257 Venous And Lymphatic Disorders Flashcards

1
Q

What is thrombosis?

How do venous thrombi form?
What is the common symptom?

A

Thrombosis = blood clod (thrombus) in a blood vessel occluding blood flow. When the clot is dislodged from its origin and travels to a distant site in circulation this is thromboembolism

  • Venous thrombi is due to one or more abnormalities developing secondary Virchow’s triad:
    1) increased coagulability (increased platelet activity or procoagulant factors, deficiencies of anticoagulant factors, or inhibited fibrinolysis); 2) vascular stasis
    3) endothelial disruption
  • often undetected as there are fewer overt abnormalities compared to arterial thrombosis
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2
Q

What is PTE?
How does Pulmonary thromboembolism (PTE) form?

What does PTE result in?

A

PTE= partial or complete obstruction of the PA or its branches by thrombi secondary to other disease processes.

Pathogenesis: based on endothelial damage, blood flow stasis, and hypercoagulable states.

  • thrombus formed in peripheral veins, vena cava, or right heart may embolism to pulmonary arterial vasculature.
  • develop in pro-thrombotic states such as nephrotic syndrome, hyper adrenocortical IMHA, thrombocytosis, cardiac disease, sepsis, DIC, HWD, and neoplasia.

PTE results in hypoxemia, bronchoconstriction, V-P mismatch, and hyperventilation.

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3
Q

What is venous varicose? How common is it? How does it form in dogs?

A
  • tortuous and dilated veins
  • rare in dogs and cats
  • accompany arteriovenous fistula or develop from chronic venous obstruction
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4
Q

How does cystic dilation of veins occur?

  • How does the thrombosis occur?
  • What PE findings might be seen?
A
  • venous dilation or aneurysm generally permits only low velocity blood flow and small lesions are asymptomatic
  • thrombosis can result from sluggish blood flow, resulting in localised swelling and tenderness.
  • larger lesions in dependent area may enlarge, causing vascular dilation, and changes to skin colour, dermal ulceration, and haemorrhage.
  • areas can be warm, soft, compressible mass.
  • pain can be present from pressure exerted on deep tissues and nerves.
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5
Q

How is cystic dilation diagnosed? And managed?

A
  • History, physical examination, and ultrasound.
  • venography or cross-sectional imaging such as CT or MRA
  • light, compressive wraps for acute management.
  • surgical excision of vessels is required, but complete resection difficult and local recurrence common
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6
Q

What is phlebitis?

What causes it? Who is susceptible?

How does phlebitis occur?

How is phlebitis related to venous thrombosis?

A
  • local inflammatory process extending from veins
  • common causes are perivenous or intravenous injection or irritating drugs, infusion of large amounts of fluid, long-term placement of IV catheter.
  • IV phlebitis occurs in
    1) chemical injury
    2) physical trauma (catheter, needle),
    3) microbial (infection).
  • Thrombophlebitis is localised and characterised by pain, swelling, and s duration.
  • Patients with serious illnesses or compromised immune systems develop sepsis, thromboembolic pneumonia, or endocarditis.
  • Phlebitis is a major cause of damage leading to venous thrombosis. The thrombosis is usually of little local consequence if localised to smaller vessels. Emboli may be carried to lung and cause PTE
  • When inflammatory disease, dehydration, or circulatory failure occurs, thrombus formation may continue in the pulmonary vessels and lead to vascular occlusion, dyspnea, pain, and death.
  • In infectious thrombophlebitis, bacterial emboli can be carrier to the lungs and cause thromboembolic pneumonia.
  • usually underlying hepatic disease, or conditions associated with prothrombotic state (PLE, immune mediated haemolytic anemia, or hyper adrenocortical) or compression is identified.
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7
Q

How does venous occlusion present?

What are some causes of cranial vena cava obstruction?
What will central venous obstruction cause?

What does obstruction of intra-abdominal or pelvic venous system cause?

What are some other causes of venous obstruction ?

A
  • edema , cyanosis, discomfort, and venous dilatation distal to obstruction site.
  • obstruction of cranial vena cava = edema in neck, head, front limbs, and dependent portions of cranial thorax.

Causes include cranial mediastinal mass, indwelling central venous catheter, and trans venous pacemaker.

