What is Proteus Syndrome?

Adult respiratory distress syndrome, also known as acute respiratory distress syndrome (ARDS), is a common medical emergency that is

Adult respiratory distress syndrome

Adult respiratory distress syndrome is the patient's original cardiopulmonary function is normal, due to severe disease process outside or inside the lung, acute osmotic pulmonary edema and progressive hypoxic respiratory failure are relayed. Although the causes are different, the pathological and functional changes of lung tissue damage are roughly the same. The clinical manifestations are acute respiratory distress and refractory hypoxemia, because they are clinically similar to infant respiratory distress symptoms, and their etiology and pathogenesis They are not the same, so they are called "adults" to show the difference. The onset of this disease is rapid and its development is rapid. If it is not diagnosed and treated early, its mortality rate is as high as 50% (25% -90%), and it often dies from multiple organ failure.

Etiology of adult respiratory distress syndrome

Adult respiratory distress syndrome, also known as acute respiratory distress syndrome (ARDS), is a common medical emergency that is

Caused by acute processes that damage the lungs, such as sepsis, primary bacteria or viral pneumonia, inhalation of bone contents, direct chest injury, continuous or deep shock, burns, fat embolism, drowning, massive blood transfusion, extracorporeal circulation, O2 The incidence of ARDS with poisoning, acute hemorrhagic pancreatitis, inhalation of smoke or other toxic gases, and absorption of certain drugs, with sepsis is estimated at more than 30%. Although called "adult" respiratory distress syndrome, it can also occur in children.

Adult Respiratory Distress Syndrome Pathophysiology

Little is known about the initial lung damage. Animal model studies suggest that activated leukocytes and platelets accumulate in capillaries, interstitial and air cavities; they release prostaglandins, toxic O2 radicals, proteolytic enzymes and other mediators (such as tumor necrosis factor and interleukins). Damage cells, promote inflammation and fibrosis, and alter bronchomotor and vascular reactivity.

When the pulmonary capillary endothelium and alveolar endothelium are damaged, plasma and blood escape to the interstitial and alveolar cavities. Causes alveolar fluid and atelectasis, which is partly due to a decrease in surfactant. This damage is not uniform, it mainly occurs in the sagging part of the lung. Within 2 to 3 days, interstitial and bronchoalveolar inflammation and epithelial and interstitial cell proliferation occur. Then, collagen quickly accumulates, causing severe interstitial fibrosis within 2 to 3 weeks. These pathological changes have reduced lung compliance, reduced functional residual capacity, imbalanced ventilation / perfusion ratios, increased physiological dead space, severe hypoxemia, and pulmonary hypertension.

Adult respiratory distress syndrome symptoms and diagnosis

ARDS usually occurs 24 to 48 hours after the initial injury or disease. Appear first

Adult respiratory distress syndrome Difficulty breathing, usually shallow speed. There may be intercostal space and depression of the upper sternal fossa when inhaling. Buns and streaks can appear on the skin, which cannot be improved by inhaling oxygen. On auscultation, snoring, snoring, or wheezing may be heard and may be normal. Early diagnosis should be highly vigilant for dyspnea occurring in situations that may cause ARDS. At this time, speculative diagnosis can be made by measuring arterial blood gas and chest X-ray immediately. This initial blood gas analysis showed acute respiratory alkalosis: PaCO2 was normal or decreased, PaO2 was significantly reduced, and the pH was increased. A chest X-ray usually shows bilateral diffuse alveolar infiltration similar to acute cardiogenic pulmonary edema, but the heart silhouette is usually normal. However, changes in X-rays are often many hours later than changes in function, and hypoxemia is much more severe than pulmonary edema seen on X-rays. Despite the inhalation of high concentrations of O2 (FiO2), extreme hypoxemia often persists, suggesting that due to atelectasis and consolidation of the lungs, shunting from right to left, which prevents ventilation.

After the immediate treatment of hypoxemia, further diagnosis should be made. Swan-Ganz catheters can help identify when symptoms are suspected to be due to heart failure. ARDS is characterized by low pulmonary wedge pressure (PAWP <18mmHg), and if elevated, it is a manifestation of heart failure (PAWP> 20mmHg). If considered like pulmonary embolism, clinical manifestations similar to ARDS should be performed after the patient has stabilized (eg, pulmonary angiography). Pneumocystis carinii pneumonia and other occasional primary lung infections can be similar to ARDS and should be considered, especially for patients with impaired immune function. Lung biopsy or bronchoalveolar lavage may be helpful.

