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STUDENT DIGITAL NEWSLETTER ALAGAPPA INSTITUTIONS |
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This disorder is a disconnection syndrome in which afferents carrying processed visual information from the right hemisphere are affected diabetes medications brand names 10 mg forxiga with mastercard, with the left angular gyrus isolated; the parietal lobe per se may not be damaged diabetes symptoms in young children forxiga 10mg low price. Anomia diabetes insipidus drug induced cheap 10mg forxiga overnight delivery, or difficulty recalling the names of objects blood sugar numbers for diabetics purchase forxiga 10mg fast delivery, occurs with left angular gyrus or left temporal polar lesions diabetes type 1 impact on health care resources purchase forxiga 10 mg otc. However diabetes medications before surgery purchase 5mg forxiga overnight delivery, different forms of anomic aphasia are seen with lesions in various parts of the cerebral cortex and are frequent early signs in degenerative dementia. Apraxias in which subjects pantomime poorly or are unable to perform gestures on command occur with lesions of the left inferior parietal lobule, left pre-motor cortex, and corpus callosum. Lesions of the right parietal lobe are frequently characterized by hemispatial neglect. In this condition the subject does not attend to stimuli in the neglected sphere contralateral to the lesion. They may ignore the left half of the visual field, the left half of their bodies, auditory stimuli from the left hemispace, or anything in the left hemiuniverse. A milder form of neglect called extinction has been described; in extinction, subjects are capable of attending to contralateral stimuli but, when presented with stimuli simultaneously on both sides, respond only to the ipsilateral side. Neglect has been reported with damage to the right dorsolateral frontal lobe, cingulate gyrus, putamen, and thalamus, but most consistently with lesions of the right inferior parietal lobule. Neglect associated with frontal lobe damage may result in a decreased tendency to react with the contralateral limb. When acute, as when caused by a stroke, neglect may be severe but then tends to recover. Neglect may also occur transiently with left parietal lobe lesions but usually resolves. Subjects may deny their left hemiparesis, hemianesthesia, or hemianopia and as a result attempt to perform activities of which they are incapable. If they are aware of their deficit, they may exhibit anosodiaphoria, or relative lack of concern regarding their impairment. Many studies have implicated a role for the parietal lobes, especially in the right hemisphere, in visuospatial functions. Specific tasks on which subjects with right parietal lesions have been shown to be more impaired include localization of points in space, estimation of line orientation, tests of topographic orientation, some tests of depth perception, and tests of facial discrimination. A common sequela of non-dominant parietal damage is difficulty dressing, which may be due to a combined hemibody neglect and spatial disorientation. A convergence of information from electrophysiologic and ablation studies in animals is suggesting that visual information initially processed in the striate cortex (Brodmann area 17 in the occipital lobe) undergoes further processing in two separate pathways. A ventral pathway passing forward into the temporal lobes is concerned primarily with identifying visual stimuli, the so-called what pathway. The dorsal pathway that involves occipitoparietal connections plays a role in determining the location of visual stimuli, the so-called where pathway. These animal data conform to human neuropsychological studies implicating a role for the parietal lobes in visuospatial functions. Disorders of visual perception may occur with lesions at the occipitoparietal or occipitotemporal borders. The isotypic primary visual receiving area (Brodmann area 17) forms the lips of the calcarine sulcus on the medial aspect of the occipital lobes. The superior lip receives afferents representing the contralateral inferior visual field, and the inferior lip receives afferents from the contralateral superior visual field. The unimodal visual association areas 18 and 19 form concentric rings around area 17. Lesions of the occipital lobes are therefore manifested as changes in visual perception, and a homonymous visual field cut is frequently seen. In part because of the small size of the occipital lobes, isolated occipital lobe syndromes are relatively rare. In complete cortical blindness, or blindness caused by bilateral destruction of the occipital lobes or their afferents, retention of pupillary responses reflects intact visual input to the brain stem. Hallucinations can occur as a result of occipital lobe injury by one of two mechanisms. When visual loss is cortical in origin, these 2037 hallucinations appear in the abnormal field and may be complex and continuous. Ictal hallucinations are rare and are a manifestation of seizures originating in the occipital lobes. Such hallucinations arising from area 17 generally consist of contralateral lights (or darkness) moving from the periphery to the center of the visual fields. Focal seizures arising from areas 18 or 19 may be motionless and pulsatile and may occur in both the ipsilateral and contralateral hemifields. More complicated visual hallucinations most likely originate in the temporal lobe. In this condition the subject is unable to attend to more than a small part of the visual field at once and consequently has difficulty understanding whole scenes. Selective deficits in perception of movement may occur with occipital lobe lesions. Alexia without agraphia was described above as a disconnection syndrome in which the left angular gyrus is isolated from visual information. The most common cause is a lesion in the occipitoparietal white matter of the left hemisphere with concomitant involvement of the splenium of the corpus callosum and optic radiations. Visual agnosia, or "a normal (visual) percept stripped of its meaning," may occur with more ventral occipital lobe damage. Agnosia has been subdivided into apperceptive agnosia, or a defect in perceiving all but the most basic aspects of visual stimuli such as color and movement, and associative agnosia, characterized by an inability to recognize stimuli despite completely intact visual perception (as demonstrated by the ability to draw the object). Patients with either type of agnosia can recognize objects through other sensory modalities. It is therefore necessary to assess language abilities, as well as the ability to recognize, in non-visual sensory modalities to characterize an agnosia. Visual agnosia is generally due to bilateral lesions in the occipitotemporal area affecting the inferior longitudinal fasciculus and is often associated with other visual disturbances. Visual agnosia has been described as resulting from lesions more anterior in the ventral visual pathway in the temporal lobes. Achromatopsia, or acquired color blindness, typically involves a single hemifield and is caused by a lesion of the contralateral occipitotemporal area. Prosopagnosia is the inability to recognize familiar faces visually, although it can also be manifested as an inability to distinguish individuals among a class of objects. The lesion is most frequently bilateral in the lingual and fusiform gyri of the ventral occipitotemporal area, although unilateral right-sided lesions can produce the syndrome. It is often associated with environmental agnosia, or the inability to recognize familiar places. Infarction in the distribution of the posterior cerebral arteries is a frequent etiology of occipital lobe damage; head injury, tumors, and many other processes can affect the occipital lobes as well. Visual field defects, particularly those caused by lesions of the non-dominant occipital