WikiVet English - User contributions [en]

Pulmonary Hypertension

2021-06-23T13:45:02Z

LauraN156: /* Diagnosis */

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== Introduction ==

Hypertension is defined as the pathological elevation of arterial blood pressure.There are two main types of hypertension, [[Systemic Hypertension|systemic hypertension]] (affects the systemic circulation) and pulmonary hypertension (affects the pulmonary circulation). Blood pressure in veterinary patients is not measured routinely; therefore hypertension is usually only diagnosed after clinical signs become apparent.

Pulmonary hypertension = increase in pulmonary arterial pressure.

'''There are two types of pulmonary hypertension:'''

1. '''Primary''' pulmonary hypertension = idiopathic pulmonary hypertension (contributing factors: drugs, toxins, genetic predisposition and infections)

2. '''Secondary''' pulmonary hypertension = pulmonary hypertension resulting from an identifiable underlying condition

[[Cor Pulmonale|'''Cor pulmonale''']] = [[Heart Failure, Right-Sided|right sided heart failure]] resulting from pulmonary hypertension.

The hypoxic conditions at high elevations or animals with chronic airway disease contribute to pulmonary hypertension through hypoxia-induced vasoconstriction.

==Signalment==

Some diseases predispose animals to secondary pulmonary hypertension. Predisposed breeds include brachycephalic dogs (chronic obstructive pulmonary disease); small breeds ([[Degenerative Mitral Valve Disease|mitral endocardiosis]]) and West Highland White Terriers (pulmonary fibrosis).

== Clinical Signs ==

Clinical signs may vary and also may be disguised by other signs of the underlying, causative disease. There is often signs of right sided heart failure, such as exercise intolerance, dyspnoea, coughing, syncope, cyanosis, abdominal distension and distended jugular veins.

== Diagnosis ==

'''Physical examination''', depending on any underlying conditions, may show a [[Heart Murmurs|heart murmur]] (mitral or tricuspid regurgitation), presence of a gallop rhythm, increased lung sounds and splitting of S2 heart sounds (see [[:Category:Arrhythmia|arrhythmias]]).

'''Blood tests''':
:Arterial blood gases may show hypoxemia if there are low oxygen conditions.
:Complete Blood Count will show an eosinophilia if ther is parasitic involvement. (Serology or Fecal Baermann tests would confirm parasitic involvement).
:Biochemistry would show hyperglobulinemia in chronic inflammation.
:A biomarker for a pulmonary hypertension is an elevated NT-proBNP.

'''Urinalysis''' may show the presence of proteinuria if systemic disease is present.

'''Radiography''' is best performed with a DV view. Signs will include right atrial and ventricular enlargement, pulmonary arteries enlargement, enlargement of the V. cava caudalis, congested pulmonary veins and signs of pulmonary disease.

'''Electrocardiography''' may show the presence of right ventricular hypertrophy (deep S-waves) and signs of myocardial hypoxia (ST segment abnormalities).

'''Echocardiography''' may be used to calculate pulmonary arterial pressures. It may also show enlargement of the right-side of the heart and enable visualisation of mitral or tricuspid regurgitation.<gallery caption="[[File:Enlarged pulmonary artery.jpg|thumb|354x354px|Enlarged pulmonary artery]]">
</gallery>
<gallery caption="[[File:Diagnosis of Pulmonary Hypertension.jpg|thumb|340x340px|Enlarged right atrium and ventricle]]">
</gallery>

== Treatment ==

'''Treat the underlying conditions:'''

*Treat right sided heart failure

*Treat pulmonary thromboembolism with heparin and then warfarin

*Treat chronic obstructive pulmonary disease

== Prognosis ==

Depends on the disease condition causing pulmonary hypertension and the ability to control it. Prognosis is poor when pulmonary drainage is irreversible.

{{review}}

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[[Category:Lungs_-_Circulatory_Pathology]] [[Category:Vascular_Diseases_-_Dog]] [[Category:Vascular_Diseases_-_Cat]] [[Category:Arterial_Pathology]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

File:Pressure gradient over the tricuspid valve.jpg

2021-06-23T13:16:18Z

LauraN156:

Source: Source: Praxis der Kardiologie Hund und Katze. Kresken J, Wendt R, Modler P, Hrsg. 2., aktualisierte Auflage. Stuttgart: Thieme; 2019. doi:10.1055/b-006-166351

File:Enlarged pulmonary artery.jpg

2021-06-23T13:12:13Z

LauraN156:

Description of the content: Enlarged pulmonary artery

Source: Praxis der Kardiologie Hund und Katze. Kresken J, Wendt R, Modler P, Hrsg. 2., aktualisierte Auflage. Stuttgart: Thieme; 2019. doi:10.1055/b-006-166351

File:Diagnosis of Pulmonary Hypertension.jpg

2021-06-23T13:04:56Z

LauraN156:

Description of the content: enlarged right atrium and ventricel

Source: Praxis der Kardiologie Hund und Katze. Kresken J, Wendt R, Modler P, Hrsg. 2., aktualisierte Auflage. Stuttgart: Thieme; 2019. doi:10.1055/b-006-166351

Seizures

2021-05-30T09:59:00Z

LauraN156:

==Introduction==

* '''Seizures''' are paroxysmal changes in cerebral cortex electrical activity that start abruptly, end suddenly and have a tendency to recur.
* '''Epilepsy''' is the occurence of recurrent seizures.

==Pathophysiology==

* Seizures occur when there is imbalance between exitatory and inhibitory processes. This may be due to :
** Inadequate neuronal inhibition.
*** Major inhibitory neurotransmitters include GABA and glycine.
** Excessive neuronal excitation.
*** Major excitatory neurotransmitters include aspartate and glutamate.

===Proposed Mechanisms===

* Defective feed-forward inhibition or feed-back initiation of inhibitory neurons in cortical circuits.
** Recurrent excitatory collaterals may be formed.
* Changes in membrane properties of neurons.
** These may include changes at:
*** Potassium, sodium, chloride and calcium ion channels
*** GABA receptors
*** Nicotinic acetyl choline receptors
*** NMDA receptors
**** Activation.
* Changes in the ionic microenvironment.

