Treating Aortic Aneurysms

Repture of an abdominal aortic aneurysm remains one of the most dangerous events in vascular surgery, the mortality being close to 100% if the condition is not treated. The diagnosis may, however, be difficult as many other life threatening conditions produce a similar clinical picture. Any delay in operating on these patients has a serious adverse effect on their outcome; many die before they reach the operating theatre, so the mortality in the community remains over 90%. The perioperative mortality has remained constant at 30-50% despite advances in anaesthetic and surgical techniques during the past two decades.

In contrast, mortality after elective repair of an aneurysm that has not ruptured is usually between 2% and 5%. Even operations on selected patients over the age of 80 have a mortality of only about 10%. The most important way of improving the poor prognosis of patients with ruptured abdominal aortic aneurysms is to diagnose the aneurysm before it ruptures. Careful assessment by surgeons and cardiologists can then be made before operation is contemplated.

The incidence of abdominal aortic aneurysm is increasing in the United Kingdom; it is more common among men than women, the ratio being about 5:1. Although the natural course is unknown, aneurysms expand at a rate of about 0.5 cm a year and this rate increases as the aneurysm enlarges. The risk of rupture increases proportionately with the diameter, but even aneurysms <4 cm have a slight risk of rupture. Less than half the patients with symptomatic aneurysms will survive a year, and asymptomatic aneurysms also carry a high risk. The average time between diagnosis and rupture is 16 months.

Ruptured abdominal aortic aneurysms are responsible for 1-1.5% of all deaths in men over the age of 65 in the Western World, with an incidence of 25-30/100 000 population.

Screening has recently been advocated to reduce the high incidence of ruptured aneurysms. The group at risk comprises men over 65, among whom there is a 2% prevalence of abdominal aneurysms .4 cm in diameter. Furthermore, a single ultrasound scan that shows an entirely normal aorta in a 60 year old man does not need to be repeated. Aneurysms <4 cm in diameter can usually be treated conservatively and followed up with six monthly ultrasound scans. Whether to operate on asymptomatic aneurysms <5 cm in diameter is controversial, but the risk of rupture was shown to be small in two recent population studies; the operation is indicated only if the aneurysms expand or start to cause symptoms.

A screening programme for men over 60 would probably be cost effective because:

* The prevalence of aortic aneurysm in this group is 20%

* Ultrasonography is a simple, cheap, and accurate test

* The mortality associated with elective surgery is between 2% and 5%–and 90% if the aneurysm ruptures

* The life expectancy after successful aortic replacement is similar to that of age matched peers, the five year survival being more than 60%.

Between 30% and 60% of abdominal aortic aneurysms are asymptomatic, and the commonest presenting symptom in the rest is low back pain caused by erosion of vertebral bodies. Erosion into the gastrointestinal tract (usually the third part of the duodenum) to form a primary aortoenteric fistula is rare, but carries a high mortality. Erosion into the vena cava is also rare and also carries a high mortality unless the diagnosis is made before operation. Distended superficial veins (which may be pulsatile), ankle oedema, cardiac failure, and raised central venous pressure in a patient with shock, together with a machinery murmur on abdominal auscultation, may alert the clinician to the diagnosis.

Pressure on peripheral nerves may cause pain in the groin or thigh and compression of adjacent veins may cause ankle oedema. The aneurysmal sac may fill with thrombus and clot, and debris may embolise distally to the legs, causing intermittent claudication or rest pain of sudden onset. Smaller emboli may occlude arterioles to the skin, causing small punctate areas of necrosis in the feet. Rarely occlusion of the mesenteric vessels may cause lef sided ischaemic colitis that presents with diarrhoea, which may be bloody. Organisms may multiply in the artheroma or thrombus within the lumen of the aneurysm and the patient may complain of non-specific symptoms such as weight loss, anorexia, and malaise.

Occasionally, dense retroperitoneal fibrosis associated with an inflammatory aneurysm may occlude the ureters, causing hydronephrosis. Inflammatory aneurysms also cause severe backache that is associated with generalised malaise and anorexia. A high erythrocyte sedimentation rate is suggestive of this and computed tomography can usually confirm the diagnosis.

A pulsatile, expansile, abdominal mass is palpable in 80-90% of patients with abdominal aortic aneurysms. In thin patients smaller swellings (4-5 cm in diameter) may easily be felt. The diagnosis may be difficult in obsese patients, however, and the size of the aneurysm is usually overestimated. An aneurysm that is tender on palpation may indicate impending rupture, and urgent referral to a vascular surgeon is mandatory.

The diagnosis is confirmed by ultrasound scanning, but inaccuracies of up to 8 mm must be expected. In addition, the neck of the aneurysm may also be incorrectly diagnosed as being above the renal arteries if an elongated tortuous aorta is twisted forwards.

Computed tomography of the abdomen provides more accurate antomical information, but is more expensive. Arteriography is essential in a patient though to have a thoracoabdominal aneurysm, abnormal renal function, or symptoms of distal occlusive disease; if the aneurysm is uncomplicated, however, it is probably unnecessary.

It is important that the patient is warned before the operation of the small but pertinent risks associated with repair of an abdominal aortic aneurysm. The mortality is 2-5%, and a rare complication is paraplegia. A more usual problem is retrograde ejaculation, but true impotence is uncommon. Sigmoid ischaemia resulting in bloody diarrhea or perforation may occur in 1-2% of patients; leg ischaemia may also arise from embolisation of the pultaceous debris in the aneurysmal sac.

The advances in anaesthetic and perioperative care during the past decade have made a great impact on results, but the operation has also been greatly simplified. In 60% of patients it is possible to insert a short Dacron tube rather than the more extensive aortobi-iliac or aortobifemoral grafts. Dissection of vessels can then be kept to a minimum and the graft laid inside the sac without disturbing surrounding structures.

Although prophylatic antibiotics are given at the time of operation, a small perentage of grafts still become infected. Patients may present with malaise, anorexia, weight loss, and fever. A gammacamera scan after injection of radiolabelled white cells may confirm the diagnosis, and computed tomography may show gas surrounding the grat. A secondary infective aortoenteric fistula may present with haematemesis and malaena and should be suspected in a patient who has had an aneurysm repaired and who presents with such symptoms. Usually the blood loss into the gastrointestinal tract is intermittent, giving time for the diagnosis to be confirmed. Treatment is by removal of the graft together with revascularisation of the legs with bilateral axillofemoral grafts.

