Cranial Nerve Palsies

Patients occasionally present with cranial nerve lesions (fifth or seventh) attributed to neurapraxia. These lesions can be caused by the implosive tissue-damaging barotraumatic effects during descent, the distension in enclosed gas spaces during ascent or both. It is possible that air could be forced into the nerve canals as the gas expands with ascent. The nerve damage varies greatly, often transitory but occasionally long-lasting. These presentations are usually associated with barotrauma symptoms and signs, as described earlier (see Chapters 7 and 8).

With the cranial nerve palsies produced by ascent, there may be a delay of many minutes after the dive, and the diver may be aware of the feeling of distension of the gas space. The relief as gas escapes may coincide with improvement in the neurapraxia. This infers that the cause may be ischaemic, with a middle ear or sinus pressure in excess of the mean capillary perfusion pressure. Oxygen inhalation may assist, or even recompression may be indicated.

Bone Cyst Barotrauma

Bone cysts causing pain during ascent and or descent
Figure 9.6 Bone cysts causing pain during ascent and or descent. (a) An x-ray study showing a translucent cyst in the right ilium, next to the sacro-iliac joint. (b) A computed tomography scan showing two air cysts in the right ilium. (Courtesy of Dr B. L. Hart.)

Occasionally, pain may develop from an intraosseous bone cyst, probably with haemorrhage into the area, during descent or ascent, and may last for hours after the dive. The pelvic bones are most often involved, in the ileum and near the sacroiliac joints. An x-ray study, computed tomography or magnetic resonance imaging scan may demonstrate the lesions (Figure 9.6). This disorder has been confused clinically with decompression sickness, but it does not respond to recompression therapy and is sometimes aggravated by it.

Pneumocephalus

Occasionally, the cranial gas spaces (mastoid, para-nasal sinuses) are affected by ascent barotrauma, when the expanding gas ruptures into the cranial cavity. This may follow descent barotrauma, when haemorrhage occupies the gas space and its orifice is blocked. The sudden bursting of gas and/or blood into the cranial cavity, usually through the tegmen tympani and the thinned petrous temporal bone into the epidural space, could cause significant brain damage.

The clinical presentation may have all the clinical features of a catastrophic intracerebral event, such as a subarachnoid haemorrhage. Excruciating headache immediately on ascent is probable, although the effects of a space-occupying lesion may supervene. Neurological signs may follow brain injury or cranial nerve lesions.

It is likely that the condition could be aggravated by excessive Valsalva manoeuvres (‘equalizing the ears’) or ascent to altitude (air travel). Diagnosis can be verified by positional skull x-ray study or computed tomography scan (Figure 9.5).

Pneumocephalus from sinus barotrauma of ascent.
Figure 9.5 Pneumocephalus from sinus barotrauma of ascent. (a) The x-ray lateral view, showing gas at the vertex. (b) A computed tomography section showing gas anteriorly. (Courtesy of Dr R. W. Goldman.)

Treatment includes the following: bed rest, sitting upright; avoidance of the Valsalva manoeuvre, sneezing, nose blowing, altitude exposure, or other manoeuvres that increase nasopharyngeal pressures; 100 per cent oxygen inhalation for many hours; and follow-up radiology or scans to verify a reduction of the air volume. If untreated, the disorder may last a week or so, and subsequent infection is possible. On theoretical grounds, recompression or craniotomy could be considered in dire circumstances.

 

Pneumoperitoneum

This disorder has been observed with pulmonary barotrauma, with movement of air from a ruptured pulmonary bulla dissecting along the mediastinum to the retroperitoneal area, and then released into the peritoneum, to track under the diaphragm. It is also possible that previous injury to the lung or diaphragm, producing adhesions, could permit the direct passage of air from the lung to the subdiaphragmatic area.

Another possible cause of pneumoperitoneum is, as described earlier, a rupture of a gastrointestinal viscus, especially with barotrauma of ascent or underwater explosions.

