In 1909, Ravenhill went to the Poderosa and Collahuasi mines in north Chile for 2 years as medical officer, or “Surgeon,” as the position was then called. The evidence for these dates is that, in his article, he states that on January 15, 1912, he had been away from the “altitudes” for 5 months, and he also states that he was there for 2 years. Thus reasonable dates of his stay in Chile would be from August 1909 to August 1911.

As a result of his period there, Ravenhill wrote his landmark paper “Some experiences of mountain sickness in the Andes” [36]. It gives excellent descriptions of acute mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema. His choice of the Journal of Tropical Medicine and Hygiene for the paper was in the tradition of reports by British physicians on diseases in colonies and other remote areas, although, of course, the subject had little to do with either tropical medicine or hygiene.

Ravenhill begins his paper by noting that mountain sickness is known as “puna” in Bolivia and “soroche” in Peru. He adds that the term “puna” is employed loosely by the inhabitants, who use the word not only to describe the illness that most people suffer on arrival at high altitude but also the dyspnea, which affects everybody who lives there. Ravenhill correctly restricts the term to the first meaning. He also points out that the location of the mines is a good place to study puna, because most newcomers come from Antofagasta on the coast by train and therefore avoid complicating factors such as fatigue and insufficient food. He includes a brief but interesting description of the rail journey.

Ravenhill then describes “puna of a normal type,” which we now call acute mountain sickness. The clinical description could hardly be bettered. He wrote

It is a curious fact that the symptoms of puna do not usually evince themselves at once. The majority of newcomers have expressed themselves as being quite well on first arrival. As a rule, towards the evening the patient begins to feel rather slack and disinclined for exertion. He goes to bed, but has a restless and troubled night, and wakes up next morning with a severe frontal headache. There may be vomiting, frequently there is a sense of oppression in the chest, but there is rarely any respiratory distress or alteration in the normal rate of breathing so long as the patient is at rest. The patient may feel slightly giddy on rising from bed, and any attempt at exertion increases the headache, which is nearly always confined to the frontal region.

Ravenhill then notes that the pulse is nearly always high and “there is at times reduplication of the pulmonary second sound.” This last is a remarkable prescience of the pulmonary hypertension associated with alveolar hypoxia, which was not described in animals until 1946 by von Euler and Liljestrand [49] and in humans at high altitude until about 1956 [43].

Ravenhill goes on to point out that the patient usually sleeps better on the second night and by the fourth day of arrival is probably very much better. He specifically notes that there is no “epistaxis or other hemorrhages, dyspnea or extreme vertigo” in puna of the normal type, “which is not a very serious condition at the altitude in question.” This is an interesting observation, because some earlier descriptions of acute mountain sickness gave prominence to bleeding from the nose and other mucous membranes, which has always been puzzling because these are not features of the modern condition.

Of course, there had been many descriptions of acute mountain sickness before Ravenhill’s, and it is interesting that he does not cite any previous references. Indeed, his paper has no references at all. Traditionally, the first extended account of acute mountain sickness is attributed to the Jesuit priest Joseph de Acosta [2], although the description is not typical and sounds more like acute gastroenteritis. Here is a section from the English translation of 1604 [3].

There is in Peru, a high mountaine which they call Pariacaca… when I came to mount the degrees, as they call them, which is the top of this mountaine, I was suddenly surprised with so mortall and strange a pang, that I was ready to fall from the top to the ground…. I was surprised with such pangs of straining and casting, as I thought to cast up my heart too; for having cast up meate, fleugme, & choller, both yellow and greene; in the end I cast up blood, with the straining of my stomacke.

Following de Acosta, there were many descriptions of high-altitude illness in the seventeenth-nineteenth centuries. The first book devoted to mountain sickness was probably that written by Meyer-Ahrens in 1854 [30]. The best compendium of early descriptions is Chap. 1 of Paul Bert’s monumental “La Pression Barométrique” [12], where he devotes 170 pages to the topic. However, none of the descriptions there rings as true as Ravenhill’s.

Following the section on puna of a normal type, Ravenhill goes on to describe two “divergent types of the disease… [1]. Those in which cardiac symptoms, and [2] those in which nervous symptoms predominate.” He describes three cases of puna of a cardiac type, which we now call high-altitude pulmonary edema. Again, the descriptions are accurate and vivid. Here is part of the description of the first case.

He seemed in good health on arrival, and said that he felt quite well, but nevertheless he kept quiet, ate sparingly, and went to bed early. He woke next morning feeling ill, with symptoms of the normal type of puna.