Aortic aneurysms that include the origins of the visceral vessels used to be considered inoperable. Following recent encouraging reports from the United States, however, surgeons in some centres in the United Kingdom are repairing thoracoabdominal aneurysms, albeit with a higher mortality than after the repair of infrarenal aneurysms. In contrast to infrarenal aneurysms, thoracoabdominal aneurysms tend to be symptomatic. Most patients present with pain, although they may have other symptoms including dysphagia, dyspnoea, hoarse voice, and chronic cough. Careful preoperative assessment f cardiac, respiratory, and renal function is necessary and the risks of death, and visceral and spinal cord ischaemia, should be explaned to the patient. Given the poor prognosis associated with these aneurysms, however, with only a quarter of the patients suriving two years, the results of surgery seem to be justified by survivial rates of 60% at two years.

Many aortic aneurysms are asymptomatic, so some form of screening is necessary to diagnose them. The most cost effective method is the routine abdominal examination of patients in the general practitioner’s surgery, and two thirds of aneurysms >4 cm will be diagnosed by careful clinical examination. There are few absolute contraindications to operation. In particular, age is no bar.


Prevention of venous thrombosis with minidose warfarin after joint replacement

Without prophylaxis 5-10% of patients having elective hip replacement develop clinically important venous thrombosis and about 5% develop symptomatic embolism, which is fatal in up to 0.5%. (1) Effective preventive methods exist, but many orthopaedic surgeons do not use them systematically because they tend to be complex, cumbersome, dangerous, or not generally available. (1) Minidose warfarin (a fixed dose of 1 mg warfarin a day) is simple, seems to be safe, prevents leg vein thrombosis after elective gynaecological surgery, (2) and prevents subclavian vein thrombosis after central venous line insertion. (3) We report a pilot study of its use in elective major joint replacement.

Patients, methods, and results

Forty five patients having elective hip replacement (35 patients) or knee replacement (10) completed the study. Thirty four were excluded because of previous thromboembolism, allergy to contrast medium, aspirin treatment, a potential drug interaction, refusal of consent by patient or surgeon, mild von Willebrand’s disease, or insufficient notice of surgery. Venography failed in five patients.

Warfarin (1 mg/day) was given for a mean of 20 (SD 3) days (range 8 to 28 days) before surgery and continued until bilateral ascending venography seven to 10 days after operation. The trial protocol was approved by the relevant clinical investigation committees. Omitting an actively treated control group was justified ethically on the grounds that no prophylaxis was routinely used by orthopaedic surgeons at either hospital, whereas thrombosis detected by routine

Venous thrombosis at routine venography 7-10 days after total hip or knee replacement (95% confidence intervals calculated for observed proportions)

Historical controls
Present study Flinders Medical Centre (4)
(n=45) (n=115)
95% 95%
Site of Confidence Confidence
thrombosis No (%) interval No (%) interval
Total hip replacement (n=35)
Calf 9(26) 12.5 to 43% 58(50) 40 to 60%
Proximal 11(31) 17 to 49% 38(33) 25 to 43%
Total 14(40) 24 to 58% 70(61) 52 to 71%
Total knee replacement (n=10)
Calf 7(70) 35 to 93%
Proximal 3(30) 7 to 65%
Total 7(70) 35 to 93%
venography could then be treated to prevent extension and embolism.


Patients had a mean age of 70 (SD 9) years (range 52-94 years) and a mean weight of 72 (SD 15) kg (range 44-119 kg); 31 (89%) hip replacements and three of 10 knee replacements were done under general anaesthesia; 20 (57%) hips were replaced with cemented prostheses and 24 (69%) replacements were done with a lateral approach. The prothrombin ratio (international normalised ratio) was normal on the day of surgery (one patient with a ratio of 1.7 on the day before surgery remained in the trial after the ratio fell below 1.5 after vitamin K was given), increased slightly on day 3 but fell on day 7. Surgical and postoperative bleeding were not excessive. The rate of venous thrombosis was 40% after hip replacement and 70% after knee replacement (table).


Our trial was a relatively unambitious pilot study, methodologically handicapped by its lack of randomised controls. Nevertheless, our findings strongly suggest that minidose warfarin cannot be recommended prophylactically in patients having elective major joint replacement.

We chose a cohort study because routine venography after hip replacement discloses a stable rate of thrombosis of about 50% in untreated patients, (1) giving us confidence that a pilot study would quickly indicate if a randomised trial would be worth while. In the event, the rate after minidose warfarin was similar to that in previous controls having hip or knee replacement (table). (1,4,5) There was perhaps a trend towards a lower rate of venous thrombosis in the calf, but the rate in proximal veins remained unchanged. In addition, although 95% confidence intervals for the observed rates of thrombosis remained wide, their lower limits (table) suggest that any prophylactic effect of minidose warfarin that might be demonstrable with a much larger randomised study is unlikely to be impressive.

We thank the radiologists, anaesthetists, orthopaedic surgeons, and ward nursing staff at Flinders Medical Centre and Royal Adelaide Hospital for their help. The study was funded in part by the National Health and Medical Research Council of Australia and the Adelaide Bone and Joint Research Foundation.

Keeping up on arthritis meds

Any time you have a sore ankle, neck, or shoulder, you have a painful reminder of what the arthritis patient suffers all the time. Except that most arthritis is more than just joint pain. It’s also a complicated systemic disease. Its treatment includes a confusing array of medication: non-steroidal anti-inflammatory drugs–NSAIDs–analgesics, anti-rheumatics, steroids, and immunosuppressives.

To help your patients understand what these drugs do, you’ve got to keep up to date on the medications available now–changes in indications, recommended dosages, interactions with other drugs, and adverse reactions–and be aware of the investigational drugs you may be giving soon. This review will help you do just that.

Aspirin is still the drug of choice

Of the commonly used NSAIDs–acetylsalicylic acid, indomethacin, and phenylbutazone–ASA is still the preferred drug for the initial management of rheumatoid arthritis and osteoarthritis. It works as both an analgesic and an anti-inflammatory. The analgesic effect benefits patients with OA, a localized condition resulting from biochemical or biomechanical changes within the joint. Its anti-inflammatory action is especially important in treating RA, a systemic connective tissure disease marked by stiff, sore joints and swelling, redness, and tenderness in the surrounding tissues.

Because aspirin is such a common medication, it’s easy to treat its prescription in an offhand way: “Just take aspirin.” But for the arthritis sufferer, the benefits of the drug are highly dependent on correct dosage. While it’s possible to obtain pain-relief from 2,300 mg–about seven regular-strength tablets a day–4,000 to 6,000 mg are often necessary to achieve anti-inflammatory action. To maintain a therapeutic blood level, your patient must get into the habit of taking the drug at regular intervals, not just when pain intensifies. The first dose should be taken upon arising. However, it may take several hours before the drug’s therapeutic effect enables a patient to carry out his usual everyday activities.

