Pulmonary edema is a serious pathological condition that threatens not only the health, but also the life of the child. Pulmonary edema in children characterized by the accumulation of fluid from blood plasma in the lung tissue. The condition is not considered as separate disease, but as a complication of a number of diseases.
In newborns, pathology develops due to prematurity and immaturity respiratory system, it can be triggered by oxygen deficiency in the prenatal period.
The main causes of edema in older children are acute inflammatory processes in the respiratory tract, foreign body or water, massive therapeutic infusions for acute pneumonia.
The condition can also be caused by other diseases:
The mechanism of development of edema in the lungs
The development of the condition is due to increased permeability vascular wall and an increase in hydrostatic pressure. The liquid part of the blood, plasma, sweats first into the interstitial and then into the alveolar tissue. Normal gas exchange is disrupted: the blood does not supply organs and tissues with oxygen, and there is no outflow of metabolic products and carbon dioxide. Acute oxygen starvation(hypoxia) leads to disruption of the functioning of all systems.
The condition often develops at night, the child takes a forced position and suffers from the following symptoms:
Interstitial and alveolar pulmonary edema
- two successive phases of one severe pathological condition. The interstitial process affects the lung parenchyma. If treatment is not received, the condition progresses to alveolar edema. Fluid from the lung parenchyma overcomes the walls of the alveoli and enters their space. At this stage, the cough changes from dry to wet and pink, foamy sputum is formed or bleeding begins. The child turns blue, breathes deeply and frequently, his face becomes puffy, and the neck veins swell. The outcome of the condition is decided by minutes, timely comprehensive intensive therapy gives a chance for recovery.
Time of development of pulmonary edema
The time it takes for harmful symptoms to develop affects the prognosis of the condition and has the following options:
An experienced doctor can predict the outcome of the condition based on the degree of moisture in the child’s skin. A dry body or light sweat on the forehead are favorable prognostic signs. Underwear wet with sweat characterizes serious condition life-threatening.
Therapeutic measures are started by ambulance workers urgently at home and continue in a hospital setting.
To avoid serious consequences of pulmonary edema, you should know what the signs, causes and methods of treating this condition in patients are. This pathology is characterized by impaired pulmonary gas exchange and the development of oxygen deficiency in the blood. In this case, hypoxia itself is accompanied by damage to the alveolocapillary membranes, which leads to their high permeability - the first stage of pulmonary edema.
Pathological condition caused by increased levels tissue fluid, called pulmonary edema. Lung pathology occurs in 2 stages:
Edema respiratory tract appears suddenly and develops quickly. TO clinical symptoms diseases in adults include:
Symptoms of pulmonary edema in a child appear clearly, so it is easy to recognize the pathology. Children have a cough with prolonged wheezing, they begin to choke, especially in a horizontal position, and thick sputum with a pink tint appears. In addition, the child refuses to eat, sleeps poorly and behaves restlessly due to chest pain. Older children about this pain syndrome They say. When fluid is retained in the lungs, parents notice ragged breathing and pale skin that may turn blue and become covered in sweat. You also need to pay attention to an increased heart rate.
What causes pulmonary edema? There are many reasons for the development of lung pathology. They are associated with cardiology, pulmonology, nephrology and other areas of medicine. So, the causes of pulmonary edema may be the following:
Main reason pulmonary disease in elderly patients there is blood stagnation, which develops due to prolonged lying down. Signs of congestion are similar to symptoms of respiratory failure. Other reasons for the development of the pathological condition include:
In a horizontal position, much less air enters the body than in a vertical position. Due to the fact that breathing activity is reduced, blood flow in the lungs decreases and congestion occurs. Thus, sputum accumulates, the expectoration of which in a horizontal position is difficult - the process of stagnation progresses. In addition, sputum contains components that cause inflammation. The gradual development of pulmonary edema is typical for many bedridden patients.
