Orbital Chloroma (Myeloid Sarcoma of the Orbit)

Orbital chloroma is a solid tumor made of immature white blood cells (myeloid blasts) that grows inside the eye socket (the orbit). Doctors also call it myeloid sarcoma or granulocytic sarcoma. It is the same disease process as acute myeloid leukemia (AML), but instead of only living in the blood and bone marrow, the cancer cells gather in a lump in the tissues around the eye. The tumor can press on the eyeball, the eye muscles, the optic nerve, and the eyelids. This pressure causes bulging of the eye, pain, double vision, swelling, and sometimes sudden vision loss. The tumor is dangerous because it usually means there is AML now or AML will appear soon. It can also mean a relapse of leukemia after earlier treatment. Because of that, orbital chloroma is a medical and oncologic emergency and needs rapid diagnosis and full-body treatment (systemic therapy), not only local treatment.

“Orbital chloroma” means a solid lump of leukemia cells that grows in or around the eye socket (orbit). Doctors today call it myeloid sarcoma (MS). It is made of immature myeloid “blast” cells—the same cells seen in acute myeloid leukemia (AML)—but here they collect outside the bone marrow as a mass. The old word “chloroma” came from the greenish color seen in some tumors due to the enzyme myeloperoxidase (MPO) inside the cells. EyeWiki

This tumor can show up in many body sites; when it forms in the eye socket, it can push the eye forward (proptosis), cause swelling or double vision, and sometimes be the first sign of leukemia, especially in children. In some patients it appears at the same time as AML, before AML, or when AML comes back. EyeWikiAJR American Journal of RoentgenologyJAMA Network

Why doctors use different names

Doctors use more than one name for this tumor:

• Myeloid sarcoma is the preferred modern name. It describes a sarcoma-like (solid) mass of myeloid cancer cells.

• Granulocytic sarcoma is an older term. It points to the granulocyte-type cells (a type of white blood cell) seen in the tumor.

• Chloroma is a very old term. The tumor sometimes looks green when cut in the lab because of the enzyme myeloperoxidase. “Chloro” means green.

All these names point to the same disease.

---

Types

Doctors sort orbital chloroma in several simple ways. These “types” help predict timing, behavior, and best tests.

1. By timing with leukemia

   • Isolated (primary) orbital chloroma: The eye mass is found before any blood cancer is known. Many of these patients develop AML later. The mass is a warning sign.

   • Concurrent with AML: The eye mass is found at the same time as AML is diagnosed. The mass is part of the leukemia.

   • Relapse after remission: The eye mass appears months or years after treatment as a return of AML, even if the blood counts look normal at first.

   • Herald of blast crisis in CML: People with chronic myeloid leukemia (CML) can suddenly worsen into blast crisis, and a new orbital mass can be the first clue.

2. By cell pattern under the microscope (immunophenotype)

   • Granulocytic / neutrophilic pattern: Cells look like early neutrophils, often myeloperoxidase-positive.

   • Myelomonocytic / monocytic pattern: Cells show monocytic features, may be lysozyme-positive, and can infiltrate tissues more readily.

   • With maturation vs. without maturation: Some tumors show a mix of early and more mature myeloid cells; others show very immature blasts only.

3. By exact spot in the orbit

   • Extraconal mass: Sits outside the muscle cone, often near the orbital walls or sinuses. It may push the eye.

   • Intraconal mass: Sits within the muscle cone, close to the optic nerve and eye muscles, more likely to impair movement or vision.

   • Optic nerve sheath involvement: Wraps or compresses the optic nerve, raising risk of sudden vision drop.

   • Lacrimal gland involvement: Feels like a firm mass in the outer upper eyelid, sometimes mimicking lacrimal tumors.

   • Preseptal / eyelid tissue involvement: Looks like dense eyelid swelling that does not behave like simple infection.

4. By imaging appearance

   • Well-circumscribed “mass”: A compact lump that enhances with contrast.

   • Diffuse infiltrative pattern: Sheet-like spread through fat and muscles, sometimes hard to separate from inflammation on imaging.

---

Causes and biological associations

“Causes” here means the disease situations and biological features that are linked with orbital chloroma. Many are not everyday “causes” like infection, but medical conditions and molecular changes that make this tumor more likely.

1. Acute myeloid leukemia (AML, de novo)
   Most orbital chloromas belong to AML. The mass is a collection of AML cells in the orbit.

