Symptoms

 

 

Signs

 

Note: The diagnosis of chronic fatigue syndrome remains hotly debated because of the lack of a gold standard. Persons with chronic fatigue syndrome meeting specific criteria (such as those from the CDC) report a greater frequency of childhood trauma and psychopathology and demonstrate higher levels of emotional instability and self-reported stress than persons who do not have chronic fatigue. Neuropsychological and neuroendocrine studies reveal abnormalities in most patients but no consistent pattern. For example, one study found widespread areas of neuroinflammation in the brain of chronic fatigue syndrome patients that were correlated with the severity of neuropsychological symptoms. A longitudinal MRI study showed no abnormal patterns in rate and extent of brain atrophy, ventricle volume, white matter lesions, cerebral blood flow, or aqueductal cerebrospinal fluid flow. Sleep disorders have been reported in 40–80% of patients with chronic fatigue syndrome, but polysomnographic studies have not shown a greater incidence of primary sleep disorders in those with chronic fatigue syndrome than in controls, suggesting that the sleep disorders are comorbid rather than causative. Veterans of the Gulf War show a tenfold greater incidence of chronic fatigue syndrome compared with nondeployed military personnel. Older patients with chronic fatigue syndrome demonstrate a greater disease impact than younger patients, perhaps secondary to their greater autonomic dysfunction, decreased baroreflex sensitivity, and prolonged left ventricular ejection time. A study found that atopy (especially numerous atopic syndromes) is associated with chronic fatigue syndrome.

 

 

  • It is currently unknown if the disease is a single pathologic condition, has different subsets, or is a nonspecific condition shared among varying pathologies.
  • Adult women are affected more than men, but in children equal ratios of males and females are affected.
  • CFS/SEID usually follows a relapsing and remitting course and there is no current cure.
  • Illness onset can be rapid or gradual and may have a preceding event or precipitating factor which may include:
    • viral, bacterial, or parasitic infection (acute or chronic)
    • environmental toxin exposure
    • recent vaccination
    • significant trauma (physical or emotional)
  • Compared to teenagers and adults, children are more likely to have:
    • neurologic symptoms (headache, cognitive impairment, or sleep disturbances)
    • autonomic dysfunction, commonly orthostatic intolerance
  • Factors which can exacerbate CFS include physical or mental overexertion, new infections, sleep deprivation, immunizations, comorbid medical conditions, and life stressors (such as financial difficulty, illness stigma, child care, marital or relationship problems).

The diagnosis of chronic fatigue syndrome remains hotly debated because of the lack of a gold standard. Persons with chronic fatigue syndrome meeting specific criteria (such as those from the CDC) report a greater frequency of childhood trauma and psychopathology and demonstrate higher levels of emotional instability and self-reported stress than persons who do not have chronic fatigue. Neuropsychological and neuroendocrine studies reveal abnormalities in most patients but no consistent pattern. For example, one study found widespread areas of neuroinflammation in the brain of chronic fatigue syndrome patients that were correlated with the severity of neuropsychological symptoms. A longitudinal MRI study showed no abnormal patterns in rate and extent of brain atrophy, ventricle volume, white matter lesions, cerebral blood flow, or aqueductal cerebrospinal fluid flow. Sleep disorders have been reported in 40–80% of patients with chronic fatigue syndrome, but polysomnographic studies have not shown a greater incidence of primary sleep disorders in those with chronic fatigue syndrome than in controls, suggesting that the sleep disorders are comorbid rather than causative. Veterans of the Gulf War show a tenfold greater incidence of chronic fatigue syndrome compared with nondeployed military personnel. Older patients with chronic fatigue syndrome demonstrate a greater disease impact than younger patients, perhaps secondary to their greater autonomic dysfunction, decreased baroreflex sensitivity, and prolonged left ventricular ejection time. A study found that atopy (especially numerous atopic syndromes) is associated with chronic fatigue syndrome.

