Endometriosis: What a Normal Scan Cannot Tell You

TL;DR: Endometriosis is when tissue like the lining of the uterus grows in places it does not belong, most often on the surfaces inside the pelvis. It can cause period pain that stops your life, pain during sex, pain with bowel movements or peeing, heavy bleeding, deep bloating, hard fatigue, and trouble getting pregnant. About 10 out of every 100 women of childbearing age have it. Most wait 5 to 12 years to be told what it is. The biggest reason for that wait is this: a normal ultrasound or a normal MRI does not rule it out. Scans are good at spotting cysts on the ovaries and deep growths, and they often miss the flat surface spots, which are the most common kind. So "your scan was normal" is an incomplete answer, and you can say so. Here is the order I would use. First, write down your symptoms and where they fall in your cycle, for 2 or 3 cycles. Second, see a doctor who will take that history, examine you, and tell you out loud what a scan can and cannot answer. Third, start treatment now instead of waiting for surgery, and check the other things that cause the same pain, like the bladder, the gut, and the pelvic floor muscles. Fourth, if you need a specialist, ask for one who treats endometriosis often, and bring your written history with you.

You have probably already been told that bad periods run in families, that your scan looked fine, and that some of this might be stress. Maybe you have been missing 2 days of work every month since you were 15. Maybe sex hurts in a way you have stopped bringing up. Maybe you collected a diagnosis of irritable bowel syndrome somewhere along the way, and a bladder infection that never grew anything on culture, and none of it ever added up to a story that explained your life.

What I want you to know is that a normal pelvic ultrasound and a normal pelvic MRI do not rule out endometriosis, that the most common form of the disease is the form imaging misses, and that a great deal can be done for you starting now, well before any operating room.

What is endometriosis?

Endometriosis is a chronic inflammatory condition in which tissue similar to the lining of the uterus grows outside the uterus. The most common locations are the peritoneum (the thin membrane lining the pelvis and abdomen), the ovaries, the ligaments behind the uterus, and the surfaces of the bowel and bladder. That tissue responds to the hormones of your cycle, bleeds, inflames the tissue around it, and over time can build scar tissue and adhesions that stick organs to one another.

The disease comes in 3 recognized forms, and the difference between them explains most of what follows on this page:

• Superficial peritoneal endometriosis. Flat lesions on the lining of the pelvis. This is the most common form.
• Ovarian endometrioma. A cyst filled with old blood inside the ovary, sometimes called a chocolate cyst.
• Deep infiltrating endometriosis. Lesions that burrow more than 5 mm below the peritoneal surface, often involving the bowel, bladder, ureters, or the ligaments behind the uterus.

Less often, endometriosis appears above the diaphragm. Thoracic endometriosis can produce chest pain, right shoulder pain, or a collapsed lung that recurs with menstruation, and cyclical shoulder or upper-abdominal pain is sometimes the only clue that it is there.

The World Health Organization estimates that endometriosis affects roughly 10% of women of reproductive age, about 190 million people worldwide. Estimates across the literature run from about 6% to 10% in the general population and much higher in specific groups: among women being evaluated for infertility, reported rates run from 25% to 50%, and roughly 30% to 50% of women with endometriosis have difficulty conceiving. Anyone who menstruates can have it, including trans men and nonbinary people.

The symptoms that should make a clinician think of it are:

• Period pain severe enough to interrupt school, work, or plans, particularly when it has been present since the teenage years
• Pelvic pain outside of your period, sometimes constant
• Pain with deep penetration during sex, and often for hours or days afterward
• Pain with bowel movements or with urination, worse around your period
• Cyclical bowel changes: diarrhea, constipation, or the marked bloating many patients call endo belly
• Heavy menstrual bleeding, which often ends in iron deficiency
• Fatigue that is out of proportion to everything else
• Difficulty getting pregnant

Family history matters more than most people realize. Having a first-degree relative with endometriosis carries a substantially higher risk, with reported estimates ranging from a roughly 5-fold to a 7-to-10-fold increase, and twin studies put the heritable contribution near 50%. If your mother or sister had brutal periods, that belongs in your history.

