Improving Patient Care (QI)

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In this episode I am joined by my friends and colleagues, Stacey Davidson and Ru Clements of VetLed, to discuss the role of Quality Improvement (QI) in improving patient care. We discuss what QI is and why you should be engaged with it. We also talk about the role of human factors and workplace culture in QI.

VetLed website
VetLed Facebook page
Veterinary Human Factors private Facebook group started by VetLed

Some terms used in the episode:

Quality Improvement:

A number of definitions describe quality improvement as a formal approach that uses specific techniques to improve quality. The RCVS definition is ‘supporting effective, patient and client-centred treatment by implementing systematic, measurable approaches to advance high-quality care’

Clinical Governance:

Essentially a framework through which organisations are accountable for continuously improving the quality of their services and safeguarding high standards of care by creating an environment in which excellence in care will improve. The RCVS definition is ‘a continuing process of reflection, analysis and improvement in professional practice for the benefit of the animal patient and the client owner’.

Clinical Audit:

The systematic critical analysis of the quality of veterinary care, including the procedures used for diagnosis and treatment, the use of resources and the resulting outcome and quality of life for the patient. This is considered a major component of clinical governance and QI.

Human Factors:

This has become a common way of referring to Human Performance in the working environment. It is scientific knowledge about the human body, mind and behaviour, specifically to understand human capabilities and limitations so that there is the best possible fit between people and the systems in which they operate.

In healthcare, clinical human factors have been described as enhancing clinical performance through an understanding of the effects of elements such as teamwork, tasks, equipment, workspace, culture and organisation on human behaviour and abilities, and application of that knowledge in clinical settings.

Non-technical skills:

Social, cognitive and personal elements of behaviour which combined with role-specific (technical) skills contribute towards successful outcomes. Examples include identifying and communicating anticipated complications prior to a procedure and awareness of cognitive bias’ during decision making.

Workplace culture:

The character and personality of your organisation. It's what makes your workplace unique and is the sum of its values, traditions, beliefs, interactions, behaviours, and attitudes. It is the unique social and psychological environment. Put simply it's measured by 'the way people do things' in any given environment and has a huge influence on the way people in that environment are likely to do things subsequently.

CRM:

Crew Resource Management is the name given to the field of human factors within aviation. It is commonly defined as the effective utilisation of all available resources (people, equipment, checklists, procedures etc.) to achieve a safe and efficient operation and passenger well-being.

Blame culture:

A culture where blame is apportioned to individuals based primarily on the severity of outcome without a willingness to understand underlying causational factors.

Growth vs. fixed mindset:

A growth mindset is a fundamental belief that you can grow, learn and change for the better – through failure and success alike. This mindset motivates you to try, to reflect, to get back up, to ask for help and to learn. 

A fixed mindset is seated in the opposite and is a belief that your qualities are not able to develop or change. It assumes that our character, intelligence, ability, talent and so on are static and that we are unable to change them in any meaningful way.

[This podcast is closely aligned with the MedEdLIFE Research Collaborative's Quality Checklist for Podcasts.]

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Sepsis and the Glycocalyx

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Sepsis

Evidence base:

Growing interest in evidence-based veterinary medicine (EBVM)
Many challenges with practical implementation; especially quantity and quality of evidence.
Sepsis is a prime example of this.

Veterinary sepsis teaching is largely extrapolated from clinical human studies +/- minimally relevant animal experimental work.
Sepsis management in human medicine remains on an evidence-based journey. Situation is even less clear in veterinary medicine.

What is sepsis?

Disease continuum with progression of severity.

Long-standing definitions:

Sepsis = systemic inflammatory response syndrome (SIRS) due to confirmed or highly suspected infection.
In veterinary patients sepsis is most often due to bacterial infection. Often gram-negative; their endotoxin (lipopolysaccharide) is a very potent trigger of inflammation. Mixed infections and gram-positive infections also described.

