Hypopyon: Description, Causes and Risk Factors:
The presence of leukocytes in the anterior chamber of the eye.
By the strictest definition, hypopyon is the accumulation of pus resulting from suppurative infection inferiorly in the anterior chamber. However, hypopyon may be neither caused by infection nor lie at 6 o'clock in the anterior chamber. Firstly, it caused by inflammatory mechanisms does not contain microorganisms. If hypopyon is due to ocular tumors, it consists largely of neoplastic cells, in which case the term pseudohypopyon is often used. However, in the clinical setting, the appearances are identical and therefore pseudohypopyon will be discussed with it. Secondly, hypopyon collects at the dependent part of the anterior chamber, so after a shift in posture it may either be dispersed or in a different orientation. The speed with which it settles again will vary according to the content of the material. Finally, macrohypopyon refers to hypopyon visible to the naked eye, whereas micro refers to hypopyon visible only microscopically. Angle hypopyon is a subcategory of microhypopyon visible in the dependent anterior chamber angle only on gonioscopy. The prevalence of hypopyon may, therefore, vary among clinical series if the stringency of diagnostic criteria for this clinical sign differ.
There is no single unifying process by which it forms. Initiating factors include infection, cellular immune reactions influenced by patterns of HLA (human leukocyte antigen) expression, and trauma. Exposure to gram-negative organisms has been implicated as a causative factor in some HLA-B27 patients with uveitis, so it is possible that hypopyon associated with infection and uveitis share the same trigger.
In all cases, the development of hypopyon depends upon the strength of local chemotaxic and activating stimuli and the degree of tissue destruction engendered by the inflammatory process concerned. Chemotaxins are derived from bacterial material, injured tissue, plasma (e.g., complement system) and PMNs. Of the leukotrienes, LTB4 is the most important PMN-chemotaxin, and it is responsible for the arrival of large numbers of PMNs. Local vascular damage and the vasodilatory influence of bradykinin—which is derived from plasma by the action of kallikrein and histamine from platelets, basophils, and mast cells — allows exudation of PNMs, necrotic debris, and inflammatory mediators into the anterior chamber from iris vessels.
In infective hypopyon the alternative complement pathway is a ubiquitous first line of defense against microbes. It is activated by bacterial endotoxin, or polysaccharide, or by PMN (polymorphonuclear) lysosomal enzymes. C3a, C5a, and the activated complex of C5, C6, and C7 are strongly chemotactic for PMNs. C8 and C9 lyse cells and bacterial membranes. Activation of PMNs in infectious disease aids phagocytic clearance of microbes. PMNs frequently appear degenerate because they turn over very quickly anyway and are also killed by exotoxins released by certain bacteria. However, PMNs are also activated in hypopyon-iridocyclitis. Anterior chamber cells from a patient with hypopyon uveitis associated with psoriasis and arthropathy were found to be activated, as judged by their ability to pass through a micropore filter compared to healthy controls. They may, therefore, be instrumental in disease activations when they show greater adhesiveness, aggregation, and deformation. Anterior chamber PMNs with late arrival of lymphocytes is also an observed characteristic of Behcet's disease.
HLA-B27-associated disease is a common cause of hypopyon. The x-ray crystallographic structure of the HLA-B27 molecule has been described. It may be possible to block the antigen-binding cleft on the molecule and thereby prevent T cell activation. Differences on the humoral arm of the immune system have also been found: raised levels of serum IgA is significantly more common in HLA-B27-positive of uveitis patients (p < 0.001) than in patients with idiopathic uveitis. With further work it will be possible to better understand the pathogenic mechanisms behind these and other uveitic phenotypes.
Pain, redness and drop of vision.
The differential diagnosis of hypopyon in the context of raised intraocular pressure includes phacolytic glaucoma, response to laser iridotomy or angleclosure glaucoma, and finally, endophthalmitisfrom a leaking filter bleb.
Endophthalmitis is the first diagnostic consideration in hypopyon following recent penetratingtrauma or surgery such as complicated cataract surgery or glaucoma surgery. In full-blown cases, theclinical picture is clearer, but it is still essential to attempt to confirm microbiological organisms by anterior chamber and vitreous tap. In lessclear-cut cases, other noninfectious causes should beconsidered. Where hypopyon clears withcorticosteroid therapy and residual chronic inflammation remains, the decision to treat conservativelyis guided by the absence of visual deterioration, discomfort, cystoid macular edema, and the absence ofa posterior capsular plaque.
Most patients with hypopyon and isolated is anterior uveitis will have HLA-B27 disease, but, rarely herpetic disease may be responsible. Posterior uveitis must be differentiated from endogenous endophthalmitis and masquerade syndromes by careful systemic history, examination, and microbiological/cytological sampling, where necessary.
Hypopyon associated with corneal disease is typically heaped up centrally and triangular in shape rather than flat. These cases should usually be investigated and treated as infectious hypopyon keratitis, although the clinician must be aware that (rarely) noninfectious causes, such as recurrent erosion syndrome, can produce similar clinical pictures. If there is a history of trauma with organic matter or ocular surface disease, then the ophthalmologist should consider the possibility of penetrating corneal keratitis/endophthalmitis due to filamentous fungi and yeasts, respectively.
In treating hypopyon, the bottom line would be to treat its cause. For example if it is due to tuberculosis, the treatment should be aimed at eliminating the pathogen causing the tuberculosis. The hypopyon itself would not require any treatment and will settle itself. If the underlying condition is not treated, the hypopyon can lead to cataract formation, visual impairment, glaucoma and even retinal detachment.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.