Capillary malformation-arteriovenous malformation (CM-AVM) syndrome is a genetic condition that causes two main kinds of blood-vessel changes. First, many people have several small, pink-to-red flat skin spots called capillary malformations (CMs). Second, some people also have deeper, fast-flow blood-vessel connections called arteriovenous malformations (AVMs) or arteriovenous fistulas (AVFs), where arteries connect to veins without the usual tiny capillary bed in between. These fast-flow lesions can steal blood, grow over time, and sometimes lead to pain, swelling, bleeding, or heart strain if large. The skin spots are usually round or oval, often 0.5–2 cm, commonly on the face and limbs, and may be present at birth or appear in childhood. The condition is usually inherited in an autosomal dominant way (one changed gene copy is enough), most often due to a change in the RASA1 gene (CM-AVM1) or the EPHB4 gene (CM-AVM2). Not everyone in a family is affected to the same degree, and some people have very mild signs. ScienceDirect+3NCBI+3MedlinePlus+3
CM-AVM is a genetic blood-vessel disorder. People develop many small, round, pink-red birthmarks on the skin called capillary malformations (CMs). Some individuals also form fast-flow vascular lesions—arteriovenous malformations (AVMs) or arteriovenous fistulas (AVFs)—where arteries and veins connect abnormally and blood rushes through too fast. These fast-flow lesions can occur in skin, muscle, bone, or the brain/spinal cord and may cause pain, bleeding, heart strain, or neurologic symptoms. CM-AVM is usually inherited in an autosomal-dominant way and is most often caused by changes in the RASA1 gene (CM-AVM1) or EPHB4 gene (CM-AVM2). MedlinePlus+2NCBI+
RASA1 makes p120-RasGAP, a “brake” on the RAS/MAPK signaling pathway that governs vessel growth; losing this brake can drive abnormal vessel connections. EPHB4 is a receptor crucial for separating arterial and venous flow during development; loss-of-function variants disturb that separation and can promote fast-flow lesions. Many patients inherit a faulty copy and then develop a “second hit” in some cells, which is why spots or AVMs appear in patches. Actas Dermo-Sifiliográficas+2American Heart Association Journals+2
Other names
CM-AVM syndrome
RASA1-related CM-AVM (also called CM-AVM type 1)
EPHB4-related CM-AVM (also called CM-AVM type 2)
Some patients with CM-AVM may overlap with Parkes Weber phenotype (high-flow limb lesions with overgrowth), but Parkes Weber can also occur from other genes; careful evaluation is needed. NCBI+2ARUP Consult+2
Types
Type 1 (CM-AVM1): due to RASA1 gene variants. People usually have multiple small CMs and may have one or more AVMs/AVFs in the skin, muscle, bone, brain, or spine. Severity ranges from very mild skin spots to serious fast-flow lesions. NCBI
Type 2 (CM-AVM2): due to EPHB4 gene variants. The skin spots and AVMs/AVFs can look similar to type 1. Some families show nosebleeds or vein changes that can resemble other vascular conditions, so genetic testing helps. American Heart Association Journals+1
Notes on inheritance and “second hits”: CM-AVM is usually autosomal dominant. Many patients inherit the variant; others are “de novo” (new in the child). Research suggests that a germline variant plus a local second hit in tissue may explain why lesions are patchy and multifocal. Mosaicism can also occur, which can make testing harder. JAMA Network+1
How doctors categorize it
CM-AVM type 1 (CM-AVM1) — RASA1 gene variants. Typical multiple small CMs; some have fast-flow lesions (AVMs/AVFs) in skin, bone, brain, or spine; a subset shows Parkes Weber features (capillary marks plus limb overgrowth due to many small AV connections). ScienceDirect+1
CM-AVM type 2 (CM-AVM2) — EPHB4 gene variants. Overlaps with CM-AVM1 but may also show telangiectasia, Bier spots (pale speckles), and nosebleeds in some families; occasionally overlaps with hereditary hemorrhagic telangiectasia-like signs. Orpha+1
Mosaic CM-AVM — the variant is present in only some cells (a “postzygotic” or somatic change), which can create patches or segments of involvement and may underlie some Parkes Weber cases. Ovid+1
CM-AVM with extracutaneous fast-flow lesions — emphasis on AVMs/AVFs in muscle, bone, brain, or spine; these need more urgent imaging and management. JAMA Network
Fetal/neonatal-onset CM-AVM — rare cases where features are seen before birth or in early infancy, sometimes with severe fast-flow lesions and high-output heart failure. MDPI
Causes
In CM-AVM, “causes” mainly refers to gene-level reasons and biological mechanisms. Environmental factors don’t cause the syndrome but can unmask or worsen lesions already “programmed” by the genes.
