The question is on a patient with ocular injury with or without retained foreign body. The answer should cover both immediate management and the after care.

Answer plan:

A detailed history is essential to ascertain the type of foreign body (FB) which may enter the body and for medicolegal purposes. Time of last meal important if surgery needed as GA is preferable. Tetanus status.

Examination:  VA, Siedel's positive?, presence of FB? Cataract? Retinal lesion? Dilate pupil to examine before cataract obscure view but hyphaema may make view difficult. 

Further examination: X-ray and CT scan if retained FB suspected. MRI to be avoided if metallic FB can't be excluded.

Management depends on the findings:

a. if laceration not full thickness, Sidel's negative, no retained intraocular FB (IOFB) and no 
    evidence of sclera laceration. Then bed rest, analgesia dilate pupil, topical antibiotic, 
    monitor intraocular pressure (IOP). Risk of angle recession and traumatic retinal problem check 
    these in the outpatient. Corneal scar may interfere with vision through opacity or irregular 
    astigmatism.
b. if full-thickness laceration and no retained IOFB, suture wound if active leakage with iris 
    prolapse. If leakage slow and no iris prolapse, bandage contact lens may be an option to allow 
    spontaneous healing. The rest of management as in a.
c. if IOFB seen, this need to be removed especially if organic or metallic FB containing iron or 
    copper. If IOFB in the vitreous cavity, vitreoretinal surgery needed to remove the FB. The lens 
    may need to be removed if cataract developed. Risk of
    glaucoma, other retina problem, corneal scar and cataract need follow up.

If iron IOFB suspected in follow-up monitor ERG and repeat CT scan.
Examine fellow eye for signs of sympathetic ophthalmitis in the follow up clinic

Although the most likely diagnosis is thyroid eye disease (TED). The answer should cover the history, differential diagnosis, investigation and management.

Answer plans:

History of the symptoms, any pain, duration, associated medical problems (especially thyroid problem, any radioactive iodine treatment), smoking? (smoker has worse TED), previous cancer, previous head trauma?

Differential diagnosis: VEIN: Vascular problem, Endocrine problem, Inflammation and Infection and Neoplasm.

Ocular examination: Red eye, conjunctival arterialization? VA, lid retraction, amount of proptosis, type of proptosis (does it vary with Valsalva manoeuvre?, reducible with pressure?), corneal changes, IOP in primary and upgaze, colour vision, afferent pupillary defect, optic disc appearance, visual field. Orthoptist assessment for baseline and prescription of prism as necessary.

Physical examination: thyroid status, signs of Grave's disease (thyroid acropachy, pretibial myoxedema), lymphadenopathy? etc.

Investigation (depends on the findings): Blood test for thyroid function test and antibodies. CT or MRI if diagnosis not certain, Chest X-ray for any secondary. If scan suggests space occupying lesion biopsy needed to confirm diagnosis. 

Management depends on the cause: 

• If TED without optic nerve compression, advise to stop smoking and control thyroid function. Monitor eyes for compressive optic neuropathy and proptosis, orthoptist follow up of eye movement. When clinical signs stable, muscle surgery may be needed or orbital wall decompression to reduce unsightly proptosis.
• If TED with signs of optic nerve compression, for immunosuprressant treatment, radiotherapy or orbital wall decrompression depending on the acuteness of the compression.
• If orbital inflammation, investigation for underlying cause and immunosuppressant or radiotherapy may be useful. Physician referral for co-management. 
• If orbital lymphoma or secondary, refer to oncologist for management. Regular follow-up for ocular functions

The answer should include ocular examination including the intraocular pressure check, risk of neovascularization. A brief discussion of the CVOS study may be useful. Physical examination to exclude cardiovascular disease such as hypertension. Blood tests to exclude diabetes mellitus, blood dyscrasia, auto-immune disorders and clotting tendency.

Answer plans:

Investigation: Look for factors that may be treatable and prevent further occurrence in the same or fellow eye. Investigation should begin with the history for any systemic illness such as hypertension, tendency of clotting, skin or joint problem, headache and jaw claudication, then examination including:

In the eyes: examine the eyes for ocular hypertension and signs of inflammation and hyperviscosity syndrome.

Systemic examination: this include systemic hypertension and diabetes mellitus (check BP and fasting blood glucose), blood dyscrasias such as polycythaemia, increased plasma proteins and leukaemia (blood tests for full blood count and serum proteins) and predisposition to clotting (checked protein S and C level). ESR and C reactive protein for any systemic inflammation.  Disorders such as sarcoidosis, SLE and Behcet's disease etc. (CXR, autoantibodies, ACE etc but the investigations should only be carried out based on the history and not blindly as the yield is low in asymptomatic patients). Temporal artery biopsy if history suggestive of giant cell arteritis.

Management:

Important to differentiate ischaemic from non-ischaemic CRVO. Close follow up important as about 1/3 of non-ischaemic CRVO can evolve into ischaemic CRVO.

Distinguishing between the two types of CRVO is clinically important. Eyes with ischaemic CRVO have a poor natural history: 67% will develop ocular neovascularization and 37% will develop neovascular glaucoma.

Pan-photocoagulation should be performed in ischaemic eye or eye with neovascularization (although the CVOS study show that PRP does not prevent iris or angle neovascularization.). Macular oedema is an important of decreased vision in both ischaemic and non-ischaemic CRVO but laser does not improve the vision.

The overall visual prognosis in eyes with CRVO is directly related to baseline visual acuity. After 3 years of follow-up, 65% of eyes with initial visual acuity of 20/40 or better retain their vision, whereas 79% of eyes with initial visual acuity less than 20/200 fail to gain visual improvement. Patients with CRVO also have a 1% annual risk for developing a vascular occlusion in their fellow eye. 

Additonal points:
The Central Vein Occlusion Study (CVOS) reported that panretinal photocoagulation (PRP) in ischemic CRVO does not prevent the development of iris or angle neovascularization. The study recommended that both nonischemic CRVO and ischemic CRVO without anterior segment neovascularization should be managed through careful observation (the former to monitor for progression to ischemic CRVO). These examinations should ideally include gonioscopy in undilated eyes because neovascularization of the angle can precede rubeosis. Once anterior segment neovascularization is detected, PRP should be performed promptly. Focal grid photocoagulation was not effective in improving visual acuity in eyes with macular edema secondary to perfused CRVO.