Critical Conditions in Pulmonary Tuberculosis in Adults - N.I. Fomichova 2010

Atelectasis

Pulmonary atelectasis is the complete collapse of alveoli, alveolar ducts, and respiratory bronchioles. All conditions localized in the Bronchi, lung parenchyma, Mediastinum, or Diaphragm can be complicated by The Development of atelectasis. Pulmonary Tuberculosis is complicated by atelectasis in 3.9% of all cases, and bronchial tuberculosis in 22.9%. As a complication in patients with respiratory tuberculosis, atelectasis ranks second in frequency of occurrence only to atelectasis caused by malignant Lung Tumors.

Pathogenesis. The primary causes of atelectasis in tuberculosis include the development of specific and nonspecific endobronchitis, impaired bronchial drainage due to the occlusion of its lumen by viscous sputum or caseous masses, compression of the bronchus by enlarged intrathoracic Lymph Nodes in Primary tuberculosis, perforation of the intrathoracic lymph node capsule with the discharge of caseous masses into the bronchial lumen and its obstruction (in tumor-like forms of intrathoracic lymph node tuberculosis), breakdown of the parenchyma in a tuberculosis-affected lung area followed by the development of pericavitary atelectasis, and cirrhotic Changes in the peribronchial zone and bronchial wall. Bleeding into and around the bronchial lumen can also cause bronchial stenosis and atelectasis. When small basal areas of the lung are affected, so-called discoid atelectasises develop.

In bronchial tuberculosis, if ulceration of a specific inflammatory focus occurs, the risk of obstruction and atelectasis increases sharply, potentially accompanied by mucosal edema and the proliferation of tuberculous granulations. Under such conditions, ulcers and granulations gradually transform into mature Connective Tissue, eventually leading to scarring and bronchial stenosis, which can trigger the development of atelectasis.

Pericavitary atelectasis can be observed as a thick-walled ring surrounding an inflated cavity. Distal cavitary atelectases are located between the cavity and the chest wall and are wedge-shaped in most cases. They occur As a result of the obstruction of bronchi located distally to the cavity. Such atelectases usually do not lead to The formation of new cavities.

Atelectasis may be caused by bronchial stenosis located near the cavity, yet proximally to it. Due to the impaired drainage function of this bronchus, the cavity cannot empty. The air within the cavity is absorbed, and its walls may collapse. This mechanism is recognized as critical for the scarring of pulmonary cavities. The same mechanism of atelectasis development operates in stenosis accompanied by the obstruction of large bronchi, typically affecting an entire segment.

Tuberculous atelectases occur more frequently on the right side, particularly in the right upper and middle lobes, which is explained by their Anatomical and physiological features. Tuberculous atelectases are rarely encountered in the lower lobe of the right lung.

Thus, the cause of atelectasis in tuberculosis is invariably obstruction, stenosis, or compression of the corresponding bronchus. Blockade of segmental bronchi by caseous masses represents a milder form of atelectasis compared to that caused by stenosis.

In the postoperative period, atelectasis may develop as a result of pulmonary hypoventilation, accumulation of significant amounts of viscous sputum, narrowing of the bronchial lumen, suppression of the cough reflex, and impaired bronchial patency.

If the cause of atelectasis is eliminated in a timely manner, the atelectasis itself will resolve, the lung tissue will regain its airiness, and conditions for the development of a pathological process within it will be eliminated. However, if atelectasis persists uncorrected for a prolonged period, a nonspecific inflammatory process joins in, further worsening the patient's condition.

Pathophysiology of Atelectasis. Atelectasis of the lung or its lobe is accompanied by impaired Respiration, cardiovascular dysfunction, Biochemical changes in the Blood, trace element alterations, and shifts in the body's immunological reactivity.

Thus, in lobar atelectasis, the respiratory rate increases, which can be explained by the reduction in the pulmonary respiratory surface and its excursion, caused by blood stasis in the atelectatic lobe, elevated body Temperature in some patients, and the shunting of venous blood into the arterial bed. Atelectasis leads to a decrease in inspiratory and expiratory reserve volumes, vital capacity (VC), minute ventilation, as well as the frequency and depth of breathing during minute ventilation. All these are signs of respiratory failure, which in atelectasis manifests as hyperventilation. As the process progresses, hyperventilation can no longer ensure the necessary oxygen saturation of arterial blood, leading to arterial hypoxemia. In pulmonary atelectasis, respiratory failure may occur even with normal arterial blood oxygen saturation maintained by hyperventilation. The degree of respiratory failure can be assessed by The Nature and severity of dyspnea. In patients with chronic pulmonary atelectasis, respiratory failure is subsequently joined by cardiac failure, which sharply deteriorates their condition.

