Category: Basic Sciences

Fluoroquinolones are widely used broad‑spectrum antibiotics, but their association with tendinopathy and tendon rupture has become a major safety concern, particularly in weightbearing tendons such as the Achilles. This essay outlines the epidemiology, pathophysiology, clinical presentation, risk factors, and management of fluoroquinolone‑associated tendon injury, with particular attention to implications for lower‑limb practice.

Overview and epidemiology

Fluoroquinolones (FQs) such as ciprofloxacin, levofloxacin, and ofloxacin achieve excellent oral bioavailability and tissue penetration, and have therefore been heavily prescribed for urinary, respiratory, and gastrointestinal infections. Despite their efficacy, post‑marketing surveillance and observational studies have consistently linked these agents to tendinopathy and tendon rupture, prompting regulatory warnings in multiple countries.

Large database studies suggest that the absolute risk of tendon rupture with FQs is low but clinically meaningful. In a cohort of over 740,000 fluoroquinolone‑exposed patients, the excess risk attributable to current FQ use was estimated at about 3.7 additional tendon ruptures per 10,000 person‑years for any tendon rupture and 2.9 per 10,000 person‑years specifically for Achilles rupture. Another UK primary‑care database study reported an incidence of any tendon rupture of 5.9 per 10,000 person‑years, with Achilles tendon rupture at 1.9 per 10,000 person‑years, and found that FQ exposure increased the relative risk compared with a non‑FQ antibiotic comparator.

Relative risk estimates vary but generally demonstrate a 1.5–5‑fold increase in tendon rupture with current fluoroquinolone exposure, with higher estimates for Achilles tendon injuries. One nested case–control analysis reported odds ratios of 1.6 for any tendon rupture, 2.7 for Achilles rupture, and 1.5 for biceps rupture with current FQ use compared with non‑exposed patients. These data underpin the current view that, while population‑level risk is modest, the consequences for affected individuals can be severe and long‑lasting, especially in active or older adults.

Pathophysiology and mechanisms

The precise mechanism by which fluoroquinolones damage tendon tissue is not fully elucidated, but several converging pathways have been identified in experimental and translational studies. Tendons depend on a highly organised collagenous extracellular matrix maintained by tenocytes and other resident cells; disturbance of this balance predisposes to micro‑damage, degeneration, and, ultimately, mechanical failure.

In vitro and animal studies demonstrate that fluoroquinolones can impair fibroblast and tenocyte function by reducing collagen synthesis and up‑regulating matrix degradation. Ciprofloxacin, for example, has been shown to decrease type I collagen production and increase activity of matrix‑degrading enzymes, shifting the tendon milieu toward net catabolism. FQs also appear to increase apoptosis in human tenocytes, reducing the viable cell population needed for ongoing repair and homeostasis.

Another proposed mechanism relates to the chelating properties of fluoroquinolones, which bind divalent cations such as magnesium. This may disrupt cell–matrix interactions and interfere with integrin‑mediated signalling that is essential for mechanotransduction and collagen organisation. Histopathological studies of affected tendons have described hyaline and mucoid degeneration, chondroid metaplasia of tenocytes, altered mucopolysaccharide content, and disorganisation of collagen fibres, findings consistent with a degenerative tendinopathy rather than pure inflammatory process.

Vascular factors may further contribute. The Achilles tendon already has relatively poor blood supply, particularly in its mid‑portion, and this perfusion appears to decline with age. Reports of narrowed vasculature and paratendinous changes in FQ‑associated tendinopathy suggest that impaired blood flow and local ischaemia could exacerbate drug‑mediated matrix damage, helping explain the predilection for the Achilles in older patients. Together, changes in gene expression, cell survival, extracellular matrix composition, and microvascular supply create a vulnerable tendon prone to symptomatic tendinopathy and rupture under normal or modest mechanical loading.

