Complications of pneumonia

The severity of the course of the disease and the tactics of managing patients with pneumonia are largely determined by the presence of pulmonary and extrapulmonary complications. The most significant of them are:

1. Pulmonary complications:
   1. acute respiratory failure;
   2. parappectonic exudative pleurisy and / or pleural empyema;
   3. abscess of the lungs;
   4. acute respiratory distress syndrome.
2. Extrapulmonary complications:
   1. infectious-toxic shock;
   2. sepsis.

[1], [2], [3], [4], [5], [6], [7],

Acute respiratory failure

Acute respiratory failure is undoubtedly one of the main indicators of the severity of the course of pneumonia and can develop within a few hours or days from the onset of the disease. Acute respiratory failure develops in 60-85% of patients with severe pneumonia, and more than half of them need artificial ventilation.

The severe course of pneumonia is accompanied by the development of a predominantly hypoxemic (parenchymal) form of respiratory failure due to several pathogenetic mechanisms:

• massive alveolar infiltration;
• a decrease in the total functioning surface of the alveolar-capillary membrane;
• violation of the diffusion of gases;
• severe violations of ventilation-perfusion relations.

The latter mechanism appears to be crucial for the emergence of patients with pneumonia of arterial hypoxemia, since the preservation of blood flow in poorly ventilated or unventilated alveoli quickly leads to the discharge of mixed venous blood into the arterial bed of a large circulation and the occurrence of alveolar shunting. Of great importance in the implementation of this mechanism is insufficient hypoxemic vasoconstriction (Eilech Lilestrandt reflex) in poorly ventilated areas of the lung, which worsens the ratio of ventilation and perfusion.

Another mechanism of formation of respiratory failure is observed in the massive inflammatory lesion of one lung. In these cases, there is a significant difference in the respiratory volumes that produce a healthy and affected lung. For reasons of retaliation, the affected (ie, more rigid) lung during inhalation receives a significantly smaller proportion of the respiratory volume, since a significantly higher filling pressure is required to overcome the airway resistance in the affected lung. This leads to an even greater violation of ventilation-perfusion relations and aggravation of arterial hypoxemia.

The described mechanism is the reason that some patients with unilateral widespread lung injury, complicated by respiratory failure, often occupy a forced position on the healthy side. This position somewhat aligns the respiratory volumes of healthy and affected lungs and, in addition, promotes some redistribution of blood flow towards the healthy lung. As a result of the violation of ventilation-perfusion ratios, oxygenation of the blood decreases and somewhat improves.

It should be added that in case of severe respiratory failure, when total impairment of pulmonary ventilation is added to the disturbances of oxygenation, for example, as a result of the expressed fatigue of the respiratory musculature, in addition to hypoxemia in the arterial blood, the stress of carbon dioxide increases and hypercapnia develops. In these cases, it is a mixed form of acute respiratory failure.

[8], [9], [10], [11], [12], [13]

Infectious-toxic shock

Infectious-toxic shock is a syndrome of acute vascular insufficiency that develops as a result of the toxic effect of an infectious agent on the vascular system. The massive effect of bacterial toxins directly on the vascular wall leads to a pronounced dilatation of venous vessels and the deposition of large volumes of blood mainly in the vascular bed of abdominal organs. As a result, the flow of blood to the right heart, bcc decreases, the shock volume (VO), cardiac output and the perfusion of peripheral organs and tissues are significantly impaired.

Thus, as a result of the action of pathogens of pneumonia on the vascular system, a hypovolemic shock develops, characterized by a decrease in BCC, cardiac output, CVP (pressure in the right atrium), and the filling pressure of the left ventricle.

In severe cases, if the toxic effect of the infectious agent continues, the hypoxia of organs and tissues, aggravated by respiratory insufficiency and hypoxemia, leads to the development of fatal disorders of microcirculation, metabolic acidosis, the onset of DIC syndrome, and a sharp disruption of vascular permeability and peripheral organs.

The clinical picture of infectious-toxic shock depends on the degree of circulatory disturbance. Signs of infectious-toxic shock often occur at the stage of resolution of severe lobar pneumonia, especially with a critical fall in the previously elevated body temperature. The patient suddenly has a sharp weakness, dizziness, noise in the ears, darkening in the eyes, nausea, the urge to vomit. Increases shortness of breath, palpitation, there is a profuse sticky cold sweat.

