Category: Module

Buerger Disease

BUERGER DISEASE


BUERGER’S DISEASE (THROMBOANGITIS OBLITERANS)

  • Buerger’s disease is a non- atherosclerotic, progressive, segmental, occlusive inflammatory disorder involving small and medium sized arteries with cell mediated sensitivity to Type I and Type II collage in upper and lower extremities.
  • Inflammatory process does involve adjacent nerves and veins.
  • Triad of thromboangitis obliterans- occlusion of small and medium sized vessels, superficial thrombophelbitis, Raynaud’s phenomenon.

ETIOLOGY-

  • Mainly seen in smokers and tobacco users.
  • Common in Jewish people
  • Hormonal influence
  • Familial nature
  • Poor hygiene

PATHOLOGY-

  • Smoke → vasospasm & hyperplasia initma → thrombus & obliteration medium sized vessels → Panarteritis → Artery, vein & nerve are involved  → Blockage leads to collateral open up → Blood supply to ishchaemic areas → Compensatory peripheral vascular disease
  • Microabscesses, giant cells are found.

CLASSIFICATION-

  • Type I- upper limb TAO (rare)
  • Type II- involving legs & infrapopliteal
  • Type III- femoropopliteal
  • Type IV- aortoiliofemoral
  • Type V- generalised

CLINICAL FEATURES-

  • Common in male smokers between 20- 40 years
  • Intermittent claudication in foot & calf progressing to rest pain, ulceration & gangrene.
  • Absence of atheromas.
  • Small & medium sized vessels such as dorsalis, pedis, posterior tibial, popliteal are commonly involved.

INVESTIGATIONS-

1. Arterial Doppler & Duplex scan

2. Transformed retrograde angiogram-

  • Shows blockage
  • Cork screw appearance of the vessel
  • Inverted tree/ spider leg collaterals
  • Severe vasospasm causing rippled artery

3. Transbranchial angiogram- if femorals are not felt then transbranchial angiogram is done.

4. USG abdomen- shows abdominal aorta for block 

TREATMENT-

  • Stop smoking
  • Vasodilators- nifedipine, xanthinol nicotinate
  • Antithrombin activity- low dose of aspirin
  • Analgesics
  • Lumbar sympathectomy- for rest pain and ulcerations
  • Omentoplasty, profundoplasty
  • Amputation in gangrene

Exam Important

PATHOLOGY-

  • Smoke → vasospasm & hyperplasia initma → thrombus & obliteration medium sized vessels → Panarteritis → Artery, vein & nerve are involved  → Blockage leads to collateral open up → Blood supply to ishchaemic areas → Compensatory peripheral vascular disease
  • Microabscesses, giant cells are found.

ETIOLOGY-

  • Mainly seen in smokers and tobacco users.
  • Common in Jewish people
  • Hormonal influence
  • Familial nature
  • Poor hygiene

CLINICAL FEATURES-

  • Common in male smokers between 20- 40 years
  • Intermittent claudication in foot & calf progressing to rest pain, ulceration & gangrene.
  • Absence of atheromas.
  • Small & medium sized vessels such as dorsalis, pedis, posterior tibial, popliteal are commonly involved.
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Ectopic Testis

ECTOPIC TESTIS


ECTOPIA TESTIS

  • An ectopic testicle descends normally through the inguinal canal but then moves into an abnormal position in the groin area.
  • The main hazard is liability to injury.
  • Sites of ectopic testis-

a) Superficial inguinal pouch

b) Perineum

c) Root of the penis

d) Femoral triangle (thigh)

  • Ectopic testis is usually fully developed

EMBRYOLOGY-

  • Testis reaches the scrotum by the scrotal tail gubernaculum.
  • The gubernaculums helps to guide the descent of the testicles.
  • Most ectopic testicles are palpable.

TREATMENT-

  • Surgical treatment after age of about 6 months but no later than 2 years
  • Orchidopexy in a new scrotal pouch.
COMPLICATIONS- 
  • Liability to injury (torsion)

Exam Important

  • Sites of ectopic testis-

a) Superficial inguinal pouch

b) Perineum

c) Root of the penis

d) Femoral triangle (thigh)

  • Ectopic testis is usually fully developed
COMPLICATIONS- 
  • Liability to injury (torsion)
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Mucocele Of Gall Bladder

MUCOCELE OF GALL BLADDER


Mucocele of the Gall bladder

  • It is one of the complications of Gall stones.
  • Caused due to obstruction of the stone at the neck of the bladder.
  • In course of time the bile is absorbed and replaced by the mucus secreted by the Gall bladder epithelium. Due to this the Gall bladder may because distended and palpable.

