Critical States in Respiratory Tuberculosis in Adults - N.I. Fomichova 2010

Pulmonary Embolism

Pulmonary embolism (PE) is the occlusion of the main pulmonary artery trunk or its branches of various calibers by a thrombus that originally formed in the Veins OF THE systemic Circulation or in the right heart chambers and was transported into the pulmonary vascular bed by the Blood flow.

PE is the most frequent and clinically significant type of embolism. Today, it is a rather common complication of numerous diseases and conditions, predominantly venous thrombosis, including in the clinical Setting of tuberculosis. According to domestic and foreign literature, PE occurs in approximately 3% of the population. Autopsy findings reveal pathomorphological signs of pulmonary embolism in 25–50% of hospitalized patients, and in many cases, this complication is the cause of death. However, during life, PE is diagnosed in only 10–20% of cases (T.J. Prendergast, S.J. Ruoss, 1999).

Etiology AND Pathogenesis. The cause of thrombosis lies in the Impairment of the general blood clotting system function, yet there are numerous factors that contribute to this process. It is known that thrombosis occurs in various infections and intoxications, postoperatively, upon endothelial integrity disruption, in inflammation of the vascular and endocardial walls, slowed blood flow, alterations in plasma protein composition and Organism reactivity, vascular spasm tendencies, and decreased anticoagulant function of the Lungs. All these factors are present in tuberculosis. However, due to the high anticoagulant and fibrinolytic activity of blood flowing through the lungs, primary pulmonary artery thrombosis is extremely rare. Even cases of spontaneous thrombolysis in pulmonary vessels with persistent peripheral venous thrombosis are known. Consequently, the main etiological factors of PE are thrombophlebitis, phlebothrombosis, or the presence of diseases causing The formation of thrombotic masses in the right heart chambers (thromboendocarditis, atrial fibrillation, Hypertension, rheumatism, ischemic heart disease, cardiomyopathies, etc.).

Three major risk factors for thrombosis are well recognized: venous stasis (low Cardiac Output syndrome, major surgical interventions, bed rest, advanced age, Pregnancy), activation of the Blood Coagulation SYSTEM (surgery, myocardial infarction, fibrinogen dysfunction, coagulopathies in general, oncological diseases, Nephrotic Syndrome, etc.), and vascular intima damage (of traumatic and non-traumatic origin). All these factors can accompany tuberculosis. On the other hand, the tuberculous process itself can create preconditions for pulmonary embolism, especially in patients with chronic forms of the disease accompanied by The Development of Chronic Cor Pulmonale, which significantly increases the risk of PE. Acute Heart Failure with a risk of PE may occur in patients with acutely progressive forms of tuberculosis, such as Miliary tuberculosis and Caseous Pneumonia. The main pathogenetic factors in this regard are hypertension in the lesser circulation due to hypoxemia, spasm of pulmonary arterioles, and their reduction in fibrocavernous, cirrhotic, and chronic disseminated tuberculous processes. In addition, in chronic forms of tuberculosis and extensive residual changes after the cure of respiratory tuberculosis, sclerotic changes in pulmonary vessels are observed, along with their deformation and prolonged vascular spasm, leading to decreased blood flow velocity, increased blood viscosity, and vascular wall damage. It is known that vasoconstriction weakens the function of the BLOOD ANTICOAGULANT SYSTEM and contributes to elevated venous pressure. A threat to the patient's life arises during relapse, exacerbation, or progression of the tuberculous process in the lungs, which worsens respiratory impairment. A generalized tuberculous process with pronounced intoxication (so-called tuberculous Sepsis) can be complicated by thrombosis—typically a manifestation of the hypercoagulable phase of DIC syndrome—and become the cause of PE. The latter is a frequent complication of the postoperative period, and the surgical method of Treatment is gaining increasing importance in the context of the spread of drug-resistant tuberculosis.

PE is divided into three categories (M. Moss, 1998):

1. Massive pulmonary artery occlusion (up to 50% of all cases).

2. Pulmonary infarction - embolization of a feeding branch of the pulmonary artery with Necrosis of a lung parenchyma area (in 10% of cases).

3. Non-infarcted PE (very difficult to diagnose as there are no specific symptoms).

Pathophysiology of PE. When a thromboembolus enters the pulmonary artery, a cascade of pathological disorders is triggered. First and foremost, hemodynamic alterations occur with an increase in pulmonary vascular resistance resulting from vascular obstruction and vasoconstriction induced by serotonin and thromboxane A2. Right ventricular afterload increases, requiring an increase in its workload. Pulmonary hypertension develops when 50% of the Pulmonary Circulation is occluded. Further increase in embolic obstruction leads to decreased cardiac output and hypoxemia (it should be noted that in chronic forms of tuberculosis, due to specific pathomorphological Changes in the Vessels of the lesser circulation, occlusion of an even smaller volume of the pulmonary circulation can lead to a life-threatening condition for the patient). A reduction in pulmonary blood flow by more than 75% represents a critical level of embolic obstruction and leads to cardiac depression, systemic arterial hypotension, Shock, and circulatory arrest. Thus, mechanical obstruction of the pulmonary Arteries is the leading factor in hemodynamic disorders during PE. In the event of a massive embolus entering the pulmonary artery, cardiac output may suddenly drop to zero, resulting in circulatory arrest.

Another important pathogenetic factor of PE is the disruption of pulmonary gas exchange. Alveolar dead space increases, ventilation-perfusion ratios in the lungs are impaired, surfactant synthesis deteriorates, alveolar stability decreases, leading to their Atelectasis and increased pulmonary blood shunting. These factors result in severe hypoxemia, often while carbon dioxide elimination is preserved. Areas of poorly perfused lung tissue are high-risk zones for the development of infarct pneumonia.

The pathomorphological picture of lung tissue lesions in PE is typically characterized by areas of necrosis and atelectasis, interstitial edema, zones of acute emphysema, compensatory-adaptive dilation and hyperemia of Pulmonary veins and bronchial arteries, as well as dystrophic changes in the myocardium, including infarctions of the right heart chambers resulting from pulmonary hypertension and hypoxemia developed during PE. Pulmonary edema occurs against the Background of pronounced Hypoxia and multiple embolization.