Depending on the reasons, causing pathology, experts distinguish 2 types of pulmonary edema:
Non-cardiogenic pulmonary edema also has subtypes, which can be used to describe the patient’s condition in more detail in order to use suitable treatment:
In addition to classification by pathogenesis, pulmonary edema is distinguished by the course of the condition. So, they highlight following forms:
The disease is a very serious pathological condition that requires timely treatment. If you do not meet the deadlines or carry out therapeutic measures incorrectly, the following dangerous complications may arise:
In order to diagnose pulmonary edema, several measures are carried out. The main methods of examination include the following:
The treatment strategy for the pathology is to eliminate the causes and signs of pulmonary edema in order to alleviate the patient’s condition. Doctors perform the following actions:
If you notice symptoms of pulmonary edema, you should immediately call doctors, and before their arrival, first aid for pulmonary edema is carried out. You should:
While performing the above actions, it is necessary to constantly monitor the patient’s pulse and breathing. Upon arrival, doctors will provide emergency therapy to reduce the load on the circulatory and respiratory systems, normalize blood pressure and reduce foaming:
If it develops pulmonary edema for heart disease, for normalization high blood pressure and if there are signs of myocardial ischemia, nitrates are used. A representative of this group is Nitroglycerin, which quickly relieves ischemic attacks and angina. Contraindications include: hypersensitivity, head injuries, pregnancy and breastfeeding ( breast-feeding). With low blood pressure, the patient is given drugs to increase heart contraction - the stimulant Dobutamine.
To remove excess fluid from the body, diuretics or diuretics are used. Lasix is a “loop” diuretic drug that enhances the excretion of water and increases the excretion of potassium, magnesium, and calcium. The drug is contraindicated in severe kidney and liver diseases, increased central venous pressure, and hypersensitivity to furosemide.
For symptoms of bronchospasm, steroid hormones are taken. One of them is Prednisolone, which has anti-inflammatory, antiallergic, and glucocorticoid effects. The drug has practically no contraindications - only the presence of fungal infections and increased sensitivity to the components of the drug.
By effective means To eliminate foaming during pulmonary edema, antifoam agents are used. Their action is to increase the surface tension of the liquid, which helps stop the formation of hemorrhagic foam. The main defoaming agents include ethyl alcohol. Air or oxygen is passed through 30-90% ethanol, after which the patient breathes it. If alcohol turns out to be ineffective, Antifomsilan solution is used.
After emergency care, the patient may experience complications. The main ones include:
Pulmonary edema contributes to the creation favorable conditions for damage to internal organs. Thus, the consequences of lung pathology are varied:
Survival after surgery pulmonary disease accounts for 50% of cases, while most patients have abnormalities in the body. If you do not see a doctor in the clinic for the next year and do not cure the cause of the lung pathology, the probability of relapse is 100%. Only the right therapeutic measures can ensure a positive prognosis. If you want to avoid such a pathology, you should carry out prevention:
Pulmonary edema in humans is an immediate threat to life and requires urgent measures before hospitalization.
This pathological process is not an independent disease. He is already developing as a complication existing disease . Therefore, in order to avoid the occurrence of swelling, adequate treatment of all existing pathologies, especially those associated with the cardiovascular system, should be carried out.
The cause may be pathologies that are accompanied by the entry of various types of toxins into the body. These include pneumonia and pleurisy, sepsis, as well as all types of poisoning (medicines, drugs, poisons, and so on). The pathological process in this case develops due to increased permeability of the alveolocapillary membrane.
Heart disease in the decompensation stage can result in the accumulation of fluid in the alveoli. This phenomenon occurs due to stagnation of blood in the pulmonary circulation. Pressure increases in the capillaries of the lung tissue, which leads to swelling. In addition to heart pathologies, bronchial asthma and emphysematous expansion of lung tissue act in the same way.
Thromboembolism can lead to pulmonary edema pulmonary artery. It is a consequence of the detachment of a blood clot from blocked veins lower limb or after operations, when there is hypercoagulation in the blood.
Most common etiology pulmonary edema - acute heart failure.
Also, the causes of this condition in adults can be those diseases in which there is a decrease in protein in the body. These include almost all kidney pathologies, as well as liver cirrhosis. By the same principle, swelling is provoked by intravenous transfusions of various solutions in large volumes.
This type of edema is caused by acute heart failure. Pathology begins to develop at night or early in the morning. It is provoked by psychological and physical nature or other sudden changes in the body. A characteristic sign of the cardiogenic form of the pathological process is decompensated cardiac dysfunction. When conducting differential diagnosis detect changes in the ECG and a decrease in ejection fraction.
This type of pathology rarely affects children, and in adults the symptoms of pulmonary edema are as follows::
Doctors can use auscultation to detect hard wheezing in a patient, which over time turns into moist wheezing of various sizes. When providing assistance, it is important to monitor blood pressure, which during pulmonary edema can drop so much that the heart stops. Doctors also stop the progression of hypoxia, which affects everything internal organs, especially the brain.
The clinical picture of toxic damage has some features that make it possible to distinguish it from other forms. Only this type of swelling can be asymptomatic, detected using laboratory and instrumental methods.Toxic edema can occur in extensive and abortive forms.
