Implant with a connective tissue disorder (EDS/hypermobility)? Anyone have experience or thoughts?

[runtsss]

M22, nearly 4 years functionless from PSSD. I’ve been through the entire treatment ladder, pills, injections, the works. On the injection side I’ve tried single agent alprostadil, bimix, and trimix. I can achieve rigidity with trimix, but without fail I end up needing to reverse it with phenylephrine, so it’s not a workable long-term solution. I’ve had several appointments with Dr. Eid and am seriously

considering moving forward with an implant.
The wrinkle is that I have a diagnosed connective tissue disorder (hypermobility spectrum, same family as Ehlers-Danlos), and I can’t find much of anything on how that affects implant surgery. Healing, tissue integrity, long-term outcomes, any of it.

Has anyone here had the procedure with EDS or a similar condition, or discussed it with their surgeon? Even if you don’t have direct experience, I’d appreciate any educated guesses or things worth thinking about. Just trying to get some light shed on this before I go further. Thanks!

[lasthope2.0]

I checked this with some bot and found the response to be quite insightful. However, only our doctors can confirm its accuracy, so please take this with a grain of salt.

• No direct evidence exists. No published data on implants specifically in EDS or hypermobility-spectrum patients.
  
• Closest tissue-level analog: case reports of penile fracture repair in EDS patients (same tunica albuginea being incised and closed) show successful healing but with adapted technique — non-absorbable sutures for the tunical closure, gentle tissue handling, meticulous hemostasis with close monitoring for hematoma, and extended post-op abstinence of at least 12 weeks instead of the standard 6 — reflecting the delayed wound healing generally seen in connective tissue disorders.
  
• Best available outcomes data: a 2022 case-control study matched 36 EDS patients to 108 controls, all undergoing genital gender-affirming surgery. Wound-healing issues and need for additional post-op intervention in the EDS group were not significantly different from controls; the study concluded an EDS diagnosis shouldn't be treated as a barrier to offering the surgery. Exact figures: major reoperation 2.8% EDS vs 5.4% controls (p=0.63); minor intervention 8.3% vs 14% (p=0.38); any wound-healing issue 28% vs 47% (p=0.04) — lower in the EDS group. Not implant-specific, but real genital-surgery data.
  
• Implant-specific mechanism: cylinder erosion is externalization of the cylinders caused by gradual weakening of the tunica albuginea, typically triggered by excessive corporal dilation or long-standing pressure from oversized cylinders. A connective tissue disorder affecting baseline tunical collagen strength is a mechanistically plausible long-term erosion/migration risk factor — but this hasn't been tested in any implant cohort.
  
• Severity gradient within the EDS family: hypermobile EDS is generally a less severe form of the syndrome than other subtypes; hypermobility spectrum disorder sits alongside it at the milder end for tissue fragility. Vascular EDS is the subtype specifically tied to surgical complications like wound dehiscence and arterial rupture; classical EDS carries more skin-specific fragility and scarring than the hypermobile/HSD end of the spectrum.