Visual acuity and intraocular pressure assessments can also yield results that are diagnostic of sickle cell retinopathy. Differential diagnosis
Sickle cell retinopathy should be differentiated from other retinal conditions that arise due to similar pathologies. The following differentials are classified by those pathologies. Additional causes of macular ischemiaDiabetic retinopathy
Retinal embolization (talc retinopathy, internal carotid artery embolism)
Retinal vascular occlusion
Infectious retinopathyInflammatory diseases leading to ischemiaSarcoidosis
Retinal vasculitis
Intermediate uveitis
Acute retinal necrosisAlternative causes of ischemic vascular diseaseProliferative diabetic retinopathy
Central retinal vein occlusion
Branch retinal vein occlusion
Ocular ischemic syndromE
Radiation retinopathy
Retinopathy of prematurityUnclassified causesIncontinentia pigmenti
Autosomal dominant vitreoretinochoroidopathy
Chronic rhegmatogenous retinal detachment
Scleral buckle
Retinitis pigmentosa

Prevention
Screening
Screening is an important pillar of prevention of sickle cell retinopathy as it provides the benefit of early detection and treatment thus reducing complications. Screening also provides an opportunity for education of families predisposed to retinopathy as a result of a family history of sickle cell disease. Screening can take the form of DNA screening at birth and Ophthalmology-related examinations later in life. DNA screening in newborns at risk of having sickle cell disease allows the early diagnosis of the disease. Families can then be educated on the possible effects of sickle cell disease at each stage of life. Ophthalmology-related examinations - dilated fundoscopic examination is recommended from the age of 10 and biannually thereafter in patients with no abnormal retinal findings. Fluorescein angiography and angioscopy is recommended for patients with abnormal findings that may be indicative of proliferative sickle cell retinopathy. The frequency of follow up appointments is determined by the ophthalmologist based on the severity of the findings.
Prevalence in post-menopausal women approaches that of men in the same age range. Women are at greater risk for developing OSA during pregnancy. Medication and lifestyle
Lifestyle factors such as smoking may also increase the chances of developing OSA as the chemical irritants in smoke tend to inflame the soft tissue of the upper airway and promote fluid retention, both of which can result in narrowing of the upper airway. Cigarettes may also have an impact due to a decline of blood nicotine levels, which alters sleep stability. Smokers thus show a higher risk to develop OSA, but the effect of cigarettes on increased OSA is reversible with the cessation of smoking. Children exposed to cigarette smoke may also develop OSA as the lymphadenoid tissue will proliferate excessively in contact with the irritants. An individual may also experience or exacerbate OSA with the consumption of alcohol, sedatives, or any other medication that increases sleepiness as most of these drugs are also muscle relaxants. Allergic rhinitis and asthma have also been shown to be implicated in the increased prevalence of adenotonsillar hypertrophy and OSA. Genetic
OSA also appears to have a genetic component; those with a family history of it are more likely to develop it themselves. Craniofacial syndromes
Of substantial recent interest is the idea that there is a general human tendency towards developing short lower jaws (neoteny) is a major cause of OSA through a combined condition called glossoptosis. The posterior “normal” tongue is displaced backwards by a smaller “abnormal” anterior tongue and lower jaw.