Pulmonary Edema
Introduction
Introduction to pulmonary edema Pulmonary edema (pulmonaryedema) 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 The lungs are full of symmetrical wet snoring sounds. X-ray chest radiographs can be seen in the blister-like blushing shadows of the two lungs. In the late stage, shock or even death may occur. The arterial blood gas analysis may have low O2, low CO2 partial pressure, and severe O2 deficiency. CO2 retention and mixed acidosis are one of the clinical critical illnesses. basic knowledge Sickness ratio: 0.05% Susceptible population: more common in patients with severe pneumonia Mode of infection: non-infectious Complications: disseminated intravascular coagulation
Cause
Cause of pulmonary edema
Environmental factors (65%):
The condition of contact with the plateau: it is the first time to enter the plateau or return to the plains for a period of time to return to the plateau, or from the plateau to another higher. The altitude of the affected area. From the time you enter the plateau to the time of onset. After the illness, there is no history of oxygenation or transfer to a low place (below 3001m). There are no similar symptoms before or after entering the plateau.
Other factors (35%):
There are no obvious incentives for the onset, such as excessive speed, physical activity, cold or climate change, hunger, fatigue, insomnia, motion sickness, emotional stress, upper respiratory tract infection and other factors.
Pathology :
The surface of the lungs is pale, the wet weight is obviously increased, and there is a large amount of fluid exudation on the cut surface. Under the microscope, extensive pulmonary congestion, interstitial space, alveolar and bronchioles are filled with protein-containing liquid, and a transparent film is formed in the alveoli, sometimes visible. Interstitial hemorrhage and alveolar hemorrhage, microthrombus formation in the pulmonary capillaries, and sometimes focal atelectasis.
Prevention
Pulmonary edema prevention
Before entering the plateau, learn more about the climate characteristics of the plateau, understand the knowledge about altitude sickness and eliminate the fear of the high altitude environment; before entering the plateau, you must make strict health checks; pay attention to keep warm and prevent cold. In the first week of the plateau, pay attention to rest, gradually increase the amount of activity, reduce and avoid strenuous exercise, avoid excessive fatigue; people suffering from high altitude pulmonary edema are prone to recurrence; drug prevention: high altitude, Rhodiola capsule.
Complication
Pulmonary edema complications Complications, disseminated intravascular coagulation
Concurrent DIC, acid-base balance disorders, various systems of various organs are damaged, and eventually lead to multiple organ failure.
Symptom
Pulmonary edema symptoms Common symptoms Snoring, breathing, dyspnea, phlegm, lung ventilation, blood flow ratio, mixed acid-base balance disorder, cardiovascular blockage, hilar shadow, cough, dyspnea, edema, difficulty in breathing, purpura, lung dysfunction
1, typical acute pulmonary edema, can be divided into four periods according to the pathological process, the clinical symptoms and signs of each period are described as follows.
(1) Interstitial edema: mainly manifested as nocturnal dyspnea at night, forced to sit with cold sweat and restlessness, cyanosis of the lips, both lungs can smell dry or wheezing, tachycardia, blood pressure rise High, at this time due to pulmonary interstitial edema and increased pressure, small bronchial pressure is narrowed and hypoxia caused by bronchospasm.
(2) Alveolar edema: mainly manifests severe dyspnea, is sitting breathing, with fear of suffocation, complexion, gray, skin and lips, cyanosis, sweating, coughing, coughing a lot of pink foamy sputum, urine Incontinence can occur, and the two lungs are full of sudden wet voice. If it is a cardiogenic person, the heart rate is fast, the arrhythmia is abnormal, the first heart sound of the apex is weakened, and the pathological third heart sound and the fourth heart sound can be heard.
(3) Shock period: a large amount of extravasation of plasma in a short period of time, resulting in a rapid decrease in blood volume in the short term, hypovolemic shock, and a significant decrease in myocardial contractility, causing cardiogenic shock, shortness of breath, and decreased blood pressure , the skin is damp cold, oliguria or anuria and other shock performance, accompanied by consciousness, change of consciousness.