 

 

 

 

A working case definition of chronic fatigue syndrome is not a homogeneous abnormality, there is no single pathogenic mechanism and no physical finding or laboratory test can be used to confirm the diagnosis.

Chronic fatigue syndrome is a condition characterized by chronic disabling fatigue, postexertional (physical, emotional, or cognitive) malaise, and symptoms including neurologic and/or cognitive impairment, orthostatic intolerance, nonrefreshing sleep, musculoskeletal pain, and altered immune or autonomic responses.

A working case definition of chronic fatigue syndrome indicates that it is not a homogeneous abnormality, there is no single pathogenic mechanism, and no physical finding or laboratory test can be used to confirm the diagnosis.1

 

 


A variety of agents and modalities have been tried for the treatment of chronic fatigue syndrome.

 Acyclovir, intravenous immunoglobulin, nystatinclonidine (in adolescent chronic fatigue syndrome), peripheral IL-1 inhibition with anakinra, and low-dose hydrocortisone do not improve symptoms. Some patients with postural hypotension report response to increases in dietary sodium as well as fludrocortisone, 0.1 mg orally daily. The immune modulator rintatolimod improved some measures of exercise performance compared with placebo in two trials (low strength of evidence). There is very limited evidence that dietary modification is beneficial.

There is a greater prevalence of past and current psychiatric diagnoses in patients with this syndrome. Affective disorders are especially common. Patients with chronic fatigue syndrome have benefited from a comprehensive multidisciplinary intervention, including optimal medical management, treating any ongoing affective or anxiety disorder pharmacologically, and implementing a comprehensive cognitive-behavioral treatment program. At present, cognitive-behavioral therapy and graded exercise are the treatments of choice for patients with chronic fatigue syndrome. Cognitive-behavioral therapy, a form of nonpharmacologic treatment emphasizing self-help and aiming to change perceptions and behaviors that may perpetuate symptoms and disability, is helpful. Although few patients are cured, the treatment effect is substantial. Response to cognitive-behavioral therapy is not predictable on the basis of severity or duration of chronic fatigue syndrome. Patients with high neuroticism or low acceptance show more improvement in mental quality of life with cognitive-behavioral therapy.

Graded exercise has also been shown to improve functional work capacity and physical function. A 2011 randomized trial (PACE trial) confirmed the independent benefits of cognitive-behavioral therapy and graded exercise; it found no benefit of adaptive pacing therapy. Physiologic studies find an altered immune response to exercise in patients with chronic fatigue syndrome.

In addition, the clinician’s sympathetic listening and explanatory responses can help overcome the patient’s frustrations and debilitation by this still mysterious illness. All patients should be encouraged to engage in normal activities to the extent possible and should be reassured that full recovery is eventually possible in most cases. Chronic fatigue syndrome is not associated with increased all-cause mortality, but one study showed a substantial increased risk of completed suicide.

 

Test Clinical Significance
complete blood count, Anemia
erythrocyte sedimentation rate, Presence of any inflammation
chemistries (blood urea nitrogen [BUN]), serum electrolytes, glucose, creatinine, calcium, liver and thyroid function tests), antinuclear antibody, urinalysis, and tuberculin skin test, and screening questionnaires for psychiatric disorders.  
   
   

 

Other tests to be performed as clinically indicated are serum cortisol, rheumatoid factor, immunoglobulin levels, Lyme serology in endemic areas, and HIV antibody. More extensive testing is usually unhelpful, including antibody to Epstein-Barr virus. There may be an abnormally high rate of postural hypotension. MRI scans may show brain abnormalities on T2-weighted images—chiefly small, punctate, subcortical white matter hyperintensities, predominantly in the frontal lobes, although a 2010 study found no such abnormalities. Brain MRI is not routinely recommended.

 

Figure 2–1.

Classification of chronic fatigue patients. ALT, alanine aminotransferase; BUN, blood urea nitrogen; Ca2+, calcium; CBC, complete blood count; ESR, erythrocyte sedimentation rate; PO4 3–, phosphate; TSH, thyroid-stimulating hormone; UA, urinalysis.

