Barotrauma

Introduction: This can be caused by an air bag rupturing during deployment, forcing high pressure gas into a person's lungs. It has also been associated with rapid ascent in military aircraft and with pressure changes associated with space exploration. Barotrauma has also be documented with tracheal intubation and fibreoptic endotracheal intubation. Fibre optic endotracheal inturbation requires insufflated oxygen, which increases airway pressure. This leads to alveolar rupture with pneumothorax and subcutaneous emphysema.

Pathophysiology:

Barotrauma caused by pressure changes are governed by Boyle and Henry laws of physics. the Boyle law states, " For any gas at a temperature, the volume of gas will vary inversely with the pressure", for example pressure rises by 1 atmosphere for every 33 feet of sea water depth. This indicates that a balloon or lungs containing a volume of 1 cubic foot of gas at 33 feet of sea water depth will have a volume of gas of 2 cubic feet at the surface. If this air is trapped, as occurs when a person holds the breath during rapid ascent, it expands with great force against the walls of that space (also known as reverse squeeze). During rapid ascent, incidents of pneumothorax and penumomediastinum as well as sinus squeeze and inner ear injuries can occur. Sinus squeeze occurs with eustachean tube dysfunction which may result in inner ear hemorrhage tearing the labyrinthine membrane or could cause perilymph fistula.

Henry law states that the solubility of a gas in liquid is directly proportional to the pressure exerted upon the gas and liquid. This is something like when the cap is removed from a bottle of soda, the soda begins to bubble as the gas is released from the liquid. When nitrogen in a diver's air trank dissolves in the diver's fatty tissue or synovial fluids at depth, nitrogen will be released from those tissues as the diver ascends to a low pressure environment. This process occurs rather slowly and gradually and if the diver ascends slowly and gradually then nitrogen enters the blood stream to the lungs and is exhaled. If the diver ascends rapidly then nitrogen exits tissues rapidly and forms gas bubbles. These bubbles can affect tissues in many ways. They can obstruct blood vessels leading to ischemic injury. If this happens in the brain the results could be disastrous. When bubbles are formed in blood stream then proteins in blood stream can cling to it and begin a clotting / inflammatory response leading to endothelial breakdown and permenant tissue damage.

Decompression sickness:

This usually results from the formation of gas bubbles, which can travel to any part of the body accounting for many disorders possible. A gas bubble forming in the back or joints can cause localized pain ( the bends). In the spinal cord / peripheral nerve tissues, a bubble may cause paresthesias, neuropraxia or paralysis. A bubble forming in the circulatory system can lead to pulmonary or cerebral gas emboli.

Some gases are more soluble in fats. Nitrogen, for example is 5 times more soluble in fat than in water. Approximately nearly half of the serious decompression injuries involve CNS. Women are at high risk of decompression sickness because they have more fat inside their bodies. Decompression sickness can also occur at high altitudes.

Types of decompression sickness:

Type I:

Is mild and not life threatening. It is characterized by pain in the joints and muscles and swelling in the lymph nodes. The most common symptom is joint pain, which is mild and worsens over time and with movement.

Type II:

This is serious and life threatening. Manifestations of this type include: Respiratory compromise Circulatory compromise Peripheral nerve compromise CNS compromise

Arterial gas embolism is the most dangerous manifestation of type II decompression sickness. Air gas embolism occurs after a rapid ascent when gas bubbles forms in the arterial blood supply. These air bubbles travels to the brain, heart, or lungs. This complication can also occur ever after ascent from even shallow depths. Patients with patent foramen ovale are at higher risk of gas passing from right to left shunt causing CNS injuries.

Medical barotrauma:

This occurs in patients receiving respiratory support via positive pressure ventilation. The risk factors for this complication include:

1. Presence of COPD

2. Age of the patient

3. Malignancy involving upper / lower airway

4. Airway trauma

5. Surgical procedures to the thoracic cavity

Complications of barotrauma due to positive pressure ventilation include:

1. Systemic air embolism

2. Air cardia tamponade due to pneumothorax

3. Pneumothorax (the most common complication)

4. Pneumomediastinum - less serious complication and could present with chest pain, mild dyspnoea, dysphagia and voice changes. This condition can be managed with supportive therapy.

5. Otitic barotrauma - This involves injury to the middle ear with ear drum rupture, hemotympanum, transient hearing loss and otalgia.

