Revision as of 14:12, 16 November 2010

Introduction

Endocarditis is defined as an inflammation of one or more of the cardiac valves. It is usually a result of a bacteraemia or pyaemia, spread from adjaent myocardium is rare. It occurs in all species and is more common in cattle, pigs and sheep than dogs and cats.

Bacterial endocarditis. Courtesy of A. Jefferies

Organisms commonly isolated include:

Pathophysiology

Vegetative Endocarditis

Predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow. Needs sustained or recurrent bacteraemia. Some bacteria have particular adherence properties and may only need a single episode of bacteraemia to set up an endocarditis. Progression to rupture of the chordae tendinae is possible, along with spread of the infection to the adjacent mural endocardium. Valves may become stenotic, incompetant or both. Death usually results from either embolisation of the vegetative material or congestive heart failure due to significant valvular damage.

Vegetative endocarditis (dog). Courtesy of T. Scase

UlcerativeEndocarditis

Commonly seen along with renal failure in dogs. Uraemia irritates and damages the endocarium, particularly in the left atrium. Oedema is seen in the sunendocardial tissue with deposition of glycosaminoglycans.

Healing may occur by fibrosis or the lesion may progress to a necrotising endcarditis and, in extreme cases, left atrial rupture. If renal sufficieny is re-established then healing of the endocardial lesion is possible.

Species differences:

Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. Congestive right sided failure is manifested as ascites (including bottle jaw) and embolisation to the lungs. Anaemia is often present as the red blood cells are damaged as they pass through the vegetation.
Pig and dog: Lesions occur particularly on the mitral valve, perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage. Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.

Contributing factors include:

Trauma: haemodynamic turbulence.
Valve tissue ageing.
Avascularity of valves; poor healing capacity.
Tissue exposure; constant contact with blood-borne pathogens.

Signalment

Clinical Signs

Diagnosis

Laboratory findings

Echocardiography

Radiography

Electrogcardiogram (ECG)

Treatment

Prognosis

References

from clinical

Infective Endocarditis

Bacterial endocarditis. Courtesy of A. Jefferies

Signalment

Present in small animals:

Dogs: (uncommon); Males & Large Breeds (e.g. German Shepherd) most affected

Cats: (rare)

Present in large animals:

Cattle: (common); Adult cattle

Swine: (very common); Young pigs

Horse: (uncommon); Males more affected

Description

Infective endocarditis is a bacterial infection of the cardiac endocardium. The infection can affect the valves (valvular endocarditis) and then spread to the heart wall (mural endocarditis).

Bacteremia is essential for the development of endocarditis. Once bacteria colonize the valvular endocardium, vegetative lesions composed of platelets and fibrin are formed on the valves. Pieces of the vegetative lesions can detach as emboli. Most often these emboli travel to the kidneys and spleen.

Diagnosis

History & Clinical Signs

-Sings of Embolization:

sudden death
lameness
seizure
arrhythmias
cold extremities

-Signs of Sepsis:

Pyrexia
Neck Pain
Joint Pain
Muscle Pain
Anorexia
Lethargy

-Signs of Cardiac Involvement:

Syncope
Weakness
Exercise Intolerance
Heart Failure
Pulmonary edema
Pulse deficits

Physical Exam

-Systolic Murmur (Mitral Valve Affected)

-Diastolic Murmur (Aortic Valve Affected)

-Pulmonary crackles (If edema is present)

Laboratory Findings

-Urine analysis

If UTI is present, could be (+/-) for the same bacteria that caused endocarditis

Proteinuria

Casts

Pyuria

Hematuria

-Blood Culture

collect blood from the jugular vein

3-4 sterile samples taken 1 hour apart over 24 hours and grown in enhancement media

Positive culture (Rare)

Negative culture is not diagnostic

-Blood Profiles:

Hematology=leukocytosis, neutrophilia, monocytosis, nonregenerative anemia, thrombocytopenia (See with development of: disseminated intravascular coagulation); clotting times may be prolonged