Why does endometriosis take years to diagnose?

The delay is the defining feature of this disease. A 2025 systematic review in BJOG pulled together 17 observational studies and found that the overall time from first symptom to diagnosis ranged from 5 to 12 years. The same review split that interval in half, and the split is the part that should bother all of us. Time from first symptom to the first medical visit ranged from 1 to 4 years. Time from that first medical visit to the diagnosis ranged from 0.3 to 8.6 years. In other words, a large share of the delay happens after a woman has already asked for help.

Several forces produce that gap, and they compound.

Period pain gets normalized on both sides of the room. Girls are taught that cramps are part of it, so they under-report. Clinicians hear "bad periods" and hand over a prescription for an anti-inflammatory or a birth control pill without ever mapping the symptoms. Symptom onset during adolescence is associated with a longer wait for the diagnosis, which is the opposite of what you would want, since that is the window where treatment does the most good.

The symptoms belong to several specialties at once. Painful bowel movements go to gastroenterology, urinary urgency goes to urology, back and hip pain go to orthopedics, and fatigue goes nowhere. Each specialist finds nothing wrong in their own organ and sends her back out. Nobody is looking at the calendar that would tie the symptoms together.

Hormonal contraception masks the picture without treating the story. Starting the pill at 16 for painful periods often works, which is a good outcome for the pain and a bad outcome for the diagnosis. The endometriosis is still there. It resurfaces years later when she stops the pill to try to conceive, and the clock on the workup starts from zero.

And the imaging trap. A normal scan gets read as a negative result and closes the file. That deserves its own section, because it is the place where most of these stories stall.

Why does a normal ultrasound or MRI not rule out endometriosis?

This is the single most useful fact on this page: negative imaging does not rule out endometriosis. In February 2026, the American College of Obstetricians and Gynecologists published a clinical practice guideline on the diagnosis of endometriosis that says so directly: neither transvaginal ultrasound nor MRI can reliably identify superficial peritoneal lesions, and negative imaging findings do not definitively exclude the disease. The 2022 ESHRE guideline says the same thing and recommends considering laparoscopy in a woman with painful symptoms whose ultrasound is negative.

The reason is anatomical. Imaging performs well for the forms of endometriosis that have bulk. Transvaginal ultrasound has high specificity for ovarian endometriomas and moderate sensitivity for deep infiltrating disease when it is done by a sonographer trained in the standardized protocol. MRI adds detail for deep disease, bowel and ureteric involvement, and surgical planning. What neither one reliably sees is a flat lesion a few millimeters across sitting on the peritoneum, and that superficial form is the most common presentation of the disease. An addendum published in 2025 by the International Deep Endometriosis Analysis group exists because superficial lesions have been so hard to characterize on ultrasound at all.

So here is what the scans can and cannot answer for you.

A pelvic ultrasound can tell you: whether you have an ovarian endometrioma, whether there are signs of deep disease at the common sites, whether there are fibroids, whether the uterus has the features of adenomyosis, and whether something else structural explains the picture. It is the right first test, and it is low-cost and widely available.

A pelvic MRI can tell you: how far deep disease extends, whether the bowel, bladder, or ureters are involved, and what a surgeon would be walking into. It is a mapping tool, ordered when the answer would change the plan.

Neither one can tell you: that you do not have endometriosis.

Blood tests do not settle it either. CA-125 rises in endometriosis, and it also rises in fibroids, pelvic inflammation, ovulation, and pregnancy, and it can be normal in significant disease. ACOG's 2026 guideline states that blood, urine, and endometrial biomarkers should not be used to diagnose endometriosis. If someone offers you a blood test that promises to answer this question, that is not where the field is.