Complications and Prognosis of Adult Respiratory Distress Syndrome

Secondary multiple pulmonary bacterial infections, especially Gram-negative bacteria (such as Klebsiella, Pseudomonas and Proteus) and Gram-positive Staphylococcus aureus, especially methicillin-resistant strains Multiple organ failure, especially

Adult respiratory distress syndrome It is renal failure; and complications of invasive life support measures lead to high disability and mortality. Tension pneumothorax associated with the placement of a central venous catheter and the use of positive pressure ventilation (PPV) and positive end expiratory pressure (PEEP) can occur suddenly. To prevent death, tension pneumothorax needs to be recognized and treated quickly, tachycardia, hypotension, and sudden increase in inspiratory peak pressure during mechanical ventilation are all related to tension pneumothorax. Tonic pneumothorax, which occurs in the advanced stages of ARDS, is an unknown sign, as it is often caused by severe lung injury and the high air pressure required. Without adequate blood volume replenishment, the reduction of venous return caused by PPV and PEEP reduces cardiac output, reduces tissue oxygen supply, and causes secondary multiple organ system failure. The survival rate of severely treated ARDS is 60%. If severe hypoxemia of ARDS is not recognized and treated, 90% of patients may suffer cardiac arrest. Patients who quickly respond to treatment usually have little or no residual pulmonary insufficiency. Pulmonary fibrosis often occurs in patients who require long-term ventilation with FiO2> 50%. In the vast majority of severe acute cases, pulmonary fibrosis can be found to disappear after several months, but the mechanism is unknown.

Adult Respiratory Distress Syndrome Treatment

Adrenal glucocorticoids for adult respiratory distress syndrome

Adult respiratory distress syndrome It is currently believed that glucocorticoids should be used as soon as possible for non-infectious adult respiratory distress syndrome such as non-infectious respiratory distress syndrome caused by irritating gas inhalation and fat embolism caused by traumatic fracture. The principle of its use is early, large amount and short course treatment. Such as dexamethasone 20-30mg, 2-3 times a day, for 2 consecutive days, if effective, continue to use for a few days and then stop. However, glucocorticoids in adults with respiratory distress syndrome associated with sepsis or severe infection should be avoided or used with caution.

Adult Respiratory Distress Syndrome Oxygen Therapy

Correcting O2 deficiency is an important and urgent measure. If O2 deficiency is not corrected, it will cause irreversible damage to important organs. Generally need to inhale high concentration of oxygen (> 50%), but should try to inhale as low as possible, as long as SaO2> 90% can prevent oxygen poisoning.

Adult respiratory distress syndrome positive end expiratory pressure ventilation

Deliver a certain volume or flow of gas to the lungs for the ventilator, inhale the airway and the alveoli at a positive pressure, and when exhaling until the end-expiratory airway opens, the oral, airway, and alveolar pressures are all higher than atmospheric mechanical ventilation Types of.

Reasonable fluid input for adult respiratory distress syndrome

On the premise of ensuring sufficient blood volume and stable blood pressure, a slight negative balance (-500ml--1000ml) is required for the volume of fluid entering and leaving. In order to promote the resolution of edema, furosemide may be given at 40-60 mg / day. When the permeability of the damaged capillaries of endothelial cells increases, colloidal fluid can penetrate into the interstitial and aggravate pulmonary edema, so it is not appropriate to supplement colloids in the early stages of adult respiratory distress syndrome. In addition to excessive bleeding due to trauma, blood must be transfused, and fresh blood should be transfused with a microfilter to avoid micro-thrombosis caused by micro-thrombosis in pulmonary capillary endothelial cells.

Nutritional Replenishment and Primary Treatment of Adult Respiratory Distress Syndrome

ARDS patients are often nutritionally deficient. Nasal feeding and intravenous nutrition should be given to maintain adequate energy supply and avoid metabolic disorders and dielectric disorders.