Letters to the Editor

Importance of an Accurate Diagnosis for Achilles Rupture

TO THE EDITOR: The article in American Family Physician on conditions of the Achilles tendon¹ points out that the frequency of ruptures is increasing as more people exercise. The high rate of ruptures that go undiagnosed or misdiagnosed should alert physicians to this condition in patients who present with ankle and leg complaints suggestive of tendon injury. The desirability and importance of early, correct diagnosis and prompt treatment is clearly seen by information that delayed diagnosis and subsequent improper (in misdiagnosed cases) or delayed treatment (longer than one month) can result in less functional recovery in some patients.²

As stated in the article, most ruptures of the Achilles tendon occur during physical activities, especially those involving certain movements that place stress on the tendon and promote rupture. Three categories of indirect injury that may result in rupture are: (1) pushing off with a weightbearing forefoot while also extending the knee, as occurs at the beginning of a sprint, running, and some forms of jumping; (2) sudden and unexpected dorsiflexion of the ankle, which may occur when a person slips off a chair or a ladder, when stumbling into a hole, or suddenly falling forward; and (3) violent dorsiflexion of a plantar-flexed foot when one falls from a height.^3,4

Although future improvements in surgical and nonsurgical treatments will undoubtedly benefit patients with a ruptured Achilles tendon, the efficacy of treatment in maximizing the functional recovery of strength, power, endurance, and mobility of the ankle joint and calf muscles (gastrocnemius and soleus) will be limited if injury to the tendon goes unnoticed or is misdiagnosed. Careful history taking of events before the injury and a complete physical examination of the foot, ankle, and leg are generally adequate to diagnose rupture. Because the incidence of rupture is expected to increase, physicians need to become more adept at diagnosing Achilles tendon ruptures, so that patients may realize the maximum benefit from available treatment options.

JAMES BRADLEY SUMMERS, M.D.
P.O. Box 16343
Mobile, AL 36616

REFERENCES

1. Mazzone MF, McCue T. Common conditions of the Achilles tendon. Am Fam Physician 2002;65:1805-10.
2. Inglis AE, Scott WN, Sculco TP, Patterson AH. Ruptures of the tendo achillis. An objective assessment of surgical and non-surgical treatment. J Bone Joint Surg Am 1976;58:990-3.
3. Hattrup SJ, Johnson KA. A review of ruptures of the Achilles tendon. Foot Ankle 1985;6:34-8.
4. Leppilahti J, Orava S. Total Achilles tendon rupture. A review. Sports Med 1998;25:79-100.

Use of Feeding Tubes in Elderly Patients with Dementia

TO THE EDITOR: Dr. Li's article, "Feeding Tubes in Patients with Severe Dementia,"¹ was an excellent review of the literature on this topic. While approximately 30 percent of percutaneous endoscopic gastrostomy (PEG) tubes are placed in patients with dementia, the author elucidates that patients with dementia have poor outcomes after PEG tube placement. Feeding tubes may ease the care for some patients but, in my opinion, they also distance the patient from human contact and take away one of their last pleasurable activities. I am concerned about our increasing elderly population and the overuse of PEG tubes in populations where their use is unproven and potentially harmful.

PEG tubes were first used in 1980, with the conclusion that they would improve nutrition, promote healing, and prevent aspiration in all patients.² Even though certain subsets of patients fare poorly with feeding tubes, I have found that few medical professionals stratify patients into different risk groups. This observation was made most clear during a chart review that I conducted with regard to spiritual history taking in chronically ill elderly patients. I reviewed the charts of 42 patients over 65 years of age who underwent PEG placement and found that almost half of them did not have an indication for the PEG and/or did not have a procedure note for the PEG in the chart. Why is PEG placement treated differently than any other surgical intervention? Why are surgeons being reimbursed for a procedure for which they do not even list an approved indication?

If placing PEG tubes in patients with advanced dementia were shown to improve quality of life, then I would recommend them in all of my patients who are malnourished or who have dementia. However, a survey of relatives of patients with PEG tubes in nursing homes in both Canada and the United States found that: (1) family members often regret having placed a PEG in their relative; (2) 60 percent did not feel it improved quality of life; and (3) 61 percent would not want a PEG for themselves in a similar situation.³

Feeding tubes are a beneficial medical intervention in select populations. Education of families, doctors, and ancillary staff about the failure of PEG tubes in elderly patients with dementia is necessary to decrease the number of unnecessary and potentially harmful procedures. As with all medical care, objective evidence rather than assumptions should guide treatment decisions regarding PEG tubes.

BRIAN J. WELLS, M.D.
Medical University of South Carolina
9298 Medical Plaza Dr.
Charleston, SC 29406

REFERENCES

1. Li I. Feeding tubes in patients with severe dementia. Am Fam Physician 2002;65:1605-10.
2. Cappell MS, Waye JD, Farrar JT, Sleisenger MH. Fifty landmark discoveries in gastroenterology during the past 50 years. A brief history of modern gastroenterology at the millenium: Part I. Gastrointestinal procedures and upper gastrointestinal disorders. Gastroenterol Clin North Am 2000;29:223-63.
3. Mitchell SL, Berkowitz RE, Lawson FM, Lipsitz LA. A cross-national survey of tube-feeding decisions in cognitively impaired older persons. J Am Geriatr Soc 2000;48:391-7.