Laparoscopy with a tissue sample remains the only way to confirm superficial peritoneal disease, and even that has a human element, since subtle lesions can look clear, white, or red rather than the classic dark powder-burn appearance, and what gets recognized depends on the surgeon's familiarity with the disease. What has changed, and changed in your favor, is that both ACOG and ESHRE now say a clinical diagnosis based on symptoms and examination is enough to start treatment. You no longer have to earn treatment by getting through an operation first.

What can primary care do while you wait for a specialist?

A great deal, and this is the part that usually goes unused. Fishtown Medicine does not perform gynecologic surgery, and I cannot confirm endometriosis without laparoscopy. What primary care can do is everything on either side of that operation, and most of the value lives there.

Take the history properly, mapped to the cycle. The highest-yield diagnostic instrument in this disease is a careful timeline, and it takes longer than a rushed visit allows. I want to know the age your periods started, when the pain started, whether it is cyclical or constant now, where it sits, what it does to your bowels and your bladder and when, whether penetration hurts and whether it hurts afterward, how many days a month you lose, what you have tried and at what dose and for how long, and what happened when you stopped birth control. A symptom-and-cycle diary kept over 2 or 3 cycles turns a vague story into a pattern that a specialist can act on.

Examine you for the findings that raise suspicion. Tenderness in the posterior fornix or nodularity along the uterosacral ligaments, a uterus that is fixed and retroverted rather than mobile, focal tenderness at a specific point rather than diffuse discomfort, and pelvic floor muscles that reproduce your exact pain when palpated. An abdominal wall source can be separated from a deeper one at the bedside with Carnett's test, where tenderness that worsens when you tense your abdominal muscles points at the wall rather than at the organs beneath it. Where an in-person exam is needed, Fishtown Medicine arranges it.

Order the imaging that helps, and say plainly what it answers. Transvaginal ultrasound first, read by someone who looks for endometriosis rather than only for cysts. MRI when deep disease is suspected or when a surgeon will need a map. Then the sentence that should follow every result and rarely does: this scan being normal does not mean you do not have this.

Work up and treat the conditions that mimic it or travel with it. More on those below. Sorting them is often what produces the first improvement a woman has had in years, and it happens without waiting for a surgical date.

Treat the bleeding and its consequences. Heavy periods drain iron, and low iron makes the uterus contract poorly, which makes the bleeding heavier. That loop is fixable, and it accounts for a good share of the fatigue and brain fog that get blamed on everything else. Checking ferritin rather than only hemoglobin is the difference between finding it and missing it.

Start symptomatic treatment now. Hormonal suppression, a pain plan built out of non-opioid tools, pelvic floor physical therapy, sleep, and the metabolic and inflammatory basics. Waiting 8 months for a surgical consult while taking nothing is a waste of 8 months of your life.

Write a referral that a specialist takes seriously. This is a skill, and it changes what happens at the other end.

What else causes this pain, and what travels alongside endometriosis?

Chronic pelvic pain is rarely a single-organ problem, and the conditions below both mimic endometriosis and coexist with it. Sorting them is most of the clinical work.

Interstitial cystitis and bladder pain syndrome. Bladder pain that builds as the bladder fills and eases after voiding, urgency and frequency, and repeatedly negative urine cultures. The overlap with endometriosis is substantial, and reported coexistence in chronic pelvic pain populations varies widely across studies, from around 15% to well over half. Antibiotics keep getting prescribed and keep failing. Bladder pain with negative cultures covers this in full.

Irritable bowel syndrome and small intestinal bacterial overgrowth. Bloating, alternating stool pattern, and pain that improves after a bowel movement. The label is often applied before anyone checks whether the symptoms track the menstrual cycle, which is the question that separates gut disease from cyclical bowel involvement. See IBS and SIBO and bloating and digestive discomfort.

Pelvic floor myofascial dysfunction. Chronically tight, tender pelvic floor muscles refer pain into the pelvis, low back, abdomen, and thighs, and they hurt with penetration. In one study of women with chronic pelvic pain, myofascial trigger points were present in over 90% of those with pain, and signs of central sensitization were most common in the group with a history of endometriosis. This one matters because it is treatable with pelvic floor physical therapy, and because it explains why some women still hurt after excellent surgery.

