Acute respiratory distress syndrome in the elderly

Introduction to acute respiratory distress syndrome in the elderly Acute respiratory distress syndrome (ARDS) is an acute, progressive respiratory failure caused by various intrapulmonary and extraclinical factors other than cardiogenic. The main pathological feature is that due to the increased permeability of pulmonary microvasculature, the alveolar is full of protein-rich liquid, which leads to pulmonary edema and transparent membrane formation, which may be associated with pulmonary interstitial fibrosis. Pathophysiological changes were mainly due to decreased lung volume, decreased lung compliance, and severe ventilation/blood flow imbalance. The clinical manifestation is an acute progressive dyspnea characterized by respiratory distress and hypoxemia. Hypoxia, which is difficult to correct by conventional oxygen inhalation, is one of the most common critical illnesses in the clinic, and the mortality rate is high. basic knowledge Sickness ratio: 0.05% Susceptible people: the elderly Mode of infection: non-infectious Complications: arrhythmia, pneumothorax, shock, heart failure, respiratory failure, electrolyte imbalance

The cause of acute respiratory distress syndrome in the elderly

Shock, trauma, severe infections and sepsis (45%):

Infectious, hemorrhagic, cardiogenic. Pulmonary or extrathoracic trauma, pulmonary fat embolism, drowning. Bacterial pneumonia, viral pneumonia, fungal infections and fungal pneumonia, rickettsial infections, tuberculosis, other infections.

Aspiration, drugs and others (10%):

Stomach contents. Inhalation of harmful gases: high concentration of oxygen, others. Anesthetic overdose, methadone, colchicine, others. Acute pancreatitis, connective tissue disease, cardiopulmonary bypass, heart rhythm conversion, organ transplantation.

Disease (5%):

Metabolic disease: Diabetic acidosis. Blood disease: multiple large blood transfusions, DIC. Obstetrics and gynecology diseases: eclampsia and preeclampsia, amniotic fluid embolism.

Pathogenesis

The pathogenesis of ARDS is complicated. Although it has been deeply understood, it has not been fully elucidated. Two major factors, including effector cells and inflammatory mediators, are involved in lung injury and play a key role in the pathogenesis of ARDS.

1. Cells involved in the reaction

(1) Polymorphonuclear leukocytes (PMNs): Normally, PMNs in the interstitial lung account for 1.6%. In the early stage of ARDS, activated complement C5a, bacteria, immune complexes, etc. can activate PMNs, which release oxygen free radicals (oxygen).

More radicals, OR), the greatest impact on the occurrence and development of ARDS, regardless of any cause of ARDS, activated PMNs become the source of the disease, first directly damage the lung tissue, and then appear in the lungs of various inflammatory cells, release A variety of inflammatory mediators, aggravating lung injury.

(2) Epithelial cells and endothelial cells: After inhalation of harmful gases, the alveolar epithelial cells are first damaged. After the damage of alveolar epithelial cells, the cell barrier is destroyed, the pores are enlarged, and the lipid layer of the original barrier is exfoliated. Increased sexual activity, when harmful substances such as endotoxin enter the blood circulation, firstly damage the pulmonary cpillary endothelial cells (PCEC), so that the monolayer permeability of the endothelial cells increases, shrinks, dies, and the endothelium is damaged for 2 hours. Pulmonary interstitial edema can occur, alveolar edema occurs after 12 to 24 hours of severe injury, thromboxane A2 (thromboxane A2), platelet activating factor (PAF) and interleukin (LTS) can be chemotaxis after endothelial cell injury More PMNs and platelets enter the lung tissue.

(3) Mononuclear-macrophage (AM) system: Recent studies have found that in pathological conditions, AM not only participates in the pathogenesis of ARDS, but also proves that pulmonary intravascular macrophage (PIM) can also be produced. OR, release of lysosomal enzymes, prostaglandins (PG), endotoxin ester polysaccharides (LPS), etc., play a role in mediating pulmonary microvascular injury and pulmonary inflammation.

2. Media involved in acute lung injury

(1) Oxygen free radicals: OR is one of the important inflammatory mediators, which can make PMN migrate to the inflammatory zone, aggregate, activate and release lysosomal enzymes, damage the vascular endothelium, and cause increased vascular permeability. Animal experiments It is found that OR increases after injury, and OR is derived from activated PMN.AM. Endothelial cells, etc., which can destroy tissues, cells and proteins, activate resting enzymes, destroy anti-trypsin (a-AT), and affect peanuts. The metabolism of enoic acid (AA) increases the production of prostaglandins (PGS), thromboxane (TXA2), and interleukin (LTS).