To provide adequate blood levels through the night, time-release ASA preparations are sometimes useful. When the medication is taken at bedtime it not only helps the patient sleep through the night, but often decreases morning stiffness and pain as well.

In the dosages required to relieve arthritis, aspirin is a potent drug, not without danger. For this reason, blood samples may be drawn every few weeks during the early stages of management to monitor serum salicylate levels and determine the right dosage. The dosage shouldn’t raise salicylate levels above 30 mg/%, the toxicity threshold. Once the safest effective dosage is determined, serum salicylate levels are drawn periodically, as determined by the patient’s response.

Even a relatively low dose of aspirin can become toxic if your patient takes it along with other products that contain hidden salicylates. For example, Pepto-Bismol can provide the equivalent of eight 5-grain aspitin tablets when taken at the dosage recommended for travelers’ diarrhea (2 tablespoons every hour or half hour). That can be enough to cause toxicity when added to salicylates prescribed for arthritis.

Even relatively low salicylate levels can cause harmful GI side effects, including irritation and bleeding. You can’t always rely on positive results from an occult blood test to confirm the presence of bleeding. The best way to monitor bleeding is to have a baseline CBC done before therapy begins, with follow-up testing every four to six months.

To reduce the risk of bleeding, give the drug with food or milk. You might also suggest that the patient be switched to enteric-coated aspirin or non-acetylated salicylates, when necessary. The non-acetylated salicylates include salsalate (Disalcid), choline salicylate (Arthropan), magnesium salicylate (Magan), and choline magnesium salicylate (Trilisate). They produce less gastrointestinal irritation, and can be administered less often than aspirin.

When other NSAIDs are indicated

Physicians often prescribe indomethacin (Indocin) as an anti-inflammatory when patients don’t respond well to milder medications such as aspirin. Some patients experience prompt relief from the drug, others may not get any relief for several weeks.

You should caution patients on indomethacin to take the drug with milk or food to prevent GI irritation. Aldo be on guard for visual and renal complications. Patients on long-term regimens need regular eye exams. Elderly patients or others with kidney problems should be closely monitored.

Another potent NSAID, phenylbutazone, is generally given for only seven days at a time to manage acute inflammatory conditions. It’s rarely used for long-term treatment of rheumatoid arthritis because of its high incidence of GI, cardiovascular, hematologic, and cutaneou side effects. Sometimes, physicians will prescribed the drug for longer periods in treating anky-losing spondylitis, a rheumaic disease characterized by back pain and eventual fusion of the spine.

Some other non-steroidal anti-inflammatory drugs are listed on the following page. Several drugs may have to be tried to find the one that’s right for the patient.

For osteoarthritis and other conditions where patients need an analgesic but not an anti-inflammatory agent, aspirin remains the ideal medication. Approximately seven regular-strength tablets–2,300 mg–are given per day, just enough to ease pain. Patients who can’t tolerate aspirin can take acetaminophen.

When neither of these drugs controls the pain, the doctor often prescribes propoxyphene (Darvon). One precaution: Remind patients not to take Darvon with alcohol, tranquilizers, sedatives, or other CNS depressants.

Narcotics are not indicated for arthritis because it’s a chronic disease. Occasionally, patients in severe pain may receive codeine either alone or in combination with aspirin, acetaminophen, or propoxyphene. However, whenever possible, urge your patients to seek non-drug alternatives such as relaxation techniques, biofeedback, or transcutaneous electrical nerve stimulation (TENS).

Anti-rheumatics are the next step

When conservative drug treatment fails to provide adequate relief from the symptoms of rheumatoid arthritis, the physician will usually try anti-rheumatic compounds such as gold stars, D-penicillamine, and hydroxychloropine. They sometimes produce excellent results because they suppress the immune system, thus decreasing the inflammatory response.

Gold salts, for example, can produce dramatic, sustaines, remission. But if the treatment–called chrysotherapy–is discontinued, the inflammation often returns. Two types of injectable gold salts are available: aurothioglucose (Solganal), in an oil suspension, and gold sodium thiomalate (Myochrysine), in a water-soluble formula. Myochrysine may cause a transient effect called nitritoid crisis, that produces dizzines, blurred vision, flushing, joint pain, and occasionally anaphylactic shock. So observe patients for at least one hour after the first injection, and at least 15 minutes after subsequent doses.

A test dose of 10 mg IM is given the first week, followed by 25 mg the second week, then 50 mg the third week. After this, patients receive 25 to 50 mg per week until they improve, which sometimes takes three to six months. Because of this delayed response, other anti-inflammatory drugs are given at the same time.

After patient and doctor observe sustained improvement, the physician gradually reduces the number of injections to once a month. Some physicians wait until a cumulative dose of 1,000 mg is reached before switching to a maintenance program. Be sure to record the dose given after each injection to keep track of the total dosage.

Advise your patient to report rashes, mucosal ulcers, hematuria, and a metallic taste in his mouth because these adverse effects can indicate blood levels of the drug in the toxic range. If the drug is continued, serious complications, including renal damage and bone marrow suppression, can occur.

To monitor these potential dangers, the physician will probably request a urinalysis and CBC before each injection. Check these reports for blood or protein in the urine and for a decreased WBC or platelet count. If test results show abnormal findings, the physician will usually discontinue the drug or lower the dose.

Fortunately, problems usually show up early and disappear when the medication is stopped. With the exception of those experiencing hematologic and renal complications, patients who have reactions can often start taking the drug again later without suffering side effects.

A new oral preparation of gold salts called auranofin (Ridaura) was approved recently by the Food and Drug Administration. It’s expected to have fewer side effects than injectable gold salts.

Another anti-rheumatic agent that helps control the systemic effects of rheumatoid arthritis is D-penicillamine. At first, the doctor prescribes low oral doses–125 to 250 mg daily. Every two to four weeks, he increases the dosage until the therapeutic range is reached. This is usually 750 mg, given in equally divided doses of 250 mg each. Rarely is more than 1,000 mg daily prescribed. Because food, antacids, and ferrous sulfate interfere with the drug’s absorption, it’s best to give it an hour and a half before or after a meal, separated from other drugs by one hour.

Instruct patients to promptly report fever, rash, diarrhea, or ulcers because these may signal a toxic reaction. Watch for hematologic, renal, and cutaneous signs of toxicity by reviewing urinalysis and CBC reports every two to four weeks for proteinuria or a decrease in WBCs and platelets.

