5. Traumatic hemothorax

than being cause by trauma and is frequently encountered in closed pneumothorax. In tension pneumothorax, there is one-way air entry into the pleural space, and the increased air pressure within the pleural space puts pressure on the lung and pushes the mediastinum to the opposite side, which ultimately applies pressure on the other lung. Pushing the mediastinum along with the heart and other vascular structures towards the opposite thoracic space is called

Figure 1. PA chest radiography of a case operated on with a right tube thoracostomy due to a developed traumatic right

Increased mediastinal shift impairs cardiac venous filling and presents a life-threatening condition, with the patient developing dyspnea, tachypnea, hypoxia, tachycardia, hypotension and agitation. Radiological imaging shows increased air pressure in the pleural space, the total collapse of the lung on the affected side, the widening of the costal intervals, the detrusion of the diaphragm and the translocation of the mediastinal structures to the opposite side. In the absence of an emergency diagnosis and tube thoracostomy, the patient may experience a dramatic course, including hypoxemia, metabolic acidosis, decreased cardiac output, cardiac

As an emergency intervention, to empty the air in the pleural space, a thoracentesis can be performed at the point of interception between the midclavicular line and the 2nd intercostal space to empty the air from the intrapleural space, thus reducing the pressure on the lungs and vital organs. After this, a tube thoracotomy should be performed as soon as possible. Of all cases of tension pneumothorax resulting from penetrating thoracic traumas, 75% can be

"mediastinal shift".

pneumothorax.

100 Trauma Surgery

arrest or even death.

treated with a tube thoracostomy [27, 28].

Hemothorax is the deposition of blood between the pleural membranes, and is most frequently caused by trauma. Traumatic hemothorax may originate from the thoracic wall, lungs, blood vessels, mediastinum or diaphragm. In blunt thoracic injuries, hemothorax frequently develops as a result of the bleeding of the pleura or the lung parenchyma, secondary to rib fractures [23]. While patients may remain asymptomatic, they may also present with hypovolemia or even shock, depending on the amount of bleeding. The development of hemothorax in structures with high blood flow, such as the heart, aorta, pulmonary artery, and vena cava inferior and superior, may very quickly become mortal [29, 30].

Hemothorax also has negative effects on the hemodynamics and respiratory system. Bleeding limits the expansion of the lung at the concerned region, and the mediastinum may shift to the opposite side if the bleeding continues. In an adult, the thorax may unilaterally be infiltrated by up to 6 L of blood. While bleeding of up to 500–750 mL can be tolerated, bleeding of 750– 1500 mL can result in the development of tachycardia and hypotension, and signs of shock start to be seen in the presence of bleeding above 1500 mL (6). Diagnosis is made based on a direct lung radiography and thoracentesis, although thoracic CT is more specific for the diagnosis of hemothorax. Recently, in emergency clinics, bedside USI has also frequently been used for the diagnosis of hemothorax [6, 26, 29, 31].

A diagnosis of hemothorax can also be made when the hematocrit level in the sample obtained from the pleural space by thoracentesis is more than 50% of the hematocrit level measured in a spontaneously obtained blood sample. In the presence of penetrating traumas, hemothorax is most frequently caused by intercostal artery injuries, which, along with internal mammarian artery injuries, are the most common injuries causing persistent bleeding, and therefore require thoracotomies. For patients who are taken for emergency thoracotomies due to hemorrhagic shock, even applying finger pressure to the bleeding artery can rapidly improve the patient's vital signs [32].

Treatment approaches to traumatic hemothorax vary, depending on whether the injury is blunt or penetrating, and on the amount of bleeding. In such cases, the first procedure to be performed should be a tube thoracostomy, as this can serve as an important guide for monitoring the amount of hemothorax and for the prevention of intrathoracic hematoma deposition. Vascular access should be established and appropriate fluid and blood product replacements, such as erythrocyte infusion, should be performed as necessary. The drainage of 1500 mL or more blood following a tube thoracostomy is considered as a massive hemothorax and represents an indication for a thoracotomy. Emergency thoracotomy indications in hemothorax: (Table 1) [23, 26, 31].