 

 

 Evaluate for infection

neoplasm

thyroid duiseae (HYpo or Hypoer???)

 

 

Psychiatric or neorologic disease

blood count, erythrocyte sedimentation rate, chemistries (blood urea nitrogen [BUN]), serum electrolytes, glucose, creatinine, calcium, liver and thyroid function tests), antinuclear antibody, urinalysis, and tuberculin skin test, and screening questionnaires for psychiatric disorders. Other tests to be performed as clinically indicated are serum cortisol, rheumatoid factor, immunoglobulin levels, Lyme serology in endemic areas, and HIV antibody. More extensive testing is usually unhelpful, including antibody to Epstein-Barr virus. There may be an abnormally high rate of postural hypotension. MRI scans may show brain abnormalities on T2-weighted images—chiefly small, punctate, subcortical white matter hyperintensities, predominantly in the frontal lobes, although a 2010 study found no such abnormalities, and brain MRI is not routinely recommended.

A variety of agents and modalities have been tried for the treatment of chronic fatigue syndrome. Acyclovir, intravenous immunoglobulin, nystatin, clonidine (in adolescent chronic fatigue syndrome), and low-dose hydrocortisone do not improve symptoms. Some patients with postural hypotension report response to increases in dietary sodium as well as fludrocortisone, 0.1 mg orally daily.

There is a greater prevalence of past and current psychiatric diagnoses in patients with this syndrome. Affective disorders are especially common. Patients with chronic fatigue syndrome have benefited from a comprehensive multidisciplinary intervention, including optimal medical management, treating any ongoing affective or anxiety disorder pharmacologically, and implementing a comprehensive cognitive-behavioral treatment program. At present, cognitive-behavioral therapy and graded exercise are the treatments of choice for patients with chronic fatigue syndrome. Cognitive-behavioral therapy, a form of nonpharmacologic treatment emphasizing self-help and aiming to change perceptions and behaviors that may perpetuate symptoms and disability, is helpful. Although few patients are cured, the treatment effect is substantial. Response to cognitive-behavioral therapy is not predictable on the basis of severity or duration of chronic fatigue syndrome. Patients with high neuroticism or low acceptance show more improvement in mental quality of life with cognitive-behavioral therapy.

Graded exercise has also been shown to improve functional work capacity and physical function. A 2011 randomized trial (PACE trial) confirmed the independent benefits of cognitive-behavioral therapy and graded exercise; it found no benefit of adaptive pacing therapy. Physiologic studies find an altered immune response to exercise in patients with chronic fatigue syndrome.

In addition, the clinician’s sympathetic listening and explanatory responses can help overcome the patient’s frustrations and debilitation by this still mysterious illness. All patients should be encouraged to engage in normal activities to the extent possible and should be reassured that full recovery is eventually possible in most cases.

When to Refer

  • Infections not responsive to standard treatment.

  • Difficult to control hyperthyroidism or hypothyroidism.

  • Severe psychological disease.

  • Malignancy.

When to Admit

  • Failure to thrive.

  • Fatigue severe enough to impair activities of daily living.