The examination pays attention to the sharp pallor of the skin and visible mucous membranes, acrocyanosis, the skin becomes moist and cold. In the study of the cardiovascular system, very characteristic signs of shock are revealed:

• tachycardia up to 120 beats. In minutes and more;
• threadlike pulse;
• decrease in systolic blood pressure to 90 mm Hg. Art. And below;
• a significant reduction in pulse blood pressure (up to 15-20 mm Hg), which is often associated with a sharp drop in cardiac output;
• pronounced deafness of heart sounds.

In severe cases, it is possible to develop a co-morbid condition and even coma. Cold, moist, pale skin acquires a peculiar earthy-gray hue, which indicates a marked violation of peripheral circulation.

Body temperature drops below 36 ° C. Dyspnea increases, the number of respiratory movements increases to 30-35 per 1 minute. Pulse is threadlike, frequent, sometimes arrhythmic. Heart sounds are very deaf. Systolic blood pressure is not higher than 60-50 mm Hg. Art. Or is not determined at all.

The decrease in renal function is manifested by oliguria, and in more severe cases by anuria, accompanied by a gradual increase in the concentration of urea and creatinine in the blood, a violation of the acid-base state (metabolic acidosis).

Sepsis

Currently, sepsis is defined as a generalized inflammatory response of the body to infection mediated by endogenous mediators and realized in organs and systems remote from the site of primary damage. The main consequence of this generalized inflammatory reaction is multiple organ failure.

In accordance with the decisions of the conciliatory conference, the American College of Chest Physicians and Society of Critical Care Medicine (1991) distinguish five stages of a single infectious and inflammatory process of the body:

• bacteremia;
• sepsis;
• severe sepsis;
• septic shock;
• multiple organ failure.

Each of these stages is distinguished by its unique clinical picture and the outcome of the disease. For example, lethality with sepsis averages 40-35%, with severe sepsis from 18 to 52% and septic shock - from 46 to 82%.

It should be remembered that the most common causes of sepsis are:

• pulmonary infections, including pneumonia (about 45% of all cases of sepsis);
• abdominal infections (about 20%);
• infection of the urino-genital organs (about 15%).

Below are the clinical and laboratory markers of the five stages of the generalized infectious inflammatory process.

Bacteremia is characterized by the presence of bacteria in the blood, detected by special laboratory methods.

Sepsis is a systemic inflammatory response of the body to infection. It is manifested by the following nonspecific signs:

• body temperature greater than 38 ° C or less than 36 ° C;
• The heart rate is more than 90 beats. In 1 min;
• CHDD more than 24 per 1 min or PaCO2 is less than 32 mm Hg. Art. (hypocapnia);
• leukocytosis more than 12 x 10 ⁹ / l or leukocytes less than 4 x 10 ⁹ / l or a stab shift to the left more than 10%

It should be emphasized that according to modern ideas, bacteraemia is not an obligatory sign of sepsis; this is just one of the initial stages of the systemic inflammatory response of the body. In a real clinical situation, bacterial culture in the blood is detected only in 30% of patients with sepsis (!).

Severe sepsis is a sepsis associated with organ dysfunction, a decrease in blood supply, or arterial hypotension (a systolic blood pressure of 120 mm Hg or a systolic blood pressure decrease of more than 40 mm Hg from the baseline level.

Septic shock is characterized by arterial hypotension, which persists despite adequate treatment, as well as the presence of pronounced violations of perfusion and hypoxia of peripheral organs and tissues and the emergence of metabolic acidosis and oliguria / anuria.

The above criteria for sepsis are not specific, so the diagnosis of this complication, at least until Until signs of tissue hypoperfusion and / or persistent arterial hypotension are present, is extremely difficult. In most cases, evaluation of the results of blood cultures for sterility also does not help, since in 1/2 or 2/3 of patients with sepsis they are generally negative.

Clinical and laboratory diagnosis of late sepsis (severe sepsis and septic shock) is more reliable, because at these stages of the progression of the septic state, clearly defined features of persistent arterial hypotension, tissue hypoperfusion and internal organ dysfunction are attached to the nonspecific signs of the inflammatory syndrome.

Recall that in the case of severe sepsis and septic shock sharply worsened clinical picture of the disease. In patients, there are signs of Iptoxication, acute respiratory failure and arterial hypotension. Strengthens weakness, shortness of breath, palpitation, there is a cold sweat. Pale or earthy color of the skin, acrocyanosis indicate a marked violation of peripheral circulation. There is a tachycardia more than 120 ud. In min, a thread-like pulse. Significantly reduced systolic blood pressure (below 90-60 mm Hg). Appears oliguria and anuria. Consciousness is obscured (sopor, coma).