(SIRS:

Activation of systemic inflammation caused by excessive production of inflammatory mediators (e.g. TNFα, IL-1, IL-6). Overwhelms anti-inflammatory mechanisms.
Most commonly triggered by infection. But there are non-infectious causes.
Excessive production of pro-inflammatory mediators disrupts homeostasis. Causes:
Loss of vascular tone with generalised vasodilation
Disruption of endothelial permeability barrier leading to vascular leak
Activation of coagulation
May progress to include acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), multiple organ dysfunction and death)

Severe sepsis = sepsis that results in organ or body system dysfunction.
Cardiovascular system often first concern. Patient with systemic hypoperfusion and confirmed/highly suspected infection has severe sepsis.
Other organs and systems may also be affected.

Septic shock = patient with hypoperfusion or hypotension that is refractory to intravenous fluid resuscitation.

SEPSIS-3 definitions:

Recently suggested updates in human medicine.
Work done by Task Force convened by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine.

New definitions:

  • Sepsis = life-threatening organ dysfunction due to a dysregulated host response to infection
  • Severe sepsis no longer used
  • Septic shock = subset of patients with sepsis and profound circulatory, cellular, and metabolic abnormalities

SOFA score and quickSOFA score used to identify organ dysfunction.

Still early days; not without critics and problems. Need to be prospectively evaluated and potentially adapted.

All much less clear in veterinary medicine!

Sepsis management:

Early goal directed therapy (EGDT):

Introduced by Emmanuel Rivers with publication of a single centre trial in The New England Journal of Medicine in 2001.
Randomly assigned patients who arrived at an urban emergency department with severe sepsis or septic shock to receive either six hours of early goal-directed therapy or standard therapy (as a control) before admission to the intensive care unit.
Ultimately concluded that early goal-directed therapy provides significant benefits with respect to outcome in patients with severe sepsis and septic shock.
Since then many other studies have been published that apparently also identified outcome benefits.

In sepsis circulatory abnormalities lead to an imbalance between systemic oxygen delivery and oxygen demand.
Abnormalities include intravascular volume depletion, peripheral vasodilatation, myocardial depression, and increased metabolism.
Result is global tissue hypoxia or shock
Physiologically, aim of management is to adjust cardiac preload, afterload, and contractility to optimise tissue oxygen delivery.

Five key parameters monitored intensively and managed aggressively to specified targets:

  • Central venous pressure (CVP)
  • Mean arterial blood pressure (MAP)
  • Urine output
  • Mixed venous oxygen saturation
  • Haematocrit

Interventions include fluid resuscitation, inopressor agents, blood product transfusion, and mechanical ventilation.

EGDT became well known and many people supported its use.
Presumptively extrapolated as gold standard best practice to veterinary medicine too. Though few able to deliver this care due to practical and resource (expertise, equipment, financial, personnel) limitations.

Some critiqued the Rivers study and the EGDT approach. E.g. not widely adopted in Australasia.

Surviving Sepsis Campaign:

First set of "Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock" published in 2004.
SSC administered jointly by the European Society of Intensive Care Medicine, International Sepsis Forum, and the Society of Critical Care Medicine.

Objective:

"to develop management guidelines for severe sepsis and septic shock that would be of practical use for the bedside clinician, under the auspices of the Surviving Sepsis Campaign, an international effort to increase awareness and improve outcome in severe sepsis." 

EGDT largely incorporated into first 6 hours of sepsis management (resuscitation bundle); disseminated internationally as standard of care for early sepsis management.
Again, extrapolated to veterinary medicine too.

Updated guidelines published every 4 years.

ProCESS (USA), ARISE (Australasia), ProMISe (UK):

Three large scale multicentre randomised controlled trials published recently. 
Reported that human sepsis mortality at an all-time low
Concluded that in a general population of human patients with severe sepsis and septic shock, EGDT did not confer a mortality benefit compared with usual resuscitation.
Ability to generalise from these studies – including to veterinary medicine – depends on consistency of treatment provided as part of usual resuscitation across individual hospitals.

Again there have been critiques of these three recent trials.

Bottom line for veterinary practice:

If we are able to deliver a high level of standard care we will be doing right by our patients. The aspects of management that are now being emphasised are ones that we should also be able to do well.

So what does that mean?

  • Early recognition of patients that are septic or at high risk of becoming septic
  • Intravenous fluids for volume resuscitation to improve systemic perfusion
  • Early use of inopressor agents
  • Starting intravenous antibiosis early
  • Looking for sources of infection. And establishing control of the source of infection as well as possible as soon as possible.
  • Close regular monitoringAnd tailored goals that make sense for the individual patient.