(4) End-stage: in a coma, often dying due to heart and lung failure.
2, different causes of different types of pulmonary edema, clinical manifestations and control measures have their commonalities, but also have individual characteristics.
(1) Cardiac pulmonary edema: a common clinical pulmonary edema caused by left heart failure or mitral stenosis, mainly characterized by difficulty breathing, cyanosis, cough, cough pink foam, and full lungs Dry voice, extensive wet voice at the bottom of the lungs, X-ray chest radiograph showing butterfly-like shadows on both sides of the lung, rheumatic valvular heart disease, hypertensive heart disease, coronary heart disease, myocardial infarction, congenital cardiovascular malformation, etc. As a common cause, left heart failure, due to insufficient left ventricular bleeding or obstruction of left atrial blood flow, resulting in increased left atrial pressure, pulmonary capillary hydrostatic pressure increased, fluid filtered through the pulmonary capillary wall to form pulmonary edema Mitral stenosis due to blood flow into the left ventricle blocked, causing increased left atrial pressure, chronic interstitial pulmonary edema, infection, severe labor, tachycardia and pregnancy can also cause acute alveolar stenosis induced by mitral stenosis Pulmonary edema, specific clinical manifestations, diagnosis, treatment as previously described.
(2) High altitude pulmonary edema: It is one of the most serious types of acute high altitude disease. It is caused by pulmonary edema caused by high altitude hypoxia, rapid ascending, severe physical labor and cold are the cause of the disease. The minimum incidence height is 2600m. However, most of the people who entered the altitude of 4000m above the first time, those who are young and not adapted to the plateau environment, or those who have adapted to return to the plateau after a few weeks of living in the lowland are more susceptible to disease, and the plateau adaptors quickly rise to higher areas. It will be complicated, and the disease is often recurred. The pathogenesis is not clear. The possible factors are: 1 hypoxia through the action of neurohumoral fluid to cause pulmonary arteriolar contraction and pulmonary hypertension; 2 extensive thrombosis in the pulmonary capillaries, making the pulmonary capillaries Wall permeability changes; 3 hypoxia causes hyperventilation, arterial blood CO2 partial pressure drops, leading to respiratory alkalosis, aggravating tissue hypoxia; 4 hypoxia causes peripheral vasoconstriction, blood redistribution leads to increased pulmonary blood volume; Exercise also increased the amount of blood in the right heart, leading to excessive lung circulation; 6 individual factors.
Clinical manifestations: patients with high altitude pulmonary edema have a special dark gray face, lips and limbs with prominent cyanosis and apathy; severe cases are awkward and extremely exhausted, with more than 80% of patients having headache, dizziness, insomnia, loss of appetite , fatigue, oliguria, chest tightness, shortness of breath, difficulty breathing and coughing, more than half of the patients have palpitations, sitting breathing, nausea, vomiting, chills, fever and coughing pink foam sputum, critical cases have a large number of bloody foam Nasal cavity and mouth gushing out, a few cases have chest pain, abdominal distension and abdominal pain, signs of typical pulmonary edema, according to the lung lesions of the high altitude pulmonary edema lesions are divided into the following three types: central type: about 25 %, characterized by the distribution of lesions along the vascular and bronchial regions of the hilar region, with speckled or patchy smear, mostly with a butterfly-like oozing shadow centered on the hilum, and an enlarged lung shadow with increased lung texture Thick, carefully observed visible floc doping in the fuzzy lung texture, focal type: about 20%, characterized by lesions confined to one side or bilateral lung fields, in both sides, The distribution of shadows in the lungs is mostly asymmetrical, and the symmetry is distributed in the lower lungs. The shadows are mostly of different sizes. The clouds of uneven density are sometimes fused into a cotton mass, the edges are blurred and are not restricted by the leaf gap. Type: about 55%, characterized by a wide range of lesions, more common in the two lungs, the lower field, or spread to the upper, middle, and lower fields, the flaky floc density is higher, sometimes blended into cotton lumps, mostly located in the middle, inside band.
