Pulmonary edema (LR) during and after surgeryintervention was recently considered one of the most serious complications, a pulmonary manifestation of heart failure or hyperinfusion. Its origin is due to the transition of the liquid part of the blood from the pulmonary capillaries into the respiratory air spaces due to a change in the normal relationship between the hydrostatic pressure in the capillaries and the oppositely acting pulmonary pressure and also the colloid osmotic pressure of the blood.
As a result of significant changes in thesefactors, the pressure gradient between the microvessels of the lungs and the gas medium of the diffusion zone of the lungs decreases, which, in fact, represents pulmonary interstitium.
Increase in permeability of alveolocapillarymembranes under the influence of various humoral factors of complicated postoperative periods (BAA, other ETS), as well as the use of prolonged aspiration from the bronchial tree during its sanation, promotes the initial transition of intravascular fluid containing protein into the gas medium of the lungs. Water on the surface of the pulmonary diffusion membrane eliminates the surface-active properties of the lung surfactant (Johnson J.W.C. et al., 1964), which dramatically reduces lung compliance and increases energy expenditure on respiration.
Transition of significant quantitiessurface-active phospholipid and protein into the respiratory liquid that bleeds into the lumen of the respiration, promotes the formation of a stable foam filling the airway zone of the lungs, which is considered to be a manifestation of alveolar OJI (Luizada AA 1965). Filling the airways with foam even more disrupts the distribution of gas in the lungs and ultimately reduces the effectiveness of pulmonary gas exchange with a significant increase in energy expenditure on respiration.
The specific genesis of early postoperative ALcomplicated. Hyperactivation of the sympathoadrenal system, especially in case of insufficient anesthesia, an increase in the level of so-called traumatic mediators and MSM, an acute decrease in the blood COD under the influence of excessive infusion of saline solutions against a background of a deficiency of plasma albumin, a direct effect of hypoxia and venous hypoxemia, acidosis, hyperfermentemia on permeability of pulmonary capillaries in combination with a decrease in cardiac output, can be combined in each specific case of AL after surgery in various combinations.
Now most resuscitators tend tothe idea that the hemodynamic causes of early AL play a significant role only in patients with initial toxic or metabolic myocardial damage, concomitant valvular heart disease or direct myocardial trauma during cardiac surgery.
Often acute hypertension of a small circleblood circulation develops a second time and can be associated with direct damage by factors of ODN (hypoxemia, hypercapnia, acidosis) of the invalid cardiac muscle. This disorder is clearly manifested against a background of increased systemic vascular resistance due to low BCC or, conversely, high blood pressure in the large circulation, which can be realistic in the near postoperative period. Early clinical observations of pulmonary surgeons A.D. Yarushevych (1955), I.S. Kolesnikova (1960) emphasize that the development of AL usually coincided with the period of the greatest instability of pulmonary gas exchange in such patients: after resection of the lungs, it appeared in the first hours and not later than the first day after the intervention.
Later postoperative OJI developsnot only against the background of hemodynamic disorders (with a significant decrease in IOC), which accompanies other postoperative complications, such as bilateral pneumonia or pneumonia of a single lung, acute myocardial infarction.
OJI is often the end of a heavy proteininsufficiency with limiting hypoproteinemia, infectious-inflammatory endotoxicosis, or decompensation of concomitant hypertensive disease on the background of cerebral circulation disorders. Such OJI develops slowly, through the stage of interstitial edema with a fluid retention in the peribronchial tissue. The intensity of water accumulation in the lungs largely depends on the magnitude of systemic blood pressure (hypertensive crisis) due to the increased rate of filtration of tissue fluid from the system of bronchial vessels (Simbirtsev, SA Serikov, VB 1985).
Clinic and diagnostics. In many cases, the initial stage of postoperative OJI occurs suddenly. Only sometimes it is preceded by a typical syndrome in the form of a feeling of pressure behind the sternum, a feeling of lack of air and especially a dry, unproductive cough. But soon the patient assumes the position of orthopnea. Inhalation is difficult, requires considerable physical effort, tachypnea more than 40 per min. With auscultation, breathing over the lungs is initially severe, often accompanied by an unproductive cough. This increases tachycardia, despite the absence of reasons for hypovolemia. The rise of systemic BP, and sometimes CVP, as well as a moderate dilatation of the pupils, indicating the excessive activation of the sympathoadrenal system and complement the picture of the complications.
