If a sufferer is seriously ill or if vomiting has commenced, the pylorus will be constricted, and oral drugs may not reach their site of absorption. The drugs must be administered parenterally. Some agents are suitable for intramuscular injection if an intravenous line is not available. Sufferers severely affected by seasickness should not dive, and they should lie down and try to sleep. A mild degree of sedation is sometimes very helpful if the patient is being supervised by someone suitably qualified. This can often be achieved by use of an antihistamine that is not only antiemetic but also sedating (e.g. cyclizine). Under these circumstances, a drug such as droperidol in very small doses may also be helpful, but there should be no diving if sedating strategies are used. If there is a prolonged period of interrupted oral intake, intravenous fluid and electrolyte replacement may be required; seagoing medical officers have observed that the fluid may be more important than the drug.
For boat passengers and sailors, acclimatization will develop if progressively increasing periods are spent at sea. Otherwise, it usually takes 2 to 3 days of continuous exposure to adapt to new conditions. The sources of vestibular and proprioceptive stimulation should be reduced to a minimum. This usually means either lying down or being as still as possible. Unnecessary head movements should be avoided. In small craft, staying along the centre line of the craft, toward the stern, incurs the least complex motion. Conflicting visual stimulation is reduced by keeping the eyes closed or by focusing on the horizon. Vulnerable individuals should definitely avoid reading, and noxious stimuli such as smells should be avoided.
Drugs for general use
Most drugs for preventing and treating seasickness are either antihistamines or anticholinergics. This reflects the importance of histaminergic and cholinergic transmission of neural inputs to the vestibular apparatus, the solitary tract nucleus and the vomiting centre itself. Drugs that target the chemoreceptor trigger zone, such as the 5-hydroxytryptamine antagonist ondansetron and the dopamine antagonist droperidol, are not considered particularly effective in motion sickness.
Commonly used antihistamines include cyclizine, dimenhydrinate, promethazine and cinnarizine; and the most commonly used anticholinergic is hyoscine or scopolamine (whose most widely available preparation is a transdermal patch). Various attempts have been made to compare the efficacy of these agents, both within and between the two classes. Graybeil and colleagues4 compared drugs alone and in combinations. They found that the best combination was promethazine hydrochloride 25 mg in combination with 25 mg ephedrine sulphate. Scopolamine was the most effective single drug, but it was more effective also when combined with ephedrine sulphate or d-amphetamine sulphate than as a single drug. In a trial reported by Pyykko and associates5, dimenhydrinate was more effective than one scopolamine patch and about equal to two and had the advantage of needing a shorter period to become effective. Other studies place cyclizine and dimenhydrinate as equal in performance but suggest that cyclizine reduced gastric symptoms and drowsiness6. Use of combined preparations (e.g. hyoscine and dimenhydrinate7) may be more effective than a single compound.
Drugs for divers
The main problem for divers is that all these drugs have some side effects, and none are truly proven safe for diving. Antihistamines may cause dry mouth and drowsiness, whereas anticholinergics also cause dry mouth, variable levels of sedation and occasionally blurred vision. The effects on arousal leave open the possibility of an interaction between motion sickness drugs and nitrogen narcosis. Another frequently cited concern is the question of whether there is any interaction between the drugs and risk of oxygen toxicity. There has been limited investigation of these issues. In hyperbaric chamber dives to 36 metres, transdermal scopolamine was not found to cause decrements in cognitive performance or manual dexterity8. Both scopolamine9 and cinnarizine10 were found not to increase risk of central nervous system oxygen toxicity in rats. Although not a trial in divers or diving, it is perhaps notable that dimenhydrinate was found to induce significant neurocognitive impairment in volunteer subjects, whereas cinnarizine and transdermal scopolamine were not.
In electing to use anti–motion sickness agents, divers must accept that the safety case for use in diving has not been comprehensively made for any drug. However, on balance (which includes consideration of the debilitating effects of seasickness on divers who nevertheless enter the water), the risk versus benefit equation probably favours use of a preventive agent in susceptible divers. At the present time, the evidence suggests that use of a non-sedating antihistamine such as cinnarizine or an anticholinergic in the transdermal form (scopolamine) is acceptable. Unfortunately, both these agents can be difficult to source in Australia and New Zealand. Use of the sedating antihistamines (e.g. cyclizine) or those shown to affect performance significantly (e.g. dimenhydrinate) should be avoided. Any drug used for this purpose must be tried previously to ensure that no untoward reactions occur.
Usually, the first sign of seasickness is pallor, although this occasionally may be preceded by a flushed appearance1. This may be followed by yawning, restlessness and a cold sweat, often noticeable on the forehead and upper lip. Malaise, nausea and vomiting may progress to prostration, dehydration and electrolyte and acid-base imbalance, although these latter and more serious manifestations usually appear only in intractable seasickness during long periods at sea. During this progression, there is often a waxing and waning of symptoms, especially before the actual development of vomiting, and vomiting itself often brings temporary relief.
Tolerance develops to a particular motion, and a person may become acclimatized to specific conditions. If there is a change in the intensity or nature of the motion, the individual may again be susceptible. Continuous exposure to constant conditions usually produces tolerance within 2 to 3 days. Tolerance can also develop to repeated shorter exposures. There is a central nervous system habituation to such a degree that after the person disembarks and the motion is stopped, the person feels that he or she is rocking at the frequency of the original ship exposure.
There is considerable variation in susceptibility to seasickness. With increasing age individuals tend to become more resistant, and at least one study suggests that girls and women are more susceptible2. This susceptibility is said to result from a lack of experience with the situations that produce seasickness. Overindulgence in food and alcohol before exposure, and especially the night before, predisposes to motion sickness. Both the number of meals and their energy content correlate with susceptibility to airsickness2.The position on board the vessel can also be important, with least stimuli if the victim is amidships and using the horizon as a visual reference. Any attempt to read aggravates motion sickness. Psychological factors play a part, especially with seasickness that develops before boarding the vessel. Once one person becomes seasick, there is often a rapid spreading among others present.
AETIOLOGY：Motion sickness is caused by a mismatch or conflict of sensorineural information3. Normally, the vestibular stimuli are consistent with the visual and proprioceptive stimuli, all informing the brain of the position of the body – even when it is in motion. When the environment starts moving as well, the information becomes conflicting. The motion sickness occurs at the onset and cessation of sensory rearrangements; when input of vision, vestibular and proprioception is at variance with the stored patterns of recent stimuli information.
Almost everybody is susceptible to motion sickness1. In general, the population can be divided roughly into one third who are highly susceptible, one third who react only under rough conditions and one third who become sick only under extreme conditions. Although anyone with a normally functioning vestibular system is susceptible, people who are totally deaf and have unresponsive vestibular systems are very resistant.
In diving, two situations predispose to seasickness. The first is on the boat going to the dive site, and the second is while the diver is in the water, particularly if attached to the boat, for example, on a shot line during decompression. Most divers are less susceptible to seasickness while swimming underwater than when they are on the boat. For this reason, many divers hurry to enter the water after exposure to adverse sea conditions en route to the dive site. Problems develop because divers are inadequately prepared and equipped as a result of haste or from the debilitating and demoralizing effects of seasickness.