  • pleural effusion = central venous obstruction.
  • obstruction of intra-abdominal or pelvic venous system cause oedema of hind limbs and scrotum. Signs depend on vessel reserve and capacity of regional lymphatics to drain interstitial and serous cavity.
  • causes of venous obstruction include thrombosis, abscesses, hematomas, tumors and lymphadenopathy.
  • ## tumors tending to invade include chemodectoma, pheochromocytoma, and hemangiosarcoma.
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8
Q

Explain how Inflammatory lymphatic disorder (lymphangitis and lymphadenitis) occur.

What are the clinical signs associated with inflammatory lymphatic disorder?

A

Lymphangitis and lymphadenitis occurs secondary to local inflammation, particularly involving skin, mucous membranes, and subcutaneous tissues.
- Lymphangitis can results from bacterial or fungal infection or adjacent neoplastic and inflammatory disease.

  • lymph nodes become obstructed, enlarged, warm, and painful.
  • affected limbs can be swollen and lame
  • pyrexia, anorexia, and depression are common and leukocytes is with acute, severe lymphangitis.

Lymphangitis:
- may be chronic when associated with granulomatous or static lesion such as foreign body or with unsuccessfully treated acute inflammation.
- associated with cutaneous coccidoidomycosis in dog and cat, intestinal lymphadenitis secondary to bite wounds, sporotrichosis, and chronic lipogranulomatous lymphangitis in chronic protein-losing intestinal disease.
-

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9
Q

What is lymphoedema? How does Lymphoedema occur?

A
  • lymphoedema specifically refers to fluid accumulation in the interstitial space resulting from abnormal lymphatic drainage. Not used for other forms of oedema such as venous obstruction or generalised hypoproteinemia.
  • pathologic fluid accumulation in the interstitial when micro vascular filtration rate exceeds lymphatic drainage.
  • in micro vascular bed there is net movement of ultrafiltrate to interstitial so when impaired lymphatic flow, the ultrafiltrate leads to lymphoedema.
  • protein rich lymphoedema 2-5g/L causes high osmotic gradient and exacerbates fluid accumulation
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10
Q

What is primary lymphoedema? How does it occur? How is it diagnosed? What is the prognosis?

A

= abnormality of lymphatic vessels or lymph nodes

Three principle morphological and functional abnormalities:

  1. Abnormaly large vessels (aplasia or hypoplasia) of thoracic duct and cisterna chyli
  2. Aplasia of peripheral lymphatic or congenital valvular incompetence
  3. Lymph node fibrosis or deficient lymph node size and number.

Dx = history and clinical signs
- age of onset (young),disease progression, pain, affected limbs, distribution of oedema, and clinical signs.
- Previous surgery, trauma, and infections.
Radiographic lymphangiography - my confirm diagnosis

Prognosis =
- guarded and depends on etiology
- some with HL oedema during neonatal period improve spontaneously, but severe oedema of trunk and legs succumb
- chronic lymph vessel dilation -> permanent valvular dysfunction and metabolic by-products accumulate and lead to collagen deposition and fibrosis.
- abrasions and infection is a problem
- hypothesis of autosomal dominant inheritance with variable expression
-

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11
Q

What is secondary lymphoedema? How does it occur?

A

= result from neoplasia, surgery, trauma, parasites, radiation therapy, or infection

  • persistent lymphoedema occurs after destruction or blockage of major lymph channels or several sequential LN with afferent or efferent lymphatics
  • inhibited venous return increases lymphatic flow by altering Starlings forces toward increased tissue fluid accumulation. This overloads lymphatics and causes fluid accumulation in interstitial space.
  • aetiologies include post traumatic, post radiation therapy or post surgical interruption of lymphatics; lymph node excision, and blockage of lymph nodes and lymph vessels by compression or invasive neoplasms.
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12
Q

What are the clinical signs of secondary lymphoedema?

A
  • depends on location and severity of obstruction
  • could be localised to extremity, or extend proximal to subcut tissue
  • lymphoedema may be accompanied by fever, anorexia, and weight loss.
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13
Q

How is lymphoedema diagnosed?

What is expected on X-ray and U/S?