Pathogenic variants in RASA1 — Loss-of-function changes disrupt a key brake on RAS/MAPK signaling, leading to abnormal vessel growth and connections. ScienceDirect+1
Pathogenic variants in EPHB4 — Changes in this receptor affect arterial–venous identity and vascular guidance; can produce the CM-AVM2 pattern with telangiectasia and nosebleeds. PubMed+1
Autosomal dominant inheritance — A parent with a pathogenic variant has a 50% chance to pass it to a child. Expression varies widely, even in the same family. NCBI
De novo variants — Some people are the first in the family with the change; parents test negative. NCBI
Mosaic (postzygotic) variants — The change occurs after conception in a subset of cells; can produce segmental or localized disease. Ovid
“Two-hit” or second-event model in lesions — A second, local somatic alteration in the same pathway may help explain why only certain spots become AVMs/AVFs. JAMA Network
Abnormal arterial–venous specification — Disturbed EPHB4/EFNB2 and RAS signaling can blur arterial vs venous identity, encouraging direct artery-to-vein channels. PubMed
Excess RAS/MAPK pathway activity — Without RASA1 restraint, growth signaling can be overactive in endothelial cells. ScienceDirect
mTOR pathway upregulation downstream of EPHB4 changes — Experimental evidence links EPHB4 loss to mTORC1 activation in vascular cells. PubMed
Defective endothelial cell migration and pruning — Vessels may not remodel properly during development, leaving enlarged capillaries or AV shunts. NCBI
Hemodynamic stress — High flow through an abnormal channel can enlarge and maintain the lesion once formed. (Physiologic principle discussed across AVM reviews.) BioMed Central
Puberty-related hormonal changes — Growth spurts and hormones can make existing lesions more noticeable or symptomatic. (Observed clinically in vascular malformations.) BioMed Central
Pregnancy — Increased blood volume and hormones may worsen symptoms or enlarge fast-flow lesions in predisposed individuals. (General AVM literature observation.) BioMed Central
Trauma or procedures — Injury can draw attention to a lesion or trigger growth in an already abnormal vascular bed. (General principle in AVM care.) BioMed Central
Inflammation — Inflammatory mediators can alter vessel tone and permeability, aggravating symptoms. (General mechanism noted in vascular anomaly reviews.) BioMed Central
Coexisting lymphatic abnormalities with EPHB4 variants — Some EPHB4-related disorders include lymphatic dysfunction that may interact with blood-vessel problems. Nature
Genetic variability (different variants different effects) — Not all variants act the same; some families show more telangiectasia, others more fast-flow lesions. ScienceDirect
Variable penetrance — Some people with a variant show few or no signs; others have many lesions—reason still being studied. NCBI
Prenatal developmental timing — Earlier second events (somatic changes) may produce broader, more severe patterns (e.g., Parkes Weber). JAMA Network
Rare additional genes or modifiers (under study) — Most cases are RASA1 or EPHB4, but research continues on other contributors and modifiers. Nature
Symptoms and signs
Multiple small pink-red skin spots (capillary malformations) — Round/oval, often 0.5–2 cm; sometimes a pale ring; may be present at birth or appear later. Usually painless. NCBI
Warmth or a subtle “thrill” over a spot — If an underlying fast-flow channel is present, a gentle vibration can sometimes be felt. JAMA Network
Audible “bruit” (whooshing) with a stethoscope — A sign of high-speed blood flow through an AVM/AVF. JAMA Network
Pain or tenderness — Can occur when fast-flow lesions expand or irritate nearby tissues. JAMA Network
Swelling or warmth of a limb — Linked to increased flow or shunting in the limb. JAMA Network
Limb overgrowth — Soft-tissue and bone hypertrophy may occur (Parkes Weber spectrum). JAMA Network
Skin ulceration or bleeding — Fragile surface vessels over AVMs can bleed. JAMA Network
Headaches, seizures, or neurologic changes — If brain AVMs are present; symptoms depend on location. JAMA Network