lobe, are often overlooked by the patient. Its lateral surface consists of the superior, middle, and inferior temporal gyri, which run longitudinally. The inferior surface is also composed of longitudinal gyri: the occipitotemporal gyrus and the more medial parahippocampal gyrus. The parahippocampal gyrus, as well as the underlying amygdala and hippocampus and the temporal pole, will be discussed below as limbic structures. Aside from this isotypic cortex, the temporal lobe consists mainly of paralimbic cortex and unimodal and heteromodal association cortex. The anterior temporal lobe connects with the orbitofrontal region via the uncinate fasciculus, and the posterior temporal lobe is connected with more lateral frontal lobe by the arcuate fasciculus. Seizure disorders frequently arise from pathology in the temporal lobes and adjacent structures. Complete destruction of the primary auditory area unilaterally does not result in appreciable hearing deficits. Acute bilateral destruction (for example, by bilateral middle cerebral artery infarction) is rare and causes cortical deafness, or lack of a behavioral response to sounds of any kind. Over time this condition generally improves such that the subject can demonstrate some hearing but may have persistent auditory agnosia, or a deficit in the ability to recognize sounds. This condition also occurs with involvement of auditory association areas anterior to and sparing areas 41 and 42 and can be manifested as an inability to grasp the meaning of sounds such as car horns or a ringing telephone. Because of the proximity of areas important for language comprehension, auditory agnosia rarely exists without a concurrent language deficit. It is therefore important to assess language function when examining for auditory abilities. A condition termed pure word deafness in which patients are unable to understand spoken language but do not have a more general auditory agnosia or aphasia occasionally occurs. It is caused by bilateral lesions separating the primary auditory areas from the posterior association cortex. Patients with this condition have intact motor output and persist in uttering nonsense phrases filled with paraphasias (incorrect word or letter substitutions) that retain grammatical structure. They are not aware that people do not understand them and may become alarmed as though believing that those around them are speaking in code. A selective amusia, or the inability to recognize or appreciate pitch and melodies, may occur with right posterior temporal or inferior parietal lesions. Deficits resulting from right temporal lobe lesions are generally subtle and require specific testing for spatial orientation, fine visual discrimination, and odor discrimination. Focal seizures arising from the temporal lobe may give rise to changes in ongoing language function and to sensory, emotional, or psychic phenomena. Auditory hallucinations arising from the superior temporal gyrus range from simple sounds to complex speech, whereas visual hallucinations arising from the temporal lobe are generally complicated scenes or visual memories. The psychic and visceral experiences that occur during seizures arising from limbic structures within the temporal lobes are discussed below. It consists of the subcallosal gyrus anteriorly, includes the cingulate gyrus curving up and around the corpus callosum, and continues down the medial and inferior aspect of the temporal lobe as the parahippocampal gyrus. Some authors include the temporal poles, pyriform region of the frontal lobes, and portions of the insular cortex in the limbic lobe. As opposed to the six-layered neocortex, the cortex of the limbic lobe consists of a three-layered archeocortex (hippocampal formation and dentate gyrus), a three-layered paleocortex (parahippocampal gyrus), and a transitional juxtallocortex (cingulate gyrus). In mammals other than primates and in non-mammalian species, the limbic lobe makes up a much larger proportion of brain volume than it does in humans. Convergence of data from anatomic investigations, animal studies, and observations in humans suggests that the limbic system plays a role in mediating the experience of emotions, visceral responses, and storage of memories. The limbic system has connections to most areas of the cortex and has intimate connections with the hypothalamus, the "head ganglion" of the autonomic nervous 2038 system. In animals, electrical stimulation of the anterior cingulate cortex and the orbital-insular-temporal cortex causes changes in blood pressure, gastrointestinal motility, pupillary dilatation, salivation, bladder contraction, and respiration. In humans, seizure activity in these same areas can cause similar autonomic changes, including orgasm. Lesions of the limbic lobe usually do not induce clinically evident autonomic changes, in part because of the independence of subcortical structures such as the hypothalamus in mediating autonomic reflexes. Characteristic visceral and psychic phenomena occur with epileptic activity arising from limbic structures. Olfactory sensations, usually of an unpleasant nature, are classically associated with involvement of the uncus in the medial temporal lobe. Autonomic and gustatory sensations are seen with involvement of the opercular area within the sylvian fissure. Psychic sensations of deja vu, jamais vu, dream-like states, and depersonalization may occur along with associated impairment in consciousness. The temporal neocortex is intimately connected to the deeper limbic structures, so it is difficult to establish whether the observed seizure phenomena are due to limbic or neocortical involvement. Bilateral anterior temporal dysfunction resulting from lobectomy or other conditions (such as blunt head trauma, stroke, or herpes encephalitis) can cause a severe deficit in the ability to form new memories. Less dramatic deficits in specific items are seen with unilateral lesions, verbal memories being more impaired with left-sided lesions and non-verbal memories such as that for faces being more impaired with right anterior temporal lobe lesions. Considerable debate has arisen over the specific structures that need to be involved to produce this memory deficit. Observations suggest that the hippocampus is required to store emotionally neutral declarative memories whereas the adjacent amygdala is necessary to store emotionally laden memories. Aside from a memory deficit, bilateral lesions of the anterior temporal lobes can also induce Klu ver-Bucy syndrome. First described in monkeys, this condition consists of hypersexuality, hypermetamorphosis (excessive exploratory behavior), emotional placidity, hyperorality, and agnosia. Since then, clinical observation and countless studies have confirmed a more important role of the left hemisphere in language production and comprehension in most individuals. Of right-handed subjects, 96 to 99% have left-sided speech representation and bilateral speech representation is rare. In people who are left-handed or of mixed handedness, the majority (70%) still have exclusively left hemisphere speech representation, with 15% having bilateral speech representation. Mild degrees of aphasia frequently result from injury to either hemisphere in left-handers, whereas the aphasia resulting from left hemisphere lesions in right-handed individuals is generally of greater severity and duration. This asymmetry applies more to expressive language inasmuch as some degree of comprehension can be demonstrated in the right hemisphere of strictly right-handed subjects. In addition to non-right-handed people, women as a group tend to exhibit less cerebral lateralization. Right hemisphere superiority has been found in such tasks as somesthetic and visual recognition of shapes, perception of orientation and perspective, aspects of arithmetic ability, and perception and expression of emotional tone. Direct damage to a neuronal structure that performs an operation will prevent that operation and thus impair the output of that region. Alternatively, a lesion may destroy white matter tracts connecting two structures, thus impairing their interaction while leaving the structures themselves intact.
