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Equine Final Year > Pericardial and Vascular Disease > Flashcards

Pericardial and Vascular Disease Flashcards

1
Q

What are the 5 categories of pericardial disease and which species is this most common?

A
  • Traumatic / Septic
  • most common from in cattle
  • Idiopathic
  • most common from in horses
  • Bacterial
  • most common form in pigs
  • Neoplastic
  • uncommon in large animals
  • Viral
  • uncommon in large animals
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2
Q

What is the pathogenesis of traumatic pericarditis?

A
  • A manifestation of hardware disease (traumatic reticuloperitonitis)
  • ingested wires migrate through the wall of the reticulum, into the peritoneal cavity and through the diaphragm into the pericardial sac
  • accumulation of septic fluid and gas within the pericardial sac
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3
Q

What are the early and later signs of traumatic pericarditis?

A
  • Early signs: non-specific
  • fever, anorexia, depression
  • stand with elbows abducted, or with forequarters elevated
  • reluctant to move
  • positive grunt test
  • Later signs: right-sided heart failure
  • venous congestion, peripheral oedema
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4
Q

What is seen on cardiac exam of traumatc pericarditis? (5)

A
  • tachycardia
  • muffled heart sounds
  • If you cant hear the heart sounds with a good stethoscope and then you ECG. Do you need to U/s?
  • splashing “washing machine” murmurs
  • Gas fluid interface – usually anaerobic bacteria
  • venous distension
  • weak pulses
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5
Q

What is the treatment of pericarditis?

A
  • The vast majority of affected cattle are culled
  • Surgical procedures to strip out the pericardium and remove septic debris have been described. And lavage – valuable breeding stock
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6
Q

What does lymphosarcoma cause in cattle? What is seen on cytology?

A
  • Right atrial infiltration (RAP increases, jugular distension)
  • May have pericardial infiltration: may have pericardial effusion- haemorrhagic in appearance
  • Cytology reveals neoplastic cells
  • Lymphocytes – sporadic lymphoma
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7
Q

What is the aetiology and pathology of pericarditis in horses?

A
  • the majority of cases are idiopathic
  • equine viral arteritis, equine influenza
  • Strep. Pneumoniae (E.Coli, Actinobacillus
  • Penicillin drug of choice initially
  • tend to develop fibrinous effusion
  • Just idiopathic once or twice – shouldn’t come back. Leaves a small hole so can just drain and be absorbed
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8
Q

What are the clinical signs of pericarditis in horses? (5)

A
  • venous distension
  • ventral oedema
  • muffled heart sounds

•pericardial friction rubs
(triphasic sounds in time with heart)

•pleural effusion

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9
Q

Hwo do you diagnose pericarditis in horses? (3)

A
  • Echocardiography
  • fluid and fibrin in pericardial sac
  • compression of cardiac chambers
  • Electrocardiography
  • small complexes – make sure your leads are in an appropriate place before you diagnose
  • main differential is obesity
  • Cytology of pericardial fluid
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10
Q

What does this show?

A

Pericarditis

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11
Q

How can you treat pericarditis in horses? (2)

A
  • Pericardial drainage and lavage are indicated if the right atrium is collapsing (i.e. cardiac tamponade is present)
  • Indwelling drain and twice daily lavage with antibiotic containing fluids greatly improves prognosis
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12
Q

What is the prognosis for pericarditis in horses?

A
  • good provided treatment is early and aggressive
  • constrictive disease may occur in chronic cases
  • Can return to full performance
  • Serosanguous – transudate or exudate; not such a good prognosis
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13
Q

What causes pericarditis in pigs?

What are the signs?

A
  • Haemophilus parasuis, Strep. Suis
  • Non-specific signs - fever, depression
  • Also fibrinous serositis and effusion in CNS, pleural, peritoneum, and synovia
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14
Q

What are the signs of non septic (2) and septic (3) jugular thrombosis?

A
  • NON-SEPTIC
  • thickening “cording” of the vein
  • reduction in patency
  • SEPTIC
  • hot
  • painful
  • discharging tracts (chronic) – burst out following catherter complication
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15
Q

What is the aetiology of jugular thormbosis?

A

•Most (all) cases of jugular thrombosis are associated with intravenous catheterisation or injection – buscopan combo, oxytet, guarphenesin, diapentone

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16
Q

What are the predisposing factors for jugular thrombosis? (5)

A
  • Systemic inflammatory response syndrome (SIRS)
  • Gram +ve and –ve
  • Multi-organ dysfunction Syndrome
  • irritant drugs
  • poor catheter placement
  • poor catheter use
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17
Q

What are the clinical signs of jugular thrombosis?

A

VENOUS OCCULSION

  • swelling in the supraorbital area
  • cheek and lips
  • tongue
  • leading to dysphagia
  • upper airway obstruction
  • Nasal airflow test
  • Affects performance
  • proximal venous distension
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18
Q

What is ultrasound used for in jugular thrombophlebitiis? (5)

A
  • assess extent of thrombus
  • identify sepsis (cavitation)
  • assess patency of vein
  • distinguish perivenous swelling from thrombosis
  • select site for aspiration
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19
Q

What can be seen on jugular thrombophlebitis?

