Early Approach to Dyspnoeic Cats, First Do No Harm!

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

Listen to Stitcher

Principles on which approach is predicated:

1. Risk-benefit assessment:

Help as much as possible, harm as little as possible
Dyspnoeic cats can be very vulnerable, easy to ‘tip over the cliff edge’

“sometimes cats are just going to do the dance of death and there is only one outcome…BUT the premise is that for a significant proportion of the dyspnoeic cats that we see there is real benefit in a rational approach to their management.”

2. Emergency Medicine philosophy:

ALSO SEE THIS BLOG POST.

Top priorities:

  • Identify and address potentially life-threatening problems
  • Make the patient feel better

Do not necessarily have to answer all the questions about what is going on with the patient early on
A slow staged approach is essential
Medical therapy or interventions may need to be provided empirically or presumptively
Judicious pattern-spotting may be appropriate

3. Individual patient approach:

Start with a rational cautious general approach, modify and pivot according to individual patient
Some dyspnoeic cats are very amenable and easy to do things to, especially with a minimal restraint hands-off approach; others require a much slower staged approach

4. Clinical confidence, reasoning and gestalt:

Approach described relies to some extent on clinician confidence in terms of examining the patient, interpreting findings, and drawing rational conclusions with all the available information.

5. Anatomical localisation:

Where in this patient’s respiratory tract do I think the cause is?

Five anatomical sites:

  • The upper respiratory tract including the proximal trachea
  • The lower respiratory tract including the distal trachea, bronchi and bronchioles
  • The lung parenchyma
  • The pleural space
  • The chest wall and diaphragm

Localisation helps to consider differential diagnoses
Multiple sites may be affected
Respiratory status can be affected by e.g. pain, raised temperature, acid-base status; typically would not cause dyspnoea, more often tachypnoea

General approach:

1. Preparedness:

Essential not just for dyspnoeic cats but all emergency patients!
Ideally clinic in a constant state of preparedness
When awaiting a dyspnoeic cat (if you know they are en route!) ensure that:

  • All potential team members that will be involved are informed
  • You know how you are going to be providing oxygen supplementation
  • Potentially indicated drugs and dose rates are to hand
  • You get thoracocentesis equipment together
  • Etc.

2. Initial period after arrival:

“When the cat arrives at the clinic he or she could potentially be at their most vulnerable depending on how well they have coped with being in the carrier and travelling.”

Triage starts immediately with observation:

  •  Respiratory status: effort, postural adaptations, pattern, subjective rate
  • External evidence of trauma
  • Some perfusion information (e.g. if the cat is sitting upright they must have some level of adequate perfusion even if not normal)
  •  Mentation

Initial period of oxygenation:

Typically hands-off in oxygen cage
In carrier with top removed or after careful removal from carrier (no time to be tipping cat out of carrier from height!)
E.g. 15-20 minutes but no prescribed period
Allows:

  • Cat time to calm down after journey: improves welfare and potentially reduces oxygen consumption
  • Improved oxygenation if compromised

Potential benefit of oxygen cage depends on individual patient:

Degree of improved oxygenation affected by existing pathology
Potentially greater benefit with pulmonary parenchymal disease (e.g. contusions, oedema) but less with pleural space disease (e.g. effusion, pneumothorax) if lungs too compressed

All cases may benefit from period of hands-off observation after stress of journey

DO NOT SCRUFF CATS IN GENERAL AND ESPECIALLY NOT DYSPNOEIC ONES – PLEASE!
Scruffing is rarely necessary and anecdotally used excessively

Brief examination:

Before putting cat in oxygen cage; or potentially after some time in oxygen cage
Flow-by oxygen supplementation – if tolerated
Key objectives:

  • Cardiovascular:
    • Sternal cardiac auscultation: murmur? Gallop sound? Other rhythm disturbance? Subjective heart rate? Muffling? Displacement?
    • +/- Concurrent pulse palpation
    • Mucous membranes
  • Respiratory:
    • Lung auscultation: dullness – ventral, dorsal, diffuse? Louder sounds – harshness, crackles, wheezes? Bilaterally symmetrical?
    • Upper respiratory tract dyspnoea?