Biochemistry=hypoalbumenemia, hypoglycemia (if septic), signs of complications from emboli

Radiography

-Usually normal unless severe damage is present

-Left atrial and ventricular enlargement (Mitral Valve Incompetence)

-Right atrial and ventricular enlargement (Aortic Valve Incompetence)

-Signs of congestive heart failure with chronic/severe valve damage

Electrocardiography (ECG)

-Usually normal

-Arrhythmias (especially ventricular premature complexes; AV node damage causes 3rd degree AV block)

Echocardiography

-Vegetative lesions on valves and/ mural surfaces

Treatment

-Antibiotic given I/V for at least five days and then given orally for at least six weeks (Broad Spectrum or Culture/Sensitivity)

-Manage secondary problems:

(e.g. septic shock, congestive heart failure, embolization, D.I.C.)

Prognosis

-Guarded

(Possibility of recurrent infections, embolic complications, congestive heart failure)

Difference between revisions of "Endocarditis"

Revision as of 14:12, 16 November 2010

Contents

Introduction

Pathophysiology

Vegetative Endocarditis

UlcerativeEndocarditis

Signalment

Clinical Signs

Diagnosis

Laboratory findings

Echocardiography

Radiography

Electrogcardiogram (ECG)

Treatment

Prognosis

References

from clinical

Infective Endocarditis

Signalment

Description

Diagnosis

History & Clinical Signs

Physical Exam

Laboratory Findings

Radiography

Electrocardiography (ECG)