A special place in the pathogenesis of PE is occupied by pulmonary infarction, which almost always occurs against the background of prior venous congestion, sometimes occult. Occasionally, against the backdrop of pronounced pneumosclerosis leading to Impaired blood supply, pulmonary infarction can be ischemic. Embolism of a vessel of any diameter is accompanied by incomplete pulmonary infarction, which is characterized by focal Hemorrhage. This explains its usually favorable outcome. Pulmonary infarction predominantly occurs 24 hours after pulmonary vessel obturation, and its full development takes 5–6 days. A decrease in surfactant production plays an important role in the development of pulmonary infarction.

In PE, activation of Fibrinolysis occurs as early as the first days, and the dissolution of fresh thromboemboli begins. This process takes 10–14 days. Complete lysis of thrombi in the pulmonary artery occurs within several weeks. However, not all emboli dissolve—sometimes the thrombus rapidly organizes, making its lysis impossible. As microcirculation in the lungs improves, surfactant production is restored, which promotes the fastest possible disappearance of pathomorphological and clinical manifestations of pulmonary infarction.

Classification and clinical manifestations. Depending on the localization of the embolic process, the following clinical and anatomical variants of PE are distinguished:

1. Embolism of the main trunk or main Branches of the pulmonary artery (massive embolism).

2. Embolism of lobar or segmental branches of the pulmonary artery.

3. Embolism of small branches of the pulmonary artery, which is most often bilateral and, as a rule, is not fatal for the patient.

Depending on the volume of embolic obstruction, PE is classified as small (occlusion of 25% of the pulmonary circulation), submassive (occlusion of up to 50% of the pulmonary circulation), massive (occlusion of over 50% of the pulmonary circulation), and fatal (occlusion of over 75% of the pulmonary circulation).

The clinical picture of PE is determined by the number and caliber of vessels excluded from circulation, The rate of Development of the embolism, and the degree of pulmonary artery obturation.

The following Clinical forms of PE are distinguished:

1. Fulminant - observed with simultaneous complete occlusion of the main trunk or both main branches of the pulmonary artery.

The most severe clinical symptoms are associated with profound disorders of vital Functions (collapse, Acute Respiratory Failure, respiratory arrest, frequently ventricular fibrillation); the disease runs an instantaneous course and results in death within several minutes. Pulmonary infarctions do not have time to develop in these cases.

2. Acute (in 30–35% of patients) - observed with rapidly progressive occlusion of the main branches of the pulmonary artery involving a greater or lesser number of its lobar or segmental ramifications.

The development of pulmonary infarction is not typical for this variant, but it does occur. The acute form of PE lasts from several hours to several days (maximum 3–5 days). It is characterized by a sudden onset and tumultuous Progressive development of symptoms of respiratory, cardiovascular, and cerebral insufficiency.

3. Subacute (in 45–50% of patients) - observed with embolism of large and medium-sized intrapulmonary branches of the pulmonary artery.

It is frequently accompanied by the development of multiple pulmonary infarctions. Subacute pulmonary embolism (PE) lasts from one to several weeks. The acute manifestations of the initial period subside somewhat, and the disease takes on a slowly progressive character with increasing right ventricular and respiratory failure. Against this background, recurrent episodes of thromboembolism may occur, which are typically characterized by an exacerbation of symptoms or the appearance of a pulmonary infarction. Death may result from a sudden recurrent embolism of the main trunk or main branches of the pulmonary artery, or from progressive cardiopulmonary failure.

4. Recurrent or chronically recurrent with varying duration of remission and numerous relapses (in 15-25% of patients).

It is characterized by repeated embolisms of lobar, segmental, and subpleural branches of the pulmonary artery. Clinically, it manifests as recurrent pulmonary infarctions or Pleurisy, and lesser circulation hypertension with the development of progressively increasing right ventricular failure.

PE can occur in severe, moderate, and mild forms. Its clinical manifestations are nonspecific, but it is precisely these manifestations that make it possible to suspect the presence of this complication. The classical triad of symptoms in PE—sudden dyspnoea, pleuritic chest pain, and haemoptysis—is observed in only 20% of cases, while these symptoms individually are diagnosed in 85%, 75%, and 30% of cases, respectively. Dyspnoea is a consequence of reflex bronchoconstriction, decreased elasticity of the pulmonary tissue, and, in late stages, progressive hypoxaemia. The respiratory rate varies from 5-8 breaths per min (which is prognostically unfavourable) to tachypnoea of the order of 60-70 respiratory cycles per 1 minute. A sudden onset of dyspnoea is characteristic.

The most characteristic subjective manifestation of the disease is retrosternal pain of various characters, which occurs unexpectedly and suddenly. Most commonly, acute knife-like pain is observed. Embolism of the main trunk of the pulmonary artery causes recurrent retrosternal pain caused by the irritation of nerve apparatuses located in the wall of the pulmonary artery. In embolism of the small branches of the pulmonary artery, pain may be absent or masked by other clinical symptoms. The duration of pain can vary from a few minutes to several hours. Pleuritic pain accompanies the development of a pulmonary infarction, which is not always confirmed during a chest X-ray Examination.

Haemoptysis most frequently occurs against the background of pulmonary parenchymal infarction and is a consequence of high pulmonary hypertension.

Occlusion of large pulmonary arteries is accompanied by signs of acute cardiopulmonary failure. The classic syndrome of massive pulmonary vessel involvement includes: sudden collapse, the onset of retrosternal pain, dyspnoea, cyanosis of the mucous membranes, Nails, face, and the upper half of the body (pronounced slate-grey cyanosis), Swelling and pulsation of the jugular veins.

Tachycardia in patients with PE is often accompanied by rhythm and conduction disorders (extrasystolic and atrial fibrillation, bundle branch blocks). In addition to tachycardia and tachypnoea, an accentuation of the second heart sound over the pulmonary artery is auscultated in PE, which is recorded when systolic blood pressure in the pulmonary circulation exceeds 50 mm Hg. Auscultation in the lungs reveals dry or moist rales of various calibres, associated with both bronchoconstriction and pulmonary parenchymal oedema.