On-going observation – can be continued more extensively once in oxygen cage

“Beyond just deciding whether lung sounds are louder or quieter than normal, it is important to consider whether the loudness of the lung sounds is appropriate for the patient’s respiratory rate and effort? Apparently normal lung sounds in a cat with marked respiratory effort may in fact be inappropriately quiet, suggesting for example pleural effusion or severe consolidation.”

How long you spend doing this brief examination – if you do it at all – needs to be tailored to the individual cat. 

3. Client communication:

Can use oxygenation period to consult with clients, get further consent
May already have reasonable idea of what is wrong with the cat, if not specific disease(s) then anatomical localisation and potential differentials, based on:

  • Signalment
  • Any known history
  • Brief examination

**Ensure cat observed by team member throughout**

Potential next steps…

4. Diagnostic Imaging:

As mentioned previously, anatomical localisation is essential in dyspnoeic patients
May have already achieved this; if not what else can be done to localise better and potentially establish specific diagnosis?

Plain radiography:

“A lot of people are very keen to radiograph dyspnoeic patients very quickly in order to try and get the information that they feel they need to be able to help the patient. And my premise is that I think in many cases it is possible to do this without needing to take radiographs early on.”

Radiographs typically provide useful information but at what risk to the patient?
THINK RISK-BENEFIT, RISK-BENEFIT, RISK-BENEFIT!
Can you delay radiography, do more to improve stability and reduce risk first?
Take steps to mitigate risk if radiography performed – prepare everything ahead of moving cat, quiet environment, ‘cat in carrier’ technique etc.

Point-of-care ultrasound (POCUS):

Getting increasing attention in human and veterinary medicine; increasing good quality clinical data in humans
Not just thoracic focused assessment with sonography for trauma (T-FAST) but for other causes of dyspnoea too
Non-invasive, minimal patient restraint
Potentially leaving cat in oxygen cage
Clipping vs. non-clipping?
Use quiet patient-friendly clippers

“what we are after with POCUS, especially in dyspnoeic cats, is to get the interpretable images that we need in the most efficient time possible and sometimes trying to do this in the cage or with no clipping is not going to get you this result. So there is a balance to be found between handling and intervening with the patient and giving yourself the best and most efficient chance of success.”

Everyone, with just a little training and practice, can identify pleural effusion
With more training and practice, may be able to evaluate left atrial size, cardiac contractility, lung parenchyma, pneumothorax
BUT start with reasonable expectations and then improve in time

5. What else?

Intravenous catheterisation:

Early IV access allows less invasive drug therapy; important if cat rapidly decompensates
But…THINK RISK-BENEFIT, RISK-BENEFIT, RISK-BENEFIT!
What can you do to make the cat more stable before catheterisation to reduce risk? E.g. thoracocentesis; empirical drug therapy
Clip at least two peripheral vein sites and apply topical local anaesthesia beforehand
Try to minimise environmental stress – quiet room, minimal traffic, etc.
Ask the most skilled team member to attempt catheterisation first

Thoracocentesis:

Empirical thoracocentesis frequently safer than radiography; do before/after POCUS according to circumstances
Diagnostic and therapeutic, potentially life-saving
Suspect pleural effusion? Target ventral third
Suspect pneumothorax? Target dorsal third
Unsure? Target midway up chest
Collective anecdotal experience suggests clinically significant iatrogenic complications of thoracocentesis are rare
Minimise risks and maximise chance of successful outcome by preparing equipment in advance, tailoring manual restraint to individual patient
Consider e.g. 0.1 mg/kg methadone (or more according to analgesia requirement) or butorphanol IV/IM beforehand: anxiolytic; thoracocentesis not totally pain-free
Some cases require more aggressive chemical restraint, e.gm ketamine/midazolam

“if you find yourself fighting with a cat trying to perform thoracocentesis, scruffing him or her or otherwise aggressively restraining the cat, then I really do think you should take a step back and consider whether this is a rational thing to be doing, is it the safest and kindest thing for the cat, and is it likely to give you the best chance of a successful outcome. I would strongly argue that it is usually a flawed approach.”