In patients with no evidence of distant metastatic disease diabetic diet resources discount forxiga 10 mg with visa, reoperative compartment-oriented lymphadenectomy may be appropriate diabetes in dogs life expectancy purchase forxiga 10mg without prescription. A detailed exposition of multiple endocrine neoplasia and the regulation of calcitonin-gene products diabetes type 2 history cheap forxiga 10 mg overnight delivery. Genotype/phenotype correlation of clinical syndromes with specific mutations of the c-ret proto-oncogene diabetes signs symptoms buy discount forxiga 10 mg online. Renal osteodystrophy encompasses a wide variety of derangements in mineral and bone metabolism diabetes diet soda link order forxiga 10mg online. With progressive loss of excretory kidney function diabetes jeopardy generic forxiga 10 mg on-line, abnormalities in divalent ions and secondary hyperparathyroidism typically develop early. However, the early stages of renal failure are marked by some signs of end-organ resistance to vitamin D, such as a mild decrease in intestinal calcium absorption and an altered calciuric response to oral supplementation of calcitriol. The exact mechanisms implicated in impaired binding of the hormone-vitamin D receptor complex to the vitamin D response element are not fully elucidated. In experimental studies on rats, alterations in the vitamin D receptor heterodimer partner (retinoid X receptor) have been observed; however, this mechanism has not been proved in humans. With more advanced nephron loss, the phosphate load of the remaining functioning nephrons progressively increases. This increased load results in inhibition of C1-alpha-hydroxylase, the enzyme responsible for the conversion of 25-hydroxyvitamin D to its active metabolite 1,25-dihydroxyvitamin D (calcitriol). Calcitriol deficiency in turn further decreases intestinal calcium absorption and thus results in hypocalcemia. Calcitriol deficiency in advanced renal failure is associated with a decreased number of vitamin D receptors, in particular, receptors in parathyroid glands. Calcium exerts its effects on parathyroid gland cells through a recently isolated G protein-coupled calcium-sensing receptor located on the cell membrane. The decreased number of calcium-sensing receptors with low circulating calcitriol may, at least in part, explain the relative insensitivity of parathyroid gland cells to calcium in patients undergoing dialysis (higher set point). When the glomerular filtration rate reaches levels of less than 25% of normal, the serum phosphorus content rises. At this level of reduced renal function, the ability of the remaining nephrons to increase phosphate excretion is exhausted. Increased serum phosphorus levels further decrease serum calcium through physicochemical binding and suppress C1-alpha-hydroxylase activity, which results in further lowering of the circulating levels of calcitriol. Monoclonal cell growth may also develop and result in the formation of tumor-like nodules that have less or no vitamin D and calcium-sensing receptors and that promote parathyroid gland resistance to calcitriol and calcium. Accumulation of aluminum in bone and other organs such as the parathyroid glands may occur in patients undergoing dialysis or before the initiation of dialysis. In addition, aluminum inhibits renal and intestinal C1-alpha-hydroxylase activity and may thus further contribute to reduced levels of calcitriol. Possible sources of aluminum include high concentrations in the water used for dialysis, prescription of aluminum-containing phosphate binders, and aluminum in drinking water, infant formula, and other liquids or solid food. Metabolic acidosis has been shown to stimulate bone resorption and suppress bone formation, thereby resulting in negative bone balance. Disturbed osteoblastic activity results in a disorderly production of collagen, which is deposited not only toward the trabecular surface but also in the marrow cavity, thereby causing peritrabecular and marrow fibrosis. Osteoid seams no longer exhibit their usual birefringence under polarized light; instead, a disorderly arrangement of woven osteoid and woven bone with a typical crisscross pattern under polarized light is seen. The mineral apposition rate and number of actively mineralizing sites are increased, as documented under fluorescent light after the administration of time-spaced tetracycline markers. Low-turnover uremic osteodystrophy is the other end of the spectrum of renal osteodystrophy. The majority of trabecular bone is covered by lining cells, with few osteoclasts and osteoblasts. Low-turnover osteomalacia is characterized by an accumulation of unmineralized matrix in which a diminution in mineralization precedes or is more pronounced than the inhibition of collagen deposition. The increased lamellar osteoid volume is due to the presence of wide osteoid seams that cover a large portion of the trabecular surface. The occasional presence of woven bone buried within the trabeculae indicates past high bone turnover. When osteoclasts are present, they are usually seen within trabecular bone or at the small fraction of trabecular surface left without osteoid coating. With adynamic uremic bone disease, the reduction in mineralization is coupled with a concomitant and parallel decrease in bone formation. Adynamic uremic bone disease is characterized by few osteoid seams and few bone cells. Mixed uremic osteodystrophy is caused primarily by hyperparathyroidism and defective mineralization with or without increased bone formation. Whereas active mineralizing surfaces increase in woven bone with a higher mineralization rate and diffuse labeling, mineralization surfaces may be reduced in lamellar bone with a decreased mineral apposition rate. Aluminum accumulates in bone at the mineralization front, at the cement lines, or diffusely. The extent of stainable aluminum at the mineralization front correlates best with histologic abnormalities in mineralization. In patients in whom an increased aluminum burden develops, bone mineralization and bone turnover progressively decrease. With progressive loss of renal function, cancellous bone volume is increased along with a loss of cortical bone. Patients undergoing chronic dialysis might have a loss or gain in bone volume depending on bone balance. In the case of negative bone balance, bone loss occurs in cortical and cancellous bone and is more rapid when bone turnover is high. When the bone balance is positive, osteosclerosis may be observed when osteoblasts are active in depositing new bone, thus superseding bone resorption. When bone turnover is low, however, positive bone balance results in hypercalcemia and possibly extraosseous calcification. Clinical manifestations are preceded, however, by an abnormal biochemical profile that should alert the physician and prompt steps to prevent more severe complications. When symptoms occur, they are usually insidious, subtle, non-specific, and slowly progressive. It may be diffuse or localized in the lower part of the back, hips, knees, or legs. Bone pain may progress slowly to the degree that patients are completely incapacitated. Occasionally, pain can occur suddenly at 1412 one joint of the lower extremities and mimic acute arthritis or periarthritis not relieved by heat or massage. Spontaneous fractures or fractures after minimal trauma may also occur in vertebrae (crush fractures) and in tubular bones. However, low-turnover osteomalacia and aluminum-related bone disease are associated with the most severe bone pain and the highest incidence of fractures and incapacity. In rickets, bowing of the long bones is seen, especially the tibiae and femora, with typical genu