Characteristic symptoms of PE are fever and leukocytosis. Complaints of cough appear already at the stage of pulmonary infarction, i.e., on the 2nd-3rd day after pulmonary embolism. Complaints of dizziness, noise in the HEAD, and tinnitus are caused by transient cerebral hypoxia, and in severe forms, by cerebral oedema. In addition, patients may complain of general weakness, nausea, vomiting, and sweating.

Thus, clinically in PE, several syndromes can be distinguished in various combinations:

1. Acute respiratory distress syndrome – objectively manifested by dyspnoea, predominantly inspiratory, not accompanied by noisy breathing and orthopnoea.

2. Moderately pronounced bronchospastic syndrome – appears quite frequently and is accompanied by dry rales in the lungs, which are a consequence of the bronchopulmonary reflex.

3. Acute vascular insufficiency syndrome – manifested by pronounced arterial hypotension. This is a characteristic sign of PE. Circulatory shock is usually associated with massive pulmonary occlusion. Arterial hypotension is caused by the blockade of pulmonary blood flow due to occlusion of the main branches of the pulmonary artery, which causes acute overload of the right heart, a sharp decrease in blood flow to the left heart with a drop in cardiac output. A drop in blood pressure is also promoted by the pulmonary-vascular reflex. Arterial hypotension is accompanied by pronounced tachycardia.

4. Acute cor pulmonale syndrome – occurs in the first minutes of the disease and is caused by massive or submassive PE. It is manifested by the following symptoms: swelling of the jugular veins; pathological pulsation in the epigastric region and in the 2nd intercostal space to the left of the Sternum; tachycardia, expansion of the right border of The Heart and the zone of absolute cardiac dullness, accentuation of the second heart sound over the pulmonary artery; increased central venous pressure; sometimes pulmonary oedema; a painful Liver, upon pressure on which the jugular veins swell; characteristic ECG changes.

5. Acute coronary insufficiency syndrome – manifested by severe retrosternal pain, extrasystole, atrial fibrillation, etc.

6. Cerebral syndrome – characterized by general cerebral or focal disorders and caused primarily by cerebral hypoxia, and in severe PE – by cerebral oedema, microfocal haemorrhages into the Brain substance and Meninges. Thus, the patient may experience vomiting, convulsions, bradycardia, a comatose state, psychomotor agitation, hemiparesis, polyneuritis, meningeal symptoms.

7. Abdominal syndrome – rarely encountered, caused by acute swelling of the liver. The liver is enlarged, painful upon Palpation. Acute pain in the right hypochondrium and vomiting are observed.

8. Febrile syndrome – an increase in body Temperature usually occurs from the first hours of the disease and is a characteristic symptom of PE. In the majority of patients, a subfebrile temperature without chills is noted, and in a smaller number of patients, a febrile one. The total duration of fever is 2-12 days. Against the background of an active tuberculous process, this syndrome has almost no diagnostic value.

9. Pleuropulmonary syndrome, i.e., pulmonary infarction, pleuropneumonia, or infarction-pneumonia – develops 1-3 days after embolism. Clinically manifested by cough and chest pain on the affected side, pain intensifies during breathing; haemoptysis; elevated body temperature; lagging of the corresponding half of the chest during breathing, decreased pulmonary excursion on the affected side; shortening of the Percussion note over the area of pulmonary infarction; in the presence of pulmonary tissue infiltration – enhanced vocal fremitus, the appearance of bronchophony, a bronchial shade of breathing, fine bubbling rales, crepitation; pleural friction rub in dry pleurisy, a dull percussion sound and weakened/absent breathing upon the appearance of exudate.

Thus, a severe form of PE is observed in 16-35% of patients, in the overwhelming majority of whom 3-5 of the above-mentioned syndromes dominate in the clinical picture with the highest degree of severity. A moderately severe form is observed in 45-57% of patients. The clinical picture is less dramatic, and the manifestations of PE usually last several days. A mild form with a recurrent course occurs in 15-27% of patients. The Clinical presentation is mild, and PE is often undiagnosed because it proceeds under the mask of an "exacerbation" of the underlying disease, etc. For the timely Diagnosis of this form of PE, the following clinical signs should be taken into account: unexplained repeated losses of consciousness; collapses with a feeling of air hunger; feelings of chest tightness with difficult breathing that occur suddenly; repeated pneumonias of undetermined etiology; pleurisy with rapid regression; the appearance or enhancement of symptoms of cor pulmonale; unexplained fever. The Diagnostic significance of these symptoms increases if they are observed in patients with heart failure, intoxications, after surgical interventions, with signs of phlebothrombosis, as well as in patients with sclerotic changes in the pulmonary vessels with their prolonged spasm, decreased blood flow velocity, increased blood viscosity, and damage to the pulmonary vessel wall.

Diagnostics (Figure 14). The key to the diagnosis lies in the necessity of constantly remembering the possibility of PE in patients of the relevant categories, especially when relevant clinical manifestations occur, as discussed above. An important diagnostic factor is the presence of deep vein Thrombosis of the lower extremities. Attention should be paid to the patient's complaints of discomfort in the upper or lower extremities, a burning sensation, pulling pain along the veins, swelling and Asymmetry of the extremities, tenderness upon palpation, and unilateral swelling by the end of the day. One should not forget about pelvic vein thrombosis, which is also a frequent source of PE. Thrombosis of these veins manifests as dysuria, tenesmus, flatulence, tenderness upon rectal examination, and sometimes swelling of the abdominal wall and genitals.

Laboratory data. A general blood test reveals neutrophilic leukocytosis with a stab shift, lymphopenia, monocytosis, and an increased ESR, which, in combination with an active tuberculous process, has no diagnostic value. A biochemical blood test reveals an increase in Lactate dehydrogenase, especially LDH₃, seromucoid, haptoglobin, fibrin, and hypercoagulation. The enzyme-linked immunosorbent assay (ELISA) reveals an increase in D-dimer (a fibrin degradation product) in Blood Plasma. The sensitivity of elevated D-dimer levels for diagnosing proximal deep vein thrombosis or PE exceeds 90%, as it indicates the presence of an acute thrombus.

A normal D-dimer level (within 500 ng/ml) almost completely rules out the diagnosis of PE or thrombosis. However, an elevated D-dimer level does not specifically confirm pulmonary artery thrombosis, since fibrin is produced in many conditions (Cancer, inflammation, infections, necrosis, etc.).

