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Medicina Oral, Patologia Oral Y Cirugia... Sep 2007A cerebrospinal fluid (CSF) rhinorrhoea occurs when there is a fistula between the dura and the skull base and discharge of CSF from the nose. CSF rhinorrhea or... (Review)
Review
A cerebrospinal fluid (CSF) rhinorrhoea occurs when there is a fistula between the dura and the skull base and discharge of CSF from the nose. CSF rhinorrhea or liquorrhoea commonly occurs following head trauma (fronto-basal skull fractures), as a result of intracranial surgery, or destruction lesions. A spinal fluid leak from the intracranial space to the nasal respiratory tract is potentially very serious because of the risk of an ascending infection which could produce fulminant meningitis. This article reviewed the causes, diagnosis and treatment of CSF leakage. A PUBMED search of the National Library of Medicine was conducted. CSF leak most commonly occurs following trauma and the majority of cases presenting within the first three months. CSF rhinorrhoea have significantly greater incidence of periorbital haematoma. This suggests that patients with head injuries and features of periorbital haematoma are at greater risk of unobserved dural tear and delayed CSF leakage. In the presence of a skull base fracture on computed tomography and a clinical CSF leak, there is no need for a further confirmatory test. In cases where a confirmatory test is needed, the beta-2 transferrin assay is the test of choice because of its high sensitivity and specificity. A greater proportion of the CSF leaks in the patients resolved spontaneously. CSF fistulae persisting for > 7 days had a significantly increased risk of developing meningitis. Treatment decisions should be dictated by the severity of neurological decline during the emergency period and the presence/absence of associated intracranial lesions. The timing for surgery and CSF drainage procedures must be decided with great care and with a clear strategy.
Topics: Cerebrospinal Fluid Rhinorrhea; Humans
PubMed: 17767107
DOI: No ID Found -
Diagnostics (Basel, Switzerland) Feb 2021Systemic dehydration due to inadequate water intake or excessive water loss, is common in the elderly and results in a high morbidity and significant mortality.... (Review)
Review
Systemic dehydration due to inadequate water intake or excessive water loss, is common in the elderly and results in a high morbidity and significant mortality. Diagnosis is often overlooked and there is a need for a simple, bedside diagnostic test in at-risk populations. Body hydration is highly regulated with plasma osmolality (pOsm) being tightly controlled over a wide range of physiological conditions. By contrast, normal tear osmolarity (tOsm) is more variable since the tear film is exposed to evaporation from the open eye. While plasma hyperosmolality is a diagnostic feature of systemic dehydration, tear hyperosmolality, with other clinical features, is diagnostic of dry eye. Studies in young adults subjected to exercise and water-deprivation, have shown that tOsm may provide an index of pOsm, with the inference that it may provide a simple measure to diagnose systemic dehydration. However, since the prevalence of both dry eye and systemic dehydration increases with age, the finding of a raised tOsm in the elderly could imply the presence of either condition. This diagnostic difficulty can be overcome by measuring tear osmolality after a period of evaporative suppression (e.g., a 45 min period of lid closure) which drives tOsm osmolality down to a basal level, close to that of the pOsm. The arguments supporting the use of this basal tear osmolarity (BTO) in the diagnosis of systemic dehydration are reviewed here. Further studies are needed to confirm that the BTO can act as a surrogate for pOsm in both normally hydrated subjects and in patients with systemic dehydration and to determine the minimum period of lid closure required for a simple, "point-of-care" test.
PubMed: 33668748
DOI: 10.3390/diagnostics11030387 -
Frontiers in Pharmacology 2021Corneal neuropathic pain can be difficult to treat, particularly due to its lack of response to standard dry eye therapies. We describe a variety of topical therapeutic... (Review)
Review
Corneal neuropathic pain can be difficult to treat, particularly due to its lack of response to standard dry eye therapies. We describe a variety of topical therapeutic options that are available to treat corneal neuropathic pain with a significant or primary peripheral component. We also describe possible mechanisms of action for such topical therapies. Topical corticosteroids and blood-derived tear preparations can be helpful. Newer therapies, including topical lacosamide and low-dose naltrexone are emerging therapeutic options that may also be considered. Corneal neuropathic pain with a significant peripheral component may be managed with a variety of topical therapeutic options.
PubMed: 35173607
DOI: 10.3389/fphar.2021.769909 -
The Ocular Surface Jul 2017Pain associated with mechanical, chemical, and thermal heat stimulation of the ocular surface is mediated by trigeminal ganglion neurons, while cold thermoreceptors... (Review)
Review
Pain associated with mechanical, chemical, and thermal heat stimulation of the ocular surface is mediated by trigeminal ganglion neurons, while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of meibomian gland secretion or mucin release have not been identified. In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with in vivo confocal microscopy.