(2) Arachidonic acid metabolites (AA): Activation of AA plays an important role in the pathogenesis of ARDS.

The experiment proved that the changes of PMN and AM producing leukotriene B4 (LTB4) in RDS dogs under hypoxic conditions showed that the concentration of LTB4 at 6h after injury was significantly higher than that before injury and the control group, showing a significant increase in PMN and LTB4. LTB4 has chemical agonism and chemotaxis, can increase vascular permeability, contract bronchial smooth muscle, cause bronchial mucosal edema, slow down its ciliary movement and promote PMN release OR. Therefore, LTS plays an important role in the pathogenesis of ARDS.

(3) Complement system: In the early stage of ARDS, the complement system is activated first, and the intermediate or terminal product is an important regulatory mediator of the disease. The total hemolytic complement activity (CH50) is significantly reduced, and the neutrophil aggregation activity (neutrophil aggregation activity) Increased (NAA) causes PMN to accumulate in the lungs and rapidly develops respiratory distress, indicating that activation of the complement system and accumulation of PMN in the lung are closely related to the pathogenesis of ARDS.

(4) The enzyme system is activated: proteolytic enzymes, collagenase and cathepsin are present in PMN, which release the basement membrane of the alveolar capillary membrane (ACM), endothelial collagen and structural proteins, resulting in increased ACM permeability. Causes pulmonary edema.

(5) Transmitter: release of various transmitters during the onset of ARDS, causing lung damage:

1 Tumor necrosis factor (TNF) is a protein produced by macrophages. Experiments have shown that TNF peak can be detected after 2 hours of endotoxin injury. Direct injection of TNF can often cause hypotension shock, death within a few hours, and activate PMN chemotaxis. , phagocytosis and release of lysosomal enzymes and OR and procoagulant damage to the lungs.

2 Interleukin (TLS), in which IL-1 and TNF are secreted by monocytes or macrophages, endothelial cells, etc., IL-1 first invades the lungs, and can be activated by PMN, promote OR release, and damage the pulmonary endothelium. The cells adhere to the endothelium, activate coagulation and fibrinolysis, promote synthesis and release of catecholamine (CA) and acute reaction protein (ARC), initiate the ARDS humoral reaction chain, and cause pulmonary edema and hemorrhage.

3 platelet activating factor (PAF), PAF can be produced by PL, PMN, AM, lymphocytes, endothelial cells, etc. Its target cells include PL, AM and endothelial cells, which play an important role in the pathogenesis of shock, and can pass PGS, LTS medium. Damage to lung tissue can lead to PMN in circulating blood. PL activates and accumulates in the lungs, releasing the medium and increasing the permeability of ACM.

(6) Pulmonary surfactant (PS): PS is synthesized in the alveolar type II epithelial cells (PC-II) lamellar bodies. It binds to the carrier protein and becomes lipoprotein, which is secreted into the alveolar cavity and formed. Thin layer, forming a gas-liquid interface, the main functions of PS:

1 reduce the surface tension of the gas-liquid interface to prevent alveolar collapse;

2 maintain proper lung compliance and reduce work of breathing;

3 to prevent pulmonary microvascular fluid from infiltrating into the alveoli and reducing pulmonary edema;

4 enhance lung defense ability;

5PS can suppress AM oxidation burst and prevent the occurrence of a large amount of OR.

Pulmonary surfactant plays an important role in maintaining alveolar stability. Patients with ARDS suffer from PC-II injury, PS synthesis is reduced or consumed excessively, activity is reduced, inactivation is fast, etc., causing PS to lose normal function, leading to alveolar trapping, massive plasma Infiltration into the alveoli, alveolar edema and clear film formation.

3, osmotic pulmonary edema

Due to the above various mechanisms, the alveolar capillaries are damaged, and the capillary permeability is increased, so that more body fluids and plasma leak into the pulmonary interstitial and alveolar spaces, resulting in osmotic pulmonary edema.

