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
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
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
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
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
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
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
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
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
10
Q
What does this show?
A
Pericarditis
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
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
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
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
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
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
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
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
19
Q
What can be seen on jugular thrombophlebitis?
A
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)
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
What is sepsis?
SIRS plus blood culture proven infection
26
What is severe sepsiss?
•Sepsis with organ hypoperfusion or dysfunction (high creatinine, low BP etc).
27
What is septic shock?
* Severe Sepsis + systemic hypotension
* Common in foals, rare in adults
28
What is multi organ dysfunction syndrome and how can we classify?
* 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
What is disseminated intravascular coagulopathy?
What is it associated with?
* “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
What are the clinical signs of DIC?
* 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
How can we diagnose DIC? (5)
* thrombocytopaenia
* Prolonged prothrombin time
* activated partial thromboplastin time
* fibrin degradation products
* antithrombin 3
32
How should you do a IV jugular injection?
* 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
What are the factors you have to consider when choosing a catheter? (10)
* 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
What do we need to do when using catheter? (7)
•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
What are the complications of IV catheterisation? (3)
* 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
Whatis aortoiliac thrombosis? and what is the aetiology?
* Partial or complete occlusion of the terminal aorta, and external and internal iliac arteries by an organising thrombus
* Aetiology unknown
37
What are the results of aortoiliac thrombosis? (4)
* 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
How do you diagnose AORTO-ILIAC THROMBOSIS? (3)
* palpate thrombus, turgid vessel on rectal examination
* visualise the thrombus with transrectal ultrasonography
* Doppler is good
* vascular phase scintigraphy
39
How do you treat AORTO-ILIAC THROMBOSIS and what is the prognosis?
TREATMENT
* non-steroidal anti-inflammatory drugs
* aspirin
* fenbendazole (larvicidal, anti-thrombotic effect?)
PROGNOSIS
•guarded
40
Where is caudal vena caval thrombosis seen and what are the signs?
* 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
What is seen in caudal vena caval thrombosis? (6)
* 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
What is vascular rupture and how common?
* 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
What is this?
Aneurism causing PA rupture
44
What are the differentials for vascular rupture? (3)
* Stress fractures
* Exertional rhabdomyolysis
* Arrhythmias
45
How do you know whetehr blood in the abdomen is from a rupture or you've hit a vein?
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
What is teh aetiology vascular rupture? (3)
* 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
When does RUPTURE OF THE UTERINE VESSELS –uterine artery, external iliac artery occur?
How do we manage? (3)
* 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
AORTO-CARDIAC FISTULA:
What is it, where is it seen?
* Congenital or acquired absence defect of the aortic wall
* Seen mainly in intact males
49
When does the rupture occur with AORTO-CARDIAC FISTULA? (2)
Excerise
Breeding
50
What are the signs of AORTO-CARDIAC FISTULA? (4)
* Sudden death
* Distress
* ventricular tachycardia
* loud continuous murmur
51
How do we diagnose AORTO-CARDIAC FISTULA and what is the prognosis?
* Diagnosis:
* Echocardiography
* Prognosis:
* Hopeless
52
What is the most important vascular disease in horses?
Jugular thrombosis