Chronic Fatigue Syndrome and Depression

TO THE EDITOR: I read with interest "Chronic Fatigue Syndrome: Evaluation and Treatment," in American Family Physician.¹ As with most reviews of chronic fatigue syndrome (CFS), Drs. Craig and Kakumanu go into great detail proposing the etiologic links with infectious, neuroendocrine, and immunologic causes. Regrettably, their article glosses over the possibility that the key etiologic factor in CFS could actually be depression. To state that "CFS...is often dismissed by physicians as ... a manifestation of clinical depression"¹ downplays the significance of depression as a disease entity. Since when is making a diagnosis of depression, which is a common illness of patients in family practice offices, a "dismissive" act?

Despite noting that two thirds of patients with CFS have signs of major depressive illness, the authors attempt to distance CFS from depression by noting that "patients with CFS also show symptoms that are not typical of clinical depression, such as sore throat, lymphadenopathy, and postexertional malaise."¹ While this may be true, it should also be noted that these symptoms, including lymphadenopathy, are often self-reported in patients with CFS, just as back pain, headache, and other somatic symptoms are often self-reported in patients with depression. In addition, the fact that "patients with CFS lack feelings of anhedonia, guilt, and decreased motivation," certainly does not mean that they are not depressed. Many patients who are clinically depressed do not exhibit these symptoms, either.

Unfortunately, it seems that many researchers of CFS are going out of their way to distance themselves from the possibility that CFS might be an atypical manifestation of clinical depression. Why is this, when clinical depression has been recognized as a biologic entity for years? Family physicians have been at the forefront of educating the public about this fact. Yet, for some reason, many researchers seem to think that linking the etiology of CFS to clinical depression somehow makes CFS less of a "disease."

As the authors note, "the diagnostic ambiguity surrounding CFS invariably leads to imprecise and inconsistent epidemiologic statistics." Despite millions of dollars of research, even the incidence of CFS is unknown. Could CFS be less of a "neuroendocrine-immunologic" process, and more of a somatized, atypical presentation of clinical depression? In my opinion, this question has never been adequately addressed.

Unfortunately, for many patients, the notion that CFS must be something more than "just" depression effectively demotes the diagnosis of clinical depression to a less-than-clinical entity. If CFS, in all of its manifestations, is found to be caused by depression, does that make it less of a true disease? Of course not.

There needs to be continued research into CFS. The dimensions and incidence of this illness must be better defined as we sift through the relative "zebras" of neuroendocrine, allergic, and immunologic potential sources.

At the same time, to continue to largely ignore the "elephant" of depression that is standing in our midst is both wasteful and ill-advised.

DONALD R. FREY, M.D.
601 North 300th St.
Omaha, NE 68131

REFERENCE

1. Craig T, Kakumanu S. Chronic fatigue syndrome: evaluation and treatment. Am Fam Physician 2002; 65:1083-90.

IN REPLY: I read Dr. Frey's letter with great interest. I agree that depression is a frequent and often overlooked disease. Patients with depression often present with somatic complaints such as fatigue. It was not the intent of our article¹ to discuss at length the role depression plays in chronic fatigue syndrome (CFS), but instead to develop and discuss CFS as a unique syndrome which, despite being heterogenous, does appear to exist. By definition, if depression is the cause of the patient's somatic complaints, the patient does not have CFS. It is only after other etiologies are eliminated and it is decided that the cause of the patient's symptoms is or appears to be idiopathic that the diagnosis of CFS can be made.

I also agree with Dr. Frey that depression is a frequent coexisting disease with CFS; however, it is often reactive, being secondary to patients' inability to maintain their previous lifestyle. In fact, the depression experienced in patients with CFS can often be differentiated by their desire to get better, whereas patients with primary depression often do not care to improve. Nonetheless, psychiatric care has proven to be a successful intervention in patients with CFS. Psychiatric care is properly indicated in most of our patients who were once functioning ideally and, for whatever reason, suddenly became incapacitated by an illness that left them dependent and poorly productive despite their earnest attempts to improve themselves.

TIMOTHY J. CRAIG, D.O.
Department of Medicine
Pennsylvania State University College of Medicine
Hershey Medical Center
500 University Ave.
Hershey, PA 17033

REFERENCE

1. Craig T, Kakumanu S. Chronic fatigue syndrome: evaluation and treatment. Am Fam Physician 2002; 65:1083-90.

Lead Poisoning Presents a Difficult Diagnosis

TO THE EDITOR: Occult lead poisoning is a difficult diagnosis to make in a primary care setting because the symptoms of plumbism are nonspecific. We would like to report a case in which unsuspected lead toxicity resulted in a delayed diagnosis and inconclusive hospital work-up.

