"Heat cramps" (exercise associated muscle cramps)

Definition, clinical presentation, and risk factors — Although muscle cramps are common in athletes, their etiology and pathophysiology remain poorly understood. The term "heat cramps" is a misnomer, as heat has not been shown to directly trigger cramping. Nevertheless, nearly all cases of cramping in athletes involve exercise at a high intensity or to exhaustion. Muscle cramps occur more often when athletes perform strenuous exercise in the heat, but they can also occur in cooler environments (eg, ice hockey, swimming). Muscle cramps are also more common in athletes engaged in novel or rarely performed exercise regimens. The treatment of heat cramps is discussed separately. (See "Exertional heat illness in adolescents and adults: Management and prevention", section on '"Heat cramps"'.)

A number of factors are thought to contribute to the development of muscle cramps in athletes [14]. Dehydration, loss of sodium and/or potassium, extreme environmental conditions, and neurogenic fatigue are suspected to play a role [14,50].

As a result of the controversy surrounding the etiology of muscle cramps, sports medicine researchers often refer to cramping that occurs during or after exercise as "exercise associated muscle cramping" (EAMC) [51]. Clinical criteria for establishing the diagnosis of muscle cramps generally include intense muscle pain (not associated with acute muscle strain or other injury) and spasm, and persistent contractions of the muscles primarily involved in the prolonged exercise. No signs of more severe illness, such as exertional hyponatremia or exertional heat stroke, may be present.

Factors that are thought to predispose to EAMC include [14,51,52]:

●Sweat with high salt concentration (ie, "salty sweaters") [53,54]

●Heavy sweating

●Dehydration

●Insufficient sodium intake prior to and during intense activity

●Lack of heat acclimatization

●Baseline (preactivity) fatigue

●History of heat cramps

Differential diagnosis — It is important to note that muscle cramps are not necessarily related to exercise. The differential diagnosis is extensive and includes medications (eg, diuretics), myopathies, and endocrine disorders. Another possible cause is sickle cell trait, which is thought to have played a role in several cases of exertional sudden death and severe rhabdomyolysis [55]. In some of these cases, reports describe antecedent cramping following brief periods of intense exercise characterized by intense pain and distinguishable from EAMC-related symptoms by the lack of spasm, suggesting the possibility of acute muscle ischemia [17,18]. (See "Myopathies of systemic disease" and "Sickle cell trait", section on 'Rhabdomyolysis and sudden death during strenuous physical activity'.)

 

 

 

 

 

 

 

 

 

 

 

 

Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.

 

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A

A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?

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The correct answer is A. You answered A.

Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.

 

Mr. Jenson is a 40-year-old man with a congenital bicuspid aortic valve who you have been seeing for more than a decade. You obtain an echocardiogram every other year to follow the progression of his disease knowing that bicuspid valves often develop stenosis or regurgitation requiring replacement in middle age. Given his specific congenital abnormality, what other anatomic structure is important to follow on his biannual echocardiograms?

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The correct answer is A. You answered A.

The answer is A. (Chap. 282) Bicuspid aortic valve is among the most common of congenital heart cardiac abnormalities. Valvular function is often normal in early life and thus may escape detection. Due to abnormal flow dynamics through the bicuspid aortic valve, the valve leaflets can become rigid and fibrosed, leading to either stenosis or regurgitation. However, pathology in patients with bicuspid aortic valve is not limited to the valve alone. The ascending aorta is often dilated, misnamed “poststenotic” dilatation; this is due to histologic abnormalities of the aortic media and may result in aortic dissection. It is important to screen specifically for aortopathy because dissection is a common cause of sudden death in these patients.

 


 

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