Class="center">FIGURE 14 DIAGNOSTIC SCHEME FOR PULMONARY EMBOLISM (PE)

ECG findings. ECG Changes in pulmonary embolism (PE) are nonspecific and inconstant, remaining absent in 25% of cases. PE most frequently manifests as sinus tachycardia and T-wave inversion, while ST-segment alterations may also occur. Typical signs of pulmonary hypertension—such as a deep S wave in lead I, along with a Q wave and an inverted T wave in lead III—are observed in only 11% of PE patients. Often, the acute ECG manifestations of PE are mistaken for a posterior Left ventricular myocardial infarction. In some instances, PE presents with complete or incomplete right bundle branch block, and various Cardiac Arrhythmias may develop as well.

Chest radiography is a mandatory component of PE diagnostics; although it fails to verify the condition in nearly 40% of cases, it remains essential for ruling out alternative pathologies.

Due to the wide variety of radiographic signs associated with PE, they are conventionally classified into several distinct groups:

1. Radiographic signs of acute cor pulmonale.

2. Radiographic signs of impaired pulmonary arterial blood flow.

3. Radiographic signs of pulmonary infarction.

4. Elevation (raising) of the diaphragmatic dome.

Radiographic signs of acute cor pulmonale in PE include transverse and anterior enlargement of the cardiac silhouette due to right-sided heart chamber enlargement (particularly the right atrium), alongside dilation of the pulmonary trunk and SUPERIOR VENA CAVA.

Consequently, a sudden enlargement of the right heart chambers, pulmonary artery arch, and superior vena cava (hallmarks of acute cor pulmonale), when accompanied by other clinical and radiological signs of pulmonary vessel occlusion, strongly points toward pulmonary embolism.

Radiographic signs of altered pulmonary blood flow. Changes in the pulmonary hilum and lung markings on the affected side are among the primary indicators of PE. Depending on the level of occlusion, the hilum may appear dilated, deformed, or reduced in size. Dilation of the pulmonary hilum on the affected side manifests as an increased transverse diameter with preserved length. Simultaneously, a attenuation of vascular markings occurs within the affected zone.

A reduction in the size of the pulmonary hilum, or the presence of "small hila," results from decreased blood filling and serves as an indicator of "growing" thrombosis.

Pulmonary markings. The oligemia sign—manifested as diminished lung markings caused by impaired patency of the occluded pulmonary artery branch—along with vessel cutoff and the "avascular" sign.

Radiographic signs of pulmonary infarction. The radiographic picture of a pulmonary infarction emerges as vascular wall damage progresses, leading to Hemorrhage into the alveolar space. Infarction typically develops 2–5 days following pulmonary occlusion. Most authors emphasize the inconstancy of pulmonary infarction manifestations, meaning there is no single pathognomonic radiological pattern. The most characteristic shapes include cuboid, meniscus-like, or "parachute" configurations, as well as nodular shadows, while triangular, rhomboid, and trapezoidal infarcts are also considered typical.

The size of a pulmonary infarction varies, though relatively small infarct shadows (3 × 4 cm) are detected most frequently.

The structural pattern of a fully formed pulmonary infarction shadow is usually homogeneous. Its density depends on both the size of the lesion and the stage of the process, as well as any secondary complications. The margins of an uncomplicated pulmonary infarction are sharp, smooth, or wavy.

Thus, it can be concluded that establishing or excluding a diagnosis of PE based solely on clinical, laboratory, and radiological data remains extremely challenging.

Echocardiography helps detect the development of acute cor pulmonale while ruling out valvular and left ventricular myocardial pathologies. It also determines the severity of pulmonary hypertension, assesses the Structural and functional status of the right ventricle, and identifies thrombi within the cardiac chambers and main pulmonary artery branches. Nevertheless, a negative echocardiographic result does not completely rule out pulmonary embolism. In the presence of echocardiographic signs of right ventricular overload when computed tomography is unavailable, a diagnosis of PE should be established in high-risk thrombosis patients. Conversely, in patients presenting with shock or hypotension, the absence of echocardiographic signs of right ventricular overload or dysfunction effectively rules out PE.

The most informative diagnostic Methods for PE include radioisotope ventilation-perfusion lung scanning, compression Ultrasonography, impedance plethysmography, pulmonary angiography, and spiral computed tomography.

Radioisotope lung scanning successfully diagnoses PE in 87% of cases, and a normal lung scan allows the condition to be ruled out. This Procedure involves sequential perfusion and ventilation scans followed by a comparative Analysis of the results. The scan reveals isotope uptake defects that correspond to areas of oligemia. Depending on the extent of pulmonary perfusion defects, the probability of PE is classified as high (> 80%), intermediate (20–79%), or low (< 19%). The complete absence of perfusion defects virtually excludes PE. Ventilation scintigraphy identifies the Location, shape, and size of unventilated lung regions. A classic hallmark of PE is a perfusion defect accompanied by preserved ventilation in the affected lung segments. If the diagnosis remains ambiguous following lung scanning, contrast pulmonary angiography is indicated.

Pulmonary angiography—particularly multidetector computed tomographic angiography of the pulmonary arteries—serves as the "gold standard" for diagnosing PE. Angiographic signs of PE include a widened pulmonary artery diameter, complete or partial lack of contrast opacification in pulmonary vessels on the affected side, filling defects within the vascular lumen, distorted pulmonary markings, and a hazy contrast pattern resulting from multiple rather than complete obstruction of lobar and segmental arteries. The diagnostic value of the method depends heavily on technical capabilities. Multidetector spiral computed tomographic angiography (with contrast enhancement) boasts a sensitivity and Specificity of 100%, allowing visualization of thrombi within the pulmonary arterial tree down to the subsegmental level. However, its routine clinical use is limited by high costs and the complication risks associated with conventional pulmonary angiography.

PE must be differentiated from Other types of pulmonary embolism (air and fat embolism), as well as pneumonia, myocardial infarction, Spontaneous pneumothorax, acute cerebrovascular accidents, acute cholecystitis and pancreatitis, Viral Hepatitis, primary pulmonary thrombosis, and lung neoplasms.

