**2. Predisposing factors**

Ocular allergy is frequently associated with keratoconus ranging from 7 to 35% [6–9]. Bawazeer et al. in a case control study demonstrated a positive correlation between keratoconus and atopy [10]. Any form of ocular allergy instigates itching, foreign body sensation, and eye rubbing [11]. This triggers a corneal intrastromal inflammation because of the increased levels of histamine, tumor necrosis factor-alpha, and interleukins [12]. It coaxes to stromal lysis and corneal thinning because of the increased levels of lysosomal and proteolytic enzymes with a simultaneous reduction in the levels of protease inhibitors [12]. This vicious cycle of inflammation and stromal lysis is exacerbated by recurrent eye rubbing [13], and the stable keratoconus eventually becomes progressive which increases the risk of acute hydrops [14].

A history of having worn the contact lenses, specially the rigid gas permeable lens, is also considered an important risk factor for acute hydrops [15]. Contact lens usage triggers ocular inflammation because of hypoxia of the corneal surface [16]. A study showed that the level of inflammatory markers present in the tear film increases after the use of contact lens [17]. This inflammation initiates the progression of keratoconus that eventually leads to acute hydrops [18].

A trivial ocular trauma plays a significant role in the rupturing of already stressed-out descemet membrane (DM) [19]. Advanced keratoconus, eccentric cone, and poor visual acuity are other important risk factors for acute hydrops in patients with keratoconus. Down syndrome increases the risk of keratoconus progression, thereby increasing the risk of acute hydrops [20]. Retinitis pigmentosa, Leber Congenital Amaurosis (LCA), floppy eye lid syndrome, and Ehler-Danlos syndrome are other risk factors for progressive keratoconus, which are followed by the incident of hydrops [21–24]. Pregnancy and lactation are also the critical but temporary risk factors [25]. However, a positive family history has been reported to have a negative correlation with the acute hydrops incidence [26].

## **3. Corneal topography and acute hydrops**

Corneal topography plays a critical role in identifying patients with keratoconus progression [27]. Various parameters are available in pentacam that must be reinvestigated after every 3 month to accurately diagnose the progression; parameters, namely, maximum keratometry, minimum pachymetry, pachymetric progression index, elevation indices of corneal front and back surfaces, anterior radius of curvature taken 3 mm surrounding the thinnest pachymetry, posterior radius of curvature taken 3 mm surrounding the thinnest pachymetry, and deviation index, must be scrutinized during every visit. Any evidence of progression should be intervened to prevent or halt the deterioration to eventually decrease the risk of acute hydrops incidence [28].

#### **4. Pathophysiology**

The progression of keratoconus initiates because of stretching of the DM that is adhered strongly to the periphery, which leads to circumferential stretching of the membrane and increased risk of its rupture [29, 30]. If the stretching extends beyond a limit, the membrane tends to rupture at the center, which leads to the seepage of aqueous fluid into the stroma and thereby causes acute hydrops [31].

**3**

*Acute Hydrops and Its Management*

**Figure 1.**

*Showing a case of acute hydrops.*

*DOI: http://dx.doi.org/10.5772/intechopen.94592*

**5. Clinical examination and manifestations**

should also be documented (**Figure 1**) [38].

**6. Grading of acute hydrops**

anterior segment is clearly visible through the clear cornea [35].

due to the blockage of light rays by the edematous cornea [39, 40].

Acute hydrops initiates with a sudden onset of poor vision and discoloration of the cornea [32]. The disease is confined to the central and paracentral regions and rarely manifests in the peripheral region in case of coexistent pellucid marginal degeneration [33]. In addition to a defective vision, pain and redness are the typical symptoms of this disease [34]. The patients exhibit a definite history of persisting poor vision since childhood and experience progressive vision loss [35]. History of spectacle use should be investigated by reviewing the old optical prescriptions or old spectacles. Past history of high astigmatism, oblique axis and poor best corrected visual acuity are considered as corroborative clinical signs of acute hydrops following progressive keratoconus. Meticulous medical history of ocular allergy, atopic dermatitis, contact lens usage, eye rubbing, and ocular trauma should be documented [36]. Contact lens history, with emphasis on the type, duration of usage, overnight usage while sleeping, and expiry date of the contact lens, is also considered essential [37]. Ocular trauma history, with emphasis on the blunt trauma not withstanding its impact or severity,

