Enophthalmos Clinical Presentation

Updated: Sep 30, 2014
  • Author: Charles NS Soparkar, MD, PhD; Chief Editor: Hampton Roy, Sr, MD  more...
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Progressive sinking in of one or both eyes over any time frame (ranging from minutes to years) may be noted in the history of patients with enophthalmos.



Bilateral enophthalmos may be difficult to determine without radiographic studies or old photographs for comparison, but unilateral enophthalmos is often obvious when comparing one eye with the other. Specific changes include the following:

  • Narrowed vertical eyelid fissure (vertical fissure may be widened or normal if associated with downward displacement of the eye, also known as hypoglobus or globe ptosis)
  • Superior sulcus deformity (deepened upper eyelid crease)
  • Lost fullness of fat bulge in upper and lower eyelids
  • Can be associated with hypoglobus (downward displaced eye), usually without significant associated diplopia (double vision) [2]
  • Other physical findings, depending on etiology
    • Skin and eyelids
      • Thinned skin, muscle, fat, or even bone in a linear array may suggest Parry-Romberg syndrome or linear scleroderma.
      • Thickened indurated skin may suggest metastatic scirrhous carcinoma.
      • Blue boggy skin might indicate associated vascular malformation with varix.
    • Fifth nerve function
      • Decreased function of second division may suggest nerve entrapment in fracture.
      • Decreased function of either of the first 2 divisions may suggest tumor infiltration or cavernous sinus involvement.
    • Exophthalmometry measurement: This is important to establish progression or stability.
    • Ocular motility: Dysmotility might suggest a mass (orbital tumor) or restrictive process (fracture).


Causes of secondary enophthalmos include the following:

  • Postnatal, inadequate, orbital cavity development
    • Bone growth arrest (eg, ionizing radiation for retinoblastoma)
    • Inadequate local tissue stimulation of orbital bone growth
      • Intraorbital (eg, phthisis bulbi, anophthalmos, fat atrophy in childhood)
      • Extraorbital (eg, maxillary bone growth problems)
  • Orbital cavity expansion
    • Outward fracture of orbital bones: In order of frequency, fracture sites are as follows: floor, medial wall, lateral wall, and roof.
    • Surgical expansion of the orbit (as in thyroid orbitopathy)
    • Silent sinus syndrome (ie, spontaneous, asymptomatic collapse of the maxillary sinus and orbital floor associated with negative sinus pressures)
    • Orbital varix with presumed slow bone erosion when the varix fills during recumbent position
  • Volumetric loss of orbital contents
    • Orbital fat atrophy
      • Following concussive trauma
      • Following severe inflammation or infection
      • Following external beam irradiation
      • Associated with wasting disorders (eg, Parry-Romberg hemifacial atrophy, linear scleroderma)
    • Contraction of orbital fat - Scirrhous carcinomas (most commonly metastatic breast, but pulmonary, prostate, and GI cancers may cause fat and globe retraction as well) [3]
    • Following surgery (as in resection of a mass lesion associated with local fat atrophy)
    • Phthisis bulbi or prephthisis bulbi
  • Pseudoenophthalmos
    • Unilateral blepharoptosis
    • Horner syndrome
    • Contralateral exophthalmos
    • Contralateral pseudoexophthalmos
    • Contralateral high myopia
    • Contralateral buphthalmos or megaloglobus
    • Contralateral eyelid retraction