===Seizure Development===

# At the onset of a seizure, abnormal neurons undergo prolonged depolarisations.
#* These depolarisations are associated with the rapid firing of repeated action potentials.
# Depolarisation of abnormal neurons recruits adjacent neurons with which they are connected.
# The electrical discharges of the large number of neurons involved become linked together.
# A storm of electrical activity results, causing a clinical seizure.
# Seizures may then spread:
#* To adjacent areas of the brain.
#* Through established anatomic pathways to other distant areas.

==Nomenclature==

* '''Status epilepticus''' is the term used to describe
** A seizure lasting longer than 5 minutes, or
** A collection of discrete seizures without full recovery of consciousness.
* '''Cluster seizures''' occur when 2 or more seizures are experienced in a brief periods, but the patient regains consciousness between them.
* Three classes of seizures are recognised:
*# Generalised seizures
*# Focal seizures
*# Focal generalising seizures

===Generalised Seizures===

* Generalised seizures may be:
** Idiopathic
** Symptomatic
*** Due to intracranial disease e.g. neoplasia, storage diseases etc.
** Cryptogenic
*** There is probably an underlying cause but it cannot be identified by the diagnostic tests available.
** Reactive
*** Due to some extracranial disorder, for example a toxin or metabolic disorder.

====Clinical Signs====

* Initial clinical signs show involvement of both cerebral hemispheres.
* Generalised seizures result in:
** Change in consciousness
** Motor activity
*** Tonic-clonic seizures are most common in dogs and cats.
** Autonomic signs
* The body's energy utilisation can increase to around 250% of the normal value during a generalised seizure.

====Stages====

# Prodromal Phase
#* The animal experiences an indication of a forthcoming seizure.
#* This occurs hours to days before the event itself.
# Aural Phase
#* This is the very start of the seizure.
#* Behaviour changes may be apparent.
# Ictal Phase
#* The seizure "proper".
# Postictal phase
#* Consists of transient neurological and behavious changes, which can last from hours to days.

====[[Idiopathic Epilepsy]]====

====Acquired Generalisd Seizures====

* Other general seizures may be acquired.
* Seizures can occur at any age, but generally occur in animals younger than 2 years and older than 5 years.
* Causes may include:
** Intracranial disease
*** Neoplasia
*** Trauma
*** Infection
*** Inflammation
** Extracranial disease (also known as "reactive epilpsy").
*** Electolyte disorders
*** Metabolic disorders
*** Toxicity

===Focal Seizures===

* Almost always an acquired disease.
* Active diseases often progress to become more general.
** Cause generalised seizures.

===Simple Focal Seizures===

* Onset occurs in a limited area of one cerebral hemisphere.
* No impairment of consciousness.

=== Complex Focal Seizures===

* Arise in a single brain region, but cause impaired consciousness.

==Causes of Acquired Seizures==

{| border="3" cellpadding="8"
!width="150"|'''Cause'''
!width="400"|'''Examples'''

|-
|Neoplasia
|Primary or metastatic
|-
|Inflammatory
|Distemper, FIP, FeLV/FIV, rabies, cryptococcosis (cats), toxoplasmosis
|-
|Traumatic
|Immediate or delayed
|-
|Vascular
|Feline ischaemic encephalopathy, thromboembolism, hypertenstion
|-
|Anomalous
|Hydrocephalus
|-
|Metabolic
|Hepatic encephalopathy, uraemia, hyperparathyroidism, hypolycaemia, hyperkalaemia, hypocalcaemia, hypoxia, acid-base disorders, hyperthermia
|-
|Toxic
|Lead, organophosphates, metaldehyde, strychnine
|}
[[File:Causes of Epilepsy in cats and dogs older than 6 years.pdf|alt=|thumb|Causes of Seizures in Cats and Dogs older than 6 Years]]

==Investigation of Seizures==

* It must first be determined whether seizure activity is in fact a seizure, rather than a non-epileptic paroxysmal event, for example:
** Syncope
** Exercise-induced weakness
** Obsessive-compulsive behaviour
** Narcolepsy
* Idiopathic epilepsy may be differentiated from secondary or reactive seizures by considering:
** Age of onset
** Breed disposition
** Partial seizures or asymmetrical post-ictal signs
*** These suggest a discrete lesion.
** Older animals (>5 years) may be more likely to have an acquired aetiology.
** Younger animals (<6 months) may be more likely to have toxic or metabolic causes.
* Useful tests include:
** Metabolic screening
** Haematology
** Serum biochemistry
** Urinalysis
** Serology.
** Bile acid stimulation test
** Serum lead
** MRI and CT scanning, and CSF analysis, help rule out cancer.
 

{{Template:Learning
|podcasts = [[Seizures podcast|RVC clinical podcast about seizures]] 
}}

[[Category:Central Nervous System - Pathology]]

File:Causes of Epilepsy in cats and dogs older than 6 years.pdf

2021-05-30T09:58:34Z

LauraN156:

Infarct:
• Blocked pipe
Bleeding:
• Pool filled with blood
Hyperviscosity
• Man wading through the viscous blood
Hypoglycemia + Hypocalcemia:
• Normally the testbox is filled with a sample of the poolwater to test the pH value and the amount of chloride
• In the picture the blood is tested for glucose and calcium, both levels are too low
Uremia/ Hepatoencephalopathy
• The Ammonium which is dropping out off the bottle and is contaminating the water is
illustrating the urinary excreted substances which are circulating in the blood vessels
Primary and sekundary Neoplasias:
• The cauliflower floating in the pool is illustrating the primary tumor
• The cauliflowers in the basket are illustrating the metastasis
• The cauliflowers in general represent tumors, because of the cauliflower-like proliferation of
some tumors

File:Epilepsy older than 6 years.pdf

2021-05-30T09:53:34Z

LauraN156:

Infarct:
• Blocked pipe
Bleeding:
• Pool filled with blood
Hyperviscosity
• Man wading through the viscous blood
Hypocalemia + Hypocalcemia:
• Normally the testbox is filled with a sample of the poolwater to test the pH value and the
amount of chloride
• In the picture the blood is tested for potassium and calcium, both levels are too low
Uremia/ Hepatoencephalopathy
• The Ammonium which is dropping out off the bottle and is contaminating the water is
illustrating the urinary excreted substances which are circulating in the blood vessels
Primary and sekundary Neoplasias:
• The cauliflower floating in the pool is illustrating the primary tumor
• The cauliflowers in the basket are illustrating the metastasis
• The cauliflowers in general represent tumors, because of the cauliflower-like proliferation of
some tumors

Degenerative Mitral Valve Disease

2021-05-11T14:16:34Z

LauraN156: Addition in clinical signs, diagnostics and treatment

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Also known as: '''''MVD — Mitral Valve Disease — Mitral Insufficiency — Mitral Endocardiosis — Myxomatous Mitral Valve Disease (MMVD) — Endocardiosis — Mitral Regurgitation — Chronic Valvular Disease'''''

== Introduction ==
Myxomatous degeneration of the mitral valve is the most common acquired cardiac disease in the dog. Degenerative mitral valve disease (DMVD) is a progressive disease and subtle changes in valve structure precede the development of clinically significant disease. The aetiology of DMVD is unknown. Genetic predisposition for development of the disease is likely, however the inheritance is complex.