The persistence of pulmonary atelectasis for a month initially leads to increased vascular resistance in the non-ventilated area, followed by capillary obliteration and the shunting of venous blood through arteriovenous anastomoses into the systemic Circulation. The volume of the additional blood portion entering the Pulmonary Veins, and consequently the additional load on the myocardium, depends on the area of lung tissue excluded from the respiratory act. Shunting increases the workload on the left ventricle, which negatively affects its function under conditions of escalating Hypoxia.

Classification. Pulmonary atelectases are classified by origin into congenital and acquired; by clinical course into acute and chronic; by the volume of involvement into total and limited (atelectasis of the lung, lobe, segment, subsegment, discoid atelectasis); by The Mechanism of development into obstructive, compressive, neuroreflex, congestive (or Shock lung); and by the functional state of respiration and circulation into compensated, subcompensated, and decompensated.

Clinical Manifestations and Diagnostics (Diagram 10). The clinical picture of atelectasis depends on the volume of affected lung tissue, concomitant diseases, and the state of cardiovascular function. Partial and total atelectases pose a threat of developing a critical condition.

A characteristic sign of atelectasis is a dry, frequent, and excessive cough. Each cough shock is accompanied by pain in the corresponding half of the chest. The cough intensifies with minor physical exertion, accompanied by progressive dyspnea, cyanosis, increased pulse rate, elevated body temperature, and the looming threat of Acute Respiratory Failure.

Physical examination reveals a lag in the expansion of the corresponding half of the chest during breathing; intercostal spaces on the side of atelectasis are narrowed, Ribs are approximated, and the chest wall appears sunken. The lung decreases in volume. Its lower border on the affected side rises upward, and the mediastinal Organs shift toward the lesion (positive "fork" sign). Percussion over the atelectatic area reveals dullness, while tympanites is heard over adjacent lung areas. Auscultation on the affected side shows markedly weakened or completely absent breath sounds, reduced vocal fremitus, and no rales.

Such distinct clinical manifestations of atelectasis in pulmonary tuberculosis are most commonly encountered during the obstruction of large bronchi by caseous masses or blood clots, as well as in stenoses.

The acute onset of total pulmonary atelectasis (in cases of main bronchus obstruction by caseous masses) is characterized by the sudden appearance of chest pain, dyspnea, tachycardia, cyanosis, and high body temperature. These factors create the prerequisites for a critical condition resulting from acute respiratory and cardiac failure.

Suspicion of atelectasis arises from the aforementioned clinical manifestations and physical examination findings. A complete blood count holds no special significance in pulmonary atelectasis. The Diagnosis is confirmed by chest X-ray Examination. Typical atelectases are detected on direct and lateral radiographs. On a plain radiograph, atelectasis is defined as a homogeneous opacity (opaque lung) with a demarcation line, prominent along one edge, often matching the boundary of the corresponding lung lobe. The diaphragmatic dome is positioned higher than usual, ribs are approximated, and intercostal spaces are narrowed. In atelectasis of the entire lung, radiographs show all its lobes significantly reduced in size, appearing as an opacity around the ROOT.

Class="center">DIAGRAM 10. DIAGNOSTIC ALGORITHM FOR PULMONARY ATELECTASIS IN PATIENTS WITH RESPIRATORY TUBERCULOSIS

When atelectasis is suspected, fiberoptic bronchoscopy is indicated. In bronchoglandular atelectasis, bronchoscopy reveals hyperemia and thickening of the bronchial mucosal wall; the inflammatory area often takes a cone-shaped form protruding into the bronchial lumen with a grayish-white color. Upon perforation of this area, caseous masses obstructing the bronchial lumen are found within it. The bronchial wall shows signs of inflammation, and the edge of the perforation opening is uneven. The bronchial lumen is significantly narrowed. Due to edema and infiltration of the mucosa surrounding the perforation, the opening in the bronchial wall is often unnoticeable. It may be obscured by granulations and mucosal ulceration.