Hydroxychloroquine (Plaquenil), an anti-material drug, also has an anti-rheumatic effect. But it’s usually reserved for patients who don’t respond favorably to medications with less serious adverse side effects. Hydroxychlorine can cause rashes, retinopathy, peripheral neuropathy, and leukopenia. These effects usually stop when the drug is discontinued, but retinopathy can be permanent. So, recommend that patients taking the drug have eye examinations every three to six months during therapy to discover problems before they become serious.

Corticosteroids for acute flare-ups

Your patient with rheumatoid arthritis may need corticosteroids to suppress acute systemic inflammation. Prednisone and prednisolone are two drugs often used for this purpose, and they have fewer side effects than other medications.

When giving corticosteroids, the lowest effective dose is the most desirable one. The longer you give the drug, however, the higher the dose needed to get the same therapeutic effect. Higher doses are also needed during emotional trauma and surgery. These increased doses increase risk of toxicity.

Side effects of corticosteroids include GI ulcers, osteoporosis, hyperglycemia, fluid retention, skin lesions, infection, thrombi, and psychosis. Patients on long-term, high-dose therapy are also susceptible to aseptic necrosis–a condition that causes sclerosis and cystic changes in bone, especially the head of the femur.

sometimes, a corticosteroid is injected directly into a joint or its surrounding tissues. The drug can reduce pain and swelling in a severely inflamed joint while you wait for slower-acting drugs to take effect. The corticosteroid is often combined with a local anesthetic and given for RA or osteoarthritis. These injections shouldn’t be repeated in the same joint more than three or four times a year nor given when joint infection, fracture, or severe osteoporosis exists.

Clean the injection site well to avoid introducing bacteria into the joint. The patient will probably experience immediate pain relief, but some complain of increased pain caused by the medication. If this happens, advice the patient to apply ice for 15 minutes every hour for 24 to 48 hours.

Remind all patients who receive an intra-articular injection not to overuse the treated joint just because it feels so much better. Overuse can damage the joint.

Immunosuppressives are a last resort

when other attempts to control severe rheumatoid arthritis fail, drugs such as methotrexate, cyclophosphamide (Cytoxan), azathioprine (Imuran), or chlorambucil (Leukeran) can help. These drugs reduce the patient’s immune response to his disease. Dosages are lower for rheumatoid arthritis than for cancer treatment, so you may see less toxicity than you would in cancer patients. But even so, the side effects can be devastating, and these drugs are still considered experimental. Adverse reactions include malignancy, chromosome damage, infection, and bone marrow suppression.

One other experimental drug worth mentioning is dimethyl sulfoxide, DMSO. Although its effectiveness and safety are still being debated, you may find a number of patients using it as a topical agent because it’s available over the counter as a commercial solvent. Warn patients you suspect of using DMSO–they’ll have a garlic-like breath odor–that in many states the commercial formulas are too concentrated and may contain dangerous impurities.

Patients will use DMSO and other unproven treatmens because they’ve had no relief from traditional treatment. Indeed, all the drug therapy discussed above is aimed at relieving pain, reducing inflammation, and impeding systemic manifestations. There is no one drug that will cure arthritis.

As long as there is no cure, new drugs will be developed to treat the symptoms. And they’ll be heralded in the news media as the latest miracle cure, raising false hope for the millions of arthritis sufferers who live with chronic pain. It’s those patients who need the up-to-date, accurate information that we can provide.

Helping an elderly patient live with CHF

Helping an elderly patient live with CHF I was working the 3-to-11 shift in our hospital’s busy CCU when I first met Esther Saver. This 69-year-old woman had just been transported to our unit from the emergency room. She was pale and short of breath, with a puffy face and 2+ pitting edema of both ankles. The diagnosis: congestive heart failure.

We managed to stabilize Esther without much difficulty. But that was only the beginning of our task. The real challenge was to prevent another cardiac emergency.

Congestive heart failure kills countless people every year, and sends many others rushing to the hospital for treatment of one cardiac crisis after another. To help your CHF patients break this vicious cycle, you’ll need to coach them on individualized exercise and nutrition regimens. You’ll also need to address the ways in which aging affects the body’s response to the medications that are prescribed for CHF.

The history and physical exam

A thorough nursing history will allow you to establish realistic goals for your elderly CHF patient. In order to accurately assess the physical and psychosocial status of a patient like Mrs. Saver, you will need to learn the answers to questions such as these:

* Does she live alone or with her family?

* What is her daily dietary intake? What are her food preferences and mealtimes?

* How many hours does she sleep at night? Does she have difficulty falling asleep?

* How much and what kinds of physical activity does she usually engage in?

* What prescribed medications and over-the-counter drugs does she use? Does she take these drugs every day or only occasionally?

* Does she have any financial problems?

* Is there a family member or a close friend whose advice she trusts?

Also ask your patient about recent deaths among her friends or relatives and any physical disabilities she has that might interfere with her ability to care for herself. The deaths of friends and personal disabilities, both frequent causes of depression in the elderly, can bring on fatigue, loss of appetite, difficulty sleeping, and lack of interest in personal hygiene and appearance. Such symptoms, if mistakenly attributed to the patient’s hearth condition, can complicate nursing care.

It’s also important to distinguish physical findings related to CHF from those attributable to some other cause. For example, dependent edema–a common sign of CHF–can also stem from protein deficiency or decreased venous return. Shortness of breath on exertion–another sign of CHF–can result from iron deficiency or a sedentary lifestyle.

An individualized exercise program

To combat the harmful effects of immobility on Mrs. Saver’s cardiovascular system, we designed an exercise program for her. Such a program can also relieve anxiety and depression, help maintain ideal weight, and reduce the need for anti-hypertensives and sedatives.

To determine whether it was safe for Mrs. Saver to exercise alone, we observed how her pulse rate and blood pressure responded when she walked around her room. These vital signs should increase with exercise unless the patient is taking a beta blocker. Falling blood pressure or failure of the heart rate to increase with exercise usually indicates severe cardiac disease requiring strict medical supervision. If the vital signs of a patient who’s not taking beta blockers fail to increase, warn her to avoid unsupervised exercise, including walking.

Any exercise program must, of course, take into account the patient’s physical limitations. The patient with severe arthritis, for example, should be advised to stick to swimming and riding a stationary bicycle, which don’t put undue pressure on weight-bearing joints.

To avoid overexertion, tell your patient to space activities throughout the day with adequate rest periods in between. This is especially important in hot weather and during large family gatherings, which can be stressful times for the elderly patient with a failing heart.

Also instruct elderly patients to protect themselves against excessive heat and cold when they exercise. Older people can overheat quickly because their sweat glands don’t function efficiently and their peripheral blood vessels don’t dilate fully to dissipate body heat. They’re also vulnerable to hypothermia because their blood vessels don’t constrict efficiently in response to cold. Either condition puts an added strain on the heart.

