Correspondence

Clinical Problem-Solving — Where Did Good Old Clinical Diagnosis Go?

N Engl J Med 1997; 337:940-942September 25, 1997

Article

To the Editor:

In their recent Clinical Problem-Solving article (May 15 issue),1 Rozenman et al. suggest that the delayed diagnosis of endocarditis was the result of a failure to follow up on an appropriate initial diagnostic hypothesis that the patient had anemia due to iron deficiency. I challenge the appropriateness of the belief that iron deficiency is common in this setting. The anemia that occurs after bypass surgery is due to acute blood loss. Average adult iron stores of about 1 g are equivalent to four to five units of blood. The net operative blood loss is less than this because of transfusion, so most patients should be able to correct the postoperative anemia without supplemental iron. In fact, elderly adults have been shown to tolerate iron losses of up to 1.5 g by phlebotomy.2 In addition, a randomized, controlled trial of iron supplementation after bypass surgery showed no benefit of iron therapy.3

Without such a high suspicion of iron deficiency, there would be no reason for an empirical trial of iron, and the results of the iron studies in this patient (though compatible with iron deficiency) might have been more appropriately interpreted as most consistent with anemia of chronic disease. The anemia would then have suggested the presence of an undiagnosed inflammatory disease in a patient with known valvular disease and symptoms of worsening heart failure, making endocarditis an obvious consideration. My experience has been consistent with this case in that it is common to label patients with anemia inappropriately as iron-deficient, occasionally causing another important diagnosis to be missed and frequently resulting in an extensive, unnecessary search for a source of bleeding.

Edward W. Greeno, M.D.
Hennepin County Medical Center, Minneapolis, MN 55415

3 References

1
Rozenman Y, Gilon D, Fuchs S. Where did good old clinical diagnosis go? N Engl J Med 1997;336:1435-1438
Full Text | Web of Science | Medline

2
Conrad ME, Crosby WH. The natural history of iron deficiency induced by phlebotomy. Blood 1962;20:173-185
Web of Science | Medline

3
Crosby L, Palarski VA, Cottington E, Cmolik B. Iron supplementation for acute blood loss anemia after coronary artery bypass surgery: a randomized, placebo-controlled study. Heart Lung 1994;23:493-499
Web of Science | Medline

To the Editor:

The discussant in the article by Rozenman et al. refers to the patient's elevated sedimentation rate and indicates that it concerns him because, as he states, “cardiac failure is usually associated with a low sedimentation rate.” As long ago as the 1940s, when I was a medical student and a house officer, I often heard that statement in the course of ward rounds but found very little substantiating evidence in the literature. Accordingly, I invited two fourth-year medical students to join me in studying the sedimentation rate in 38 patients with acute congestive heart failure; we determined the rates during the acute stage, as well as after recompensation. Twenty-six of the 38 patients in acute cardiac failure had elevated sedimentation rates, and by and large the elevations persisted after recompensation.1

The February 7, 1991, issue of the Journal included a more extensive study of this topic by Haber et al.2 They studied patients with chronic heart failure and concluded that the sedimentation rate was “of limited value in the clinical management of this disorder.”

Robert J. Glaser, M.D.
525 Middlefield Rd., Menlo Park, CA 94025

2 References

1
McGinnis AE, Lansche WE, Glaser RJ. Observations on the erythrocyte sedimentation rate in congestive heart failure. Am J Med Sci 1953;225:599-604
CrossRef | Web of Science | Medline

2
Haber HC, Leavy JA, Kessler PD, Kukin ML, Gottlieb SS, Packer M. The erythrocyte sedimentation rate in congestive heart failure. N Engl J Med 1991;324:353-358
Full Text | Web of Science | Medline

To the Editor:

I enjoyed the article by Rozenman et al., but I broke into a profuse sweat when I came across the word “diaphoresis” in the first paragraph. Although I am proud of the contribution of the Greek language to the vocabulary of medicine, I have strong antibodies against some words. “Diaphoresis” is one of them.

This term is nowhere to be found in Greek dictionaries or British textbooks of medicine. Its use appears to be almost exclusively American. Dorland's Illustrated Medical Dictionary defines the term as “perspiration, especially profuse perspiration.”1 In Greek the word literally means “trans-carriage” or “carrying through” (cf. “electrophoresis”). It bears no etymologic relation to sweating, for which the correct Greek term is “ephidrosis.” We already use “anhidrosis” to denote the absence of sweating, so it would be only appropriate to use the correct word for its presence.