Atelectases following hemorrhages in patients with respiratory tuberculosis develop by the end of the first day or on the second day, accompanied by a deterioration in general condition, worsening dyspnea, fever, and the presence of blood clots during bronchoscopy. Systematic radiological monitoring is required for their timely diagnosis.

If pulmonary tuberculosis is complicated by bronchial tuberculosis, and the latter leads to bronchial obstruction, the tuberculous lesion of the bronchial mucosa is visualized during bronchoscopy as bright reddening of the bronchial mucosal wall with localized infiltration. Against the Background of infiltration, erosions, ulcers, granulations, and tubercles covered with purulent deposits may be detected. The bronchus is stenosed, and its lumen is indiscernible.

EMERGENCY CARE

Emergency care should be aimed at restoring pulmonary ventilation (Diagram 11).

Patients with pulmonary tuberculosis complicated by atelectasis caused by occlusion of the draining bronchus with mucus, sputum, blood, or caseous masses undergo urgent bronchoscopy and are prescribed expectorants and mucolytic agents. Enzyme and antiseptic solutions are instilled into the tracheobronchial tree, along with catheterization of the affected bronchus. Aspiration of the bronchial contents through a bronchoscope and bronchial lavage with saline restore bronchial patency and resolve the atelectasis. If atelectasis is complicated by acute cardiopulmonary failure, immediate emergency measures must be taken to correct it.

In cases of tuberculous lesions of the bronchial mucosa and its edema, prednisolone is prescribed at 30 mg 3 times a day for 2-3 days endobronchially, followed by a tapered dose and transition to oral administration. Once the emergency condition is resolved, subsequent appropriate intensive tuberculosis therapy is indicated, including endobronchial instillation of anti-tuberculosis drugs, bronchial lavage with antiseptic solutions 1-2 times a week, breathing exercises, chest massage, anti-inflammatory drugs, maintenance of effective coughing, and broad-spectrum Antibiotics. For extensive and complicated atelectases that do not respond to conservative Treatment, surgical resection of the affected lung area is indicated.

DIAGRAM 11 EMERGENCY CARE ALGORITHM FOR TOTAL OR PARTIAL ATELECTASIS IN PATIENTS WITH PULMONARY TUBERCULOSIS

CASE STUDY

Patient L., aged 18, was admitted to a general somatic hospital with a presumptive diagnosis of community-acquired right-sided upper lobe pleuropneumonia. Her condition was severe. The respiratory rate was up to 40 breaths per minute, pulse 100 beats per minute, arrhythmic. Body temperature was 39.5°C; she suffered from a painful, dry cough that persisted day and night with a "bitonal" character, triggered by minor physical exertion. The patient complained of pronounced night sweats, poor appetite, weight loss, and weakness.

The medical history revealed that the disease had developed gradually over a month, but she had not sought medical attention, believing she had an acute respiratory viral infection, and received no treatment. Only the onset of the aforementioned symptoms prompted the patient to call an ambulance, which hospitalized her. It turned out that the patient had been living in a first-category tuberculosis infection focus for the past year, but had never had tuberculosis herself and had not received Chemoprophylaxis as a contact person. Furthermore, it was established that the girl had received two BCG revaccinations at ages 7 and 14, with post-vaccination scars of 4 mm and 2 mm, respectively. The dynamics of tuberculin Skin reactions (Mantoux test with 2 TU) were as follows: age 15 — 6 mm papule, age 16 — 3 mm papule, age 17 — hyperemia, age 18 (directly in the hospital) — 12 mm papule with a vesiculonecrotic reaction.

The patient's condition was very severe, with progressive signs of acute respiratory and cardiac failure. Percussion over the upper lobe of the right lung revealed dullness, while tympanic Resonance was noted over adjacent areas. Auscultation over the same lobe of the right lung showed almost absent breath sounds, decreased vocal fremitus, and no rales.

A chest X-ray showed intense homogeneous opacification of the upper lobe of the right lung; the lower contour of the shadow was sharp and merged with the shadow of the mediastinum, which was shifted toward the lesion and widened. The right diaphragmatic dome was at the level of the 4th rib, and the left at the level of the 6th rib. The root of the right lung was elevated, its outer contour polycyclic, merging with the aforementioned opacification in the upper lobe. Tomography of the right lung root revealed enlarged tracheobronchial and bronchopulmonary lymph nodes with sharp, semicircular, convex contours.