The condition may be detected by chest x-ray study or positional abdominal x-ray study (gas under the diaphragm, in the erect position).
Treatment is by administration of 100 per cent oxygen with a non-pressurized technique. Usually, complete resolution occurs within hours. Management of the cause (pulmonary or gastrointestinal) is required, and surgical management of a ruptured gastrointestinal viscus may be needed.

Localized Surgical Emphysema

This disorder may result from the entry of gas into any area where the integument, skin or mucosa is broken and in contact with a gas space. Although the classical site involves the supraclavicular areas in association with tracking mediastinal emphysema from pulmonary barotrauma, other sites are possible.

Orbital surgical emphysema, severe enough to occlude the palpebral fissure completely, may result from diving with facial skin, intranasal or sinus injuries. The most common cause is a fracture of the naso-ethmoid bones. The lamina papyracea, which separates the nasal cavity and the orbit, is of egg-shell thickness. When these bones are fractured, any increase in pressure in the nasal cavity or ethmoidal sinus from ascent or a Valsalva manoeuvre may force air into the orbit (see Chapter 8 and Plate 3).

Surgical emphysema over the mandibular area is common with buccal and dental lesions. The surgical emphysema, with its associated physical sign of crepitus, can be verified radiologically as it tracks into loose subcutaneous tissue.

Treatment is by administration of 100 per cent oxygen with a non-pressurized technique, and complete resolution occurs within hours. Otherwise, resolution may take many days. Recompression is rarely indicated, but diving should be avoided until this resolution is complete and the damaged integument has completely healed.

Gastrointestinal Barotrauma

Gas expansion occurs within the intestines on ascent and may result in eructation, vomiting, flatus, abdominal discomfort and colicky pains. It is rarely severe, but can occasionally cause syncopal and shock-like states, stomach rupture and even death.
Inexperienced divers are more prone to aerophagia, predisposing to this condition. Swallowing to equalize middle ear pressures is one cause of aerophagia.

Performing the Valsalva manoeuvre while in the head-down position may also cause air to pass into the stomach. Carbonated beverages and heavy meals can contribute and are best avoided before and during exposure to hyperbaric conditions.
Treatment involves slowing the rate of ascent, stopping ascent or even recompression. The simple procedure of releasing tight-fitting restrictions such as belts, girdles and so forth may give considerable symptomatic relief.

Although not common, notable examples of gastrointestinal barotrauma are recorded. Two Norwegian divers were badly affected during 122-metre dives using helium-oxygen, on H.M.S. Reclaim in 1961. An Australian lad, responding very well to hyperbaric oxygen therapy for gas gangrene, drank a ‘flat’ celebratory lemonade at 2.5 ATA and deteriorated into a shock state with abdominal distension and pains before ascent was terminated. A group of officials celebrating the successful construction of a caisson in the United Kingdom experienced a similar embarrassing fate, from imbibing flat champagne.

Stomach rupture

Rarely, with a large and rapid expansion of gas in the stomach, this organ may rupture with ascent. A review was conducted of 12 cases associated with relatively deep dives, more than 30 metres, with rapid ascents. The abdominal pain and distension were constant, with various other symptoms including vomiting (25 per cent), belching (16 per cent), haematemesis (33 per cent) and dyspnoea (50 per cent). Guarding of the abdomen and shock occasionally developed.

On x-ray examination, pneumoperitoneum was present in all cases, but sometimes this extended to include a pneumomediastinum and even pneumothorax. These radiological abnormalities can, of course, also be produced by pulmonary barotrauma.

Gastroscopy allowed identification and localization of the lesions, and laparoscopy usually showed these to be full thickness, usually on the lesser curvature of the stomach.

Treatment of rupture of the stomach is essentially a surgical procedure; however, breathing 100 per cent oxygen as a first aid measure and even hyperbaric oxygen as an initial treatment may have some value under some circumstances. As a general rule, decompression of the pneumoperitoneum is best achieved using surgical techniques.

If there has been a full-thickness tear, then gastric contents are likely to be present in the peritoneal cavity, and the treatment must then be on general medical and surgical grounds.

In the patients reviewed, an amount of approximately 4 litres or more of gas was necessary before rupture of the stomach would develop, and it usually required a pressure of 96 to 155 mm Hg. The reason given for the localization to the lesser curvature is that there the gastric wall is composed of only one muscular layer, compared with the three layers elsewhere.

