Still, he could make two weeks’ wages in a day, he said. If he could last a month, he would have enough to live on for a year. But by the fifth or sixth day, he had terrible shooting pains in his ears and he was told he might be going deaf. An Irishwoman he was boarding with in a shanty beside Central Park fixed up a remedy—“a roasted onion cut in two and clapped tight on each ear with a flannel bandage.” Harris said it worked like magic, relieving his pain in minutes. But not many days later he saw one of the men fall and writhe on the ground, blood spurting from his nose and mouth, and that was enough to decide young Harris, who quit soon after and who later took the literary license to say that the man’s legs were “twisted like plaited hair.”
Smith assumed medical charge of the caisson workers on January 25, 1872, and was on duty until May 31, when he resigned. During that time there were 110 cases of sickness that he could attribute directly to compressed air and that were severe enough to require treatment. Not by any means, however, did every man suffering pain or discomfort report to him—as he was well aware. The feeling was that a man might not get hired again at some future time if it was known he had had a dose of the Grecian Bends. (It was a feeling that would also persist among future and supposedly more enlightened generations of “sand hogs,” a term not yet in use in the 1870’s.) As Roebling would write in his own report, scarcely any man escaped without being affected by intense pain in one form or other. Martin and Collingwood both suffered attacks. Charles Young, the foreman who had collapsed in the Brooklyn caisson the same time Roebling did, had again become so much affected by the compressed air that on the advice of his own doctor he resigned, taking a job overseeing work on the dock instead.
But those cases Smith was able to treat and study, he described at some length in his notebooks:
Case 11—E. Riley. Taken sick Feb. 16th, one hour after leaving the caisson. Pressure 26 lbs. Epigastric pain and pain in the legs. No loss of sensibility. Profuse cold perspiration. Pulse, when I saw him, two hours after the commencement of the attack, was 96. The pain, which at first was very severe, had by this time become much less. Gave him an ounce of brandy and a teaspoonful of fluid extract of ergot. In 10 minutes the pulse had fallen to 82. Was able to resume work the next day.
Case 12—Joseph Brown, foreman, American, aged about 28. Taken on the 28th of February, about an hour after coming up from a three hours’ watch. Excessive pain in left shoulder and arm, coming on suddenly, “like the thrust of a knife.” Pain continued until he went down again for the afternoon watch, when it ceased immediately….
Case 13—Henry Stroud, a diver by occupation, began work on the morning of April 2d. Half an hour after coming up from the first watch, was taken with numbness and loss of power in the right side, also dizziness and vomiting. This was followed by severe pain over the whole body. Excessive perspiration. Was treated with stimulants and ergot, and in five hours was well enough to return home.
Case 14—John Barnabo, Italy, 42, reports on the 13th of March, while in a car returning home, he was taken with severe pain in both arms. This was followed by dimness of sight and partial unconsciousness. Extremities very cold. Remained in this condition for two hours. Was obliged to keep to his bed for three days. For a week afterward was unable to work, feeling very much oppressed about the chest. Had no medical attendance. Had a similar but less severe attack about a month previously.
Savage cramps in the legs were the most common first sign. Sometimes the pain lasted all night, in the knees mostly, and it felt as though the joint was being violently twisted apart and every muscle torn away from the bones—or worse. There was really no way to describe the pain, most men said. A modern medical textbook describes the pain as deep and relentless, and not throbbing. “When it is severe, local numbness, weakness, and faintness resemble the sickening pain of a blow on the testicle.”
In one out of four cases the attack was accompanied by dizziness, double vision, and repeated vomiting. All of a sudden a man would begin to stagger, bend double, retch horribly, and fall. Sometimes there was no pain at all, just a massive numb feeling and an inability to walk or to stand upright.
The victim of an attack always looked the same, whether there was pain or not, the face a leaden color with cold beads of sweat standing out all over, which were probably signs of impending shock. Men complained, too, of excruciating pains in the chest and bowels. Some had their speech affected, as though they had had a stroke. In numerous cases the joints—knees, wrists, elbows—were swollen all out of shape, burning hot to the touch, badly discolored, and extremely tender.
By the first week of April the caisson was down past sixty feet, still descending steadily, and conditions had grown very serious indeed. The remedies Smith employed were all very simple. To alleviate pain he promptly administered ergot and often in quantity. Or he doled out whiskey and ginger. Or he gave injections of atropine, a poisonous alkaloid used as an antispasmodic. When nothing else worked, he used morphine. Since the average attack generally lasted only a few hours, his solution for severe cases was simply to drug the patient so heavily that he felt little or nothing.
He applied hot poultices to swollen joints. Paralyzed legs were soaked in hot baths, arms were packed in ice, spines were doused with ice water. Men with heaving stomachs were spoon-fed bits of ice or “a scruple of calomel,” i.e., twenty grains of a white tasteless purgative. Sometimes these things worked, or seemed to. But the prevailing attitude among the workers and the engineers in charge was that it did not matter much what Smith did. As Collingwood noted at a gathering of the American Society of Civil Engineers later that spring, almost every man recovered eventually anyway, regardless, it seemed, of how much or how little was done for him.