Abdominal wall pain. Nerve entrapment or trigger points in the abdominal wall, sometimes after a cesarean or laparoscopy, produce focal pain that is easy to attribute to an organ. Carnett's test separates them in about 30 seconds.

Adenomyosis. Endometrial tissue growing into the muscular wall of the uterus. The classic picture is heavy bleeding with a bulky, boggy, tender uterus and progressively worsening cramps, and it frequently coexists with endometriosis. Unlike superficial endometriosis, adenomyosis usually is visible, on ultrasound using the MUSA criteria or on MRI, which is one of the arguments for imaging even when you already suspect endometriosis. See heavy periods and anemia and abdominal and pelvic imaging.

Ovarian cysts, fibroids, pelvic inflammatory disease, hip and sacroiliac pathology, and inflammatory bowel disease round out the differential. Two or three of these are often present at once, which is why a plan that addresses only the endometriosis frequently underdelivers.

Is endometriosis part of the hypermobility, POTS, and mast cell cluster?

You will see this claim everywhere, so here is what the evidence supports and where it runs out.

What is established. The clustering of hypermobile Ehlers-Danlos syndrome, postural orthostatic tachycardia syndrome, and mast cell activation problems is well described in the literature, and Fishtown Medicine sees that triad often enough to have built a page for each of them. Separately, mast cells are present in higher numbers inside endometriotic lesions, frequently in a degranulated state, and they sit close to nerve fibers within those lesions. That has been documented since Anaf and colleagues published on pain, mast cells, and nerves in 2006, and more recent work has described the signaling between mast cells and sensory nerves that appears to amplify pain locally.

What is not established. Endometriosis belonging to that same clinical cluster is a hypothesis under investigation rather than a settled association, and much of what circulates about it online traces back to specialty-clinic blogs rather than to primary literature.

Take the pieces one at a time. The mast cell work in endometriosis is mechanistic: tissue studies, cell experiments, animal models, and reviews. That is different from evidence that women diagnosed with mast cell activation syndrome have more endometriosis, which has not been shown in a population study. For hypermobile Ehlers-Danlos, the primary literature has not established a significant association with endometriosis; a figure of 6% to 23% gets repeated online and traces to a 2022 conference presentation rather than to a peer-reviewed cohort. For POTS, the most direct data available points the other way: a 2025 cross-sectional survey of 167 young women in the Long-Term POTS Outcomes Survey found that endometriosis was not reported at higher rates than in the general population, alongside the finding that POTS symptoms worsened around menses in about 72% of them.

A different overlap is well documented, and it is the one that changes a treatment plan. A 2024 cross-sectional survey of 525 women with chronic pelvic and abdominal pain, 133 of whom reported endometriosis, measured chronic overlapping pain conditions, the group that includes fibromyalgia, irritable bowel syndrome, interstitial cystitis, temporomandibular disorder, chronic fatigue syndrome, migraine, vulvodynia, and chronic low back pain. A quarter of the women with endometriosis carried 3 or more of those conditions, against 12% of the women who had pelvic pain without endometriosis, and fibromyalgia, chronic fatigue syndrome, and temporomandibular disorder were each more common in the endometriosis group. Their pain was more severe, interfered more with daily life, and had a larger effect on work and relationships. The result that matters clinically is that the number of overlapping conditions predicted how badly a woman was doing whether or not endometriosis was among them. That survey was online and cross-sectional and relied on self-reported diagnoses, the endometriosis diagnosis included, so it describes an association rather than proving one. It still points somewhere useful: treating the lesions and stopping there leaves a large part of the pain load untouched in the women carrying several of these at once.

