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Herpetic infections have plagued humanity for thousands of years, but only recently have advances in antiviral medications and supportive treatments equipped physicians to combat the most keratitiis manifestations of disease. Prompt recognition and treatment can be life-saving in the care of patients with herpes simplex-1 virus encephalitis, kerwtitis most commonly identified cause of sporadic encephalitis worldwide.

Clinicians should be able to recognize the clinical signs and symptoms of the infection and familiarize themselves with a rational diagnostic approach and therapeutic modalities, as early recognition and treatment are key to improving outcomes.

Clinicians should also be vigilant for the development of acute complications, including cerebral edema and status epilepticus, as well as chronic complications, including the development of autoimmune encephalitis associated with antibodies to the N -methyl-D-aspartate receptor and other neuronal kegatitis surface and synaptic epitopes.

Herein, we review the pathophysiology, differential diagnosis, and clinical and radiological features of herpes simplex virus-1 encephalitis in adults, including a discussion of the most common complications and their treatment.

Herpes Simplex Virus-1 Encephalitis in Adults: Pathophysiology, Diagnosis, and Management

While great progress has been made in the treatment of this life-threatening infection, a majority of patients will not return to their previous neurologic baseline, indicating the need for kratitis research efforts aimed at improving the long-term sequelae. The online version of this article doi: Encephalitis is inflammation of the brain parenchyma with neurologic dysfunction, and can result from infectious, postinfectious, and noninfectious causes [ 1 ].

Herein, we review the clinical sakep radiological manifestations, diagnostic evaluation, and treatment of herpes simplex virus-1 HSV-1 encephalitis HSVEthe most common infectious cause of sporadic encephalitis. Herpetic infections have been recognized since the time of ancient Greece. Goodpasture [ 3 ] and others demonstrated that material from keragitis lip and genital lesions produced encephalitis when introduced into the scarified cornea or skin of rabbits.

In the s, the Mathewson commission was among the earliest reports to suggest HSV caused encephalitis in humans [ 4 ]. The first pediatric case report of HSVE was published in [ 5 ]. The first adult case, a year-old man who presented with headache, fever, aphasia, and left pupillary dilatation, was reported in [ 6 ]. On postmortem pathological examination, there were numerous petechiae and ecchymoses with perivascular lymphocytic cuffing in the left temporal lobe, midbrain, and pons.

Significant progress in the pathobiology, diagnosis, and treatment of HSVE has been made since these early reports. The herpesviruses are large, double-stranded DNA viruses that are well-adapted to human infection as they establish lifelong infection, rarely cause death of the host, and are readily spread between individuals. HSV initially gains access to host tissues through mucous membranes or damaged skin. After primary infection of the mucosal or skin epithelium, the virus infects sensory neurons via interactions with cell-surface glycosaminoglycans such as heparan sulfate [ 7 ], and cell adhesion molecules such as nectin-1 [ 89 ], and travels to the neuronal cell body in the dorsal root ganglion via fast retrograde axonal transport [ 1011 ].

The mechanisms by which HSV gains access to the central nervous system CNS in humans are unclear, and this remains an area of debate. The most likely routes include retrograde transport through the olfactory or trigeminal nerves [ 91213 ], or via hematogenous dissemination. The viral tropism for the orbitofrontal and mesiotemporal lobes argues against hematogenous dissemination in most cases. Experimental evidence in animals supports transmission to the CNS via either or both the trigeminal and olfactory routes, and suggests that virions can spread to the contralateral temporal lobe via the anterior commissure [ 13 ].

Unlike other cranial nerves with sensory functions, the olfactory nerve pathways do not route through the thalamus but connect directly to the frontal and mesiotemporal lobes including the limbic system.

There is some evidence to support olfactory spread to the CNS in humans, but definitive data are lacking [ 1214 — 16 ]. The trigeminal nerve innervates the meninges, and spread to the orbitofrontal and mesiotemporal lobes could also occur through this route [ 17 ].

However, as the sensory nuclei of the trigeminal nerve are located in the brainstem, one would expect the relatively rare occurrence of brainstem encephalitis associated with HSVE to be more common if this were the primary route of entry to the CNS in most cases [ 18 — 20 ]. Whether HSVE is a reactivation of latent virus or caused by primary infection is also an area of contention; both may occur.

Proposed pathogenic mechanisms include reactivation of latent HSV in the trigeminal ganglia with subsequent spread of infection to the temporal and frontal lobes, primary CNS infection, or perhaps reactivation of latent virus within the brain parenchyma itself [ 1721 — 23 ].