valgum that becomes more severe with adolescence. Long-standing secondary hyperparathyroidism in children may be responsible for slipped epiphyses secondary to impaired transformation of growth cartilage into regular metaphyseal spongiosa. This complication most commonly affects the hips, becomes obvious in pre-adolescence, and causes limping but is usually painless. When the radius and ulna are involved, ulnar deviation of the hands and local swelling may occur. In adults, skeletal deformities can be observed in cases of severe osteomalacia or osteoporosis and include lumbar scoliosis, thoracic kyphosis, and recurrent rib fractures. Proximal muscle weakness is fairly common in dialysis patients, particularly those with aluminum toxicity, severe hyperparathyroidism, or osteomalacia. Proximal myopathy is manifested by difficulty rising out of a chair or climbing stairs. Pruritus can occur before the institution of dialysis and can disappear after regular dialytic therapy. However, symptoms more often begin about 6 months after the start of dialysis and persist thereafter. Several possible factors have been implicated (alone or in combination), such as secondary hyperparathyroidism, hypercalcemia, and increased calcium phosphate production, in addition to dry skin (xeroderma), intradermic microprecipitation of divalent ions, peripheral neuropathy, allergic reactions, hypersensitivity, histamine, proliferation of skin mast cells, hypervitaminosis A, iron deficiency, and abnormal fatty acid metabolism. Soft tissue calcification may occur in the eyes and be manifested as band keratopathy in the sclerae or induce an inflammatory response known as the red eye syndrome in the conjunctiva. These types of calcifications are usually associated with hyperparathyroidism or increased calcium phosphate product. Calcium deposits are also found in the lungs and lead to restrictive lung disease. Deposits in the myocardium might cause arrhythmias, annular calcifications, or myocardial dysfunction. Most soft tissue calcifications are attributed to secondary hyperparathyroidism or to the increased calcium phosphate product associated with it. This diversity could be explained by increased calcium and/or phosphate release from bone in patients with severe hyperparathyroidism and an inability to maintain normal mineral accretion in patients with adynamic bone disease. Tumoral calcinosis is a form of soft tissue calcification that usually involves the periarticular tissues. Calcium deposits may grow to enormous size and interfere with the function of adjacent joints and organs. Although this type of calcification is usually associated with high calcium phosphate product, its exact pathogenesis is poorly understood. Similar to soft tissue calcification, it is observed with severe hyperparathyroidism and low-turnover bone disease. The syndrome of calciphylaxis is characterized by vascular calcification in the tunica media. These calcifications induce painful violaceous skin lesions that progress to ischemic necrosis. Calciphylaxis has been associated with high serum calcium phosphate product and severe secondary hyperparathyroidism. The pathogenesis of calciphylaxis is probably multifactorial because hyperparathyroidism, high calcium phosphate production, steroid therapy, vitamin D therapy, iron overload, aluminum toxicity, and protein C deficiency have all been implicated. Clinically, dialysis dementia is a form of progressive neurologic abnormality and includes dysarthria, dysphagia, amnesia, apraxia, mutism, myoclonic jerks, facial grimacing, seizures, and ultimately, severe dementia and death. It determines, on the same bone sample, the precise level of bone formation, mineralization, bone resorption, bone turnover, and extent of bone aluminum deposition, if present. The results serve as a basis for appropriate use of tailored therapeutic regimens. In the absence of bone biopsy, the physician needs to estimate the level of bone turnover, the presence of osteomalacia, and the possibility of bone aluminum toxicity. Abnormalities in serum calcium, phosphorus, and alkaline phosphatase levels indicate severe renal osteodystrophy but are useless when used alone to indicate bone turnover or osteomalacia. Hypercalcemia may be observed in severe hyperparathyroidism or adynamic bone disease, especially with vitamin D therapy. Hyperphosphatemia is an indication of non-compliance with phosphate binders and/or severe hyperparathyroidism secondary to increased release of phosphorus from bone. High serum levels of alkaline phosphatase are usually seen in both osteomalacia and predominant hyperparathyroidism. Skeletal radiographic abnormalities are seen when the disease is advanced and include erosive cortical defects in the skull (pepper pot skull), acro-osteolysis of the clavicula, and erosion of the terminal finger phalanges. A rugger-jersey appearance of the spine and a ground-glass appearance of the skull, ribs, pelvis, and metaphysis of tubular bones reflect advanced cancellous changes. In severe hyperparathyroid bone disease, pseudocysts or brown tumors may be observed. However, signs of increased bone resorption may be seen on radiographs reflecting past resorption activity, which may have been succeeded by the accumulation of osteoid. Because osteoid is radiolucent, the superimposed osteomalacia will be missed by x-ray examination. Looser zones that are straight bands of radiolucency abutting onto the cortex and running perpendicular to the long axis of bone are of relatively low sensitivity and low specificity for the diagnosis of osteomalacia. Although correlations exist between random serum aluminum levels and the extent of stainable aluminum in bone, no threshold value allows a clear-cut distinction between patients with and patients without aluminum-related bone 1413 disease. The deferoxamine infusion test is advocated to improve the sensitivity of random serum aluminum levels. An increase in serum aluminum levels of greater than 200 mug/L 48 hours after a standardized infusion constitutes a positive result. This test does improve the sensitivity of predicting aluminum-related bone disease, but the specificity is greatly reduced. However, the sensitivity is greatly reduced and many patients will have false-negative results. Secondary hyperparathyroidism can be prevented by avoiding deviations of serum phosphorus and calcium levels from normal. None of the available dialytic methods is efficient in removing phosphorus because of compartmentalization and slow efflux of phosphorus from the intracellular space. However, because phosphate is present in most protein-containing food products, phosphate restriction is limited by the need for appropriate dietary protein intake.
Although other studies may be suggestive diabetes type 2 research order 10mg forxiga with visa, angiography is required for the definitive antemortem diagnosis of a mycotic aneurysm diabete 0 90 discount 5 mg forxiga. Cardiac catheterization can provide important information and should not be avoided when indicated in selected patients with endocarditis for fear of dislodging emboli managing diabetes nz ltd cheap forxiga 10mg visa. Coronary angiography is used to assess the presence of significant coronary artery disease before elective placement of prosthetic cardiac valves in patients who are older than 40 years and have additional atherogenic risk factors blood glucose 105 forxiga 10 mg low price. Computed tomography or magnetic resonance imaging is used to define the cause of focal neurologic findings and identify metastatic suppurative infection or embolic events that can impede clinical or bacteriologic therapeutic responses diabetes xango purchase 10mg forxiga fast delivery. After obtaining blood cultures blood glucose watch monitor cheap forxiga 5 mg line, empirical antimicrobial therapy should be initiated. If echocardiography reveals vegetations, valvular destruction or its hemodynamic effects, valve