Clinical features and risk factors

Fluoroquinolone‑associated tendon injury typically presents as an acute or subacute onset of pain, swelling, and stiffness in a tendon region within days to weeks of drug exposure, although onset can be delayed. The Achilles tendon is most commonly involved, accounting for nearly 90% of reported cases, but other sites such as the biceps brachii, supraspinatus, triceps, extensor pollicis longus, and various hand and shoulder tendons have also been described. Symptoms may be unilateral or bilateral and often include focal tenderness, impaired function, and difficulty with tasks that load the tendon (e.g., push‑off in gait or climbing stairs).

Several risk factors substantially amplify the likelihood of tendon injury in the setting of fluoroquinolone therapy. Advancing age is consistently associated with higher risk; epidemiological analyses show greater absolute risk in older adults, reflecting age‑related changes in tendon vascularity and matrix quality. Concomitant systemic corticosteroid therapy is a particularly potent enhancer, with studies indicating a materially increased risk of Achilles tendon rupture when FQs and steroids are used together compared with FQs alone. Other reported risk factors include chronic kidney disease and renal transplantation (with reduced drug clearance and higher tissue exposure), diabetes, and pre‑existing tendon disorders, as well as high levels of physical activity or sudden changes in loading.

From a podiatric perspective, a typical clinical scenario might involve an older patient treated with levofloxacin for pneumonia while on oral prednisolone for chronic obstructive pulmonary disease, presenting one to two weeks later with sudden posterior heel pain and difficulty weightbearing. If not recognised promptly and the antibiotic continued, this tendinopathy can progress to partial or complete rupture, often during relatively low‑demand activities such as walking.

Diagnosis and management

Diagnosis of fluoroquinolone‑associated tendinopathy is primarily clinical, based on a compatible symptom pattern, localisation to a tendon, and a history of recent or current FQ use in the absence of alternative causes. Ultrasound and MRI are not mandatory but can be valuable for confirming tendon involvement, characterising partial tears, and excluding other pathology, particularly for deep or less accessible tendons. Typical ultrasound features include tendon thickening, hypoechoic areas, and increased neovascularity on Doppler imaging, mirroring changes seen in non‑drug‑induced tendinopathy.

Once suspected, immediate cessation of the fluoroquinolone is recommended, even if the antibiotic course is incomplete, and an alternative non‑FQ agent should be selected whenever feasible. Early management centres on rest and load reduction for the affected tendon, often using heel lifts, counterforce bracing, walking aids, or short periods of immobilisation for Achilles involvement to reduce tensile stress. In Achilles cases, guidelines describe protecting the tendon for several weeks to months, with progressive re‑loading guided by pain and function.

Physical therapy plays a major role in rehabilitation once acute pain has settled. Protocols based on principles of connective tissue remodelling and eccentric loading, such as Alfredson’s heel‑drop programme, have been successfully adapted for FQ‑induced Achilles tendinopathy. Case reports describe meaningful improvements in pain and functional scores over 3–11 months with structured physiotherapy, sometimes combined with adjunctive modalities such as extracorporeal shockwave therapy when rest alone failed. Most cases of tendinosis recover over several weeks and typically within two months after discontinuation of the drug, although some patients experience more prolonged symptoms.

When tendon rupture occurs, management parallels that of non‑drug‑related ruptures and may be operative or non‑operative depending on patient factors, tendon involved, and local expertise. Early orthopaedic or sports medicine referral is appropriate, as delayed recognition can compromise outcomes. Importantly, individuals who have experienced fluoroquinolone‑associated tendon injury should generally avoid future exposure to this drug class, and prescribers should carefully evaluate the risk–benefit ratio before initiating FQs in patients with recognised risk factors.

Overall, fluoroquinolones exemplify the tension between antimicrobial efficacy and musculoskeletal safety. For clinicians working with the lower limb, recognising early tendon symptoms in patients recently treated with these agents, particularly older adults and those on corticosteroids, is critical to preventing progression from reversible tendinopathy to disabling rupture.