(3) Neurogenic pulmonary edema: It is a pulmonary edema that occurs after various central nervous system injuries, but no primary heart, lung, kidney and other diseases, also known as "brain-derived pulmonary edema". Common causes are Acute and severe cerebrovascular diseases, such as cerebral hemorrhage, cerebral embolism, subarachnoid hemorrhage, hypertensive encephalopathy, meningeal and brain inflammation, brain tumors, brain abscess, convulsions or status epilepticus, and cranial brain injury The disease with increased internal pressure has not yet been elucidated. It is currently considered to be related to the following factors:
1Intracranial pressure caused by various acute central nervous system injury, high intracranial pressure caused hypothalamic dysfunction, sympathetic nerve excitation, catecholamine release, causing severe contraction of blood vessels around the body, increased blood flow resistance, and a large amount of blood in the body circulation Entering the pulmonary circulation, the blood volume of the pulmonary circulation increases sharply. At the same time, the vasoactive substances such as prostaglandins, histamine and bradykinin are released in large amounts, which increases the permeability of the pulmonary capillary endothelium and alveolar epithelium, and increases the hydrostatic pressure of the pulmonary capillaries. The arterio-venous shunt increases the burden on the left heart and causes left heart failure to further aggravate pulmonary congestion.
2 cerebral hypoxia, animal experiments show that cerebral hypoxia can also cause reflex, pulmonary edema occurs in the pulmonary venules through the autonomic nervous system. There are data showing that pulmonary edema has occurred 2 hours after acute cerebral ischemia.
3 In the acute injury of the central nervous system, vomiting aspiration of acidic gastric juice with pH <2.5 can cause damage to lung tissue.
4 damage and free radical theory, after severe damage to the central nervous system, can promote free radical-induced lipid peroxidation, resulting in secondary brain damage, aggravating brain edema and pulmonary edema.
Clinical manifestations of acute central nervous system injury, sudden dyspnea, respiratory rate > 35 times / min, three concave signs and cyanosis, cough, cough pink or white foamy sputum; blood pressure increased, at 26.7/14.7 Above kPa, lower in the late stage, the body can be smelled and the lungs are wet or wheezing; the chest radiograph shows enhanced lung texture, butterfly-like or intrapulmonary flake shadows; blood gas analysis has different degrees of PaO2 reduction and PaC02 is elevated.
(4) Relapsing pulmonary edema: refers to the intrapulmonary fluid leakage caused by impaired pulmonary capillary wall integrity during or after resuscitation of the lungs after multiple stages of lung collapse at various times due to various causes. Move into the alveoli, resulting in acute non-cardiac unilateral pulmonary edema, more common in a large number of pneumothorax or chest hydraulic lung tissue and rapid venting or drainage, and due to huge tumor compression or blood clots obstructive atelectasis It is rare to induce recurrent pulmonary edema after total re-expansion. The longer the lung collapse time, the higher the incidence of pulmonary edema after re-expansion. It is reported that the incidence of pulmonary edema is 17% after 3 days of lung collapse. 85% after 8 days,
(5) Oxygen-induced pulmonary edema: Oxygen poisoning is a long-term inhalation of high concentration (>60%) of oxygen can cause lung injury, inhalation of pure oxygen at normal pressure for 12 to 24 hours or under high pressure oxygen for 3 to 4 hours. Poisoning, tissue damage caused by oxygen poisoning is caused by the lungs. Due to the sudden increase of oxygen concentration in the alveoli, a large amount of reactive oxygen species can be generated. Under high oxygen environment, the neutrophils are aggregated and activated by the activation of the complement system, producing a large amount of active oxygen. When the scavenging capacity of the antioxidant system is exceeded, pulmonary capillary endothelial cells, pulmonary interstitial and alveolar epithelial cells may be damaged, and the permeability of the alveolar