EMERGENCY CARE

The onset of clinical signs of PE is invariably life-threatening and mandates immediate therapeutic interventions (Protocol 15), occasionally requiring cardiopulmonary resuscitation and frequently necessitating mechanical ventilation. Patients suspected of having any clinical form of PE must be urgently hospitalized—transported on a stretcher in a supine or semi-upright position—to an intensive care unit (preferably with a cardiovascular focus) for comprehensive evaluation and ongoing management.

Prehospital emergency care (most frequently administered to patients with a subacute course of PE) is primarily symptomatic in nature and comprises the following measures:

1. Pain management. The following medications are administered via intravenous bolus injection in 10–15 mL of isotonic sodium chloride solution: 1–2 mL of a 0.005% fentanyl solution (providing analgesia) combined with 2 mL of a 0.25% droperidol solution (providing neuroleptic effects)—a neuroleptanalgesia technique; for a systolic blood pressure below 100 mm Hg, only 1 mL of droperidol is administered; alternatively, 1–2 mL of a 2% promedol solution, a 1% morphine solution, or 3 mL of a 50% analgin solution combined with 1 mL of a 2% promedol solution may be used.

Pain relief prevents the development of reflex pain shock. Droperidol has a favorable effect on microcirculation, reduces spasm of the pulmonary arteries and arterioles, and calms the patients.

2. Intravenous administration of heparin (for patients with a high probability of pulmonary embolism).

Administer 10,000–15,000 IU of heparin in 10 mL of isotonic sodium chloride solution.

SCHEME 15 PROTOCOL FOR EMERGENCY CARE IN PULMONARY EMBOLISM

3. Intravenous administration of 10 mL of 2.4% aminophylline solution in 10–20 mL of isotonic sodium chloride solution, very slowly (over 5 minutes).

If systolic BP is below 100 mmHg, aminophylline is not administered. Intravenous infusion of aminophylline relieves bronchospasm, reduces pulmonary hypertension, and relieves pulmonary artery spasm.

In heart failure and collapse, strophanthin K (0.5–0.75 mL of a 0.05% solution), mesaton (0.5–1.0 mL of a 1% solution), and glucocorticoids (prednisolone) are administered. Once blood pressure normalizes, ganglion blockers may be prescribed.

Fulminant and acute forms of pulmonary embolism have a severe course and result in death within 8–10 minutes. Effective medical assistance is possible only when the condition develops in hospitalized patients. An attempt can be made to perform endotracheal intubation with mechanical ventilation, closed-chest cardiac massage, and intravenous bolus or drip administration of analgesics, antispasmodics, and fibrinolytic agents. If mechanical ventilation is impossible, inhalation Oxygen therapy via a nasal catheter or Mouth-to-mouth artificial Respiration is applied.

Resuscitation measures should be performed rapidly, preferably by a specialized team. Subsequent management of pulmonary embolism is a highly challenging task. Treatment must be combined with measures aimed at identifying the source of embolic thrombosis and preventing recurrent thromboembolism.

Depending on the patient's condition, drugs are administered intravenously as a bolus (for more massive pulmonary embolism and an acute course) or as an infusion (for less massive pulmonary embolism and a subacute course).

In the intensive care unit, subclavian vein catheterization is performed due to the need to infuse thrombolytic and other drugs, as well as to measure central venous pressure. Sometimes, intravenous drug administration into the cubital vein can be established via routine puncture.

Thrombolytic therapy is the primary treatment modality and must be initiated immediately. It is more effective than anticoagulant therapy. Thrombolytics are particularly indicated in cases of right ventricular failure resulting from pulmonary embolism. However, clinical practice does not always adhere to this principle because thrombolytic therapy carries a high risk of bleeding in the first place. According to various authors, 93% of patients have contraindications to thrombolytic therapy. Furthermore, it must be administered within the first 7 days of thrombosis onset; otherwise, its efficacy decreases significantly. Unfortunately, the onset of pulmonary embolism is very often not diagnosed in a timely manner.

Modern thrombolytic agents can be administered into the general circulation via both central and peripheral veins. Streptokinase, urokinase, and tissue plasminogen activator (t-PA) are used as thrombolytics.

The initial dose of streptokinase is 250,000 IU over 30 minutes, followed by an infusion at a rate of 100,000 IU/hour or 4,400 IU/kg/hour.

The Use of thrombolytics is highly effective (complete or partial thrombus lysis is observed in 90% of patients) but hazardous, as it causes significant hemorrhagic complications, which is particularly critical for patients with destructive, chronic forms of Pulmonary Tuberculosis. Consequently, systemic thrombolytic therapy is not recommended for the majority of patients with pulmonary embolism. It is also advisable to limit the use of systemic thrombolysis in patients with unstable hemodynamics.

Absolute contraindications to thrombolytic therapy include:

✵ Active internal bleeding;

✵ BP > 200/120 mmHg;

✵ Aortic dissection;

✵ Allergic reaction to thrombolytic drugs;

✵ Hemorrhagic stroke.

The duration of therapeutic thrombolysis is typically 2–3 days.

In most cases of embolism of the lobar and segmental branches of the pulmonary artery, adequate anticoagulant therapy is sufficient. The pulmonary circulation possesses high compensatory reserves and a high probability of spontaneous lysis of small thromboemboli due to the activation of endogenous fibrinolytic systems. Administering anticoagulant drugs in adequate doses prevents recurrent thrombosis in the pulmonary vessels.

Immediately after diagnosing pulmonary embolism, heparin should be administered intravenously at a dose of 80 IU/kg. Subsequently, if thrombolytic therapy is not required, heparin is infused intravenously in 500 mL of isotonic sodium chloride solution at a rate of 18 IU/kg/h. The dose is calculated based on body weight and activated partial thromboplastin time (aPTT). The primary criterion is an increase in aPTT by 1.5–2.5 times (rather than the Glass-slide clotting time). The aPTT should be measured every 6 hours. The total duration of heparin therapy is 5–14 days. Indirect anticoagulants (warfarin) are prescribed prior to reducing the heparin dose.

To treat pulmonary embolism (PE), low-molecular-weight heparins can be administered: Clexane at 1 mg/kg twice daily, Fraxiparine at 0.1 ml/10 kg twice daily, and Fraxiparine Forte at 0.1 ml/10 kg once daily.

