Fever of unknown origin

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Cracked mercury dental amalgam as a possible cause of fever of unknown origin: a case report

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Hospital-acquired sinusitis is a common cause of fever of unknown origin in orotracheally intubated critically ill patients...

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Fever is the most common presenting sign of liver abscess. Some patients, particularly those with associated disease of the biliary tract, have symptoms and signs localized to the right upper quadrant, including pain, guarding, punch tenderness, and even rebound tenderness. Nonspecific symptoms, such as chills, anorexia, weight loss, nausea, and vomiting, may also develop. Only 50% of patients with liver abscesses, however, have hepatomegaly, right-upper-quadrant tenderness, or jaundice; thus, half of patients have no symptoms or signs to direct attention to the liver.

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Abducens Nerve The sixth cranial nerve innervates the lateral rectus muscle. A palsy produces horizontal diplopia, worse on gaze to the side of the lesion. A nuclear lesion has different consequences, because the abducens nucleus contains interneurons that project via the medial longitudinal fasciculus to the medial rectus subnucleus of the contralateral oculomotor complex. Therefore, an abducens nuclear lesion produces a complete lateral gaze palsy, from weakness of both the ipsilateral lateral rectus and the contralateral medial rectus.

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Oculomotor Nerve The third cranial nerve innervates the medial, inferior, and superior recti; inferior oblique; levator palpebrae superioris; and the iris sphincter. Total palsy of the oculomotor nerve causes ptosis, a dilated pupil, and leaves the eye "down and out" because of the unopposed action of the lateral rectus and superior oblique. This combination of findings is obvious. More challenging is the diagnosis of early or partial oculomotor nerve palsy.

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Myogenic Ptosis The causes of myogenic ptosis include myasthenia gravis (Chap. 381) and a number of rare myopathies that manifest with ptosis. The term chronic progressive external ophthalmoplegia refers to a spectrum of systemic diseases caused by mutations of mitochondrial DNA. As the name implies, the most prominent findings are symmetric, slowly progressive ptosis and limitation of eye movements. In general, diplopia is a late symptom because all eye movements are reduced equally. In the Kearns-Sayre variant, retinal pigmentary changes and abnormalities of cardiac conduction develop.

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Orbital Cellulitis This causes pain, lid erythema, proptosis, conjunctival chemosis, restricted motility, decreased acuity, afferent pupillary defect, fever, and leukocytosis. It often arises from the paranasal sinuses, especially by contiguous spread of infection from the ethmoid sinus through the lamina papyracea of the medial orbit. A history of recent upper respiratory tract infection, chronic sinusitis, thick mucous secretions, or dental disease is significant in any patient with suspected orbital cellulitis. Blood cultures should be obtained, but they are usually negative.

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Melanoma and Other Tumors Melanoma is the most common primary tumor of the eye (Fig. 29-18). It causes photopsia, an enlarging scotoma, and loss of vision. A small melanoma is often difficult to differentiate from a benign choroidal nevus. Serial examinations are required to document a malignant pattern of growth. Treatment of melanoma is controversial. Options include enucleation, local resection, and irradiation. Metastatic tumors to the eye outnumber primary tumors. Breast and lung carcinoma have a special propensity to spread to the choroid or iris.

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Central Serous Chorioretinopathy This primarily affects males between the ages of 20 and 50. Leakage of serous fluid from the choroid causes small, localized detachment of the retinal pigment epithelium and the neurosensory retina. These detachments produce acute or chronic symptoms of metamorphopsia and blurred vision when the macula is involved. They are difficult to visualize with a direct ophthalmoscope because the detached retina is transparent and only slightly elevated.

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Glaucoma results in "cupping" as the neural rim is destroyed and the central cup becomes enlarged and excavated. The cup-to-disc ratio is about 0.7/1.0 in this patient. In acute angle-closure glaucoma, the eye is red and painful due to abrupt, severe elevation of intraocular pressure. Such cases account for only a minority of glaucoma cases: most patients have open, anterior chamber angles. The cause of raised intraocular pressure in open angle glaucoma is unknown, but it is associated with gene mutations in the heritable forms.

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Stroke This occurs when interruption of blood supply from the posterior cerebral artery to the visual cortex is prolonged. The only finding on examination is a homonymous visual field defect that stops abruptly at the vertical meridian. Occipital lobe stroke is usually due to thrombotic occlusion of the vertebrobasilar system, embolus, or dissection. Lobar hemorrhage, tumor, abscess, and arteriovenous malformation are other common causes of hemianopic cortical visual loss. Factitious (Functional, Nonorganic) Visual Loss This is claimed by hysterics or malingerers.