A
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20
Q

How can you diagnose jugular thrombophlebitits? (4)

A
  • catheter tip; take it out sterile can culture it
  • ultrasound-guided aspirate fluid pocket from within thrombus
  • swab from discharging tracts
  • Contamination from the skin
  • blood culture (take from other jugular vein in culture media)
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21
Q

How can you treat jugular thrombosis? (7)

A
  • Nursing! Most important with time
  • Feed from high to prevent head swelling
  • Hot packs
  • Compagel - break thrombus
  • Broad spectrum antibiotics
  • Anti-inflammatories
  • Systemic
  • aspirin
  • other NSAIDs
  • Topical
  • DMSO
  • hot packs
  • Heparin
  • Or analogues
  • Vasodilators
  • Gyleryltrinitrate
  • Raise head
  • Aspirin – stop the clot forming. Prevent platelets forming – give every 3 days
22
Q

How can you manage jugular thrombosis?(3)

A
  • Alternative venous access
  • lateral thoracic
  • cephalic
  • With bilateral thrombosis, tracheostomy may be required
  • Surgical procedures to strip and/or graft the vein have been described but are rarely undertaken
23
Q

What are the jugular thrombosis complications? (4)

A
  • Embolic disease
  • Bacterial endocarditis
  • Septic Pneumonia
  • Long-term poor performance due to:
  • Recurrent laryngeal neuropathy
  • Due to the anatomical location cf the jugular
  • Upper airway oedema during exercise
24
Q

What is SIRS and what is it triggered by?

A
  • A self-amplifying dysregulated systemic inflammatory response
  • Triggered by
  • Bacterial toxins
  • Lipopolysaccharide derived from gram negative bacteria, but gram positive is also identified now
  • S aureus
  • Burns, Neoplasia, Pancreatitis (not equine)
  • Can result in coagulopathies
  • Previously referred to as endotoxaemia (not helpful as not the endotoxin causing the problems – it’s the inflammation)
  • Inflammation leading cell death and apoptosis
  • LPS has some direct roles
  • Includes non-LPS bacteria
25
Q

What is sepsis?

A

SIRS plus blood culture proven infection

26
Q

What is severe sepsiss?

A

•Sepsis with organ hypoperfusion or dysfunction (high creatinine, low BP etc).

27
Q

What is septic shock?

A
  • Severe Sepsis + systemic hypotension
  • Common in foals, rare in adults
28
Q

What is multi organ dysfunction syndrome and how can we classify?

A
  • Altered organ function in an acutely ill animal such that haemostasis cannot be maintained without intervention (can get renal failure as a result)
  • Classified as either primary or secondary
  • Primary
  • resulting from well-defined insult where organ dysfunction occurs early and is a direct consequence of the insult itself
  • Eg burns and neoplasia
  • Secondary
  • Organ failure not in direct response to the insult but as a consequence of a host response (SIRS)
29
Q

What is disseminated intravascular coagulopathy?

What is it associated with?

A
  • “Consumptive coagulopathy”
  • Pathological activation of coagulation
  • microvasculature clotting
  • haemorrhagic diathesis
  • consumption of procoagulants
  • Associated with
  • SIRS, SEPSIS, SEPTIC SHOCK
  • MODS
  • systemic neoplasia
  • enteritis and colitis

More likely to see thrombosis In horses not haemhorrhage

30
Q

What are the clinical signs of DIC?

A
  • In large animals, DIC is usually manifested by thrombosis rather than spontaneous haemorrhage
  • petechial haemorrhages
  • bleeding at following trauma
  • Venipuncture
  • surgical sites
  • nasogastric intubation
  • DIC in horses – abnormal bleeding following trauma
31
Q

How can we diagnose DIC? (5)

A
  • thrombocytopaenia
  • Prolonged prothrombin time
  • activated partial thromboplastin time
  • fibrin degradation products
  • antithrombin 3
32
Q

How should you do a IV jugular injection?

A
  • Inject in the proximal one third of the neck (lower you go the closer to the CA and you will give the drug to the brain – will seizure, due or recover). O think it’s a drug reaction.
  • avoids the carotid artery
  • which is less superficial
  • Remove the needle from the syringe – put needle in first. You will know if you have hit the carotid.
  • 18 gauge, 1/5 inch needle
  • Push the needle right into the hub
33
Q

What are the factors you have to consider when choosing a catheter? (10)

A
  • catheter insertion
  • sterile technique
  • minimal trauma
  • secure appropriately in jugular furrow – don’t want it coming out
  • catheter material
  • catheter design
  • catheter use
  • sterile insertion
  • catheter material
  • cheaper but more thrombogenic (nylon, PVC or Teflon):
  • teflon, nylon and polyvinylchloride
  • Only leave 1-2days
  • more expensive but less thrombogenic
  • Polyurethane
  • Long stay put in over a wire
  • Can stay for up to 28 days
  • catheter design
  • catheter use
34
Q