capillary membrane may be increased to cause osmotic pulmonary edema, and the active oxygen may also occur. Inactivation of 1-antitrypsin, increased protease activity, increased malondialdehyde and arachidonic acid metabolites, etc., exacerbate pulmonary alveolar capillary damage and cause pulmonary edema. In addition, oxygen poisoning also damages type II alveoli. Epithelial cells reduce the alveolar surfactant and increase the surface tension of the alveoli, causing the fluid in the pulmonary capillaries to infiltrate the alveoli, aggravating pulmonary edema, clinically tight under the sternum, and chest pain is the first to oxygen poisoning. Symptoms, with dry cough, gradual dyspnea, fever, respiratory function changes, lung compliance, right to left shunt, causing hypoxemia, extensive wet voice in the lungs, fine mesh on X-ray Weaving or flaky shadows, severe glassy changes, oxygen poisoning inhibit airway mucus-cilia clearance, often induce respiratory infections, clinical oxygen therapy must always be alert to the possibility of oxygen poisoning, oxygen concentration to maintain PaO2 at 8.0kPa Low safety level, unless there is absolute indication, the oxygen concentration does not exceed 60%, hyperbaric oxygen treatment, such as at 2 atmospheres, inhalation of pure oxygen does not exceed 4h, 3 atmospheres, no more than 2h, when oxygen poisoning aura occurs Take measures such as continuous pressurized breathing or positive end expiratory pressure and correspondingly reduce the oxygen concentration.
(6) Inhaled pulmonary edema: Inhalation of the food, stomach contents or other hydrocarbon liquids into the respiratory tract can cause bronchial-pulmonary damage, cause aspiration pneumonia, and can also cause pulmonary edema. The main predisposing factors are:
1 Reflex protection dysfunction: If the mind is unclear, the pharyngeal reflection of the inhalation is weakened, most commonly during surgical anesthesia, easy to inhale the stomach contents; also seen in drunkenness, vomiting, anesthesia sedative overdose, cerebrovascular accident, Myasthenia gravis, infectious polyradiculitis, and central nervous system diseases such as epilepsy.
2 pathological anatomical abnormalities: such as congenital, traumatic or cancerous bronchial-esophageal fistula, esophageal diverticulum, achalasia and so on.
3 iatrogenic factors: such as gastric tube (nasal feeding tube affects the reflection of epiglottis and stimulates vomiting, tracheotomy sleeve inhibits pharyngeal movement, may lead to vomit inhalation into the respiratory tract, the severity of inhaled pulmonary edema and inhalation The pH, the amount of inhalation, the toxicity of the inhalation, the osmotic pressure of the inhalation, and the severity of the primary disease and the patient's reactivity. Inhalation of gastric contents containing hydrochloric acid is particularly prone to pulmonary edema and gastric acid irritations. Inflammatory cell infiltration around the bronchi and bronchi, alveolar epithelial cell damage, destruction of capillary endothelial cells, exudation of intravascular fluid into surrounding tissues, leading to extensive hemorrhagic bronchial pneumonia with destruction of alveolar capillary membrane, pulmonary interstitial congestion Edema, alveolar edema, the patient can have no obvious symptoms within 1 to 3 hours after inhalation, followed by a sudden increase in shortness of breath, followed by cyanosis, palpitations and hypotension, bloody foam and lungs, inhalation In the early stage, X-ray performance can be normal, with the appearance of symptoms, showing a diffuse patch of lung infiltration shadow, due to type II lung Destruction of vesicular epithelial cells and pulmonary edema fluid should be used for tracheal intubation plus mechanical respiration, commonly used for positive end-expiratory breathing (PEEP), suitable for colloidal fluids such as dextran 40 (low molecular dextran) and human serum albumin (albumin) In order to reduce pulmonary edema, but should pay attention to avoid excessive burden of left ventricular and leakage of colloidal fluid into the interstitial lung, aggravate pulmonary edema, early application of adrenal cortex hormones, diuretics, etc., the disease prevention is more important than treatment.