We eased Mrs. Savier into her exercise program by startling her on simple warm-up activities, then gradually increasing the time she spent walking. We encouraged her to join the YWCA or a local spa after discharge. Some local schools also have special exercise programs for senior citizens.

The challenge of a balanced diet

Patients with congestive heart failure usually require a low-sodium diet to reduce water retention. This restriction adds one more obstacle to the already difficult task of maintaining adequate nutrition. Since the sense of taste decreases with advancing age, restricting salt intake only makes matters worse. To compensate for the absence of salt, encourage patients to season their food with lemon peel or an herb and spice mixture.

Financial problems force some elderly people to forgo fresh fruits, vegetables, and meat in favor of canned and processed foods–all high in sodium. Such was the case with Mrs. Saver. Since she couldn’t avoid canned foods altogether, we urged her to buy items marked low sodium or no salt added.

We also warned her not to use laxatives or antacids without first checking the sodium content. Some contain large amounts of sodium.

Changes in the elderly patient’s gut can interfere with absorption of essential nutrients. CHF compounds digestive problems by decreasing circulation to the stomach and small intestine. This causes food to move slowly through the GI tract and produces a feeling of fullness or distention. To compensate, encourage small, frequent meals of high-protein, high-calorie foods that supply adequate bulk.

In addition to their other benefits, exercise and good diet help build resistance to infection, a danger to which CHF patients are particularly susceptible. Warn your CHF patients to avoid anyone with an upper respiratory infection. To bolster their resistance, encourage them to get a flu shot.

Special precautions for giving drugs

Patients like Mrs. Saver often take medications such as digitalis and diuretics to treat their heart condition. Aging alters the way the body absorbs, uses, and excretes these drugs. For example, gastrointestinal changes–including decreased acid production, prolonged stomach-emptying, and decreased intestinal motility–can cause variations in the absorption rate. To prevent adverse effects and ensure that the patient is getting therapeutic doses, you’ll need to check blood levels and monitor how well CHF symptoms are being controlled.

The aging process exacerbates decreased renal blood flow caused by CHF. This means you’ll have to pay extra attention when your patient’s taking any drug excreted primarily by the kidneys. Again, therapeutic levels for such drugs should be determined by monitoring serum drug levels.

Hepatic blood flow also decreases in congestive heart failure. This can lead to abnormally high blood levels of drugs that are detoxified by the liver, such as propranolol (Inderal) and theophylline. Watch for side effects and signs of toxicity even at low doses of these drugs.

Another problem you may encounter in elderly patients with CHF is the tendency to medicate themselves with OTC drugs or with prescription drugs shared with friends. We told Mrs. Saver of the dangers of this practice, stressing in particular the risks of OTC expectorants. These drugs can worsen heart failure by increasing the heart’s workload. We also reminded Mrs. Saver that a dry, non-productive cought occurring at night and clearing during the day is a symptom of the fluid overload of CHF, not a cold.

Fortunately, Mrs. Saver followed our advice. She also stuck to her exercise regimen and diet after she was discharged. As a result, she’s now doing well at home.

While not all elderly CHF patients are able to live with their disease as successfully as Mrs. Saver, chances are that thorough assessment and patient teaching will at least help them to do better.

Be ready for Lyme disease in your own backyard

Summer is coming, and with it an increasing number of cases of this potentially devastating disease-which is spreading at an alarming rate. Fred Hammersmith, a Midwestern farmer, noted an expanding circular rash on his shoulder. His wife,alerted by reports in the local newspaper about a tick-borne disease, realized the rash might be the hallmark of Lyme disease. A three week course of oral tetracycline resolved Fred’s Lyme infection without complications.

Several years after being treated for Rocky Mountain spotted fever, Mary Leonard developed problems with her left knee. Steroids eased the inflammation and stiffness, but Mary couldn’t walk without crutches. A rheumatologist ordered blood tests. They showed she’d been exposed to the bacterium that causes Lyme-undoubtedly the real cause of the chills and fever she’d been treated for earlier. With IV penicillin her condition began to improve. Though she experienced several relapses, she now walks normally.

An active 9-year-old, Jonathan Lee began having trouble concentrating in school. He was tired all the time, and his left hip hurt. His doctor considered such diagnoses as emotional trauma and Paget’s disease. When Jonathan was finally hospitalized, an astute intern suggested drawing a Lyme titer to measure the concentration of antibodies to the bacterium in his blood. The test results were positive, and IV antibioties were begun immediately. Within a few weeks Jonathan was ready to resume a full schedule of schoolwork and play.

Variations on these scenarios are being played out with increasing frequency in many parts of the country. A disease that did not even have a name a few years ago has now made its appearance in nearly every state. Between 1983 and 1986 some 1,500 cases a year were reported to the Centers for Disease Control; in 1987, 2,000 cases were reported in Wisconsin alone.

The public’s reaction to an outbreak often borders on hysteria, where everything from flu to summer doldrums is suspected of being Lyme disease. It’s past time for nurses to know the facts about the disease and to help communicate them accurately.

What is Lyme disease?

In the mid-1970s, researchers investigating a cluster of arthritis cases in children living in the area around Old Lyme, Conn., named the puzzling disease Lyme arthritis. It soon became clear, however, that arthritis was only one manifestation of a syndrome that includes cardiac and neurological complications as well.

The carrier of the disease was identified as a tiny deer or bear tick called Ixodes dammini. As it feeds, the tick infects its host with the spirochete Borrelia burgdorferinamed for Willy Burgdorfer, the scientist who initially recognized the organism. The western blacklegged tick, I. pacificus, was later tied to the disease on the West Coast, and two or three other ticks have now been implicated as well.

This baffling disease has few certainties in its presentation. Most people bitten by an infected tick never get sick. Many of those who do contract the disease don’t develop the characteristic skin rash. And a person may present in the later stages of the disease without ever experiencing the early symptoms.

Like some other spirochetal illnesses, Lyme disease has been divided into stages. Asymptomatic periods may separate them, or they may overlap.

Stage I. Within a few weeks of the tick bite a rash may appear at the site. Called erythema migrans (EM), it varies greatly in appearance. The classic rash resembles a bull’s eye or target, but a great many don’t fit this pattern, and more variations are seen each year. The less typical rashes are easily confused with hives or cellulitis.

Even the classic rash varies greatly in size. It is usually painless, though it may feel hot, burn, or itch. The most common locations are the moist areas of the groin and armpit, or behind the knee. You may see secondary lesions, similar to the primary ones, on other parts of the body, and the lymph glands may be swollen. The rash may go away in a few days or last for a month or more. If Lyme disease is untreated at this stage, the lesions may reappear later.

