This paper is an update on the assessment and management of dry eye disease (DED). According to the second International Dry Eye Workshop 2017, “Dry eye is a multifactorial disease of the ocular surface characterised by a loss of homoeostasis of the tear film, accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation damage, and neurosensory abnormalities have aetiological roles”. Assessment of patients with DED comprises recording of symptoms and observations which include tear secretion, tear clearance, ocular surface damage, tear film stability, tear volume, lipid layer assessment and tear osmolarity. The Ocular Surface Disease Index consists of 12 questions and is used for measuring the subjective severity of DED. The Oxford Scheme is often used for grading ocular surface staining in steps from 0 to 5, using fluorescein and rose bengal or lissamine green. Tear film stability is assessed by fluorescein break-up time and can be measured at the slit-lamp. Meibomian glands can be imaged by scanning the everted lid with an infrared light source. Tear osmolarity is however the single best marker of dry eye disease severity. It uses the TearLab Osmometer. The accepted threshold for mild to moderate dry eye disease is at 308 mOsm/l. Schirmers test is cheap, quick, universally available and clinically remains a useful measure of tear production. The principles of DED management start with controlling the ocular environment. This means advising the patient to avoid dry atmospheres, high airspeeds including fans, car heaters and air conditioning, and being aware of the effects of concentration on blink rate. Concentration includes reading, working at the computer screen, and the use of digital devices. Most over-the-counter artificial tear preparations are similarly effective. Treating the closed eye with a liposome-containing spray may allow the drug to cross the lid margins after a few blinks and then, with the ability of phospholipids to generate surface monolayers, thickens the lipid layer of the tears for 60-90 min. Autologous serum, prepared from the patient’s own blood, is very similar to natural tears, being of the correct pH and containing nutrients, vitamins, fibronectin, epithelial, and nerve growth factors, but there are legal hurdles involved in its preparation and it is very expensive. Steroids have been used for many years in DED where there is significant inflammation. Short periods of use and the ‘less-penetrating’ drugs are to be preferred. Newer drugs are at various stages of development including clinical trials. Lifitegrast, an integrin inhibitor that downregulates T-lymphocyte-mediated inflammation was licenced recently. Lid hygiene remains one of the mainstays of the management of meibomian gland dysfunction and there is still little evidence that commercial alternatives are superior. Warm compresses are soothing and may liquefy solidified meibomian secretions. In the UK systemic tetracyclines are used, however, there is no evidence to support the use of oral antibiotics in the management of ocular surface disease. Topical macrolides, specifically azithromycin, show promise.