When Long COVID Walks into the Office: Recognizing Foot and Ankle Manifestations

By Mikel D. Daniels, DPM, MBA, President and Chief Medical Officer, WeTreatFeet Podiatry

A Patient walks into the office with generalized foot pain. Taking a history, you learn the patient has fatigue, or myalgias in other muscles, or feels weak all the time. What are the usual diagnoses?

Long COVID has changed how I approach foot and ankle pain in these patients. I no longer believe we can safely evaluate lower-extremity symptoms without at least considering its potential role. When patients tell me their feet “haven’t been right” since having COVID, I don’t dismiss the comment. I treat it as a meaningful clinical clue. This does require some outside-the-box thinking, and we all need to start taking a deeper dive.

In my own practice, the pattern has become hard to ignore. Since the start of the pandemic, I have seen an increasing number of patients who present with burning feet, dysesthesias, swelling, color changes, or stubborn tendon and fascia pain that doesn’t go away. Histories indicate this began during a SARS-CoV-2 infection, or within months afterward. Some of them are diabetic. Many are not. Early on, I caught myself trying to fit these complaints into familiar boxes: classic length-dependent diabetic neuropathy, idiopathic neuropathy, garden-variety plantar fasciitis, overuse tendinopathy. But then the timeline and the risk factors just didn’t fit in that box. Heel pain was random, not first thing in the morning. Tendons would throb at random times, not just with use or just at rest. Bilateral symptoms that were not symmetrical and with varying degrees of severity. By themselves, a normal day in the office. However, traditional treatments didn’t work.

As the Long COVID literature has matured, those clinical observations have started to make more sense. We now have evidence that persistent spike protein, immune dysregulation, microclot formation, and small fiber neuropathy exist in Long Covid patients. These are no longer fringe theories, but recurrent findings in subsets of patients with post-acute COVID-19 syndrome. The lower extremities sit right at the intersection of those mechanisms. They are at the end of the vascular tree, packed with small sensory and autonomic fibers, and loaded with muscles and tendons that decondition quickly. So, it should not surprise any of us that the feet and ankles are often where Long COVID quietly shows itself first

I want to discuss this as a physician and lower extremity clinician, not as a virologist, and certainly not as someone claiming to have all the answers. The truth is that I look at the feet as an early-warning system, and my core message is simple. Going forward, we have to recognize the role of Long COVID in foot and ankle pain and dysfunction, or we are going to miss a meaningful piece of the puzzle in a lot of patients.

Long COVID by the Numbers, and Why That Matters for Feet

Long COVID prevalence estimates vary, but across large U.S. data sets the numbers are not small. A 2024 national survey estimated that roughly 17.8 million adults in the United States had experienced Long COVID. This represents close to 7% of the adult population. A 2026 analysis of nearly 458,000 patients across multiple health systems reported a prevalence closer to 16%, which extrapolates to the order of 50 million Americans with potentially persistent symptoms. Other cohort and registry studies suggest that at least 10% of people infected with SARS-CoV-2 develop symptoms that persist for months or longer beyond the acute phase.

From a lower extremity standpoint, the exact percentage is less important than the order of magnitude. Tens of millions of people with a chronic post-viral condition means that every foot and ankle practice, every wound center, every PT clinic, and every primary care office will encounter Long COVID patients. If even a fraction of those patients has symptoms in the distal lower extremity, that becomes our problem whether we claim it or not.

How Long COVID Reaches the Feet: What the Science Suggests

To understand why the feet are so commonly involved, I had to step back and look at the proposed mechanisms. The details are still evolving, and some of this remains controversial, but several themes in the literature keep repeating.