Blood tests:

THINK RISK-BENEFIT, RISK-BENEFIT, RISK-BENEFIT!

“When you are considering doing a blood test on a dyspnoeic cat, stop for a second and consider how the results of that test will change your current plan…ask yourself how the results of those tests will help you to help the patient in their current circumstances; do the results help you to stabilise the cat or could you postpone doing those tests for now?”

Take-home messages:

  • Appreciate that dyspnoeic cats can be very vulnerable and easily tipped over the cliff edge.
  • Even more so than normal, pay acute attention to the risk-benefit assessment at all times.
  • Understand that each cat is clearly going to be an individual patient with their own set of circumstances and behaviour, but that a hands-off, slow, staged approach is likely to be the least risky and most beneficial in most cases.
  • Continue to improve your ability and confidence in examining these cases paying attention to trying to anatomically localise the cause of the dyspnoea; this will allow you to make the most sensible decisions in terms of how to help the patient.
  • Don’t be in a hurry to x-ray dyspnoeic cats until and unless you feel like you have done all you can to make them as stable as possible beforehand.
  • And, lastly engage more with POCUS, point-of-care ultrasound, if you are not already.

Please do get in touch using the contact form on website, via email at shailenjasani@gmail.com, via Twitter @VetEmCC or via Facebook at the Veterinary ECC Small Talk page. I would love to hear what you think of my views expressed in this episode, what you agree with and indeed what you might disagree with.

And don’t forget to join the new Veterinary ECC Small Talk private Facebook group:

CLICK THE IMAGE TO JOIN THE FACEBOOK GROUP!!!

CLICK THE IMAGE TO JOIN THE FACEBOOK GROUP!!!

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

Journal Papers: PORV in dogs, Lactate in cats, and 'All in a tangle'

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

Listen to Stitcher

Davies JA, Fransson BA, Davis AM, et al. Incidence of and risk factors for postoperative regurgitation and vomiting in dogs: 244 cases (2000–2012). J Am Vet Med Assoc 2015. 246(3):327-335.

ABSTRACT

Objective — To determine the incidence of and risk factors for postoperative regurgitation and vomiting (PORV) in dogs.
Design — Retrospective cohort study.
Animals — 244 client-owned dogs.

Procedures — Dogs referred for nonelective surgery in the first 3 months of 2000 and 2012 were included. Breed; sex; age; weight; body condition score; emergency status; food withholding status; history of vomiting or regurgitation; American Society of Anesthesiologists score; presence of diabetes or hypothyroidism; preoperative PCV and total solids concentration; anesthesia protocol; corticosteroid, opioid, neuromuscular blocking agent, and nitrous oxide usage; anesthesia time; surgery time; type of surgery; and occurrence of vomiting or regurgitation within 24 hours after recovery from anesthesia were recorded. Data were analyzed by means of the Fisher exact test, Wilcoxon rank sum test, and logistic regression.

Results — 30 of 244 (12.3%) dogs meeting study inclusion criteria developed PORV. There was no significant difference in the incidence of PORV between the 2000 (12/111 [10.8%]) and 2012 (18/133 [13.5%]) cohorts, although the incidence of regurgitation was higher in 2012. Univariate logistic regression identified the most significant risk factors as gastrointestinal surgery (OR, 11.15; 95% confidence interval [CI], 3.11 to 40.03), premedication without strong sedatives including either an α2-adrenoceptor agonist or acepromazine (OR, 5.36; 95% CI, 1.89 to 15.17), American Society of Anesthesiologists score of 4 (OR, 5.25; 95% CI, 1.05 to 26.15), history of vomiting or regurgitation (OR, 5.12; 95% CI, 1.83 to 14.31), emergency surgery (OR, 4.08; 95% CI, 1.29 to 12.90), neurologic surgery (OR, 3.18; 95% CI, 1.02 to 9.92), sevoflurane inhalation anesthesia (OR, 2.78; 95% CI, 1.25 to 6.13), and being sexually intact (OR, 2.37; 95% CI, 1.07 to 5.27). Multivariate analysis was not clinically useful owing to the low sensitivity and specificity of the model.

