ABCs                                      CANALITH REPOSITIONING                             DIX-HALLPIKE MANEUVER

BPV                                         CHICAGO                                                                LYMPHADENOPATHY

BRIGHT RED BLOOD        COLONOSCOPY                                                    VERTIGO
 

THE ABCs OF LYMPHADENOPATHY: The Mayo Clinic recently published a general review of lymphadenopathy in clinical practice. ⁽¹⁾ While the article itself is not entertaining reading, the authors do manage to reduce almost everything you need to know about lymphadenopathy to two mnemonics- CHICAGO and the ABCs (ABCDEFGHIJKLMNOPQRSTUVWXYZ), which is quite a feat.

In general, the causes of lymphadenopathy are summarized by CHICAGO:
 

C Cancers

H Hypersensitivity syndromes: serum sickness, drug reaction, silicone reaction, vaccination reaction, or graft vs. host disease.

I Infections: EBV, CMV, infectious hepatitis, postvaccinial lymphadenitis, adenovirus, herpes, HIV, cutaneous bacterial infections (staph, strept), cat-scratch disease, chancroid, melioidosis, TB, atypical TB, syphilis, chlamydia (LVG), toxoplasmosis, coccidioidomycosis, scrub typhus, and filariasis.

C Connective tissue diseases: RA, SLE, dermatomyositis, mixed connective tissue disease, and Sjogren syndrome

A Atypical lymphoproliferative disorders: Giant lymph node hyperplasia (Castleman disease), Wegener's granulomatosis, lymphomatoid granulomatosis, angioimmmunoblastic lymphadenopathy with dysproteinemia, and angiocentric immunoproliferative disorders.

G Granulomatous disorders: TB, histo, mycobacterial, crypto, silicosis, berylliosis, and cat-scratch disease.

O Other: inflammatory pseudotumor of lymph nodes, histiocytic necrotizing lymphadenitis (Kikuchi lymphadenitis), sinus histiocytosis with massive lymphadenopathy, vascular transformation of sinuses, progressive transformation of germinal centers.
 

The differential diagnosis of lymphadenopathy can be summarized by the alphabet:

A AIDS, actinomycosis, allergic bronchopulmonary aspergillosis, amyloidosis, asbestosis, autoimmune syndromes.

B Bite wound infection, BCG, blastomycosis, borreliosis, brucellosis, bubonic plague.

C Cancer, cellulitis, chronic leukemia, cat-scratch disease, chancroid, chlamydia (LGV), cold agglutinin syndrome, common variable immunodeficiency, CMV, crypto, & corynebacteria.

D Drugs: allopurinol, carbamazepine, Dilantin, gold, hydralazine, primidone, sulfonamides.

E EBV, eosinophilic granuloma, exanthem subitum, extramedullary hematopoiesis.

F Familial Mediterranean fever, Felty syndrome, filariasis

G Granulomatous diseases: (histo, atypical TB, sarcoid, TB, Gaucher disease, glanders.

H Hodgkin disease, histo, heavy-chain disease, Henoch-Schonlein purpura, hepatitis A, herpes, histiocytosis X, HIV, hypersensitivity syndromes, and hyperthyroidism.

I Infectious mono, idiopathic retroperitoneal fibrosis, inflammatory pseudotumor.

J Juvenile rheumatoid arthritis (Still disease)

K Kaposi sarcoma, Kawasaki disease, Kikuchi syndrome, Kimura disease.

L Leukemia, leishmaniasis, Lyme disease, lymphomatoid granulomatosis.

M Mycobacterial infections, mastocytosis, measles, melioidosis, mixed essential cryoglobulinemia, mixed connective tissue disease, mucocutaneous lymph node syndrome, multiple myeloma, mycosis fungoides, mesenteric lymphadenitis (Yersinia, Salmonella)

N Non-Hodgkin lymphomas, neurodermatitis, Niemann-Pick disease

O Occult malignancy

P Peetoom-Meltzer syndrome (arthralgia-purpura-weakness), postvaccination lymphadenitis, psittacosis, pulmonary alveolar proteinosis.