Major complications of traumatic hemothorax include thrombus/hematoma in the pleural space, pleural infection, pleural effusion and chylothorax. Clotting blood should be replaced within 1 week following the trauma, or else the hemothorax starts to be organized and the risk of infection increases (Figure 2) [7, 22].

Table 1. Emergency thoracotomy indications in hemothorax.

pneumothorax, and towards the posterior and lateral for hemothorax. After the tube thoracostomy is complete, the position of the chest tube and the status of the air and/or fluid in the pleural space should be evaluated through a direct lung radiography. The chest tube should never be clamped for any reason while the patient is being transported or transferred outside the emergency unit. The tube thoracostomy is removed under the control of a lung radiography after the air leakage stops or drainage drops below 100 mL/day [22, 31, 34].

Emergency and Current Approaches to Thoracic Traumas

http://dx.doi.org/10.5772/intechopen.74713

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Emergency care thoracotomies are considered to be life-saving procedures for a limited patient group. Nowadays, the already effective and still developing emergency transport methods, and the fact that resuscitative interventions are performed before the patients arrive at the hospital, mean that a higher number of almost-morbid patients actually arrive at the hospital. The rate of survival following an emergency care thoracotomy has been reported to vary between 0 and 64%, with the best outcomes achieved for isolated penetrating cardiac injuries. On the other hand, this rate varies between 1 and 3% in cases of blunt and multiple trauma, for which the time of transfer to a hospital is longer. Emergency care thoracotomies are performed on almost-morbid patients in the emergency unit by making a left anterolateral incision between the 4th and 5th intercostal space. Emergency care thoracotomies should not be confused with thoracotomies performed in an operating room or in intensive care during the first hours following the initial injury [35, 36]. The reasons for an emergency care thoracotomy include the drainage of the pericardial tamponade, the control of intrathoracic or cardiac bleeding, the control of massive bronchovenous air embolisms, or bronchopleural fistula, open cardiopulmonary resuscitation or temporary occlusion of the descending thoracic aorta (cross-

Contraindications for emergency care thoracotomies include cardiopulmonary resuscitation lasting longer than 15 minutes for penetrating chest traumas, cardiopulmonary resuscitation lasting longer than 5 minutes for blunt chest traumas, non-traumatic arrest, severe head trauma, severe multi-system injuries, the absence of appropriately trained staff and insufficient equipment. The preferable incision for emergency care thoracotomy is an anterolateral thoracotomy, which is carried out on the side with the predicted injury following a physical examination. The incision is performed transversely, the chest cavity is entered through the

• Prehospital cardiopulmonary resuscitation that lasts less than 15 min in patients exposed to penetrating trauma • Prehospital cardiopulmonary resuscitation that lasts less than 5 min in patients exposed to blunt trauma

Serious continuous systolic hypotension after injury (≤60 mmHg) caused by:

• Bleeding (intrathoracic, intraabdominal, extremity, cervical)

Table 2. Indications of emergency care thoracotomy.

7. Emergency care thoracotomy

clamp placement) (Table 2) [36].

Rescuable cardiac arrest after injury

• Cardiac tamponade

• Air embolism

Figure 2. Thorax CT: Hemothorax following thoracic trauma.

### 6. Tube thoracostomy

A tube thoracostomy is performed for the treatment of traumatic pneumothorax and/or hemothorax, and it is an essential surgical intervention in cases requiring drainage of the pleural cavity in patients suffering a chest trauma. A tube thoracostomy is indicated for all open thoracic injuries, for pneumothorax of more than 10% and for radiologically-confirmed hemothorax. Even if there is no apparent pneumothorax and/or hemothorax, a tube thoracostomy could still be performed in intensive care patients with severe chest traumas who require mechanical ventilation. If a patient with penetrating or blunt chest trauma is transferred to the emergency unit when the vitals are completely lost, or about to be lost, it would not be erroneous to perform an emergency bilateral tube thoracostomy [9, 13, 33].