Here is where that leaves the question. Mast cells are part of how endometriosis lesions generate pain, and that is documented tissue biology. Whether endometriosis belongs in the same clinical cluster as hypermobility, dysautonomia, and mast cell activation syndrome is unresolved, and the direct data is thin and partly contradictory. In the clinic the picture is mixed in the same way: some of our patients do carry the cluster alongside endometriosis, and most of the people we see for hypermobility and dysautonomia have no cycle-related or fertility concerns at all.

What that means for your care is simple and does not depend on resolving the question. If you have several of these things, each one gets evaluated on its own criteria and treated on its own merits. A Beighton score, an active stand test, and an endometriosis symptom map are 3 separate pieces of work, and skipping any of them because a cluster label felt like an explanation is how people end up under-treated for the piece that was most fixable.

Which treatments have evidence behind them?

Treatment aims at pain, at bleeding, at fertility when that is the goal, and at the overlapping conditions. Here is where the evidence sits.

Hormonal suppression is first-line, and the evidence is stronger for some options than others. Combined hormonal contraception has been the default for decades, and the trial evidence supporting it is thinner than its popularity suggests. Progestins have better randomized data: norethindrone acetate and dienogest both carry regulatory approval for endometriosis, and oral progestin-only treatment has randomized evidence for pelvic pain. The levonorgestrel intrauterine system is effective for endometriosis-associated symptoms with fewer systemic effects than oral options, and randomized comparisons against dienogest show similar quality-of-life improvement. Which one fits depends on your bleeding pattern, your contraceptive needs, your mood history, and what you have already tried.

GnRH agonists and antagonists are second-line. Oral GnRH antagonists like elagolix and relugolix reduce dysmenorrhea, non-cyclical pelvic pain, and pain with sex in randomized trials, and current guidelines reserve them for symptoms that first-line treatment did not control. They induce a low-estrogen state, so hormonal add-back therapy is standard to protect bone density and limit hot flashes.

Anti-inflammatories are widely used and thinly studied. The Cochrane review of NSAIDs for endometriosis pain found the evidence inconclusive, with a single small trial of 24 women available for analysis. That does not mean naproxen or ibuprofen fails you; it means nobody has done the trial. Taking an anti-inflammatory starting a day before the pain rather than after it has begun is a reasonable, low-cost approach with a plausible mechanism and no strong data behind the timing.

Pelvic floor physical therapy earns its place. Given how common myofascial dysfunction and central sensitization are in this population, a skilled pelvic floor therapist often produces more day-to-day change than a medication does. Kegels are the wrong move when the floor is already too tight, and prescribing them anyway is a common mistake that makes symptoms worse.

Neuromodulators are a mixed picture. Gabapentin was tested head-to-head against placebo for chronic pelvic pain in women in the GaPP2 trial published in The Lancet in 2020, and it did not outperform placebo, with more side effects. Amitriptyline and duloxetine are used for centrally mediated pain with evidence borrowed from other conditions rather than generated in endometriosis.

Low-dose naltrexone is something we prescribe, and its evidence base in endometriosis is close to empty. Naltrexone is an opioid antagonist rather than an opioid, so it sits fully inside our prescribing policy, and at low doses it appears to act on glial cells and inflammatory signaling rather than on pain receptors. The one phase 3 randomized trial testing low-dose naltrexone alongside standard hormonal treatment, NCT03970330, was terminated when the investigator left and funding ran out, and it never reported results. Systematic reviews of low-dose naltrexone across chronic pain describe small trials with limited replication. It is a reasonable option to trial in the right person, with a clear plan for deciding whether it helped, and it is not a proven endometriosis therapy. Our low-dose naltrexone guide goes deeper.

Diet and supplements: modest signal, weak evidence, honest framing. The best-supported supplement finding is a 2024 systematic review and meta-analysis of 5 randomized trials in which combined vitamin C and vitamin E supplementation reduced chronic pelvic pain, dysmenorrhea, and pain with sex. The trials are small and the effect sizes look larger than one would expect, so I hold it loosely. Beyond that pairing, a 2026 critical review of 34 studies covering omega-3, vitamin D, curcumin, resveratrol, N-acetylcysteine, alpha-lipoic acid, zinc, and magnesium found the results mixed and much of the human evidence limited, with several signals coming from animal work. Anti-inflammatory eating patterns help some women and have not been tested rigorously. None of this substitutes for treatment, and any page selling you a supplement protocol as an endometriosis cure is ahead of the data.