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In at least half of HSVE cases, the viral strain responsible for encephalitis is different from the strain that causes herpetic skin lesions in the same patient, an observation that suggests the possibility of primary CNS infection [ 24 ]. Infection with HSV triggers a robust response from the innate immune system until adaptive immunity is able to assist in clearing active infection.

Early in the course of the immune response to HSV, pattern recognition receptors, called Toll-like receptors TLRslocated on cells of the innate immune system, recognize and bind to conserved viral motifs known as pathogen associated molecular patterns [ 25 ].

This triggers dimerization of the TLRs, which subsequently activates signaling pathways that initiate the production of proinflammatory cytokines such as interferons IFNstumor necrosis factor, and various interleukins [ 26 ]. IFNs contribute to host resistance to viral proliferation through activation of the Jak-Stat signaling pathway [ 27 ], and by triggering production of both RNAse enzymes that destroy cellular RNA both host and viral and double-stranded RNA-dependent protein kinase, which halts cellular translation [ 28 ].

Deficiencies in the immune response to HSV e. The inflammatory cascade recruits innate immune cells and primes adaptive immunity, which can lead to necrosis and apoptosis of infected cells. While the host immune response is critical to eventual viral control, the inflammatory response, particularly recruitment of activated leukocytes, may contribute to tissue destruction and consequent neurologic sequelae [ 3233 ].

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After primary infection, the virus establishes a latent state for the life of the host and remains quiescent unless reactivated [ 34 ]. In order to establish and maintain latency, a number of complex processes must be balanced.

These include silencing of viral lytic-phase genes, abrogation of keratktis cellular defense mechanisms e. During reactivation, the expression of viral genes occurs in a temporally organized fashion, kedatitis reviewed recently [ 38 ].

Once reactivated, the virus can infect neighboring neurons and travel to tissues innervated by the infected dorsal root ganglia to cause recurrent disease and shed infectious viral particles that can be transmitted to others. Akep only rarely manifesting as encephalitis in infected individuals, HSV-1 is consistently the single most common cause of sporadic encephalitis worldwide [ 42 — 52 ].

Encephalitis must be distinguished from encephalopathy, a broader term that refers to a clinical state of disorientation, confusion, behavioral, and other cognitive changes that can occur in the setting of encephalitis, as well as numerous other noninflammatory conditions. Many patients present with prodromal symptoms, suggesting upper respiratory tract or other systemic infection. keratiits

Herpes Simpleks Keratitis

Signs and symptoms of encephalitis asiep progress over the course of several days in most cases of HSVE [ 5758 ]. The most common manifestations include encephalopathy, fever, seizures, headaches, and focal neurological deficits kerattiis 57 — 62 ].

Although clinical features of HSVE have been well described in multiple large epidemiological studies, the clinical manifestations lack specificity. Immunocompromised patients present a greater diagnostic challenge.

In the largest series to date, Tan et al. In that study, immunocompromised patients were less likely to present with prodromal symptoms or with focal neurologic deficits.

They had more extensive brain involvement that was more often distributed outside the temporal lobes and it was not uncommon to observe a lack of pleocytosis in the CSF. Morbidity and mortality were significantly higher in the immunocompromised group, with In the setting of suspected encephalitis, the value of a thorough history and physical examination cannot be overstated, and a thoughtful approach is critical to narrowing the differential.

Weight loss and infectious symptoms, including low-grade fever, rash, and so on, and neurologic or psychiatric abnormalities such as aphasia, behavioral changes and seizure-like activity should also be reviewed. Full neurologic and general medical examinations are critical and may uncover clues to the diagnosis. Patterns of neurologic dysfunction may help to suggest an etiology, for example cranial neuropathies and autonomic instability may suggest a brainstem encephalitis, which can help to narrow the differential diagnosis [ 65 ].

Aaskep, movement disorders, keeatitis other signs referable to the basal kerqtitis may also assist in guiding the differential [ 65 ]. Differentiating encephalitis from aekep mimics can be especially challenging in the elderly and the immunocompromised.

Focused laboratory testing and prompt neuroimaging assist greatly in the diagnostic approach. Serum laboratory studies that should be obtained on all adults with encephalitis include complete blood count with differential, electrolytes, measures of renal and liver function, blood cultures, HIV testing consider RNAand treponemal testing. HSV serologies are generally not clinically helpful in the acute setting [ 66 ].

In patients at risk for tuberculosis, such as the immunocompromised and homeless individuals, skin or blood testing for Mycobacterium tuberculosis should be considered.

Unless contraindicated see acute complications; edemalumbar puncture should be obtained in all patients with encephalitis, but should not delay the administration of empiric antimicrobials. The opening pressure in HSVE is generally normal or slightly elevated.

