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Edema comeal

Hydroxychloroquine administration may result in irritability, nervousness, anorexia, nausea, vomiting, and diarrhea This drug also may have adverse effects on the eye, including blurred vision, comeal edema, halos around lights, and retinal damage. Hematologic effects, such as aplastic anemia and leukopenia, may also be seen. [Pg.193]

The drug may cause burning in the eye, ptosis (drooping of tiie upper eyelid), lid edema, itching, comeal edema, browache photophobia, dryness of the eye, tearing, and blurring of vision. [Pg.626]

Stroke patients who require mechanical ventilation are not necessarily destined for a poor outcome. In a study by Santoli et al., 58 patients underwent mechanical ventilation and 16 survived. Eleven achieved a Barthel Index (BI) score of 60, indicating a good outcome. Within this study population, those patients with bilaterally absent comeal and pupillary reflexes had uniformly poor outcomes, underscoring the need for careful assessment of brainstem reflexes in intubated stroke patients. Other factors that have been associated with poor outcome in intubated stroke patients are advanced age and lower Glasgow Coma Score (GCS) at the time of intubation, as well as seizures and pulmonary edema. ... [Pg.164]

Idoxuridine may cause local irritation, mild edema, itching, and photophobia. Comeal clouding and small punctate defects in the corneal epithelium have been reported. Allergic reactions are rare. [Pg.574]

Its action on the comeal transparency only visible in case of pathology, the part played by the intraocular pressure is to be considered separately. Indeed, the big increase of the intraocular pressure may cause a stromal edema and this might happen after a chemical eye bum with lesion at the level of the trabeculum. [Pg.57]

The penetration into the tissue follows the initial breakdown of the epithelial barrier. This results in an immediate and strong edema of the conjunctiva, known as chemosis, due to a water influx from the surrounding tissue, vascular leakage, tears, and applied fluids. The cornea itself loads up with ions to a measured osmolarity of 1,830 mOsmol/kg after a 1 mol NaOH bum for 30 s [24]. The penetration of strong alkali has been systematically tested on sodium hydroxide by means of evaluation of the anterior chamber pH. This pH change typically occurs within 2 min after exposure of the comeal surface. The change of the cornea... [Pg.68]

There are several most interesting observations concerning osmolarity. We have found that there is an important difference of osmolarity between the hyperosmolar stroma with 420 mOsmol/kg and the extra and intraocular fluids with lower osmolarities of about 320 mOsmol/kg. This results in an inversion of the water flux, when barriers like endothelium and epithelium are damaged. The immediate result of any membrane damage is that water starts to flow from the outside into the comeal stroma. This results in a corneal edema with turbidity. This is an indirect proof of the pumping function of the endothelium. [Pg.79]

We have observed the following pattern (Fig. 6.2) of decrease of the tissne osmolarity after eye bnms within the comeal stroma. This confirms the chnical finding of severe edema of the stroma and was snstained by work of Kompa et al. [8], who have found the alteration of the comeal sweUing and comeal osmolarity by the eye bnm itself and changes due to different fluids used for rinsing of the cornea thereafter. [Pg.79]

The edema of the cornea is the diminution or even the complete loss of the comeal transparency (Fig. 7.9). [Pg.96]

At such a step and every 48 h, there must be a thorough clinical examination of the comeal edema, because it is certainly a cause of the noncicatrization of the cornea. A good illustration of this phenomenon is the image of a roof collapsing because it is supported by a too weak stmcture. The epithelial... [Pg.99]

Persistent comeal edema, limiting the visual acuity and mainly reserving the long-term functional, even anatomical, prognosis of this burned eye... [Pg.101]

Bums can cause an edema due to a toxic necrosis of the endothelial cells, an opacification of the comeal stroma, and a thinning of the stroma, which generates an important irregular astigmatism. The aim of the TK is to restore the comeal transparency. [Pg.107]

Retinotoxic effects associated with iontophoresis have been evaluated by slit lamp microscopy, indirect ophthalmoscopy, light and electron microscopy. Commonly reported toxic effects include slight retinal and choroidal bums and retinal pigment epithelial and choroidal necrosis, comeal epithelial edema, persistent corneal opacities and polymorphonuclear cell infiltration. Disadvantages of iontophoresis include side-effects such as itching, erythema and general irritation. Although the technique is found to be suitable for a... [Pg.317]

Chicken 12 Inhalation 1,000 2 wk At 3 d, animals had photophobia and nasal secretion. At 8 d, comeal opacity evident. Pathologic examination at 2 wk revealed pulmonary congestion, edema, hemorrhage congestion of liver and spleen. LOAEL 1,000 Anderson et al. 1964... [Pg.72]

Vapor contact with the conjimctiva may be the victim s first symptom. Severe eonjimctival irritation and blepharospasm result upon eye contact leading to loosening of comeal epithelial cells and swelling and edema of the cornea. [Pg.114]

In addition to opacification, additional comeal effects from particulate CN exposure include possible penetration of the comeal stroma, severe scarring and ulceration, and deficits in the comeal reflex (Blain, 2003 Scott, 1995). Penetration of the comeal stroma may lead to stromal edema and later vascularization, resulting in further ocular complications. These may include pseudopterygium, infective keratitis, symblepharon, trophic keratopathy, cataracts. [Pg.163]