Back pain, weakness, or sensory changes — Possible signs of spinal AV shunts. JAMA Network
Nosebleeds, lip/mouth telangiectasia — More often described in EPHB4-related disease. Orpha
Pale macules (“Bier spots”) — Speckled pale areas that become obvious with limb positioning; reported in CM-AVM2. Orpha
Heart palpitations, shortness of breath, fatigue — Large or multiple AVFs can cause high-output heart failure, especially in infants. JAMA Network
Cosmetic distress or anxiety — Visible spots can affect self-image and quality of life. (General CM-AVM experience.) Cincinnati Children’s
Iron-deficiency symptoms — Chronic small bleeds can lead to anemia with tiredness or dizziness. JAMA Network
Prenatal signs — Rarely, fetal hydrops or very high-flow lesions detected on ultrasound. MDPI
Diagnostic tests
A) Physical examination (bedside checks)
Full skin inspection — The doctor maps the number, size, and look of capillary spots and checks for the pale halo typical of CM-AVM. This helps decide if genetic testing and imaging are needed. BioMed Central
Palpation for warmth and “thrill” — Using fingertips, the clinician feels for warmth or vibration that suggests high-flow blood under a lesion. JAMA Network
Auscultation for a bruit — Listening with a stethoscope over suspicious areas can detect the whooshing sound of an AVM/AVF. JAMA Network
Limb length and girth measurements — Serial tape and ruler measurements identify overgrowth or swelling, which can point to deeper fast-flow changes. JAMA Network
Focused neurologic exam — Strength, sensation, reflexes, and gait are checked if brain or spine involvement is possible. Findings guide urgent imaging. JAMA Network
B) Manual/office tests (simple, non-lab tools)
Diascopy (blanching test with a clear slide) — Gentle pressure turns capillary marks pale and then they refill; this helps distinguish them from bruises or pigmented spots. Cincinnati Children’s
Handheld Doppler assessment — A small probe can detect fast blood-flow signals in the clinic; a strong continuous signal suggests an AVF/AVM. (Screening step; imaging still needed.) BioMed Central
Segmental limb pressures / plethysmography — Cuffs and sensors compare flow and volume changes along a limb; unusual patterns hint at shunting. BioMed Central
Nailfold capillaroscopy (where available) — A microscope inspects tiny nailfold vessels; abnormal patterns can support a vascular-malformation phenotype in the right context. BioMed Central
Epistaxis and mucosal check — Visual inspection for lip or oral telangiectasia and inquiry about nosebleeds, especially in EPHB4-related disease. Orpha
C) Laboratory and pathological studies
Germline genetic testing for RASA1 and EPHB4 — A blood or saliva test looks for variants that confirm CM-AVM1 or CM-AVM2. Panel or exome tests are commonly used. Results guide counseling and family screening. ARUP Consult
Targeted testing for mosaic/somatic variants — If blood is negative but suspicion remains, testing DNA from the lesion can find postzygotic changes. Ovid
Complete blood count (CBC) and iron studies — If there are frequent nosebleeds or skin bleeds, labs check for iron-deficiency anemia. JAMA Network
Coagulation profile (PT/INR, aPTT) — Ordered when bleeding is a concern or before a procedure near a lesion. JAMA Network
Brain natriuretic peptide (BNP) or NT-proBNP — If a large AVF is suspected in an infant or adult with shortness of breath or fatigue, these heart-strain markers may help triage urgency. JAMA Network
Skin biopsy (rarely needed) — Most cases do not need a biopsy. If performed, it shows enlarged superficial capillaries; however, biopsy can bleed and is generally avoided unless diagnosis is unclear. Actas Dermo-Sifiliográficas
D) Electrodiagnostic / physiologic tests
Electrocardiogram (ECG) — Looks for heart strain or rhythm issues if a large shunt is taxing the heart. JAMA Network
Noninvasive plethysmography / pulse volume recordings — Sensors track limb blood-volume changes with each heartbeat; high-flow shunts create characteristic waveforms. BioMed Central
E) Imaging tests
