From The Editor

Chronic inflammation is especially critical in the posterior pole

Statistics support the assertion that we are an inflamed society. According to Medscape, over 70 million NSAID prescriptions are written annually in the U.S. If you factor in over-the-counter drugs, more than 30 billion doses of NSAIDs are consumed annually (Weigand).

Given that inflammation isn’t always a bad thing, it’s difficult to estimate just how many Americans suffer from chronic inflammation. Whether it’s pain, heat, redness, swelling or loss of function, we all experience varying degrees of inflammation on a daily basis. However, if we consider persistent pain as a surrogate marker, the Institute of Medicine estimates that over 100 million Americans suffer from chronic pain, resulting in about $600 billion in direct costs and lost productivity annually.

Acute inflammation is part of the body’s immune response to threatening stimuli. Whether sparked by an injury or infection, our body initiates an acute inflammatory cascade to expedite tissue repair. Things get a little tricky when inflammation lingers too long. As the body’s response shifts from acute to chronic, the inflammatory mechanism takes on a different tack – one that results in progressive tissue fibrosis and necrosis. In short, chronic inflammation equates more with damage than healing. This mechanism is believed to be operative in a variety of chronic conditions, including cardiovascular disease, diabetes, inflammatory bowel disease, arthritis and even depression.

In optometry we witness our share of inflammatory ocular sequelae, ranging from dry eye to macular edema. Like other disciplines within medicine, we struggle in understanding, identifying, treating and reigning it in.

Michael D. DePaolis

While extinguishing chronic ocular inflammation is important regardless of the target tissue, the stakes are especially high when the posterior pole is involved. Given the macula’s delicate structure and intricate function, it’s essential that we do everything to protect it. Fortunately, we have sophisticated diagnostic technologies, affording us the ability to recognize even the subtlest degree of swelling or loss of function. Additionally, with an ever-expanding array of treatment options we are better able to manage inflammatory maculopathies. The challenge lies in knowing when inflammation is acute – self-limiting and likely to resolve on its own – or when it’s chronic and a harbinger of irreversible damage.

This month we asked colleagues to address this topic in our feature article. While providing a contemporary overview of various posterior pole inflammatory states, they also provide sage advice for when to monitor and when to refer. In the final analysis, it’s really about getting the upper hand on inflammation before it gets the better of us.

Statistics support the assertion that we are an inflamed society. According to Medscape, over 70 million NSAID prescriptions are written annually in the U.S. If you factor in over-the-counter drugs, more than 30 billion doses of NSAIDs are consumed annually (Weigand).

Given that inflammation isn’t always a bad thing, it’s difficult to estimate just how many Americans suffer from chronic inflammation. Whether it’s pain, heat, redness, swelling or loss of function, we all experience varying degrees of inflammation on a daily basis. However, if we consider persistent pain as a surrogate marker, the Institute of Medicine estimates that over 100 million Americans suffer from chronic pain, resulting in about $600 billion in direct costs and lost productivity annually.

Acute inflammation is part of the body’s immune response to threatening stimuli. Whether sparked by an injury or infection, our body initiates an acute inflammatory cascade to expedite tissue repair. Things get a little tricky when inflammation lingers too long. As the body’s response shifts from acute to chronic, the inflammatory mechanism takes on a different tack – one that results in progressive tissue fibrosis and necrosis. In short, chronic inflammation equates more with damage than healing. This mechanism is believed to be operative in a variety of chronic conditions, including cardiovascular disease, diabetes, inflammatory bowel disease, arthritis and even depression.

In optometry we witness our share of inflammatory ocular sequelae, ranging from dry eye to macular edema. Like other disciplines within medicine, we struggle in understanding, identifying, treating and reigning it in.

Michael D. DePaolis

While extinguishing chronic ocular inflammation is important regardless of the target tissue, the stakes are especially high when the posterior pole is involved. Given the macula’s delicate structure and intricate function, it’s essential that we do everything to protect it. Fortunately, we have sophisticated diagnostic technologies, affording us the ability to recognize even the subtlest degree of swelling or loss of function. Additionally, with an ever-expanding array of treatment options we are better able to manage inflammatory maculopathies. The challenge lies in knowing when inflammation is acute – self-limiting and likely to resolve on its own – or when it’s chronic and a harbinger of irreversible damage.

This month we asked colleagues to address this topic in our feature article. While providing a contemporary overview of various posterior pole inflammatory states, they also provide sage advice for when to monitor and when to refer. In the final analysis, it’s really about getting the upper hand on inflammation before it gets the better of us.