Capsaicin causes conjunctivitis, periorbital edema/ erythema, ophthalmodynia, blepharospasm, blepharitis, corneal abrasions, and lacrimation. In a retrospective study of 81 patients who presented to the emergency department following aerosol exposure from law enforcement use of OC, 56% of individuals developed ophthalmodynia, 44% conjunctivitis, 40% conjunctival erythema, 13% lacrimation, and 9% comeal abrasions (Watson et al, 1996). Another study involved exposure of 47 human volunteers to OC for evaluating effects on the cornea and conjunctivae (Zolhnan et al, 2000). All subjects reported significant eye pain, blurred vision, and lacrimation 10 min after exposure to OC pepper spray, but symptoms improved by 1 h later. Comeal abrasions were not apparent, but 21% of subjects showed evidence of punctate epithelial erosions and reduced comeal sensitivity. Comeal abnormalities were absent 1 week after exposure. Another human study identified 23% of subjects (7 of 30) with comeal abrasions following aerosol exposure to OC spray (Watson et al, 1996). In mice, a single subcutaneous injection of 12.5, 25,... [Pg.164]

The toxieity of both neat and vapor exposures of SM to the eye is highly predictable. After a time period of no symptoms, laerimation begins and quickly progresses to eonjunetivitis, pain, blepharospasm, and photophobia. Comeal edema follows rapidly as a result of the loss of the epithelium, whieh allows water to enter the stroma from the preeomeal tear film (Slatter, 1990). By 24 h after exposure, it is not unusual to see a 100 to 300% increase in comeal thiekness evident by a substantial increase in opacification. Fluorescein staining at 24 h will reveal ulcers that may eover a majority of the eomeal surface. By 48 h, evidence of healing is seen, and by 96 h, it is not imusual to have... [Pg.580]

Once the toxic effects of SM have resulted in epithelial loss, the progression of comeal edema is rapid and persistent for weeks. As noted in Table 39.2, 1 week after exposure to a 0.8 p.1 (1 mg) challenge, the average thickness of the rabbit corneas increased almost 2.5 times and remained at more than twice the thickness of the control contralateral naive eye for more than 5 weeks. By 6 weeks, although not as thick, most of the exposed corneas were still above the baseline thickness values of a typical cornea (Babin et al, 2004)... [Pg.580]

Ocular absorption happens within minutes. With mild ocular exposures, conjunctivitis and lacrimation begin about 4 to 12 h after exposure. Moderate ocular exposures produce conjunctivitis, blepharospasm, lid inflammation, comeal damage, and eyelid edema about 3 to 6 h post-exposure. Severe ocular exposures will lead to marked swelling of lids, comeal ulceration, comeal opacification, severe pain, and miosis in 1 to 2 h (Requena et al, 1988). [Pg.724]

Dermal, ocular, and respiratory lesions are similar to those caused by mustard gas. Inhalation and oral absorption may cause respiratory tract irritation, dyspnea, and pulmonary edema. Dermal lesions are erythematous and extremely painftil. With ocular exposure to phosgene oxime, very low concentrations can cause lacrimation, inflammation, and temporary blindness, while high concentrations can cause permanent comeal lesions and blindness (Sidell et al, 1997 NATO, 1996 USACHPPM, 2001c). Death is generally due to respiratory arrest. [Pg.726]

The objective for any ophthalmology consultation on pediatric HD injuries involving the eye is prevention of scarring and infection (Sidell et al, 1997). Eyes exposed to HD should be irrigated to remove traces of vesicant. Severe ocular involvement requires topical antibiotics (tobramycin OD) applied several times a day. Topical steroids may be useful in the first 48 h after exposure. Temporary loss of vision may also occur after mustard exposure (Sidell et al, 1997 Azizi and Amid, 1990 Motakallem, 1988). The patient should be reassured that vision loss is not permanent and is due to palpebral edema and not comeal damage. [Pg.938]

Various agents can reduce comeal edema, including corn symp, glucose, gum cellulose, sodium chloride, and glycerin. Only a few of these have proved clinically useftil and acceptable to most patients. Sodium chloride and glycerin (Table 15-1) are the preferred agents in clinical practice. [Pg.279]

Luxenberg MN, Green K. Reduction of comeal edema with topical hypertonic agents.AmJ Ophthalmol 1971 71 847-853 Mishima S, Hedbys BO. Physiology of the cornea, hit Ophthalmol Clin 1968 8 527-560. [Pg.282]

Payrau P, Dohhnan CH. Medical treatment of comeal edema. Int Ophthalmol Clin 1968 8 601-610. [Pg.282]


See other pages where Edema comeal is mentioned: [Pg.804]    [Pg.804]    [Pg.100]    [Pg.242]    [Pg.1178]    [Pg.68]    [Pg.79]    [Pg.82]    [Pg.101]    [Pg.242]    [Pg.408]    [Pg.408]    [Pg.211]    [Pg.255]    [Pg.161]    [Pg.163]    [Pg.163]    [Pg.168]    [Pg.575]    [Pg.577]    [Pg.577]    [Pg.579]    [Pg.588]    [Pg.588]    [Pg.732]    [Pg.905]    [Pg.165]   
See also in sourсe #XX -- [ Pg.1114 ]




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