Early recognition of patients that are septic or at high risk of becoming septic:

Spectrum of severity; keep your radar on
Some patients are severely compromised with marked hypoperfusion and obvious infection; straightforward diagnosis (e.g. really sick dogs with septic peritonitis)
Some patients have severe infection that is yet to cause systemic consequences
Some patients have systemic abnormalities but elusive focus of infection

Effects on major body systems (cardiovascular, respiratory, central nervous system (especially brain)):

Especially signs of systemic cardiovascular compromise, hypoperfusion, hypotension, possibly full blown shock
Major cause of hyperdynamic distributive shock in dogs; but some dogs with sepsis have a hypodynamic picture.
Cats classically have hypodynamic picture

Not every septic patient is pyrexic. Temperature may be inappropriately ‘normal’, or hypothermic.

Lactate:

Complex relationship between sepsis and blood lactate
Inappropriately high lactate for given cardiovascular/perfusion status possible flag for sepsis.
Not every septic patient has notable hyperlactataemia

Intravenous fluids for volume resuscitation to improve systemic perfusion:

Synthetic colloids were previously used early and commonly in septic patients
Recent evidence in human patients and experimental +/- clinical animal studies suggests negative risk-benefit assessment. Potential harms in critically ill patients including acute kidney injury. No proven benefits.
Side-lined for majority of human patients with sepsis
Conclusions extrapolated to veterinary practice

So intravascular volume resuscitation involves using a replacement isotonic crystalloid with a bolus strategy.
Less aggressive approach advocated in recent times due to increasing recognition of harms of excessive fluid administration/over-resuscitation.
Again, extrapolated to veterinary practice.

Albumin:

Natural colloid
Has been used extensively in human sepsis management
Canine albumin still not widely available and using human albumin in dogs and cats creates additional risks.

Early use of inopressor agents:

Hypoperfusion in sepsis due to hypovolaemia, peripheral vasodilation and myocardial depression
In addition to volume replacement, early inopressor use makes sense to squeeze vessels (especially venous capacitance) and boost cardiac pump
Noradrenaline (norepinephrine) current agent of choice in human medicine where available and affordable. Albeit not total consensus.
Extrapolated by some to veterinary practice.

Dopamine fallen out of favour in human medicine due to negative risk-benefit assessment.

Starting intravenous antibiosis early:

Early aggressive antibiosis justified in patients with confirmed sepsis.
Likewise in patients with suspected sepsis. But must be reasonable and think critically in terms of index of suspicion. Not carte blanche to adopt ‘just in case’ approach in all patients!
Antibiotics massively overused in veterinary and human medicine. Significant bacterial resistance challenges.

Broad-spectrum, including gram-negative coverage where involvement suspected
Do not withhold until samples collected for microbiology; but do collect samples for microbiology!

Looking for sources of infection. And establishing control of the source of infection as well as possible as soon as possible: 

Prioritise resuscitation, stabilisation and maintenance of stability
Identifying focus of infection may involve e.g. good thorough physical examination, point of care ultrasound, diagnostic imaging, and/or collection of fluid and cell samples.
In some patients antibiotics and own immune system will be curative
In other cases other interventions are required (e.g. exploratory laparotomy; abscess drainage).
Some early though non-definitive source control may be possible with modern non-invasive techniques 

Close regular monitoring
And tailored goals that make sense for the individual patient.

Looking for improvement in, and ultimately normalisation of, physical examination perfusion parameters.
Likewise blood pressure. Generally cited blood pressure targets: mean systemic arterial blood pressure > 65-70 mmHg, systolic blood pressure > 90mmHg.
Also normalisation of or significant improvement in hyperlactataemia. Slow lactate clearance may indicate worse prognosis.

Urine output can also help to inform perfusion status and response to treatment.
Urinary catheter placement not recommended in all patients with confirmed/suspected sepsis:
Foreign body
Carries risk of ascending potentially resistant hospital-acquired infection
Causes patient discomfort
Placement may require sedation
Helpful when present though.

Other treatments not discussed include: blood product transfusion; treatment for critical illness related corticosteroid insufficiency (CIRCI).

Glycocalyx

What is the glycocalyx?

