Closed atraumatic flexor hallucis longus tendon rupture following hallux valgus correction repaired using a turn down flap

A case report of closed atraumatic rupture of flexor hallucis longus (FHL) tendon few months after hallux valgus correction in a high functioning individual is presented. There have been only two cases of FHL tendon rupture reported following hallux valgus correction in literature till now. Our patient underwent Hallux valgus corrective osteotomy, 4 months after which he presented with rupture of the FHL tendon, he subsequently underwent successful surgical turn down flap repair with good clinical outcome. Closed atraumatic rupture of FHL tendon as an isolated injury is a rare event evidenced by systematic review reporting only 10 cases in literature till now. Low clinical suspicion of FHL rupture in closed foot injuries could be one factor resulting in fewer cases being reported in literature. Acute rupture of FHL tendon following open foot injuries and partial closed rupture due to tendinitis in dancers have been reported frequently in literature. In conclusion, we emphasize careful handling of FHL tendon while performing corrective osteotomy of the hallux in any patient. Although, turn down flap is a well-documented technique to bridge gaps and repair chronic tendo-achilles rupture, we were able to replicate the same technique in our patient and produce good functional result using this effective tendon repair technique to bridge segmental gap as evidence by return of almost normal power of great toe plantar flexion

Aplastic anemia in a patient with chronic liver disease

The association of aplastic anemia with chronic liver disease is rare. We report the case of a 47-year-old male patient who presented with bleeding gums and melena. He was found to have pancytopenia and on evaluation, had an aplastic bone marrow. He also had cirrhosis with portal hypertension (cryptogenic cirrhosis) for which no cause could be ascertained. This case illustrates that in a patient with cirrhosis and pancytopenia, we must look for causes other than hypersplenism

Creutzfeldt-Jakob disease: A great masquerade in neurology, a rare case report from South India

Creutzfeldt-Jakob disease (CJD) is a rare, fatal neurodegenerative disease caused by an infectious protein called prion and is characterized by spongiform changes, neuronal loss, reactive astrocytic proliferation, and accumulation of pathologic cellular protein. Clinical presentation of CJD is characterized by rapidly progressive dementia, neurologic symptoms and visual impairment, and the development of akinetic mutism, which can mimic many neurological conditions. The diagnosis is based on clinical presentation, electroencephalogram, and typical cerebrospinal fluid and magnetic resonance imaging (MRI) findings. Literature on the incidence and prevalence of CJD is lacking in South India. We report the case of a 57-year-old woman with progressive dementia and typical neurologic symptoms, myoclonic jerks, and MRI findings of CJD. This case highlights the need for a high index of suspicion to diagnose CJD