What do we need to do when using catheter? (7)

A

•extension sets to avoid excessive
manipulation of hub

  • swab injection ports
  • change ports and fluid lines q24hrs?
  • Change fluid bags in sterile manner
  • appropriate life-span
  • PVC - 72 hours
  • polyurethane - 7 - 21 days
  • covering and application of antiseptic are controversial - helpful in foals to stop them scratching the catheter out, may increase risk of infection. This is usually to prevent them pulling it out rather than a clean thing
  • Always keep an eye on the catheter
35
Q

What are the complications of IV catheterisation? (3)

A
  • jugular thrombosis
  • catheter breakage
  • May be attached to jugular wall, therefore can remove
  • adults - travel to lungs and rarely cause problems
  • foals - stick within heart and require surgical removal
36
Q

Whatis aortoiliac thrombosis? and what is the aetiology?

A
  • Partial or complete occlusion of the terminal aorta, and external and internal iliac arteries by an organising thrombus
  • Aetiology unknown
37
Q

What are the results of aortoiliac thrombosis? (4)

A
  • Poor performance
  • Exercise-associated hindlimb lameness (i.e. exacerbated by exercise: differential for extertional rhabdomyolysis)
  • Breeding failure in stallions
  • After exercise
  • Cold limb
  • Weak pulses
38
Q

How do you diagnose AORTO-ILIAC THROMBOSIS? (3)

A
  • palpate thrombus, turgid vessel on rectal examination
  • visualise the thrombus with transrectal ultrasonography
  • Doppler is good
  • vascular phase scintigraphy
39
Q

How do you treat AORTO-ILIAC THROMBOSIS and what is the prognosis?

A

TREATMENT

  • non-steroidal anti-inflammatory drugs
  • aspirin
  • fenbendazole (larvicidal, anti-thrombotic effect?)

PROGNOSIS

•guarded

40
Q

Where is caudal vena caval thrombosis seen and what are the signs?

A
  • Production animal disease – due to poor diet. Loss of rumen integrity due to acidosis. Bacteria cross.
  • Formation of thrombus in the caudal vena cava following extension of sepsis from a liver abscess
  • Young, beef cattle
  • Early signs vague, may appreciate distension in the superficial epigastric veins without jugular distension
  • Respiratory signs
  • Severe epistaxis
41
Q

What is seen in caudal vena caval thrombosis? (6)

A
  • Palatable high energy diet, low roughage, less saliva
  • Increase in SCFA, lactic acid increase
  • Incorrect bacterial population
  • Rumen pH <5.5
  • Reduction in rumen motility, hyperkeratosis, loss of mucosal integrity
  • Bacteria = hepatic portal vein = liver abscessation
42
Q

What is vascular rupture and how common?

A
  • Any intra-abdominal or intra-thoracic vessel can rupture
  • aorta and pulmonary artery appear to be most common sites
  • Vascular rupture is the commonest form of sudden death during exercising horses, accounts for around 30% of cases
43
Q

What is this?

A

Aneurism causing PA rupture

44
Q

What are the differentials for vascular rupture? (3)

A
  • Stress fractures
  • Exertional rhabdomyolysis
  • Arrhythmias
45
Q

How do you know whetehr blood in the abdomen is from a rupture or you’ve hit a vein?

A

Blood in the abdomen which has been sat there for a while – so there are no platelets in this. This is how you know it is haemoabdomen not just hitting a vein

46
Q

What is teh aetiology vascular rupture? (3)

A
  • pre-existing aneurysm
  • medial degeneration
  • congenital
  • parasitic
  • large strongyles are more likely to affect the cranial mesenteric arteries and be associated with colic
  • the role of migrating strongyles in other vascular diseases may have been over-emphasised
47
Q

When does RUPTURE OF THE UTERINE VESSELS –uterine artery, external iliac artery occur?

How do we manage? (3)

A
  • Occurs in periparturient broodmares, particularly immediately before or after foaling, but up to three weeks after
  • Colic
  • Mass palpable in the broad ligament, or may bleed directly into abdomen
  • Management
  • conservative
  • support circulation
  • Analgesics
  • If its bad enough you need to do something about it – it is too late…
  • If it is small enough – don’t worry about it
48
Q

AORTO-CARDIAC FISTULA:

What is it, where is it seen?

A
  • Congenital or acquired absence defect of the aortic wall
  • Seen mainly in intact males
49
Q

When does the rupture occur with AORTO-CARDIAC FISTULA? (2)

A

Excerise

Breeding

50
Q

What are the signs of AORTO-CARDIAC FISTULA? (4)

A
  • Sudden death
  • Distress
  • ventricular tachycardia
  • loud continuous murmur
51
Q

How do we diagnose AORTO-CARDIAC FISTULA and what is the prognosis?

A
  • Diagnosis:
  • Echocardiography
  • Prognosis:
  • Hopeless
52
Q

What is the most important vascular disease in horses?

A

Jugular thrombosis

Equine Final Year (102 decks)

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