Treatment

  • The t/t is early cholycystectomy.
  • If early t/t is not done following complications can occur
  • Empyema
  • Perforation
  • Gangrene

Exam Important

  • It is one of the complications of Gall stones.
  • Caused due to obstruction of the stone at the neck of the bladder.
  • In course of time the bile is absorbed and replaced by the mucus secreted by the Gall bladder epithelium. Due to this the Gall bladder may because distended and palpable.

Treatment

  • The t/t is early cholycystectomy.
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Hemoglobinopathies

HEMOGLOBINOPATHIES


HEMOGLOBINOPATHIES

  • It is the family of genetic disorders caused by production of a structurally abnormal hemoglobin molecule, synthesis of insufficient quantities of normal hemoglobin, or, rarely, both.
  • variants leading to hemoglobinopathies may be either alpha chain variants or beta chain variants.
  • Abnormalities in the primary sequence of globin chains lead to hemoglobinopathies,e.g. HbS (qualitative hemoglobinopathy)
  • Abnormalities in the rate of synthesis would result in thalassemias (quantitative hemoglobinopathy).

Sickle cell anemia (Hb S), hemoglobin C disease (Hb C), hemoglobin SC disease (Hb S + Hb C), and the tha-lassemia syndromes are representative hemoglobinopathies that can have severe clinical consequences.

1.Sickle syndromes

A. Sickle-cell trait (AS):

  • heterozygous (AS) condition, 50% of Hb in the RBC is normal. Therefore the sickle cell trait as such does not produce clinical symptoms.
  • hypoxia may cause manifestation of the disease. Chronic lung disorders may also produce hypoxia-induced sickling in HbS. trait.
  • HbS affords protection against Plasmodium falciparum infection

In sickle cell trait, both the bands of HbA and HbS can be noticed in electrophoresis.

B. Sickle-cell disease with SS, SC, SD, SO varieties and S beta thalassemia.

  • glutamic acid in the 6th positionof beta chain of HbA is changed to valine in HbS causing a distortion of cell into sickle shape.
  • HbA and HbF will prevent sickling, because they do not co-polymerize with HbS. sickling occurs under deoxygenated state.
 2.Unstable hemoglobins

Congenital Heinz body anemia:

  • Unstable Hb variants have an increased tendency to denature which lead to increased hemolysis.
  • Heinz bodies are stained purple with cresyl violet. Their occurrence in RBC indicates that the cells have been subjected to oxidative stress.
  • Heinz bodies alter the surface of the red cells, creating indentations. As a result, they have a tendency of getting trapped in the spleen.(life-span of RBC reduced).

3. Hemoglobins with abnormal oxygen affinity
A. High affinity—Polycythemia (familial): Hb Chesapeake. Hb binds oxygen, but has difficulty in unloading. The ODC is shifted to the left, with a diminished Bohr effect. So, tissues suffer from hypoxia.
B. Low affinity—Cyanosis (familial): HbM–>occurs in the proximal or distal histidine residues of alpha or beta chains.

–> Alpha 58 His →Tyr (Hb M Boston)
–> Beta 92 His →Tyr (Hb M Hyde Park)

4. Structural variations leading to thalassemia

A. Alpha thalassemia—Hb Constant spring, delta beta thalassemia, Hb Lepore
B. Beta thalassemia: Hb Quong sze

5. Non-symptomatic hemoglobin variants:- HbP, Q, N, J, etc.

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Gene Therapy

GENE THERAPY


GENE  THERAPY

  •  It is  a technique  for  correcting  defective  gene  responsible  for  disease  development. It implies to correct the basic genetic abnormality.
  • Gene therapy is a procedure involving inserting (or sometimes deleting) portions of gene in diseased patients for the purpose of cure.
  • Antisense gene therapy or gene silencing selectively inactivate (or turn off) a mutated gene by RNA interference using short synthetic double stranded siRNA (small interfacing RNA).