The '''mitral apparatus''' consists of the mitral '''valve leaflets''', valve '''annulus''', '''chordae tendinae''' and '''papillary muscles'''. The mitral valve leaflets are known as '''anterior''' and '''posterior''' leaflets. In the normal dog, these are thin, translucent structures that are anchored to the papillary muscles by chordae tendinae. Both papillary muscles (anterior and posterior) arise from the left ventricular free wall. The mitral valve prevents the backflow of blood from the left ventricle to the left atrium during systole. In early systole, when left ventricular pressure exceeds left atrial pressure, the mitral valve leaflets close. In normal dogs, the chordae tendinae tether the leaflets to prevent them prolapsing into the left atrium. When the mitral valve is incompetent, there is ''regurgitation'' of blood from the left ventricle to the left atrium. Mitral regurgitation may be mild, with no clinical consequence, or may be severe. The severity of mitral regurgitation is determined primarily by the size of the orifice, that results from incomplete apposition of the mitral valve leaflets, and the relationship between left ventricular and left atrial systolic pressures. Mitral regurgitation causes an increase in left atrial pressure, which over time can lead to left atrial dilation. In diastole, the left ventricle is filled by both pulmonary venous return and blood that has been regurgitated into the left atrium. Therefore, both the left atrium and left ventricle become volume overloaded. This may result in '''ventricular dilation and eccentric hypertrophy'''. In severe cases, increased left ventricular and left atrial filling pressures may result. This leads to an increase in pulmonary venous pressure and may result in [[Heart Failure, Left-Sided|left-sided congestive heart failure]].

==Signalment==

Degenerative mitral valve disease tends to affect middle-aged and older dogs, particularly males. The disease more commonly affects small breed dogs, with Cavalier King Charles Spaniels, Chihuahuas, Boston Terriers, Poodles, Pomeranians and Bull Terriers being predisposed. The disease is also recognized in large breed dogs.

==History and Clinical Signs==
Animals may remain asymptomatic for years, the disease is usually clinically silent until it is advanced.

In most affected dogs, DMVD does not cause clinical signs and the disease is detected by the auscultation of a cardiac murmur at routine health checks.

In cases where DMVD becomes clinically significant, a '''cough''' is usually the first clinical sign noticed by the owner. The coughing is likely of multifactorial aetiology and may be related to pulmonary oedema, stimulation of the juxtapulmonary (J) receptors that are associated with pulmonary capillaries and detect increases in pulmonary venous pressure, compression of a mainstem bronchi by an enlarged left atrium and concurrent airway disease. Occasionally, '''syncope''' is the first sign of clinically significant DMVD. This may occur due to arrhythmias or on exertion where mitral regurgitation limits stroke volume and therefore cardiac output.

Other symptoms that may occur include increased exercise intolerance and efficiency, tachypnea or dyspnea during exercise, ascites, weight loss, anorexia and thromboembolisms.

== Diagnosis==
===Physical Examination===
* Systolic murmur with point of maximal intensity over the left apex. Murmur grade is usually correlated with severity of mitral regurgitation, severe regurgitation causes a loud murmur.
* Mid-systolic click, associated with mitral prolapse. In many dogs, clicks are a precursor to mitral regurgitation.

Other findings will depend on the stage of disease. Crackles may be detected on thoracic auscultation in patients with pulmonary oedema, resulting from [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Abdominal palpation is usually normal, but ascites and hepatomegaly may be present when there is concurrent [[Heart Failure, Right-Sided|right-sided congestive heart failure]].

Primary respiratory disease, such as chronic bronchitis, is also common in older small breed dogs. It is important to distinguish between the patient with clinically significant respiratory disease and incidental DMVD from the patient with clinically significant DMVD. Respiratory sinus arrhythmia, indicating vagal influence on heart rate and rhythm, is usually not present in severe cardiac disease. In contrast, sinus arrhythmia is usually preserved or accentuated when respiratory disease is the cause of clinical signs.

===Diagnostic Imaging===
====Radiography====
Early in the course of DMVD, thoracic radiographs will be normal. As the disease progresses, cardiomegaly will become apparent. There may be evidence of left atrial enlargement, with or without dorsal displacement of the trachea and narrowing of the mainstem bronchus. Pulmonary venous distension may be observed if there is increased pulmonary venous pressure. Interstitial pulmonary oedema may precede alveolar pulmonary oedema. Evidence of [[Heart Failure, Right-Sided|right-sided congestive heart failure]] may be present in severe cases, radiographic findings include distension of the caudal vena cava, hepatomegaly, ascites and pleural effusion.

====Echocardiography====
* Thickened mitral valve leaflets
* Prolapse of mitral valve leaflets into the left atrium during systole
* Tricuspid leaflets may also be affected, though usually not as severely as the mitral valve
* Increased diastolic left ventricular diameter
* Hyperdynamic left ventricle
* Colour Doppler jet of mitral regurgitation
*(Flail leaflet)

Thickening of the mitral valve leaflets is usually diffuse, but most pronounced at the leaflet edges. With myxomatous degeneration, the mitral valve becomes stiffer and distorted. The conformation of the valve remains constant throughout the cardiac cycle. Normally, the mitral valve leaflets do not extend beyond a line across the mitral annulus in systole. In dogs with DMVD, the mitral leaflets prolapse towards the left atrium during systole. Colour Doppler can be used to demonstrate the jet of mitral regurgitation. The size of the jet is related to the severity of mitral regurgitation. Most mitral regurgitation jets in DMVD are eccentric.

The more severe the DMVD, the greater the degree of left ventricular and left atrial dilation.