ring abscess or a fistula, or a predisposing valvular lesion and/or clinical evidence of left-sided or right-sided endocarditis. Even if another potential source for the bacteremia is present and no echocardiographic or clinical evidence of endocarditis but the organism isolated is likely to cause endocarditis, such as S. If no apparent source is found for the bacteremia, even if echocardiographic and clinical evidence is lacking, the patient should still be considered to possibly have endocarditis. If blood cultures remain negative after 1 week of incubation, the patient may be discharged from the hospital without echocardiography, unless clinical evidence of left-sided or right-sided endocarditis is present, in which case the diagnosis of endocarditis should nevertheless be suspected. In patients with bacteremia related to intravascular devices, such as an arteriovenous fistula or graft for hemodialysis, indwelling central intravenous line, cardiac assist balloon pump, or pacemaker wire, the device should be removed, especially with S. Catheter-associated coagulase-negative staphylococcal nosocomial bacteremia, which rarely eventuates in native valve endocarditis, should not be investigated with echocardiography after antibiotics are begun unless a prosthetic cardiac valve is present. Indeed, catheter removal may not be necessary to cure coagulase-negative staphylococcal catheter-associated bacteremia. Catheter-associated nosocomial fungemia should probably be investigated with echocardiography after the catheter is removed and antifungal chemotherapy begun, regardless of whether clinical evidence of endocarditis is present. In a recent study, 43% of patients with a prosthetic valve in whom fever and bacteremia developed had or subsequently acquired prosthetic valve endocarditis. Any organism in blood cultures in these patients must be taken seriously as a potential cause of endocarditis. In those with clinical evidence suggestive of prosthetic valve endocarditis, empirical antibiotic therapy can be initiated after three or four sets of blood cultures are obtained. After antimicrobial therapy is started, blood cultures should be repeated to assess for clearance of bacteremia. In bacteremic patients with no evidence of endocarditis despite these studies, antimicrobial therapy has traditionally been recommended for 2 weeks, but new data suggest that even therapy continued beyond 2 weeks may not prevent prosthetic valve endocarditis from occurring as a result of the initially transient bacteremia. Effective antimicrobial therapy for endocarditis optimally requires identification of the specific pathogen and assessment of its susceptibility to various antimicrobial agents. Therefore, every effort must be made to isolate the pathogen before initiating antimicrobial therapy, if clinically feasible. In patients who are in immediate danger of death, empirical antibiotic therapy should be started as soon as possible after obtaining blood cultures. Empirical therapy should be targeted at the most likely pathogens in that particular clinical setting (see Table 326-4). The minimal requirements for an effective antimicrobial regimen include the following: 1. Bacteriostatic agents are not able to clear the pathogen from infected tissues unaided by host defenses such as polymorphonuclear leukocytes, antibody, and complement. Because host defenses are thought to not operate within vegetations (except in tricuspid valve vegetations, in which polymorphonuclear leukocytes may aid the effect of an antimicrobial agent), clearing bacteria from these vegetations requires bactericidal action from antibiotics. In fact, complete eradication of pathogens from the vegetation by the antimicrobial drug is thought to be essential to cure endocarditis. If any bacteria remain after completion of antibiotic therapy, the residual organisms regrow and result in relapse. Table 326-7 (Table Not Available) shows the various antimicrobial agents that have bactericidal activity. The enterococcus illustrates the problems in selecting appropriate bactericidal therapy for endocarditis. Unlike viridans streptococci, which are killed by relatively low concentrations of penicillin, penicillin G alone, even at concentrations of up to 1000 mug/mL, is only inhibitory or at best slightly bactericidal against enterococci. The aminoglycosides are also poorly effective at low concentrations (<500 to 1000 mug/mL) because of inadequate permeability of the bacterial cell. Antibiotic synergism does occur, however, as the result of enhanced intracellular uptake of the aminoglycoside in the presence of a beta-lactam (such as penicillin, ampicillin, or piperacillin) or a glycopeptide (such as vancomycin or teicoplanin), the so-called cell wall-active antibiotics. The definition of synergism requires that the reduction in bacterial count at 24 hours with the drug combination be at least 100-fold greater than that with the cell wall-active antibiotic alone. Synergism is predicted on routine screening of strains by inhibition of growth with 500 mug/mL of gentamicin or 1000 mug/mL of streptomycin (see Table 326-6) (Table Not Available). In addition to determination of susceptibilities to high levels of streptomycin and gentamicin, all enterococci causing endocarditis should be tested for beta-lactamase production and susceptibility to penicillin and vancomycin to select optimal therapy. Doses of the antimicrobial agent must achieve blood concentrations of the antimicrobial agent high enough to facilitate passive diffusion of the antimicrobial agent into the depths of the vegetation where microcolonies of the pathogen are located. Over 90% of the microbial population in the vegetation is non-growing and metabolically inactive once the infection has become well established. Non-growing organisms are more likely to be found in the central portions of the microcolonies in the deeper regions of the vegetation. As a result, microorganisms in vegetations for the most part are not susceptible to commonly used antibiotics such as the beta-lactams and aminoglycosides, which are effective only against actively growing bacteria. Optimally, the antimicrobial agent should be active against non-growing microorganisms. However, when the drug is active only against growing microorganisms, each dose of the bactericidal drug is able to effect a reduction in the microbial count only in that minor portion (<10%) of the population that happens to be growing at the time of drug administration. The duration of drug therapy must therefore be prolonged to completely clear the pathogen from the vegetation. The duration of therapy varies with the specific pathogen, the site of the infection, and the type of antibiotic. For example, bacterial clearance is more rapid for viridans streptococci than for staphylococci, in tricuspid than in aortic vegetations, with antistaphylococcal beta-lactams than with vancomycin, or with combinations of cell wall-active agent plus aminoglycoside than with single drugs. More rapid clearance in these special circumstances may permit a shorter course of therapy to achieve cure. The organisms that remain after brief in vitro exposure to an aminoglycoside or a beta-lactam antibiotic frequently exhibit a post-exposure delay in further in vitro growth, the so-called post-antibiotic effect. Unfortunately, no such effect occurs with some organisms such as enterococci 1638 or P. Standardized regimens have been recommended for the most common pathogens-viridans streptococci, enterococci, and staphylococci on native and prosthetic valves (Table 326-8) (Table Not Available). In vitro susceptibility testing should be performed for these organisms and the patient treated with the regimen that demonstrates the best bactericidal activity. In patients who are hemodynamically unstable, emergency cardiac valve replacement should not be delayed to allow further antibiotic therapy. Patients with valve ring abscess should be