Echocardiography

Treatment

Prognosis

Navigation menu

Search

@@ Line 1: / Line 1: @@
+{{unfinished}}
 ==Introduction==
-[[Image:Bacterial endocarditis.jpg|right|thumb|200px|<small><center>'''Bacterial endocarditis'''. Courtesy of A. Jefferies</center></small>]]
-Endocarditis is defined as an inflammation of the cardiac endocardium. The infection can affect the valves (valvular endocarditis) and then spread to the heart wall (mural endocarditis). It is usually a result of a bacteraemia or pyaemia, spread from adjacent myocardium is rare. It occurs in all species and is more common in cattle, pigs and sheep than dogs and cats.
+Endocarditis is defined as an inflammation of one or more of the cardiac valves. It is usually a result of a bacteraemia or pyaemia, spread from adjaent myocardium is rare. It occurs in all species and is more common in cattle, pigs and sheep than dogs and cats.
+[[Image:Bacterial endocarditis.jpg|right|thumb|125px|<small><center>'''Bacterial endocarditis'''. Courtesy of A. Jefferies</center></small>]]
 Organisms commonly isolated include:
-*Cattle: ''[[Actinomyces pyogenes]]''
+*Cattle: [[Actinomyces pyogenes]]
-*Pigs: [[Erysipelothrix_rhusiopathiae|''Erysipelothrix spp.'']]
+*Pigs: [[Erysipelothrix_rhusiopathiae|Erysipelothrix spp.]]
-*Sheep: [[:Category:Streptococcus species|''Streptococci'']]
+*Sheep: [[:Category:Streptococcus species|Streptococci.]]
-*Dogs: [[:Category:Streptococcus species|''Streptococci'']], [[:Category:Staphylococcus species|''Staphylococci'']] and ''[[E. coli]]''
 ==Pathophysiology==
 ===Vegetative Endocarditis===
-[[Image:vegetative endocarditis.jpg|right|thumb|200px|<small><center>'''Vegetative endocarditis (dog)'''. Courtesy of T. Scase</center></small>]]
+Predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow.  Needs sustained or recurrent bacteraemia.  Some bacteria have particular adherence properties and may only need a single episode of bacteraemia to set up an endocarditis. Progression to rupture of the chordae tendinae is possible, along with spread of the infection to the adjacent mural endocardium. Valves may become stenotic, incompetant or both. Death usually results from either embolisation of the vegetative material or congestive heart failure due to significant valvular damage.
-It is predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow. Mechanical trauma can cause such damage, such as jet lesions from turbulent blood flow or endocardial injury from a catheter extending into the heart. Highly virulent bacteria or a heavy bacterial load increase the risk of cardiac infection, and normal valves can be invaded by virulent bacteria. Bacteremia is essential for the development of endocarditis. Diseases that impair immune responses or cause hypercoagulability or endothelial disruption are thought to increase the endocarditis risk. Once bacteria colonise the valvular endocardium, vegetative lesions composed of platelets and fibrin are formed on the valves. Progression to rupture of the ''chordae tendinae'' is possible, along with spread of the infection to the adjacent mural endocardium. Valves may become stenotic, incompetent or both. Congestive heart failure commonly results from valvular insufficiency and volume overload. Because the mitral and aortic valves are typically affected, pulmonary oedema is the usual manifestation. Death usually results from either embolisation of the vegetative material or congestive heart failure due to significant valvular damage. Metastatic infection of other body sites commonly occurs.
+[[Image:vegetative endocarditis.jpg|right|thumb|125px|<small><center>'''Vegetative endocarditis (dog)'''. Courtesy of T. Scase</center></small>]]
+===UlcerativeEndocarditis===
+Commonly seen along with renal failure in dogs.
+Uraemia irritates and damages the endocarium, particularly in the left atrium.  Oedema is seen in the sunendocardial tissue with deposition of glycosaminoglycans.
+Healing may occur by fibrosis or the lesion may progress to a necrotising endcarditis and, in extreme cases, left atrial rupture.
+If renal sufficieny is re-established then healing of the endocardial lesion is possible.
-===Ulcerative Endocarditis===
-Commonly seen along with renal failure in dogs. [[Uraemia]] irritates and damages the endocarium, particularly in the left atrium. Oedema is seen in the subendocardial tissue with deposition of glycosaminoglycans. This may progress to a necrotising endocarditis and, in extreme cases, left atrial rupture. If renal sufficiency is re-established then healing of the endocardial lesion is possible.
-==Species differences==
-'''Cattle''': the disease predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. Common underlying causes include liver abscesses, [[Traumatic Reticulitis|traumatic reticulitis]], metritis, mastitis, navel abscesses and 'joint ill'. Congestive right sided failure is manifested as ascites (including '''bottle jaw''') and embolisation to the lungs. [[:Category:Anaemia|Anaemia]] is often present as the red blood cells are damaged as they pass through the vegetation.