Fractional shortening may be increased (hyperynamic left ventricle). This is because, in the setting of mitral regurgitation, impedance to ventricular emptying is reduced (blood can be ejected into the low pressure left atrium)and end-diastolic ventricular stretch is increased by the addition of the regurgitant fraction, increasing the force of contraction.

A serious complication of DMVD is '''chordae tendinae rupture''', resulting in a 'flail leaflet' and acute worsening of mitral regurgitation. A leaflet segment typically 'flails' back into the left atrium during systole.

'''Left atrial rupture''' is a major complication of DMVD. Left atrial endocardial and endomyocardial splits are usually multiple and may heal or perforate the atrial wall, causing haemopericardium or an acquired atrial septal defect depending on their depth and location.

===Electrocardiogram (ECG)===
Electrocardiography is primarily used to diagnose arrhythmias, but can provide evidence of chamber enlargement. Most arrhythmias in DMVD are supraventricular in origin and occur secondary to left atrial stretch. Ventricular arrhythmias may develop in association with left ventricular dilation and fibrosis.

* P-mitrale: wide P waves in leads II, III and aVF, indicates left atrial enlargement
* high R-wave
* Stage C2-D: (supra-) ventricular extrasystoles

===Laboratory Tests===
Pro-brain natriuretic peptide ('''NT-proBNP''') concentration is associated with severity of DMVD. Elevated NT-proBNP levels are useful in discriminating patients with respiratory distress caused by heart failure from those with primary respiratory tract disease.

==Staging==
Staging according to American College of Veterinary Internal Medicine (ACVIM) is as follows:
* '''Stage A''': Dog predisposed to the development of DMVD
* '''Stage B''': Subclinical disease
** ''B1'': Without cardiac remodeling
** ''B2'': With cardiac remodeling
* '''Stage C''': Current or prior clinical signs
* '''Stage D''': Refractory heart failure

== Treatment ==
===Stage B===
There is no therapy demonstrated to be beneficial in dogs with stage B1 disease. Nevertheless the cardiac function should be controlled after 12 months or earlier if the general condition gets worse.

The results of the EPIC study demonstrated that administration of '''Pimobendan''' to dogs with stage B2 disease resulted in prolongation of the asymptomatic phase of disease by approximately 15 months. Dogs receiving Pimobendan were around 33% less likely to go into congestive heart failure or suffer a cardiac death than those not receiving the drug. Pimobendan appears safe and well-tolerated. The cardiac function should be controlled after 6-12 months.

Based on findings of the EPIC study, dogs with typical mitral valve murmurs of grade III/VI or higher should be investigated to look for evidence of cardiomegaly. If cardiomegaly is apparent, then the dog may benefit from starting Pimobendan, as opposed to the 'watch and wait' approach that was previously recommended.

===Stage C===
Medical management is intended to alleviate clinical signs and prolong life.

'''Furosemide''' is a potent first-line diuretic that can be administered orally or parenterally, depending on the clinical status of the patient. Most patients with congestive heart failure secondary to DMVD require lifelong diuretic therapy.

The addition of an '''ACE inhibitor''' is considered standard therapy. The benefits of ACE inhibitors are related to their vasodilator action and also protecting the heart from the detrimental effects of RAAS activation.

'''Pimobendan''' is phosphodiesterase inhibitor and calcium sensitiser that is both a ''positive inotrope'' and ''vasodilator'' (inodilator). A randomized clinical trial (QUEST) demonstrated a survival benefit associated with Pimobendan administration, when evaluated relative to treatment which was considered at that time to be the gold standard; benazepril. Use of triple therapy with furosemide, an ACE inhibitor and Pimobendan is recommended. When financial or compliance concerns limit the therapeutic choices, evidence suggests that Pimobendan is superior to an ACE inhibitor.

Aldosterone may contribute to the development of myocardial fibrosis. Complete suppression of RAAS is generally not achieved by ACE inhibition alone. Therefore the addition of '''Spironolactone''' may be beneficial.

Surgical mitral valve repair in dogs is currently being performed. However, availability is limited by the expense, required expertise and cardiopulmonary bypass facilities.

If the patient shows supraventricular tachycardia '''Digoxin''' can be prescribed. If that does not work effectively '''calcium canal blockers''' can be added.

Relevant ventricular extrasystoles can be treated with '''sodium canal blockers.'''

Syncopes or acsites can be treated with '''Sildenafil.'''

'''Amlodipin''' can be used to treat systemic hypertension that occurs as a result to the valvular degeneration.

''Clinical Example:''

A patient is presented in an acute cardiac crisis. He is staged as C3-D. The therapy goal is to get him to C1.

# inpatient admission
# '''Furosemide'''
#* depending on the degree of severity: 2-4 mg/kg body weight, parenteral, every 2-6 hours
#* better is an intravenous drip that covers half of the conservation needs (1 mg/kg body weight per hour), can be reduced by half when the breathing rate has normalized
# '''Pimobendan'''
#* 0,15 mg/kg body weight once i.v.;
#* when the symptoms persist the injection can be repeated after 12 hours
# Oxygen
# thoracocentesis if there is a liquidothorax
# punction of the ascites if there is a right heart failure
# '''Dobutamin''': 5–10µg/kg body weight/min (Stadium D)
# '''Nitroglycerin''' with an atomizer: 1–2 pumps in the mouth (cave: do not breath in, wear gloves!)
# '''ACE inhibitors''' and '''Spironolactone''' should be added as soon as oral treatment is possible

'''''When the patient is stabilized:'''''

# treatment can be continued at home
# '''Sildenafil''' for the pulmonary hypertension

===Stage D===
If congestive heart failure signs are not controlled by high doses of Furosemide, addition of a thiazide and Spironolactone should be considered. Together these drugs have a synergistic action, by providing sequential nephron blockade, allowing lower doses of the individual agents.

==Monitoring and Follow Up==
For dogs in stage B, owners should be made aware of signs of congestive heart failure. In dogs with Stage B2 disease where congestive heart failure is imminent, it is useful to give the owner Furosemide to administer if the dog develops signs of respiratory distress. Owners of Stage B2 and Stage C dogs should be educated on how to measure sleeping respiratory rate and should begin recording this regularly.