Q Q fever

R Rheumatologic disorders, relapsing fever, rheumatic fever, rubella.

S Sarcoid, strept infections, salmonella. schistosomiasis, Sezary syndrome, silicone, Sjogren syndrome , sporotrichosis, Still disease, storage diseases, SBE, Sutton syndrome (periadenitis mucosa necrotica recurrens), Sweet syndrome, syphilis, SLE, systemic mastocytosis.

T Toxoplasmosis, toxic oil syndrome, TB, tularemia, trypanosomiasis

U Ulceroglandular fever, unknown.

V vascular transformation of sinuses.

W Waldenstrom macroglobulinemia, Wegener granulomatosis, Whipple disease

X X-linked lymphoproliferative disease

Y Yaws, yersinia infections

Z Zahorsky syndrome (exanthem subitum).
 

COMMENT: We confront lymph node enlargement on a fairly regular basis, so this short, systematic review of the differential is a useful list to keep somewhere. Another practical tip is that benign reactive inguinal lymphadenopathy is more common in patients who walk shoeless outdoors (which makes perfect sense-I just never saw it explicitly stated before).
 

THE CANALITH REPOSITIONING PROCEDURE FOR BPV IN PRIMARY CARE: Benign positional vertigo (BPV) is the most common cause of vertigo with an estimated annual incidence of BPV is 160,000 new cases per year in the U.S. Free-moving particles in the endolymph of the posterior semicircular canals make them sensitive to position changes and cause symptoms of positional vertigo with head movement. Support for the canalithiasis theory comes from direct intraoperative observation of these free-floating particles. BPV is characterized by a history of positional vertigo and by positional nystagmus (generally torsional with a vertical component) elicited by a head-hanging maneuver, usually called the Dix-Hallpike maneuver.

One form of therapy was described by Epley in 1992-the canalith repositioning procedure (CRP); this involves a 5-position cycle in which the patients head is moved about in such a way as to displace theoretically any loose material in the posterior semicircular canal into the utricle of the vestibular labyrinth. To date, however, validation studies of this maneuver (and its somewhat less gentle equivalent, the Semont maneuver) have been confined to subspecialty clinics and may not represent the patients that we see in primary care. This study assessed the outcome of CRP therapy in 50 patients from an Urgent Care Center with a history of positional vertigo and with unilateral positional nystagmus on physical examination; no vestibular or other laboratory studies were performed. ⁽²⁾ Patients were randomized to either CRP or a sham maneuver. 
 

Step 1. Move patient from a sitting to a reclining position. Extend patient's head over the end of

the table at a 45 ^o angle.

Step 2. Turn the patient's head to the opposite side.

Step 3. Roll the patient over onto that side. The head is slightly angled while the patient is

looking down at the floor.

Step 4. Return the patient to a sitting position.

Step 5. Tilt the patient's chin down.
 

The time that each patient spent in each position was equal to the latency plus the duration of the positional nystagmus observed during the initial diagnostic Dix-Hallpike maneuver. The 5-position cycle was repeated until no positional nystagmus was elicited during any of the position changes or until a total of 5 cycles had been performed.

All patients were provided with a cervical collar and were asked to sleep sitting up for the first 2 nights after treatment. They were told to wear the collar only at night and only for the first 2 nights. Patients were also asked not to sleep on the symptomatic side for an additional 5 days and to avoid excessive turning of the head for 1 week. 

In the CRP group the patients were treated with a median of 3 cycles of the maneuver. Patients were not premedicated before the CRP. Three (13%) of the CRP group had persistent positional nystagmus throughout 5 cycles of treatment and were considered an immediate treatment failure.