4, PS reduction leads to alveolar collapse, atelectasis

Due to lack of oxygen, acidosis and some toxic substances can damage PC-II, inhibit PS metabolism, inhaled high concentration of oxygen and mechanical ventilation, severe infection, and insufficient pulmonary perfusion, pulmonary capillary embolism, etc., so that alveolar epithelial type II The phospholipid metabolism disorder of cells affects the synthesis of PS, and the vicious circle that promotes lung collapse is one of the pathophysiological changes of respiratory distress.

5, increased intrapulmonary shunt, decreased lung compliance, impaired lung function

Due to decreased PS or decreased activity in patients with ARDS, and alveolar edema, alveolar atelectasis, the alveoli are in a state of hypoventilation, resulting in a imbalance in the proportion of severe ventilatory blood flow, so that the blood of the alveolar capillaries is not fully oxygenated, resulting in partial mixed veins The blood returns to the left heart and forms a shunt. Due to the decrease of PS, the pulmonary interstitial and alveolar edema, the alveolar atelectasis, the lung compliance decreases, the proportion of ventilation/blood flow decreases, and the lung diffuses dysfunction.

6, general observation

The lungs are obviously full and swollen, with reduced gas content, and focal hemorrhage on the surface of the lungs. The weight is obviously increased, generally increasing by 3 to 4 times. The lung section has obvious congestion, hemorrhage, edema or atelectasis.

7, change under the optical microscope

(1) pulmonary interstitial and alveolar edema, hemorrhage: pulmonary interstitial edema first, followed by alveolar edema, edema is evident in the formation of small bronchial or small blood vessels around the sleeve edema or bleeding.

(2) Focal atelectasis: Most of the autopsy cases showed focal atelectasis.

(3) Transparent film formation: The transparent film often occurs on the basis of obvious exudation, and it is a dark red uniform film attached to the alveolar, alveolar and respiratory bronchioles in a ring or half ring. Shaped or strip-like, transparent membrane is one of the typical lesions of ARDS.

(4) Diffuse inflammatory cell infiltration in the lung: Sometimes there is PMN infiltration in the early stage of the disease, but it can be observed at 48 hours. Interstitial pneumonia can be seen after 3 to 4 days, and almost 100% secondary lungs after 5 days. Infectious inflammation.

(5) Fibrosis of pulmonary interstitial and terminal airway: diffuse interstitial collagen fibrosis can be seen at an early stage, and obvious fibrosis can be seen in advanced cases, and the mechanism or fibrosis of lung exudate and transparent membrane is The course of disease can be seen for more than 3 days, and more than 7 days of fibrosis, so it is called acute pulmonary fibrosis, which seriously affects lung function. In the advanced stage, large fibrosis may occur, and late lung may be a honeycomb lung.

Prevention of acute respiratory distress syndrome in the elderly

The prevention of this disease is mainly to actively treat the primary disease, prevent complications, reduce the mortality rate, and encounter traumatic diseases, such as chest trauma, to treat immediately, prevent hypoxemia and extensive lung injury, and prevent fat embolism in fracture patients. Etc., infection is a common complication, and aggravating the condition, increasing mortality, should actively prevent and treat infection, common complications include pneumothorax, liver and kidney dysfunction, gastrointestinal bleeding, reasonable use of ventilator during treatment, strict Monitor clinical and laboratory indicators to prevent complications and be corrected in a timely manner.

Complications of acute respiratory distress syndrome in the elderly Complications arrhythmia pneumothorax shock heart failure respiratory failure electrolyte disorder

Common complications include infection (especially Gram-negative bacilli infection), liver and kidney dysfunction, gastrointestinal bleeding, arrhythmia, pneumothorax, etc.

Symptoms of acute respiratory distress syndrome in the elderly Common symptoms Difficulty in breathing, three concave signs, pink foamy sputum, cough, irritability, restlessness, sorrow, expression, indifference, cough, snoring, difficulty in breathing, cyanosis

ARDS is often complicated by severe trauma, shock, sepsis, aspiration, toxic gas inhalation and serious infections, and its symptoms are acute and even sudden.

1, breathing difficulties

Frequent respiratory rate, respiratory distress is the main clinical manifestation of ARDS, usually the respiratory rate occurs within 1 to 2 days of onset, progressive increase, often more than 28 times / min, critically ill respiratory rate up to 60 times / min, breathing difficulties are very obvious , showing symptoms of respiratory distress.

2, cough, cough, irritability and ambition

Cough, cough and sputum sputum is one of the typical symptoms of ARDS. Due to hypoxia, respiratory distress, most patients with ARDS begin to have irritability, ambiguity or apathy in the early stage.