The frequency of follow-up examinations is dependent on the severity of disease and owner compliance. For dogs with preclinical disease, rechecks can be recommended every 6-12 months depending on the severity of mitral regurgitation and cardiac remodeling. Following hospitalization for control of acute congestive heart failure, dogs should receive a follow up examination within 2 weeks to check for resolution of clinical signs, hydration status, electrolytes and renal function. For dogs in stage C with stable disease, re-checks can be every 3-6 months.

== Prognosis ==

Asymptomatic patients may live for many years. Dogs with stage B2 disease have a median of 27 months before developing congestive heart failure. Once heart failure occurs, life expectancy is usually around 6-12 months, although some patients remain stable for longer. Risk factors for progression include severity of valvular lesions, increased age and male gender. Risk factors for onset of congestive heart failure include severity of mitral regurgitation, left atrial enlargement and elevated NT-proBNP. Development of complications such as atrial fibrillation or chordae tendinae rupture are associated with a poor prognosis.

{{Learning
|videos = [http://www.cardioacademy.cevalearn.com/en/Programme/Sessions/1-Pathophysiology-of-Mitral-Valve-Disease video on mitral valve disease from Cardio Academy]
|flashcards = [[Endocardial Pathology Flashcards]]
|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Mitral+Valve+Dysplasia%22&occuring1=title&rowId=2&options2=OR&q2=%22Mitral+Valve+Disease%22&occuring2=title&rowId=3&options3=OR&q3=%22Mitral+insufficiency%22&occuring3=title&rowId=4&options4=OR&q4=%22endocardiosis%22&occuring4=title&x=36&y=9&publishedstart=yyyy&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Mitral Valve Dysplasia publications]

[http://www.cabdirect.org/search.html?it=any&q2=%22Mitral+Valve+Disease%22&q1=%22Mitral+Valve+Dysplasia%22&calendarInput=yyyy-mm-dd&q4=%22endocardiosis%22&q3=%22Mitral+insufficiency%22&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&rowId=4&options1=AND&options2=OR&occuring4=title&options3=OR&options4=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:(ft+OR+fr+OR+fa+OR+fv+OR+fw+OR+fx+OR+gf+OR+ga+OR+b1+OR+b2+OR+b3+OR+b4+OR+b5+OR+b6)&y=9&x=36 Other MDV Full Text Articles]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103219945.pdf ''' Myxomatous degenerative mitral valve disease: an update.''' Disatian, S.; Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, Thai Journal of Veterinary Medicine, 2010, 40, 2, pp 151-157, many ref.]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093114836.pdf ''' Latest information about canine mitral valve disease: results of the QUEST trial.''' Häggström, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 188-191, 10 ref. - '''Full Text Article''']

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017845.pdf ''' Treatment of mitral valve disease in dogs.''' French, A.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 107-108]

[http://www.cabi.org/cabdirect/FullTextPDF/2009/20093017847.pdf ''' Prognostic variables in canine mitral valve disease.''' Häggstrom, J.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 112-113, 7 ref.]
}}

==References==
* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2016) '''Manual of Canine and Feline Cardiology (Fifth Edition)''' ''Saunders''.
* Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) '''BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (Second Edition)'''
* Boswood, A. et al. Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study - A Randomized Clinical Trial. JVIM, September 2016. DOI: 10.1111/jvim.14586

{{review}}

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[[Category:Cardiovascular_System_-_Degenerative_Pathology]] [[Category:Endocardial_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Cat]] [[Category:Cardiac_Diseases_-_Dog]]
[[Category:Cardiac_Diseases_-_Horse]]
[[Category:Cardiovascular_System_-_Developmental_Pathology]]
[[Category:Cardiology Section]]

Pulmonary Hypertension

2021-05-11T13:01:56Z

LauraN156: Update on Diagnostics

{{OpenPagesTop}}
== Introduction ==

Hypertension is defined as the pathological elevation of arterial blood pressure.There are two main types of hypertension, [[Systemic Hypertension|systemic hypertension]] (affects the systemic circulation) and pulmonary hypertension (affects the pulmonary circulation). Blood pressure in veterinary patients is not measured routinely; therefore hypertension is usually only diagnosed after clinical signs become apparent.

Pulmonary hypertension = increase in pulmonary arterial pressure.

'''There are two types of pulmonary hypertension:'''

1. '''Primary''' pulmonary hypertension = idiopathic pulmonary hypertension (contributing factors: drugs, toxins, genetic predisposition and infections)

2. '''Secondary''' pulmonary hypertension = pulmonary hypertension resulting from an identifiable underlying condition

[[Cor Pulmonale|'''Cor pulmonale''']] = [[Heart Failure, Right-Sided|right sided heart failure]] resulting from pulmonary hypertension.

The hypoxic conditions at high elevations or animals with chronic airway disease contribute to pulmonary hypertension through hypoxia-induced vasoconstriction.

==Signalment==

Some diseases predispose animals to secondary pulmonary hypertension. Predisposed breeds include brachycephalic dogs (chronic obstructive pulmonary disease); small breeds ([[Degenerative Mitral Valve Disease|mitral endocardiosis]]) and West Highland White Terriers (pulmonary fibrosis).

== Clinical Signs ==

Clinical signs may vary and also may be disguised by other signs of the underlying, causative disease. There is often signs of right sided heart failure, such as exercise intolerance, dyspnoea, coughing, syncope, cyanosis, abdominal distension and distended jugular veins.

== Diagnosis ==

'''Physical examination''', depending on any underlying conditions, may show a [[Heart Murmurs|heart murmur]] (mitral or tricuspid regurgitation), presence of a gallop rhythm, increased lung sounds and splitting of S2 heart sounds (see [[:Category:Arrhythmia|arrhythmias]]).

'''Blood tests''':
:Arterial blood gases may show hypoxemia if there are low oxygen conditions.
:Complete Blood Count will show an eosinophilia if ther is parasitic involvement. (Serology or Fecal Baermann tests would confirm parasitic involvement).
:Biochemistry would show hyperglobulinemia in chronic inflammation.
:A biomarker for a pulmonary hypertension is an elevated NT-proBNP.

'''Urinalysis''' may show the presence of proteinuria if systemic disease is present.

'''Radiography''' is best performed with a DV view. Signs will include left (isn't it the right heart that is enlarged, because of the backlog of the pulmonary arteria?) atrial and ventricular enlargement, pulmonary arterial enlargement, enlargement of the V. cava caudalis, congested pulmonary veins and signs of pulmonary disease.