Conclusions and Clinical Relevance — Between 2000 and 2012, there was no change in the incidence of PORV for dogs undergoing neurologic, orthopedic, and soft tissue surgical procedures; however, the proportion of dogs that regurgitated increased significantly in 2012. Preoperative antiemetic prophylaxis should be considered in dogs undergoing gastrointestinal surgery and in those in which other risk factors are present.

Reineke EL, Rees C, Drobatz KJ. Association of blood lactate concentration with physical perfusion variables, blood pressure, and outcome for cats treated at an emergency service. J Am Vet Med Assoc 2015. 247(1):79-84.

ABSTRACT

Objective —To determine the association of blood lactate concentration with physically assessed perfusion variables, systolic arterial blood pressure (SAP), and outcome in cats evaluated by an emergency service.
Design — Prospective, observational study.
Animals — 111 cats.

Procedures — Initial blood lactate concentration and SAP (prior to any therapeutic interventions) as well as physically assessed perfusion variables (mucous membrane color, capillary refill time, peripheral pulse quality, heart rate, and rectal temperature) were determined. Cats were categorized as having no shock, mild to moderate shock, or severe shock. Outcomes were recorded. Associations between lactate concentration and these variables were assessed.

Results — Median initial blood lactate concentration was 2.7 mmol/L (range, 0.5 to 19.3 mmol/L); cats with white mucous membranes, abnormal peripheral pulse quality, and hypothermia had significantly higher lactate concentration than did cats without these findings. Median lactate concentration for cats with SAP < 90 mm Hg (3.3 mmol/L) was significantly higher than that of cats with SAP ≥ 90 mm Hg (2.35 mmol/L). Cats with severe shock had significantly higher lactate concentration (4.3 mmol/L) than did cats in other shock categories. Median initial lactate concentration at admission did not differ between cats that did (2.45 mmol/L) and did not (3.2 mmol/L) survive to discharge from the hospital. Change in lactate concentration during hospitalization (when applicable) was not associated with outcome.

Conclusions and Clinical Relevance — Findings indicated that blood lactate concentration, together with physical examination findings and SAP, may be a useful tool for identifying abnormalities in tissue oxygen delivery in cats. However, lactate concentrations were not associated with outcome in the present study.

Boveri S, Brearley JC. All in a tangle: a mishap with an oesophagostomy tube in an intubated cat. Vet Anaes Analg 2015. 42(2):227-229.

If you would like a copy of these papers or of the case report, please do get in touch using the contact form on the website, via email at shailenjasani@gmail.com, via Twitter @VetEmCC or via Facebook at the Veterinary ECC Small Talk page.

And don’t forget to join the new Veterinary ECC Small Talk private Facebook group:

CLICK THE IMAGE TO GO THROUGH TO THE FACEBOOK GROUP!

CLICK THE IMAGE TO GO THROUGH TO THE FACEBOOK GROUP!

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

A Critical Patient Daily Checklist

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

Listen to Stitcher

Critically ill patients almost by definition have a number of different problems and management considerations. They can be high maintenance requiring intensive care and it is easy to accidentally overlook different aspects of their care; this is especially the case when you are looking after more than one critically ill patient and/or working in an otherwise busy practice environment. 

Using some form of checklist on a daily basis is a quick and easy way of being reminded of all the different aspects of the care of critically ill patients and hopefully minimises how often treatment considerations are overlooked and sub-optimal care provided.

In this episode I discuss my version of a daily checklist for critically ill patients including aspects such as monitoring, analgesia, nursing care and non-clinical considerations.

To download a COPY OF THE CHECKLIST for free, go HERE.