As the day drew on he began to feel very ill indeed. In the afternoon his pulse-rate was 144, respirations 40. Later in the evening he became very cyanosed, had acute dyspnoea, and evident air hunger, all the extraordinary muscles of respiration being called into play. The heart sounds were very faint, the pulse irregular and of small tension. He seemed to present a typical picture of a failing heart. This condition persisted during the night; he coughed up with difficulty. He vomited at intervals. This condition persisted during the night; he had several inhalations of oxygen; strychnine and digitalis also were given. Towards morning he recovered slightly, and as there was luckily a train going down to Antofagasta in the early morning, he was sent straight down.

I heard that when he got down to 12,000 ft. he was considerably better, and at 7000 ft. he was nearly well. It seemed to me that he would have died had he stayed in the altitudes for another day.

A surprising omission is auscultation of the chest, which presumably would have been rewarded with rales. Indeed, these were reported in the third case. The rapid improvement on descent is typical of high-altitude pulmonary edema.

Ravenhill did not personally see the second case, a patient who died while being carried down from a neighboring mine. The third case is interesting because it was a young Turk, aged 23, who had lived in the district for some months before but who had been at sea level for some weeks and developed puna the day after his return to high altitude. Ravenhill was asked to see him on the fifth day, when he was “profoundly dyspnoeic, respirations being 60, pulse 144, and hardly perceptible.” He died that night. The case is interesting, because the illness occurred in someone who had been living at high altitude but went to sea level and then returned to altitude. This sequence of events has been described many times since.

These are the first convincing descriptions of high-altitude pulmonary edema. Angelo Mosso, in his book “Fisiologia dell’Uomo Sulle Alpi”, 1897 [31] [English translation: “Life of Man on the High Alps”, 1898 [32]] described two cases of what he called “inflammation of the lungs,” and while these may have been high-altitude pulmonary edema, the descriptions are not typical. The first was Dr. Jacottet who died on Mont Blanc in 1891, and the description included “violent shivering fits” (fort frissons). The diagnosis at postmortem examination was “capillary bronchitis and lobular pneumonitis,” with the immediate cause of death being “suffocative catarrh accompanied by acute edema of the lung”.⁴

Mossoʼs other case was a fit young soldier named Pietro Ramella who developed “inflammation of the lungs” at the Capanna Margherita, altitude 4559 m. The man survived without being taken down, and no pathology is available. The clinical description could fit high-altitude pulmonary edema, although the rectal temperature rose to 39.9 °C, and the sputum was thought to be typical of a lung infection.⁵ Thus Ravenhill may not have seen the first case of high-altitude pulmonary edema but he did give the first typical clinical description.

It is not surprising that Ravenhill attributed high-altitude pulmonary edema to cardiac failure, although we now know that this was an error. The pulmonary arterial wedge pressure has repeatedly been shown to be normal [53], and the left atrial pressure is also normal [15]. In fact, recent work shows that the normal left ventricle tolerates the hypoxemia of extreme altitude extraordinarily well, maintaining normal contractility up to altitudes of 8000 m [42, 47]. Interestingly, early climbers on Mt. Everest who became fatigued were sometimes diagnosed as having “dilatation” of the heart. Indeed, as late as 1934, Leonard Hill stated that “degeneration of the heart and other organs due to low oxygen pressure in the tissues, is the chief danger which the Everest climbers have to face” [19].

The second divergent type of puna described by Ravenhill was puna of a nervous type. He noted that this was a “rare divergence from the normal.” However, he added that “the nervous symptoms may develop to such a degree as to become alarming.” Ravenhill goes on

The most marked case I had was a young Chileno, aged 19. He arrived at the neighboring mine in the usual way; three days later I was called to see him. He was then unable to speak, there were violent spasmodic movements of the limbs, and he resisted examination. The face was blanched, the lips almost white, the pupils slightly dilated. Temperature and respiration were normal; the pulse 140. He was unable to stand or walk. I was told that he had been in this condition almost since his arrival, and that he had been delirious, talking all sorts of nonsense. I could find nothing organically wrong on physical examination. He was sent down the same day; three days later, i.e., by the time he had reached the coast, he had quite recovered.

This seems to be a typical description of high-altitude cerebral edema, except for the spasmodic movements of the limbs. The rapid recovery on going to lower altitude is certainly characteristic. Ravenhill described two other cases. One was a young man whom he did not see personally. The patient had marked convulsions but recovered on being sent down and had no recollection of being at high altitude at all. In another case, vertigo was the most prominent symptom.

Again, Ravenhill must be given credit for first recognizing the condition that we now call high-altitude cerebral edema. Indeed, this was not described again until many years later [14], notably when a large series of Indian troops were airlifted to altitudes of ~ 5500 m in the 1960s [46].