3, signs

The respiratory rate is fast, and as the symptoms worsen, there is a cyanosis, inhalation "three concave signs", and some patients can smell the dry and wet voices in the lungs.

The typical clinical course of ARDS can be divided into four phases: the first phase, also known as the acute injury phase, is the incubation period, mainly the clinical manifestations of the primary disease; the second phase, also known as the stable phase, after the onset of 24-48 hours, breathing The frequency increased, the lungs could smell wet and the voice was decreased, PaO2 decreased; the third stage, acute respiratory failure, rapid development of the disease, increased difficulty in breathing, respiratory distress, progressive decline of PaO2, difficulty in correcting oxygen, typical chest radiograph The diffuse haze infiltrates the shadow; the fourth phase, severe hypoxia and carbon dioxide retention, eventually leading to heart failure, shock, coma, severe hypoxia leading to death.

There are more than 100 kinds of primary diseases of ARDS, and the pathogenesis is complicated. At present, the clinical diagnosis is based on medical history, clinical manifestations and arterial blood gas analysis. There is no unified diagnostic criteria, but the clinical process of ARDS is hidden, combined with ARDS. The mortality rate is as high as 50%, so early diagnosis is very important.

Examination of acute respiratory distress syndrome in the elderly

PaO2 decreased, and PaO2 <8 kPa is an important indicator for the diagnosis of ARDS when the inhaled oxygen concentration reaches 60%.

Chest X-ray signs, patch shadows or large patches of interstitial or alveolar lesions.

Diagnosis and diagnosis of acute respiratory distress syndrome in the elderly

Diagnostic criteria

1, with the primary disease that can cause ARDS, such as aspiration, infection, trauma and so on.

2, respiratory symptoms, respiratory rate > 28 times / min or respiratory distress.

3, abnormal blood gas analysis, hypoxemia, PaO2 <8kPa (60mmHg).

4, heart failure, but exclude left heart failure of chronic primary heart.

Early diagnosis

The mortality rate of ARDS is as high as 50%. The main reason is the lack of early diagnostic criteria, and it is difficult to carry out effective early prevention and treatment. In recent years, around the pathological basis of ARDS, some active substances and metabolites that can cause acute lung injury are used as markers of ARDS. The study was carried out to initially show certain clinical significance.

1. Close monitoring of high-risk patients with ARDS: In 1982, Pepe et al. proposed the following 8 conditions for concurrent ARDS: 1 sepsis sepsis; 2 aspiration; 3 pulmonary contusion; 4 multiple long bones and pelvic fractures; 5 a large number of blood transfusions in a short period;; 7 acute pancreatitis; 8 persistent hypotension.

2. Looking for early diagnostic criteria:

(1) Cellular Polysaccharide (LPS) and Tumor Necrosis Factor (TNF): LPS and TNF are widely used inflammatory mediators. Dmarks et al. found in sepsis shock, elevated plasma TNF, incidence of ARDS, and mortality. Significantly increased, so high concentrations of LPS and TNF have certain predictive and monitoring effects on ARDS.

(2) Alveolar capillary membrane (ACM) permeability measurement: ARDS patients have increased ACM permeability before X-ray can show pulmonary edema.

(3) Factor VIII-related antigen and lactate dehydrogenase (LDH): In the case of ARDS, a large number of markers of lung tissue are released due to extensive lung injury. Monitoring the concentration of these markers in body fluids can reflect the lung injury of ARDS. Occurrence and development.

Differential diagnosis

1, cardiogenic pulmonary edema

Common in high blood pressure, coronary heart disease, aortic valve disease, myocarditis, rheumatic heart disease and other left heart failure, combined with medical history, physical signs, electrocardiogram and correction of heart failure treatment, generally easy to identify.

2, acute pulmonary embolism

Surgery, trauma, long-term bed-riding history, acute onset of the disease, as well as difficulty breathing, chest pain, hemoptysis, cyanosis, shock, etc. are the main clinical manifestations, and the chest radiograph shows a typical circular or triangular shadow.

3. Diffuse pulmonary interstitial fibrosis

The disease is mostly chronic, and a few are subacute. The lungs often have bursty wet voices in the lungs. The chest radiographs have reticular nodules in the lungs, and the lung function is a restrictive ventilatory disorder.

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