Against the backdrop of the advanced stage of AL over pulmonaryfields with percussion reveals a high tympanitis, especially over their upper sections, a huge number of wet wheezes are audible, which are sometimes audible at a distance. The heart sounds of such a patient are barely discernible. Breathing quickly becomes bubbling with the departure of white, yellowish or pink foamy sputum, the amount of which within 1-2 hours can reach 2-3 liters.
In the terminal phase of OJI, when confused orloss of consciousness, cyanosis of the skin, bubbling breath, sometimes of the agonal type and the release of large amounts of sputum, a marginal tachycardia (140-180 contractions per minute) is recorded, and sometimes, on the contrary, a bradycardia, an unstable systemic BP is registered against a persistent and significant increase in CVP.
With pulse oximetry and laboratory monitoring inthe initial stage of OA arterial hypoxemia is combined with a significant hypocapnia, and in the terminal - hypocapnia shortly before death is replaced by hypercapnia. With the X-ray inspection of the lungs, non-homogeneous shading, recorded earlier in the lower parts of the lungs, gradually fills all the pulmonary fields. If pulmonary arteries are catheterized for intensive hemodynamic monitoring in a given patient, or if it is possible to use such access for monitoring as needed (through a central venous catheter), pulmonary capillary pressure (jam pressure) is examined. At the height of the true alveolar OJI, it is higher than 28-30 mm Hg.
The main areas of therapy for postoperative OL are in treatment activities that provide several areas of therapeutic effect:
- restoration of the usual ratio of pressures in the pulmonary capillaries and gas environment of respirons;
- elimination of foaming and hypoxemia;
- removal of excitation and hyperactivity of the sympathoadrenal system;
- Reduction of the overload of a small circle and light liquid;
These effects are complemented by measures to reduce plasma hydration and restore RCD, normalizing the permeability of the alveolocapillary membrane.
Inhalation of O2 through an anesthesia machine underpressure of 10-15 mm Hg. (14-20 cm H2O) or other device providing DM diarrhea is used in those cases of OJI when the complication has predominantly hemodynamic origin. Excessive pressure increase in the airways (above 18-20 mm Hg) is unacceptable, since significant resistance to blood flow in the pulmonary capillaries and a violation of the right atrial filling increase hemodynamic disorders in such patients.
OJI treatment often begins with eliminationfoaming and restoring the activity of pulmonary surfactants. The most accessible for this purpose is the inhalation of ethyl alcohol vapors, which are obtained by passing 02 through 96 ° ethanol, poured into a conventional bubbling humidifier.This enriched with ethyl alcohol and oxygen gas mixture is given to the patient through nasopharyngeal catheters.
The duration of this inhalation session is 30-40min with 15-20 min interruptions. When using an oxygen-air mixture during SD with PD, ethanol is poured into the vaporizer of the anesthesia apparatus. Less often, in more difficult conditions, they simply pour 2-3 ml of ethyl alcohol into the trachea with a syringe piercing the thyroid-cricoid ligament, especially if the patient's consciousness is inhibited. It is also possible to use aerosol inhalations of 20-30% aqueous ethanol solution created by an ultrasonic fogger.
The most effective extinguishing of pulmonary foam is the derivativepolysiloxane - antifosilane. The effect of defoaming in such circumstances depends on compliance with the basic conditions for its use: rapid nasotracheal aspiration of the foam from the trachea and a gradual adaptation to the inhalation of the drug. Oxygenotherapy with antifensilane antifoam for 15-20 min allows to reduce the phenomenon of expressed alveolar OJI, which rightly allows to relate this remedy to specific analeptics.
Rapid relief of alveolar OJI allowscalm environment to conduct the necessary examination of the patient and establish with a certain degree of probability the cause of the complication. Adynamic patients tolerate inhalation of antifosilane easily; in sharply excited - the inhalation of a defoamer is difficult and therefore ineffective.
At this stage, mental excitement is eliminatedintravenous administration of midazolam (dormicum, flormidal) 5 mg, rarely sibazone (up to 0.5 mg / kg MT of the patient), sodium oxybutyrate (70-80 mg / kg MT), even less often droperidol (up to 0.2 mg / kg MT ) or 2-3 ml of talamonal in adult patients, supplementing sedation with antihistamine H-blockers (diphenhydramine, diprazine).