2. AML relapse
   An orbital mass can be the first sign that AML is back, even before the blood shows it.

3. Core-binding factor AML (t(8;21))
   AML with the RUNX1::RUNX1T1 fusion often has extramedullary disease, including the orbit.

4. Core-binding factor AML (inv(16)/t(16;16))
   AML with CBFB::MYH11 can also form tissue masses, including chloromas.

5. KMT2A (MLL) rearranged AML (11q23)
   This genetic group is prone to tissue infiltration, raising the risk of chloroma.

6. Monocytic / myelomonocytic AML (FAB M4/M5)
   These subtypes invade tissues more readily and can seed the orbit.

7. NPM1-mutated AML
   Some NPM1-mutant cases show extramedullary disease, including orbital sites.

8. FLT3-ITD–high burden AML
   Very proliferative AML can spread beyond marrow, making masses more likely.

9. Chronic myeloid leukemia (CML) in blast crisis
   When CML transforms, blast cells can form an orbital mass.

10. Myelodysplastic syndromes (MDS) transforming to AML
    During transformation, blasts can leave the marrow and create chloromas.

11. Myeloproliferative neoplasms (MPN) transforming to AML
    As MPNs progress, myeloid blasts can collect in the orbit.

12. Therapy-related AML (after chemo or radiation)
    Prior cancer therapy can lead to AML that is more likely to spread into tissues.

13. Post–stem cell transplant extramedullary relapse
    After a transplant, AML can reappear in “sanctuary” sites like the orbit.

14. CD56 (NCAM) expression on leukemic blasts
    CD56 on AML cells is linked with extramedullary disease, including chloroma.

15. High matrix-degrading enzymes (MMPs) in blasts
    These enzymes break tissue barriers, helping cells invade the orbit.

16. Chemokine receptor CXCR4 up-regulation
    This receptor guides cell migration to tissues, including orbital fat and muscle.

17. Tissue “homing” to sinus-rich orbit
    The orbit sits near paranasal sinuses, giving rich blood and tissue pathways for myeloid cells.

18. Pediatric age
    Children can present with isolated orbital chloroma as the first sign of leukemia.

19. Immune evasion in protected spaces
    The orbit can act as a relative sanctuary, allowing blasts to escape immune attack.

20. Delayed systemic control of leukemia
    When AML treatment is insufficient or interrupted, blasts persist and seed the orbit.

---

Symptoms and signs

1. Bulging eye (proptosis)
   The mass pushes the eyeball forward, so the eye looks more prominent.

2. Eyelid swelling and fullness
   The lids look puffy and firm, not soft like allergy swelling.

3. Eye pain or pressure
   The mass stretches tissues and can cause deep ache behind the eye.

4. Double vision (diplopia)
   The tumor restricts eye muscles, so the two eyes do not align.

5. Limited eye movement
   Looking up, down, or sideways can be blocked or painful.

6. Decreased vision
   If the optic nerve is squeezed, vision can blur or dim.

7. Loss of color brightness
   Colors look washed out, a sign the optic nerve is affected.

8. Afferent pupillary defect (RAPD)
   The pupil reflex is weaker in the sick eye, a fast bedside clue.

9. Tearing or watery eye (epiphora)
   Tumor pressure can distort the tear system, causing overflow.

10. Red eye and chemosis
    The eye surface can look red and swollen, mimicking infection.

11. Firm, non-tender mass in the eyelid or orbit
    The lump often feels solid and does not move easily.

12. Headache or facial pressure
    Tumor near the sinuses can create facial pain.

13. Nose symptoms if sinus spread
    There may be nasal blockage or nosebleeds if the mass extends.

14. Swollen lymph nodes (occasionally)
    Nodes near the jaw or neck can enlarge as part of systemic disease.

15. General “blood cancer” symptoms
    Fatigue, fever, night sweats, easy bruising, and frequent infections suggest leukemia involvement.

---

Diagnostic tests

Doctors use exam, bedside tests, lab work, pathology, and imaging together. Because orbital chloroma is tied to AML, the team usually includes ophthalmology, hematology/oncology, radiology, and pathology. The goal is to confirm the tumor type, protect vision quickly, and stage the whole body for the right systemic treatment.

A) Physical examination

1. Visual acuity testing
   You read letters on a chart. This shows how sharp your vision is and whether it is dropping because of optic nerve or macular involvement.

2. Color vision testing (e.g., Ishihara plates)
   You identify colored dot patterns. Early optic nerve damage often shows up first as poor color discrimination.