Atrial fibrillation (AF) can profoundly impact the foot and lower limb through its cardiovascular, circulatory, and systemic complications, with podiatrists playing a crucial role in early detection, risk reduction, and patient management.

How Atrial Fibrillation Impacts the Foot and Lower Limb

Atrial fibrillation is the most common cardiac arrhythmia, characterized by rapid and irregular heart rhythms. While primarily a cardiac problem, AF’s downstream consequences frequently manifest in the lower limbs.

• Impaired Circulation and Peripheral Arterial Disease (PAD): AF increases the risk of peripheral arterial disease due to shared underlying conditions like atherosclerosis and systemic vascular inflammation. Up to 21% of patients with AF demonstrate PAD when screened with ankle-brachial index (ABI), significantly higher than the general population. PAD leads to poor blood flow, leg and foot pain, intermittent claudication, numbness, slow wound healing, and—in severe cases—gangrene or limb ischemia.
• Arterial Embolism and Acute Limb Ischemia: AF increases the risk of blood clot formation in the atria. Emboli can travel to distal arteries, causing acute occlusion—most commonly in the legs. Patients may present with sudden foot pain, pallor, paresthesia, pulselessness, and risk of irreversible muscle and tissue damage if not treated rapidly. Case reports highlight limb-threatening embolic events directly linked to AF, requiring emergency intervention to restore blood flow and prevent amputation.
• Venous Complications and Edema: AF-induced heart failure results in fluid accumulation, leading to swelling of feet, ankles, and lower legs. This can cause discomfort, skin changes (e.g., stasis dermatitis), and increased susceptibility to ulcers and infection. Chronic edema can exacerbate existing lower limb conditions and hinder podiatric interventions.
• Chronic Lower Limb Symptoms: Signs associated with AF include muscle fatigue, weakness, and lower extremity swelling. These symptoms may limit mobility and reduce quality of life, especially in older adults or those with comorbid diabetes or PAD.

Mechanisms Connecting AF With Lower Limb Pathology

Several underlying mechanisms link AF to foot and lower limb pathology.

• Atherosclerosis: Both AF and PAD frequently occur due to atherosclerosis—a chronic process involving vessel inflammation, lipid accumulation, and structural change. Systemic atherosclerosis raises the risk for both cardiac arrhythmia and vascular insufficiency in the extremities.
• Thromboembolism: Rapid irregular heartbeat in AF leads to stasis of blood in the atria, promoting clot formation. These clots may embolize to peripheral arteries supplying the legs, producing acute ischemic episodes with potentially catastrophic outcomes.
• Heart Failure: The inability of the heart to efficiently pump blood because of AF leads to venous congestion and fluid leak into the tissues, commonly seen as lower limb edema.
• Impaired Perfusion and Healing: Chronic low cardiac output, coupled with PAD, deprives foot and leg tissues of adequate oxygen and nutrients, impairing wound healing, increasing infection risk, and worsening diabetic foot outcomes

Clinical Presentation in the Foot and Lower Limb

AF’s manifestations in the lower limbs can be subtle or dramatic:

• Sudden onset of calf pain, pallor, and paresthesia (sensory disturbances) may signal acute embolic arterial occlusion
• Chronic symptoms include fatigue, chronic leg pain, intermittent claudication, and persistent swelling.
• Ulcers, delayed healing, and recurrent infection are frequent in patients with coexisting AF and PAD.
• Irregular pulse and diminished pedal pulses may be noted during routine foot examination.

The Role of Podiatrists

Podiatrists play an essential interdisciplinary role in the management of patients with AF, often serving as the first point of contact for those with undiagnosed cardiac arrhythmia.

Early Detection and Opportunistic Screening

• Pulse Checks: Podiatrists can detect irregular pedal pulses during routine vascular assessments of the foot. Simple palpation or use of Doppler ultrasound for 30 seconds can identify rhythm disturbances suggestive of AF.
• Targeting High-Risk Populations: Patients with diabetes, advancing age, or known vascular disease are at elevated risk of AF and PAD. Podiatrists routinely encounter these groups in clinical practice, allowing opportunistic screening during foot checks.
• Technology-Assisted Screening: Initiatives in some healthcare systems have integrated digital single-lead ECG testing into podiatry clinics, allowing prompt diagnosis and referral for cardiac evaluation if AF is suspected.