Gel-like acellular epithelial layer endothelium of blood vessels (and part of heart, lymphatics)
Important in fluid dynamics and various pathophysiological states
Meshwork of glycoproteins, proteoglycans and various soluble molecules
In a dynamic equilibrium with adjacent flowing blood
Constantly changing in thickness and composition; sheds and regenerates

What are the functions of the glycocalyx?

1) Key determinant of vascular permeability:

Integrity important for normal microvascular fluid exchange
Disrupted by inflammatory cells and cytokines, and ischaemia-reperfusion
Increases vascular permeability leading to oedema
Hallmarks of SIRS and sepsis as well as other disease states
Ubiquitous nature of glycocalyx helps explain why localised infection can have widespread consequences.

2) Mechanical protection for endothelium
3) Creates a microenvironment for receptor binding, local growth and repair. Protects the vascular wall.
 

What is the relevance of all this?

Traditional Starling model of vascular fluid exchange has been revised.

"In the last 5 years or so, we have had a better understanding of capillary fluid dynamics, particularly in conjunction with an appreciation of the glycocalyx. We now know that the glycocalyx normally ‘traps’ about a litre and half of plasma water in it (due to its hydrophilic chemical composition!) and that normally in the capillaries, there is a central moving layer of plasma and a relatively immobile layer closer to the endothelium….the bit that is bound to the glycocalyx. This explains the differences in measured capillary and venous hematocrit values, and also why Crystalloid : Colloid equivalence is 1.3 : 1 rather than 4: 1 as previously thought.
We have also acquired a better understanding of the mechanisms of edema formation in critical illness and more importantly, the magical phenomenon of improved diuresis that we have all marvelled at, during the recovery phase.
In short, we have kinda debunked the original Starling theory of fluid dynamics in the capillary.
We now know that the colloid osmotic pressure in the intravascular space will only oppose the outward movement of water, and increasing the colloid osmotic pressure by synthetic colloids will not reverse the flow and draw fluid from the interstitial to the intravascular space. ( Multiple trials , starting with the SAFE trial have proved the futility of using synthetic colloids !) What they end up doing is, probably drawing water from the glycocalyx in the intravascular space itself and dehydrating and then disintegrating this vital layer. As a result you will find a transient improvement in blood pressures, but afterwards, a lot of this fluid will track into the extravascular space. Any hyperosmolar solution can do this including Soda Bicarb….we have all seen the very transient increase in blood pressure after bicarb which has always been incorrectly attributed to ‘reversal of acidosis’…bah!!
Extravasation of fluid from the capillaries is predominantly dependant on capillary hydrostatic pressure and not on decreased intravascular colloid osmotic pressure— because we have realised that interstitial and intravascular colloid osmotic pressures are very close to each other.
The way to prevent overloading and thus extravasation would be to minimise rapid increases in capillary hydrostatic pressure. How can we do that? – By small volume crystalloid boluses and early use of alpha1 agonists—the latter work by afferent arteriolar constriction and thus minimising huge increases in capillary hydrostaic pressures. This is where Marik’s argument takes a strong foothold.
Albumin is needed for the integrity of glycocalyx, — explaining why albumin is making a comeback into our fluid armamentarium.
The lymphatics have assumed a pivotal role in the normal mechanisms that prevent edema formation. We have realised that they are a very active conduit to return of interstitial fluid to the central circulation, and they they have contractile collecting ducts and passages that are calcium dependant. They are inhibited by the terrible twins ANP and BNP—therefore shutting down in active sepsis, where the twins tend to dominate. (This also partly explains the peripheral edema commonly seen with Ca channel blockers when they are used as antihypertensives). Once the sepsis resolves, ANP and BNP levels drop and the lymphatics recover their contractile elements. All the interstitial fluid can now be returned to the central circulation causing an improved diuresis.
In any case, fluids should only be used as any other drug should be— only if needed. We need to realise that fluid requirement and fluid responsiveness are two completely different things and focus on appropriate fluid balance rather than branding it as either restrictive or liberal." (John, retired human intensivist)

Does this affect how we manage our patients clinically, and if so, how?
Can the glycocalyx serve as a novel therapeutic target?