Blast injury:

This occurs from an external explosive force causing localized increase in atmospheric pressure. This is also known as primary blast injury. Blast injuries can be divided into secondary, tertiary and quaternary. Secondary is impact with flying debris, tertiary deals with the person being thrown by the force of the blast. Primary blast injuries could involve respiratory, digestive, auditory and nervous systems.

Repiratory primary blast injury: could produce immediate fatal injury. Pulmonary contusion, systemic air embolism, disseminated intravascular coagulation and acute respiratory distress syndrome are commonly caused. Primary blast injury can also cause injury to thorax causing slowing down of heart, stroke volume and cardiac index leading on to hypotension without associated increase in the systemic vascular resistance.

Primary blast injury involving gastrointestinal tract produces contusion of the organ / rupture of the organ. Hemorrhage, peritonitis, mesenteric emboli and organ failure. These injuries can be occult in the begining hence the physician should keep re evaluating the patient.

Auditory primary blast injury includes rupture of ear drum, ossicle disruption and hemotympanum.

Neurological primary blast injury produces post concussion syndrome to cerebral oedema, hematoma, and intracranial hemorrhage. Aggressive treatment (craniotomy decompression) will decrease mortality.

Clinical examination:

This should be tailored to the history described by the patient. A complete general examination is performed with emphasis on ears, sinuses and neck. Pulmonary, cardiovascular and neurologic systems should also be examined. Extremities should be inspected and palpated. All joints should be tested for varying range of motion.

Patients with sinus squeeze:

Nasal mucosa should be inspected for the presence of polypi, hemorrhage or other lesions.

Individual sinuses should be palpated to elicit tenderness.

Transillumination test should be performed to rule out hemorrhage into the sinuses.

Upper teeth should be percussed with a tongue blade to test for sinus tenderness.

Patient with Ear squeeze:

The ear drum should be inspected carefully for the following signs:

1. Amount of congestion around the umbo

2. Percentage of ear drum involvement

3. Amount of hemorrhage behind the ear drum

4. Evidence of rupture of ear drum

Patient's balance and hearing should be tested. Ear drum should be evaluated using Teed scale.

Teed 0 - No visible damage (normal ear)

Teed 1 - Congestion around umbo. This occurs with a pressure differential of 2 pounds per square inch

Teed 2 - Congestion of entire ear drum. This occurs with a pressure differential of 2-3 pounds per square inch

Teed 3 - Hemorrhage into the middle ear

Teed 4 - Extensive middle ear hemorrhage with blood bubbles visible behind the ear drum. There could be rupture of ear drum

Teed 5 - Entire middle ear is filled with dark (deoxygenated) blood.

Decompression sickness type I:

Inspect for swelling or effusion in the affected joint

Test for range of motion both actively and passively

Palpate the affected area for crepitus and compartment tightness

Neurovascular status should be evaluated by performing complete neurological examination. Findings of this examination should be documented and should be used as a baseline to determine improvement in post drive chamber treatment.

Decompression sickeness type II:

Evaluate cardiovascular and pulmonary systems

Note neck vein distention / petichiae on the head and neck

Palpate skin for crepitus

Auscultate lungs and heart for decreased breath and muffled heart tones. Presence of cardiac murmurs if any is to be noted.

Neurological status be be evaluated including gross motor, sensory and cerebellar examinations.

Causes of decompression sickenss include:

1. Multiple daily dives

2. Poor adherence to the dive tables

3. Breath holding

4. Rapid ascent

5. Flying / traveling to high altitudes within 24 hours after diving

Lab investigations:

Complete blood count. Patients with a hematocrit values of 48% and more would have persistent neurologic sequelae 1 month after the injury.

Arterial blood gas determination

Serum creatine phosphokinase level - Increase in levels of CPK indicate tissue damage associated with barotrauma. Rising CPK levels indicate increasing tissue damage due to micro emboli.

Imaging:

Chest radiographs

Radiographs of joints / extremities

Spiral CT is the most sensitive method to evaluate pneumothorax

Echocardiography and ultrasonography of abdomen also need to be performed.

Immediate care:

1. Adequate oxygenation and perfusion to be maintained

2. Intubation is preferred if the patient is unstable or has persistent hypoxia despite breathing 100% oxygen

3. Thoracostomy can be performed to evacuate pneumothorax / hemothorax

4. Needle decompression of chest to be performed in suspected cases of tension pneumothorax

Recompression therapy: Recompression therapy should be performed at a dive chamber by a dive medical officer.

Sinus squeeze and middle ear sqeeze to be treated symptomatically