(7) Infectious pulmonary edema: pulmonary edema secondary to systemic infection and/or pulmonary infection, sepsis caused by Gram-negative bacilli infection is the main cause of pulmonary edema, increased pulmonary capillary permeability As a result, there is no bacteria in the lungs to multiply, pulmonary edema can also be secondary to viral infections, such as influenza virus and varicella virus, the main cause of pulmonary edema is the increased permeability of the pulmonary capillary wall, onset 24 ~ After 48 hours, the patient's cough, dyspnea, hemoptysis, high fever, physical examination and chest X-ray showed typical pulmonary edema changes, treatment mainly for the cause, active anti-infection and oxygen therapy.
(8) Other:
1 excessive anesthesia poisoning can cause pulmonary edema, seen in morphine, methadone (mesophage), barbiturate and other poisoning, the mechanism of the respiratory center is extremely inhibited, severe hypoxia, leading to increased capillary wall permeability; The stimulating response of oxygen to the hypothalamus causes contraction of peripheral blood vessels, and redistribution of blood leads to an increase in pulmonary blood volume.
2 drowning pulmonary edema refers to pulmonary edema caused by fresh water and seawater drowning. After a large amount of inhalation of hypotonic fresh water, it quickly enters the blood circulation through the alveolar-capillary membrane, causing a sudden increase in blood volume. If the myocardial function is impaired, the left ventricle Pulmonary edema can be induced when the load required for blood volume increase cannot be increased; seawater is hyperosmotic. After entering the lungs, a large amount of water is circulated from the blood into the alveoli causing pulmonary edema, and pulmonary edema caused by hypoxia caused by pulmonary edema Endothelial cell damage leads to increased permeability, which intensifies pulmonary edema.
3 uremic pulmonary edema, renal dysplasia often occurs in patients with renal failure, the main factors are: A. hypertension, atherosclerosis caused by left heart failure; B. oliguria caused by water or excessive infusion of blood Increased volume; C. Increased permeability of pulmonary capillary wall may be due to allergic reaction; D. Reduced plasma protein, decreased intravascular colloid osmotic pressure, increased gap between hydrocapillary hydrostatic pressure and colloid osmotic pressure, promotes lung Edema is formed.
4 gestational toxic pulmonary edema, pregnancy-induced poisoning patients with pulmonary edema are related to the following factors.
A. Endocrine or biochemical factors associated with placenta cause extensive contraction of peripheral arteries and hypertension, left heart failure and increased pulmonary venous pressure.
B. Aldosterone, secretion of vasopressin and renal sodium, water retention.
5 pulmonary edema after cardioversion, electroacupuncture treatment of arrhythmia within 1 to 3 hours after a few patients with pulmonary edema, and all have occurred in the case of sinus rhythm, may be caused by electric shock to inhibit left atrial function, Also considered to be caused by pulmonary embolism.
6 Occupational toxic pulmonary edema refers to pulmonary edema caused by occupational exposure to irritating harmful gases or poisons. Industrial gases that are prone to pulmonary edema mainly include nitrogen dioxide, chlorine, chlorine oxides, phosgene, ammonia, and fluorine. Compound, ozone, sulfur dioxide, cadmium oxide, selenide, dimethyl sulfate, formaldehyde, etc., the pathogenesis is related to the following factors: A. Allergic reaction caused by irritating gas or direct damage increases the permeability of pulmonary capillary wall; Damage to alveolar surfactants; C. Pulmonary vein contraction and lymphatic fistula caused by neurohumoral factors; D. Organophosphorus pesticides combined with cholinesterase inhibiting enzymes, causing accumulation of acetylcholine in the body leading to massive secretion of bronchial mucus, bronchi Hemorrhoids, respiratory muscles and respiratory center paralysis cause hypoxia and increased permeability of the pulmonary capillary wall.
