Lecture Inhalation injury

Smoke inhalation is the primary cause of death in about 60% to 80% of the 8,000 victims of burn injuries each year in the United States . Airway injury occurs in up to one third of those with major burns and the risk of concurrent pulmonary damage is directly related to the extent of surface burns present Inhalation injury greatly increases the incidence of respiratory failure and acute respiratory distress syndrome. It is also the cause of most early deaths in burn victims. The mortality rate following smoke inhalation ranges from 45% to 78% .

Definition Inhalation trauma may be defined as an acute damage of the respiratory tract caused by the inhalation of combustion products or steam, as a rule in a closed space. Pathophysiology: The 3 primary mechanisms that lead to injury are thermal damage, asphyxiation, and pulmonary irritation. 1-Thermal damage (Damage from Heat Inhalation) Thermal damage usually is limited to the oropharyngeal area. This is due to the poor conductivity of air and the high amount of dissipation that occurs in the upper airways. thermal injury is confined to the upper airways.

2-Asphyxiation (Damage from Systemic Toxins): Tissue hypoxia can occur secondary to decreasing the ambient concentration of oxygen to as low as 10-13%. Carbon monoxide (CO) causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Toxin poisoning can cause permanent damage to organs including the brain. Carbon Monoxide poisoning can appear symptomless up until the point where the victim falls into a coma.

3-Pulmonary irritation (Damage from Smoke Inhalation) Irritants can cause direct tissue injury, acute bronchospasm, and activation of the body's inflammatory response system. Activated leukocytes and/or humoral mediators, such as prostanoids and leukotrienes, produce oxygen radicals and proteolytic enzymes.

Mechanisms of injury Pulmonary injury following smoke inhalation occurs in two phases. The initial cellular and exudative phase is characterized by an influx of neutrophils, elaboration of oxygen-free radicals, liberation of complement degradation products and production of inflammatory mediators.The constituents of smoke can cause atelectasis by destroying lung surfactant, increasing pulmonary vascular resistance, and contributing to edema. Airflow limitation can result from bronchospasm, upper airway narrowing from laryngeal edema, bronchorrhea, ciliary dysfunction, and inspissation of desquamated cells.

CLINICAL PICTURE After exposure to products of combustion, reaction occurs at three levels: Supraglottic region: The latter responds by the rapid development of oedema (within several minutes to three days Symptoms: hoarseness, tendency to cough, respiratory insufficiency, imminent laryngospasm (Fig. 1).

Fig. 1 - Supraglottic region - pathophysiology; respiratory insuficiency 5th hour - 3rd day.

2. Tracheobronchial damage: Slower development of oedema 2. Tracheobronchial damage: Slower development of oedema. Greater risk of development of ARDS and pneumonia, imminent bronchospasm. Symptoms: urge to cough, bronchorrhoea, sings of respiratory insufficiency usually appear the third to fifth day (Fig. 2).

Fig. 2 - Tracheobronchial region - pathophysiology; respiratory insuficiency 3rd - 7th day postburn.

3. Intoxication by combustion products (most frequently carbon monoxide C0): Carbon monoxid is linked very actively to haemoglobin and thus takes up the binding sites for Oxygen. The transport capacity of haemoglobin for Oxygen is impaired even in the Gase of good partial Oxygen pressure in arterial blond and this results in hypoxia. N.B inhalation injury usually appears within 2-48 hours after the burn occurred. Indications may include: The patient faints Fire or smoke present in a closed area Evidence of respiratory distress or upper airway obstruction Soot around the mouth or nose Nasal hairs, eyebrows, eyelashes have been singed

Burns around the face or neck Circumferential burns in the cervical area cause extrinsic upper airway occlusion from encircling eschars. Management  Diagnosis . Clinical manifestations vary among victims depending on their susceptibility to injury and degree of exposure. Injury may be limited to the upper airways (eg, nasopharyngeal irritation, hoarseness, stridor, cough) may extend distally with tracheobronchial and alveolar destruction (eg, dyspnea, chest discomfort, hemoptysis). Inhalation injury is likely in the presence of facial and upper cervical burns, singed eyebrows and nasal vibrissae, bronchial breath sounds, wheezing, rales, cyanosis, and carbonaceous sputum.

1-Chest films taken soon after smoke inhalation injury are often normal, but abnormalities ranging from patchy atelectasis to diffuse interstitial and alveolar involvement may be seen 24 to 36 hours later.. 2-Pulmonary function testing can confirm obstructive or restrictive ventilatory defects. 3-Bronchoscopy is considered the "gold standard" for early evaluation of upper airway injury, but the best results are obtained within the first 24 hours. 4-Bronchoalveolar lavage, which typically reveals an increased number of polymorphonuclear cells and alveolar macrophages, 5-Transbronchial biopsy, which can be used to diagnose bronchiolitis obliterans and interstitial fibrosis

TREATMENT Treatment of patients with Inhalation injuries involves supportive treatment apart from the specific treatment of some intoxications.In the majority of Gases, Inhalation trauma is associated with extensive dermal burns. Immediately after injury and on admission to a specialized department, basic measures are essential to take:

1. Ensuring free airways - prompt endotracheal intubation:In case of deep skin burns on the neck and trunk, releasing incisions must be made as soon as possible. 2. Ensuring adequate ventilation and oxygenation of peripheral tissues: moistened oxygen, artificial pulmonary ventilation in case of respiratory insufficiency. 3. Treatment of shock, involving haemodynamic stabilization of the patient , it means adequate intravenous volume resuscitation as a prevention of hypovolaemic shock. In inhalation trauma, during the first 24 hours the need of crystalloids is 40-75 % greater than in patients with dermal burns only. 4. Careful analgosedation is essential.

5. Specific antibodies (if known) and oxygen therapy. 6. Promotion of mobilization and evacuation of secretions and detritus from the tracheobronchial tree and lungs (airway suction and lavage, humidification, chest physiotherapy, regular positioning of the patient, mucolytics, bronchodilatating substances). 7. Antioedematous treatment (elevation of head and trunk on the bed, escinum etc.). 8.Maintenance of airway patency, 9.Adequate oxygenation and ventilation,aggressive pulmonary toilet, and stabilization of hemodynamic status are the cornerstones of therapy for smoke inhalation injury. 10.Patients with altered mental status or documented upper airway injury are at risk for airway obstruction.

11.Early intervention and respiratory support are essential.   12.The cervical spine must be protected during endotracheal intubation in neurologically impaired patients. Inhaled bronchodilators help reduce bronchospasm, and humidification can relieve excessive airway drying or mucous plugging. 13.High-flow oxygen should be administered to all patients with smoke inhalation. In severe cases, mechanical ventilatory support, 14.Chest physiotherapy, early ambulation to reduce post-injury atelectasia, consolidation, and pneumonia

Prognosis Patients with smoke inhalation injury may have complications caused by a number of pulmonary sequelae, including persistent chest tightness and shortness of breath. Chronic cough and wheezing may reflect underlying hyperreactive airways. Chronic bronchitis, bronchiectasis, bronchial stenosis, pulmonary fibrosis, and bronchiolitis obliterans may also occur.