Outcomes were assessed in 10 days. Resolution of symptoms was reported in 50% of the CRP patients and 19% of the sham treatment group. The Dix-Hallpike maneuver was negative for positional nystagmus in 67% of patients in the CRP group and in 38% in the sham group at 10 days.

COMMENT: This is another common problem whose management many of us are hazy about. This article provides very specific guidance. To reiterate the important points:

1. History and physical examination (Dix-Hallpike maneuver) is all that is required for diagnosis. No lab or other vestibular testing is necessary. Note that their definition of BPV is based on unilateral positional (torsional with a vertical component) nystagmus. Patients were excluded if they had a positive Dix-Hallpike maneuver for both ears. The authors comment that empirical use of CRP for patients with positional vertigo who can lateralize their symptoms but who lack objective positional nystagmus may be reasonable but cannot be supported by this study.

2. To test for positional nystagmus affecting the right ear have the patient lie down, extend his/her head 45 o over the edge of the table and turn it to the right.

3. The duration of each of the 5 steps described above should be equal to the latency plus duration of the positional nystagmus observed during the initial Dix-Hallpike maneuver
 

DO YOU NEED COLONOSCOPY FOR BRIGHT RED RECTAL BLEEDING? Another common problem is the young healthy person who presents with an episode of mild rectal bleeding. Do you need to visualize the colon? To answer this question these Canadian researchers report their findings in 186 patients who did undergo colonoscopy for their bright red rectal bleeding. ⁽³⁾ A source of bleeding was identified in 143 patients. Among 61 patients below the age of 55, 3 cancers were identified, and 1 was found more than 60 cm from the anus (i.e., beyond the reach of a flexible sigmoidoscope) in a patient with massive acute bleeding. Among the 82 older patients, 18 cancers were found, 4 of which were located more than 60 cm from the anus. The authors conclude that simple fiberoptic sigmoidoscopy may be an appropriate initial investigation for persons under the age of 55 with limited bright red rectal bleeding. An editorialist on this study expresses a preference for performing full colonoscopy in patients who are 40 or older. 

For another report of experience evaluating bright red blood per rectum consider this report in Am J Gastroenterol. The authors evaluated whether the 'bright red' color ensured that a lesion was in the sigmoid colon. They evaluated 163 men and 149 women with a complaint of blood in the stools and had them match the reported color of the blood they observed with 4 color cards (bright red, dark red, maroon, and black). All patients underwent colonoscopy (of course!). They found that the likelihood of a distal source of bleeding decreased as the color of the blood seen darkened, but even in the group with bright red bleeding 6 of 24 cancers were in the proximal colon, mostly near the hepatic flexure. Even in the group of 45 patients younger than 40 with bright red bleeding, 3 of 5 cancers were in the proximal colon. The authors believe that initial colonoscopy is associated with slightly lower costs and lower rates of perforation than initial sigmoidoscopy followed by colonoscopy, if negative. COMMENT: The endoscopy decision is, of course, a patient's choice. These articles are useful for informing younger patients what the relative risks of "something bad" are (very low but not zero). I rarely order even sigmoidoscopy in patients under 40 who have only 1 or 2 episodes of light bleeding and normal hematocrits. Three strikes, however, and they're out and off for endoscopy of one kind or another (their choice). Time magazine recently ran the sad story of Katie Kouric's husband who died of colon cancer in his 40's; she'd like colonoscopy for everyone-symptoms or not; this would hardly be the best use of our health care dollars (although very popular with the gastroenterologists). No matter what you do, you're not going to prevent or 'catch' 100% of colon cancer (or any other kind of cancer); we just have to resign ourselves to what's 'reasonable,' if we can ever figure out what that is. Remember, if you recommend a lot of colonoscopies, you'll find a lot of polyps, and the patient will never get off of the polyp detection treadmill. Be sure to tell them that! 