Examine
Pulmonary edema examination
1, laboratory tests: including blood, urine routine, liver, kidney function, cardiac zymogram and electrolyte examination, provide clues for the diagnosis of infection, hypoproteinemia, kidney disease, heart disease.
2, arterial blood gas analysis : oxygen partial pressure in the early stage of the disease mainly showed hypoxia, oxygen can make PaO2 significantly increased, carbon dioxide partial pressure in the early stage of the disease mainly showed low CO2, late in the emergence of high CO2, respiratory acidosis and Metabolic acidosis.
3, X-ray examination : only when the extra-pulmonary fluid volume increased by more than 30%, the chest X-ray examination showed abnormal shadows.
(1) Ordinary fluoroscopy: the main X-ray findings of interstitial pulmonary edema:
1 Interval line: It is an important X-ray performance. There are more opportunities in A and B lines, and the diagnosis is easier. The rapid change of appearance and disappearance is a characteristic of acute pulmonary edema. Its appearance time is often earlier than clinical symptoms. A very valuable indicator of the degree and efficacy of left heart failure, line A: a line-like shadow from the periphery of the lung field to the hilar, about 4 cm long, 0.5 to 1 mm wide, more common in the upper lung field, acute left heart failure More common, B line: more common in the rib angle, is about 2 ~ 3cm horizontal horizontal line, width is also 0.5 ~ 1mm, is the most common in the interval line, more common on the right side, C line: rare, for each other Interlaced into a grid-like linear shadow, visible in any part of the lung, D line: often from the front pleural surface to the back, about 4 ~ 5cm long, 2 ~ 4mm wide, more common in the tongue and middle leaves, so in the lateral position The chest radiograph shows better.
2 subpleural edema: pleural thickening at the pleural and rib angles between the leaves, sometimes a small amount of pleural effusion.
3 hilar shadow: blurred and enlarged.
4 Peri-bronchial and perivascular shadow enhancement (cuff sign): The outer diameter of the bronchial and vascular sections is increased and the edges are blurred.
5 other: heart changes, thickening of the lungs and enlargement of the upper pulmonary veins.
(2) Ordinary fluoroscopy: There are many types of X-ray manifestations of alveolar pulmonary edema, the same characteristics are rapid changes in the short-term, typical X-ray manifests as a fan-shaped shadow extending from the hilum to the lung field, in the bilateral hilum The outer side forms a butterfly shape, and unilateral pulmonary edema may also occur. The X-ray manifests as a unilateral or a leafy patchy shadow, which is easily misdiagnosed and is common in long-term bedridden patients, especially those lying on the side.
Alveolar pulmonary edema:
1 Alveolar solid shadow, early nodular shadow, about 0.5-1cm size, blurred edges, and soon merge into patch or large shadow, with air bronchoscopy image. Uniform density.
2 The distribution and morphology are diverse, which can be central, diffuse and limited. The central type is characterized by large symmetrical shadows in the two lungs. The density of the hilar region is high. Wing sign, limited type can be seen on one side or one leaf, more common on the right side, in addition to the flaky shadow, it can also show one or several large circular shadows, and the contour is clear like a tumor.
3 dynamic changes: pulmonary edema initially occurs in the lower part of the lungs, the medial and posterior, and soon to the upper part of the lung, the lateral and anterior development, the lesion often changes significantly within a few hours.
4 pleural effusion: more common, mostly a small amount of effusion, bilateral.
5 heart shadows increase.
In addition to the above image features, renal pulmonary edema can also have the following characteristics:
1 pulmonary blood vessel shadows are generally thickened.
2 vascular pedicle widening.
3 diffuse distribution: seen in chronic nephritis uremia, with more shadows in the lungs.