Risk Factor Modification and Prevention

• Addressing Comorbidities: Podiatrists support management of risk factors such as diabetes, hypertension, obesity, and peripheral arterial disease—modifying the underlying pathways that contribute to AF and lower limb vascular events.
• Patient Education: Education on the signs and symptoms of acute ischemia and chronic vascular insufficiency is fundamental. Podiatrists teach patients to recognize new or worsening lower limb symptoms requiring medical attention.

Multidisciplinary Referral and Care Coordination

• Referral Pathways: When an irregular lower limb pulse is detected, podiatrists initiate timely referral to cardiac or vascular specialists for formal diagnostic evaluation and intervention.
• Interdisciplinary Communication: Integrated care ensures that podiatric findings prompt comprehensive cardiac assessment and anticoagulation therapy, reducing risk of recurrence and long-term complications.

Lower Limb Preservation and Advanced Management

• Monitoring and Wound Care: Patients with AF, especially those on anticoagulant therapy, may have delayed healing and increased risk of bleeding. Podiatrists play an ongoing role in wound management, infection control, and limb preservation, particularly in those with chronic foot ulcers.
• Surveillance for Edema and Tissue Health: Routine assessment for chronic fluid accumulation, skin breakdown, and infection helps reduce the risk of lower limb complications secondary to AF-induced heart failure.

Practical Examples and Evidence of Podiatric Involvement

Real-world initiatives have demonstrated how podiatrists can contribute to AF detection and improved patient outcomes.

• In the United Kingdom, podiatry departments have embraced technology, implementing opportunistic AF screening during routine appointments and referring patients for further cardiac evaluation when irregular pulses are identified.
• Studies have shown that integration of point-of-care testing and robust referral pathways enhances the early diagnosis of AF and reduces major adverse events such as stroke and limb loss.

Atrial fibrillation has far-reaching consequences for foot and lower limb health, contributing to arterial embolism, PAD, chronic edema, impaired healing, and increased risk of amputation. Podiatrists occupy a pivotal role through opportunistic screening, education, risk modification, and care coordination—helping to bridge the gap between systemic cardiac disease and limb preservation. Through vigilance and collaborative care, podiatrists serve as a frontline defense against the silent threats of AF in the lower limb.

Medical terminology, the specialized language used in healthcare, has a rich and complex history rooted in the development of science, language, and culture. Its evolution reflects centuries of discovery, intercultural influence, and the need for clarity and precision in communication. Understanding its derivation not only sheds light on how medicine developed as a profession but also helps learners navigate and decode unfamiliar terms.

The Historical Roots of Medical Terminology

Medical terminology originated thousands of years ago, with the earliest recorded terms found in ancient Egyptian hieroglyphs inscribed on medical papyrus scrolls. These early documents described diseases, treatments, and anatomical structures in a rudimentary form, marking the dawn of a specialized medical language. Greek medicine, heavily influenced by philosophers like Hippocrates and later the Alexandrian school, made pioneering advances in medical description and observation. Many terms for diseases, anatomical parts, and clinical phenomena were first coined in Ancient Greek, thanks to early attempts to systematically categorize illnesses and organs.

When the Romans conquered Greece around 400 BCE, the Latin language intertwined with Greek medical writing, birthing a hybrid diction that persists today. Influential Greek physicians such as Hippocrates—often called the “Father of Medicine”—and Galen contributed many root words and concepts to what would become the international language of medicine. Galen, in particular, revived Greek methods in Rome, emphasized clinical observation, and helped propagate Greek-rooted terminology through his teachings and writings. Over time, Roman physicians Latinized Greek terms, embedding them into medical practice.