3. Pupil examination for RAPD
   The doctor shines a light in each eye. A weaker constriction in one eye suggests optic nerve compression from the tumor.

4. Ocular motility and alignment exam
   You follow the doctor’s finger in 9 gaze positions. Restricted movement or misalignment points to muscle or nerve involvement by the mass.

B) Manual / bedside functional tests

5. Hertel exophthalmometry
   A simple device measures how far the eye protrudes. A larger reading on one side supports proptosis from an orbital mass.

6. Globe retropulsion test
   The doctor gently presses the eye backward through the closed lid. A stiff, resistant feel suggests a space-occupying lesion behind the eye.

7. Confrontation visual fields (manual)
   You cover one eye and count fingers in different quadrants. Field cuts imply optic nerve or pathway compression.

8. Cover–uncover and alternate cover tests
   The doctor covers one eye and watches how the other eye refixes. This exposes hidden misalignment due to muscle restriction from the mass.

C) Laboratory and pathological tests

9. Complete blood count (CBC) with differential
   Looks for anemia, low platelets, and circulating blasts. These findings support leukemia when present.

10. Peripheral blood smear
    A lab expert looks at blood under a microscope for myeloblasts and Auer rods. This gives direct visual evidence of myeloid disease.

11. Bone marrow aspiration and trephine biopsy
    Samples from the pelvic bone show the cellularity, blast percentage, and overall marrow health. This confirms AML and its subtype.

12. Histopathology of the orbital mass (biopsy)
    A small piece of the mass is examined. The tumor shows sheets of myeloid blasts, often myeloperoxidase-positive. This is the gold standard to prove myeloid sarcoma.

13. Immunohistochemistry (IHC) and flow cytometry
    Special stains and markers (e.g., myeloperoxidase, lysozyme, CD68, CD33, CD117, CD34, CD43; sometimes CD56) define the myeloid nature and help distinguish from lymphoma or small round blue-cell tumors.

14. Cytogenetic and molecular testing
    Tests look for t(8;21), inv(16)/t(16;16), KMT2A rearrangements, NPM1, FLT3-ITD, and other AML-related changes. These results guide prognosis and therapy and explain why the tumor formed in tissue.

D) Electrodiagnostic tests

15. Visual evoked potentials (VEP)
    You watch a checkerboard pattern. Electrodes on the scalp measure how fast and how strong signals travel from the eye to the brain. Delayed or reduced signals mean optic nerve compression.

16. Electroretinography (ERG)
    Measures retinal function. It helps separate retinal disease from optic-nerve compression, which is important when vision falls but the retina looks normal.

E) Imaging tests

17. MRI of the orbits with contrast (and brain)
    This is the best imaging test for soft tissues. It shows tumor size, exact location (intra- vs extraconal), optic nerve involvement, and how the mass enhances. It also checks brain and meningeal spread.

18. CT scan of the orbits and paranasal sinuses
    CT shows bone and sinus detail. It helps when surgery or biopsy planning needs to know if bone is thinned, eroded, or intact.

19. Orbital ultrasound (B-scan, with Doppler if needed)
    A quick, bedside way to see a solid mass, its vascularity, and its relation to the globe. It is useful when MRI is delayed.

20. Whole-body staging with PET-CT or contrast CT chest/abdomen/pelvis
    Because chloroma is part of a systemic blood cancer, doctors must look for other sites. PET-CT finds hidden deposits and helps plan systemic therapy.

Non-pharmacological treatments (therapies & other measures)

(Each lists purpose & “how it works” in simple terms.)

1. Urgent referral to an experienced leukemia center – ensures prompt AML-level care; MS is treated like AML. www2.tri-kobe.org

2. Radiation therapy (RT) to the orbital mass – used with systemic therapy or when quick local control is needed; typical effective dose ~24 Gy in 12 fractions for MS provides excellent local control by damaging leukemia cell DNA so they cannot grow. BioMed CentralFrontiersAsh Publications

3. Protect the cornea (lubricating drops/gel, moisture chamber, taping at night) – prevents exposure keratopathy when the eye protrudes; keeps the surface wet and safe. (Standard ophthalmic care.)

4. Elevate head of bed & cool compresses – reduces eyelid/orbital swelling by lowering venous congestion.

5. Temporary occlusion or prism lenses – eases double vision by aligning or resting the visual system.

6. Low-vision aids and contrast-rich lighting – supports reading and daily tasks if vision is reduced.

7. Nutritional support with safe-food handling – keeps weight and strength up; strict hygiene lowers infection risk during neutropenia.