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

The Shock Index in Veterinary Patients

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

 

Listen to Stitcher

Shock Index = Heart Rate divided by Systolic Arterial Blood Pressure

Healthy human adults: 0.5-0.7

Shock, Heart Rate and Blood Pressure

Shock = significant reduction in systemic tissue oxygen delivery
Most often due to systemic reduction in tissue blood flow or systemic hypoperfusion
Most commonly four types of hypoperfusion-related shock identified: hypovolaemic, distributive, cardiogenic and obstructive; more than one type may exist concurrently.

Uncomplicated hypovolaemic shock in dogs:

Low effective circulating volume triggers sympathetic nervous system-driven compensatory mechanisms: increased heart rate (positive chronotropy), increased force of cardiac contraction (positive inotropy), peripheral vasoconstriction.
Aim to improve effectiveness of circulation and hence oxygen delivery to key organs and tissues

Note:

1. Heart rate during hypovolaemia potentially also influenced by other factors, e.g. pain
2. Findings may be less predictable in other types of shock
3. ‘Shocky’ cats are typically relatively bradycardic regardless of predominant type of shock – hence shock index cannot be used.

Systolic arterial blood pressure:

Blood pressure is not the same thing as blood flow/perfusion; used as a surrogate for perfusion
Systemic hypotension may be late in onset during worsening hypovolaemia; physical perfusion parameters may suggest hypoperfusion despite measured normotension.
Treat blood pressure as an adjunct to perfusion assessment that is supplementary to but not more important than or does not replace cardiovascular exam
May also be affected by other influences, e.g. pain

The Shock Index

Can it help us in the earlier detection and/or treatment of dogs in shock?
Can it allow us to suspect occult hypoperfusion?

Some questions about the shock index:

  • What is it meant to do? How is it meant to help us in our clinical practice? Is it being suggested as something that helps us to improve our management in a way that has an impact on the patients in terms of their progression and outcomes? Could it help us with prognostication?
  • Is it something that can be used for all types of shock, across all disorders that might lead to shock, or do we need to be more granular than that?  
  • What is the evidence around the clinical use of the shock index?
  • What are the implications of using the shock index? Is it quick and easy to do? Does it require any equipment or additional training or resources? And does it end up costing the pet’s carers any extra money? 

“Detecting dogs that are in the late compensatory or early decompensatory stage of hypovolaemic shock may not be particularly challenging but we know that the sooner we can pick up on changes in perfusion that have triggered compensatory responses the sooner we can intervene and reverse the situation…At least in theory this improves patient-centred outcomes. Especially bearing in mind…the potential pitfalls with heart rate changes and with blood pressure then maybe combining these two parameters into one index allows us to smooth or cancel out some of these pitfalls, allows us to detect early compensation sooner and to intervene sooner.”

Human Medicine Literature

Shock index papers from 1980s and indeed earlier
Typically evaluating use of shock index in specific scenarios, e.g. haemorrhagic hypovolaemic shock, especially post-traumatic; obstetric patients; acute coronary syndrome, etc.
Has been evaluated:

  • To see whether it correlates with higher mortality and injury severity after trauma
  • As a predictor for length of hospital stay, number of ventilator days and likelihood of ICU admission
  • In healthy human adult blood donors

Suggests it is necessary to account for patient-specific circumstances that might influence ability to show compensatory heart rate and/or blood pressure responses; e.g. age, concurrent drug therapies such as calcium channel or beta-blockers, diseases that tend to cause hypertension, etc.

These sorts of confounding factors essentially raise two questions:

  • Firstly is there a role for the shock index across all human patients?
  • But secondly, how does it need to be modified for the different patient populations? Do you need a slightly different index or threshold depending on the specific patient population? In other words is a ‘one size fits all’ shock index actually appropriate?