'''Electrocardiography''' may show the presence of right ventricular hypertrophy (deep S-waves) and signs of myocardial hypoxia (ST segment abnormalities).

'''Echocardiography''' may be used to calculate pulmonary arterial pressures. It may also show enlargement of the right-side of the heart and enable visualisation of mitral or tricuspid regurgitation.

== Treatment ==

'''Treat the underlying conditions:'''

*Treat right sided heart failure

*Treat pulmonary thromboembolism with heparin and then warfarin

*Treat chronic obstructive pulmonary disease

== Prognosis ==

Depends on the disease condition causing pulmonary hypertension and the ability to control it. Prognosis is poor when pulmonary drainage is irreversible.

{{review}}

{{OpenPages}}

[[Category:Lungs_-_Circulatory_Pathology]] [[Category:Vascular_Diseases_-_Dog]] [[Category:Vascular_Diseases_-_Cat]] [[Category:Arterial_Pathology]] [[Category:Expert_Review]]
[[Category:Cardiology Section]]

Seizures

2021-04-13T07:15:54Z

LauraN156:

==Introduction==

* '''Seizures''' are paroxysmal changes in cerebral cortex electrical activity that start abruptly, end suddenly and have a tendency to recur.
* '''Epilepsy''' is the occurence of recurrent seizures.

==Pathophysiology==

* Seizures occur when there is imbalance between exitatory and inhibitory processes. This may be due to :
** Inadequate neuronal inhibition.
*** Major inhibitory neurotransmitters include GABA and glycine.
** Excessive neuronal excitation.
*** Major excitatory neurotransmitters include aspartate and glutamate.

===Proposed Mechanisms===

* Defective feed-forward inhibition or feed-back initiation of inhibitory neurons in cortical circuits.
** Recurrent excitatory collaterals may be formed.
* Changes in membrane properties of neurons.
** These may include changes at:
*** Potassium, sodium, chloride and calcium ion channels
*** GABA receptors
*** Nicotinic acetyl choline receptors
*** NMDA receptors
**** Activation.
* Changes in the ionic microenvironment.

===Seizure Development===

# At the onset of a seizure, abnormal neurons undergo prolonged depolarisations.
#* These depolarisations are associated with the rapid firing of repeated action potentials.
# Depolarisation of abnormal neurons recruits adjacent neurons with which they are connected.
# The electrical discharges of the large number of neurons involved become linked together.
# A storm of electrical activity results, causing a clinical seizure.
# Seizures may then spread:
#* To adjacent areas of the brain.
#* Through established anatomic pathways to other distant areas.

==Nomenclature==

* '''Status epilepticus''' is the term used to describe
** A seizure lasting longer than 5 minutes, or
** A collection of discrete seizures without full recovery of consciousness.
* '''Cluster seizures''' occur when 2 or more seizures are experienced in a brief periods, but the patient regains consciousness between them.
* Three classes of seizures are recognised:
*# Generalised seizures
*# Focal seizures
*# Focal generalising seizures

===Generalised Seizures===

* Generalised seizures may be:
** Idiopathic
** Symptomatic
*** Due to intracranial disease e.g. neoplasia, storage diseases etc.
** Cryptogenic
*** There is probably an underlying cause but it cannot be identified by the diagnostic tests available.
** Reactive
*** Due to some extracranial disorder, for example a toxin or metabolic disorder.

====Clinical Signs====

* Initial clinical signs show involvement of both cerebral hemispheres.
* Generalised seizures result in:
** Change in consciousness
** Motor activity
*** Tonic-clonic seizures are most common in dogs and cats.
** Autonomic signs
* The body's energy utilisation can increase to around 250% of the normal value during a generalised seizure.

====Stages====

# Prodromal Phase
#* The animal experiences an indication of a forthcoming seizure.
#* This occurs hours to days before the event itself.
# Aural Phase
#* This is the very start of the seizure.
#* Behaviour changes may be apparent.
# Ictal Phase
#* The seizure "proper".
# Postictal phase
#* Consists of transient neurological and behavious changes, which can last from hours to days.

====[[Idiopathic Epilepsy]]====

====Acquired Generalisd Seizures====

* Other general seizures may be acquired.
* Seizures can occur at any age, but generally occur in animals younger than 2 years and older than 5 years.
* Causes may include:
** Intracranial disease
*** Neoplasia
*** Trauma
*** Infection
*** Inflammation
** Extracranial disease (also known as "reactive epilpsy").
*** Electolyte disorders
*** Metabolic disorders
*** Toxicity

===Focal Seizures===

* Almost always an acquired disease.
* Active diseases often progress to become more general.
** Cause generalised seizures.

===Simple Focal Seizures===

* Onset occurs in a limited area of one cerebral hemisphere.
* No impairment of consciousness.

=== Complex Focal Seizures===

* Arise in a single brain region, but cause impaired consciousness.

==Causes of Acquired Seizures==

{| border="3" cellpadding="8"
!width="150"|'''Cause'''
!width="400"|'''Examples'''

|-
|Neoplasia
|Primary or metastatic
|-
|Inflammatory
|Distemper, FIP, FeLV/FIV, rabies, cryptococcosis (cats), toxoplasmosis
|-
|Traumatic
|Immediate or delayed
|-
|Vascular
|Feline ischaemic encephalopathy, thromboembolism, hypertenstion
|-
|Anomalous
|Hydrocephalus
|-
|Metabolic
|Hepatic encephalopathy, uraemia, hyperparathyroidism, hypolycaemia, hyperkalaemia, hypocalcaemia, hypoxia, acid-base disorders, hyperthermia
|-
|Toxic
|Lead, organophosphates, metaldehyde, strychnine
|}
[[File:Causes of Seizures in Cats and Dogs older than 6 Years updated .pdf|thumb|Causes of Seizures in Cats and Dogs older than 6 Years]]

==Investigation of Seizures==

* It must first be determined whether seizure activity is in fact a seizure, rather than a non-epileptic paroxysmal event, for example:
** Syncope
** Exercise-induced weakness
** Obsessive-compulsive behaviour
** Narcolepsy
* Idiopathic epilepsy may be differentiated from secondary or reactive seizures by considering:
** Age of onset
** Breed disposition
** Partial seizures or asymmetrical post-ictal signs
*** These suggest a discrete lesion.
** Older animals (>5 years) may be more likely to have an acquired aetiology.
** Younger animals (<6 months) may be more likely to have toxic or metabolic causes.
* Useful tests include:
** Metabolic screening
** Haematology
** Serum biochemistry
** Urinalysis
** Serology.
** Bile acid stimulation test
** Serum lead
** MRI and CT scanning, and CSF analysis, help rule out cancer.
 