A long-term recommendation to use against the backgroundof the expanded OJI pattern in agitated patients, morphine intravenously has sufficient functional bases: in addition to the necessary sedation in such cases, this opiate at a dose of 10-20 mg causes an increase in the tone of respiratory bronchioles, creating a higher level of pressure in the diffusion zone of the lungs.
Antihistamines andpathogenetic action, namely reduce the permeability of the alveolocapillary membrane. For which also prescribe SCS (prednisolone, dexomethasone), vitamins P and C in significant doses, as well as a 30% urea solution at a rate of 1-1.5 g / kg MT of the patient.
Infusion of a solution of lyophilized urea (withabsence of azotemia!), unlike the infusion of mannitol or sorbitol, does not create an overload of the vascular bed, is well tolerated by patients and not only condenses the alveolocapillary membrane of the lungs, promotes resorption of the edematous fluid into the blood, but also has a positive inotropic effect on the myocardium.
Excess intravascular volume of the fluid is reduced by saluretics (40-60 mg of lasix, 20 mg of unate, 1-2 mg of buphenox intravenously) in combination with measures that reduce blood flow to the right heart:
- superposition of venous tourniquets (better pneumatic cuffs) on limbs for 25-30 min;
- Controlled hypotension (arfonade, nitroglycerin, less often pentamine), especially with hypertensive AD reaction against OJI;
- widespread blockade with local anesthetics in the presence of a patient in a catheter in the epidural space, delivered with other purposes.
The action of saluretics, especially of Lasix,is determined not only by their diuretic effect: OJI phenomena often subsided even before the diuretic effect of the drug appears. With a high hematocrit, bloodletting with an autoblood preform on a citrate preservative is especially indicated and a part of the blood being removed is replaced with oncotically active blood substitutes.
If there is evidence of hyperhydration of the bodybackground of normal or decreased intravascular volume and hypoalbuminemia, it is desirable to use concentrated protein blood substitutes followed by mild vasoplegia. The decisive effect for excretion of a patient from OJI, especially resistant to conventional therapy, sometimes has GF (rarely isolated ultrafiltration of blood). It is indicated with a low index of hematocrit and clear signs of hyperhydration of tissues with a high index of the blister sample.
Often, based on the "respiratory" genesis of the earlyOJI, with the progression of respiratory failure (tendency to hypercapnia, mixed acidosis, edema-pneumonia development), confusion, a decision should be made to transfer the patient to controlled ventilation in the PERP mode (Castanig, G. 1973) using midazolam, diazepam drugs for endotracheal intubation, rohypnol or steroid anesthetics (altezin).
The emergence of OL in the late postoperativeperiod usually occurs against a background of persistent other pulmonary or extrapulmonary life-threatening complications: pneumonia, coma, sepsis, etc.
In these cases, preference should be given to(Kassil VL Ryabova NM 1977) in a rare rhythm (14-18 cycles per minute) with a high DO (at least 700 ml in an adult patient) and a high Fi02, which is decreased as the arterial resolution is resolved hypoxemia.
Such a regime makes it possible to achieve effectiveoxygenation of the blood in the lungs and the resorption of edematous fluid from the surface of the pulmonary diffusion membrane, reduces the filling of the pulmonary blood channel and reduces the energy expenditure of the patient for ventilation, which any SD method can not provide in the PD regime. In such cases, there is no need to suck off the foamy fluid from the airways. Therapy of late postoperative OJI with the use of PEEP with ventilation should be complemented by measures to increase the plasma blood plasma COD, stabilize myocardial contractility, prevent pulmonary infection.
Sometimes a clinical picture resembling AL,may be a consequence of a so-called "silent" regurgitation, whose frequency can be 8-15% for all patients operated under general anesthesia with the deactivation of protective glotto-guttural reflexes (Blitt et al., 1970; Turndorf et al., 1974). Regurgitation of gastric contents most often occurs in emergency abdominal surgery, with limited ability to prepare the gastrointestinal tract, but it can also occur in patients who are sufficiently well prepared for routine operations.
"Silent" regurgitation is facilitated by a difficultexhalation with increased intra-abdominal pressure, esophagectasis or a large esophageal diverticulum, and the use of depolarizing muscle relaxants for intubation of the trachea without special measures to prevent the fibrillation of arbitrary muscles when administered to anesthesia, for example, using precurarization with a non-reflexing dose of one of the nondepolarizing relaxants (pavulon, arduan) .