Duplex Doppler ultrasound — First-line imaging for suspected fast-flow lesions. It shows vessel anatomy and measures flow to spot AVMs/AVFs; it is painless and radiation-free. BioMed Central
MRI with MRA (and, when needed, MRV) — MRI shows soft tissues and nerves; MRA maps arteries; MRV maps veins. This combination defines the extent and depth of a lesion, especially in the brain, spine, head-and-neck, or limbs. BioMed Central
CT angiography (CTA) — Useful when MRI is not possible or for certain bones/lungs; it outlines vessels quickly but uses radiation and contrast. BioMed Central
Catheter (digital subtraction) angiography — The gold standard for detailed vessel mapping when a procedure (embolization) is planned. A tiny catheter injects dye directly into arteries; images guide therapy. BioMed Central
Echocardiography — Ultrasound of the heart to look for high-output changes or heart failure in patients with large shunts (common in severe infant cases). JAMA Network
Prenatal ultrasound and fetal echocardiography — In rare fetal cases, imaging can show high-flow lesions and heart strain before birth, guiding delivery and care. MDPI
Targeted brain/spine MRI — For headaches, seizures, weakness, or sensory changes, this looks for intracranial or spinal AVMs/AVFs that need early management. JAMA Network
Whole-body MRI (selected centers) — Some centers screen for deep lesions when the clinical picture and genetics suggest higher risk; protocols vary. BioMed Central
Treatment overview
There is no single FDA-approved drug specifically for CM-AVM. Care is individualized by a multidisciplinary vascular anomalies team (dermatology, interventional radiology, surgery, genetics, cardiology/neuro). Options range from observation and skin laser to embolization and staged surgery. Some systemic agents targeting mTOR (sirolimus/everolimus) or MAPK/MEK (trametinib) pathways are used off-label in complex cases, supported by growing—but still limited—evidence. BioMed Central+2PubMed Central+2
Non-pharmacological treatments (therapies & others)
Education & watchful waiting – Many tiny CMs are harmless. Families learn danger signs (sudden pain, swelling, bleed, neuro signs). Early reporting prevents complications. Follow-up schedules spot growth or new fast-flow changes. NCBI
Sun and skin care – Gentle moisturizers, SPF, avoid trauma over thin skin covering AVMs. Good skin care reduces bleeding risk and improves comfort. MedlinePlus
Compression therapy (custom garments) – Graduated compression for limb AVMs can reduce pain, swelling, and venous hypertension; used carefully in fast-flow lesions under specialist guidance. Journal of Vascular Surgery
Activity pacing & limb elevation – Short rest and elevation after exertion reduce throbbing and edema around lesions. Athletes adjust training with team input. BioMed Central
Laser therapy for capillary malformations – Pulsed-dye or similar lasers lighten color and sometimes reduce bleeding of superficial lesions; multiple sessions often needed. Journal of Vascular Surgery
Sclerotherapy (specialist) – Image-guided injection (e.g., ethanol, polidocanol, bleomycin) targets nidus or outflow channels in selected components; often staged and combined with embolization. PubMed Central
Endovascular embolization – Catheter-based occlusion of AVM feeders/nidus using coils, liquid embolics; usually staged and sometimes followed by surgery to reduce recurrence. PubMed Central
Surgery (conservative, staged) – Resection works best after pre-op embolization in well-defined lesions; aims to remove nidus and reconstruct tissue while protecting function. Journal of Vascular Surgery
Pain management (non-opioid first) – Structured plan with acetaminophen/NSAIDs if safe, neuropathic agents for nerve pain, plus physical therapy; refer to pain specialists for complex cases. PubMed Central
Wound care – For ulcers/bleeds: gentle cleansing, non-adherent dressings, treat infection early; coordinate with interventional team if wounds reflect high-flow. BioMed Central
Cardiac monitoring in large shunts – Periodic echocardiograms if high-output concerns; early management prevents heart strain. BioMed Central