The first signs of pulmonary edema are reflex disorders, in which patients note tearfulness, hacking cough, headaches, general weakness and dizziness. At this time, the risk of death from cardiac or respiratory arrest is high. Then several hours pass latent period edema, in which there is no clinical picture, but the condition progressively worsens.
This form of the pathological process is characterized by the presence of a period where there is a high risk of re-accumulation of fluid. This is due to the phenomena of heart failure, which can develop against the background of the first attack of edema. Therefore, toxic damage requires the longest observation in a hospital.
Pulmonary edema can be divided into 4 main forms of course: acute (the peak occurs within 2-4 hours), subacute (up to 12 hours), fulminant (death within a few minutes) and prolonged.
With a protracted form of the pathological process, the increase in symptoms continues for more than a day.
This pulmonary edema manifests itself gradually, beginning to bother the patient with attacks of shortness of breath during physical exertion. Gradually the condition progresses, tachypnea develops. Breathing increases up to 40-50 times per minute. Patients complain of dizziness and general malaise. Over time, the clinical picture worsens and develops into typical symptoms of an acute pathological process.
However, already at the very beginning of fluid accumulation in patients, gurgling wheezing in the lungs can be heard. This indicates a small amount of transudate in the alveoli. In addition, there are signs of pulmonary emphysema. If the doctor reacts at this stage of the development of the condition, he will be able to avoid taking many potent drugs and prevent serious hypoxia of the body.
A protracted course of the pathological process is typical for people with chronic diseases. For example, heart failure or kidney pathology. Gradually progressive liver cirrhosis also leads to slowly progressive pulmonary edema.
First of all, swelling can be recognized by its typical clinical picture. You can also ask the patient or people nearby about the events that preceded the deterioration of the condition. It's important to know about serious illnesses patient. At the emergency stage medical care emergency measures begin without obtaining additional examination data.
In bedridden patients, edema progresses faster, so treatment begins with simultaneous clinical studies.
First of all, the phenomena of hypoxia during edema are identified by determining the partial pressure of oxygen and carbon dioxide. Then a biochemical blood test is performed, which can indirectly indicate the etiology of the edema. Biochemistry is also taken to clarify the diagnosis and confirm myocardial infarction if its presence is suspected. An important study is a coagulogram, which allows you to detect increased blood clotting and pulmonary embolism.
Most instrumental methods are aimed at identifying problems in the heart. These include: electrocardiography, echocardiography, and so on. In addition, using pulse oximetry, blood oxygen saturation is detected (if edema is below 90%).
Chest X-ray is the leading test for lung swelling. It is used to detect fluid in the lung tissue. Swelling can be bilateral or unilateral. Additionally, pulmonary artery catheterization can be performed, but this requires certain indications.
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Acute pulmonary edema is a violation of blood and lymph circulation, which causes active release of fluid from the capillaries into the tissue of the said organ, which ultimately provokes a violation of gas exchange and leads to hypoxia. Acute edema grows quickly (the duration of the attack is from half an hour to three hours), which is why even with timely started resuscitation actions it's not always possible to avoid fatal outcome.
Acute pulmonary edema - the cause of death in many patients - develops as a result of infiltration into the lung tissue, where it accumulates in such quantities that the ability to pass air is greatly reduced.
Initially, the named edema has the same character as edema of other organs. But the structures that surround the capillaries are very thin, which is why fluid immediately begins to enter the cavity of the alveoli. By the way, she also appears in pleural cavities, however, to a much lesser extent.
Acute pulmonary edema is a cause of death in many diseases, although in some cases it can still be controlled with medication.
Diseases that can provoke pulmonary edema include pathologies of the cardiovascular system, including damage to the heart muscle due to hypertension, birth defects and stagnation in big circle blood circulation
No less common causes of pulmonary edema are severe skull injuries of various etiologies, as well as meningitis, encephalitis and various brain tumors.
It is natural to assume the cause of pulmonary edema in diseases or lesions such as pneumonia, inhalation of toxic substances, chest injuries, allergic reactions.
Surgical pathologies, poisoning, and burns can also lead to the described swelling.
Patients most often experience two main, radically different types of pulmonary edema:
However, despite the fact that the causes of their occurrence are different, these edemas can be very difficult to differentiate due to similar clinical manifestations attack.
Emergency care provided in time for pulmonary edema still gives the patient a chance to survive. To do this, it is important to know all the symptoms of this pathology. They appear quite clearly and are easy to diagnose.