• The issue of persistent spike protein and viral remnants can’t be ignored. Multiple studies have found circulating spike protein in subsets of Long COVID patients. These are even months after the initial infection, and often in the absence of ongoing viral replication. One explanation is the presence of tissue reservoirs, particularly in the gut and possibly other immune-active sites, that continue to shed antigen. This is not universally accepted, and the direct clinical implications are still being worked out, but it does offer a plausible source of chronic immune stimulation.
• The microvascular story. SARS-CoV-2 uses the ACE2 receptor to enter cells, and ACE2 is richly expressed on endothelial cells throughout the vascular tree. Endothelial injury and dysfunction are now widely described in acute COVID. Several groups have reported “amyloid-like” fibrin microclots in plasma that appear resistant to normal fibrinolysis, along with evidence of a persistent thrombo-inflammatory state. If you think about the smallest capillaries in the feet, where perfusion is already most vulnerable, the idea that microclots and endothelial dysfunction could impair oxygen and nutrient delivery is not a stretch.
• Most relevant for what I see in the exam room, is the nervous system. There is now fairly strong evidence linking Long COVID to small fiber neuropathy. A large 2025 analysis of 977 Long COVID patients found that over half reported neuropathic symptoms, and among those who underwent skin biopsy (not everyone did), more than half had confirmed small fiber neuropathy affecting both epidermal sensory fibers and autonomic fibers. Importantly, many of these patients did not have the usual risk factors we would expect for neuropathy, such as diabetes or heavy alcohol use.

Other cohort and histologic studies have reinforced that association. Several groups have documented reduced intraepidermal nerve fiber density, abnormal autonomic sweat fiber function, and microneurographic evidence of unmyelinated fiber dysfunction in Long COVID cohorts. Some patients also exhibit elevated anti-ganglioside antibodies, suggesting an autoimmune component similar in flavor to other post-infectious neuropathies. Not every study agrees on prevalence or mechanism, but taken together, the data make it very hard to ignore.

The musculoskeletal side also needs to be addressed. Studies have reported that sometimes years after infection, a significant minority of Long COVID patients report persistent myalgias and arthralgias, sometimes a years after infection. There are studies that indicate structural changes in key lower extremity muscles, including the tibialis anterior and gastrocnemius. Some patients have concomitant post-viral fatigue and exercise intolerance. When those muscles change, gait changes, plantar pressure shifts, and tendons see loads they were not conditioned to handle. All of that can land in the foot and ankle as pain, even before we get to explicit neuropathy.

Again, none of these mechanisms are completely settled science. There is active debate about how often viral remnants persist, how directly microclots contribute to symptoms. Questions remain about what proportion of neuropathy in these patients is truly COVID-specific versus unmasking other conditions?

The Symptom Patterns I Listen for Now

In day-to-day practice, I have gradually built a mental checklist for possible Long COVID involvement whenever a patient presents with lower extremity symptoms that feel “out of proportion” or poorly explained. The details vary, but the themes are fairly consistent with what has been reported in the literature.

Burning feet and length-dependent dysesthesias are at the top of the list. Patients describe electric shocks, pins and needles, or a deep burning pain that is often worse at night and not clearly linked to a mechanical trigger. Sometimes there is allodynia, or a mix of numbness and pain. Objectively, the exam can be frustrating. Monofilament may be normal or only mildly abnormal. Larger fibers may test fine. Yet the patient is clearly uncomfortable, and the distribution is classic for small fiber involvement.

Color changes and temperature asymmetry raise another flag. I have seen toes with intermittent livedo-like patterns, patchy erythema, or purplish discoloration that waxes and wanes, similar to CRPS symptoms. Sometimes in nerve conduction studies it looks like traditional pernio. Others resemble the “COVID toes” I saw in the hospitalize COVID patients during the pandemic. Histopathologic studies of these lesions have shown vascular and perivascular inflammation. So differential diagnoses include autoimmune vasculitis, hypersensitivity reactions, or infections disease. Nothing that is specific to SARS-CoV-2.

Swelling and dependent edema—particularly in patients who also report orthostatic symptoms—may offer another piece of the puzzle. Soft-tissue complaints can also present in unexpected ways. When musculoskeletal deconditioning, inflammatory changes, and altered pain processing from a systemic post-viral syndrome converge in the same patient, standard diagnostic algorithms often fail to capture the full clinical picture.

Putting This Together Into a Practical Approach

Recognizing possible Long COVID involvement does not mean that every patient with foot pain after 2020 has Long COVID. I remind myself of that often. It does mean that I take a more structured history and I am quicker to ask specific questions when the story feels even slightly suspicious.

I routinely ask about the timing of symptom onset relative to any known COVID infection. I want month and year if they remember it. I ask whether the symptoms began during the acute illness, within the first three months afterward, or later. I ask about the character of the pain in plain language first. I ask whether the symptoms climb up the leg, whether they are worse at night, and whether anything clearly relieves or worsens them.

