Complications of pneumonia

The severity 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 these are:

1. Pulmonary complications:
   1. acute respiratory failure;
   2. parapleural exudative pleurisy and/or pleural empyema;
   3. lung abscess;
   4. acute respiratory distress syndrome.
2. Extrapulmonary complications:
   1. infectious toxic shock;
   2. sepsis.

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Acute respiratory failure

Acute respiratory failure is undoubtedly one of the main indicators of the severity 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 require artificial ventilation.

Severe pneumonia is accompanied by the development of a predominantly hypoxemic (parenchymatous) form of respiratory failure, caused by several pathogenetic mechanisms:

• massive alveolar infiltration;
• reduction of the total functioning surface of the alveolar-capillary membrane;
• violation of gas diffusion;
• severe disturbances in ventilation-perfusion relationships.

The latter mechanism is apparently of decisive importance for the development of arterial hypoxemia in patients with pneumonia, since the preservation of blood flow in poorly ventilated or non-ventilated alveoli quickly leads to the discharge of mixed venous blood into the arterial bed of the systemic circulation and the development of alveolar shunting. Of great importance in the implementation of this mechanism is insufficient hypoxemic vasoconstriction (Eilech-Liljestrandt reflex) in poorly ventilated areas of the lung, which worsens the ventilation-perfusion ratio.

Another mechanism of respiratory failure formation is observed in case of massive inflammatory damage of one lung. In these cases, there is a significant difference in the respiratory volumes received by the healthy and damaged lungs. For obvious reasons, the damaged (i.e. more rigid) lung receives a significantly smaller part of the respiratory volume during inhalation, since significantly greater filling pressure is required to overcome the resistance of the airways in the damaged lung. This leads to an even greater disruption of ventilation-perfusion relations and worsening of arterial hypoxemia.

The described mechanism is the reason why some patients with unilateral widespread lung damage complicated by respiratory failure often take a forced position on the healthy side. This position somewhat equalizes the respiratory volumes of the healthy and affected lungs and, in addition, contributes to some redistribution of blood flow towards the healthy lung. As a result of the violation of ventilation-perfusion relations, blood oxygenation decreases and improves somewhat.

It should be added that in severe respiratory failure, when oxygenation disorders are accompanied by a total reduction in pulmonary ventilation, for example as a result of severe fatigue of the respiratory muscles, in addition to hypoxemia, the carbon dioxide tension in the arterial blood increases, and hypercapnia develops. In these cases, we are talking about a mixed form of acute respiratory failure.

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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. Massive impact of bacterial toxins directly on the vascular wall leads to pronounced dilation of venous vessels and deposition of large volumes of blood mainly in the vascular bed of the abdominal organs. As a result, blood flow to the right heart chambers, circulating blood volume decreases, stroke volume (SV) and cardiac output fall, and perfusion of peripheral organs and tissues is significantly impaired.

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

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

The clinical picture of infectious toxic shock depends on the degree of circulatory failure. Signs of infectious toxic shock often appear at the stage of resolution of severe lobar pneumonia, especially with a critical drop in previously elevated body temperature. The patient suddenly experiences severe weakness, dizziness, tinnitus, darkening of the eyes, nausea, and vomiting. Shortness of breath and palpitations increase, and profuse sticky cold sweat appears.

During examination, attention is drawn to the sharp pallor of the skin and visible mucous membranes, acrocyanosis, the skin becomes moist and cold. When examining the cardiovascular system, very characteristic signs of shock are revealed:

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

In severe cases, a soporous state and even coma may develop. Cold, damp, pale skin acquires a peculiar earthy-gray hue, which indicates severe disturbances of peripheral circulation.

Body temperature drops below 36°C. Shortness of breath increases, the number of respiratory movements increases to 30-35 per 1 min. The pulse is threadlike, frequent, sometimes arrhythmic. Heart sounds are very muffled. Systolic blood pressure is not higher than 60-50 mm Hg or is not determined at all.