8. Oral care protocol – soft brush, alcohol-free rinses; reduces mouth sores and infection risk during chemotherapy.

9. Physical activity as tolerated – light, regular movement supports energy, mood, and lowers blood-clot risk.

10. Psychological counseling – helps anxiety, sleep, coping for patients and family.

11. Infection prevention – hand hygiene, avoid crowds when counts are low, masks in high-risk settings; lowers serious infection risk.

12. Vaccination planning – inactivated vaccines when appropriate; avoid live vaccines during immunosuppression; follow oncology timing. (General AML standards.)

13. Eye-shield or protective glasses – protects a protruding eye from trauma.

14. Manage sinus/nasal health – saline rinses and ENT input if sinuses are involved; reduces local infection.

15. Sleep positioning (on the back with support) – minimizes pressure on the affected orbit.

16. Smoking cessation and no second-hand smoke – better wound healing and infection control.

17. Sun/UV protection – some drugs and RT increase photosensitivity; hats and sunglasses protect tissues.

18. Social work and financial counseling – helps maintain treatment access and adherence.

19. Palliative care alongside active treatment – improves symptom control and quality of life at any stage.

20. Clinical trial consideration – may provide access to newer, targeted strategies. (General AML guidance.) Cancer.gov

---

Drug treatments

Important: Doses below are typical examples to show scale and timing. Actual regimens vary by age, genetics, organ function, and protocols. Treatment must be led by a hematology/oncology team.

1. Cytarabine (Ara-C) – backbone of AML therapy.
   When/Time: Induction (often “7” in “7+3”) and high-dose for consolidation.
   How it works: blocks DNA synthesis in blasts.
   Typical dosing examples: 100–200 mg/m²/day IV continuous infusion × 7 days for induction; HiDAC 1.5–3 g/m² IV q12h on days 1,3,5 in consolidation (varies).
   Common side effects: low blood counts, mucositis, fever; high-dose can affect the cerebellum and eyes (needs monitoring). Cancer.gov

2. Daunorubicin (or idarubicin) – anthracycline partner in induction.
   Time: days 1–3 (“+3”).
   Mechanism: intercalates DNA; topoisomerase-II blocker.
   Typical dosing: daunorubicin ~60–90 mg/m² IV daily × 3 days in adults (per trials).
   Key risks: low counts, cardiac toxicity (dose-related). NCBI

3. Azacitidine (hypomethylating agent).
   Use: for patients not fit for intensive chemo or as part of venetoclax combos.
   Mechanism: epigenetic re-programming that re-activates tumor suppressors.
   Dosing: common schedule 75 mg/m²/day SC/IV × 7 days in 28-day cycles.
   Effects: cytopenias, nausea, fatigue. Cancer.gov

4. Decitabine (another HMA).
   Use/Mechanism: similar to azacitidine.
   Dosing: e.g., 20 mg/m²/day IV × 5 days q28d.
   Effects: cytopenias, infections. Cancer.gov

5. Venetoclax (BCL-2 inhibitor).
   Use: with azacitidine/decitabine for many older or unfit patients.
   Mechanism: triggers leukemia-cell apoptosis.
   Dosing: oral daily with ramp-up; cycles with HMA.
   Risks: tumor lysis, neutropenia—requires close monitoring. Cancer.gov

6. Midostaurin (for FLT3-mutated AML).
   Use: added to induction and consolidation; sometimes maintained.
   Mechanism: FLT3 tyrosine-kinase inhibitor.
   Dosing: oral during chemo days (protocolized).
   Risks: GI upset, QT changes; drug interactions. Cancer.gov

7. Gilteritinib (FLT3 inhibitor) for relapsed FLT3-AML.
   Use: single-agent in relapse.
   Mechanism: targeted FLT3 blockade.
   Side effects: LFT changes, cytopenias. Cancer.gov

8. Ivosidenib (IDH1) / Enasidenib (IDH2).
   Use: for AML with IDH1 or IDH2 mutations.
   Mechanism: fixes abnormal cell metabolism, promotes differentiation.
   Key risk: differentiation syndrome (needs steroids). Cancer.gov

9. Gemtuzumab ozogamicin (GO) (anti-CD33 antibody-drug).
   Use: in selected CD33+ AML, sometimes with induction.
   Mechanism: delivers a toxin directly into leukemia cells.
   Key caveat: timing around transplant because of sinusoidal obstruction syndrome risk. cme.ahn.org

