INFECTIONS PRESENTING AS STROKE SYNDROMES
Saturday, August 16, 2008
Essentials of Diagnosis
• History: known or recently acquired valvular heart disease plus prior infectious processes (eg, staphylococcal sepsis), genitourinary or dental procedures, or intravenous drug use; presence of indwelling intravenous catheters; immunocompromised host predisposed to fungal infections.
• Antecedent signs of infection: fever and chills, heart murmurs.
• Signs of systemic embolism: ocular (Roth spots and other hemorrhages); skin or mucosal (petechiae, Osler's nodes); renal (hematuria); splenic (abdominal pain).
• Laboratory studies: imaging of brain, CSF analysis, cardiac echo studies, blood cultures.
Infections as a cause of stroke are uncommon but must be considered in young individuals, in patients with valvular or congenital cardiac disease, or in immunocompromised hosts. Stroke in young individuals is less often due to atherosclerosis or hypertension and more often related to thrombosis or endocarditis complicating congenital or acquired valvular heart disease as a result of intravenous drug use, right-to-left cardiac shunts, or combinations of the above.
Bacterial Endocarditis
Bacterial endocarditis must always be considered in at-risk individuals, particularly if there is intravenous drug use or if the patients have recently undergone oral or genitourinary surgery or have a prosthetic cardiac valve (see Chapter 11). Embolic infarctions of brain in these individuals, although dominantly in the middle cerebral distribution, can occur in any vascular distribution and are often multiple, frequently in the distal territories of the cerebral vessels, and most frequently encountered when the causative organism is S aureus. The formation of mycotic aneurysms at the site of embolism is not uncommon, and may occur late in the course of the condition. Rupture of the mycotic aneurysm with subarachnoid hemorrhage is uncommon, but, when it occurs, is frequently fatal. The management of these problems, if caused by infective endocarditis, requires prolonged intravenous optimal antibiotic therapy and often repair or replacement of damaged cardiac valves.
Clues to the presence of subacute bacterial endocarditis include known previous congenital or rheumatic heart disease or rheumatic fever and the development of anorexia, backaches, myalgia, or signs of emboli in the spleen, kidney, eyes, or skin. The foregoing signs may all be easily overlooked if attention is devoted exclusively to the neurological phenomena. Repeated blood cultures may be required to identify the causative organism; identification and determination of the organism's susceptibility to antibiotics is of critical importance in determining the nature and duration of treatment with intravenous antibiotics.
Fungal Infections
Immunocompromised hosts, particularly if neutropenic or diabetic, are susceptible to fungal diseases and, of these, Candida, Aspergillus, and Mucor species have a predilection for invading the walls of cerebral blood vessels, resulting in stroke syndromes. The source for Aspergillus infection of cerebral vessels is often in the respiratory tract (see Chapter 75). Candida infection with involvement of cerebral vessels is seen in association with prolonged use of intravenous lines and in intravenous drug users (see Chapter 73). Mucor infections are characteristically seen in diabetic patients with frequent episodes of acidosis (see Chapter 75). Branches of the internal carotid artery, cranial nerves III through VI, and orbital tissues are often involved.
Other Meningeal Infections
Stroke syndromes may be seen in a variety of meningeal infections as a result of the involvement in the inflammatory exudate of penetrating vessels at the base of the brain. Often such vascular involvement is seen relatively late in the course of a meningeal infection and is related perhaps to the duration and intensity of the inflammatory process. It is also seen in acute bacterial meningitides caused by pneumococci (see Chapter 47) or H influenzae (see Chapter 56), in subacute meningitides caused by tuberculosis or fungal infections, and in low-grade chronic meningeal infections such as those caused by syphilis (see Chapter 64). It is rarely observed in viral meningitides but can be seen in the aftermath of herpes zoster (see Chapter 33) when it affects the trigeminal nerves, presumably resulting from a zoster infection of adjacent cranial vessels.
• History: known or recently acquired valvular heart disease plus prior infectious processes (eg, staphylococcal sepsis), genitourinary or dental procedures, or intravenous drug use; presence of indwelling intravenous catheters; immunocompromised host predisposed to fungal infections.
• Antecedent signs of infection: fever and chills, heart murmurs.
• Signs of systemic embolism: ocular (Roth spots and other hemorrhages); skin or mucosal (petechiae, Osler's nodes); renal (hematuria); splenic (abdominal pain).
• Laboratory studies: imaging of brain, CSF analysis, cardiac echo studies, blood cultures.
Infections as a cause of stroke are uncommon but must be considered in young individuals, in patients with valvular or congenital cardiac disease, or in immunocompromised hosts. Stroke in young individuals is less often due to atherosclerosis or hypertension and more often related to thrombosis or endocarditis complicating congenital or acquired valvular heart disease as a result of intravenous drug use, right-to-left cardiac shunts, or combinations of the above.
Bacterial Endocarditis
Bacterial endocarditis must always be considered in at-risk individuals, particularly if there is intravenous drug use or if the patients have recently undergone oral or genitourinary surgery or have a prosthetic cardiac valve (see Chapter 11). Embolic infarctions of brain in these individuals, although dominantly in the middle cerebral distribution, can occur in any vascular distribution and are often multiple, frequently in the distal territories of the cerebral vessels, and most frequently encountered when the causative organism is S aureus. The formation of mycotic aneurysms at the site of embolism is not uncommon, and may occur late in the course of the condition. Rupture of the mycotic aneurysm with subarachnoid hemorrhage is uncommon, but, when it occurs, is frequently fatal. The management of these problems, if caused by infective endocarditis, requires prolonged intravenous optimal antibiotic therapy and often repair or replacement of damaged cardiac valves.
Clues to the presence of subacute bacterial endocarditis include known previous congenital or rheumatic heart disease or rheumatic fever and the development of anorexia, backaches, myalgia, or signs of emboli in the spleen, kidney, eyes, or skin. The foregoing signs may all be easily overlooked if attention is devoted exclusively to the neurological phenomena. Repeated blood cultures may be required to identify the causative organism; identification and determination of the organism's susceptibility to antibiotics is of critical importance in determining the nature and duration of treatment with intravenous antibiotics.
Fungal Infections
Immunocompromised hosts, particularly if neutropenic or diabetic, are susceptible to fungal diseases and, of these, Candida, Aspergillus, and Mucor species have a predilection for invading the walls of cerebral blood vessels, resulting in stroke syndromes. The source for Aspergillus infection of cerebral vessels is often in the respiratory tract (see Chapter 75). Candida infection with involvement of cerebral vessels is seen in association with prolonged use of intravenous lines and in intravenous drug users (see Chapter 73). Mucor infections are characteristically seen in diabetic patients with frequent episodes of acidosis (see Chapter 75). Branches of the internal carotid artery, cranial nerves III through VI, and orbital tissues are often involved.
Other Meningeal Infections
Stroke syndromes may be seen in a variety of meningeal infections as a result of the involvement in the inflammatory exudate of penetrating vessels at the base of the brain. Often such vascular involvement is seen relatively late in the course of a meningeal infection and is related perhaps to the duration and intensity of the inflammatory process. It is also seen in acute bacterial meningitides caused by pneumococci (see Chapter 47) or H influenzae (see Chapter 56), in subacute meningitides caused by tuberculosis or fungal infections, and in low-grade chronic meningeal infections such as those caused by syphilis (see Chapter 64). It is rarely observed in viral meningitides but can be seen in the aftermath of herpes zoster (see Chapter 33) when it affects the trigeminal nerves, presumably resulting from a zoster infection of adjacent cranial vessels.
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