Neuro-surveillance – Imaging and neurology follow-up for brain/spinal AVMs to reduce risk of hemorrhage and seizures; emergency plans in place. MedlinePlus
Psychological support – Visible lesions and procedures can be stressful; counseling improves coping and quality of life. BioMed Central
Multidisciplinary case review – Regular tumor-board-style discussions align laser, sclerotherapy, embolization, surgery, and systemic agents. PubMed Central
Genetic counseling – Explains inheritance (50% chance to pass on), testing for relatives, and reproductive options. NCBI
Pregnancy planning – Fast-flow lesions can enlarge in pregnancy; pre-pregnancy imaging and plan reduce bleeding risk. BioMed Central
Dental/ENT care – Mouth/nasal lesions bleed; inform dentists, adjust procedures, and have hemostasis plans. BioMed Central
School/work accommodations – Avoid heavy trauma to affected limb, allow rest breaks, and provide emergency instructions for bleeding. BioMed Central
Physiotherapy – Gentle strength and flexibility protect joints and reduce pain in involved limbs; avoid high-impact stress on fragile tissues. BioMed Central
Patient-support networks – Connecting with vascular anomalies centers and rare-disease groups improves access to expert care. BioMed Central
Drug treatments
Important: The FDA has not approved any medication specifically for CM-AVM. Below are drugs used for related vascular anomalies or theoretical pathway targets. When a drug is off-label for CM-AVM, I state it clearly and cite the official FDA label plus clinical evidence where available.
Sirolimus (Rapamune) – mTOR inhibitor; off-label for complicated vascular anomalies including some AVMs. Typical adult doses are individualized with trough-level monitoring (per label for transplant). Trials/series show sirolimus can shrink lesion bulk, reduce pain/bleeding, and help as an adjunct to embolization in complex AVMs. Label: transplant rejection prophylaxis; adverse effects include mucositis, hyperlipidemia, infection risk. FDA Access Data+2PubMed Central+2
Everolimus (Afinitor/Afinitor Disperz) – mTOR inhibitor; off-label for complex malformations. Pediatric-friendly formulation exists; label indications include SEGA in tuberous sclerosis and various cancers. Side effects resemble sirolimus (stomatitis, infection risk). Evidence for AVMs is extrapolated from mTOR-pathway benefit in slow/complex malformations. FDA Access Data+1
Trametinib (Mekinist) – MEK inhibitor; off-label for some extracranial AVMs harboring MAP2K1 or RAS-MAPK activation. Case reports and early pilot studies show angiographic and clinical responses in difficult AVMs. Label indications are oncology (e.g., BRAF V600E/K tumors); adverse effects include rash, edema, cardiomyopathy, ocular events. FDA Access Data+2PubMed Central+2
Alpelisib (Vijoice) – PI3Kα inhibitor; approved for PROS, not CM-AVM, but highlights pathway-directed therapy in vascular anomalies. Accelerated approval was based on reduction in lesion volume and symptoms in PROS; adverse effects include hyperglycemia and rash. Not a standard for CM-AVM unless a PI3K pathway mutation is present. U.S. Food and Drug Administration+2PubMed Central+2
Propranolol (Hemangeol) – Beta-blocker approved for infantile hemangioma, not for AVMs; occasionally tried symptomatically for flow-related flushing or pain but not standard for CM-AVM. Risks include bradycardia and hypoglycemia in infants. FDA Access Data
Topical/Intralesional sirolimus – Investigational/off-label for superficial components; aims to reduce color and bleeding with lower systemic exposure; data are limited. (Systemic sirolimus data extrapolated.) PubMed Central
Doxycycline (anti-angiogenic properties) – Off-label adjunct explored in some vascular anomalies; evidence is limited; monitor photosensitivity and GI effects. (No FDA indication for AVMs.) PubMed Central
Bevacizumab (Avastin) – Anti-VEGF; off-label case reports for refractory AVMs (systemic or intra-lesional) exist, but bleeding/HTN risks and limited data make this non-routine. (FDA-approved in oncology; consult label for boxed warnings.) PubMed Central