A progressive deterioration in patients with massive PE requires emergency surgery—embolectomy—which is indicated for patients with substantial thromboembolism of the pulmonary trunk or both of its main branches, accompanied by persistent arterial hypotension refractory to vasopressors, or a right ventricular systolic BP exceeding 60 mmHg in the presence of high end-diastolic pressure.

Nonspecific therapy for PE involves a set of management measures primarily aimed at improving cardiovascular and respiratory function. In PE patients presenting with reduced cardiac output, arterial hypotension, or shock, non-glycoside positive inotropic agents and vasopressors are predominantly used (dobutamine IV 5–20 mcg/kg/min, dopamine IV 5–30 mcg/kg/min, norepinephrine IV drip 2–30 mcg/kg/min, levosimendan IV 0.05–0.2 mcg/kg/min, among others), alongside plasma expanders (up to 500 ml of Reopoligליukin [or rheopolyglucukin], isotonic sodium chloride solution, etc.). Fluid administration in PE patients must be monitored using the cardiac index.

To lower pressure in the lesser circulation, intravenous injections of papaverine hydrochloride or No-Spa are recommended, in addition to an intravenous aminophylline drip. However, if acute right ventricular failure develops (neck vein engorgement, hepatomegaly, right ventricular dilatation on echocardiography, etc.), the use of vasodilators (nitrates, sodium nitroprusside, etc.) is contraindicated because, by reducing preload and cardiac output, they can trigger severe systemic hypotension. This limitation can be overcome by the inhaled administration of prostacyclin, nitric oxide, or levosimendan.

To support myocardial contractility, patients are prescribed rapid-acting Glycosides (strophanthin K, corglycon). For cardiac arrhythmias, beta-blockers and potassium supplements are used. To improve pulmonary ventilation, aminophylline, isadrin, and atropine sulfate are indicated. Oxygen therapy and the normalization of blood acid-base balance are of paramount importance in Pulmonary Thromboembolism.

In the event of infarction pneumonia, broad-spectrum antibiotic therapy is prescribed.

The Prevention of thrombosis and pulmonary embolism in patients with pulmonary tuberculosis—especially those scheduled for surgery, those with chronic forms of the disease, or those with significant residual post-tuberculosis changes that lead to chronic cor pulmonale and substantially increase the risk of both thrombosis and PE (in the presence of other risk factors)—involves the timely gradual mobilization from bed rest in the postoperative period, active and passive lower extremity exercises, and the early Diagnosis and treatment of peripheral thrombophlebitis and other conditions that may cause PE.

Thus, in tuberculosis patients at risk for PE, applying a compression bandage with external pressure over the ankle joint and malleolus (creating a pressure of 18 mmHg) and the thigh (8 mmHg) prior to surgery is recommended (S.Z. Goldhaber, M. Marpurgo, 1992). A more effective method is intermittent pneumatic compression delivering 25 mmHg of pressure to the ankles and 20 mmHg to the thigh (G.P. Clagget et al., 1992).

Arteriovenous impulse therapy is an effective, albeit uncommon, method of PE prophylaxis in Ukraine.

Vena cava filter placement is indicated for patients at high risk of proximal femoral vein thrombosis or in the presence of the following factors: widespread chronic pulmonary tuberculosis; limited forms of respiratory tuberculosis accompanied by severe concomitant lung disease; pulmonary hypertension; contraindications to anticoagulants; or the development of PE despite anticoagulant therapy. When a vena cava filter is present, the incidence of PE does not exceed 3%.

The most common method of PE prevention is anticoagulant therapy. Unfractionated heparin (UFH) as well as low-molecular-weight heparins (LMWHs) are prescribed for this purpose. Notably, in patients with destructive forms of pulmonary tuberculosis, heparin is incorporated into the pathogenetic treatment regimens for the specific disease process. Recently, low-dose UFH has been recommended for the prevention of thrombosis and PE. Typically, surgical patients receive it 2 hours before surgery at a dose of 5,000 IU, followed by postoperative subcutaneous administration every 8–12 hours at the same dose. UFH therapy is monitored via blood clotting tests, platelet counts, and activated partial thromboplastin time (aPTT).

In patients with chronic forms of pulmonary tuberculosis and significant residual post-tuberculosis changes in the lung tissue and Pleura—particularly in the presence of chronic cor pulmonale and other risk factors for thrombosis—LMWHs are more effective. These include enoxaparin sodium, nadroparin sodium, dalteparin sodium, Clexane, and Fraxiparine. They offer certain advantages over UFH: a higher anticoagulant potential at lower doses, higher bioavailability and a longer duration of action, a lower risk of thrombocytopenia, no requirement for routine coagulation monitoring, and suitability for outpatient use. LMWHs are administered in the following doses: Clexane at 20–40 mg; Fraxiparine at 0.3 g subcutaneously twice daily, subsequently reduced to once daily for 7 days.

In addition to LMWHs, patients at high risk for PE are indicated prophylactic infusions of dextran-40 or hydroxyethyl starch solutions. The use of acetylsalicylic acid for this purpose is currently considered to have low efficacy.

CASE STUDY

Patient R., 60 years old, has been hospitalized in a tuberculosis dispensary for 2 weeks. Pulmonary tuberculosis was newly diagnosed upon presentation. The medical history reveals that the patient has suffered from hemorrhoids for about 10 years. He was evaluated by a surgeon.

Clinical diagnosis: Newly diagnosed pulmonary tuberculosis ( infiltrative, upper lobe of the right lung) (25.10.2008), Dest+ MBT+M+K0, Resist0, Hist0, Cat. 1, Cog. 4 (2008), hemorrhoids, phlebothrombosis of the external and internal deep rectal veins, grade II.

Upon admission, the patient complained of a cough with sputum production, generalized weakness, nocturnal hyperhidrosis, and a body temperature elevation up to 38.3 ⁰C. In addition, the patient reported constant pain and a feeling of heaviness in the rectum, pain during defecation accompanied by bright red rectal bleeding. The patient was prescribed treatment According to the protocol for medical care of tuberculosis patients, as well as hemorrhoid treatment. Intoxication and bronchopulmonary syndromes persist 2 weeks after the initiation of anti-tuberculosis therapy, although the body temperature has dropped to subfebrile levels. Clinical manifestations of hemorrhoids have barely decreased.