A decrease in kidney function is manifested by oliguria, and in more severe cases - anuria, accompanied by a gradual increase in the concentration of urea and creatinine in the blood, and a violation of the acid-base balance (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 consensus conference of the American College of Chest Physicians and the Society of Critical Care Medicine (1991), five stages of a single infectious and inflammatory process in the body are distinguished:

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

Each of these stages is distinguished by its own unique clinical picture and outcome of the disease. Thus, the mortality rate for sepsis is on average 40-35%, for severe sepsis from 18 to 52% and for 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%);
• genitourinary infections (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 manifests itself with the following non-specific signs:

• body temperature greater than 38°C or less than 36°C;
• Heart rate greater than 90 beats per 1 min;
• Respiratory rate greater than 24/min or PaCO2 less than 32 mm Hg (hypocapnia);
• leukocytosis more than 12 x 10 ⁹ /l or leukocytes less than 4 x 10 ⁹ /l or band shift to the left more than 10%

It should be emphasized that, according to modern concepts, bacteremia is not a mandatory sign of sepsis; it is just one of the initial stages of the body's systemic inflammatory response. In a real clinical situation, bacterial culture in the blood is detected in only 30% of patients with sepsis (!).

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

Septic shock is characterized by arterial hypotension that persists despite adequate treatment, as well as the presence of severe perfusion disorders and hypoxia of peripheral organs and tissues and the occurrence of metabolic acidosis and oliguria/anuria.

The listed criteria for sepsis are not specific, so the diagnosis of this complication, at least until there are signs of tissue hypoperfusion and/or persistent arterial hypotension, is extremely difficult. In most cases, the assessment of the results of blood cultures for sterility is also of no help, since in 1/2 or 2/3 of patients with sepsis they are generally negative.

Clinical and laboratory diagnostics of the late stage of sepsis (severe sepsis and septic shock) is more reliable, since at these stages of progression of the septic condition, non-specific signs of inflammatory syndrome are joined by fairly clearly defined signs of persistent arterial hypotension, tissue hypoperfusion and dysfunction of internal organs.

Let us recall that in case of development of severe sepsis and septic shock the clinical picture of the disease sharply worsens. Patients show increasing signs of hyptoxication, acute respiratory failure and arterial hypotension. Weakness, dyspnea, palpitations increase, cold sweat appears. Paleness or sallow color of the skin, acrocyanosis indicate severe disturbances of peripheral blood circulation. Tachycardia over 120 beats per minute, threadlike pulse appear. Systolic blood pressure significantly decreases (below 90-60 mm Hg). Oliguria and anuria appear. Consciousness is clouded (stupor, coma).

Recently, some new laboratory parameters have been used to diagnose sepsis. These include determination of the concentration of cytokines, 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 - TNF-a (TNF) has been shown. Nevertheless, it is necessary to take into account 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.

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 has been 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 dynamic assessment of the state of tissue perfusion and the effectiveness of treatment of patients with sepsis, it is recommended to determine the following indicators:

• lactate concentration in the blood (normally less than 2 mEq/l);
• determination of PCO2 of the gastric mucosa during gastric tonometry (normally less than 45 mm Hg);
• determination of mixed venous blood saturation (normal 70-80%);
• determination of oxygen delivery (normally more than 600 ml/min/m2 ⁾.

Finally, for individual adequate therapy of septic shock, in many cases it is indicated to determine a number of hemodynamic parameters dynamically, including using catheterization of the right heart with a Swan-Ganz catheter.

Multiple organ failure

Multiple organ failure syndrome is the final stage of progression of the generalized inflammatory response of the body (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 common immediate cause of death in patients hospitalized in intensive care units.

Progressive dysfunction of various organ systems is caused, first of all, by a generalized increase in vascular permeability and endothelial damage as a result of the impact of excessively high levels of cytokines, leukotrienes, active O2 metabolites, and arachidonic acid products on organs. Most often, dysfunction of the central nervous system, liver, and kidneys, DIC syndrome, and acute respiratory distress syndrome develop. At the same time, damage to one organ system against the background of sepsis increases the risk of a fatal outcome by an average of 15-20%.

Assessment of the severity of pneumonia

An objective assessment of the severity of pneumonia is necessary to develop optimal patient management tactics, primarily to decide on the advisability of hospitalizing patients with pneumonia in a hospital or in the intensive care unit (ICU). The severity of pneumonia is determined by many factors: the biological properties of the pathogen, 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 patients, their social status, etc.

Currently, the most widely used scale among clinicians is the Pneumonia PORT (The Patient Pneumonia Outcomes Research Team - PORT), developed by M. Fine and his colleagues in 1997. The M. Fine scale allows for rapid stratification of a patient with pneumonia by severity of the disease and prognosis. The scale takes into account the age and gender 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.