The X-ray manifestations of interstitial phase of pulmonary edema are mainly due to blurred and increased pulmonary vascular texture, unclear hilar shadow, decreased lung translucency, widened interlobular septal space, and perpendicular pleural effusion in both lung ribs. Kerley B line, occasionally the upper lung is curved oblique lung door Kerer A line longer than Kerley B line, alveolar edema mainly manifests as acinar dense shadow, irregularly blending fuzzy shadows, diffuse distribution or limited to one Side or a leaf, or outward from the lung door to gradually fade into a typical butterfly-like shadow, sometimes with a small amount of pleural effusion, but the lung content increased by more than 30% can appear above.
4, cardiac catheterization: Swan-Ganz catheter examination bed intravenous Swan-Ganz catheter examination of pulmonary capillary wedge compression (PCWP), can be identified pulmonary pulmonary hypertension increased pulmonary edema, but PCWP height is not necessarily associated with pulmonary edema The degree is consistent, Swan-Ganz catheter is often retained for several days, as a monitoring of cardiogenic pulmonary edema, guiding clinical treatment, maintaining PCWP between 1.9 ~ 2.4kPa.
5, other examination methods : in the past many methods of measuring extravascular water (EVLW), such as X-ray, thermal indicator dilution technology, soluble gas inhalation, transpulmonary electrical impedance, CT, magnetic resonance imaging, etc., pulmonary edema microvascular-alveolar Early judgment of barrier damage is not sensitive. In recent years, the permeability of pulmonary vascular endothelium was evaluated by in vitro determination of the net flow of isotope-labeled proteins (usually 99mTc) through the pulmonary capillary endothelium; by measuring alveolar isotope small molecules (radiolabeled proteins) , 99mTc-DTPA) clearance, evaluation of alveolar epithelial permeability, can determine the extent of lung injury earlier, these methods provide an advanced and effective means for early diagnosis of pulmonary edema, but still need further improvement.
Diagnosis
Diagnosis of pulmonary edema
diagnosis
According to medical history, clinical symptoms, signs and X-ray findings, general clinical diagnosis is not difficult, but there is still no satisfactory, reliable early quantitative diagnosis of pulmonary edema, clinical symptoms and signs as a basis for diagnosis, low sensitivity, when the pulmonary vessels When the external fluid is increased by 60%, abnormal signs appear in the clinic. X-ray examination only shows abnormal shadow when the lung water volume increases by more than 30%. CT and MRI can help quantitative diagnosis and distinguish between pulmonary congestion and pulmonary edema. Colloid osmotic pressure-pulmonary capillary wedge pressure gradient measurement, radionuclide scanning, indicator dilution method for measuring pulmonary extravascular fluid, chest electrical impedance measurement, etc., are helpful for early diagnosis, but have not been used in clinical, blood gas analysis has Helps to understand the severity of arterial oxygen partial pressure, carbon dioxide partial pressure and acid-base balance imbalance, and can be used as a follow-up indicator of dynamic changes.
Differential diagnosis
1, according to medical history, symptoms, physical examination and X-ray findings can often make a clear diagnosis of pulmonary edema, but due to increased lung water content more than 30% can appear obvious X-ray changes, if necessary, CT and MRI can be applied To help early diagnosis and differential diagnosis, thermal conduction dilution method and plasma colloid osmotic pressure pulmonary capillary wedge pressure gradient measurement can calculate pulmonary extravascular water content and determine the presence or absence of pulmonary edema, but need to indwell the pulmonary artery catheter, for traumatic examination, with 99mTc When human hemoglobin microcapsules or 113mIn transferrin are used for lung perfusion scan, if the vascular permeability is increased, it can accumulate in the interstitial lung, and the permeability-enhancing pulmonary edema is particularly obvious. In addition, the cardiogenic and non-cardiac Primary pulmonary edema differs in handling.
2, also with lung diseases such as acute lung infarction, bronchial asthma, tension pneumothorax and other differential diagnosis.