Topics: Animals; Cornea; Dry Eye Syndromes; Nociceptors; Pain; Sensation; Thermoreceptors
PubMed: 28736339
DOI: 10.1016/j.jtos.2017.05.002 -
Experimental Eye Research Dec 2013Tear proteins are potential biomarkers, drug targets, and even biotherapeutics. As a biotherapeutic, a recombinant tear protein might physiologically rescue the ocular... (Review)
Review
Tear proteins are potential biomarkers, drug targets, and even biotherapeutics. As a biotherapeutic, a recombinant tear protein might physiologically rescue the ocular surface when a deficiency is detected. Such a strategy pays more attention to the natural prosecretory and protective properties of the tear film and seeks to alleviate symptoms by addressing cause, rather than the current palliative, non-specific and temporary approaches. Only a handful of tear proteins appear to be selectively downregulated in dry eye, the most common eye disease. Lacritin and lipocalin-1 are two tear proteins selectively deficient in dry eye. Both proteins influence ocular surface health. Lacritin is a prosecretory mitogen that promotes basal tearing when applied topically. Levels of active monomeric lacritin are negatively regulated by tear tissue transglutaminase, whose expression is elevated in dry eye with ocular surface inflammation. Lipocalin-1 is the master lipid sponge of the ocular surface, without which residual lipids could interfere with epithelial wetting. It also is a carrier for vitamins and steroid hormones, and is a key endonuclease. Accumulation of DNA in tears is thought to be proinflammatory. Functions of these and other tear proteins may be influenced by protein-protein interactions. Here we discuss new advances in lacritin biology and provide an overview on lipocalin-1, and newly identified members of the tear proteome.
Topics: Dry Eye Syndromes; Eye Proteins; Glycoproteins; Humans; Lipocalin 1; Proteome
PubMed: 23769845
DOI: 10.1016/j.exer.2013.05.020 -
Scientific Reports Jul 2022The purpose of this study was to evaluate any alterations in the tear film and ocular surface beyond the early postoperative period following penetrating keratoplasty...
The purpose of this study was to evaluate any alterations in the tear film and ocular surface beyond the early postoperative period following penetrating keratoplasty (PK) and deep anterior lamellar keratoplasty (DALK). This cross-sectional, contralateral-eye study compared ocular surface and tear film parameters of eyes with a previous PK or DALK in one eye and no prior surgery in the contralateral eye. Overall, 14 (87.5%) participants underwent PK, and 2 (12.5%) underwent DALK using a mechanical dissection. The median time from surgery was 3.4 years (range 1.5 to 38.7 years). The indication for unilateral keratoplasty was keratoconus in 15 (94%) participants, and corneal scarring in 1 (6%) eye, secondary to microbial keratitis. Operated eyes exhibited poorer non-invasive tear film breakup time, lower corneal sensitivity, lower sub-basal nerve density and more severe fluorescein staining scores than unoperated fellow eyes (all Q < 0.05). There were no significant differences in tear film lipid layer quality, tear meniscus height, conjunctival hyperaemia, lissamine green staining score, or meibography grade between operated and fellow eyes (all Q ≥ 0.20). Higher corneal esthesiometry threshold (lower corneal sensitivity) was correlated with shorter non-invasive tear film breakup time (Spearman's rho = - 0.361, p = 0.04) and increased fluorescein staining score (Spearman's rho = 0.417, p = 0.02). Keratoplasty can induce persistent changes in the ocular surface and tear film, including: increased fluorescein staining, decreased tear film breakup time, decreased corneal sub-basal nerve plexus density, and reduced corneal sensitivity.
Topics: Corneal Transplantation; Cross-Sectional Studies; Fluoresceins; Humans; Keratoplasty, Penetrating; Tears
PubMed: 35835841
DOI: 10.1038/s41598-022-16191-6 -
Acta Ophthalmologica Mar 2014To perform a comprehensive evaluation and comparison of tear function in diabetic and non-diabetic patients. Research related to tear function in diabetic and... (Meta-Analysis)
Meta-Analysis Review
To perform a comprehensive evaluation and comparison of tear function in diabetic and non-diabetic patients. Research related to tear function in diabetic and non-diabetic patients was gathered using PubMed, EBSCO, OVID. Two reviewers independently conducted the literature search. The quality assessment and the data extraction were performed in accordance with exclusion criteria and cross-checking. RevMan 5.1.7 software was used for the meta-analysis. The tear film break-up time was studied in eight articles with a total of 1449 samples. Through a random-effects model analysis, the combined weighted mean difference (WMD) was -4.44 [-5.87, -3.01]. The time in diabetic patients was shorter than that in the non-diabetic group (p < 0.00001). The basal tear secretion test was studied in seven articles with a total of 949 samples. The combined WMD was -3.96 [-5.70, -2.23], and the difference between the diabetic group and control group was statistically significant (p < 0.00001). The total tear secretion test was studied in five articles with a total of 921 samples. The combined WMD was -3.96 [-7.43, -0.50]. The difference between the diabetic and control groups was statistically significant (p = 0.03). The corneal sensitivity was compared in eight studies with a total of 976 samples. Through a random-effects model analysis, the standardized mean difference (SMD) was -5.14 [-6.99, -3.29]. The corneal sensitivity was lower in diabetic patients than the control group (p < 0.00001). Our study suggests that the tear functions are worse in diabetic patients compared with the control group. Moreover, patients with PDR are more predisposed to impaired tear functions.
Topics: Cornea; Diabetes Mellitus; Diabetic Retinopathy; Dry Eye Syndromes; Humans; Tears
PubMed: 23782539
DOI: 10.1111/aos.12063