10. Intrathecal chemotherapy (methotrexate/cytarabine ± steroid)
    Use: selected patients with CNS risk or involvement.
    Mechanism: bathes the CNS to prevent/treat leukemia spread.
    Risks: headache, chemical meningitis (specialist-directed). (General AML practice). Cancer.gov

Big picture: Even if the tumor is surgically removed or irradiated, systemic AML-type chemotherapy is usually recommended—because MS behaves like AML outside the marrow. Local therapy alone often isn’t enough. PMCwww2.tri-kobe.org

---

Dietary “molecular” supplements

Supplements can interact with chemo. Use them only if your clinicians agree. Doses below are typical nutrition ranges (not cancer cures).

1. Vitamin D3 – 800–1,000 IU/day (or per level). Supports bone/immune function via vitamin-D receptor signaling.

2. Calcium – 1,000–1,200 mg/day (diet first). Bone health; pair with vitamin D.

3. Protein (whey or food) – 20–30 g per meal; supplies amino acids to maintain muscle, immune proteins.

4. Omega-3 (EPA/DHA) – ~1 g/day; may help inflammation and appetite.

5. Zinc – 8–11 mg/day (RDA); supports enzyme and immune function.

6. Selenium – 55 mcg/day (RDA); antioxidant enzyme cofactor (avoid high doses).

7. Vitamin B12 / Folate – RDA levels only, and only if deficient; supports normal blood cell production.

8. Vitamin C – 75–90 mg/day (RDA); avoid high-dose antioxidants during chemo unless your team approves.

9. Glutamine (nutrition support) – diet-based or 5–10 g/day powder sometimes used for mucosal support; evidence mixed—ask your team.

10. Electrolyte solution (ORS on sick days) – as directed; prevents dehydration during fevers/diarrhea.

(These are supportive nutrition ideas, not treatments for the tumor.)

---

Regenerative / stem-cell–related” support drugs

1. Filgrastim (G-CSF) – ~5 mcg/kg/day SC after chemo until neutrophils recover; purpose: shortens neutropenia; mechanism: stimulates granulocyte production; risks: bone pain, rare splenic issues.

2. Pegfilgrastim – single 6 mg SC dose per chemo cycle; long-acting G-CSF; similar purpose/mechanism/risks.

3. Sargramostim (GM-CSF) – ~250 mcg/m²/day; stimulates broader myeloid recovery; risks include fever, aches.

4. Intravenous immunoglobulin (IVIG) – 0.4 g/kg/day × 5 days or protocol; purpose: passive antibodies for recurrent serious infections/low IgG; risks: headache, thrombosis risk in some.

5. Plerixafor – 0.24 mg/kg SC for stem-cell mobilization with G-CSF when transplant collection is planned; mechanism: blocks CXCR4 to release stem cells.

6. Palifermin – 60 mcg/kg/day for 3 days pre- and 3 days post-transplant conditioning; purpose: reduces severe mouth/throat mucositis; mechanism: keratinocyte growth factor; risks: rash, taste change.

---

Surgeries

1. Incisional biopsy via anterior orbitotomy – a small cut to remove a piece of the mass to confirm the diagnosis with stains and genetics.

2. Lateral orbitotomy (deep biopsy/debulking) – side approach to a deeper tumor; why: safe access for tissue, sometimes modest decompression.

3. Orbital decompression (select emergencies) – remove small bits of bone/fat to relieve optic-nerve pressure when vision is at immediate risk; used rarely because systemic therapy works quickly.

4. Temporary tarsorrhaphy (eyelid-partial closure) – protects the cornea if the eye protrudes and won’t close fully.

5. Central venous port placement – surgical insertion of a long-term IV port to safely deliver chemotherapy and draw blood.

---

Prevention tips

There’s no proven way to prevent orbital myeloid sarcoma itself. Prevention focuses on complications and relapse monitoring:

1. Get care at a leukemia-experienced center; follow the treatment plan closely. www2.tri-kobe.org

2. Keep every follow-up (eye checks, labs, marrow tests) to catch recurrence early.

3. Infection control during low counts: hand hygiene, safe food, masks in high-risk spaces.

4. Vaccines—plan inactivated vaccines with oncology; avoid live vaccines until cleared.

5. Report vision changes immediately (blur, color washout, double vision).

6. Protect the eye—safety glasses, avoid contact sports while the eye protrudes.

7. Good oral care to lower mouth infections.

8. Avoid herbal or high-dose antioxidant supplements unless cleared by your team (drug interactions).

9. No smoking; avoid second-hand smoke.

10. Maintain nutrition, sleep, and activity to support recovery.

---

When to see a doctor now

• Sudden worsening bulging, new double vision, or vision loss.