It is postulated that rapid distension of the stomach will increase the angle of His and compress the cardia against the right diaphragmatic pillar, thus making the oesophageal-gastric junction act like a one-way valve, obstructing eructation.

Suit Barotrauma of Ascent (‘Blow up’)

Figure 9.4 ‘Blow up’. Suit barotrauma of ascent.

During ascent in a standard diving (‘hard hat’) suit, the expanding gas must be able to escape. If it does not, then the whole suit will expand like a balloon and cause increased buoyancy and a rapid and uncontrolled ascent to the surface (Figure 9.4). This may result in barotrauma of ascent, decompression sickness, imprisonment of the diver and physical trauma.

Figure 9.4 ‘Blow up’. Suit barotrauma of ascent.
Figure 9.4 ‘Blow up’. Suit barotrauma of ascent.

With the decreasing use of standard diving suits, this emergency is now not often encountered, but a variant is likely with divers who use a drysuit. It also can occur with other inflatable objects, such as a buoyancy vest or salvage/lift bag if inflated excessively or from failure to deflate during ascent.

A clinically dissimilar and relatively minor manifestation is noticed by divers in an upright position who are using rebreathing equipment that has a counterlung, or breathing bag, positioned below the head and neck. The pressure gradient from the bag to the diver’s head results in a sensation of head and neck distension and bulging of the eyes.

Head and Body Barotrauma of Descent (Diver’s Squeeze)

Figure 9.3 Barotrauma of descent. Total body squeeze. Diagrammatic representation.

A rigid helmet, as used in standard diving, may permit this trauma (Figure 9.3). If extra gas is not added during descent to compensate for the effects of Boyle’s Law, the suit and occupant may be forced into the helmet, thus causing fractured clavicles, bizarre injuries and death. The sequence of events may occur dramatically if the heavily weighted diver falls off his or her stage. There is a similar result when the diver loses compressed air pressure, e.g. as a result of a compressor or supply line failure. To prevent this, a non-return valve is inserted in the air supply line.

Figure 9.3 Barotrauma of descent. Total body squeeze. Diagrammatic representation.
Figure 9.3 Barotrauma of descent. Total body squeeze. Diagrammatic representation.

The clinical features include the following: dyspnoea and a heavy sensation in the chest; a bulging sensation in the head and eyes; swelling in the areas associated with rigid walls, e.g. the helmet, and then oedema and haemorrhages within the skin of the face, conjunctiva, neck and shoulders; and bleeding from the lungs, gastrointestinal tract, nose, ears and sinuses. These pathological changes are caused by the effects of barotrauma on the enclosed gas spaces and by a pressure gradient forcing blood from the abdomen and lower extremities into the thorax, head and neck because of the negative pressure differential in the helmet. Similarly induced haemorrhages occur in the brain, heart, respiratory mucosa and other soft tissues.

Genito-Urinary Barotrauma

A variant of suit barotrauma is the genital ‘squeeze’ from the P-valve, used to assist male divers to urinate out of the drysuit during long-duration dive exposures. The condom catheter is exposed to the same pressure gradients as the drysuit, as may be the female equivalent (the ‘she-P collecting system’). A squeeze (a descent barotrauma equivalent) and a pneumatization of the urine (an ascent barotrauma equivalent) are possible, as is a subsequent urinary infection from organisms incubated in the drysuit tubing, usually Pseudomonas species. These problems may be reduced, but not eliminated, by use of a balanced P-valve, which adds a one-way valve into the system. Adequate equalization of the drysuit pressure during descent may also assist. Another problem with this equipment is flooding of the drysuit from tubing disconnection.

Skin Barotrauma of Descent (Suit Squeeze)

This condition is encountered mainly with drysuits (especially if the air inlet hose is not functional) or poorly fitting wetsuits. During descent the air spaces are reduced in volume and trapped in folds in the suit. The skin tends to be sucked into these folds, leaving linear weal marks or bruises. The condition is usually painless and clears within a few days.