Patients often experience malaise, fever and chills, nausea, headache, stiff neck, joint pain, or low back pain. Some of these symptoms come and go from hour to hour, and are so commonplace that patients with early-stage Lyme disease are often diagnosed as having the flu or a viral illness. Like the rash, flulike symptoms may recur.

Stage II. Complications in the second stage of the disease are more serious. Some 10% of patients develop heart block or other cardiac problems. Symptoms include weakness, lightheadedness, chest pain, and dyspnea upon exertion.

Another 10% will have neurological disturbances, most often Bell’s palsy-a sudden paralysis of one side of the face. The paralysis is temporary in 95% of treated cases.

An occasional patient develops aseptic meningitis, encephalitis, or polyradiculitis. Second-stage Lyme disease can also mimic GuillainBarre syndrome and benign intracranial hypertension. In these cases there tend to be spontaneous remissions and relapses.

As with syphilis, another spirochetal disease, Lyme disease may damage the eye through inflammation including conjunctivitis, iritis, and optic neuritis.

Stage III. Manifestations of third-stage Lyme disease may occur as early as four weeks after the bite or years later. Arthritis characterizes this stage. It usually involves the larger joints-the knee, ankle, hip, elbow, or wrist. About half the victims of Lyme disease experience arthritic episodes; some 10% develop chronic joint pain.

If Lyme remains untreated long enough, chronic neurologic problems may develop. The symptoms are not well-defined but include severe fatigue and muscle weakness, numbness or pain in the arms or legs, and short-term memory loss.

As with other spirochetal illnesses, Lyme disease has the potential to cross the placenta and harm the fetus. A pregnant woman who suspects she’s been bitten by a tick should call her obstetrician for advice.

Diagnosis and treatment

It’s easy to see why Lyme disease is so often mistaken for other illnesses. Unless a patient remembers being bitten by a tick or develops EM, it’s nearly impossible to diagnose early-stage Lyme disease. Blood tests are not helpful until antibodies form, some four to eight weeks after exposure. Even then, tests are not standardized and are sometimes inconclusive. False negatives and lab errors do occur.

On the other hand, a positive test does not necessarily mean that the patient has the disease; it simply indicates the presence of antibodies to the Lyme disease bacterium. Each institution has its own reference value for a titer range that indicates current infection.

Most patients with second- and third-stage Lyme disease will have clearly elevated Lyme titers. Aspirated fluid from an arthritic joint may contain fibrinous exudates, white blood cells, and immune complexes. Biopsy of the synovium may show lymphocytic infiltrates.

Antimicrobial protocol. Though it’s agreed that antibiotic therapy is the proper treatment, the precise regimen may vary from institution to institution. The following protocol is the one we use at the Marshfield Clinic:

If the patient presents during Stage I, a 21 -day course of oral antibiotics is prescribed. The treatment of choice for adults is 100 mg of doxycycline bid; alternatively, 500 mg of penicillin V potassium (Pen-Vee K) may be given qid orperhaps less effective-500 mg of erythromycin qid.

Children over the age of eight receive the same course as adults, with dosage adjusted to weight. A younger child is given a 21-day oral course of 50 mg/kg of Pen-Vee K daily, 125 mg/kg of amoxicillin tid, or 40 mg/kg of erythromycin qid.

During Stages 11 and 111, patients who are acutely ill receive a 14-day course of intravenous antibiotics. Adults are given 24 million units of IV penicillin or 2 grams of ceftriaxone (Rocephin) daily, Children receive 250,000 units of IV penicillin or 100 mg/kg of ceftriaxone daily.

In late-stage cases where chronic neurologic problems have developed, adults take 100 mg of doxycycline bid, 500 mg of tetracycline qid, or 500 mg of penicillin qid in a six-week oral course. Children receive weight-appropriate doses of the adultmedication orally for six weeks or a 14-day IV course.

Prognosis. If they are treated during Stage 1, most victims recover completely. If the disease progresses to the later stages, some tissue damage may be irreversible. It is not known whether the damage is done by the spirochete itself or the immune system’s response.

Even with adequate treatment, however, symptoms can recur, although later attacks tend to be less severe. Follow-up blood tests showing declining Lyme titers are considered an indication that the illness was successfully treated. Some patients, however, continue to show an elevated titer, and clinicians are unsure about the significance of those elevations. Although one bout of Lyme does not confer immunity, it is thought to make the patient more resistant to the disease.

Ounce of prevention is the best protection

The I. dammini tick, a member of the spider class, lives in grassy, sandy, and wooded areas. During its two-year life, it survives by sucking blood from warm-blooded animals. If the larval tick feeds on a spirochete-infected mammal-its favorite prey is the field mouse-it can pass on the infection during either of the next two stages.

It’s during the nymphal stage that the tick is most likely to choose a human restaurant, attaching itself to an unsuspecting person walking through tall underbrushor even across the lawn. Ticks don’t fly or jump onto a host. Instead, they wait on top of vegetation until a mammal brushes by, then attach themselves to skin, fur, or clothing. The adult tick generally feeds on larger mammals like deer.

To feed, the tick attaches its mouth to the host, a process that usually takes from six to 12 hours. If it can be removed during this time, it probably will not infect its victim. Once attached, it sucks its meal for from one to three dayssometimes for up to a week. Typically, the tick feeds painlessly and drops off unnoticed.

Pets can also bring home the disease: An unattached tick may brush off a dog or cat onto its master. Small wild animals and birds may deposit ticks in the backyard. The spirochete has also been found in horse flies, deer flies, fleas, and mosquitos, but we don’t know if these insects are capable of transmitting the disease.

It’s possible to get Lyme disease at any time of year, but the incidence-at least in the northern part of the country-is greatest from May through August, when people spend more time out of doors and wear fewer clothes, and the tick is in the nymphal stage.

Preventing tick bites. In a tickinfested area, your best protection is to wear sturdy shoes, long pants with cuffs tucked into socks, and long-sleeved shirts with cuffs-not the most comfortable attire in the middle of summer, to be sure. You’ll be able to spot ticks more easily if your clothing is lightcolored.

You can protect yourself further with tick-repelling sprays that contain permethrin (Permanone) or D.E.E.T. Be sure to apply the spray to clothing, not directly on the skin. Put flea and tick collars on pets.

Try to avoid walking where you will brush against low vegetation. Keep the lawn and shrubs around your home trimmed.

Inspecting for ticks. When you return home make it a habit to conduct “tick cheeks” on yourself, your children, and your pets. Remember that ticks like to feed in creases.