Surgery, when it is indicated, means excision by someone who does it often. Fishtown Medicine does not perform it, and getting you to the right surgeon is part of the job. Surgery is most compelling for deep infiltrating disease, endometriomas affecting fertility, obstructive disease involving bowel or ureters, and pain that has not responded to well-run medical treatment.

On opioids. Fishtown Medicine does not prescribe opioids for any indication, and for a pain problem that may be with you for decades, they are the wrong long-term instrument regardless. Pain control here is built out of hormonal suppression, anti-inflammatories, physical therapy, neuromodulation where it fits, sleep, and treatment of the overlapping conditions.

Should you freeze eggs before endometriosis surgery?

This question arrives when a woman is told she needs an endometrioma removed and nobody has mentioned what that operation costs her ovary. It has a deadline attached, because the sequence matters and the reserve does not come back.

Start with what the disease does before any surgeon is involved. Somewhere between 30% and 50% of women with endometriosis have difficulty conceiving, and endometriomas, the ovarian cysts filled with old blood, are present in 17% to 44% of women with the disease. Those cysts damage the ovary around them on their own. Anti-Müllerian hormone, the blood marker that estimates how many eggs remain, runs lower in women with endometriosis, and in an ovary carrying an endometrioma the antral follicle count is lower than in the same woman's other ovary before she has had any operation.

Surgery then takes more. Removing an endometrioma by stripping the cyst wall away from the ovary carries off healthy ovarian tissue with it, and AMH falls after the operation across multiple studies and meta-analyses. Reported rates of the ovary failing altogether after cystectomy run from 2.4% to 13%. The decline is steeper when both ovaries carry endometriomas, and a second operation on the same ovary costs more reserve than the first while doing less for fertility.

Freezing unfertilized eggs is the technique that fits this situation, because it needs no partner, takes nothing further from the ovary, and leaves the decision about what to do with the eggs for later. In the published series, women with endometriosis stored around 9 eggs per patient on average, and those who had already had ovarian surgery stored fewer. Close to 4 in 10 needed more than one round of stimulation to reach a workable number. Among 485 women who came back to use what they had frozen, 83% of the eggs survived thawing and 46% went on to a live birth, with age moving that figure more than anything about the endometriosis did.

The reassuring finding in that same work is that when the same number of eggs was stored, women with endometriosis had live birth rates matching women who froze eggs for other reasons. The disease appears to cost a woman eggs rather than egg quality, which is why the number banked carries so much weight.

The situations where this is most worth raising are bilateral endometriomas heading for surgery, an endometrioma that has come back on the other side after a previous operation, a low AMH before any surgery has happened, and age over 35. Ovarian stimulation for egg freezing has not been shown to make endometriosis progress, so that is not a reason to hold back.

Two things belong in the same breath. No major society guideline names endometriosis specifically as an indication for fertility preservation, though a 2015 joint ESHRE and ASRM expert meeting listed it among the benign conditions where the option should be discussed. And egg freezing is paid out of pocket in most cases. This is a conversation to have before the surgical date is set, and our fertility page covers what the workup looks like here.

What does endometriosis mean for the rest of your health?

Endometriosis is a systemic inflammatory condition, and a few long-term associations are supported well enough to act on.

Ovarian cancer. The 2021 meta-analysis in Human Reproduction Update found a summary relative risk of 1.93 for ovarian cancer across 24 studies, concentrated in the clear cell and endometrioid subtypes. Because ovarian cancer is uncommon to begin with, at a lifetime risk of a bit over 1% in the general population, roughly doubling that relative risk still leaves the absolute risk low. The same analysis found a very small positive association with breast cancer and no significant association with colorectal or endometrial cancer or melanoma. This is a reason for informed awareness rather than alarm, and no ovarian cancer screening strategy has been shown to improve outcomes in this group.