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

Characteristic	Points
Demographic data
Age of the man	Age in years
Age of the woman	(Age in years - 10)
Staying in a nursing home	+ 10
Associated diseases
Malignant tumors	+ 30
Liver diseases	+ 20
Congestive heart failure	+ 10
Cerebrovascular diseases	+ 10
Kidney diseases	+ 10
Impaired consciousness	+ 20
Pulse >125 bpm	+ 10
Respiratory rate > 30 per min	+ 20
Systolic BP < 90 mmHg	+ 20
Body temperature < 35°C or > 40°C	+ 15
Laboratory and radiological data
Hematocrit < 30%	+ 30
PH < 7.35	+ 30
Serum urea > 10.7 mmol/L	+ 20
Serum sodium <130 mEq/L	+ 20
Serum glucose > 13.9 mmol/L	+ 10
Pa0 2 < 60 mm Hg. Art. (or saturation 0 2 < 90%)	+ 10
Pleural effusion	+ 10

According to the M. Fine scale, all patients with pneumonia can be classified into one of 5 pneumonia severity classes, which differ in the number of balloons assigned.

• Class I - less than 70 points (patients are under 50 years old, there are no concomitant diseases or unfavorable clinical and laboratory signs);
• Class II - more than 70 points;
• Class III - 71-90 points;
• IV class - 91-130 points;
• Class V - more than 130 points.

A close correlation was shown between the M. Fine scale class and the mortality rate of patients with community-acquired pneumonia. Thus, the mortality rate of patients with classes I - III ranges from 0.1% to 2.8%, increases to 8.2% in patients with class IV and increases sharply in patients with class V, reaching 29.2%. Thus, patients with a mild course of 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 pneumonia (classes III and IV) are shown treatment in a specialized hospital. Patients assigned to class V are distinguished by the most severe course of pneumonia, a high risk of death and, of course, require hospitalization in the ORIG.

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

Class	Number of points	Mortality, %	Recommendations for treatment location
I	<70 Age under 50, no additional points	0,1	Outpatient
II	<70	0.6	Outpatient
III	71-90	2.8	In hospital
IV	91-130	8.2	In hospital
V	>130	29.2	In hospital (ICU)

In general, the PORT scale quite satisfactorily reflects the severity of community-acquired pneumonia, but in practice it cannot always be used for the purposes of rapid stratification of patients, especially in outpatient settings, since its implementation requires a number of laboratory tests. Therefore, other, more accessible recommendations for assessing the severity of pneumonia are used in practical work.

Thus, the American Thoracic Society has developed criteria for identifying a group of patients with severe pneumonia requiring unconditional hospitalization in the intensive care unit. In this case, major and minor signs of severe pneumonia are identified;

Minor criteria include:

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

Major criteria include:

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

The criteria for severe hospital-acquired pneumonia given in the work of S. V. Yakovlev (2002) are worthy of attention. According to these criteria, to assess pneumonia as severe, it is necessary to have at least one main and additional sign presented in the table.

Criteria for severe community-acquired pneumonia (according to S. V. Yakovlev, 2002)

Main criteria	Additional criteria (if laboratory testing is possible)*
Acute respiratory failure (respiratory rate > 30 bpm and hemoglobin oxygen saturation < 90%)	Leukopenia
Arterial hypotension (systolic BP < 90 mmHg and/or diastolic BP < 60 mmHg)	Hypoxemia
Bilateral or multilobar lung disease	Hemoglobin <100 g/l
Acute renal failure	Hematocrit < 30%
Impaired consciousness
Severe concomitant pathology (congestive heart failure, liver cirrhosis, decompensated diabetes mellitus, chronic renal failure)
Extrapulmonary source of infection (meningitis, pericarditis, etc.)

* to assess pneumonia as severe, the presence of at least one main and additional symptom is necessary.

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

It should be added that approximately 10% of community-acquired pneumonia and about 25% of nosocomial pneumonia can be classified as severe pneumonia, which requires treatment in the intensive care unit.

The most common pathogens that cause severe pneumonia are:

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

Pneumonia caused by these microorganisms, especially Pseudomonas aeruginosa, Staphylococcus aureus, and Klebsiella, has a very high mortality rate (31% to 61%). Haemophilus influenzae, Mycoplasma, and Chlamydia very rarely cause severe pneumonia.

These data also need to be taken into account when assessing the risk of possible adverse outcomes of pneumonia.

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