A complete blood count showed lymphopenia, moderate leukocytosis without a left shift, monocytosis, and a slightly elevated ESR.

Analysis of the medical history and diagnostic results led to the Conclusion that the condition could not be Pneumonia. The patient was indicated for urgent fiberoptic bronchoscopy to clarify the diagnosis.

During bronchoscopy, the lumen of the right upper lobe bronchus was barely visible due to external compression. The bronchial mucosa above the compression site was hyperemic. Smear Cell/15.html">Microscopy of the bronchial washings revealed *Mycobacterium tuberculosis*.

Thus, in a young woman previously uninfected with MTB, a tuberculin skin test conversion ("shift") occurred due to her residing in a focus of tuberculosis infection, as evidenced by the dynamics of her test results. The patient had not received chemoprophylaxis, and the primary infection progressed to intrathoracic lymph node tuberculosis. When the first symptoms appeared—most likely initially presenting as infiltrative tuberculous bronchoadenitis—she did not consult a doctor, and an X-ray examination was not performed in a timely manner. Without specific treatment, the tuberculous process progressed, and hyperplastic changes in the affected lymph nodes transformed into caseous necrosis. Significantly enlarged lymph nodes compressed the wall of the adjacent bronchus, impairing its patency and causing atelectasis.

Thus, the clinical course, medical history, tuberculin skin testing, radiological, laboratory, and bronchoscopic findings established the diagnosis: Newly Diagnosed Tuberculosis of the right tracheobronchial and bronchopulmonary lymph nodes, tumorous form, Destr-, MTB+ M+ K0, Resist 0, Hist0, Cat. 1, tuberculosis of the right upper lobe bronchus, infiltrative form, atelectasis of the right upper lobe, respiratory failure grade II–III.

The patient was transferred to the tuberculosis dispensary and prescribed intensive anti-tuberculosis therapy combined with broad-spectrum antibiotics, prednisolone, cardiac medications, bronchodilators, and detoxification therapy. Antiseptic solutions, soluble anti-tuberculosis drugs, and mucolytics were administered endobronchially.

By the third day of treatment, the patient's temperature dropped, the cough decreased, and coarse moist rales appeared in the right lung against the background of bronchial breathing. X-ray imaging showed partial clearing of the upper lobe of the right lung. Once every five days, the patient underwent bronchial lavage with normal saline followed by the instillation of 5 ml of a 10% isoniazid solution.

After 6 months of treatment, chest X-rays and tomograms showed: clear lung fields bilaterally throughout, a decrease in the size of the right lung root, improved differentiation of its structural elements, and compaction of the affected lymph nodes. The bronchological picture normalized. The patient continued her treatment.

METABOLISM/35.html">Selection/41.html">Review Questions and TASKS WITH ANSWER KEYS

Clinical Problem. Patient K., 43 years old, was returning home from work when she suddenly developed a dry paroxysmal cough, right-sided chest pain, hemoptysis, and shortness of breath. The woman went to the hospital. A chest X-ray was performed, which revealed opacification of the upper lobe of the right lung. The physician found out that the patient had suffered from tuberculosis in her adolescence and had undergone prolonged treatment with a good outcome. She had not been under the supervision of a phthisiatrician for a long time, though she underwent annual fluorography. She had felt well for a long time and could not explain her current condition. Consequently, with a suspected tuberculosis relapse, the patient was referred to the tuberculosis dispensary.

Objective status: The patient's condition was moderately severe due to pronounced bronchopulmonary syndrome. Hemoptysis persisted. The patient was agitated. Respiratory rate was 28 breaths per minute, pulse rate 82 beats per minute. Percussion over the right lung from the apex to the 3rd rib revealed dullness; auscultation in the same area showed sharply decreased breath sounds, with no rales heard. Heart sounds were muffled, rhythm regular. No pathology was detected in other organs and systems.

The patient underwent a right lateral chest X-ray, tomography at the level of the lung roots, and fiberoptic bronchoscopy. Comprehensive radiological examination established that the upper lobe of the right lung was homogeneously opacified and reduced in volume, the interlobar fissure was clearly defined at the level of the 3rd rib, the Trachea was shifted to the right, and the right diaphragmatic dome was almost 3 cm higher than the left. The right root was somewhat deformed, sclerotically altered, elevated, and contained inclusions in the form of multiple, high-intensity, large focal opacities of irregular shape with sharp contours.

