The patient, male and aged 78, had received coil embolization in 2006 for subarachnoid hemorrhage caused by a ruptured basilar tip aneurysm, and subsequently had a VP shunt inserted in February 2012 due to progressive hydrocephalus (
Fig. 1). Afterwards, the patient's progress seemed satisfactory until April 2015, when the scalp skin flap surrounding the VP shunt collapsed and showed signs of necrosis, exposing part of the shunt catheter (
Fig. 2). The attending neurosurgeon, focusing only on skin necrosis and not on flap retraction or collapse, attempted to revise the wound by debriding the area, inserting a plate to support the skin flap overlying the shunt, and repairing; when the repair site displayed signs of necrosis again within 2 weeks the case was referred to the Department of Plastic Surgery, albeit without any mention of the original flap collapsing and only stating hardware exposure and flap necrosis. On visual inspection, the recently-inserted metal plate was exposed as the scalp area surrounding the repair site grew thinner. Total debridement of all necrotic and unstable portions resulted in a 5×4 cm defect, and as we had no prior knowledge of flap sinkage and thinking the patient to be a rather simple case of infection or hardware exposure, we covered the defect with a radial forearm free flap elevated from the patient's left arm with the right-sided superficial temporal artery as a recipient vessel, judging that the free flap's robust blood supply would prevent infection and necrosis (
Fig. 3). Since the Neurosurgery department had already conducted several surgical procedures on the patient, free flap coverage was considered to be a better choice than a simple local flap operation anticipating the possibility of compromised scalp flap viability and adhesion to underlying bone. The thin radial forearm flap was chosen over a muscle flap to reduce operative time, considering the patient's old age, and for superior scalp contour. After free flap coverage, the patient's postoperative course was uneventful, and was lost to follow-up after 3 weeks, ignoring outpatient clinic appointments. However, after 4 months, the patient visited our outpatient clinic stating that the inserted plate was again visible (
Fig. 4). The free flap site was showing signs of gradual sinking while the vascularity of the flap remained unimpaired, with clear arterial sounds audible with handheld Doppler probing. The flap covering the hardware had grown substantially thinner and appeared as if a skin graft had been directly applied to the plate. No signs of infection were detected. There was also no evidence suggesting disorders of collagen metabolism such as nutritional deficiency, malignancy or liver cirrhosis that could lead to flap thinning and weakening [
2]. Accordingly, we discussed with the Neurosurgery department the possibility of the VP shunt creating a constant negative pressure gradient on the overlying flap leading to its collapse, and the options of re-locating the shunt for pressure adjustment. An agreement was reached to remove the shunt device and observe the patient for any neurological symptoms, and after the shunt and covering metal plate were removed and the previous cranial opening filled with fibrin glue by Neurosurgery, we debrided the deteriorated flap and provided coverage with 2 large opposing rotational flaps. Considering the patient's old age, the possibility of recurrent flap sinking and collapse made a second free flap transfer procedure seem too risky, and the smaller size of the new post-debridement defect allowed local flap coverage without previous scarring and adhesion causing much trouble. Both the patient and the surgical site recovered as expected with no complications until discharge, and during 2 months' outpatient follow-up no neurological symptoms appeared, the scalp flap displayed slight depression, but remained in good condition (
Fig. 5); the patient has declined from any further follow-up since.