ANGINA, STABLE                                 EXERCISE                                        PTCA

CARDIAC ARREST                               HEPARIN                                         REHABILITATION, CARDIAC

CORONARY SYNDROMES, ACUTE  LMWH                                              TELEMETRY

ECG READING                                       OBESITY                                          UNSTABLE ANGINA
 

DOES TELEMETRY SAVE LIVES? CCUs were born in the 1960s and has spread the use of telemetry way beyond its original intentions. Remote telemetry for non-cardiac problems (e.g. GI bleeding, syncope, stroke, etc.) has become common. These Canadian researchers asked whether all this trouble and expense improves any outcomes. ⁽⁴⁾ They reviewed the survival of cardiac arrest patients admitted to a cardiac telemetry unit over a 5-year period. A total of 8,932 patients were admitted to the unit, and 20 (0.2%) suffered cardiac arrests, of whom 3 survived to discharge; 2 of these 3 were on monitors at the times of their arrests. Thus the monitor-signaled arrest survival rate is about 1 in 5000 (0.02%). Of the 17 patients who did not survive, 9 had monitor-signaled arrests. Survival did not differ significantly for patients with monitor-signaled arrests. COMMENT: If the yield is so low even for the patients at highest risk (i.e. those who have already had one cardiac arrest), the yield in any lower risk patients must be about as close to zero as you can get. In case of doubt, don't order telemetry!
 

CAN RESIDENTS (OR ANYONE ELSE) READ EKGs? The authors of this study evaluated the EKG reading skills of 61 residents from 6 family practice residency programs. Ten EKGs with 18 findings obtained from a community hospital were given to the residents for interpretation. The residents failed to identify the correct EKG reading 33% of the time. The lowest scores were found on some common findings: rate-uncontrolled atrial fibrillation (37% incorrect), rate-controlled atrial fibrillation (42%), old MI (48%), LVH (33%), acute MI (21%), and right axis deviation (RAD, 59%). ⁽⁵⁾ COMMENT: This is either shocking or reassuring. It is indeed surprising that there is a high missed diagnosis rate for such common and fairly obvious abnormalities like atrial fibrillation and old MI; this probably indicates that these readings were done in a hurry, probably in situations where the suspicion of cardiac disease was low. (And if the suspicion is low, why are you ordering the EKG in the first place, and why would you waste your time reading it thoroughly?) The reassuring news is two-fold. First, if you're missing one-third to one-half of your EKG diagnoses, you don't need to feel bad, you're average! Second, we don't have any evidence that these missed readings mattered or adversely affected outcomes, so who cares? The primary family practice responsibility is to correlate an EKG with acute symptoms, an issue about which this study has no information.
 

TREATMENT OF UNSTABLE ANGINA: THE CASE FOR AN INVASIVE STRATEGY: The FRISC II trial compared an early invasive with an early non-invasive strategy in unstable CAD. ⁽⁶⁾ Within 10 days of initial presentation 71% of the invasive group and 9% of the non-invasive group underwent revascular- ization; these percentages increased to 78% and 43% by the end of the first year. By the end of the first year 2.2% of the invasive group and 3.9% of the noninvasive group died (P=0.016) and 8.6% vs 11.6% had MI (P=0.015). There were also reductions in readmission (37% vs 57%) and revasculari-zation after the initial admission (7.5% vs 31%) in the invasive group. These authors conclude that after 1 year in 100 patients, an invasive strategy saves 1.7 lives, prevents 2 non-fatal MIs, and 20 read- missions. This strategy also provides earlier and better symptoms relief at the cost of 15 more patients under- going CABG and 21 more patients undergoing PTCA. They believe that an invasive approach should be the preferred strategy in patients with unstable CAD and signs of ischemia on EKG or raised levels of biochemical markers of myocardial damage. COMMENT: These are fairly persuasive data. It is difficult to argue that an invasive strategy is not appropriate for this particularly high-risk group. But what about other, lower risk groups? See below.
 