The remainder of Ravenhill’s paper deals with conditions that influence puna, its treatment, and the effects of acclimatization. He was of the opinion that puna was most common in the first 3 months of the year, when the weather was often stormy. Imbibing alcohol increased the severity as did physical exertion. Aspirin was very useful for puna of a normal type, but he was not impressed by herbal remedies such as “Chacha Como” and “Flor de Puna,” which were used by local Indians. Giving oxygen was not particularly efficacious, although one reason may have been that he had to prepare his own by heating a mixture of potassium chlorate and manganese dioxide! By far the best treatment was descent to lower altitude, and this is current practice today. He recognized the value of acclimatization, although he made the point that everyone at these altitudes experienced dyspnea on exertion, whether acclimatized or not. Visitors to the mine who took the fast train from the coast (which took only 42 h) were more likely to develop puna than those who ascended over a period of a week.

One of the most remarkable features of Ravenhill’s paper was how it disappeared from sight to be discovered some 50 years later. This is all the more remarkable because high-altitude pulmonary edema began to be recognized in the 1930s and 1940s in the Peruvian Andes [6–9, 24, 25, 28], not so very far from where Ravenhill worked. By contrast, the condition was not described in the North American and European literature until the 1960s.

Herbert Hultgren, a cardiologist at Stanford University School of Medicine, visited Peru in early 1959 and deserves credit for alerting the English-speaking world to the work that was being done there on high-altitude pulmonary edema. He visited the Chulec General Hospital at La Oroya at an altitude of 3700 m in the Andes not far from Lima. This was the central medical facility for the United States-owned corporation, the Cerro de Pasco Corporation. There he had the opportunity of reviewing the clinical records of a series of patients who had developed pulmonary edema after arriving at high altitude [21].

Hultgren pointed out that Hurtado had possibly recognized the condition in 1937 [24]. In that publication, he described a resident of Casapalca (altitude 4200 m), who developed acute pulmonary edema on return from a trip to Lima. However, signs of cardiac failure persisted, and it is likely that the patient had underlying cardiac disease. Hurtado also referred to the same patient in a later publication [25]. In 1952, Lundberg, who was Chief of Medicine at Chulec General Hospital, reported six cases to the Asociacion Medica de Yauli, but this was not published. Shortly afterward, Lizarraga carried out a study of 14 patients at the Chulec General Hospital for his Bachelor’s Thesis, which was subsequently published [28]. Other Bachelor Theses by Lopez and Marticorena evaluated many cases in adults and children but were not otherwise published. Bardález published additional cases [6, 8, 9], and in 1956 a brief English summary appeared as a “foreign letter” in the Journal of the American Medical Association [7]. This last reference has caused some confusion, because the full name of the author was Arturo Bardález Vega and the report is sometimes cited by his motherʼs maiden name Vega rather than the correct Bardález. With the exception of this brief report, which was generally overlooked, all the papers were in Spanish, and the condition was essentially unknown in the English literature.

In 1960, Charles S. Houston, an internist in Aspen, Colorado, reported a case of “acute pulmonary edema of high altitude” in the New England Journal of Medicine and thus brought the condition into prominence in the English-speaking literature [20]. At the time, he was apparently unaware of the South American studies because these were not cited. However, in the following year, Hultgren, Spickard, Hellriegel, and Houston published an extensive study giving full credit to the Peruvian work [22]. Many other reports including hemodynamic measurements in the condition soon followed [5, 15, 23, 35, 44, 45].

All this time, Ravenhill’s beautiful description lay unnoticed, waiting for its rediscovery. This occurred in June 1964 when William H. Hall of the US Army Research Institute of Environmental Medicine carried out an extensive literature search in Boston prior to writing a paper on acute mountain sickness. Together with colleagues, he had studied Indian troops deployed in Ladakh during the India-China border war. The publication [17] was the first to cite Ravenhill’s article according to the Science Citation Index. At about the same time, Drummond Rennie apparently independently came across Ravenhill’s article while he was doing a literature search for his M.D. thesis, but he did not cite it. Ravenhill’s paper was subsequently cited on many occasions, and it was included in an anthology of high-altitude papers in 1981 [54].

It is not clear what prompted Ravenhill to go to the mines in north Chile in 1909. A search for advertisements in medical journals of the time has not been successful. However, it was not uncommon for young men to go abroad at that time; as indicated earlier, Ravenhill’s younger brother spent a period of several years in Canada on a farm. A living relative has suggested that life in general practice in Bordesley must have been rather grim, with living-in assistants being trained and four sisters at home. Perhaps it is not surprising that Ravenhill wanted to get away. Nevertheless, there was presumably some event or some person who prompted this. A detailed study of his period at King Edward’s School by one of the librarians there has pointed out that the most popular school club was the Natural History Society, and while Ravenhill was at school the Society made seven visits to local mines, which, according to accounts in the school chronicle, greatly impressed those who participated. Another event that possibly influenced Ravenhill was that in 1901 Dr. Walter Myers, who was an Old Edwardian, died while leading a yellow fever expedition in Brazil for the Liverpool School of Tropical Medicine. He was only 28. A commemorative plaque was unveiled at Birmingham University in the same year, and Ravenhill was there at the same time.