{{Template:Learning
|podcasts = [[Seizures podcast|RVC clinical podcast about seizures]] 
}}

[[Category:Central Nervous System - Pathology]]

File:Causes of Seizures in Cats and Dogs older than 6 Years updated .pdf

2021-04-13T07:14:53Z

LauraN156:

Infarct:
• Blocked pipe

Bleeding:
• Pool filled with blood

Hyperviscosity:
• Man wading through the viscous blood

Hypocalemia + Hypocalcemia:
• Normally the testbox is filled with a sample of the poolwater to test the pH value and the amount of chloride
• In the picture the blood is tested for potassium and calcium, both levels are too low

Uremia/ Hepatoencephalopathy
• The Ammonium and the Urea which are dropping out off the bottle and are contaminating the water are illustrating the urinary excreted substances which are circulating in the blood vessels

Primary and sekundary Neoplasias:
• The cauliflower floating in the pool is illustrating the primary tumor
• The cauliflowers in the basket are illustrating the metastasis
• The cauliflowers in general represent tumors, because of the cauliflower-like proliferation of some tumors

File:Causes of Seizures in Cats and Dogs older than 6 Years.pdf

2021-04-13T07:08:53Z

LauraN156:

Infarct:
 Blocked pipe

Bleeding:
 Pool filled with blood

Hyperviscosity
 Man wading through the viscous blood

Hypocalemia + Hypocalcemia:
 Normally the testbox is filled with a sample of the poolwater to test the pH value and the amount of chloride
 In the picture the blood is tested for potassium and calcium, both levels are too low

Uremia/ Hepatoencephalopathy
 The Ammonium and the Urea which are dropping out off the bottle and are contaminating the water are illustrating the urinary excreted substances which are circulating in the blood vessels

Primary and sekundary Neoplasias:
 The cauliflower floating in the pool is illustrating the primary tumor
 The cauliflowers in the basket are illustrating the metastasis
 The cauliflowers in general represent tumors, because of the cauliflower-like proliferation of some tumors

Seizures

2021-04-10T10:56:46Z

LauraN156: /* Causes of Acquired Seizures */

==Introduction==

* '''Seizures''' are paroxysmal changes in cerebral cortex electrical activity that start abruptly, end suddenly and have a tendency to recur.
* '''Epilepsy''' is the occurence of recurrent seizures.

==Pathophysiology==

* Seizures occur when there is imbalance between exitatory and inhibitory processes. This may be due to :
** Inadequate neuronal inhibition.
*** Major inhibitory neurotransmitters include GABA and glycine.
** Excessive neuronal excitation.
*** Major excitatory neurotransmitters include aspartate and glutamate.

===Proposed Mechanisms===

* Defective feed-forward inhibition or feed-back initiation of inhibitory neurons in cortical circuits.
** Recurrent excitatory collaterals may be formed.
* Changes in membrane properties of neurons.
** These may include changes at:
*** Potassium, sodium, chloride and calcium ion channels
*** GABA receptors
*** Nicotinic acetyl choline receptors
*** NMDA receptors
**** Activation.
* Changes in the ionic microenvironment.

===Seizure Development===

# At the onset of a seizure, abnormal neurons undergo prolonged depolarisations.
#* These depolarisations are associated with the rapid firing of repeated action potentials.
# Depolarisation of abnormal neurons recruits adjacent neurons with which they are connected.
# The electrical discharges of the large number of neurons involved become linked together.
# A storm of electrical activity results, causing a clinical seizure.
# Seizures may then spread:
#* To adjacent areas of the brain.
#* Through established anatomic pathways to other distant areas.

==Nomenclature==

* '''Status epilepticus''' is the term used to describe
** A seizure lasting longer than 5 minutes, or
** A collection of discrete seizures without full recovery of consciousness.
* '''Cluster seizures''' occur when 2 or more seizures are experienced in a brief periods, but the patient regains consciousness between them.
* Three classes of seizures are recognised:
*# Generalised seizures
*# Focal seizures
*# Focal generalising seizures

===Generalised Seizures===

* Generalised seizures may be:
** Idiopathic
** Symptomatic
*** Due to intracranial disease e.g. neoplasia, storage diseases etc.
** Cryptogenic
*** There is probably an underlying cause but it cannot be identified by the diagnostic tests available.
** Reactive
*** Due to some extracranial disorder, for example a toxin or metabolic disorder.

====Clinical Signs====

* Initial clinical signs show involvement of both cerebral hemispheres.
* Generalised seizures result in:
** Change in consciousness
** Motor activity
*** Tonic-clonic seizures are most common in dogs and cats.
** Autonomic signs
* The body's energy utilisation can increase to around 250% of the normal value during a generalised seizure.

====Stages====

# Prodromal Phase
#* The animal experiences an indication of a forthcoming seizure.
#* This occurs hours to days before the event itself.
# Aural Phase
#* This is the very start of the seizure.
#* Behaviour changes may be apparent.
# Ictal Phase
#* The seizure "proper".
# Postictal phase
#* Consists of transient neurological and behavious changes, which can last from hours to days.

====[[Idiopathic Epilepsy]]====

====Acquired Generalisd Seizures====

* Other general seizures may be acquired.
* Seizures can occur at any age, but generally occur in animals younger than 2 years and older than 5 years.
* Causes may include:
** Intracranial disease
*** Neoplasia
*** Trauma
*** Infection
*** Inflammation
** Extracranial disease (also known as "reactive epilpsy").
*** Electolyte disorders
*** Metabolic disorders
*** Toxicity

===Focal Seizures===

* Almost always an acquired disease.
* Active diseases often progress to become more general.
** Cause generalised seizures.

===Simple Focal Seizures===

* Onset occurs in a limited area of one cerebral hemisphere.
* No impairment of consciousness.

=== Complex Focal Seizures===

* Arise in a single brain region, but cause impaired consciousness.