Kerr  CW  et al. Effects of methylphenidate on fatigue and depression: a randomized, double-blind, placebo-controlled trial. J Pain Symptom Manage. 2012 Jan;43(1):68–77. 
[PubMed: 22208450] 
CrossRef
Larun  L  et al. Exercise therapy for chronic fatigue syndrome. Cochrane Database Syst Rev. 2015 Feb 10;2:CD003200. 
[PubMed: 25674924] 
Nakatomi  Y  et al. Neuroinflammation in patients with chronic fatigue syndrome/myalgic encephalomyelitis: an 11C-(R)-PK11195 PET study. J Nucl Med. 2014 Jun;55(6):945–50. 
[PubMed: 24665088] 
CrossRef
Stocchi  F  et al; FORTE Study Group. Prevalence of fatigue in Parkinson disease and its clinical correlates. Neurology. 2014 Jul 15;83(3):215–20. 
[PubMed: 24928125] 
CrossRef
Sulheim  D  et al. Disease mechanisms and clonidine treatment in adolescent chronic fatigue syndrome: a combined cross-sectional and randomized clinical trial. JAMA Pediatr. 2014 Apr;168(4):351–60. 
[PubMed: 24493300] 
CrossRef
Vogelaar  L  et al. Fatigue management in patients with IBD: a randomised controlled trial. Gut. 2014 Jun;63(6):911–8. 
[PubMed: 23884638] 
CrossRef
Wang  XS  et al. Prevalence and characteristics of moderate to severe fatigue: a multicenter study in cancer patients and survivors. Cancer. 2014 Feb 1;120(3):425–32. 
[PubMed: 24436136] 
CrossRef
Wiborg  JF  et al. Towards an evidence-based treatment model for cognitive behavioral interventions focusing on chronic fatigue syndrome. J Psychosom Res. 2012 May;72(5):399–404. 
[PubMed: 22469284] 
CrossRef
Wright  J  et al. Fatigue. Med Clin North Am. 2014 May;98(3):597–608. 
[PubMed: 24758963] 
CrossRef

A variety of agents and modalities have been tried for the treatment of chronic fatigue syndrome. Acyclovir, intravenous immunoglobulin, nystatin, clonidine (in adolescent chronic fatigue syndrome), and low-dose hydrocortisone do not improve symptoms. Some patients with postural hypotension report response to increases in dietary sodium as well as fludrocortisone, 0.1 mg orally daily. The immune modulator rintatolimod improved some measures of exercise performance compared with placebo in two trials (low strength of evidence).

There is a greater prevalence of past and current psychiatric diagnoses in patients with this syndrome. Affective disorders are especially common. Patients with chronic fatigue syndrome have benefited from a comprehensive multidisciplinary intervention, including optimal medical management, treating any ongoing affective or anxiety disorder pharmacologically, and implementing a comprehensive cognitive-behavioral treatment program. At present, cognitive-behavioral therapy and graded exercise are the treatments of choice for patients with chronic fatigue syndrome. Cognitive-behavioral therapy, a form of nonpharmacologic treatment emphasizing self-help and aiming to change perceptions and behaviors that may perpetuate symptoms and disability, is helpful. Although few patients are cured, the treatment effect is substantial. Response to cognitive-behavioral therapy is not predictable on the basis of severity or duration of chronic fatigue syndrome. Patients with high neuroticism or low acceptance show more improvement in mental quality of life with cognitive-behavioral therapy.

Graded exercise has also been shown to improve functional work capacity and physical function. A 2011 randomized trial (PACE trial) confirmed the independent benefits of cognitive-behavioral therapy and graded exercise; it found no benefit of adaptive pacing therapy. Physiologic studies find an altered immune response to exercise in patients with chronic fatigue syndrome.

In addition, the clinician’s sympathetic listening and explanatory responses can help overcome the patient’s frustrations and debilitation by this still mysterious illness. All patients should be encouraged to engage in normal activities to the extent possible and should be reassured that full recovery is eventually possible in most cases. Chronic fatigue syndrome is not associated with increased all-cause mortality, but one study showed a substantial increased risk of completed suicide.

 

 

Most people with pyelonephritis do not have complications if appropriately treated with bacteria-fighting medications called antibiotics.

In rare cases, pyelonephritis may cause permanent kidney scars, which can lead to chronic kidney disease, high blood pressure, and kidney failure. These problems usually occur in people with a structural problem in the urinary tract, kidney disease from other causes, or repeated episodes of pyelonephritis.

Infection in the kidneys may spread to the bloodstream—a serious condition called sepsis—though this is also uncommon.

 

 

Content 3

Content 13

Content 11

 

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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