A
  • dx based on Hx and PE.
  • survey radiographs of suspicious areas. Soft tissue masses or destructive bony lesions can be detected.
  • subclinical pleural effusions in cases of peripheral oedema suggests a more generalised lymphatic disorder.
  • US: soft tissue masses identifies LN peripherally and in abdomen.
  • lymphangiography, lymphoscintigraphy, or CTA may evaluate venous and lymphatic anatomy and luminal integrity if diagnosis is unclear.
  • some lymphatics are hypoplasic, and cannot be found for radiocontrast injection.
  • lymphangiography of primary lymphoedema include LN aplasia and small lymphatics that end blindly or anastomoses into collateral vessels around locations when LN would be
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14
Q

What are the differential diagnosis for dogs with oedema?

All 4 limbs?

Both forelimbs?

Bilateral HL?

A
  • inflammation, trauma, vascular bed obstruction, haemorrhage, cellulitis, phlebitis, and AV fistula
  • All 4 limbs DDx= hypoproteinemia, CHF, renal failure, portal hypertension, or lymphatic neoplasia (lymphangiosarcoma)
  • Both forelimbs = thrombosis or compression or invasion of cranial vena cava by mediastinal mass. Mass will also cause head and neck oedema.
  • bilateral HL = obstruction of sub lumbar LN by neoplasia, right side CHF, and pericardial effusion.
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15
Q

What treatments are available for lymphoedema?
medical?

surgical?

What is contra-indicated?

A
  • Goal is to keep animal comfortable and reduce swelling
  • infection = antimicrobials
  • neoplasia = chemotherapy or radiation therapy
  • heavy bandage and physical therapy to encourage lymphatic flow and reduce SC lymph accumulation
  • benzopyrones (e.g. Rutin) are drugs that have been advocated to reduce high-protein lymphedema by stimulating macrophages, promote proteolysis, and enhance absorption of protein fragments, but proof in treatment is lacking.
  • Diuretic treatment is contraindicated: as it reduces interstitial fluid and concentrated proteins in residual interstitial space and promotes tissue injury

Surgical options include:

  1. Facilitate lymph drainage from limbs i.e. lymphangioplasty, bridging procedures, shunts, o mental transposition
  2. Excise abnormal tissue

Short term NSAIS, bandaging, and physical therapy may help trauma or post surgical lymphedema

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16
Q

What is lymphangioma? How are they categorised?

A
  • Lymphangiomas are benign tumors of small-caliber lymphatic vessels ad thought to develop when primitive lymphatic sacs fail to establish venous communication.
  • very rare
    Three categories:
    1. Capillary lymphangiomas composed of network capillary-sized lymphatic channels
    2. Cavernous lymphangiomas composed of dilated lymphatics that infiltrate surrouning tissue
    3. Cystic hygromas
17
Q

How do lymphangioma’s present?

what problems can they cause?

A
  • preset on extremities, metacarpal pads, nasopharynx, axilla, inguinal and mammary region, retroperitoneal space, and skin of dogs.
  • exert pressure on surrounding structures and can interfere with muscle function, breathing (compress trachea), urination, or intestinal function.
  • lymph can ooze to skin surface through single or multiple fistulous tracts
18
Q

What are the differential Dx for lymphangioma? What is the prognosis?

A

DDx: space-occupying mass such as abscess, enlarged LN, neoplasms, and congenital cysts of non lymphopenia origin.

  • good after surgical excision, marsuplisation, or radiation therapy.
  • recurrence is high due to inherent inability o identify boundaries.
19
Q

What is lymphangiosarcoma? What are the clinical signs?

A
  • originated from lymphatic endothelial cells
  • rare malignant tumor in dogs and cats, and frequently reported secondary to chronic lymphedema in humans
  • metastasis estimated to be 1/3 - 1/2 cases at diagnosis.
  • pitting edema of extremities, inguinal region, axilla, and head and neck.
20
Q

What is challenging about diagnosing lymphangiosarcoma?

A
  • shares features under light microscopy wth hemangiosarcoma
  • distinguish by lack of erythrocytes in vascular space of lymphangiosarcoma.
  • immunohistochemical stains are better at distinguishing cells
  • diagnosis confirmed by obtaining a biopsy specimen
21
Q

What is the prognosis of lymphangiosarcoma?

A
  • guarded to poor, with a high rate local recurrence and metastasis.
  • optimal therapy is unknown