At present, mostly discussion and theorising
Recognition of the glycocalyx and its complexity helps to:
Better understand the pathophysiology of sepsis
Explain some of what we see in clinical patients
Explain why no single magic bullet has been found for the treatment of sepsis; too complex for this. 

Sepsis damages the glycocalyx. Management should aim to minimise further damage, e.g.

Avoid fluid over-resuscitation while simultaneous improving systemic perfusion (and therefore hopefully microcirculatory blood flow) adequately
Address infection promptly to minimise further stimulation of inflammation

If physiological corticosteroids are beneficial in CIRCI, this may be through an effect on the glycocalyx (unproven).

Much work underway looking for potential therapies to help bolster and repair damaged glycocalyx. Unlikely to be a single magic bullet; rather multiple therapies and small gains.

Even if such a treatment is identified and supported by good evidence in human patients, does not mean same effect will be recognised in veterinary patients.

References/Resources:

SEPSIS-3 definitions:

Singer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315:801-10

PulmCrit - Top ten problems with the new sepsis definition
http://emcrit.org/pulmcrit/problems-sepsis-3-definition/ 

Vincent JL, Martin GS, Levy MM. qSOFA does not replace SIRS in the definition of sepsis. Critical Care 2016; 20:210
http://ccforum.biomedcentral.com/articles/10.1186/s13054-016-1389-z

Reading J. The Third International Consensus Definitions for Sepsis and Septic Shock,
https://bloggingforyournoggin.wordpress.com/2016/11/27/the-third-international-consensus-definitions-for-sepsis-and-septic-shock/ 


EGDT, Surviving Sepsis Campaign, Recent trials:

Rivers E, Nguyen B, Havstad S, et al. Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock. N Engl J Med 2001; 345:1368-1377
http://www.nejm.org/doi/full/10.1056/NEJMoa010307#t=article

Surviving Sepsis Campaign Guidelines

2016 Surviving Sepsis Guidelines: A Review and Analysis

Nguyen B, Jaehne AK, Jayaprakash N, et al. Early goal-directed therapy in severe sepsis and septic shock: insights and comparisons to ProCESS, ProMISe, and ARISE. Critical Care 2016; 20:160
https://ccforum.biomedcentral.com/articles/10.1186/s13054-016-1288-3

The PRISM Investigators. Early, Goal-Directed Therapy for Septic Shock — A Patient-Level Meta-Analysis. N Engl J Med 2017; 376:2223-2234
http://www.nejm.org/doi/full/10.1056/NEJMoa1701380

Veterinary lactate study:

Cortellini S, Seth M, Kellett-Gregory LM. Plasma lactate concentrations in septic peritonitis: A retrospective study of 83 dogs (2007-2012). J Vet Emerg Crit Care (San Antonio). 2015 May-Jun;25(3):388-95.
http://onlinelibrary.wiley.com/doi/10.1111/vec.12234/full

Glycocalyx: 

Scott Weingart. Think You Understand Fluids – Cause I don’t have a grasp yet.
EMCrit Blog. Published on November 29, 2013. Accessed on September 14th 2017.
Available at [https://emcrit.org/emcrit/best-fluids-comment-ever/]. 

Woodcock TE, Woodcock TM. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Brit J Anaesthesia 2012. 108 (3): 384–394.

Chelazzi C, Villa G, Mancinelli P, et al. Glycocalyx and sepsis-induced alterations in vascular permeability. Critical Care 1025; 19(1)

[This podcast is closely aligned with the MedEdLIFE Research Collaborative's Quality Checklist for Podcasts.]
 

Tweet: Check out FREE audio podcasts from @VetEmCC http://ctt.ec/UqL8b+ Also available in iTunes/Stitcher. #veterinary #podcast

Feline Hypertension

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Episode based on:

ISFM Consensus Guidelines on the Diagnosis and Management of Hypertension in Cats. J Fel Med Surg 2017. 19:288–303.

1. Evidence base:

Guidelines based on comprehensive review of currently available literature; where clinical studies and scientific data were not available the Guidelines represent consensus opinion of the Panel.
Many areas where more data is required which may either confirm recommendations in these Guidelines or cause some to be modified.

