Caisson Disease Also Known As Acute Decompression Sickness Or Compressed Air Illness

Caisson disease is a disorder which occurs in divers who have been brought to the surface rapidly without conforming to the safety precautions. Some workmen are particularly susceptible. Nitrogen being more lipid soluble, more bubbles are formed in the nervous tissue and hence neurological symptoms predominate. The spinal cord is most commonly affected, the brainstem and cerebral hemispheres are affected to a lesser extent. Autopsy shows hemorrhages in the white matter and micro infarcts. Other tissues involved include the joints, skin and lungs.

Clinical features: Symptoms start within three hours of surfacing, but rarely they may be delayed by several hours. Mild cases show pains and cutaneous lesions. In the severe types neurological and pulmonary lesions are prominent. An apparently mild case may rapidly become severe and hence the initial presentation may be misleading. Early cutaneous manifestations include pruritis, erythematous skin lesions and cyanotic patches, and these should alert the physician of the impending disease. The commonest presenting symptom is joint pain (bends) felt over the knees, shoulder, hips and elbows.

More serious features are retrosternal pain (chokes) and neurologic manifestations. Tachypnoea, hypotension and shock may follow the onset of chest pain and the patient may die in coma. The neurologic symptoms include parasthesiae, girdle pains, varying degrees of motor and sensory deficits, headache blurring of vision, diplopia, papillary abnormalities, dysarthria, and vestibular dysfunction characterized by vertigo, nystagmus, nausea and vomiting (staggers).

Diagnosis: The condition is likely to be missed by the unwary physician. History, the circumstance of the case and the physical manifestations should suggest the possibility of decompression sickness. Delay in onset of symptoms should not go against the diagnosis if other features are suggestive.

Course and prognosis: The course is unpredictable sine mild cases may rapidly become serious and die. Prognosis depends upon the promptness and adequacy of recompression and graded decompression. This measure should be instituted without delay even in hopeless cases. Many a time, the recovery is remarkable. Neurological deficits tend to persist if treatment is delayed. Early recompression can prevent the development of neurological lesions. In fairly suggestive cases, valuable time should not be wasted by undertaking detailed clinical examination before recompression.

Treatment: Specific treatment is to institute immediate recompression in a pressure chamber as an emergency measure. Respiratory depressants like morphine should be avoided. The pressure equivalent and the duration of recompression have to be decided by personnel trained in recompression techniques. Usually, a pressure of 2.8 atmospheres (283.7 KPa) is beneficial. Hyperbaric oxygen helps in improving oxygenation of ischemic tissues.

In patients with neurological deficits, shock, or cerebral edema, corticosteroids are beneficial. Low molecular weight dextran (dextran 40) helps in reducing vascular sludging. Infusion of appropriate fluids helps in restoring blood volume, improve the circulatory state, and mobilize trapped bubbles. After suitable recompression, the patient should be carefully decompressed, allowing sufficient periods at each stages to prevent recurrence of bubble formation. Susceptible persons should refrain from diving till recovery is complete.