A tube thoracostomy is generally performed from the anterior axillary line, at the level of the 5th intercostal space from the lateral edge of the pectoralis major muscle. This is the region where the chest wall is at its thinnest, and is ideal for a tube thoracostomy. After local anesthesia, a skin incision is made 1–2 cm below the space where the chest tube is to be inserted, and using a clamp, the intercostal muscles are separated from the lower ribs to allow entry to the pleural space. Generally, a 28 or 32 F chest tube is inserted through this obliquely formed tunnel, and a closed underwater drainage system is formed by connecting the tube to the chest bottle. The chest tube should be directed as far as possible towards the apex for

pneumothorax, and towards the posterior and lateral for hemothorax. After the tube thoracostomy is complete, the position of the chest tube and the status of the air and/or fluid in the pleural space should be evaluated through a direct lung radiography. The chest tube should never be clamped for any reason while the patient is being transported or transferred outside the emergency unit. The tube thoracostomy is removed under the control of a lung radiography after the air leakage stops or drainage drops below 100 mL/day [22, 31, 34].


**1. Introduction**

Since the original publication in 1992 [1], many researchers have tried to explain the mechanisms and substrate that causes an abnormal electrocardiographic (ECG) pattern and ventricular arrhythmias in Brugada syndrome (BrS) and few therapeutic options have been found. Initially three hypotheses were proposed for explain the mechanism and arrhythmias in BrS, the abnormal repolarization theory [2], the abnormal depolarization theory [3] and the abnormal expression of neural crest cells during cardiac development [4].

BrS is characterized by an elevated ST segment in the right precordial leads (V1–3) on the ECG and risk of sudden cardiac death (SCD) [1, 5]. The ECG 1 pattern is frequently intermittent and can be unmasked by the administration of a sodium channel blocker (**Figure 1**). The incidence of SCD in subjects with Brugada type 1 ECG pattern and no previous cardiac arrest is 2 per 1000 patients per year [6, 7].

At present, there are just two therapeutic strategies, which include implantable cardioverterdefibrillator (ICD) and/or chronic quinidine therapy [6, 7]. However, quinidine is not effective

**Figure 1.** Characteristic BrS ECG. A. In the N°3 patient the ECG at baseline show spontaneous and intermittent type 1 ECG BrS pattern. B. After flecainide test (400 mg, orally) [19].

in many patients and its use is frequently associated with intolerable adverse effects. ICD implantation may be effective in preventing SCD, and is currently recommended as a class I indication for symptomatic patients with type 1 Brugada ECG pattern. Unfortunately, ICD therapy in many patients is associated with inappropriate shocks (overall ICD complication rate is 9.1% and inappropriate shocks in BrS occur in 13.7%), lead fractures/failure, device infections and frequent ICD discharges by electric storms [6, 8, 9].

As an autosomal dominant disease with incomplete penetrance, BrS was initially linked to mutations in the SCN5A gene [9]. Currently, more than 450 pathogenic variants have been identified in 24 genes encoding sodium, potassium, and calcium channels or associated proteins [10, 11]. Known BrS-susceptibility genes can only partially explain the clinically diagnosed cases; therefore, many patients (65–70%) remain "genetically unresolved" [8, 9]. For many years, BrS has been considered a purely electric disease even if, more recently some authors have shown the presence of morphological and functional abnormalities (regional conduction slow in the endocardium and epicardium), predominantly located in the right ventricle outflow tract (RVOT) [12–14].

Radiofrequency ablation (RFA) has recently emerged as a therapeutic option in BrS patients of high risk. RFA in two previous reports was effective in preventing ventricular fibrillation (VF) in BrS [15, 16]. Two studies have recently shown fractionated systolic electrograms (EGMs) in epicardium of RVOT and RF normalized the ECG pattern and prevented ventricular fibrillation and ventricular tachycardia (VT/VF) occurrence in a short follow-up [17, 18].