TREATMENT OF STABLE ANGINA: THE CASE AGAINST AN INVASIVE STRATEGY: In a recent issue of BMJ Bucher and colleagues report a meta-analysis of randomized controlled trials comparing PTCA and medical treatment for non-acute coronary artery disease. ⁽⁷⁾ Of the drug treatments, there is evidence that only beta-blockers reduce both angina and cardiac events. Aspirin, coumadin, and statins have no antianginal properties but do reduce cardiovascular events. CABG provides a better prognosis than medical treatment only in high risk patients with main stem or 3-vessel disease. Since the CABG trials were performed in the 1970s when statins were not available and aspirin and beta-blockers less frequently used, the difference are probably much less today. Comparisons of PTCA and CABG suggest that mortality and infarction rates are comparable. 

Considering the enormous number of these procedures that are carried out each year, the author finds it surprising that only around 2000 patients have been studied in 6 trials which meet modern standards. The major finding of this meta-analysis is that PTCA may reduce angina more than medical treatment but at the cost of more CABG procedures. PTCA does substantially improve the quality of life as perceived by patients.

It is a disadvantage of medical treatment that it does not reverse coronary stenosis and often does not completely relieve symptoms. ?Although nitrates and calcium antagonists reduce vasoconstriction, the effects of medical treatment on structural vascular changes are limited, even with statins. Only CABG and PTCA restore flow. It is also likely that the true antianginal effect of PTCA is underestimated in trials since patients with severe symptoms are not randomized; the randomization rates of most trials are < 10%. One trial (AVERT) in which medical treatment with atorvastatin (Lipitor) compared favorably with PTCA enrolled only patients with mild symptoms. Furthermore, the studies analyzed did not include the use of stenting as is currently practiced, which should lead to an even more favorable outcome for PTCA. 

On the downside, the complication rates of PTCA ranged from 0.01% to 2.8% for MI and from 1.5% to 2.8% for immediate CABG. There was only 1 death. 

But even with the improved acute results in the short term, PTCA is unlikely to improve prognosis. Patients with coronary disease have numerous lesions, but only a few cause angina. The probability of plaque rupture and coronary occlusion is determined by the biological features of a lesion and not by the degree of stenosis. Treatment of a single lesion is unlikely to affect prognosis unless it is located in a proximal dominant vessel (main stem or LAD). 

The author of this editorial concludes, "We will not harm patients by using drug treatment first and using percutaneous transluminal coronary angioplasty only if symptoms persist." 

COMMENT: Unfortunately, this is an option that your cardiologist will rarely offer.
 

LMWH FOR ACUTE CORONARY SYNDROMES WITHOUT ST ELEVATION: This is a meta-analysis comparing the use of unfractionated heparin and low-molecular weight heparin (LMWH) in patients with acute coronary syndromes without ST-segment elevation in 12 trials involving a total of 17,157 patients. ⁽⁸⁾ The authors conclude that in aspirin-treated patients with acute coronary syndromes without ST elevation, short-term unfractionated heparin or LMWH halves the risk of MI or death. There is no convincing difference in efficacy or safety between LMWH and unfractionated heparin. Long-term LMWH has not been proven to confer benefit additional to aspirin. There is no evidence to support its use after the first 7 days. COMMENT: To me this says go ahead and use LMWH for 1 week since it is so much more convenient to use.
 