==Causes of Acquired Seizures==

{| border="3" cellpadding="8"
!width="150"|'''Cause'''
!width="400"|'''Examples'''

|-
|Neoplasia
|Primary or metastatic
|-
|Inflammatory
|Distemper, FIP, FeLV/FIV, rabies, cryptococcosis (cats), toxoplasmosis
|-
|Traumatic
|Immediate or delayed
|-
|Vascular
|Feline ischaemic encephalopathy, thromboembolism, hypertenstion
|-
|Anomalous
|Hydrocephalus
|-
|Metabolic
|Hepatic encephalopathy, uraemia, hyperparathyroidism, hypolycaemia, hyperkalaemia, hypocalcaemia, hypoxia, acid-base disorders, hyperthermia
|-
|Toxic
|Lead, organophosphates, metaldehyde, strychnine
|}

#
#

[[File:Causes of Seizures in cats and dogs younger than 6 months.pdf|thumb|2x2px|Causes of Seizures in Cats and Dogs '''younger than 6 months''']]

==Investigation of Seizures==

* It must first be determined whether seizure activity is in fact a seizure, rather than a non-epileptic paroxysmal event, for example:
** Syncope
** Exercise-induced weakness
** Obsessive-compulsive behaviour
** Narcolepsy
* Idiopathic epilepsy may be differentiated from secondary or reactive seizures by considering:
** Age of onset
** Breed disposition
** Partial seizures or asymmetrical post-ictal signs
*** These suggest a discrete lesion.
** Older animals (>5 years) may be more likely to have an acquired aetiology.
** Younger animals (<6 months) may be more likely to have toxic or metabolic causes.
* Useful tests include:
** Metabolic screening
** Haematology
** Serum biochemistry
** Urinalysis
** Serology.
** Bile acid stimulation test
** Serum lead
** MRI and CT scanning, and CSF analysis, help rule out cancer.
 

{{Template:Learning
|podcasts = [[Seizures podcast|RVC clinical podcast about seizures]] 
}}

[[Category:Central Nervous System - Pathology]]

File:Causes of Seizures in cats and dogs younger than 6 months.pdf

2021-04-10T10:48:24Z

LauraN156:

1. Hepathoencephalopathy
2. Infections
3. Congenital
4. Lysosomal Storage Disorder
5. Intoxication
6. Trauma

Epileptic Emergency Treatment

2021-04-08T16:38:36Z

LauraN156: I added the source of the treatment plan

1. Ask the Owner '''2 questions'''

* Is the patient a known epilepticer who’s getting KBr or Phenobarbital (PB)?
* Does the patient have diabetes and is taking insulin?

Why is that relevant?

* If he isn’t getting KBr —> i.v. full electrolyte infusion
* If he is already getting KBr —> i.v. 0,9% NaCl + 5% Glucose (1:1)
* If he has diabetes he’s probably hyperglycemic

2. First Step in Treatment is '''Diazepam (0,5 mg/kg i.v.)'''

* Onset of action: 1-2 Minutes
* If the first dose isn’t working the treatment can be repeated 2-3 times

If an i.v.- access isn’t possible try Diazepam rectal tubes

* If he isn’t getting PB already: 1 mg/kg
* If he is getting PB: 2 mg/kg
* Onset of action: 15-20 Minutes

OR

'''Midazolam''' intranasal with an atomizer (0,2 mg/kg)

* Onset of action: 1-5 Minutes

3. Next Step: '''Phenobarbital (10 mg/kg i.v.)'''

* Give PB even if Diazepam worked, because the effect of Diazepam will only last for 20-30 minutes
* Can be repeated once if the patient isn’t already getting PB
* Onset of action: 15-20 Minutes

'''CAVE: If the Patient is already getting PB always check the blood level before treating him with PB!'''

4. If the seizures persist or occure again within the next '''2''' hours: '''Levetiracetam (20 mg/kg slowly i.v.)'''

* Can be repeated 2 times

5. Start '''Diagnostics'''

* Hypoglycemia: 3-5 ml/kg 20% Glucose i.v.
* Hypocalcemia: 0,5 – 1 ml/kg 10% Ca-Carbonat slowly i.v. (CAVE: Bradycardia)
* Temperature: > 40 degree Celcius —> cool him down < 39,5 degree Celcius —> stop or will cool down too much

6. If the Seizures persist or occur again ask yourself if Diazepam worked the first time

If '''YES''':

'''Diazepam'''
* 0,5 mg/kg i.v. Bolus followed by…
* 0,1 – 0,5 mg/kg/h (continous infusion), 30 mg Diazepam in 250 ml 5% Glucose
* If it works reduce Diazepam in 6-8 hours
* If it doesn’t work put him under anaesthesia

If '''NO''':

'''Pentobarbital'''
* 1-2 mg/kg i.v. Bolus followed by…
* 1-5 mg/kg/h continous infusion

'''Propofol'''
* 4-8 mg/kg i.v. Bolus followed by…
* 4-8 mg/kg/h continous infusion

'''Cave: Both those drugs can cause depression of breathing, so the patient has to be under surveillance all the time!'''

'''Inhalation anaesthesia '''

Simultaneous to all 3 of them: PB on maintenance dose of 2,5 mg/kg i.m. (2x/day)
Wake the patient up after 6-8 hours

{{#ev:soundcloud|https://soundcloud.com/laura-nipperdey/how-to-save-a-life-epilepsy-version}}

Step one, you say we need to talk

Two things, you ask, be quick, keep it short

Thirst you really must be sure

If the dog has had seizures before

So listen up, cause if he did

Ask if he takes potassium bromid.

Or maybe he gets other meds

For example barbiturats.

Now start your treatment

With diazepam

PB is next, on the treatment plan

And now you should stay up with him all night

And that is how to save a life

If it still does not improve

Breath in, breath out and make another move

Try Levetiracetam

Next step would be Diazepam

If that hasn‘t worked before

You still got other things in store

Anesthesia makes him sleep

But careful that will not be cheap

Now that’s your treatment

Haven’t lost him yet

He’s save for now and he will be

But still you should stay up with him all night

And that is how to save a life

Based on the treatment plan by Prof. Dr. Thomas Flegel (University of Leipzig, Germany)

First Aid

2021-03-17T14:20:53Z

LauraN156: I added a section called „Epilepsy Treatment“. There I want to upload the Song „How to save a Life“ with a changed lyrics.

{{unfinished}}
*[[Shock]]

*[[:Category:Transfusion Medicine|Transfusion medicine]]
*Epilepsy Treatment

[[Category:Clinical Techniques]]