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Computed tomographic CT imaging is generally inadequate for the evaluation of encephalitis, but, in practice, is often obtained as the initial neuroimaging study in the encephalopathic patient and may suggest an alternate etiology.

CT findings suggestive of HSVE include hypodense lesions typically in the temporal lobeedema, or contrast enhancement [ 70 — 72 ]. However, CT is unable to differentiate between HSVE and many of its mimics, and lacks sensitivity, particularly early in the course of the illness. MRI with and without contrast is the neuroimaging study of choice in the evaluation of encephalitis and is abnormal in the vast majority of cases of HSVE [ 73 ].

As,ep is the most sensitive and specific imaging method for HSVE, particularly early in the course of the illness [ 74 ]. Typical findings on MRI include asymmetric hyperintense lesions on T2-weighted sequences corresponding to areas of edema in the mesiotemporal and orbitofrontal lobes and the insular cortex [ 75 ].

Accumulating evidence suggests that diffusion restriction on diffusion-weighted imaging DWI is frequently seen early in the course of HSVE and may be among azkep earliest neuroradiologic manifestations [ kegatitis ]. More reports demonstrating improved sensitivity of DWI over fluid-attenuated inversion recovery FLAIR sequences were soon to follow in adults [ 78 ], children [ 79 ], and neonates [ 8081 ].

One report demonstrated correlation between DWI lesions and clinical response to treatment [ 82 ]. FLAIR signal abnormalities appeared more prominent later in the course. Overall, DWI changes in the temporal or frontal lobes in the appropriate clinical setting should be considered a clue to the diagnosis of HSVE. While traditional teaching has emphasized bilateral temporal involvement as characteristic of HSVE, this has not held true in contemporary studies.

On the contrary, a recent study of cases of encephalitis with temporal lobe abnormalities found that bilateral temporal lobe involvement was associated with lower odds of HSVE compared with all other etiologies and when directly compared with autoimmune etiologies [ 84 ]. In that study of immune competent adults, patients with HSVE, as compared with other infectious or autoimmune etiologies of their temporal lobe encephalitis, were more likely to be older and oeratitis, and to present acutely and with fever, seizures, and upper respiratory symptoms.

In addition to bilateral temporal lobe involvement, lesions outside the temporal lobe adkep limbic region suggested an alternate diagnosis. In the acute setting, a number of electrographic findings have been associated with HSVE, including periodic discharges, focal or generalized slowing, and electrographic seizures, including status epilepticus SE [ 8586 ]. Seizures and epilepsy in the setting of HSVE have recently been reviewed [ 87 ].

Periodic discharges in HSVE have been observed generally between days 2 and 15 and may manifest before structural lesions can be observed on CT [ 8889 ]. While EEG is recommended as part of the diagnostic evaluation of patients with encephalitis, there are few studies characterizing the contribution of Zskep to diagnosis and prognosis in these patients, particularly in the era of MRI.

Patients with HSVE were significantly more likely to have periodic discharges and focal slowing in the frontotemporal and occipital areas compared with patients with encephalitis of other etiologies, consistent keratltis previous studies [ 9192 ].

InWhitley et al. Among the most common treatable mimics were other infections viral, bacterial, mycobacterial, and fungalmalignancy, vascular disease more often hemorrhagic than thromboticand a few cases of toxic or metabolic disease. No diagnostic studies, alone or in combination, were felt to be sufficiently characteristic to be diagnostically useful. However, even with contemporary diagnostic modalities, the identification of HSVE mimics remains challenging.

Numerous infectious agents and autoimmune syndromes may present similarly to HSVE. There are 3 things to consider. This can lead to insufficient testing i. As noted above, multiple studies have demonstrated that immunocompromised patients are less likely to have CSF pleocytosis [ 6395 — 97 ]. The first priority on presentation is to recognize and treat any emergent issues Fig. This includes rapid evaluation of hemodynamic and respiratory sufficiency, which is particularly important in the setting of decreased level of consciousness.

Rapid evaluation for other potentially reversible causes of encephalopathy such as hypoglycemia, hypercarbia, electrolyte abnormalities, and so on, can readily be performed in the emergency setting, and abnormalities should be treated promptly. After initial stabilization, the patient should be appropriately triaged and may require admission to the intensive care unit ICU [ ]. Decreased level of consciousness, severe comorbidities, and autonomic dysfunction are some of the indications for ICU admission.

Whenever possible, a dedicated neurological ICU is recommended; barring this, admission to a medical ICU or rapid transportation to the closest neurological ICU should be considered.