RUMORS THAT EXERCISE IS GOOD FOR CORONARY ARTERY DISEASE: These authors state that it is time to reevaluate risk stratification guidelines for medically supervised exercise training in patients with coronary artery disease. ⁽⁹⁾ Compared with other currently available therapies for CAD, the 25% risk reduction observed with exercise is comparable with the 20% achieved with aspirin, the 20% achieved with beta-blockers, and the 15% observed with ACE-inhibitors. Specifically, their quibble is about current cardiology practice guidelines which, in conjunction with increasing insurance restrictions, are tending to reduce the availability of supervised exercise programs for post-MI patients. The Am Assn of Cardiovascular and Pulmonary Rehabilitation and the Am Coll of Cardiology suggest that supervision and ECG monitoring can be limited for intermediate- and low-risk patients and the ACP and AHA guidelines suggest that low-risk patients need neither. Less than 20% of eligible patients use supervised exercise-cardiac rehabilitation services because of the inadequate number of programs available and because of geographic barriers imposed by travel distance to the program. Recent guidelines would deny services under the ACP and AHA guidelines to 55% of MI patients and 74% according to the ACC guidelines. One argument they make for the benefit of increased supervision is the observation that the mortality rate for supervised cardiac rehabilitation (1 in 784,000 patient-exercise hours) is less than half of what has been observed for those in the general public who jog (1 in 396,000). In addition, exercise as a therapy addresses a disease manifestation for which there is no other t treatment, namely sudden cardiac death. A 43% reduction in out-of-hospital sudden cardiac death was observed in patients randomly assigned to exercise in both a single trial and a meta-analysis. While the mechanism responsible for this effect of exercise provides a unique contribution to the treatment of coronary artery disease not currently available via other therapies. Finally, recent studies suggest that cardiac rehabilitation services are cost-effective by reducing recurrent hospitalization and health care expenditures with 1 study reporting a net cost savings of $70 per patients. Another study demonstrates that despite a greater financial expenditure, a comprehensive cardiac rehabilitation program results in an expenditure of $9200 per quality-adjusted life-year saved (an amount comparable to that of hypertension treatment ($16,000) and CABG ($7900). Two independent meta-analyses of randomize controlled exercise trials performed predominantly in post-MI patients suggest that a minimum of 12 weeks of exercise training reduces mortality by 20-25%, an effect that is not evident in programs of lesser duration. This survival benefit has been demonstrated to be maintained for up to 10 years, and possibly for 19 years! COMMENT: Exercise is the most powerful and underused therapy in modern medicine. Why would anyone want to restrict its availability, and most particularly so, for the highest of high-risk patient set of post-MI patients? I believe one of the most important benefits of the supervised exercise programs is that at a critical time it begins the life-style change required to make exercise a regular, daily part of life, and this is the real goal.
 

TREATMENT OF OBESITY-EXERCISE OR WEIGHT LOSS? Given the difficulty of getting patients to lose weight, this is an extremely important question. This study attempted to determine the effects of equivalent diet- or exercise-induced weight loss and exercise without weight loss on subcutan- eous fat, visceral fat, skeletal muscle mass, and insulin sensitivity by means of a randomized, controlled trial in obese men. ⁽¹⁰⁾ Participants were randomly assigned to one of four study groups (diet-induced weight loss, exercise-induced weight loss, exercise without weight loss, and control) and were followed for 3 months. Body weight decreased by 7.5 kg (8%) in both weight loss groups and did not change in the exercise without weight loss and control groups. Cardiovascular fitness in the exercise groups im- proved by 16% (P < 0.01). Total fat decreased in both weight loss group (P < 0.0091), but the aver- age reduction was 1.3 kg greater in the exercise-induced wight loss group. Similar reductions in abdominal subcutaneous, visceral, and visceral fat-to-subcutaneous fat ratios were observed in the weight loss groups ( P < 0.001). Abdominal and visceral fat also decreased in the exercise without weight loss group (P=0.001). Average improvement in glucose disposal was similar in the diet-induced weight loss group and the exercise-induced weight loss group. The authors conclude that weight loss induced by increased daily physical activity without caloric restriction substantially reduces obesity (particularly abdominal obesity) and insulin resistance in men. Exercise without weight loss reduces abdominal fat and prevents further weight gain. COMMENT: This is the best evidence I've yet seen supporting exercise, rather than the nearly impossible weight loss, as a primary strategy for treating obesity. The authors recommend walking briskly for approximately 60 minutes a day (without caloric restriction). Medically, a fit fat person is far more desirable than a thinner, deconditioned one.

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