Thalidomide/Lenalidomide – Anti-angiogenic; off-label, anecdotal use for bleeding control in vascular malformations; neuropathy and thrombosis risks limit use. (Oncologic labels.) PubMed Central
ACE inhibitors/ARB (e.g., enalapril/losartan) – Supportive, not lesion-shrinking; may help heart load in high-output failure from very large shunts, guided by cardiology. (Labels standard for hypertension/heart failure.) BioMed Central
Diuretics (e.g., furosemide) – For symptomatic fluid overload in high-output states; symptomatic only. BioMed Central
Anticonvulsants – For seizure control due to brain AVMs; drug choice per neurology. BioMed Central
Analgesics (acetaminophen/NSAIDs) – Pain control; avoid NSAIDs if bleeding risk is high; plan individualized. PubMed Central
Antibiotics (as needed) – For ulcer or secondary infection near lesions, not as a routine CM-AVM therapy. BioMed Central
Tranexamic acid (selected bleeding scenarios) – Off-label for mucosal bleeding control; assess thrombosis risk carefully. PubMed Central
Topical hemostatic agents – For minor, superficial bleeding with wound care protocols. BioMed Central
Proton-pump inhibitors – Only if GI bleeding occurs from visceral lesions (rare); symptom-directed, not lesion-directed. BioMed Central
Iron supplementation – For iron-deficiency anemia from chronic bleeding; oral or IV per labs. BioMed Central
Vaccinations (standard schedule) – Important if immunosuppressants like sirolimus/everolimus are used; follow label cautions for live vaccines. FDA Access Data+1
Antiplatelet/anticoagulants – Generally avoided unless a separate indication exists; may worsen bleeding in AVMs; specialist decision only. Journal of Vascular Surgery
Reality check: For CM-AVM, the most evidence-supported systemic option to date for complicated lesions is sirolimus (mTOR) used off-label, often as an adjunct to embolization/surgery; early data on trametinib (MEK) are promising in selected, mutation-defined AVMs but remain investigational. JAAD+3PubMed Central+3PubMed Central+3
Immune-booster / regenerative / stem-cell drugs
There are no approved stem-cell or “immune-booster” medicines for CM-AVM. Below is what you may hear about and why clinicians are cautious:
Sirolimus (immune-modulating mTOR inhibitor) – actually immunosuppressive, not a booster; used off-label to calm abnormal vessel signaling; infection risk requires monitoring and vaccines planning. FDA Access Data
Everolimus – similar to sirolimus; chosen when pediatric formulations or specific tolerability issues favor it; also immunosuppressive. FDA Access Data
Trametinib (MEK inhibitor) – targeted anti-proliferative signaling; not immune-boosting; investigational for AVMs. FDA Access Data
Alpelisib (PI3Kα) – targeted pathway drug; approved for PROS, not CM-AVM; may be discussed only when molecular findings support PI3K involvement. U.S. Food and Drug Administration
IV iron – restorative when anemia from bleeding exists; supports oxygen delivery but doesn’t treat AVM biology. BioMed Central
Stem-cell therapies – Not approved and not recommended for CM-AVM; no robust clinical evidence. (Patients should avoid unregulated clinics.) BioMed Central
Surgeries (procedures & why)
Staged AVM resection after embolization – Embolization shrinks blood flow; surgery removes the nidus to reduce recurrence and bleeding. Chosen for well-localized lesions. Journal of Vascular Surgery
Debulking of overgrown tissue – Improves function and appearance when overgrowth impairs movement or causes pain; often combined with prior endovascular control. PubMed Central
Reconstruction/skin grafting – For ulcers or skin loss after AVM treatment; aims to restore durable coverage. Journal of Vascular Surgery
Neurosurgical/endovascular treatment for brain AVMs – Combination of embolization, microsurgery, or radiosurgery depending on Spetzler-Martin grade and risk. Lippincott Journals
Orthopedic procedures – For significant limb asymmetry or bone involvement affecting gait; always coordinated with vascular team to control flow first. PubMed Central
Prevention tips
Protect skin from cuts/trauma over lesions.
