**Background:** Nutritional deficiencies, particularly vitamin deficiencies, can have significant adverse effects on systemic health and lead to end-organ damage if untreated. The eye is especially vulnerable to vitamin deficiencies because vitamins play essential roles in metabolism, cellular integrity, and homeostasis. Ocular manifestations can sometimes be the first presenting signs of a vitamin deficiency, making it crucial for ophthalmologists to understand these associations. This review aims to summarize the key ophthalmic findings associated with deficiencies in vitamins A, B1, B2, B9, B12, C, D, E, and K, covering their functions, epidemiology, ocular manifestations, workup, and management.
**Methods:** This is a comprehensive review of the literature. The authors searched MEDLINE, EMBASE, and Google Scholar using keywords including "vitamin" AND "deficiency OR hypovitaminosis" AND "eye OR ocular" AND "manifestation OR presentation OR disease." Only papers published or available in English were considered. A total of 487 peer-reviewed publications were initially considered; 46 were removed due to lack of access or language, and 159 peer-reviewed publications were ultimately included in the analysis.
**Key Results:** The review details ocular manifestations for each vitamin deficiency:
- **Vitamin A:** Deficiency leads to xerophthalmia, which includes conjunctival and corneal xerosis, Bitot spots, corneal ulceration and scarring, and nyctalopia. The global prevalence of hypovitaminosis A is approximately 30% in children under 5 years, contributing to about 2% of deaths in that demographic. In the US, prevalence is only 0.3%, but it can reach 16% in developing countries with Crohn's disease and 70% in liver cirrhosis. Treatment involves 50,000–200,000 IU of vitamin A (IM or oral) based on age.
- **Vitamin B1 (Thiamine):** Deficiency causes Wernicke's encephalopathy, characterized by nystagmus (found in 97% of patients in one study), ophthalmoplegia, diplopia, and papilledema. A study of 56 cases found 35.7% had nystagmus, 7.1% diplopia, 3.6% blurred vision, and 1.8% decreased visual acuity. Treatment is 200 mg IV or oral thiamine TID until symptoms resolve, then 10 mg daily maintenance.
- **Vitamin B2 (Riboflavin):** Deficiency is associated with blurred vision and nyctalopia. A 2022 study identified retbindin, a retina-specific riboflavin binding protein, linking deficiency to night blindness. Treatment is 5–100 mg oral riboflavin daily.
- **Vitamin B9 (Folate):** Deficiency can cause optic neuropathy and is linked to increased risk of age-related macular degeneration (AMD) and retinoblastoma. An epidemiological study found that those with B9 deficiency (<11 nmol/L) had a 75% and 89% increased risk of early and any AMD over 10 years. Treatment is 1–5 mg oral folic acid daily.
- **Vitamin B12 (Cobalamin):** Deficiency leads to optic neuropathy, increased risk of AMD, and dry eye disease. Prevalence in those over 60 is about 6% in the US and UK, rising to nearly 20% with age. In vegetarians, deficiency can be as high as 45% in infants. Treatment is 1000 µg IM weekly for up to 4 weeks.
- **Vitamin C (Ascorbic Acid):** Deficiency (scurvy) causes hemorrhages, including subconjunctival and orbital hemorrhages. The AREDS trial showed that vitamin C (with other antioxidants) reduced progression of advanced AMD. Treatment for ocular hemorrhages follows scurvy guidelines: 1–2 g daily for 3 days, then 500 mg for a week, then 100 mg daily for 3 months.
- **Vitamin D:** Deficiency is linked to dry eye disease, diabetic retinopathy, optic neuritis, and thyroid eye disease. Prevalence is estimated at 24% in the US, 37% in Canada, and 40% in Europe. Treatment: infants 400 IU daily, adults 400–2000 IU daily.
- **Vitamin E:** Deficiency can cause ophthalmoplegia, strabismus, nystagmus, and retinopathy, and may exacerbate AMD. The AREDS formulation includes 400 IU vitamin E daily. Treatment for symptomatic deficiency is up to 2000 mg oral vitamin E daily.
- **Vitamin K:** Deficiency leads to vitamin K deficiency bleeding (VKDB), which can cause retinal hemorrhages. Incidence of early VKDB ranges from 0.25 to 1.7 per 100 live births. Treatment: infants 1 mg IM at birth; adults 90 µg/day (women) and 120 µg/day (men).
**Clinical Implications:** This review provides a practical guide for clinicians to recognize, assess, and treat ophthalmological conditions associated with vitamin deficiencies. Early detection and treatment are crucial, as many ocular manifestations are reversible if addressed promptly. For example, vitamin A deficiency can lead to irreversible corneal scarring if not treated before the corneal xerosis stage. The review emphasizes the importance of targeted history-taking, including dietary intake, medical history (e.g., malabsorption), and social factors, along with appropriate laboratory workup (e.g., serum vitamin levels, PT for vitamin K). Management includes specific supplementation regimens and, in some cases, adjunctive therapies like topical antibiotics for corneal ulcers or lubricating eye drops for dry eye. The findings underscore the need for ophthalmologists to maintain a high index of suspicion for vitamin deficiencies, especially in at-risk populations such as children, pregnant women, the elderly, and those with restricted diets or malabsorption disorders.