If you find a tick, grasp it firmly with fine tweezers as close to the skin as possible. Gently but firmIy-the tick’s mouth parts have barbs-pull it straight out. Don’t grab its bottom or crush it, or you may inject the spirochetes into the bite. Thoroughly wash the bite area and your hands with an antiseptic solution. Consult your physician if you’re unable to remove the tick completely.

Save the tick, wrapped in a moist piece of tissue paper, in a jar labeled with the date, the location on the body from which you removed the tick, and the place where you think you picked up the tick. If you develop a rash or flu-like symptoms, your physician may be able to have a lab cheek the tick for spirochetes to help confirm a diagnosis. Even if you have no immediate problems, remember the tick bite if you develop mysterious symptoms in the future.

The patient who gets Lyme disease today is luckier than his counterpart of a decade ago. We know what causes Lyme, we’re getting better at recognizing its manifestations and we can usually treat it effectively. In time, our testing methods will improve, and a vaccine may someday be developed.

Such advances are no cause for complacency, however. This year many more people than last year will contract Lyme disease, and many of them will be misdiagnosed or untreated. The facts you know about the disease will help your patients get proper treatment-and maybe even prevent a case or two.

All that is The Shoulder

Trauma to the shoulder is common, although the type of injury varies considerably in different age groups. Clavicular fractures are common in childhood and early adulthood, glenohumeral dislocation and acromioclavicular disruption are frequent between the ages of 15 and 40 years, and fracture of the humeral head is often seen in elderly people. This chapter describes the features of these types of injury and a system of radiological interpretation to ensure that many of the subtle signs associated with them are not missed.

Important anatomical considerations


The shoulder consists of three bones and three joints. The acromion, coracoid process, and clavicle are linked by the shoulder ligaments. The coracoclavicular ligament is important as it is the main ligamentous attachment of the upper limb to the trunk. The acromioclavicular ligament is of secondary importance, but it is where radiographic evidence of injury is initially sought.

The inferior cortex of the most lateral aspect of the clavicle usually lies in same plane as the inferior cortex of the acromion. The distance from the coracoid process to the undersurface of the clavicle is 11-13 mm, with a difference in sides greater than 5 mm indicating rupture. The humeral head has two tuberosities and two necks; the surgical neck is the constricted portion distal to the level of the tuberosities. The neurovascular bundle (axillary artery and vein and median, ulna, and radial nerves) lies anterior to the glenohumeral joint and can be injured in anterior dislocation of the shoulder joint or in displaced fractures of the surgical neck.

Children and development

The three epiphyseal centres of the humeral head, greater tuberosity, and lesser tuberosity fuse with one another in the sixth year and with the shaft of the humerus in the 20th year.

The apophysis at the acromion appears at the age of 15 and is united within five years. The ossification centre at the interior angle of the scapula is generally seen between the ages of 15 and 25 years.

Common injury arising from trauma


Injury to the acromioclavicular/coracoclavicular ligament complex is classified according to the degree of disruption. Grade 1 injury is stable as the coracoclavicular ligament remains intact. As the injuring force increases, the acromioclavicular ligament is completely torn, with the coracoclavicular ligament either remaining intact or partially disrupted (grade 2). Stress views of the joint may be required to diagnose grade 1 and 2 injuries. Complete disruption of both acromioclavicular and coracoclavicular ligaments is termed grade 3.

Sternoclavicular disruption is uncommon but important because of associated vascular damage. This joint is not adequately seen in standard radiographs of the shoulder and specific views are therefore required if this injury is suspected clinically. Injury is usually suspected if chest radiography shows superior displacement of the medial end of the clavicle.

Glenohumeral dislocation

The shoulder is the most frequently dislocated joint of the body. Dislocations are usually clinically evident but radiography is needed to determine the direction of dislocation and the presence of any associated fracture or loose body. Dislocations are classified according to the position of the humeral head with respect to the glenoid fossa.

Anterior dislocations usually occur during excessive external rotation with the arm in abduction. Occasionally the injury is due to a direct posterolateral blow. Recurrent anterior dislocation is common and is indirectly related to age (80% in people aged below 20 years and 10% in those over 40).

About 60% of patients with anterior dislocations will also have compression fractures of the upper aspect of the humeral head, resulting in a flattened segment referred to as a hatchet deformity (Hill-Sachs). The fracture is caused by forceful impaction of the superolateral aspect of the humerus against the anterior or inferior rim of the glenoid fossa. It is often only seen in an axial or postreduction radiograph and is best seen with internal rotation of the arm. Anterior dislocation can also be associated with fractures of the greater tuberosity of the humerus (15%) and with fractures of the anterior rim of the glenoid fossa.

Direct posterior dislocation of the shoulder is uncommon but is a major diagnostic problem. Up to half are not recognised in the initial anteroposterior film. The posterior dislocation is typically associated with an anteromedial fracture of the humeral head. Simultaneous bilateral posterior dislocations are infrequent, occurring most commonly in patients with epilepsy.


Fractures of the shoulder can occur at the proximal humerus or glenoid fossa and may be associated with dislocation (figs 6 and 8). Fractures can be classified as non-displaced, displaced, or impacted. Intra-articular fractures are often associated with joint effusions or lipohaemarthrosis.


Clavicular fractures are common and usually follow a fall on the shoulder or outstretched hand. About 80% of fractures occur at the mid-third of the clavicle and are transverse (fig 4). Typically there is overriding of the fracture with the distal fragment being displaced inferiorly by the weight of the upper limb. Fractures of the outer third of the clavicle are also usually transverse but non-displaced because of stabilisation from the acromioclavicular/coracoclavicular ligament complex. A raised proximal fragment suggests disruption of the coracoclavicular ligament.


Fractures of the body of the scapula usually result from a direct crush-type injury and, with neck fractures, are the commonest injury of this bone. Fracture of the coracoid process is rare.

Non-traumatic lesions

Acute or severe shoulder pain and the painful arc syndrome are often due to inflammation of a periarticular bursa or tendon. Calcification of periarticular soft tissue or of the rotator cuff muscles is often associated with this acute inflammation. Pathological fractures of the humerus through benign or malignant bone lesions may occur spontaneously or with minimal trauma.

Types of view

The anteroposterior radiograph is the routine view performed in all patients (fig 2). The axial projection can be modified and taken with only minimal abduction and is therefore possible in most patients, even those with severe shoulder pain.

Occasionally the radiographer is unable to position the patient for a formal axial view. In these cases a through the chest lateral view (lateral transthoracic) may be taken, although this view is most useful for assessing alignment of humeral fractures and not dislocation. The axial view provides the most information and should be taken in all patients with trauma to the shoulder (fig 11).