Use SPF and moisturizers.
Avoid unnecessary piercings/tattoos over malformations.
Treat minor bleeds early with pressure and proper dressings.
Keep scheduled imaging follow-ups.
Share an emergency plan with school/work.
Maintain dental hygiene and tell dentists about oral lesions.
Plan pregnancy with the team.
Keep vaccines up-to-date, especially before any immunosuppressive therapy.
Exercise regularly but avoid high-impact trauma to affected areas. BioMed Central
When to see a doctor (or go to emergency care)
Immediately: sudden severe pain/swelling, uncontrollable bleeding, new neurologic symptoms (seizure, weakness, severe headache), shortness of breath/heart racing, or fever with open wounds. Urgent: persistent ulcer, rapidly enlarging lesion, new limb asymmetry, or pregnancy with known lesions. Routine reviews every 6–12 months with the vascular anomalies clinic help catch changes early. BioMed Central
Diet: what to eat & what to avoid
What to eat (10): iron-rich foods (lean meats, legumes), vitamin-C sources with iron meals, high-protein foods to support wound healing, whole grains for energy, omega-3-containing fish for inflammation balance, calcium/vitamin-D for bone health, hydration for tissue perfusion, fruits/vegetables for micronutrients, yogurt/kefir if antibiotics are used, and balanced meals to maintain weight during procedures. BioMed Central
What to avoid (10): smoking/vaping (impairs healing), heavy alcohol (bleeding risk), crash diets (slow healing), excess NSAIDs if bleeding risk is high (confirm with your team), energy drinks before interventions (BP/HR effects), contact sports targeting involved limbs, unregulated “stem-cell” clinics, herbal products that raise bleeding risk (e.g., ginkgo) before procedures, tanning/heat on lesions, and self-treating ulcers without guidance. BioMed Central
FAQs
Is CM-AVM cancer? No. It’s a developmental blood-vessel disorder, not a cancer. MedlinePlus
Will every person get an AVM? No. Some have only skin spots; others develop fast-flow lesions. Risk varies by person and family. NCBI
How is it inherited? Autosomal dominant—each child of an affected parent has a 50% chance. NCBI
What test confirms it? A genetic panel including RASA1 and EPHB4. NCBI
Why do lesions appear in patches? A second genetic “hit” in some cells triggers local malformation growth. Belgian Journal of Paediatrics
Are there approved drugs for CM-AVM? No targeted drug is FDA-approved for CM-AVM; sirolimus or trametinib may be used off-label in select cases. PubMed Central+1
Does propranolol help? It’s approved for infantile hemangioma, not AVMs; not a standard CM-AVM treatment. FDA Access Data
What about alpelisib? Approved for PIK3CA-related overgrowth (PROS), not CM-AVM; rarely considered unless PI3K pathway involvement is proven. U.S. Food and Drug Administration
Is laser a cure? Laser can lighten CMs; it doesn’t cure deep AVMs. Journal of Vascular Surgery
Is surgery one-and-done? AVMs often need staged therapy and careful planning to limit recurrence. Journal of Vascular Surgery
Can AVMs occur in the brain? Yes; brain/spinal involvement needs neuroimaging and specialized treatment. MedlinePlus
Can CM-AVM cause heart problems? Very large shunts can strain the heart; cardiology follows for high-output states. BioMed Central
Can children be tested? Yes—genetic counseling helps families decide timing and implications. NCBI
Will lesions grow in pregnancy? They can; pre-pregnancy planning and monitoring are important. BioMed Central
Where should I get care? At a vascular anomalies center with dermatology, interventional radiology, surgery, and genetics expertise. PubMed Central
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: November 10, 2025.
Parkes Weber Syndrome (PWS)