Linguistic Foundations: Greek and Latin

The backbone of medical terminology is its neoclassical composition: most terms derive from Ancient Greek and Latin. This tradition continued into the Renaissance and the Age of Enlightenment, when Latin was the universal language of science and scholarship in Europe. Because so many foundational works in medicine were written in Greek or Latin, later scholars continued to use these languages when inventing new terms. Accordingly, medical words are typically international and translingual, with shared elements across modern European languages and even beyond.

For example, medical words relating to the kidney utilize two root words: “nephr(os)” from Greek and “ren(es)” from Latin. This duality is widespread; Latin and Greek roots often coexist in parallel for the same anatomical or pathological concepts, enriching the vocabulary but sometimes creating confusion for students and practitioners.

The Structure of Medical Terms

Medical terms are often built from three essential morphemes: a root (or stem), a prefix, and a suffix. Understanding how these components function can unlock the meaning of thousands of terms.

• Root: The central core that provides the basic meaning or refers to a particular body part, system, or condition. For example, “cardi-” refers to the heart, “hepat-” to the liver, and “neur-” to nerves.
• Prefix: Placed before the root, it conveys information about location, quantity, time, or status. Common medical prefixes include “hypo-” (below/deficient), “hyper-” (above/excessive), and “brady-” (slow).
• Suffix: Attached to the end of a root, it modifies the meaning by indicating procedures, conditions, disorders, or diseases, such as “-itis” (inflammation), “-ectomy” (removal), or “-logy” (study of).
• Combining Vowel: Frequently included (often “o”), it connects roots to suffixes or other roots to facilitate pronunciation, particularly when joining complex word elements.

This modular system allows for precision: a relatively small set of roots, prefixes, and suffixes can be combined to describe nearly every conceivable medical condition or procedure. For example, “hypoglycemia” breaks down into “hypo-” (less/below), “glyc” (sugar), and “-emia” (blood condition), literally meaning a deficiency of sugar in the blood.

Patterns and Examples

Most medical words can be dissected as follows:

Word	Prefix	Root	Suffix	Meaning
Cardiology	–	cardi	-ology	Study of the heart
Hypotension	hypo-	tensi	-on	Low blood pressure
Dermatitis	–	dermat	-itis	Inflammation of the skin
Myopathy	–	myo	-pathy	Disease of muscle

Suffixes and prefixes reveal the nuance of a term:

• “-lysis”: dissolution or destruction (e.g., spondylolysis—breakdown of a vertebrae).
• “-malacia”: softening (e.g., spondylomalacia—softening of the vertebrae).msdmanuals
• “peri-”: around (e.g., pericardium—tissue surrounding the heart).

From Tradition to Modernity

In recent decades, the creation of new medical terms has shifted away from strict Greek and Latin roots. Contemporary terms often borrow directly from everyday English, especially with innovations in technology and procedures (e.g., “bypass operation,” “screening”). Nonetheless, classical roots remain crucial for understanding and coining many of these terms.

The international nature of scientific vocabulary means that healthcare professionals in many parts of the world share a common linguistic foundation, supporting global communication and collaboration. The process of term formation has also been influenced by other languages and cultures over centuries, resulting in a vibrant and adaptable vocabulary.

Why Understanding Medical Terminology Matters

Mastering medical terminology is essential for anyone entering the health professions. It enables clear, accurate, and efficient communication throughout healthcare systems—a crucial requirement where misunderstandings can lead to errors in patient care. By breaking down words into their roots, prefixes, and suffixes, healthcare workers can deduce the meaning of unfamiliar terms, assess patient records confidently, and stay current with new developments.

Medical terminology, derived from Ancient Greek and Latin and shaped by centuries of scholarship and practice, forms a universal language in medicine. Its structure—based on roots, prefixes, and suffixes—enables great specificity and adaptability, reflecting the evolving needs of medical science. Whether found in established diagnoses or emerging procedures, this shared lexicon is central to the precision, safety, and progress of modern healthcare.