A 24-year-old man experienced high-grade fever, chills, and headaches for 2 months. From August 18 to 28, 2021, he received intraperitoneal treatment, then remained at home. One month passed before he underwent external ventricular drainage for hydrocephalus. Two days later, he presented with vomiting, altered sensorium, and a foreign body sensation. Upon examination, the patient's vitals were stable. Clubbing was noted on all digits. He was afebrile but had an abnormal central nervous system exam with a Glasgow Coma Scale score of E4V3M5. He was disoriented and nonresponsive to commands. The patient had no relevant past medical history and was generally healthy, but a previous blood culture identified Pseudomonas. He had no prior respiratory issues or admissions. His diagnosis included multiple cerebral abscesses, ventriculitis, and hydrocephalus. The underlying reason? A pulmonary arteriovenous malformation in the left lung.

A 33-year old woman presented with a slowly progressive but asymptomatic nail disorder of the left index finger. MRI and histological examination revealed a subungual neurofibroma as the cause of this single digit clubbing. Surgical removal resulted in good recovery with preservation of the nail.

Single-digit clubbing is a rare physical sign, with only a few cases reported in the literature. The causes of single-digit clubbing are myxoid cyst, osteoid osteoma, enchondromas, myxochondromas, superficial acral fibromyxoma, sarcoidosis, median, and ulnar nerve injury. We hereby report a case of solitary digital clubbing of the toe due to an underlying occult fracture.

Nail changes are seen in some individuals with alopecia areata, with the most common variants including pitting and trachyonychia. The nail findings are presumed to be due to the same lymphocytic infiltration seen in hair bulbs in individuals with AA. Baricitinib is an immunomodulatory drug that acts as a selective and reversible inhibitor of JAK proteins and is indicated for adult patients with moderate to severe rheumatoid arthritis who have not responded to other disease-modifying antirheumatic drugs. The FDA has also approved baricitinib to treat patients hospitalized with COVID-19 and severe alopecia areata. In this report, we present a case of a patient with persistent AA-associated nail changes who has been successfully treated with baricitinib. The patient has been suffering from alopecia for several years. She presented with periungual inflammation in conjunction with persistent fingernail ridges and pitting of her right fourth digit. The nail dystrophy persisted despite treatment with tacrolimus ointment, clobetasol ointment, or oral fluconazole. Patient was started on a trial of baricitinib for alopecia areata, which was the suspected cause of the nail changes. After 4 months of treatment with baricitinib, the patient's nail showed mild improvement of nail dystrophy with some clubbing and pitting still present. Within 11 months of treatment, her nail was normalized in appearance and texture. There are no established guidelines to treat AA-associated nail changes. Our patient's AA-associated nail changes were normalized after 11 months of treatment with baricitinib. Further research is needed to determine which alopecia areata patients may benefit from treatment with baricitinib and when treatment should be initiated. Baricitinib may be an effective treatment option for AA-associated nail changes in some patients.

It is not uncommon for congenital heart defects to occur in clusters. Those involving a right to left heart shunt commonly cause cyanosis and finger clubbing. Differential clubbing involving only the lower limb digits is a strong pointer to the presence of patent ductus arteriosus with reversal of shunt. We report a case of 25-year-old man with effort intolerance and differential clubbing. He was found to have the uncommon triad of patent ductus arteriosus, ventricular septal defect and supravalvular ring mitral stenosis. The presence of differential clubbing on a background of patent ductus arteriosus usually indicates a reversal of shunt and negates surgical intervention. This general rule may however not apply with co-existing mitral stenosis as the elevated pulmonary pressure may be predominantly post-capillary. The finding of mitral stenosis in a patient with patent ductus arteriosus and differential limb clubbing may signify a good prognostic surgical outcome.

The prevalence of patent foramen ovale (PFO) is 20-25% among adults. The role of right-to-left shunting through the PFO in systemic hypoxemia remains poorly understood. Right-to-left shunting through the PFO can occur either due to elevated right atrial pressure (pressure-driven) or directed venous flow toward the PFO (flow-driven). Herein, we report a rare case of flow-driven right-to-left shunting via the PFO in a patient with traumatic tricuspid regurgitation. A 45-year-old Chinese woman was admitted due to progressive dyspnea for 3 years, presenting with cyanosis and digital clubbing. She was hypoxic, with an oxygen saturation of 83% on room air, and arterial blood gas showed an oxygen tension of 53 mmHg. Echocardiography showed severe tricuspid regurgitation with ruptured chordae tendinea, causing regurgitant jet flow directed toward the interatrial septum, leading to intermittent right-to-left shunting between the septa primum and secundum. Swan-Ganz catheterization revealed normal-high right atrial pressure and excluded pulmonary hypertension. The patient underwent tricuspid valve repair and PFO closure. Her oxygen saturation returned to 95% and her symptoms resolved. Right-to-left shunting through the PFO could cause systemic hypoxemia via a flow-driven mechanism, occasionally manifesting as cyanosis and clubbing digits. PFO closure and treatment of underlying disease are effective in improving hypoxemia.

Clubbing of the nails is soft tissue swelling of the terminal phalanx resulting in straightening of the angle that exists between the nail bed and the nail.[1] The association of clubbing of the fingers with an underlying disease was known since the time of Hippocrates. Clubbing occurs in combination with other dermatologic and skeletal findings but can also less commonly occur in isolation. Although clubbing can present in many diverse conditions, it can be idio­pathic or familial; the familial form frequently transmits as a dominant trait.

Digital clubbing has been regarded as an important sign in medicine. A 33-year-old woman with no history of hepatic, pulmonary, or malignant disease was referred to our hospital. She had been taking lubiprostone every day for three years for constipation. Clubbing in her upper and lower limb digits began gradually about two years ago. The results of laboratory investigations were almost normal. We suspected the clubbed digits were a side effect of lubiprostone and confirmed that the levels of urinary prostaglandin E2 (PGE2), which can cause clubbed digits, were elevated. Thus, we instructed the woman to stop taking lubiprostone and monitored this lab value. However, the value continued to rise over 2 months to 41.9 μg/g Cr. During that time, she had been taking sennoside A B calcium instead of lubiprostone for constipation. Since sennoside A B calcium also has the effect of increasing PGE2, we ordered the discontinuation. Her urinary PGE2 to creatinine level normalized, and the clubbing improved after the discontinuation of these two medications.