-'''Horse''': Lesions occur mainly on the mitral valve. The site of sepsis is often not identified but may be a sequale to septic jugular thrombophlembitis.
+''Species differences:''
+*Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver.  Congestive right sided failure is manifested as ascites (including '''bottle jaw''') and embolisation to the lungs.  Anaemia is often present as the red blood cells are damaged as they pass through the vegetation.
+*Pig and dog: Lesions occur particularly on the mitral valve, perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage.  Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.
+Contributing factors include:
+*Trauma: haemodynamic turbulence.
+*Valve tissue ageing.
+*Avascularity of valves; poor healing capacity.
+*Tissue exposure; constant contact with blood-borne pathogens.
-'''Pig''' and '''Dog''': Lesions occur particularly on the mitral valve (71% of cases in dogs), perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage. Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.
 ==Signalment==
-Endocarditis is rare in dogs but males and large breeds (e.g. German Shepherds) are most affected. Dogs with subaortic stenosis are more at risk of developing the disease. It is very rare in cats.
+==Clinical Signs==
-The disease mainly affects adult cattle and young pigs. In horses, males are more commonly affected than females.
+==Diagnosis==
+===Laboratory findings===
+===Echocardiography===
+===Radiography===
+===Electrogcardiogram (ECG)===
+==Treatment==
+==Prognosis==
+==References==
-==History & Clinical Signs==
-Clinical signs are often vague and rarely referable to congestive heart failure. The following clinical signs are seen related to sepsis:
+=from clinical=
+{{dog}}{{cat}}{{horse}}{{cow}}{{pig}}
+===Infective Endocarditis===
+[[Image:Bacterial endocarditis.jpg|right|thumb|125px|<small><center>'''Bacterial endocarditis'''. Courtesy of A. Jefferies</center></small>]]
+====Signalment====
+'''Present in small animals:'''
+Dogs: (uncommon); Males & Large Breeds (e.g. German Shepherd) most affected
+Cats: (rare)
+'''Present in large animals:'''
+Cattle: (common); Adult cattle
+Swine: (very common); Young pigs
+Horse: (uncommon); Males more affected
+====Description====
+*Infective endocarditis is a bacterial infection of the cardiac endocardium.  The infection can affect the valves (valvular endocarditis) and then spread to the heart wall (mural endocarditis).
+*Bacteremia is essential for the development of endocarditis.  Once bacteria colonize the valvular endocardium, vegetative lesions composed of platelets and fibrin are formed on the valves.  Pieces of the vegetative lesions can detach as emboli.  Most often these emboli travel to the kidneys and spleen.
+====Diagnosis====
+=====History & Clinical Signs=====
+-Sings of Embolization:
+*sudden death
+*lameness
+*seizure
+*arrhythmias
+*cold extremities
+-Signs of Sepsis:
 *Pyrexia
-*Lameness
 *Neck Pain
-*Lethargy/Anorexia
+*Joint Pain
-*Weight loss
+*Muscle Pain
-*Epistaxis
+*Anorexia
+*Lethargy
+-Signs of Cardiac Involvement:
+*Syncope
+*Weakness
+*Exercise Intolerance
+*Heart Failure
+*Pulmonary edema
+*Pulse deficits
+=====Physical Exam=====
+-Systolic Murmur (Mitral Valve Affected)
+-Diastolic Murmur (Aortic Valve Affected)
+-Pulmonary crackles (If edema is present)
+=====Laboratory Findings=====
+-'''Urine analysis'''
+*If UTI is present, could be (+/-) for the same bacteria that caused endocarditis
+*Proteinuria
+*Casts
+*Pyuria
+*Hematuria
+-'''Blood Culture'''
+*collect blood from the jugular vein
+*3-4 sterile samples taken 1 hour apart over 24 hours and grown in enhancement media
+*Positive culture (Rare)
+*Negative culture is not diagnostic
+-'''Blood Profiles:'''
-Signs of embolisation to other organs may also be seen and those of congestive heart failure (dyspnoea, poor pulses, pale mucous membranes, tacchycardia, pulmonary crackles)
+*Hematology=leukocytosis, neutrophilia, monocytosis, nonregenerative anemia, thrombocytopenia (See with development of: disseminated intravascular coagulation); clotting times may be prolonged
-==Physical examination==
+*Biochemistry=hypoalbumenemia, hypoglycemia (if septic), signs of complications from emboli
-A variable murmur depending upon the valve affected. It may be noted that murmur has recently arisen or changed. Other clinical examination findings include joint effusions, lymphadenopathy, pyrexia and in advanced cases signs associated with [[Disseminated Intravascular Coagulation|disseminated intravascular coagulopathy]] (D.I.C) such as bleeding diathesis and petechiation.
+=====Radiography=====
+-Usually normal unless severe damage is present