Early yesterday morning, the patient began complaining of sudden dyspnea, retrosternal and left-sided chest pain, hemoptysis, nausea, and palpitations; by evening, his body temperature rose to 38.5 ⁰C.

Objective Examination: the patient's condition is severe; Skin is pale ash-colored with cyanosis of the mucous membranes and nail beds. Pulse is 106 bpm, regular, of satisfactory volume. BP is 105/65 mmHg. Heart sounds are muffled, with an accentuated second heart sound over the pulmonary artery. Respiratory rate is 32 breaths/min. Percussion reveals dullness over the upper lobe of the right lung, as well as shortened percussion note along the posterior axillary line over the lower lobe of the left lung. Breath sounds are harsh over the lungs, with scattered dry rales; fine moist rales are auscultated over the upper lobe on the right, while pleural friction rub and isolated fine bubbling rales are heard over the lower lobe on the left along the posterior axillary line.

Blood test: Hb 110 g/L, WBC 13.6×10⁹/L, E 3%, Stab 10%, Seg 59%, L 18%, M 10%, ESR 40 mm/h. Direct smear Cell/15.html">Microscopy of sputum revealed Mycobacterium tuberculosis (5–7 per field of view). Urinalysis: straw-yellow color, specific gravity 1020, protein 0.003‰, leukocytes 3–5 per field of view.

Chest X-rays (posteroanterior and right lateral projections) performed upon hospital admission show: on the right, in S₁–S₂, a medium-intensity focal shadow measuring 3.5×5 cm with indistinct, irregular contours and an inhomogeneous Structure containing a central radiolucency 1.5×2.0 cm in diameter. The shadow is connected to the right ROOT. On the left, there are no pathological changes in the lung parenchyma or root.

Due to the patient's clinical deterioration, additional laboratory and instrumental tests were ordered: blood tests for seromucoid, haptoglobin, lactate dehydrogenase, and a coagulogram, along with chest X-rays (posteroanterior and left lateral projections) and an ECG. Results: seromucoid 0.33 g/L (normal: 0.22–0.28 g/L), haptoglobin 3.1 g/L (normal: 0.83–2.67 g/L), lactate dehydrogenase 6 µmol/(h·L) (normal: 0.8–4.0 µmol/(h·L)), prothrombin index 110%, fibrinogen B (+++).

Chest X-rays in posteroanterior and left lateral projections reveal: the finding in the right S₁–S₂ is stable. On the left, in the PROJECTION OF THE lower lobe (in S₉), There is a massive homogeneous triangular infiltration of the lung parenchyma with its apex pointing toward the root and its base located subpleurally. The opacity measures 5.0×3.5 cm. The left pulmonary root is deformed and widened, and the left pulmonary vascular pattern is depleted.

ECG revealed sinus tachycardia, T-wave inversion, and a deep S wave in lead I.

Based on the additional diagnostic workup, the patient was diagnosed with a complication: pulmonary artery branch thromboembolism complicated by pulmonary infarction. In this case, the source of embolism in the patient with Infiltrative pulmonary tuberculosis was hemorrhoidal veins (phlebothrombosis), and the complication developed As a result of inadequate Treatment of the latter. Against the background of anti-tuberculosis therapy, the patient received emergency medical care (pain relievers, aminophylline, anticoagulants) and was prescribed broad-spectrum Antibiotics. The patient's condition gradually improved.

METABOLISM/35.html">Selection/41.html">Review Questions and TASKS WITH MODEL Answers

Case Study. Patient D., 66 years old, has been undergoing inpatient treatment at a tuberculosis dispensary for 2.5 months. He has had pulmonary tuberculosis for several years. His most recent hospitalization was due to the progression of the tuberculous process. Two years ago, he suffered a myocardial infarction and was treated in a specialized inpatient unit. Clinical diagnosis: Multidrug-resistant tuberculosis (05.09.2008), bilateral fibro-cavitary, Destr + (infiltration and dissemination phase), MBT + M + C +, Resist (I) HRS, Resist (II) 0, HIST 0, Cat 4 (treatment after failure of the 2nd course of Chemotherapy, 1st line), Cog 3 (2008), chronic cor pulmonale, Post-infarction cardiosclerosis, atrial fibrillation, stage II A circulatory failure.

Upon admission, the patient complained of general weakness, malaise, nocturnal hyperhidrosis, body temperature rising to 38.5 ⁰C–39.0 ⁰C, poor appetite, weight loss, cough with up to 50 mL per day of odorless mucopurulent sputum, dyspnea upon mild physical exertion, and chest pain. These symptoms had troubled the patient previously, but over the 2 months preceding hospitalization, they became very pronounced, and the patient consented to inpatient treatment at the tuberculosis dispensary.

A chest X-ray taken upon admission to the hospital revealed: in the upper lobe of the right lung, a thick-walled, deformed cavity measuring 3.5 x 4.0 cm with a clear inner contour and an infiltrated outer contour. The lung tissue surrounding the cavity showed fibrous changes, and the lobe was reduced in volume. In the middle and lower lung fields, multiple medium- and low-intensity focal shadows with blurred contours were observed, in some places coalescing to form non-homogeneous infiltrates. On the left, in the perihilar region, an irregular, thick-walled cavity up to 2.0 cm in diameter was detected, surrounded by a zone of perifocal infiltrative shadowing. Multiple dissemination foci surrounded the cavity. The right root was deformed and pulled upward. Apical pleura on the right was thickened. The left costophrenic sinus was obliterated.

After 2.5 months of treatment, in accordance with the protocol for medical care of a patient with chronic multidrug-resistant pulmonary tuberculosis, the manifestations of intoxication and bronchopulmonary syndromes significantly decreased. However, complaints of dyspnea, low-grade fever, cough, and chest pain persisted.

Seven hours ago, the patient suddenly experienced severe retrosternal pain, a sharp increase in dyspnea, a rise in body temperature to 38.5°C, nausea, vomiting, acute pain in the right hypochondrium, dizziness, tinnitus, and aggravated general weakness.