2. Secondary versus primary hypertension:

Feline hypertension more commonly diagnosed in association with another disorder, i.e. secondary hypertension more common than primary (idiopathic) hypertension.
Most common associated disorder is chronic kidney disease followed by hyperthyroidism; there are others but they are much less common.
Unlike in humans, prevalence of hypertension in cats with diabetes mellitus is typically low, but often confounded by concomitant conditions such as CKD.

In secondary hypertension “the relationship between the hypertension and the underlying disease may not always be understood.”
Concurrent underlying disease must be managed as well as possible – which will help management of hypertension as well.

3. Target organ damage:

Can be severe and potentially irreversible
Main target organs: eyes, heart and vasculature, brain, kidneys
Problem(s) relating to TOD may be reason for presentation; especially vision impairment due to hypertensive ocular changes.

“Hypertensive ocular changes have been reported in approximately 50% of hypertensive cats…However, the high prevalence of reported ocular lesions may reflect the relatively late diagnosis of hypertension in many studies.”

“The retina and choroid have separate blood supplies and both can suffer hypertensive damage…with an array of fundic lesions visible on ophthalmoscopy”.

“Many cats with severe hypertensive ocular damage present with blindness and bilateral mydriasis resulting from complete retinal detachments and/or intraocular haemorrhage; the changes are often irreversible…Lesions that are not associated with an impaired menace response or pupillary light deficits...are much more amenable to anti-hypertensive treatment…highlighting the importance of early diagnosis and management. Detection of early hypertensive ocular lesions requires an ocular examination to be performed on all cats at risk of developing lesions.”

4. Monitoring and Underdiagnosis:

Early diagnosis followed by appropriate therapeutic management should help reduce hypertension-associated morbidity associated; however authors suggest monitoring is generally performed infrequently probably leading to underdiagnosis.
Encouraged to identify and monitor patients at risk of developing hypertension.

5. Which cats should we monitor blood pressure in?

Authors’ recommendations:

  • Any cat that has been diagnosed with a recognised risk factor for hypertension, such as chronic kidney disease or hyperthyroidism, should have their blood pressure measured at the time this diagnosis is made and then every 3-6 months thereafter.
  • Any cat that has an unexplained disease compatible with hypertensive target organ damage should also have their blood pressure measured immediately and then every 3-6 months thereafter.
  • Check blood pressure at least every 6–12 months in healthy cats aged eleven years or older.
  • Check blood pressure every 12 months in healthy cats aged 7-10 years.

Should we consider checking blood pressure every 12 months in healthy adult cats 3–6 years of age? “The main purpose of monitoring in this age group is to obtain baseline measurements for the individual cat. As few cats in this age category have hypertension, great care is needed in the interpretation of elevated BP measurements, especially in the absence of [target organ damage] or a clear underlying disease.”

5. Ensure BP is measured as accurately as possible with a reproducible technique:
   
Major take-home message alert!!!

“Indirect measurement of BP in cats can be readily performed, although care is needed with both the choice and use of the equipment to ensure meaningful and accurate results are obtained.”

Recommend using either Doppler sphygmomanometry or high-definition oscillometry; HDO is more accurate, reliable and consistent and easier to perform than traditional oscillometry.

Only systolic blood pressure measurements should be used for clinical assessment. Diastolic and mean arterial pressure readings are less accurate and should generally be ignored.

Use of standardised protocols imperative to improve accuracy and reproducibility of measurements.

Guidelines include extensive recommendations by the Panel covering:

  • Cat’s environment
  • Acclimatisation
  • Personnel
  • Restraint and positioning
  • Choice and position of cuff
  • Actual use of equipment
  • Taking and interpreting measurements

Consistency is essential.

“Blood pressure is labile and varies considerably within and between cats, depending in part on their level of arousal, activity or stress.”

Clinical assessment of systolic blood pressure is also affected by many external variables including:

  • Operator
  • Conditions
  • Environment
  • Equipment
  • Position of the cat
  • Size of the cuff
  • Site of measurement

6. ‘White coat hypertension’:

Temporary physiological increase in blood pressure due to excitement- or more likely anxiety-related sympathetic activation associated with veterinary visit.

7. Defining normal blood pressure:

“Establishing reference intervals for estimated [systolic blood pressure] in healthy cats using Doppler or oscillometric equipment is fundamental to the clinical diagnosis of hypertension, and also for determining therapeutic targets in affected cats.”