A slightly different picture is presented by toxic pulmonary edema. It is caused by poisoning with barbiturates, alcohol, as well as the penetration of poisons into the body, heavy metals or nitric oxides. A burn of lung tissue, uremia, diabetes, can also provoke the described syndrome. Therefore any severe attack suffocation occurring in these situations should lead to suspicion of pulmonary edema. Diagnosis in these cases must be thorough and competent.
Toxic edema quite often occurs without characteristic symptoms. For example, with uremia, very scanty external signs in the form of chest pain, dry cough and tachycardia do not correspond to the picture visible with x-ray examination. The same situation is typical in toxic pneumonia and in the case of poisoning by metal carbonites. And nitrogen oxide poisoning can be accompanied by all the signs of edema described above.
If a patient has symptoms accompanying pulmonary edema, emergency care should be provided to him before being admitted to the intensive care unit. The necessary measures are carried out by the ambulance team on the way to the hospital.
The variety of manifestations accompanying an attack has led to the use in medicine of many medications that can relieve acute edema lungs. The cause of death may lie not only in the pathological condition, but also in incorrectly selected treatment.
One of the medications used to relieve edema is morphine. It is especially effective if the attack was caused by hypertension, mitral stenosis or uremia. Morphine reduces shortness of breath by depressing the respiratory center and relieves tension and anxiety in patients. But at the same time he is able to increase intracranial pressure, which is why its use in patients with cerebrovascular accidents should be very careful.
To reduce hydrostatic intravascular pressure during pulmonary edema, Lasix or Furosemide are used intravenously. And to improve pulmonary blood flow, heparin therapy is used. Heparin is administered as a bolus (bolus) in a dose of up to 10,000 units intravenously.
Cardiogenic edema, in addition, requires the use of cardiac glycosides (“Nitroglycerin”), and non-cardiogenic edema requires glucocorticoids.
Severe pain is relieved with the help of the drugs Fentanyl and Droperidol. If the attack can be stopped, therapy for the underlying disease begins.
Even if the relief of pulmonary edema is successful, treatment does not end there. After such an extremely difficult condition for the entire body, patients often develop serious complications, most often in the form of pneumonia, which in this case is very difficult to treat.
Oxygen starvation affects almost all organs of the victim. The most serious consequences of this may be cerebrovascular accidents, heart failure, cardiosclerosis and ischemic lesions organs. These conditions cannot be avoided without constant and enhanced drug support; despite the suppressed acute pulmonary edema, they are the cause of death large quantity sick.
Pulmonary edema develops due to the passage of protein-rich fluid from the pulmonary capillary system through the endothelium into the interstitial space, exceeding the capacity lymphatic system return it to the venous bed.Listed below pathogenetic mechanisms determining the development of pulmonary edema:
Increased pressure in the pulmonary capillaries
- Heart failure
- Hypoxia
- Increased pulmonary blood flow
- Reduced blood flow to the lungs
Reduced blood osmotic pressure during hypoproteinemia
- Prematurity
- Congenital hydrops
- Excessive fluid administration
- Increased losses squirrel
- Inadequate nutrition
Damage to the lymphatic system
- Interstitial emphysema
- Bronchopulmonary dysplasia
- High central venous pressure
Damage to the capillary endothelium
- Hyaline membrane disease
- Pneumonia
- Senticemia
- Toxic effect of oxygen
- Pulmonary emboli
Conditions in which intravascular hydraulic pressure increases or decreases osmotic pressure blood, cause the transition of fluid from the capillaries into the interstitial space. Impaired lymphatic drainage or damage to the capillary endothelium also contributes to the development of edema. When the volume of accumulated fluid exceeds the capacity of the interstitium, protein-rich fluid begins to flow into the alveoli through the epithelium, which normally restricts the passage of fluid. This sequence of events explains the 2 main definitions of pulmonary edema: interstitial and alveolar.
In every single clinical case possible simultaneous action of several pathogenetic mechanisms. For example, in premature infants the pressure in the pulmonary circulation may be increased, resulting in fluid filtration. The reason for this is hypoxia and patent ductus arteriosus. Hypoproteinemia is often observed in prematurity. In addition, oxygen therapy and barotrauma during mechanical ventilation can adversely affect lymph flow and damage the capillary endothelium.
A number of conditions are described below: causing swelling lungs. Many of these conditions have similar pathogenetic mechanisms.