Recently, some new laboratory indicators have been used to diagnose sepsis. Among them is the definition of cytotoxic concentration, which play a leading role in the pathogenesis of the generalized inflammatory response of the body to infectious (or non-infectious) damage. A significant increase in the concentration of cytokines - IL-1, IL-6, IL-8, IL-10, as well as tumor necrosis factor-TNFa (TNF) was shown. Nevertheless, the universal role of cytokines in the pathogenesis of other pathological processes and the possibility of increasing their concentration in heart failure, pancreatitis, after massive operations, etc. Should be considered.

Another diagnostic test used to confirm the diagnosis of sepsis is the determination of the content of one of the acute phase proteins, procalcitonin. It was shown that the content of this protein above 5 mg / ml is a more sensitive and specific marker of sepsis than the level of cytokines, C-reactive protein and some clinical indicators.

For a dynamic assessment of the state of tissue perfusion and the effectiveness of treatment of patients with sepsis, the following is recommended:

• the concentration of lactate in the blood (normally less than 2 meq / l);
• determination of PCO2 of the gastric mucosa with gastric tonometry (normally less than 45 mm Hg);
• determination of saturation of mixed venous blood (in the norm of 70-80%);
• determination of oxygen delivery (normally more than 600 ml / min / m ² ).

Finally, for individual adequate treatment of septic shock, in many cases, a determination has been made in the dynamics of a number of hemodipamic indicators, including using the catheterization of the right heart with the Swan-Ganz catheter.

Multiple organ failure

The syndrome of multiple organ failure is the final phase of the generalized inflammatory reaction of the organism (sepsis). The syndrome is characterized by severe dysfunction of two or more organ systems in a patient with an acute infectious disease (including pneumonia), when homeostasis can no longer be maintained without external interventions. Multiple organ failure is the most frequent direct cause of death of patients hospitalized in the ICU.

Progressive dysfunction of various organ systems is caused, first of all, by a generalized increase in vascular permeability and damage to the endothelium as a result of exposure to organs of an excessively high content of cytokines, leukotrienes, active metabolites of O2, arachidonic acid products. Most often develops dysfunction of the central nervous system, liver, kidneys, DIC-syndrome and acute respiratory distress syndrome. In this case, the defeat of one organ system against the background of sepsis increases the risk of developing a lethal outcome by an average of 15-20%.

Assessment of the severity of pneumonia

An objective assessment of the severity of the course of pneumonia is necessary to develop optimal tactics for patients, primarily to decide whether to hospitalize patients with pneumonia in the hospital or in the intensive care unit (ICU). The severity of the course of pneumonia is determined by many factors: the biological properties of the causative agent of the disease, the possible mechanisms of its penetration into the respiratory sections of the lungs, the prevalence of the inflammatory process in the lungs, the presence of complications, severe concomitant diseases, the age of the patients, their social status, etc.

At present, the most widespread among clinicians is the Pneumonia PORT (The Patient Pneumonia Outcomes Research Team - PORT), developed by M. Fine and co-workers in 1997. The M. Fine scale allows rapid stratification of a patient with pneumonia according to the severity of the disease and the prognosis. The scale takes into account the age and sex of patients, the presence of concomitant diseases and clinical and laboratory data reflecting the severity of the inflammatory process in the lungs and the presence of the most significant complications.

Score assessment of severity of patients with community-acquired pneumonia (PORT) (according to M. Fine et al., 1997)

Characteristic	Points
Demographics
Age of the man	Age in years
Age of the woman	(Age in years - 10)
Stay in a nursing home	+ 10
Accompanying illnesses
Malignant tumors	+ 30
Diseases of the liver	+ 20
Congestive heart failure	+ 10
Cerebrovascular diseases	+ 10
Kidney Diseases	+ 10
Impairment of consciousness	+ 20
Pulse> 125 in minutes	+ 10
Respiratory rate> 30 min	+ 20
Systolic blood pressure <90 mm Hg. Art.	+ 20
Body temperature <35 ° C or> 40 ° C	+ 15
Laboratory and X-ray data
Hematocrit <30%	+ 30
PH <7.35	+ 30
Urea in serum> 10.7 mmol / l	+ 20
Sodium in serum <130 meq / L	+ 20
Glucose in serum> 13.9 mmol / l	+ 10
Pa0 2 <60 mm Hg. Art. (or saturation 0 2 <90%)	+ 10
Pleural effusion	+ 10

According to M. Fine scale, all patients with pneumonia can be referred to one and. 5 classes of severity of pneumonia, differing in the number of balloons awarded.