Divided into
1. Somatic cell gene therapy-Gene is introduced into somatic cells.
2. Germ cell gene therapy (Transgenic animal).

several  approaches maybe  used:

  1. Replacement:-  Mutant (abnormal)  gene  is  removed  and replaced  by  normal  gene.
  2.  Augmentation:– Introduction  of foreign  gene  into  a cell to  compensate  for  the  defective  mutated gene.
  3. correction:–  Pathological  change  in  the  nucleotide sequence  is  repaired.

Gene  of  interest is administered  in two vectors:-

i)   Viral vedors:- Retrovirus,adenovirus, adeno-associated virus, lentivirus.
ii)  Non-viral plasmid liposome, (Cationic-lipid) comptex

Transfer of genes into cells are :-

i) Site directed recombination
ii) Intranuclear microinjection
iii) Transduction by using viruses
iv) Transfection
v) Electroporation

Severe combined immunodeficiency disease (SCID) was the first disease treated successfully by gene therapy.

Methods of  Gene  Delivery

A- Chemical  methods:

DEAE-dextran:- Diethylaminoethyl-dextran (DEAE Dextran) is a poly cationic derivative of the carbohydrate polymer, dextran.

Calcium  Phosphate: Mixing DNA with calcium chloride, then adding this mixture to a phosphate buffered saline solution followed by incubation at room temperature.

Cationic  Lipids (Lipofection):- When liposomes were added to cells growing in vitro, some of the liposomes(lipids  mixed  with DNA in  water) would fuse with cellular plasma membranes and be taken up into the cells via endocytosis.

Polymers:  most popular polymer is the polycation, polyethylenimine (PEI). PEI is an organic macromolecule that possesses a high cationic charge density,(proton  spong

B- Physical  Methods 

Microinjection: It entails the direct iniection of DNA into the nuclei of target cells using fine glass needles under microscopy.

Electroporation: method of introducing nucleic acids into cells by exposing the cells to a rapid pulse of high-voltage current, causing pores in the cell membrane to open temporarily.

  • the gene transfer efficiency is relatively low, and electroporation frequently results in a high incidence of cell death.

Gene  Gun:  Plasmid DNA is coated onto metal microparticles and then blasted into cells using either electrostatic force or gas pressure.

  • This technique is fast, simple and safe, and it can transfer genes to a wide variety of tissues.

Gene therapy clinical trials addressed in:

1. Cancer (67%)-Most common
2. Vascular Disease (8.9%)
3. Monogenic Disorders (8.6 %)

Exam Important

  • Antisense gene therapy or gene silencing selectively inactivate (or turn off) a mutated gene by RNA interference using short synthetic double stranded siRNA (small interfacing RNA)
  • Replacement;-  Mutant (abnormal)  gene  is  removed  and replaced  by  normal  gene.

Gene  of  interest is administered  in two vectors:-

i)   Viral vedors:- Retrovirus,adenovirus, adeno-associated virus, lentivirus.
ii)  Non-viral plasmid liposome, (Cationic-lipid) comptex

Techniques of transfer of genes into cells are :

i) Site directed recombination
ii) Intranuclear microinjection

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Venous Ulcers

VENOUS ULCERS


VENOUS ULCERS

  • Venous ulcers are situated on the medial side of lower half of the leg above medial malleolus (gaitre’s zone)
  • It is a complication of varicose veins and DVT.

ETIOLOGY-

  1. Fibrin cuff theory-
  • High venous pressure –> pericapillary infiltrate –> fibrin –> fibrosis –> cuffs –> diffusion block –> tissue damage
  1. White cell trapping –> reactive oxygen species –> free radicals –> tissue damage

PATHOGENESIS-

  • Varicose veins or DVT –> Chronic venous hypertension around ankle –> haemosiderin deposition –> eczema –> dermatitis –> lipodermatosclerosis –> fibrosis –> anoxia –> ulceration

CLINICAL FEATURES-

  • Venous ulcer is vertically in shape, solitary, sloping edges and never penetrates deep fascia.
  • Painless
  • Discharge is sloughing with high exudates

INVESTIGATIONS-

  • Duplex ultrasound- IOC for deep and superficial veins
  • Bipedal ascending phelography

TREATMENT-

  • Compression bandaging regiemen

Exam Important

  • Venous ulcers are situated on the medial side of lower half of the leg above medial malleolus (gaitre’s zone)
  • It is a complication of varicose veins and DVT.

