Not quite an excerpt: Where the Light Enters

Over the coming months I will be posting bits and pieces about Where the Light Enters to help tide you over until publication.  This first time I’ve got a piece of my research to share. These real estate/rental ads are from the New York Times in 1884. The two outlined in yellow are relevant to the story. 

And they are, in my view of things, just plain interesting. The rental market has sure changed. 

click for larger size

Did I mention…

that I finished Where the Light Enters?  It will be 2019 before it hits the shelves, I’m sorry to say. But I did deliver it to my editor.

Help Me Name a Character

It often takes me a really long time to settle on a name for a character.  For example:  there is one young woman in Where the Light Enters whose name still is not right. I have some time to fix this — until the copy editing phase closes — but I’m at a loss. 

If you had 100+ daughters, you’d likely run out of names, right? Think of it that way. Elizabeth, Hannah, Martha, Lily, Jennet, Anna, Sophie, Rosa, Lia, Laura, Margaret, Nora – all unavailable.  

Sometimes I try to get my imagination going by looking at old census records, reading old newspaper stories, or considering fictional characters from 19th century novels. I also spend time looking at paintings from the right time period.  This painting  by the swedish artist Carl Larsson, (1853-1919, so just about Anna and Sophie’s age) is the kind of thing I mean — it really captures the detail of farming life in the later 1800s. Looking at the clothing of the women working in the fields.

Unfortunately, none of those methods has worked for this new character, who name, right now, is Betty Miller. And that is not right.

Lisbeth, by Carl Larsson

What I can tell you about her: she grew up in an orphan asylum, and will eventually come into her own.  Where Carl Larsson’s Lisbeth is healthy and happy, my Betty Miller is not either of those things, to start. But hopefully will get there, one day.  

So I’d like to hear suggestions, first names or even first and last names. Remember, this is somebody born ca. 1865 so Tiffany or Jordan or Montana won’t work.

Let your imagination run riot, please. If I use the name you come up with, I will thank you in the acknowledgements. 




Medical Research and the Historical Novelist

If you are writing historical fiction about doctors who are professionally active, you have few options.

First, you can jump over what they do with and for their patients, for example: “Difficult surgery today, I’ll have trouble sleeping.”  Sometimes this is fine; you don’t want to overwhelm the readers with gore. 

Other times you need to be more specific. In order to establish the time and place, you have to draw a picture, in words. And to do that you have to know what actually went on. 

So I was thinking about a surgery at the New Amsterdam. The patient would first be seen by Elise in her role as a medical student in training, and then later by Anna, in surgery.  I searched around for something that would work, and came up with the idea of a carbuncle. Carbuncles are not pleasant. Basically you’re talking about a very large abscess, and abscesses are full of pus, and pus has to be drained.  The standard line “Ubi pus, ibi evacua” has been around for a long time (for example, see this 1891 discussion).

The detailed discussion of treatment and surgery of a carbuncle I found is dated 1914, which wasn’t ideal — medical science advanced quite a lot between 1884 and 1914 — but I could extract the information I needed and leave things like leukocyte count out of the picture. 

I thought it might be useful for readers who are interested in the history of medicine to see this article. In part because it seems to be a transcript of the attending physician’s lecture to the interns who are accompanying him on rounds. He repeats himself and goes off on tangents, which professors have always done and will always do (and how do I know that?).  But there’s a world of useful information here, if you are writing about this surgery. My version lasted maybe three short paragraphs.  When the novel comes out you’ll be able to see how I interpreted it to my own ends. 

But it is fairly graphic, so be warned. I have not included all the diagrams from the medical journal article.

Murphy, John B., ‘Carbuncle of the Arm — Septicemia — Metastatic Pleurisy — Death’, The Clinics of John B. Murphy at Mercy Hospital, Chicago, IV (1915), 145–53.


The patient, twenty-seven years, entered the hospital July 5, 1914, with the following history: About two weeks ago a small crop of boils appeared on the patient’s left shoulder, and rapidly grew to carbuncles. There were three carbuncles in all. Two of them opened of their own accord, and one was opened with a knife by a doctor on July 3, 1914. Pus drained from each one. On July 4th the third carbuncle was opened again by the doctor, and drained pus. The patient’s temperature July 4th was 103° F. at the first reading, and, two hours later, 104° F. He had chilly sensations all that day, but no distinct chill. To-day (July 5th) he complains of much pain in the left side of the chest, and also some difficulty in breathing, the pain being especially marked on deep inspiration. He complains also of a dull, aching pain in his back. This pain runs down his spine to the level of the iliac crest. Late in the day yesterday the carbuncle was opened again, but no more pus was found.  What was the leukocyte count yesterday?