Pathogenesis. In most cases, massive hemorrhage into the lungs is a form of fulminant hemorrhagic edema with the transition of blood plasma and red blood cells from the capillaries to the alveolar spaces. Most probable cause increased pressure in the pulmonary capillaries - left ventricular failure due to asphyxia. This is facilitated, on the one hand, by factors that cause increased fluid filtration (hypoproteinemia, massive transfusions, surfactant deficiency) and, on the other hand, by factors that provoke damage to lung tissue (infections, mechanical ventilation, oxygen therapy). The pressure in the pulmonary capillaries can increase so much and so quickly that bleeding occurs due to the rupture of the capillaries. Pathologically, hemorrhage can be interstitial (early stage) and alveolar (late stage).
Clinical signs. The disaster develops suddenly: skin pale, cyanosis of the lips, bradycardia, drop in blood pressure, apnea. Hemorrhagic edematous fluid, often foamy, with a hematocrit of less than 10%, enters the trachea in almost every second case; this is the most pathognomonic sign. Radiographs show a granular-mesh or large-nodular pattern of the lungs. In severe cases, homogeneous darkening of both lung fields is observed. These signs of the disease appear within the first 24 hours after birth, and most deaths- 48 hours after birth.
Treatment. Treatment can be successful if artificial ventilation is started immediately with high pressure at end expiration and fresh blood transfusion or fresh frozen plasma. If blood clotting defects are detected, appropriate measures are necessary. Despite active supportive therapy, the prognosis is extremely pessimistic.
Most patients, however, are not hypervolemic, and phlebotomy is indicated only if central venous pressure remains elevated after resuscitation measures and exchange transfusion. Specified curative measures are aimed at reducing acidosis, hypoxia and anemia.
Pathogenesis. The mechanisms that determine the closure of the ductus arteriosus at birth in full-term newborns and the causes of delay in premature infants are not fully understood.
The initial functional closure of the duct is caused by contraction of its smooth muscle. This is followed by the stage of final closure, during which the endothelium is destroyed, the cells of the underlying layers proliferate, and develop connective tissue and the gap is overgrown. In premature infants, the muscular layer of the duct is poorly expressed, the subendothelial layer that obliterates the lumen during the constriction phase may be absent, and the internal elastic membrane remains intact - all this leads to long-term functioning of the duct. The tone of the ductus arteriosus is determined by the ratio of contractile (for example, oxygen) and relaxing influences. The functioning of the duct in premature infants appears to be due to hypersensitivity this vessel to prostaglandins, rather than reducing the response to oxygen.
Clinical picture. Most characteristic feature systolic or constant heart murmur, which is heard over the entire anterior surface of the chest. However, according to Valdez, published in 1981, a heart murmur is heard in only 50% of newborns with a patent ductus arteriosus. The pathophysiological signs of the disease depend on the extent to which the blood shunts from left to right and the changes in the condition of the heart and lungs in response to the shunt.
Among typical symptoms tachycardia, increased apical impulse, increased pulse pressure or racing pulse, tachypnea and wheezing in the lungs. Impaired pulmonary function is indicated by increasing apnea attacks and bradycardia.
Already against the background of mechanical ventilation, newborns often need increased ventilation and increased oxygen supply. X-ray reveals cardiomegaly and signs of pulmonary edema, from a moderate decrease in the transparency of the pulmonary fields to their complete darkening.
Diagnosis. To assess the condition of the heart in FAP, the following echocardiographic indicators are used: the ratio between the diameter of the left atrium and the aortic mouth, the size of the left atrium, the diastolic size of the left ventricle, the duration of the systolic intervals of the left ventricle. However, echocardiography only shows enlargement of the heart cavities and indirectly reflects the function of the heart. Limiting fluid administration prevents dilation of the cavities, and assisted ventilation reduces pulmonary venous return. Therefore, determining the time interval of systole is the most reliable way detect hemodynamic disturbances when shunting blood from left to right through a FAP, even against the background of mechanical ventilation and limited fluid administration.
Treatment. In cases that do not require auxiliary ventilation, carry out drug treatment until ductus arteriosus will not close spontaneously. In case of congestive heart failure, fluid administration is limited (up to 75% of the required amount) and, in addition, diuretics are used. Slow and careful administration of packed red blood cells is necessary to maintain the hematocrit above 40%.
Forecast. At asymptomatic the condition of newborns with FAP is good even without treatment. However, FAP worsens and prolongs the course of HMB, so early treatment FAP for respiratory distress is quite reasonable. If the duct remains open 3 days after birth (according to contrast echocardiography), the likelihood of death increases, the period of mechanical ventilation is prolonged, and the risk of bronchopulmonary dysplasia is greater. Long-term observation of this category of patients did not reveal any late complications treatment with indomethacin.
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