I also ask targeted systemic questions. Fatigue that feels disproportionate to activity level, post-exertional “crashes,” brain fog, palpitations, exertional tachycardia, and non-specific shortness of breath. All of these make me think harder about a broader Long COVID picture. I want to know about prior work-ups or tests like nerve conduction studies? Any skin punch biopsy? Any vascular imaging? Many of these patients have seen multiple clinicians by the time they reach a podiatry or lower extremity clinic, and our job often involves collecting and analyzing scattered data, rather than starting from scratch.

On exam, I look at light touch, vibration, temperature, and monofilament testing, with an awareness that small fiber symptoms can precede clear large-fiber or monofilament changes. I look for subtle asymmetry in color, capillary refill, skin texture, hair distribution, and sweating. I check pulses and, when indicated, order objective vascular studies if indicated. Gait analysis, range of motion, and palpation of typical pain generators still matter. Long COVID does not exempt patients from “ordinary” pathology. It may even layer on top of it

Where I think the Controversy and Uncertainty Really Sit

While the association between Long COVID and neuropathic or vascular symptoms is now well described, there is still real uncertainty about causality in individual patients. Ongoing debate about the relative importance of different mechanisms still exist. Some patients may have had subclinical neuropathy that COVID unmasked. Others may have independent autoimmune processes that happen to co-occur. Some will have neuropathic symptoms with normal biopsy and no clear structural explanation. We do not have a blood test that says, “This is Long COVID neuropathy,” so getting to a definitive diagnosis is difficult.

There is also controversy around treatments. Various nutraceutical and pharmacologic protocols have been proposed in preclinical or small human studies, but robust randomized trials are limited. Equally important to note is that long-term safety and efficacy data isn’t prevalent. I am careful not to over-promise here. When I talk with patients, I distinguish clearly between established standards of care for neuropathic pain, vascular disease, and musculoskeletal conditions versus emerging strategies that still need confirmation

What This Means for Our Everyday Practice Going Forward

For me, the practical takeaway is not that Long COVID replaces our usual differentials. It is that it joins them. When a patient with diabetes presents with a new ulcer and a history of Long COVID with neuropathic symptoms, I assume their neurovascular reserve may be more complicated than usual. When a non-diabetic patient presents with burning feet that began after COVID, I do not shrug and call it idiopathic just because nerve conduction study is normal. I consider small fiber involvement, I think about biopsy, and I counsel them that we may be dealing with a post-viral neuropathy that requires time, symptom management, and sometimes specialty input.

In the rehab setting, I have become more careful with exercise progression in patients with clear post-viral fatigue or post-exertional symptom exacerbation. A standard approach that would be appropriate for plantar fasciitis can backfire in a patient with Long COVID who then crashes for two days after a mildly aggressive session. I find that pacing, lower-intensity start points, and close symptom monitoring are safer for many of these patients. That is not unique wisdom; it is consistent with broader Long COVID rehab principles

Most importantly, I have stopped viewing these patients as “difficult” or “mystery” cases when their symptoms resist simple explanations. The biology is complex. The science is still catching up. But their experience is valid, and our exam findings often have more to tell us when we look at them through a Long COVID lens. We do not need to label everything as Long COVID. We do need to recognize that it is here to stay, and that it will continue to walk into our offices in the form of foot and ankle pain. If we do not train ourselves to see it, we will miss opportunities to understand our patients, and to build care plans that reflect the true complexity of what they are living with.

Dr. Mikel Daniels is a board-certified podiatrist and healthcare executive with more than two decades of experience in foot and ankle surgery, wound care, and medical economics. As President and Chief Medical Officer of WeTreatFeet Podiatry, he has grown the practice from 1 office into a regional network of surgical centers, and retail health services across Maryland, Pennsylvania, and Washington, D.C.

Dr. Daniels earned his Doctor of Podiatric Medicine from Temple University and an MBA in Healthcare Administration, combining clinical expertise with business strategy to deliver efficient, patient-centered care. His work focuses on complex reconstructive procedures, diabetic limb salvage, sports injuries, and minimally invasive techniques designed to accelerate recovery.

A Fellow of the American College of Foot and Ankle Surgeons and the American Professional Wound Care Association, Dr. Daniels also consults for biomedical technology firms and serves as a principal investigator in clinical research. His insights have appeared in Forbes, Parade Magazine, and CNN, and through his writing and mentorship, he continues to advance innovation.