CLINICAL FEATURES-

  • Venous ulcer is vertically in shape, solitary, sloping edges and never penetrates deep fascia.
  • Painless
  • Discharge is sloughing with high exudates

INVESTIGATIONS-

  • Duplex ultrasound- IOC for deep and superficial veins
  • Bipedal ascending phelography
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Lymphangiosarcoma

LYMPHANGIOSARCOMA


  ANGIOSARCOMA (LYMPHANGIOSARCOMA)

  • Lymphangiosarcoma arises from lymph vessel endothelium.
  • They are high grade and aggressive tumours.
  • It usually occurs after radical lymph node dissection (Stewart – Treves syndrome)
  • It may develop as a complication of a long standing lymphodema.

CLINICAL FEATURES-

  • Most of them occur in head and neck, breast, liver.
  • Acute worsening of oedema
  • Hameorrhage and ulceration.

TREATMENT-

  • Surgery (excision) followed by radiotherapy and combination of chemotherapy.

Exam Important

  • Lymphangiosarcoma arises from lymph vessel endothelium.
  • They are high grade and aggressive tumours.
  • It usually occurs after radical lymph node dissection (Stewart – Treves syndrome)
  • It may develop as a complication of a long standing lymphodema.

CLINICAL FEATURES-

  • Most of them occur in head and neck, breast, liver.
  • Acute worsening of oedema
  • Hameorrhage and ulceration.
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Grafts

GRAFTS


GRAFTS

  • Graft is transfer of tissue from one area to other without blood supply or nerve supply.
  • It can be-

a) Autograft- tissue transferred from one location to another on the same patient.

b) Isograft- tissue transferred between two genetically identical twins.

c) Allograft- tissue transferred between two genetically different members (kidney transplant)- (homograft)

d) Xenograft- tissue transferred from a donor of one species to a recipient of other species. (heterograft) 

SKIN GRAFT

  • Skin graft is transferred from one site to another site (autograft).

TYPES-

A) Partial Thickness Graft (Split- thickness skin graft- SSG)-

  • Also called as Thiersch graft.
  • It is removal of full epidermis + part of dermis from the donor area.
  • It is usually harvested by using Humby’s knife.
  • Prefered donor area is thigh
  • Beta hemolytic Streptococci can destroy split skin grafts completely, presence of this organism is a contraindication to grafting.
  • Cannot be done over bone, tendon, cartilage, joints.
  • Grafts used can be mesh graft or stamp graft.
  • Meshed skin grafts are split-thickness grafts cm 7.5
  • Meshing can be done using a machine which creates regular slits in the graft, allowing it to be expanded. Thus it can cover larger areas. The slits also allow blood from the wound to escape to the surface,reducing the chances of hematoma and therefore improving graft take.
  • Meshed grafts are particularly valuable in burned patients where large areas of skinneed to be covered.

Types of SSG are-

i) Thin SSG

  • Epidermis + thin layer of dermis
  • Resurfacing large wounds like post burn wounds

ii) Intermediate SSG-

  • Epidermis + half thickness of dermis
  • E.g. tumour excision (large raw areas with clean base)

iii) Thick SSG

  • Epidermis + major part of dermis
  • Rarely used
  • Better for cosmetics

B) FULL THICKNESS GRAFT-

  • Epidermis + full thickness of dermis
  • Harvested using ordinary scapel
  • Used over face, eyelid, hands, finger and over the joints. (used for cosmetic results)
  • Donor area needs primary suturing or SSG
  • Color match is good, no contracture.
  • Can only be used for small areas.
  • Common sites for donor area are-

i) Post- auricular area

ii) Supraclavicular area

iii) Groin crease area  

STAGES OF GRAFT INTAKE-

1. Stage of plasmatic imbibitions-

  • Thin, uniform, layer of plasma forms between recipient bed and graft.
  • Graft survives upto first 48 hours because of plasma imbibitions

2. Stage of inosculation: Linking of host and graft which is temporary.

  • Donor and recipient capillaries are aligned during inosculation which completes 4-5 days.

3. Stage of neovascularisation: New capillaries proliferate into graft from the recipient bed which attains circulation later.