INTERN: 11,200.

DR. MURPHY: This is one of those dangerous spreading streptococcus infections deep in the fascia beginning as a carbuncle. The respiratory symptoms which the patient shows, taken in connection with his high fever and great prostration, even in the absence of definite findings on auscultation, incline us to the belief that this streptococcus infection has already extended along the deep lymphatics to the left pleura, spreading down, perhaps, to   the pericardium also. This region of the shoulder is a bad place to develop one of these large carbuncles. It lies in close proximity to the deep set of lymphatics which passes upward out of the axilla, and it is, therefore, dangerous to life because of the great likelihood of rapid spread of the streptococcus infection along these wide-open pathways.

[Dr. Murphy made a deep crucial incision through the entire extent of the lesion and down to the deep fascia. The entire focus of pus-riddled tissue was turned into one large cavity by the use of a dull curet.]

There is where it (the carbuncle) is situated commonly. It extends clear down to the deep fascia covering the muscles, but did not penetrate into the deltoid bursa. See the foci of necrotic material as we break them up. See the pus welling out of the wound. Here is another deep pus pocket which I am emptying.

[Completes the toilet Of the wound]

This defect is not to be closed now, but will be left wide open with a loose packing of iodoform gauze, and allowed to drain. These silkworm-gut sutures are being put in for closure subsequently, but are now left long and will not be tied until the suppuration has been controlled. Let the record show that the superficial tissues were all infiltrated with the products of inflammation clear down to the deep fascia covering the muscles, and that necrosis had extended through the skin into the subcutaneous tissues, involving both structures en masse.

REPORT TO THE CLINIC NEXT DAY DR. MURPHY (July 7, 1914): A patient who has a furunculosis of the upper lip always has a rather high temperature and a high leukocyte count. A furuncle on the upper lip is always a very serious lesion—enormously different in course and prognosis from what it would be on the arm or forearm or on the back of the neck. It always puts the patient in a dangerous situation. It may, in fact, be stated as a general truth that whenever a furuncle or a carbuncle occurs in a rich lymphatic zone, the patient’s life be comes enormously endangered by it. A carbuncle, however, on the upper lip is, as a rule, fatal, and very promptly fatal, and  this rule, too, may be generalized to the effect, namely, that a carbuncle in any zone richly supplied with lymphatics is, usually, fatal. We have in the hospital now as a patient a young man who has developed recently a large carbuncle near the angle of his shoulder, on its anterior surface, extending into the axilla. Not only does this carbuncle lie in a zone relatively rich in lymphatics, and, therefore, dangerous to life, but it lies adjacent to a still richer lymphatic zone, the axilla. The carbuncle made its appearance on Tuesday or Wednesday of last week. The patient had something of a chill on Saturday (July 4th), rapidly followed by fever up to 103° or 104° F. That was a sign of the extension of the infection. Sunday he was breathing at the rate of from 50 to 60 respirations a minute, and his pulse-rate was 120 per minute. His temperature has ranged from 103° F. upward, but the striking symptom in the case has been his rapid, panting breathing. The method of his breathing, the fact that he breathes rapidly for a few seconds, then fixes his lower chest, breathing only with the upper portion of his chest, and then after another five or ten seconds starts his panting breathing again, is peculiar.  He complained also of pain in his chest; then he complained of severe pain in his mediastinum; and, finally, he complained of severe periodic pain in the same location.

We incised and evacuated the carbuncle yesterday morning, but without obtaining any material improvement in his general condition. The pain in the mediastinum is continuing, and his respirations last night were ranging between 56 and 60 per minute, his temperature remaining around 103° F. His pulse-rate this morning is 128.

