Objetivos Específicos

An inhalation injury can be broadly classified according to the site of the injury[2].

1. Airway Injury Above the Larynx (obstruction) 2. Airway Injury Below the Larynx (pulmonary damage) 3. Systemic Intoxication (cell hypoxia)

A patient may have one or a combination of these types of injury.

Management of the airway aims at providing a patent and protected airway first and foremost. The airway may also need to be secured to improve oxygenation and ventilation in the setting of respiratory failure.

1. Airway Injury above the Larynx (obstruction)

These are actually thermal burns produced by the inhalation of HOT GASES, and so occur in those patients who have no alternative but to breathe these gases. This is most likely to occur in an enclosed space, if trapped in a fire, or with the inhalation of steam.

These burns produce the same pathophysiological changes that are produced by thermal injury to skin with damage proportional to exposure. Inflammatory mediators cause oedema of the tissues which leads to obstruction initially, and later loss of the protective functions of the mucosa [42].

Respiratory obstruction often develops as a result of soft tissue swelling and may persist beyond the time of maximal wound oedema (between 12 and 36 hours). A burn to the skin of the neck may

aggravate this obstruction by producing neck oedema[2]. The latter is much more likely to occur in children who have relatively narrow airways and short necks with soft tissues that are readily distorted by oedema.

It should be remembered that burns involving more than 20% TBSA result in a systemic inflammatory response, even when there is no direct injury to the tissues. The airway mucosa may become oedematous, especially if large volumes of fluid are required for resuscitation, and this may further compromise the airway.

The upper respiratory tract has such an efficient ability to conduct heat away that it is only after extreme heat exposure that direct heat damage to the lower respiratory tract occurs.

2. Airway Injury below the Larynx (pulmonary damage)

These burns are produced by the inhalation of the products of combustion. Fires cause oxidation and reduction of compounds containing carbon, sulphur, phosphorus and nitrogen. The list of chemical compounds produced includes carbon monoxide and dioxide, cyanide, esters and complex organic compounds, ammonia, phosgene, hydrogen chloride, hydrogen fluoride, hydrogen bromide and the oxides and aldehydes of sulphur, phosphorus, and nitrogen [42]. Polyvinyl chloride (PVC), for example, produces at least 75 potentially toxic compounds when burnt [51]. Acids and alkalis are produced when these compounds dissolve in the water contained in respiratory mucous and tissue fluids. These compounds produce a chemical burn. In addition, the particles of soot less than 1µm are aerosolised. They also contain similar irritant chemicals and can produce damage to the alveolus [42]. These compounds contact the airway mucosa and lung parenchyma initiating the production of inflammatory mediators and reactive oxygen species. This results in oedema and potentially shedding of the trachea-bronchial mucosa. The lower airways too are involved with cast formation and plugging that may result in distal airway obstruction. The lung parenchyma may be affected with disruption of the alveolar-capillary membrane, the formation of inflammatory exudates and loss of surfactant. This results in atelectasis, interstitial and pulmonary oedema causing hypoxaemia and reduced lung compliance [51, 52].

A number of pathophysiological factors contribute to lung injury, leading to impaired gas exchange [47]:

· Obstruction due to…

- bronchoconstriction - mucus production - cast formation

· Alveolar dysfunction and shunting due to…

- emphysematous alveolar destruction - atelectasis / alveolar collapse

· Alveolar fluids…

- non-cardiac pulmonary oedema / chemical pneumonitis - secondary bacterial pneumonia

3. Systemic Intoxication (cell hypoxia)

The two common intoxications occurring in association with inhalational burns are caused by carbon monoxide and cyanide[42].

Carbon monoxide (CO)

This is produced by incomplete oxidation of carbon. Carbon monoxide (CO) is a colourless odourless gas which diffuses rapidly into the blood stream. It combines readily with haemoglobin (Hb), having a greater affinity for haemoglobin than oxygen (240 times greater) and forms carboxyhaemoglobin (COHb). This binding to form COHb effectively reduces the oxygen carrying capacity of the blood. CO causes tissue hypoxia by reducing oxygen delivery and utilisation at a cellular level [42]. It also dissociates from Hb less readily than does oxygen and so occupies an oxygen-binding site for a long period of time [42].

In addition to binding preferentially with haemoglobin, CO also binds with great affinity to other haem- containing compounds, most importantly the intracellular cytochrome system. It may also have a direct toxic effect. This causes abnormal cellular functioning which is a major component of CO toxicity. [53]. Post intoxication encephalopathy may be a serious sequel of poisoning; the exact mechanism of how this develops is not fully understood but may be due to cerebral lipid peroxidation.

The usual indicators of hypoxia may not be present:

· Haemoglobin not carrying O2 causes skin to have a blue colour (cyanosis). COHb gives false reassurance with a normal pink colour (some say ‘cherry red’)

· A pulse oximeter (O2 saturation probe) cannot distinguish between COHb and O2-Hb (oxyhaemoglobin) so even in severe poisoning, the oxygen saturation will read as normal

· A standard blood gas machine measures PaO2 as the amount of oxygen dissolved in the blood. The dissolved oxygen in the plasma remains unaffected so the PaO2may be normal.

Blood gas analysers using co-oximetry are the only reliable way to assess oxyhaemoglobin and carboxyhaemoglobin levels[54]. Carboxyhaemoglobin dissociates slowly, having a half-life of 250 minutes in room air.

Patients who have CO intoxication are often confused and disorientated, exhibiting symptoms similar to those of hypoxia, head trauma and acute alcohol intoxication. It is important to consider CO intoxication in this clinical setting.

Table 4.1

Carbon Monoxide Intoxication[9, 42, 53].

Carboxyhaemog lobin (%)

Symptoms

0 –15 None - (Smokers, long distance lorry drivers) 15 – 20 Headache, Confusion

20 –40 Nausea, Fatigue, Disorientation, Irritability 40 –60 Hallucination, Ataxia, Syncope, Convulsions, Coma

> 60 Death

Patients with an altered state of consciousness after burns have CO intoxication unless proven otherwise.

Cyanide Poisoning (HCN)

This may occur because of the production of hydrogen cyanide from burning plastics[2] or glue used in furniture. It is absorbed through the lungs, and binds readily to the cytochrome system, inhibiting its function resulting in anaerobic metabolism. It causes loss of consciousness, neurotoxicity and convulsions. It is gradually metabolised by the liver enzyme rhodenase. Blood cyanide levels are not readily available and their usefulness is debated. Smokers will often have levels of 0.1mg/L, while lethal levels are 1.0 mg/L. In practice, pure HCN poisoning is rare, most patients suffering mixed HCN and CO poisoning.