of the lungs was pale, the wet weight increased significantly, and a large amount of liquid exuded from the cut surface. Microscopically, extensive pulmonary congestion can be seen. The interstitial space, alveolar and bronchioles are filled with protein-containing fluids. There are transparent membranes in the alveoli. Sometimes interstitial hemorrhage and alveolar hemorrhage can be seen. Microthrombus formation can be seen in the pulmonary capillaries. Visible atelectasis.
Examine
an examination
According to the history, symptoms, physical examination and X-ray findings, pulmonary edema can be clearly diagnosed, but obvious X-ray changes can occur when the lung water content increases by more than 30%. CT and MRI can be used to help early stage if necessary. Diagnosis and differential diagnosis.
Diagnosis
Differential diagnosis
1. According to the history, symptoms, physical examination and X-ray findings, pulmonary edema can be clearly diagnosed, but obvious X-ray changes can occur when the lung water content increases by more than 30%. CT and MRI can be applied if necessary. Help early diagnosis and differential diagnosis.
Heat transfer dilution method and plasma colloid osmotic pressure: Pulmonary capillary wedge pressure gradient measurement can calculate pulmonary extravascular water content and determine whether there is pulmonary edema, but need to indwell the pulmonary artery catheter for traumatic examination. When the lung perfusion scan is performed with 99mTc human hemoglobin microcapsules or 113mIn transferrin, if the vascular permeability is increased, it can accumulate in the pulmonary interstitium, and the permeability-enhancing pulmonary edema is particularly obvious. In addition, cardiogenic and non-cardiogenic pulmonary edema are treated differently, and both should be identified.
2. It is also differentially diagnosed with lung diseases such as acute lung infarction, bronchial asthma, and tension pneumothorax.