• I class - less than 70 points (age of patients less than 50 years, concomitant diseases and unfavorable clinical and laboratory signs are absent);
• II class - more than 70 points;
• III class - 71-90 points;
• IV class - 91-130 points;
• V class - more than 130 points.

A close correlation was shown between the M. Fine class and the mortality of patients with community-acquired pneumonia. Thus, the lethality of I-III patients varies from 0.1% to 2.8%, increases to 8.2% in class IV patients, and increases dramatically in patients in Class V, reaching 29.2%. Thus, patients with mild pneumonia, belonging to classes I and II, have a very low risk of death and can receive treatment on an outpatient basis. Patients with moderate severity of pneumonia (III and IV classes) are treated in a specialized hospital. Patients classified as class V are characterized by the most severe course of pneumonia at high risk of death and, of course, require hospitalization in ORIG

Mortality of patients with community-acquired pneumonia, depending on the grade of severity of the disease (according to M. Fine et al., 1997)

Class	Number of points	Mortality,%	Recommendations for on-site treatment
I	<70 Age less than 50 years, no additional points	0.1	Ambulatory
II	<70	0.6	Ambulatory
III	71-90	2.8	In the hospital
IV	91-130	8.2	In the hospital
V	> 130	29.2	In the hospital (ICU)

In general, the PORT scale quite satisfactorily reflects the severity of community-acquired pneumonia, but in practice it can not always be used for rapid stratification of patients, especially on an outpatient basis, since a number of laboratory tests are required to implement it. Therefore, in practical work, other more accessible recommendations are used, but the severity of the course of pneumonia.

Thus, the American Thoracic Society has developed criteria for the isolation of a group of patients with severe pneumonia, requiring unconditional hospitalization of patients in the ICU. In this case, large and small signs of severe pneumonia are prominent;

Small criteria include:

• number of respiratory movements> 30 per min;
• severe degree of respiratory failure (PaO2 / FiJ2 <250);
• bilateral or multilobar pneumonia;
• systolic blood pressure <90 mm Hg. P.
• diastolic blood pressure <60 mm Hg. Art.

Major criteria include:

• the need for ventilation (see Chapter 2);
• an increase in the infiltrate volume in the lungs by 50% or more within 48 hours from the start of therapy;
• acute renal failure (diuresis <80 ml for 4 hours or serum creatinine> 2 mg / dL in the absence of anamnestic indications of the presence of CRF);
• septic shock or the need for vasopressors for more than 4 hours.

The criteria for the severe course of pediatric pneumonia, cited in the work of CB Yakovlev (2002), deserve attention. According to these criteria, for the evaluation of pneumonia as severe it is necessary to have at least one basic and additional trait presented in the table.

Criteria for severe course of community-acquired pneumonia (according to CB Yakovlev, 2002)

Main criteria	Additional criteria (if laboratory testing is possible) *
Acute respiratory failure (breathing rate> 30 min and saturation of hemoglobin with oxygen <90%)	Leukopenia
Arterial hypotension (systolic blood pressure <90 mm Hg and / or diastolic blood pressure <60 mm Hg)	Hypoxemia
Bilateral or multi-lobe lesion of the lungs	Hemoglobin <100 g / l
Acute kidney failure	Hematocrit <30%
Impairment of consciousness
Severe concomitant pathology (congestive heart failure, cirrhosis, decompensated diabetes mellitus, chronic renal failure)
Extrapulmonary focus of infection (meningitis, pericarditis, etc.)

* for the evaluation of pneumonia as severe it is necessary to have at least one basic and additional trait.

The table shows that the proposed criteria take into account the recommendations of M. Fine et al. And American Thoracic Society, but favorably differ from them in the simplicity and practical orientation of stratification of patients with pneumonia, which can be successfully carried out even at the outpatient and in the inpatient department of hospitals.

It should be added that approximately 10% of community-acquired and about 25% of nosocomial pneumonia can be attributed to severe pneumonia that require treatment in the ICU.

The most frequent pathogens of severe pneumonia are:

• pneumococcus pneumoniae (Sfrepfococcus pneumoniae);
• legionella (Legionella spp.) .;
• Staphylococcus aureus (Staphylococcus aureus);
• Pseudomonas aeruginosa;
• Klebsiella.

Pneumonia caused by these microorganisms, especially Pseudomonas aeruginosa, Staphylococcus aureus and Klebsiella, have a very high risk of death (31% to 61%). Hemophilus rod, mycoplasma and chlamydia rarely lead to severe pneumonia.

These data should also be taken into account when assessing the risk of a possible adverse outcome of pneumonia.

[14], [15], [16], [17], [18], [19], [20]