What does all that mean? Just exactly what it would have meant in the case of a carbuncle on the lip. Whenever you find that type of infection in a rich lymphatic zone, always look out for a further regional lymphatic spread or distant metastasis by way of the circulation. Such patients frequently develop a septic endocarditis. Then, either from the original focus, or from the endocardial vegetations, the patients rapidly develop metastatic foci of suppuration in other positions in the body. This boy has developed such metastatic processes in his diaphragm and pleura. That is why he breathes in that peculiar way. He holds his breath as long as he can. Then he takes a few short, quick respirations, and stops at the height of respira tion with a sudden “catch” or grunt. Then he holds his breath again. And so the cycle is repeated. Remember, the diaphragm is the piston of respiration in the cylinder of the chest. The patients with a diaphragmatic pleurisy stop breathing as long as they can and, when forced to, make shallow, quick excursions, in order to put the diaphragm under the least possible tension and suspend pleural friction. The predominating feature in the clinical picture presented by this patient this morning and Sunday was the left-sided pleurisy, confined apparently at first to the upper diaphragmatic surface, and then gradually extending upward, particularly along the lateral wall. This is probably a metastatic pleurisy from which the patient is suffering. He may develop also a metastatic arthritis in one or more joints, a metastatic pericarditis, or a metastatic endocarditis. These conditions terminate fatally in a large percentage of the cases. If he develops metastatic foci in addition to his pleural infection, he will undoubtedly die.

I remember a very striking case of that type that I was called to take care of when I first started private practice. The patient was a west-sider, who had acquired a Neisserial infection of his urethra. He ran the usual course until the twentieth day, when he had a chill. Then he developed a pleurisy, a pericarditis, suppurations in his joints, and a suppurative peritonitis, all before he died. All these infections were metastatic from his urethritis. Such complications are not common with a urethritis, but at the same time they are usual enough. I cite that case merely to point out the common locations in which these metastatic infections appear, not only with urethritis, but also with furuncles and carbuncles, which arise in a richly supplied lymphatic zone.

I wish, further, to call your attention to the serious results of defective treatment of a few comparatively minor surgical conditions, which are frequently inefficiently treated. Carbuncle is one of them.

What do we mean by “inefficiently  treated” in such cases? Making in the carbuncle a little slit which just goes through the derma is ill treatment. In a carbuncle a clean-cut incision should be made clear down to the fascia, and even beneath it, if necessary; then a transverse incision at right angles to the first cut, and then curetment of the entire necrotic focus or dissection upward of the flaps. The former method endangers the patient’s life, whereas the second saves it. Always make the incision in a carbuncle deep enough to expose the underlying fascia. In opening a carbuncle re member that it is not a superficial infection.

A furuncle is a superficial infection, but when it extends to form a carbuncle, it develops deep roots. These deep roots may be compared to the deep tap roots of the eucalyptus tree, which shoot downward until they strike rock and then spread like the banyan in every direction. Much the same course of events occurs in the development of a carbuncle, and that is what distinguishes it from a furuncle. The line of infection in a carbuncle extends down ward in a relatively straight direction until it meets the deep fascia; then it spreads out along the surface of the fascia beneath the fat. That is why a superficial incision in the skin does no good. One does not reach the center of the infection. One must incise a carbuncle clear down to the fascia. One can easily trace the course of the necrosis down to the fascia, where it spreads out.

To get rid of the necrotic focus and to give the patient an opportunity to get well, one must make the incision include the entire depth of the infected tract. The pathologic process in a carbuncle is not a lymphangitis: it is a necrosis. Necrosis occurs very early in the course of the inflammation, and the greater the delay in instituting proper treatment, the more extensive will the necrosis be. The route of infection is probably usually by way of a hair-follicle—since carbuncles occur almost exclusively in hairy regions. That it may occasionally occur by way of the sweat-glands also is a possibility which cannot well be denied. At any rate, once the hair-follicle or the sweat-gland is infected, the pus breaks loose into the surrounding columna adiposa, if it does not find a ready vent to the outside. The pent-up infection then rapidly descends along the   loose fatty tissue of the columna adiposa until it reaches the deep layer of the superficial fascia, which stops further downward progress and forces the infection to spread laterally, which it does with relative ease, the loose fatty tissue of the panniculus offering little resistance to its progress. As the infection proceeds laterally it infects the roots of various columnae adiposze, and these secondary infections extend upward toward the skin, where they frequently point and make the multiple tiny pus points surrounding the central original focus of infection. Superficial necrosis occurs relatively early because the spreading deep phlegmon early cuts off the blood supply to the fat, superficial fascia, and skin. The fat and fascia die early, but the epidermis, because of its great vitality, may live after the dermis and fat have been destroyed. The carbuncle continues to spread laterally until either an effective leukocyte wall is formed or appropriate treatment instituted. To drain a carbuncle properly the deep phlegmon must be opened widely by a crucial incision, extending laterally a little beyond the peripheral zone of infiltration, and clear down to the deep layer of the fascia. The four flaps thus made should then be dissected back to their bases with the knife or curet. Thus the whole area of the phlegmon is laid wide open and is packed loosely with moist or vaselinated or iodoform gauze to keep up free drainage. Do not cut away the skin! Let it fall back over the gauze. If it lives,—~and it usually does,—subsequent skin-grafting becomes unnecessary.