monitored for conduction abnormalities, which may require placing a transvenous pacemaker because of the risk of high-grade heart block. Prosthetic valve placement in an intravenous drug user is problematic because the prosthetic valve places the patient at continued risk of prosthetic valve endocarditis. Alternatively, for tricuspid valve endocarditis, tricuspid valve resection without prosthetic replacement can be tolerated hemodynamically for extended periods in many of these patients. The surgical indications for prosthetic valve endocarditis are the same as those outlined for native valve endocarditis and include relapse after a course of appropriate antibiotic therapy. Intrathoracic, intra-abdominal, or peripheral mycotic aneurysms usually require surgical excision. If symptomatic, cerebral aneurysms should be monitored closely with serial angiography and may require surgery if enlarging or bleeding. Myocardial revascularization should be performed at the time of elective valve surgery if significant coronary artery disease is present. However, patients who require emergency placement of a prosthetic valve for hemodynamic decompensation secondary to acute endocarditis usually cannot tolerate the dye load necessary for coronary angiography and the additional bypass surgery. Anticoagulant therapy, although it may impede further enlargement of a vegetation, is relatively contraindicated in endocarditis because of conversion of an unsuspected cerebral infarct into an intracerebral bleed. Having a focal infection that would require more than 2 weeks of antimicrobial therapy, prosthetic valve endocarditis, and significant renal or eighth nerve impairment precludes the use of short-course beta-lactam-aminoglycoside combination therapy. Absorption of orally administered agents may be unreliable, and oral therapy is generally not recommended. In streptococcal endocarditis, heart failure, if not present on admission, rarely initially develops during therapy. Emboli most often occur before or within the first few days of antimicrobial therapy. Before considering outpatient therapy, most patients should initially be evaluated and stabilized in the hospital, although some patients may be managed entirely as outpatients. The standard regimens used to treat penicillin-sensitive streptococci require either continuous infusion of penicillin or frequent intravenous administration. A single daily dose of ceftriaxone is an attractive alternative to penicillin for antibiotic therapy at home. Because of its long half-life and good potency against these streptococci, serum levels of ceftriaxone remain well above the minimal inhibitory and bactericidal concentrations for over 24 hours. The size of the vegetation on echocardiography should stabilize or gradually diminish. However, the erythrocyte sedimentation rate, anemia, and renal function may take weeks to months to improve. Circulating immune complexes and related serologic findings, including hypocomplementemia, mixed cryoglobulinemia, and rheumatoid factor, also tend to resolve with effective antibiotic therapy. Blood cultures for streptococci and enterococci should become sterile after 1 to 2 days of appropriate therapy and for S. If no organism is isolated from blood but the clinical response to an empirical antimicrobial regimen is good, empirical therapy should be continued in the patient thought to have endocarditis (see Table 326-5) (Table Not Available). If no organism is isolated and no clinical response is seen to empirical therapy after 1 to 2 weeks, endocarditis caused by a fastidious pathogen. If the pathogen is initially isolated from blood and appropriate antimicrobial therapy started but fever persists or recurs, blood cultures should be repeated to assess persistent or relapsing infection, among other possibilities, which include most commonly pulmonary or systemic embolization (Table 326-9). Measuring vancomycin or aminoglycoside serum levels may be helpful to ensure adequate but non-toxic antibiotic levels. The relapse organism should be evaluated for the development of antibiotic resistance. Following cure of one episode of endocarditis, patients remain at increased risk for reinfection. For example, only about half of cases have recognizable predisposing cardiac lesions, most cases do not follow an invasive procedure, and only about two thirds of cases are due to microorganisms (viridans streptococci and enterocci) against which prophylactic regimens are directed. However, in patients who are known to have a risky cardiac lesion (see Table 326-1) (Table Not Available) and are to undergo a procedure that is likely to induce bacteremia (see Table 326-3) (Table Not Available) with organisms having predictable susceptibility to antibiotics with minimal inconvenience, toxicity, and cost, the American Heart Association has made the recommendations shown in Table 326-11 (Table Not Available). Additional preventive measures are minimizing invasive procedures, avoiding intravascular catheters (a major predisposing event for prosthetic valve endocarditis), aggressively treating focal infections, and maintaining good dental hygiene in patients at increased risk for endocarditis. Discusses prevention as a complex issue involving diverse aspects of medicine, microbiology, dentistry, surgery, epidemiology, and decision analysis. This multiauthored text is a thorough, up-to-date review of every aspect of infective endocarditis, written by experts. This issue highlights important new developments in pathogenesis, diagnosis, and treatment. Archer Staphylococcus aureus has been recognized as one of the most important and lethal human bacterial pathogens since the beginning of this century. However, over the past 20 years, coagulase-negative staphylococcal infections have emerged as one of the major complications of medical progress. They are currently the pathogens most commonly isolated from infections of indwelling foreign devices and are the leading cause of hospital-acquired bacteremias in United States hospitals. This ascendancy of staphylococci as pre-eminent nosocomial pathogens also has been associated with a major increase in the proportion of these isolates that are resistant to multiple antimicrobial agents. If the trend continues, we may be forced to revisit the serious staphylococcal infections of the preantibiotic era that textbooks had long since relegated to medical history. The name "staphylococcus" means "bunch of grapes" and describes the clusters and clumps of gram-positive cocci seen on Gram stain of both infected material and organisms recovered from culture bottles and agar plates. Staphylococci produce catalase, breaking down hydrogen peroxide to H2 O and O2; streptococci do not. The latter characteristic predicts that these organisms should grow equally well in both aerobic and anaerobic media. Coagulase-negative staphylococci are found as normal skin flora on all mammals, and currently, 31 different and distinct species are recognized. Of these, 15 species are found colonizing the cornified squamous epithelium and mucous membranes of humans. Because many laboratories report specific species of coagulase-negative staphylococci to clinicians, a list of the most prevalent human pathogenic species is shown in Table 327-1. Because only 60 to 70% of coagulase-negative species identified from specimens processed by the clinical laboratory are S. Carriage can be transient, lasting hours to days; intermittent, lasting weeks to months; and recurring or chronic, persisting for months to years despite attempts at eradication. Intact cornified squamous epithelium will not support intermittent or chronic carriage of S. However, transient hand carriage clearly occurs and is an important means of exchange between patients and hospital personnel. Certain conditions have been described, however, that markedly increase skin carriage as well as nasal carriage of S.