Cardiovascular and stroke risk. In the Nurses' Health Study II, women with laparoscopically confirmed endometriosis had higher rates of coronary heart disease, including myocardial infarction, angina, and revascularization. A prospective analysis in Stroke in the same cohort found a 34% greater risk of incident stroke, with a meaningful portion of the association mediated by hysterectomy, oophorectomy, hormone therapy, and hypertension. This is why the 2024 stroke prevention guideline names endometriosis among the sex-specific risk factors clinicians should screen for. In practice it means your blood pressure, ApoB, lipids, glucose, and inflammatory markers deserve attention earlier than the standard age-based schedule would suggest.

Autoimmune conditions. A systematic review and meta-analysis in Human Reproduction Update covering 26 studies found associations between endometriosis and several autoimmune diseases, including lupus, Sjögren syndrome, rheumatoid arthritis, autoimmune thyroid disease, celiac disease, multiple sclerosis, and inflammatory bowel disease. The authors were careful to point out that only 5 of the 26 studies were high quality, so treat this as a reason to keep your ears open for new autoimmune symptoms rather than as an established causal chain.

Fertility. Roughly 30% to 50% of women with endometriosis have difficulty conceiving. If pregnancy is in your plans, that changes the timing of the conversation, and it belongs on the table early rather than after 2 years of trying.

Iron and energy. Heavy bleeding drives iron deficiency, and iron deficiency without anemia is a common and correctable cause of the exhaustion, hair shedding, and brain fog that get attributed to the pain alone.

How do you get a referral that gets taken seriously?

Who you are referred to matters as much as whether you are referred. What you are looking for is a gynecologic surgeon who treats endometriosis frequently, performs excision rather than only ablation of superficial disease, and works alongside pelvic floor physical therapy and pain management. It is a fair question to ask a practice directly how many endometriosis cases they handle in a year and whether they excise.

What makes a referral useful at the other end is specificity. A letter that says "pelvic pain, please evaluate" produces a different appointment than one that carries:

1. The cycle-mapped symptom history. What hurts, where, and where in the cycle it falls, with the duration in years.
2. The functional cost. Days of work or school missed per month, effect on sex and on your relationship, effect on sleep.
3. The examination findings. Uterosacral nodularity, a fixed uterus, focal tenderness, pelvic floor findings, Carnett's result.
4. The imaging already done and its interpretation. The report itself, plus a sentence saying that the negative study does not exclude superficial disease.
5. What has already been tried, at what dose, for how long, and what happened. This is the item most often missing and the one that most changes the specialist's plan.
6. The specific question being asked. Diagnostic laparoscopy, surgical planning for deep disease, fertility evaluation, or a second opinion on medical management.
7. Your goals. Pain relief, fertility, or both, because the plan diverges depending on the answer.

Bring your own copy of that document to the appointment. Patients who arrive with a written 2-page history get a different visit than patients who are asked to recall 12 years from memory in 15 minutes.

How Fishtown Medicine approaches endometriosis

Fishtown Medicine is a direct primary care practice in Philadelphia, and this condition is one where the structure of the practice changes the medicine available to you. The first visit runs 60 to 90 minutes, which is what a 12-year symptom history requires. Follow-up happens through secure messaging, phone, and video, so titrating a medication or reacting to a bad cycle is a same-week conversation rather than a 3-month wait.

The work runs in this order. We take the full history and map it to your cycle. We examine for the findings that raise or lower suspicion, arranging an in-person exam where it is needed. We order transvaginal ultrasound, and MRI when deep disease is on the table, and we tell you what each one can and cannot settle. We work up and treat the mimics and the companions in parallel: bladder, bowel, pelvic floor, thyroid, iron. We start hormonal and symptomatic treatment while everything else is in motion. We screen the cardiometabolic picture earlier than the standard schedule, because of the stroke and coronary associations above. And we write the referral, coordinate it, and stay in the conversation after you have seen the specialist, which is where most referrals go quiet.