  • After 5 days
  • Graft demonstrates both arterial and venous outflow.
The current procedure in skin graft storage involves wrapping the meshed autograft on a piece of ringer lactate or normal saline-moistened gauze, transferring it into a sterile container and storing it in a 4° C for 2 weeks
 

Exam Important

TYPES-

A) Partial Thickness Graft (Split- thickness skin graft- SSG)-

  • Also called as Thiersch graft.
  • It is removal of full epidermis + part of dermis from the donor area.
  • It is usually harvested by using Humby’s knife.
  • Prefered donor area is thigh
  • Beta hemolytic Streptococci can destroy split skin grafts completely, presence of this organism is a contraindication to grafting.
  • Cannot be done over bone, tendon, cartilage, joints.
  • Grafts used can be mesh graft or stamp graft.
  • Meshed skin grafts are split-thickness grafts cm 7.5

Types of SSG are-

  • Meshing can be done using a machine which creates regular slits in the graft, allowing it to be expanded. Thus it can cover larger areas. The slits also allow blood from the wound to escape to the surface, reducing the chances of hematoma and therefore improving graft take.
  • Meshed grafts are particularly valuable in burned patients where large areas of skin need to be covered.

i) Thin SSG

  • Epidermis + thin layer of dermis
  • Resurfacing large wounds like post burn wounds

ii) Intermediate SSG-

  • Epidermis + half thickness of dermis
  • E.g. tumour excision (large raw areas with clean base)

iii) Thick SSG

  • Epidermis + major part of dermis
  • Rarely used
  • Better for cosmetics

B) FULL THICKNESS GRAFT-

  • Epidermis + full thickness of dermis
  • Harvested using ordinary scapel
  • Used over face, eyelid, hands, finger and over the joints. (used for cosmetic results)
  • Donor area needs primary suturing or SSG
  • Color match is good, no contracture.
  • Can only be used for small areas.
  • Common sites for donor area are-

i) Post- auricular area

ii) Supraclavicular area

iii) Groin crease area 

STAGES OF GRAFT INTAKE-

1. Stage of plasmatic imbibitions-

  • Thin, uniform, layer of plasma forms between recipient bed and graft.
  • Graft survives upto first 48 hours because of plasma imbibitions

2. Stage of inosculation: Linking of host and graft which is temporary.

  • Donor and recipient capillaries are aligned during inosculation which completes 4-5 days.

3. Stage of neovascularisation: New capillaries proliferate into graft from the recipient bed which attains circulation later.

  • After 5 days
  • Graft demonstrates both arterial and venous outflow.
The current procedure in skin graft storage involves wrapping the meshed autograft on a piece of ringer lactate or normal saline-moistened gauze, transferring it into a sterile container and storing it in a 4° C for 2 weeks

 

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Malignant Melanoma

MALIGNANT MELANOMA


MALIGNANT MELANOMA (MELANOCARCINOMA)

  • Malignant melanoma is a malignant tumour arising from epidermal melanocyte derived from neural crest.
  • Most aggressive cutaneous malignant tumour.
  • DOPA REACTION-

SITES FOR MALIGNANT MELANOMA-

  • Head & neck
  • Lower extremity
  • Trunk
  • Upper limb
  • Choroid of the eye
  • Genetalia
  • MC site for men- front or back of the trunk
  • MC site for female- leg
  • More common in whites than black

 ETIOLOGY-

  • UV rays
  • Albinism
  • Xeroderma pigmentosa- AR (Chromosome 9q)
  • Genetic factors-