Fiberoptic bronchoscopy revealed the following: the right upper lobe bronchus was deformed, its mucosa was inflamed, its diameter significantly narrowed due to infiltration and edema, and a dense, grayish-white formation protruded into the lumen, substantially impairing patency.

The clinical blood count was normal. Smear microscopy of bronchial washings revealed no MTB, and atypical Cells were absent. Histological examination of the tissue sample from the affected bronchial area showed signs of a nonspecific inflammatory process.

The patient received appropriate care, and 2 days later, a repeat chest X-ray was performed, which showed that the upper lobe of the right lung had normal transparency, its pulmonary pattern was sclerotically altered, a single high-intensity focal shadow with sharp contours was visible beneath the clavicle, and the right diaphragmatic dome was at the level of the 6th rib. Multiple calcifications were present in the right lung root.

Question 1. What happened to the patient, and What is the diagnosis? Choose the correct answer.

A. Tuberculosis relapse.

B. Central Lung Cancer.

C. Infarction of the upper lobe of the right lung.

D. Atelectasis of the upper lobe of the right lung.

E. Encapsulated Pleurisy.

Question 2. Which additional examination will definitively clarify the diagnosis?

A. Repeated examination of bronchial washings for MTB and atypical cells.

B. Repeat fiberoptic bronchoscopy.

C. Pleural puncture.

D. Blood Coagulation study.

E. Chest computed tomography.

Question 3. How should the data obtained from the latest chest X-ray be interpreted?

A. Normal radiographic findings.

B. Focal tuberculosis of the upper lobe of the right lung in the consolidation phase.

C. Residual changes of clinically cured focal tuberculosis of the upper lobe of the right lung.

D. Intrathoracic lymph node tuberculosis on the right, complicated by bronchial tuberculosis.

E. Residual changes of a clinically cured Primary tuberculous complex of the right lung.

Question 4. What type of atelectasis has developed in this patient?

A. Acute, acquired, partial, obstructive.

B. Acute, acquired, partial, compressive, compensated.

C. Acute, acquired, partial, segmental, subcompensated.

D. Acute, limited, neuroreflex, subcompensated.

E. Acute, acquired, discoid, decompensated.

Question 5. What emergency condition poses the greatest immediate threat to this patient if treatment for atelectasis is not provided?

A. Pulmonary Hemorrhage.

B. Intoxication syndrome.

C. Acute respiratory failure.

D. Spontaneous pneumothorax.

E. Acute Heart Failure.

Question 6. What is the primary cause of atelectasis in this patient?

A. Development of endobronchitis.

B. Bronchial obturation by a calcified lymph node (broncholith).

C. Bronchial compression by calcified lymph nodes.

D. Bronchial obturation by a blood clot.

E. Deformation, scarring, and stenosis of the bronchus.

Question 7. What should be the emergency management for this patient?

A. Removal of the broncholith, aspiration of bronchial secretions, broad-spectrum antibiotics, isoniazid, bronchodilators, antiseptic lavage of the bronchi, and cessation of hemoptysis.

B. Intensive anti-tuberculosis therapy, including endobronchial administration of medications and aspiration of bronchial secretions.

C. Chest massage, active coughing exercises, anti-tuberculosis therapy.

D. Resection of the affected lung lobe and removal of calcifications from the root.

E. Removal of the broncholith, aspiration of bronchial secretions, cessation of hemoptysis, antitussive agents, and intensive anti-tuberculosis therapy.

Answers and Rationale.