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Currently blood glucose number chart generic 10 mg forxiga free shipping, erythromycin or tetracycline (either as 2 g daily in divided doses) is standard therapy (Table 320-3) blood glucose readings order 10 mg forxiga amex. Doxycycline and the newer macrolides (azithromycin and clarithromycin) can substitute for tetracycline and erythromycin diabetes mellitus greek purchase forxiga 10mg without a prescription, respectively lipoatrophy definition diabetes purchase 10mg forxiga with visa, and offer the advantage of greater patient convenience diabetes mellitus birth defects cheap forxiga 10 mg fast delivery, but at increased cost blood glucose journal pages cheap 5mg forxiga fast delivery. Although most recommendations are for 10 to 14 days of therapy, longer courses of treatment. Prophylaxis of contacts does not prevent infection but can prevent clinical disease. Tetracyclines should be avoided in children younger than 8 years and pregnant patients but are preferable if the differential diagnosis includes psittacosis, Q fever, or Mycobacterium fermentans (see below). Correspondingly, erythromycin is preferred if the differential diagnosis includes legionellosis. Quinolones show good in vitro activity (see Table 320-3), but clinical experience is limited and they can not be recommended at this point as primary therapy. These drugs should be avoided in children and adolescents under 18 and in woman who are nursing or pregnant. Mycoplasma hominis is a commensal of the genitourinary tract, especially in women. It also causes post-abortal and postpartum fever, wound infection following cesarean section, and postpartum retroperitoneal obscess. Infection of surgical wounds should be suspected if a purulent exudate is negative on Gram stain and culture. Other sites of extragenital infection include the brain, lung, prosthetic devices, skin, peritoneum, and joints (especially in patients with hypogammaglobulinemia). Although these organisms are not visible on Gram stain, some investigators have identified them in infected joint fluid with acridine orange stain and immunofluorescent staining. The organism may grow on routine media but is easily overlooked, and if it is suspected, the laboratory should be alerted. This organism has been recovered from the lower genital tract of men and women, the oropharynx, and the lower respiratory tract. This organism is resistant to erythromycin and should be treated with doxycycline or a quinolone (see Table 320-3). A growing number of other mycoplasmas are thought to possibly cause disease, especially in immunosuppressed patients; M. Other human mycoplasmas, as noted in Table 320-1, are presently considered commensals. Ureaplasma urealyticum colonizes the genital tract of 75% of women and 45% of men who are sexually active (see Chapter 361). In an adult, it may cause non-gonococcal urethritis, as well as salpingitis and pelvic inflammatory disease; outside the genitourinary tract, it can infect joints (especially in patients with hypogammaglobulinemia), transplant sites, and surgical wounds. In the neonate, it is associated with chorioamnionitis and with chronic lung disease of prematurity, but it is not strongly associated with prematurity, and treatment to eradicate it during pregnancy does not reduce the incidence of premature birth or low birth weight. Tetracyclines are agents of choice, with erythromycin or possibly quinolones as alternatives (see Table 320-3). Taylor-Robinson D: Infections due to species of Mycoplasma and Ureaplasma: An Update. These organisms are not highly virulent respiratory pathogens but strike instead individuals whose defense mechanisms have been diminished by acute or chronic disease. Over the 1613 next 1 or 2 days secretions become more purulent, gas exchange worsens, and new infiltrates appear on the chest radiograph. Colonization increases swiftly among healthy persons undergoing elective surgical procedures from essentially zero to 35 to 50% within 24 hours after surgery. The organisms responsible for colonization vary from one study to another but are only rarely attributable to demonstrable environmental sources. Colonization rates among populations with chronic disease, such as alcoholics and residents of skilled nursing facilities, may approach 50%. Because lung defenses are often impaired by the same underlying conditions that promote changes in cell resistance to adherence and colonization, the ability of the lungs to handle this bacterial inoculum is insufficient, and pneumonia results. The specific lung defense mechanism that might be impaired in a given patient varies with the nature of underlying illness. For example, patients with chronic airway obstruction have impaired mucociliary transport and alveolar hypoxia that hinders the effectiveness of phagocytic cells. This phenomenon has been associated with the presence of nasogastric tubes, which allow reflux of gastric material into the esophagus. The role of gastric acid neutralization for prophylaxis of stress ulceration is controversial; bacterial concentrations in the stomach increase dramatically as the pH rises, and some studies have associated such prophylaxis with higher rates of pneumonia, although this has been an inconstant finding. All the others together, including Enterobacteriaceae (Escherichia coli, Klebsiella, Enterobacter, Serratia, and Proteus), Pseudomonas, and Acinetobacter, account for 10 to 20% of community-acquired pneumonias, and these occur almost exclusively in patients with serious underlying disease. It was the first such organism to be recognized as a pulmonary pathogen, and the pneumonia it caused was distinct from that caused by the pneumococcus, especially in its lack of response to early forms of treatment and its predilection to cause upper lobe pneumonias in alcoholic men. However, the classic features of Klebsiella pneumonia as described in the earlier literature, such as "currant jelly" sputum (a mixture of blood and mucus), the bulging fissure associated with upper lobe consolidation, and the syndrome of "chronic cavitary pneumonia," are rarely observed today. With the advent of disposable nebulizers and other control strategies, this problem has been largely eliminated. Thus, these infections are most likely to be found in postoperative patients or patients who require intensive care for other reasons. The clinical manifestations of infection are influenced by the nature of the associated processes. The illness tends to be abrupt and associated with prominent systemic signs and symptoms, such as mental confusion, vomiting, and hypotension. Physical examination reveals rales in most patients, but the classic findings of dense consolidation are uncommon. Radiographic infiltrates may involve any lobe and are bilateral in about one third of patients. Although cavitation is most likely to occur in pneumonia caused by Klebsiella, it also occurs commonly with Pseudomonas infections and occasionally with other organisms. Laboratory features include leukocytosis or leukopenia, either of which is characteristically associated with a marked left shift. Often the patient is in respiratory failure, intubated, and receiving mechanical ventilation. Finally, the patient becomes febrile and develops new radiographic infiltrates and worsening hypoxemia. Postoperative pneumonias are most common after lateral thoracotomies (especially combined thoracoabdominal procedures) and upper abdominal incisions. As a result, the organisms are often resistant to antimicrobial agents used frequently in that particular hospital, reflecting acquisition of nosocomial strains such as Acinetobacter, Pseudomonas, and Stenotrophomonas. These and other organisms have shown the capacity to develop high-level resistance to virtually all antimicrobial agents in frequent use, an observation that supports the concept of restricting the use of certain antibiotics for periods of time. Pulmonary infiltrates in that