Objective examination: the patient's general condition is severe. Respiratory rate: 10 breaths/min, pulse: 102 bpm. Blood pressure: 85/55 mm Hg. Cardiac Activity is arrhythmic, heart sounds are muffled, accentuation of the second sound is noted over the pulmonary artery. The patient is pale, skin is moist, cyanosis of the mucous membranes, nail beds, and face is observed, along with pulsation and engorgement of the cervical veins. The right heart border and the zone of absolute cardiac dullness are enlarged. Auscultation of the lungs reveals harsh breathing accompanied by scattered dry rales. Over the right upper lobe, amphoric breathing and a focus of coarse bubbling rales are heard. The liver is enlarged by 4 cm and is tender upon palpation.

Based on the presented clinical manifestations, the physician suspected a myocardial infarction.

ECG and echocardiography revealed signs of right ventricular overload, as well as incomplete right bundle branch block. A follow-up chest X-ray showed a stable picture compared to the one taken upon admission. The patient was prescribed analgesic therapy, vasodilators, cardiac glycosides, and prednisolone. However, the patient's condition deteriorated, and he died 10 hours later.

Question 1. What complication developed in the patient with chronic pulmonary tuberculosis according to the findings?

A. Spontaneous pneumothorax.

B. Acute atelectasis.

C. Intrapleural hemorrhage.

D. Pulmonary embolism or thrombosis of the pulmonary artery branches.

E. Myocardial infarction.

Question 2. What clinical form of pulmonary artery thrombosis (confirmed at autopsy) most likely occurred in the patient?

A. Fulminant.

B. Acute.

C. Subacute.

D. Chronic.

E. Impossible to determine.

Question 3. In your opinion, which pathogenetic factor was the most crucial in the development of pulmonary artery thrombosis in this patient?

A. Advanced age of the patient, presence of chronic cor pulmonale, atrial fibrillation, post-infarction cardiosclerosis.

B. Spasm of the pulmonary arterioles and their reduction in fibro-cavitary tuberculosis.

C. Sclerotic changes in the pulmonary vessels, their deformation, prolonged vascular spasm, and decreased pulmonary blood flow velocity.

D. Increased blood viscosity, vascular wall damage, and decreased pulmonary anticoagulation function.

E. All of the above.

Question 4. Which factors indicated a high clinical probability of pulmonary embolism in this patient?

A. Presence of a chronic form of pulmonary tuberculosis.

B. Presence of multidrug-resistant chronic pulmonary tuberculosis.

C. Hypotension, tachycardia, myocardial injury, signs of right ventricular overload, sudden dyspnea and retrosternal chest pain, cyanosis.

D. Sudden acute substernal chest pain, dyspnea, cyanosis, neck vein edema and pulsation.

E. Cyanosis of the mucous membranes, nail beds, and face, fever, dry and moist rales in the lungs.

Question 5. What should have been the emergency management if pulmonary embolism had been diagnosed intravitally in this patient?

A. Analgesics, thrombolytics, non-glycoside positive inotropic agents, antitussives, oxygen inhalation.

B. Analgesics, vasodilators, broad-spectrum antibiotics, non-steroidal anti-inflammatory drugs, cardiac glycosides.

C. Thrombolytics, vasodilators, glucocorticoids, mechanical ventilation.

D. Analgesics, antipyretics, bronchodilators, heparin, plasma volume expanders, oxygen inhalation.

E. Vasodilators, anticoagulants, broad-spectrum antibiotics, analgesics.

Question 6. Which clinical signs should have been considered the primary diagnostic criterion for pulmonary embolism in a patient at high risk for its development, when multidetector computed tomography was not feasible?

A. Presence of post-infarction cardiosclerosis and atrial fibrillation.

B. Presence of febrile and abdominal syndromes.

C. Presence of acute respiratory failure syndrome.

D. Signs of right ventricular overload on echocardiography, especially when combined with hypotension.

E. Presence of chronic respiratory tuberculosis.

Answers and Rationale.

ANSWERS TO QUESTIONS: 1D, 2B, 3E, 4C, 5A, 6D

1. According to the studies conducted—specifically general clinical, radiological, ECG, and echocardiographic evaluations—a patient with chronic Pulmonary tuberculosis combined with post-infarction cardiosclerosis, atrial fibrillation, and stage IIA circulatory failure had strong grounds for diagnosing a complication such as thrombosis or thromboembolism of the pulmonary artery. There were neither clinical nor radiological grounds for diagnosing spontaneous pneumothorax, acute Pulmonary atelectasis, or intrapleural hemorrhage. ECG and echocardiography revealed signs of right ventricular overload and incomplete right bundle branch block, which, combined with hypotension, corresponding clinical manifestations, and a high risk of pulmonary embolism in this patient, provided the basis for diagnosing precisely this complication.

2. The patient developed an acute form of pulmonary embolism, as it typically lasts from several hours to a few days, characterized by a sudden onset and rapid progressive development of symptoms related to respiratory, cardiovascular, and cerebral insufficiency. The development of pulmonary infarction is not typical for this variant, which was confirmed by radiological data.

3. All of the listed factors were present in this clinical case and served as a significant cause for the development of pulmonary artery thrombosis specifically.

4. Hypotension, tachycardia, myocardial injury, signs of right ventricular strain, sudden dyspnea and retrosternal chest pain, cyanosis. The absence of echocardiographic signs of right ventricular strain in the presence of these clinical manifestations would make the diagnosis of pulmonary embolism highly unlikely.

5. Analgesics, thrombolytics, non-glycoside positive inotropic agents, antitussives, oxygen inhalation. The patient presents with severe pain that necessitates the administration of analgesics to prevent reflex pain shock, alleviate anxiety and agitation, and thereby improve the patient's tolerance to hypoxia; thrombolytic therapy forms the cornerstone of pulmonary embolism management, as it rapidly dissolves thrombus obstruction and positively affects hemodynamic parameters, leading to an increased cardiac index and reduced pulmonary arterial pressure. Because the patient has developed symptoms of acute right ventricular failure, the use of vasodilators is contraindicated, as they reduce preload and cardiac output, potentially precipitating severe systemic hypotension. Following the correction of systemic hypotension, inotropic support is advisable to increase cardiac output and improve oxygen delivery. Antitussive medications should be prescribed to suppress the cough reflex, prevent elevated pulmonary arterial pressure, and minimize the risk of hemorrhage.

6. Echocardiographic evidence of right ventricular strain, particularly when combined with hypotension (according to the guidelines of the European Society of Cardiology).