Stress views

When the acromioclavicular ligament is completely disrupted but the coracoclavicular ligament remains intact, separation of the bones may not occur unless the joint is stressed. If such an injury is suspected specialised stress views should be taken with the patients holding weights. The non-injured shoulder should be examined in a similar manner to act as a control.

As with other radiographs the ABCs approach to interpretation is recommended.

Check the adequacy and quality of the radiograph

To take an anteroposterior shoulder view the patient is rotated slightly so that the glenohumeral joint is seen face on. The upper third of the humerus, outer half of the clavicle, and lateral aspects of the ribs should be visible.

Check alignment of bones

Firstly, check the humeral head is lying in the glenoid fossa. Then check the alignment of the acromioclavicular joint for disruption. Trace the inferior cortex of the clavicle across to the inferior cortex of the acromion. Remember partial or complete rupture of the acromioclavicular ligament can exist without disruption of the coracoclavicular ligament and can be detected only in stress views.

Check bone margins and density

Systematically trace the margins of the individual bones included in the anteroposterior projection: clavicle, humerus, scapula, and the ribs. Start at the upper aspects of each bone and work clockwise round its margin. Once you have assessed the cortex, examine the internal structure of the bones for distortion of the trabecular pattern. Difficult areas due to overlying structures include:

Humeral head–Posterior dislocation is typically associated with an anteromedial fracture of the humeral head, which is identified as a curvilinear density superimposed on the humeral head, parallel to the articulating cortex (trough sign–fig 8).

The glenoid fossa, coracoid process, and body of the scapula because of overlying ribs. An avulsion fracture of the anteroinferior lip of the glenoid fossa is a common complication of dislocation of the shoulder.

Fractures of the inner third of the clavicle are uncommon and may be missed because of superimposition of the ribs.

Check cartilage and joints

The glenohumeral joint should be examined carefully as posterior dislocation of the shoulder joint may look almost normal on this view. When posterior dislocation is suspected subtle radiographic signs should be sought. Always take an axial view to exclude or confirm such a dislocation. The distance from the humeral head to the anterior margin of the glenoid fossa is usually equal from top to bottom. Asymmetry can be due to dislocation or fracture. Anterior dislocation of the humerus is the most common (fig 6). Intra-articular fractures commonly cause haemarthroses or effusions which displace the head of the humerus inferolaterally–so called pseudosubluxation (fig 9).

Acromioclavicular joint–Check the acromioclavicular joint and distance from the tip of the coracoid process to the clavicle. If there is minimal widening of the joint take stress views. When the acromioclavicular joint is completely torn (grade 2) there is usually widening of the joint as well as superior displacement of the clavicle. In grade 3 injury abnormal widening of the acromioclavicular joint and increased distance between the clavicle and coracoid process can be seen on the standard anteroposterior radiography (fig 5).

Check soft tissues

Disruption of the acromioclavicular joint is usually associated with swelling above the joint, which can be seen with the aid of a bright light. In patients who have not experienced trauma the soft tissues should be examined for calcification, although this may overlie the bones (fig 10). Look for lipohaemarthroses or effusions around the joint capsule (fig 9).

This is a notoriously difficult radiograph to interpret because of its unusual projection and overlying structures (fig 3). Nevertheless, by following an ordered system the anatomy and any abnormality can be detected.

Check the adequacy and quality of the radiograph

The coracoid process, glenoid fossa, acromion process, spine of the scapula, and less tuberosity of the humeral head should be identifiable.

Check alignment of bones

Identify the coracoid process anteriorly and the acromion process posteriorly. The glenoid fossa is projected between these structures. The humeral head should sit within the fossa (fig 3b).

Check bone margins and density

Trace the margins of the clavicle, humerus, and scapula (spine, acromion, glenoid fossa, and coracoid process) clockwise. Fractures of the coracoid process and infraspinous processes of the scapular body are clearly seen in the axial view.

Check cartilage and joints

Examine the acromioclavicular and glenohumeral joints for separation or dislocation.

Check soft tissues

Calcification of the rotator cuff can be seen more clearly in axial views.

Do I have heel spurs – And do I need surgery

Do I have heel spurs? And do I need surgery? “Probably not” may very well be the answer to both questions. “Heel spurs don’t usually cause pain,” says Charles E. Graham, MD, clinical associate professor of surgery (orthopedics) at the University of Texas Health Science Center at Dallas, and a specialist in foot and ankle surgery. A number of conditions can cause heel pain, including nerve entrapment, bursitis, arthritis, and Reiter’s syndrome; and stress fractures are a frequently overlooked possibility. “The muscle that attaches to the heel holds together better than the bone. When stressed, the muscle pulls the bone, resulting in a stress fracture.” Dr. Graham and his colleagues want to disabuse the public of the notion that heel pain means heel spurs. “It is very important that a patient get a second opinion before consenting to heel spur surgery,” says Dr. Graham.

A jogger and a victim of a stress fracture himself, Dr. Graham found that many patients whose heel pain had been attributed to bone spurs did not actually have any. Bone scans revealed that some of these individuals had hot spots–which suggested fractures–on the painful heel, but not on the unaffected side. Eventually, Dr. Graham devised a method for demonstrating the stress fracture on an X-ray, eliminating the need for a bone scan. When heel spurs were present, they were not related in any consistent way to pain. Dr. Graham’s studies, which he has been conducting since 1983, involved more than 400 patients.(*)

Most stress fractures are related to sports, particularly jogging, aerobics, and similar exercise. The majority of the other fractures can be traced to a weight gain of 9-14 kg (20-30 lb) over a 5-6 month period. Other causes include minor injuries sustained while climbing or standing on narrow-rung ladders or those incurred by using a foot to push a shovel into the ground.

Dr. Graham has formulated a treatment program that involves a moderate amount of exercise and a plantar fascial stretch: Put your hands on a wall and lean against them. Place the uninjured foot on the floor in front of you and the injured foot behind so that its heel does not touch the floor and then stretch or bounce gently. He also recommends walking 2 miles per day to strengthen the surrounding bones and muscles. “Swimming and cycling are also beneficial,” he adds. The pain will probably get worse until the muscle stretches out. Dr. Graham says that he continued jogging, though at a less rigorous pace, during his own recuperation.

In the follow-up to one of his studies, 50-60% of the joggers who returned questionnaires had healed within 3 months and all but eight respondents healed within the year. “Maybe those who did not heal didn’t adhere to their program,” he speculated.

Dr. Graham is emphatic about the need for thoroughly investigating the causes of heel pain and not automatically assuming that heel spurs are the culprit. He is willing to train interested physicians in his X-ray techniques.