i) Tumour suppressor gene mutation 9q 21

ii) Deletion or rearrangement of chromosome 10 & 8p

iii) Dysplastic naevus syndrome

  • Pre- existing mole
  • Immunocompromised- HIV, Hodgkin’s disease

CLASSIFICATION-

I) Breslow classification-

  • According to maximum thickness at the centre of the lesion-

a) Stage I- thickness less than 0. 75 mm

b) Stage II- 0.75 mm to 1.5 mm

c) Stage III- 1.5 mm to 3.0 mm

d) Stage IV- more than 3 mm

II) Clark’s Classification-

  • According to the basis of the depth of the invasion

a) Stage I- Melanoma restricting to epidermis and appendages

b) Stage II- invading papillary dermis without filling it

c) Stage III- reach interface of papillary and reticular dermis

d) Stage IV- invading reticular dermis

e) Stage V- invading subcutaneous tissue

III) According to clinical types-

a) Lentigo malignant melanoma-

  • Benign
  • MC- face

b) Superficial spreading-

  • MC type
  • MC site- torso

c) Nodular-

  • Most malignant
  • MC site- head, neck, trunk

d) Acral lentiginous-

  • Least common with worst prognosis
  • MC site- sole, mucosa

CLINICAL FEATURES-

  • Can spread from mother to foetus
  • Asymmetry, border irregularity, color variation and diameter >6mm (ABCD)
  • Microsatellites (0.05mm)- separated from main body tumour by normal dermal collagen or subcutaneous fat
  • Macrosatellites associated with increase risk of regional LN
  • MC site of systemic metastasis- liver
  • Choroidal melanoma is the most common primary malignant intraocular tumor and the second most common type of primary malignant melanoma in the body and may produce  exudative retinal detachment.
  • In melanoma cells, numbers of mutations and/or dysregulated expression of B-Rof N-Ras, CDK2A, MDM2, PTEN, p53 have been recognized”

SPREAD-

  • Through lymphatics (MC)
  • In- transit or satellite nodules
  • Through blood 

INVESTIGATIONS-

  • Chest X-ray- cannonball secondaries
  • USG abdomen- secondary in liver
  • FNAC- detects spreading & stages of the disease
  • Serum LDH levels- indicate metastatic disease
  • HHB- 4S- premelanosomal protein is specific immunohistochemical marker for melanoma
  • Full thickness excisional biopsy- confirms MM

TREATMENT-

  • Surgical excision with sentinel LN biopsy
  • Block dissection to be done when sentinel node is involved

Exam Important

According to clinical types-

a) Lentigo malignant melanoma-

  • Benign
  • MC- face

b) Superficial spreading-

  • MC type
  • MC site- torso

c) Nodular-

  • Most malignant
  • MC site- head, neck, trunk

d) Acral lentiginous-

  • Least common with worst prognosis
  • MC site- sole

CLINICAL FEATURES-

  • Can spread from mother to foetus
  • Asymmetry, border irregularity, color variation and diameter >6mm (ABCD)
  • Microsatellites (0.05mm)- separated from main body tumour by normal dermal collagen or subcutaneous fat
  • Macrosatellites associated with increase risk of regional LN
  • MC site of systemic metastasis- liver
  • Choroidal melanoma is the most common primary malignant intraocular tumor and the second most common type of primary malignant melanoma in the body and may produce  exudative retinal detachment.
  • In melanoma cells, numbers of mutations and/or dysregulated expression of B-Rof N-Ras, CDK2A, MDM2, PTEN, p53 have been recognized”

SPREAD-

  • Through lymphatics (MC)
  • In- transit or satellite nodules
  • Through blood

INVESTIGATIONS-

  • Chest X-ray- cannonball secondaries
  • USG abdomen- secondary in liver
  • FNAC- detects spreading & stages of the disease
  • Serum LDH levels- indicate metastatic disease
  • HHB- 4S- premelanosomal protein is specific immunohistochemical marker for melanoma
  • Full thickness excisional biopsy- confirms MM

TREATMENT-

  • Surgical excision with sentinel LN biopsy
  • Block dissection to be done when sentinel node is involved
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Mondor Disease

MONDOR DISEASE


MONDOR’S DISEASE

  • Mondor disease is a spontaneous thrombophlebitis of the superficial veins of the breast and anterior chest wall.
  • Also called as String phlebitis due to tender, cord like structure.

ETIOLOGY-

  • Unknown

 CLINICAL FEATURES-

  • Presented as a thrombosed subcutaneous cord (3cm) attached to skin.
  • On raising arm, shallow subcutaneous grooves appear alongside cord like thrombosed vein.
  • Frequently involved veins are-

a) Lateral thoracic vein

b) Thoracoepigastric vein

c) Superficial epigastric vein

  • Self limiting disease
  • Pain in lateral aspect of breast or anterior chest wall.

INVESTIGATIONS-

  • Biopsy is indicated

TREATMENT-

  • NSAIDS and warm compresses
  • Restriction of motion and brassiere support of breast

Exam Important

  • Mondor disease is a spontaneous thrombophlebitis of the superficial veins of the breast and anterior chest wall.
  • Also called as String phlebitis due to tender, cord like structure.
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