• Eye pain plus swelling, fever, or redness.

• New headache, vomiting, or neurologic symptoms.

• Unusual bleeding, nosebleeds, large bruises, or fevers during treatment.

• Any new mass in the eyelid or orbit—especially in a person with current or past AML.

---

What to eat” and “what to avoid

1. Eat: well-cooked proteins (fish, eggs, pulses). Avoid: raw/undercooked meats or eggs when counts are low.

2. Eat: soft fruits you can peel (bananas, oranges). Avoid: unwashed raw produce; wash thoroughly.

3. Eat: whole-grain breads/cereals if tolerated. Avoid: unpasteurized dairy/juices.

4. Drink: clean, safe water; oral rehydration if ill. Avoid: street ice or untreated water.

5. Choose: small, frequent meals if nauseated. Avoid: heavy, greasy meals that worsen nausea.

6. Use: mild seasonings and gentle cooking methods. Avoid: very spicy or acidic foods if you have mouth sores.

7. Add: omega-3 sources (cooked fish, flax). Avoid: high-dose fish-oil pills unless approved.

8. Include: yogurt-style taste only if pasteurized—avoid live probiotics during neutropenia unless your team okays them.

9. Favor: iron- and folate-rich foods as advised. Avoid: iron pills unless prescribed (can upset stomach and interact).

10. Plan: diet with a registered dietitian if possible. Avoid: fad diets that restrict major food groups during treatment.

---

Frequently Asked Questions

1) Is orbital chloroma cancer?
Yes. It’s a leukemia tumor outside the marrow, made of AML-type blasts. It behaves like AML and needs AML-level treatment. SEER

2) Can it be the first sign of leukemia?
Yes. In some people—especially children—it may appear before or with AML. JAMA Network

3) How is it diagnosed for sure?
By biopsy and special stains/flow showing myeloid markers (like MPO, CD117, CD68/CD163), plus imaging and blood/marrow tests. PMC

4) Is surgery enough?
Usually no. Surgery is mainly for biopsy or urgent decompression. Systemic chemotherapy is usually required. PMCwww2.tri-kobe.org

5) Does radiation help?
Yes—for local control or vision-saving urgency. Typical effective dosing is about 24 Gy in 12 sessions, alongside systemic treatment. BioMed CentralFrontiers

6) What chemotherapy is used?
Standard AML regimens (e.g., cytarabine + an anthracycline for induction), with targeted drugs based on mutations (FLT3, IDH1/2) when present. Cancer.gov

7) Will targeted drugs work on the orbital mass?
They can help systemic disease that drives the mass; adding them when mutations exist (e.g., FLT3, IDH) can improve responses. Cancer.gov

8) Is stem-cell transplant ever needed?
Yes, for some higher-risk or relapsed cases, after remission is achieved, based on risk models and genetics. Cancer.gov

9) What are the chances of saving vision?
Early treatment can relieve pressure and protect the optic nerve; outcomes vary by speed of therapy and tumor location. (Clinical principle; radiation and chemo can rapidly shrink masses.) BioMed Central

10) Could it come back in the eye?
It can, especially if systemic control is incomplete. Regular follow-up and systemic therapy reduce this risk. Red Journal

11) How is it different from “leukemia cutis”?
Leukemia cutis involves skin; myeloid sarcoma is a tumor mass in any tissue outside marrow—including the orbit. NCBI

12) What do MRI/CT usually show?
A homogeneously enhancing soft-tissue mass that often spares bone early; MRI helps map relation to muscles and the optic nerve. AJR American Journal of Roentgenology

13) Are children more affected?
Orbital involvement is well described in children and can be an early sign; adults can be affected too. JAMA Network

14) Why was it called “chloroma”?
Because some tumors look green from MPO (a green enzyme in myeloid cells). EyeWiki

15) Which medical teams should be involved?
Hematology/oncology, ophthalmology (oculoplastics), radiation oncology, radiology, pathology, transplant team, and supportive care.

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: August 18, 2025.

PDF Document For This Disease Conditions References