I realize, of course, that established terms are difficult to change. Until this happens, people will continue to earn their daily bread by the sweat of their brows (and not by the diaphoresis of their supraorbital ridges), and my antidiaphoretic antibodies will continue to give me a paradoxical sweaty reaction.

Anthony Papagiannis, M.D.
Gregoriou E' 42, GR 542 49 Thessaloniki, Greece

1 References

1
Dorland's illustrated medical dictionary. 25th ed. Philadelphia: Saunders, 1974.

To the Editor:

The article “Where Did Good Old Clinical Diagnosis Go?” could more aptly have been titled “Whatever Happened to the Problem List?” The value of carefully delineating all the problems and searching for the unifying syndrome that explains them all cannot be overestimated. In the patient described, the formulation of a problem list — unexplained anemia, worsening congestive heart failure, and increasing mitral regurgitation after open-heart surgery — should have prompted a systematic differential diagnosis that included infectious as well as neoplastic causes before the lytic bone lesion developed.

Unfortunately, in the day-to-day practice of medicine, the problem list exists but is often relegated to the front of the chart as a document intended to satisfy administrative requirements. Instead of consulting the list and searching for a syndrome with each new problem, we tend to apply imprecise algorithms widely — for example, anemia equals gastrointestinal blood loss; lytic bone lesion equals cancer — rather than to assess accurately how the new problem fits into the patient's overall clinical findings.

Catherine Reinis Lucey, M.D.
Washington Hospital Center, Washington, DC 20010-2975

To the Editor:

Until I read “Where Did Good Old Clinical Diagnosis Go?” I believed that most physicians guided their diagnostic thinking by some variation of a clinical pearl I received from one of my medical school professors, a pediatric nephrologist. I wish to share it, because it has served me well by saving time, money, and, I believe, a life or two:

There are three diagnoses for every disease: the one that pulls all the history together; the one you can't afford to miss; and the one that it actually is. Sometimes, if you are lucky, the first two and the third are the same, but usually they are not.

Grammatical incorrectness aside, this earthy statement embodies the practical essence of applied differential diagnosis. When one checks the “all-the-history” diagnosis against the “can't-afford-to-miss” diagnosis, their common and contradictory points emerge. As a next check, the “common-things-being-common” rule is applied to distinguish among multiple “can't-afford-to-miss” choices. As a next step, the “can't-afford-to-miss” diagnoses are eliminated, in the order of their acuity and temporal danger to the patient, by definitive diagnostic testing. Finally, a skeptical mind is maintained, even in the face of elegant thinking, for what is probable and what is possible are never really the same thing.

Vincent J. Kopp, M.D.
University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7010

Author/Editor Response

The authors reply:

To the Editor: We agree that iron supplementation does not have to be routinely prescribed to patients after coronary-artery bypass surgery. However, because transfusion practices are highly variable,1 iron deficiency should be considered in patients who received few, if any, blood products after surgery, and especially when (as in our patient) aspirin therapy is started despite a history of peptic ulcer disease.

Since the classic paper of Wood2 suggested that the erythrocyte sedimentation rate is low in patients with uncomplicated chronic heart failure, this observation has become part of medical lore.3 The study by Dr. Glaser and his colleagues is interesting, but most of their patients had acute, rather than chronic, heart failure. Even though Haber et al.4 concluded from their study of chronic heart failure that the “lack of discriminatory power [of the sedimentation rate] greatly limits the value of the test in the routine management of this disorder,” they also state that their data “provide objective evidence . . . that depression of the sedimentation rate reflects a state of severe cardiac decompensation.”

We agree with Dr. Lucey that a careful formulation of a problem list and a search for a unifying diagnosis might have led to an earlier diagnosis. In fact, this was one of the main messages of our article.

Yoseph Rozenman, M.D.
Dan Gilon, M.D.
Shmuel Fuchs, M.D.
Hadassah University Hospital, 91120 Jerusalem, Israel

4 References

1
Goodnough LT, Johnston MF, Toy PT, Transfusion Medicine Academic Award Group. The variability of transfusion practice in coronary artery bypass surgery. JAMA 1991;265:86-90
CrossRef | Web of Science

2
Wood P. The erythrocyte sedimentation rate in diseases of the heart. Q J Med 1936;29:1-20

3
Kassirer JP, Kopelman RI. A man with severe valvular heart disease. Hosp Pract 1985;20:56, 61-56, 63
Web of Science

4
Haber HL, Leavy JA, Kessler PD, Kukin ML, Gottlieb SS, Packer M. The erythrocyte sedimentation rate in congestive heart failure. N Engl J Med 1991;324:353-358
Full Text | Web of Science | Medline

Citing Articles (1)