Examination using a diffused torchlight reveals a whitish lesion over the central or paracentral regions with intense photophobia (**Figure 1**). Conjunctiva shows a sign of circumciliary congestion, and palpebral conjunctiva may be congested depending upon the presence of allergic conjunctivitis. In the absence of oculi allergy, eyes are less susceptible to palpebral congestion. The iris or anterior segment is not visible in case of central hydrops but in cases of paracentral hydrops, the

Slit lamp examination with an oblique slit shows an abnormally thick cornea with clefts in the intrastromal area and Obscuration of Descemet Membrane (DM)

Acute hydrops can be graded depending on the corneal region involved. Corneal

edema can be graded by drawing an imaginary circle around the cornea [41].

*Eyesight and Imaging - Advances and New Perspectives*

Ocular allergy is frequently associated with keratoconus ranging from 7 to 35% [6–9]. Bawazeer et al. in a case control study demonstrated a positive correlation between keratoconus and atopy [10]. Any form of ocular allergy instigates itching, foreign body sensation, and eye rubbing [11]. This triggers a corneal intrastromal inflammation because of the increased levels of histamine, tumor necrosis factor-alpha, and interleukins [12]. It coaxes to stromal lysis and corneal thinning because of the increased levels of lysosomal and proteolytic enzymes with a simultaneous reduction in the levels of protease inhibitors [12]. This vicious cycle of inflammation and stromal lysis is exacerbated by recurrent eye rubbing [13], and the stable keratoconus eventually becomes progressive which increases the

A history of having worn the contact lenses, specially the rigid gas permeable lens, is also considered an important risk factor for acute hydrops [15]. Contact lens usage triggers ocular inflammation because of hypoxia of the corneal surface [16]. A study showed that the level of inflammatory markers present in the tear film increases after the use of contact lens [17]. This inflammation initiates the progres-

A trivial ocular trauma plays a significant role in the rupturing of already stressed-out descemet membrane (DM) [19]. Advanced keratoconus, eccentric cone, and poor visual acuity are other important risk factors for acute hydrops in patients with keratoconus. Down syndrome increases the risk of keratoconus progression, thereby increasing the risk of acute hydrops [20]. Retinitis pigmentosa, Leber Congenital Amaurosis (LCA), floppy eye lid syndrome, and Ehler-Danlos syndrome are other risk factors for progressive keratoconus, which are followed by the incident of hydrops [21–24]. Pregnancy and lactation are also the critical but temporary risk factors [25]. However, a positive family history has been reported to have a negative correlation with the acute hydrops

Corneal topography plays a critical role in identifying patients with keratoconus progression [27]. Various parameters are available in pentacam that must be reinvestigated after every 3 month to accurately diagnose the progression; parameters, namely, maximum keratometry, minimum pachymetry, pachymetric progression index, elevation indices of corneal front and back surfaces, anterior radius of curvature taken 3 mm surrounding the thinnest pachymetry, posterior radius of curvature taken 3 mm surrounding the thinnest pachymetry, and deviation index, must be scrutinized during every visit. Any evidence of progression should be intervened to prevent or halt the

The progression of keratoconus initiates because of stretching of the DM that is adhered strongly to the periphery, which leads to circumferential stretching of the membrane and increased risk of its rupture [29, 30]. If the stretching extends beyond a limit, the membrane tends to rupture at the center, which leads to the seepage of aqueous fluid into the stroma and thereby causes acute hydrops [31].

deterioration to eventually decrease the risk of acute hydrops incidence [28].

sion of keratoconus that eventually leads to acute hydrops [18].

**3. Corneal topography and acute hydrops**

**2. Predisposing factors**

risk of acute hydrops [14].

incidence [26].

**4. Pathophysiology**

**2**

**Figure 1.** *Showing a case of acute hydrops.*