In a few instances, when a man reported back to the job after recovering from an attack, Smith told him to find other work. Patrick Rogers, for example, a forty-year-old Irishman from Brooklyn, was on his way home on the ferry one night when all at once he had no feeling at all in his right side and very quickly after that was unable to stand up or move a muscle. When the boat docked, he was placed in a horse cab and taken home. As with most of the cases Smith recorded, the pain Rogers was in, terrible as it was, lasted less than twelve hours. But when he returned to the caisson, ready to go down again, he told Smith of a continued “trembling” in his chest and Smith advised him to go away and not come back.
A number of other Brooklyn men were sent by Smith to the Brooklyn City Hospital, where, interestingly, the cases became the special fascination of a young intern there, Dr. Walter Reed, later to be one of the best-known physicians in the world as a result of his research on yellow fever. Like Smith, Reed also kept extensive notes on each caisson victim to come under his care and these he subsequently turned over to Smith. As Roebling would write, it was hoped that Smith’s efforts and conclusions would be made public eventually “for the benefit of future works.”
Smith never used the term “bends.” He called it the caisson disease, a name he was the first to employ and that is still used as the formal designation. He did a commendable amount of original research into the history of the subject and was thoroughly familiar with what Jaminet had written in a lengthy report published in St. Louis the previous year. * Smith described Jaminet’s observations as “exceedingly valuable,” but found it “especially to be regretted” that Jaminet’s basic remedial routine had been merely to keep the patient lying on his back with his feet elevated slightly and to administer whiskey or beef broth.
From what he read and from his own observations Smith put together a number of theories, several of which were the same as conclusions reached in France some twenty-five years earlier. The disease, he decided, depended upon increased atmospheric pressure, but always developed after the pressure was removed. Attacks never occurred while the men were still under pressure, only afterward—as had become obvious to almost everyone. So there was a very good chance, he decided, that the principal cause of the trouble was “locking out”
too rapidly. “Indeed,” he wrote, “it is altogether probable that if sufficient time were allowed for passing through the lock, the disease would never occur.” This, he knew, jibed with what the French mining engineer M. B. Pol had concluded in 1845 and later expanded on in a most interesting memoir published in 1854. “Experience teaches,” Pol wrote, “that the ill effects are in proportion to the rapidity with which the transition is made from the compressed air to the normal atmosphere.” In St. Louis Jaminet too had hit upon the same idea after being taken by a terrible seizure himself, but Jaminet thought it even more important to increase the pressure slowly when the men were going in. Smith it seems never suffered any discomfort from his time in the caisson.
To make things easier for the men after they emerged from the lock, Smith recommended that no climb up a long flight of stairs be necessary at that point. To have put the locks at the bottom of the shaft as Eads had was a serious mistake, he said. The arrangement in Brooklyn had been better. That way the climb was made “in the compressed air, instead of immediately after leaving the lock, when the system is more or less prostrated.” The elevator Roebling installed had been a wise measure, but it had not wholly alleviated the problem.
But Smith did not see how, in all practicality, the locking-out procedure could be changed much. What might be sufficient time in the lock for one man, he reasoned, would be too short for another, and far less work would be accomplished if the time in the lock were prolonged greatly. Delays would be very expensive for the Bridge Company. Besides, the men themselves would want no part of it. About all that could be done, he concluded, was to make the time required in the lock proportionate to the pressure. But even that time could only be “as great as is consistent with the circumstances.” For the New York caisson Smith established a regulation that at least five minutes more in the lock would be allowed for each additional “atmosphere,” or for every additional 14.7 pounds of pressure, which meant that for every three pounds of pressure added inside the caisson, Smith wanted the men to take a minute longer coming out. So at a depth of, say, sixty-five feet, with the pressure at thirty pounds, the men should spend five minutes in the lock on their way out; at seventy-five feet, with the pressure at thirty-three pounds, they would spend perhaps six minutes. Smith was not asking for very much, in other words. Even so, the regulation was followed only infrequently. “The natural impatience of the men to reach their homes,” he wrote in a tone of despair, “makes the delay in the lock irksome, and great firmness is required on the part of the lock tender to prevent the escape cocks being opened more widely than is consistent with safety.” One of the first steps in such work, he said, ought to be the employment of reliable lock tenders.
But despite his recognition of rapid decompression as the chief cause of the mysterious sickness, Smith remained convinced that susceptibility was still largely a matter of “special predisposition,” as he called it. Some people, he said, were simply more susceptible than others. It was commonly known, he said, that certain people had a predisposition to pains in the joints just prior to a thunderstorm. These pains, as he said, were generally considered to be of rheumatic character and caused by dampness, but Smith now thought differently. The pains suffered by his caisson workers were precisely the same, he said, only, of course, immensely intensified. So very likely anyone who could feel weather in his bones was actually feeling shifts in atmospheric pressure, and just as some people could feel such things and others could not, so some people would fall victim to the caisson disease while others would not.