+-Left atrial and ventricular enlargement (Mitral Valve Incompetence)
+-Right atrial and ventricular enlargement (Aortic Valve Incompetence)
+-Signs of congestive heart failure with chronic/severe valve damage
-==Diagnosis==
-Diagnosis can be difficult but a presumptive diagnosis is made on two or more positive blood cultures in addition to either echocardiographic evidence of vegetations or valve destruction, or the documented recent onset of a regurgitant murmur.
-===Laboratory findings===
-'''Blood profiles''': Not all cases will have altered blood changes. Possible changes include:
-::Haematology - [[Neutrophilia]], left shift, monocytosis, [[thrombocytopaenia]] and prolonged clotting times if developing D.I.C.
-::Biochemistry - [[Hypoalbuminaemia]] and hypoglycaemia.
-'''Urinalysis''' : may have proteinuria, casts, pyuria. A urinary tract infection may be present with the same organism as is responsible for the endocarditis.
-'''Blood cultures''' : Requires 3-4 sterile samples collected from the jugular vein at least 1 hour apart over a 24 hour period. Negative cultures do not rule out the possibility of bacterial endocarditis.
+=====Electrocardiography (ECG)=====
-===Echocardiography===
+-Usually normal
-Structural abnormalities and vegetations may be visible on the valves although it is difficult to differentiate from [[endocardiosis]].
-===Radiography===
+-Arrhythmias (especially ventricular premature complexes; AV node damage causes 3rd degree AV block)
-Radiography is often unremarkable. There may be evidence of cardiomegaly or congestive heart failure if valvular damage is chronic or severe. Evidence of a focus of infection such as discospondylitis may be visible.
-===Electrocardiogram (ECG)===
-ECG may be normal. Arrhythmias detectected are often ventricular in origin (e.g. ventricular premature complexes) and represent extension of the inflammatory focus to involve the myocardium. 3rd degree heart block may be present if the AV node is affected.
-==Treatment==
+=====Echocardiography=====
-Antibiotic treatment with either a broad spectrum antibiotic or an appropriate antibiotic based on culture and sensitivity results. Antibiotics should be administered intravenously for the first 5 days of therapy followed by a prolonged course (>4 weeks) of oral medication.
-<br>Common Protocols use [[Penicillins|Ampicillin]] in combination with a [[Fluoroquinolones|Fluoroquinolone]] such as Enrofloxacin or an aminoglycoside.
-<br>Secondary problems such as septic shock, D.I.C., congestive heart failure and embolisation need to be managed. Treatments commonly include diuretics or vasodilators to control the oedema, reduce valvular regurgitation and improve cardiac output.
-==Prognosis==
+-Vegetative lesions on valves and/ mural surfaces
-Long term prognosis is guarded to poor. Possible complications include septic shock, disseminated intravascular coagulation, congestive heart failure and embolisation to other organs.
-{{Learning
-|literature search = [http://www.cabdirect.org/search.html?q=title:(%22endocarditis%22)&fq=sc:%22ve%22 Endocarditis publications]
-[http://www.cabdirect.org/search.html?q=title:(%22endocarditis%22)+AND+od:(cattle)&fq=sc:%22ve%22 Endocarditis in cattle publications]
+====Treatment====
-[http://www.cabdirect.org/search.html?q=title:(%22endocarditis%22)+NOT+od:(cattle)&fq=sc:%22ve%22 Endocarditis in other veterinary species publications]
+-Antibiotic given I/V for at least five days and then given orally for at least six weeks
-|flashcards = [[Small Animal Emergency and Critical Care Medicine Q&A 01]]
+(Broad Spectrum or Culture/Sensitivity)
-}}
-==References==
+-Manage secondary problems:
-Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial''
-Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
+(e.g. septic shock, congestive heart failure, embolization, D.I.C.)
-Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) '''Manual of Canine and Feline Cardiology''' ''Saunders''.
-Elwood, C.M., Cobb, M.A., Stepien, R.L., (1993) Clinical and echocardiographic findings in 10 dogs with vegetative bacteria endcarditis. '''Journal of small animal practice'''. 34,  pp420-427.
+====Prognosis====
+-Guarded
-{{review}}
+(Possibility of recurrent infections, embolic complications, congestive heart failure)
-==Webinars==
-<rss max="10" highlight="none">https://www.thewebinarvet.com/cardiology/webinars/feed</rss>
-[[Category:Endocardial_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category:Cardiac Diseases - Cattle]][[Category:Cardiac Diseases - Pig]][[Category:Cardiovascular Diseases - Sheep]]
+[[Category:Endocardial_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category:Cattle]][[Category:Pig]][[Category:Sheep]]
-[[Category:Expert_Review - Farm Animal]][[Category:Expert Review - Horse]][[Category:Cardiac Diseases - Dog]][[Category:Cardiac Diseases - Horse]]
+[[Category:To_Do_-_Cardiovascular]]
-[[Category:Cardiology Section]]