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Vitreous Degeneration This occurs in all individuals with advancing age, leading to visual symptoms. Opacities develop in the vitreous, casting annoying shadows upon the retina. As the eye moves, these distracting "floaters" move synchronously, with a slight lag caused by inertia of the vitreous gel. Vitreous traction upon the retina causes mechanical stimulation, resulting in perception of flashing lights. This photopsia is brief and confined to one eye, in contrast to the bilateral, prolonged scintillations of cortical migraine.

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Papilledema This connotes bilateral optic disc swelling from raised intracranial pressure (Fig. 29-12). Headache is a frequent, but not invariable, accompaniment. All other forms of optic disc swelling, e.g., from optic neuritis or ischemic optic neuropathy, should be called "optic disc edema." This convention is arbitrary but serves to avoid confusion. Often it is difficult to differentiate papilledema from other forms of optic disc edema by fundus examination alone. Transient visual obscurations are a classic symptom of papilledema.

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Disorders of Gait The heterogeneity of gait disorders observed in clinical practice reflects the large network of neural systems involved in the task. There is the potential for abnormalities to develop, and walking is vulnerable to neurologic disease at every level. Gait disorders have been classified descriptively, based on the abnormal physiology and biomechanics. One problem with this approach is that many failing gaits look fundamentally similar. This overlap reflects common patterns of adaptation to threatened balance stability and declining performance.

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Source: From a study of 347 patients referred to the National Institutes of Health from 1961 to 1977 with a presumptive diagnosis of FUO of 6 months' duration (R Aduan et al. Prolonged fever of unknown origin. Clin Res 26:558A, 1978). More than 200 conditions may be considered in the differential diagnosis of classic FUO in adults; the most common of these are listed in Table 19-3. This list applies strictly to the United States. Geographic considerations are paramount.

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Infections, especially extrapulmonary tuberculosis, remain the leading diagnosable cause of FUO. Prolonged mononucleosis syndromes caused by Epstein-Barr virus, cytomegalovirus (CMV), or HIV are conditions whose consideration as a cause of FUO is sometimes confounded by delayed antibody responses. Intraabdominal abscesses (sometimes poorly localized) and renal, retroperitoneal, and paraspinal abscesses continue to be difficult to diagnose. Renal malacoplakia, with submucosal plaques or nodules involving the urinary tract, may cause FUO and is often fatal if untreated.

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Acknowledgments Sheldon M. Wolff, MD, now deceased, was an author of a previous version of this chapter. It is to his memory that the chapter is dedicated. The substantial contributions of Charles A. Dinarello, MD, to this chapter in previous editions are gratefully acknowledged. Further Readings Bleeker-Rovers CP et al: A prospective multicenter study on fever of unknown origin: The yield of a structured diagnostic protocol. Medicine 86:26, 2007 [PMID: 17220753] de Kleijn EM et al: Fever of unknown origin (FUO): I.

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Nosocomial FUO (See also Chap. 125) The primary considerations in diagnosing nosocomial FUO are the underlying susceptibility of the patient coupled with the potential complications of hospitalization. The original surgical or procedural field is the place to begin a directed physical and laboratory examination for abscesses, hematomas, or infected foreign bodies. More than 50% of patients with nosocomial FUO are infected. Intravascular lines, septic phlebitis, and prostheses are all suspect.

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In any FUO workup, the erythrocyte sedimentation rate (ESR) should be determined. Striking elevation of the ESR and anemia of chronic disease are frequently seen in association with giant-cell arteritis or polymyalgia rheumatica—common causes of FUO in patients 50 years of age. Still's disease is suggested by elevations of ESR, leukocytosis, and anemia and is often accompanied by arthralgias, polyserositis (pleuritis, pericarditis), lymphadenopathy, splenomegaly, and rash.

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Specialized Diagnostic Studies Classic FUO A stepwise flow chart depicting the diagnostic workup and therapeutic management of FUO is provided in Fig. 19-1. In this flow chart, reference is made to "potentially diagnostic clues," as outlined by de Kleijn and colleagues; these clues may be key findings in the history (e.g., travel), localizing signs, or key symptoms. Certain specific diagnostic maneuvers become critical in dealing with prolonged fevers.

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