instance usually represent non-cardiogenic pulmonary edema or the adult respiratory distress syndrome (see Chapters 88 and 92) and not actual pneumonia, with bacteremia arising from a non-pulmonary source such as the gastrointestinal or urinary tract. Blood cultures are positive in 20 to 30% of patients with community-acquired infections but in as few as 8% of those with nosocomial pneumonias. Similarly, although pleural effusion is usually not present, the yield of positive cultures from such fluid when it is present is about 30%, and a diagnostic thoracentesis should be performed if a sufficient volume of fluid is identified radiographically. Transthoracic needle aspiration is rarely used in critically ill patients because of concern about complications, especially pneumothorax. The finding of bacteria phagocytosed by more than 7% of lavaged cells seems to have predictive importance and has been used to guide empirical therapy until culture results are known. A reasonable strategy has emerged in recent years as experience has been gained with these techniques. Despite the ready availability of bronchoscopy, the etiology of nosocomial pneumonias is often frustratingly difficult to establish with certainty. Evaluation of the efficacy of treatment is confounded by the severity of underlying disease present in most of these patients; mortality rates of 20 to 30% are not uncommon among patients treated with agents that have demonstrated in vitro activity against the infecting organism. Agents other than fluoroquinolones must be given parenterally and in adequate dosage. The results of monotherapy rival those of multidrug regimens when broad-spectrum agents such as third-generation cephalosporins (ceftazidime or cefotaxime), carbepenems (imipenem or meropenem), beta-lactam/beta-lactamase inhibitor combinations (piperacillin/tazobactam or ticarcillin/clavulanate), or fluoroquinolones (ciprofloxacin or alatrofloxacin) are used. Dosages of 5 mg/kg every 24 hours for gentamicin and tobramycin; 15 mg/kg every 24 hours for amikacin. Treatment of nosocomial infection is made more difficult by previous antimicrobial therapy, and drug susceptibility studies are critically important. However, empirical therapy usually must be initiated before the results of such studies are available. Factors to consider when selecting appropriate therapy include knowledge of local resistance patterns, previous culture results, and prior treatment. Amikacin is often used in this setting because of less frequent resistance to this agent. A single daily dose of an aminoglycoside has been shown to be equally as effective as more frequent dosing and may be less nephrotoxic. Prospective studies have shown that carefully chosen empirical regimens are inadequate in up to 73% of cases when invasive sampling techniques are used to determine the etiologic organisms. Causes of inadequacy are the presence of resistant organisms singly or in polymicrobial infections; up to 40% of nosocomial pneumonias are polymicrobial. When the pathogenic organisms have been identified and the susceptibility patterns are known, modifications can be made to optimize antibiotic therapy. Ideally, antibiotics with the narrowest spectrum of activity, the least toxicity, and the best lung penetration should be chosen. In neutropenic patients and in seriously ill patients with pneumonia caused by resistant organisms such as P. Duration of therapy should be based on clinical response, but a minimum of 2 to 3 weeks is usually required. The observed level of mortality depends on the population studied and has been reported as high as 91%, but it is more commonly in the range of 20 to 50%. That adequate therapy did not reduce mortality in some studies is explained by the fact that underlying disease is the main predictor of survival for many patients. Early, broad-spectrum therapy that covers all of the organisms present in the lung is important for patients with survivable illnesses. Important complications include empyema, lung necrosis, superinfections, and multiple organ failure; metastatic seeding of infection to other sites is an uncommon complication. Criteria for the diagnosis of empyema, besides the presence of gross pus, include the presence of bacteria on Gram stain, pleural fluid pH less than 7. Each of these criteria indicates a condition that is unlikely to respond to antimicrobials alone and that usually requires drainage of the pleural space as well. Thus the term complicated effusion has gained favor over empyema to identify pleural fluid collections for which drainage needs to be considered. The occurrence of a complicated effusion generally prevents the recovery of the patient until it is recognized and effectively treated. If pleural fluid is identified on upright posteroanterior and lateral chest radiographs, thoracentesis should be performed; useful studies of the fluid obtained include measurements of pH and glucose, white blood cell count, Gram stain, and cultures for aerobic and anaerobic organisms. If the fluid qualifies as a complicated effusion, prompt placement of a thoracostomy tube should be considered. Alternative approaches (principally, repeated thoracentesis) are less successful, owing to loculation of the pleural space. Surgical drainage of the pleural space, using localized resection of an overlying rib with creation of a larger drainage tract, is reserved for patients who do not respond to tube drainage and are not candidates for a larger operation. Decortication of the pleura may be necessary if the clinical signs of uncontrolled infection are not ameliorated by simple drainage plus antimicrobial therapy. In such patients, radiographic 1615 evidence of effusion persists, along with continued fever and leukocytosis. At surgery, the pleural space is found to contain numerous loculated pockets of pus. The timing of intervention with these techniques requires excellent clinical judgment, because the patients are usually seriously ill and poor candidates for surgical treatment of any kind; on the other hand, they will not recover unless the pleural space is adequately drained. Extensive lung necrosis has been termed lung gangrene because of the rapid occurrence of pulmonary cavitation associated with marked systemic toxicity and the appearance of extensive devitalization of lung tissue at necropsy. Occasionally, an entire lung appears to dissolve within a few days, leaving multiple cavities with air-fluid levels. Extensive lung necrosis may be followed by massive hemoptysis, continued suppuration because of inadequate drainage of the massively disrupted lung parenchyma, or bronchopleural fistula caused by extension of the necrotizing process through the pleura. The last must be promptly treated by placing a chest tube because of the attendant pneumothorax. However, the definitive treatment of extensive lung necrosis is surgical resection of the involved lobe or lobes. The major question is usually whether a new complication such as oliguria is due to the underlying disease, to the current treatment, or to the infection. The guiding principles are to treat the infection aggressively and to correct life-threatening complications as they occur. If the patient is responding well and appears to be improving, the new culture results can be disregarded for the time being. On the other hand, if the new cultural data correspond to a worsening clinical course, the process of evaluation and revision of treatment must be begun again. Empirical therapy was judged to be inadequate in 73% of 60 cases with positive cultures, leading to a later change in treatment. This study reports an analysis of 241 cases of Klebsiella bacteremia, emphasizing the frequent presence of severe underlying disease and overall poor response to therapy. Aspiration of oropharyngeal liquids into the lungs is a key step in the pathophysiology of many pulmonary disorders.
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