Answers to the questions: 1 D, 2 B, 3 E, 4 A, 5 C, 6 B, 7 A

1. The patient has atelectasis of the upper lobe of the right lung. This is evidenced by the sudden deterioration of her condition (against a background of complete well-being) presenting with a pronounced bronchopulmonary syndrome (dry paroxysmal cough, right-sided chest pain, hemoptysis, dyspnea); absence of intoxication syndrome; physical examination data (dullness of percussion sound over the right lung from the apex to the 3rd rib, auscultation revealing sharply diminished breath sounds in the same area, with no rales heard); typical radiological findings (homogeneous, intensely opacified upper lobe of the right lung, reduced in volume, interlobar Pleura clearly defined at the level of the 3rd rib, trachea shifted toward the lesion, right dome of the diaphragm and root pulled upward); fiberoptic bronchoscopy findings (the right upper lobe bronchus is narrowed, deformed, sclerotically altered, the mucous membrane is inflamed and edematous, and a dense, grayish-white formation is visualized in the bronchial lumen, significantly impairing its patency); normal complete blood count, which contradicts an inflammatory Etiology of the process in the lung tissue; absence of MTB and atypical cells in bronchial washings; signs of non-specific inflammation of the bronchial mucosa according to histological examination; very rapid normalization of the radiological picture in the upper lobe of the right lung after emergency treatment; and a history of tuberculosis involving intrathoracic lymph nodes which, after the patient's recovery, turned into large calcifications that continuously exerted pressure on the wall of the adjacent, sclerotically altered bronchus, leading to its inflammation, perforation, and obturation.

2. Repeated fiberoptic bronchoscopy will definitively clarify the diagnosis because, after the removal of the broncholith and anti-inflammatory therapy (broad-spectrum antibiotics, antiseptic bronchial lavage, etc.), bronchial patency should be restored, which must be confirmed by rapid positive radiological dynamics. Therefore, the presence of lobar atelectasis will be unquestionable if the dynamics of the radiological findings (restoration of transparency in the affected lung lobe) coincide with the findings obtained during repeat fiberoptic bronchoscopy (restoration of patency in the corresponding bronchus).

3. Residual changes of a clinically cured Primary tuberculosis complex of the right lung. This is indicated, firstly, by the anamnestic data of having had tuberculosis in adolescence and recovering from it; secondly, by the presence of chest X-ray findings characteristic of residual tuberculosis changes in the right root and the upper lobe of the right lung—multiple petrifications and a single high-intensity shadow with clear contours, respectively, with no current radiological signs of active tuberculosis; thirdly, by the absence of clinical signs of active tuberculosis—no intoxication syndrome, normal blood count, absence of MTB in bronchial washings, and histological examination of the affected bronchial mucosa showing no signs of a specific process.

4. Acute, acquired, partial, obstructive. The atelectasis is acute because it occurred suddenly for the first time; acquired, as it is a consequence of residual changes from cured primary tuberculosis; partial, because the entire upper lobe of the right lung is affected; obstructive, because the impairment of bronchial patency occurred due to obturation by a calcified bronchopulmonary lymph node.

5. As a result of the collapse of alveoli, alveolar ducts, and respiratory bronchioles throughout the entire upper lobe of the lung, the patient is primarily at risk of developing acute respiratory failure. Acute heart failure can be secondary to acute respiratory failure. Intoxication syndrome is unlikely, as its development requires specific conditions—namely, an inflammatory process in the atelectatic lung lobe. Since the patient complains of hemoptysis, There is a certain risk of pulmonary hemorrhage, although this complication may not develop, especially given that emergency care has been provided. The patient is least at risk of developing a spontaneous pneumothorax at present, as there are no significant prerequisites for it.

6. The primary cause of atelectasis in the patient was specifically the obturation of the bronchus by a calcified intrathoracic lymph node, which was confirmed by fiberoptic bronchoscopy data (meanwhile, no blood clots were visualized in the bronchial lumen). Through the fistula that formed, following a cough during inspiration, the broncholith entered the bronchial lumen and caused its obstruction. Bronchial deformation with stenosis (resulting from past primary tuberculosis), which the patient had long experienced, had not previously impaired bronchial patency. Endobronchitis with mucosal edema is also a consequence of compression followed by perforation of the bronchus by the broncholith.

7. Based on the direct cause of atelectasis, the presence of local non-specific inflammation and edema of the bronchial mucosa, the absence of an active tuberculosis process but the possibility of its reactivation specifically in the bronchi, the management strategy should be as follows: removal of the broncholith, aspiration of bronchial contents, broad-spectrum antibiotics, isoniazid for prophylactic purposes, bronchodilators, washing the bronchi with antiseptics, and stopping hemoptysis. Due to the rapid achievement of positive dynamics, resection of the affected lung lobe is not required. Chest massage and cough augmentation are contraindicated due to the presence of hemoptysis and generally do not constitute an emergency care method in this clinical situation.