A healthy 57-year-old man developed abdominal pain and lower back pain over the course of several days. He had no significant medical history, took no medications, and had no known allergies. He denied having any antecedent trauma and reported no other symptoms. His vital signs were normal and physical examination was unremarkable. Rapid office tests revealed a hemoglobin level of 9.7 g per dL (97 g per L) and blood on urine dipstick. The patient was admitted to the hospital for nephrolithiasis work-up and treatment. Despite an extensive three-day hospital evaluation, work-up was inconclusive.

At follow-up after discharge, the patient continued to have the same symptoms; he then revealed that he was a welder exposed to lead fumes. A whole blood lead level obtained at that time was greater than 100 mcg per dL (4.83 µmol per L), and he was re-admitted to the hospital for chelation therapy with dimercaprol (or BAL) and edetate calcium sodium (CaNa²EDTA). Chelation was continued for five days. The patient's symptoms resolved, and the worksite evaluation was completed.

Symptoms of lead poisoning are often nonspecific¹ and include nausea, vomiting, abdominal pain, headache, back pain, paresthesias, limb weakness, and malaise. In severe cases, patients may present with encephalopathy. Without a history of exposure, lead poisoning has been mistaken for acute viral
illness, sickle cell vasoocclusive crisis, gastroenteritis, acute appendicitis, nephrolithiasis, and Guillain-Barré syndrome.¹

Lead is primarily absorbed by the ingestion or inhalation of dust particles. Elevated lead levels greater than 10 mcg per dL (0.48 µmol per L) are associated with neurocognitive delays in children, and chronic lead intoxication in adults has resulted in hypertension, anemia, peripheral neuropathy, and nephropathy. Lead-induced nephropathy is one of the oldest described manifestations of plumbism, and it has been linked to adult-onset hypertension in several population surveys.^2,3 Some centers have treated renal insufficiency and hypertension with routine chelation of body lead stores, although the long-term efficacy of such therapy still requires further evaluation.⁴

Since lead toxicity is so nonspecific, it should be considered in patients when diagnosis is unclear. Occupational exposure is the most common source for lead poisoning among adults. High-risk occupations include welding, batter manufacturing, mining, firing range maintenance, ship repair, glass blowing, and pottery glazing.¹ The Occupational Safety and Health Administration requires removal from the worksite for a single surveillance level greater than 60 mcg per dL (2.90 µmol per L). Other common sources of lead poisoning in adults include lead-glazed dishes, food supplements contaminated with lead, herbal folk remedies, and moonshine whiskey.^5,6 Unexplained anemia, basophilic stippling on the peripheral smear, and elevated creatinine are laboratory clues suggesting plumbism; the most important diagnostic maneuver is obtaining a whole blood lead level when plumbism is suspected. All patients recognized to have plumbism warrant immediate environmental intervention.

TRICIA L. HETTMANSBERGER, B.S.
University of Illinois College of Medicine
950 Wolcott
Chicago, IL 60612

MARK B. MYCYK, M.D.
1900 West Polk Street
Suite 500, Toxikon Consortium/Cook County Hospital
Chicago, IL 60612

REFERENCES

1. Heneretig F. Lead. In: Goldfrank LR. Goldfrank's Toxicologic emergencies. 6th ed. Stamford, Conn: Appleton & Lange; 1998:1277-1309.
2. Loghman-Adham M. Renal effects of environmental and occupational lead exposure. Environ Health Perspect 1997;105:928-39.
3. Cheng Y, Schwartz J, Sparrow D, Aro A, Weiss ST, Hu H. Bone lead and blood lead levels in relation to baseline blood pressure and the prospective development of hypertension: the Normative Aging Study. Am J Epidemiol 2001;153:164-71.
4. Lin JL, Ho HH, Yu CC. Chelation therapy for patients with elevated body lead burden and progressive renal insufficiency. A randomized, controlled trial. Ann Intern Med 1999;130:7-13.
5. Anderson NR, Gama R, Kapadia S. Herbal remedy poisoning presenting with acute abdomen and raised urine porphyrins. Ann Clin Biochem 2001; 38(Pt 4):408-10.
6. Morgan BW, Todd KH, Moore B. Elevated blood lead levels in urban moonshine drinkers. Ann Emerg Med 2001:37:51-4.

Send letters to Jay Siwek, M.D., Editor, American Family Physician, 11400 Tomahawk Creek Pkwy., Leawood, KS 66211-2672; fax: 913-906-6080; e-mail: afplet@aafp.org. Please include your complete address, telephone number, and fax number. Letters should be submitted on disk, double-spaced, fewer than 500 words, and limited to one table or figure and six references. Please submit a word count. Letters submitted for publication in AFP must not be submitted to any other publication. Possible conflicts of interest must be disclosed at time of submission. Submission of a letter will be construed as granting the AAFP permission to publish the letter in any of its publications in any form. The editors may edit letters to meet style and space requirements.