The downward spread of the infection in a carbuncle is not unlike the downward spread of the infection of the finger-tip which results in the formation of a felon. An infection beneath the epidermis on the palmar surface of the fingers follows down the columnar adiposae to the periosteum of the phalanx, and then spreads along the bone until it is checked proximally by the joint-capsule, laterally by the attachments of the flexor profundus tendons, and distally by the skin of the finger-tip. Hence pus accumulates under pressure in this closed space, with what result? The blood-supply to the diaphysis of the phalanx is shut ofl, the periosteum and subcutaneous fat and connective tissue become necrotic, and the diaphysis of the phalanx dies and makes a sequestrum, which must ultimately be removed before healing will take place. The old idea of Roux that the lymphatics in the finger-tips run from the skin directly downward to the sub periosteal zone, and that a felon is due to the lymphatic transmission of infection to the subperiosteal zone by this lymphatic route, is no longer tenable.  In the first place, we do not know that the lymphatics follow this route. In the second place, Sharpey’s fibers run down into the osseous tissue here in such a way that it is practically impossible for the periosteum to be separated and differentiated as it is on other bones. In the third place, the proximal epiphysis of the phalanx is practically always spared, because its blood-supply is separated from that of the shaft and does not enter the closed space of the finger-ball. If a felon were a subperiosteal phlegmon, we should expect the whole bone to be destroyed. The pus which eventually forms beneath the periosteum is due to the presence of a sequestrum. Of course, besides this ischemia the necrobiotic and toxic effects of the in fecting microorganisms play an important role in the production of the necrosis. In opening a felon always make a lateral incision, so as to spare the nerves of sensation in the skin of the finger-tip, and make the incision down through the periosteum to let out the pus from the osteomyelitis focus beneath it. If the dead fragment has already separated, remove it at once, as well as the pool of pus in which it lies. It is remarkable how well the skin usually survives in these cases, and how relatively slight the disability in such a finger may be in spite of the shortening of the terminal phalanx due to the loss of the bone. I learned the great desirability of the lateral incision for felon from a patient who was none other than Dr. Lee, with whom I was so long associated. Dr. Lee had one of his associates incise a felon, which was located on the doctor’s right index-finger. The young man made an oblique palmar incision, knowing no better, and Dr. Lee himself knowing no better at the time. The incision, of course, divided the nerve-supply to the tip of the finger, and return of sensation never occurred, although the  finger made an otherwise perfect recovery. Every time in later years that Dr. Lee threaded a needle or tried to carry out some delicate procedure with that index-finger he used to call down anathema on that unlucky assistant and on himself as well. Seamstresses are an unfortunate class who not infrequently develop felons in the course of their work, and then have their earning capacity decreased by the similar incorrectly placed incisions of careless or inexperienced surgeons. It is important not to confound a paronychia with a felon. The former commences on the dorsum of the finger, usually in the nail-fold, and spreads around the sides and base of the nail, and often underneath it. For its relief it needs the exposure of the root of the nail or the extraction of the nail, or both. I spoke about carbuncle and the significance of it when it commences on the lip. I recall a man whom I visited some years ago in a suburb a short distance from Chicago. He had a carbuncle on his upper lip, and I had him come into Chicago to the hospital, although I said it was not anything serious, and that he would be all right in forty-eight hours. I was not so familiar then with the danger of this condition as I am now. We opened it up at the hospital promptly, but he was dead in thirty-eight hours as the result of a rapidly spreading streptococcus thrombo phlebitis starting from it. That gives you some idea of the great danger latent in alip carbuncle, and the speed with which it may, occasionally, prove fatal.

[NOTE.——No further metastases developed in the patient with the shoulder carbuncle. The streptococci were never isolated from the blood. The patient’s toxemia rapidly increased, and he died on the evening of July 9, 1914, about forty-eight hours after operation. No autopsy.—ED.]