Lab work and imaging are ordered through Quest, Labcorp, and local imaging centers and can be billed to your insurance in the usual way. The visits themselves are covered by membership or a care package rather than billed to insurance, which is what buys the time this condition needs.

If you are in Philadelphia and have been carrying this for years while being told your scans were fine, that history is worth reopening with someone who has time to read it. The way to start is to tell Dr. Ash what your cycles have been doing.

Guidance from the Clinic

"The sentence I hear most in these visits is some version of 'they did an ultrasound and it was normal, so they said it wasn't endometriosis.' That sentence has cost women years. A normal scan tells me you probably don't have an endometrioma or big deep disease, and it tells me nothing about the flat lesions that are the most common form of this. When I say that out loud in the room, people sometimes cry, because they have spent a decade believing a test had ruled them out when it never could. My job in that first visit is to take the history nobody had time for, sort out what else is contributing, start you on something that helps this month, and write the referral that gets you in front of the right surgeon with your story already assembled."

Related at Fishtown Medicine

• Painful periods that everyone told you were normal - sorting ordinary period pain from the kind with a cause underneath it, and how to time an anti-inflammatory so it works
• Adenomyosis, when periods are heavy and cramping is deep - the uterine-wall condition this one is most often confused with, and most often accompanies
• Bladder Pain When Every Urine Culture Comes Back Negative - interstitial cystitis, the condition that most often travels with this one
• IBS and SIBO - when the gut label was applied before anyone checked the cycle
• Bloating and Digestive Discomfort - including the cyclical bloating many patients call endo belly
• Heavy Periods and Anemia - breaking the iron loop that drives the fatigue
• Abdominal and Pelvic Imaging - what each study answers and when it is worth ordering
• Low-Dose Naltrexone - mechanism, dosing, and where the evidence is thin
• POTS, MCAS, and Hypermobility - the cluster this question keeps coming up alongside
• Hypermobility and hEDS Care - how the hypermobility evaluation is done
• When You Feel Dismissed by Your Doctor - why this pattern of delay happens and how to be heard
• Stroke Prevention - the sex-specific risk factors that now include endometriosis
• PCOS Is Now PMOS - another under-diagnosed condition women wait years to have named
• Women's Hormone Health - the fuller hormonal picture across life stages

Scientific References

1. American College of Obstetricians and Gynecologists. "Diagnosis of Endometriosis." ACOG Clinical Practice Guideline. Obstetrics & Gynecology, published online February 19, 2026.
2. ESHRE Endometriosis Guideline Development Group. "ESHRE guideline: endometriosis." Human Reproduction Open. 2022;2022(2):hoac009.
3. De Corte P, Klinghardt M, von Stockum S, Heinemann K. "Time to Diagnose Endometriosis: Current Status, Challenges and Regional Characteristics, A Systematic Literature Review." BJOG. 2025;132(2):118-130.
4. World Health Organization. "Endometriosis." WHO Fact Sheet.
5. Guerriero S, Condous G, Rolla M, et al. "Addendum to consensus opinion from the International Deep Endometriosis Analysis (IDEA) group: sonographic evaluation of superficial endometriosis." Ultrasound in Obstetrics & Gynecology. 2025. doi:10.1002/uog.29288
6. Anaf V, Chapron C, El Nakadi I, et al. "Pain, mast cells, and nerves in peritoneal, ovarian, and deep infiltrating endometriosis." Fertility and Sterility. 2006;86(5):1336-1343.
7. Stratton P, Khachikyan I, Sinaii N, Ortiz R, Shah J. "Association of Chronic Pelvic Pain and Endometriosis With Signs of Sensitization and Myofascial Pain." Obstetrics & Gynecology. 2015;125(3):719-728.
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