Provide results from three different studies but: “there is a wide discrepancy between different studies; this reflects, at least in part, the different populations examined, and differences in types of equipment and the way equipment was used. Thus, having a standardised technique is of paramount importance.”

Categories proposed by The International Renal Interest Society (IRIS):

  • Systolic blood pressure (SBP) <150mmHg = normotensive with minimal risk of target organ damage
  • SBP 150-159mmHg = borderline hypertensive with low risk of target organ damage
  • SBP 160-179mmHg = hypertensive with moderate risk of target organ damage
  • SBP >=180mmHg = severely hypertensive with high risk of target organ damage

Strict categorisation is problematic as blood pressure is labile and target organ damage is not only related to severity of hypertension but also duration and relative change.

8. Criteria for therapeutic intervention and appropriate therapeutic targets:

Criteria as per the Guidelines:

“While individual circumstances should always be carefully assessed, based on current knowledge the Panel suggests that antihypertensive therapy is generally justified if SBP is measured carefully and when:

a. Indirect SBP is ≥150 mmHg on a single occasion, and there is clear evidence of ocular or neurological TOD [target organ damage].

Note: if clinical signs do not respond appropriately to adequate antihypertensive therapy, the diagnosis should be reassessed and other potential causes of the signs investigated.

b. Indirect SBP is ≥160 mmHg on at least two separate occasions, and there is evidence of TOD including ocular, neurological, cardiac or kidney damage.

c. Indirect SBP is ≥170 mmHg on at least two separate occasions, and the clinician does not consider ‘white coat hypertension’ is likely to be the cause.

d. Indirect SBP is <150 mmHg, but there is clear evidence of active ocular TOD.

Note: cats should be monitored carefully. If there is any doubt about the diagnosis of hypertension, the need for long-term therapy should be reassessed by trial withdrawal of therapy once stable, and monitoring of BP and clinical signs.

Cats with SBP <150 mmHg and evidence of potential TOD should have their clinical signs and BP monitored carefully, and other possible causes of the signs investigated.”

Therapeutic target:

SBP <160mmHg generally associated with decreased risk of target organ damage and hopefully an improvement in patient’s health
Indeed may be more prudent to aim for <150mmg in long-term

9. What treatment should you use?

“Based on current data, amlodipine besylate is the treatment of choice to manage feline hypertension and is effective in the majority of cats, but the dose needed to successfully manage hypertension varies between individuals.”

Guidelines also cover approach to amlodipine dosing and routine BP monitoring.

“It is worth noting that the Guidelines were supported financially by an educational grant from Ceva to the ISFM and Ceva is a manufacturer of amlodipine; however I don’t think this invalidates the statement about amlodipine being the current treatment of choice.” (Shailen)

Amlodipine causes vasodilation (peripheral arterial dilator) via calcium channel blockade; good response seen in many hypertensive cats suggests increased vascular tone may be a common component of feline hypertension.

Adjuvant therapy required in some cats:

E.g. ACE inhibitors, angiotensin receptor blockers (ARBs), beta-blockers
Less effective; typically used in addition to not instead of amlodipine.

“The choice of adjunctive therapy to help manage hypertension may in part be dictated by any concurrent or underlying disease. For example, ACE inhibitors or ARBs may be indicated in CKD patients to help manage proteinuria”.

NB. Whenever hypertension is diagnosed, it is important to search for, and treat, underlying diseases as most cases of feline hypertension are secondary.

10. Emergency treatment of hypertension:

Hypertension generally chronic; acute presentations may be due to:

Acute onset of clinical signs due to target organ damage
Acute elevations of blood pressure (e.g. possible in acute kidney injury (AKI))

Aggressive intervention with oral +/- parenteral antihypertensive therapy may be tempting/seem rational but lack of definitive evidence to support positive risk-benefit assessment. 
Uncontrolled abrupt reduction in systolic blood pressure or development of hypotension can precipitate myocardial, cerebral or renal ischaemia and should be avoided.

[This podcast is closely aligned with the MedEdLIFE Research Collaborative's Quality Checklist for Podcasts.]
 

Tweet: Check out FREE audio podcasts from @VetEmCC http://ctt.ec/UqL8b+ Also available in iTunes/Stitcher. #veterinary #podcast