Fat people and heavy drinkers, he was convinced, were more susceptible than anyone else. Men new to the work also stood a greater chance of being hit by an attack than those who had been going into the caisson for a length of time and so had had the pressure build up on them slowly. New hands suffered worst during the first week he noted. The ideal caisson worker in his view was a spare man of medium height in his twenties or thirties, a description that would have applied to Washington Roebling, among others.
But of more importance was Smith’s contention that the amount of pressure a man was exposed to and length of time spent in the caisson were as much a part of the problem as rapid decompression. So in this he agreed completely with Eads, Jaminet, and Roebling. “The testimony of all observers,” he wrote, “is that the liability to attack is directly as the duration of the stay in the caisson.” The common explanation given for Roebling’s collapse in the Brooklyn caisson the night of the fire was not that he had been coming up too fast, but that he had been staying down too long. Smith concurred with the explanation. In fact, the explanation followed perfectly out of the conclusion he had come to concerning the real root of the problem.
14
The Heroic Mode
As it is now demonstrated that the method of compressed air is applicable to a great range of engineering operations, and offers many peculiar advantages, it is extremely desirable that the principal objection to its employment, viz., the discomfort and danger to the workmen, should be reduced to a minimum. To this end I offer the following suggestions…
—ANDREW H. SMITH, M.D.,
The Effects of High Atmospheric Pressure, Including the Caisson Disease
SMITH said the caisson disease could be explained on mechanical principles. He said it was caused by the effect of abnormally high atmospheric pressure on the circulatory system. Under pressure, the blood was not distributed according to the normal physiological demands of the body, “but in obedience to overpowering physical force.” As he saw it the envelope of heavy air in the caisson pressed against the surface of the body forcing the blood into the center of the body. The blood “retreats,” he wrote, “from the surface to the center, and accumulates there until an equilibrium of pressure is produced.”
Smith held, however, that a man’s circulation could adjust somewhat to such unnatural conditions if the conditions were experienced by degrees. And the longer a man stayed down in the heavy air, and the heavier the air, the more the circulatory system would be affected. But when the pressure was removed suddenly—if a man were to waste no time getting through the air lock—then the blood vessels would fail to assume their natural condition in an instant, proper circulation would not be restored quickly enough, and “disturbance of function will result.”
Smith was quite right that rapid decompression was the secret to the mystery, but his explanation of why was wrong. His call for slower decompression was a commendable step in the right direction certainly, and seemed radically cautious at the time. (In St. Louis, for example, Dr. Jaminet wanted his men to spend an extra minute in the lock for every six new pounds of pressure, indicating that perhaps Smith’s convictions on the matter were twice as strong.) But even so, as a preventive measure, Smith’s new locking-out procedure, even when it was followed, was so inadequate as to be of little real consequence.
The mystifying disease was, in fact, caused by the effect of too rapid decompression on circulation, but for reasons other than Smith had arrived at. The leg pains, the paralysis, the swollen joints, the agonizing stomach cramps, were caused by the liberation of nitrogen bubbles from solution in the blood stream and in the tissues of the body upon the sharp reduction of atmospheric pressure.
Under pressure the normal nitrogen gas in the blood dissolves to a high degree, then returns to a gaseous state—in the form of bubbles—when and if the pressure is suddenly relieved. Set free in the body fluids such bubbles can cause great damage. If liberated in the spinal cord, for example, they can cause total paralysis. But if pressure is relieved gradually, the gas comes out of solution slowly and is removed by the lungs.
The savage pains of the bends are caused by a stoppage of the oxygen supply in the blood stream. The nitrogen bubbles released by too rapid decompression create blocks in the blood stream—the same as mechanical blocks—that keep the oxygen in the red blood cells from reaching the tissue. The red cells fail to get past the nitrogen bubble, the tissue is denied the oxygen it must h
ave, and the result is dreadful pain. This denial of oxygen-bearing blood—called ischemia—is much the same as what happens in a heart attack. So an attack of the bends might be likened to a heart attack in different parts of the body, most often the limbs and joints.
The level of pressure in the caisson and the time spent by an individual in the caisson do have a direct bearing on the problem and so Smith was right to keep the work shifts as short as possible, a policy that is still adhered to in caisson and tunnel work when pressures are extreme. Smith’s nine rules were also sound policy, in that they contributed to the over-all fitness and health of the men and fit, healthy men are less likely to be victims of the bends than those who are not. Fat men are also more prone to attacks, as Smith surmised, since the nitrogen bubbles tend to collect and dissolve in fat tissue. And from all that is now known about the bends—from subsequent experience in construction work, from underwater research and the space program—it appears that some people are indeed more susceptible to the disease than others, just as Smith declared.
The Great Bridge Page 34