“Shock Index for prediction of critical bleeding post-trauma: A systematic review” from Emergency Medicine Australasia in 2014:

“Early diagnosis of haemorrhagic shock (HS) might be difficult because of compensatory mechanisms. Clinical scoring systems aimed at predicting transfusion needs might assist in early identification of patients with HS. The Shock Index (SI) – defined as heart rate divided by systolic BP – has been proposed as a simple tool to identify patients with HS. This systematic review discusses the SI's utility post-trauma in predicting critical bleeding (CB).”

Their focus was largely on how they could use the shock index to help predict transfusion requirements.

“The SI being simple and repeatable, appears to be useful in predicting CB. Recommendations for the ideal cut-off were varied, with most studies using a cut-off of ≥0.9. However, the cut-off of ≥1.0 was observed to have higher specificity”.

“The Shock Index revisited – a fast guide to transfusion requirement? A retrospective analysis on 21,853 patients derived from the TraumaRegister DGU®” from Critical Care 2013:

Trauma registry of German Trauma Society
Aims: “to characterize four groups of worsening SI based upon a large cohort of multiply injured patients, to report transfusion requirements and outcomes within these four groups, and to compare this SI-based classification in its ability to risk-stratify patients according to their need for early blood product transfusion”.
Four groups:

  • No shock; SI < 0.6
  • Mild shock; SI ≥ 0.6 - < 1.0
  • Moderate shock; SI ≥ 1.0 - < 1.4
  • Severe shock; SI ≥ 1.4

“The SI upon ED arrival may be considered a clinical indicator of hypovolemic shock with respect to transfusion requirements, hemostatic resuscitation and mortality.” And they quite liked their four-group classification system!

“Correlation of Shock Index and Modified Shock Index with the Outcome of Adult Trauma Patients: A Prospective Study of 9860 Patients” from the North American Journal of Medical Sciences in 2014:

“Triage at emergency department is performed to identify those patients who are relatively more serious and require immediate attention and treatment. Despite current methods of triage, trauma continues to be a leading cause of morbidity and mortality…This study was to evaluate the predictive value of shock index (SI) and modified shock index (MSI) for hospital mortality among adult trauma patients.”

Modified shock index (MSI):

Less attention to date
= Heart Rate divided by Mean Arterial Blood Pressure
Using MAP incorporates diastolic blood pressure – some suggestion this may be better than just using systolic

“the present prospective study results show that MSI, as a potential marker for predicting the mortality rate is significantly better than HR, SBP, DBP, and SI alone. Thus, MSI emerges as a better and improved predictor for prediction of hospital mortality in adult trauma patients in the emergency room.”

“Utility of the shock index in patients with sepsis” from the American Journal of Medical Sciences 2015:

“have reviewed and summarized studies that have correlated the SI with other parameters of disease severity and outcomes in patients with sepsis to determine if it has utility in the management of these patients or the prediction of outcomes.”

“The SI provides an integrated assessment of cardiovascular responses in patients with critical illness; its predictive value and simplicity are important considerations that should promote its use in the field, EDs and ICUs. The authors offer a flow diagram for its use in patients with possible sepsis.”

“Is the shock index a universal predictor in the emergency department? A cohort study”

Poster presentation at the 35th International Symposium on Intensive Care and Emergency Medicine
“The shock index…is a widely reported tool to identify acutely ill patients at risk for circulatory collapse in the emergency department (ED). Because old age, diabetes, essential hypertension, and β-/Ca2+ channel-blockers might reduce the compensatory increase in heart rate and mask blood pressure reductions in shock or pre-shock states, we hypothesized that these factors weaken the association between SI and mortality, reducing the utility of SI to identify patients at risk.”

Cohort study from Odense University Hospital of all first-time visits to the ED between 1995 and 2011 (n = 111,019)
Outcome was 30-day mortality

“SI is independently associated with 30-day mortality in a broad population of ED patients. Old age, hypertension and β-/Ca2+ channel-blockers weaken this association, but the association remains prognostic. SI ≥1 suggests substantial risk of 30-day mortality in all ED patients.”

Veterinary Literature

Two studies identified in clinical canine patients; both from September/October 2013 issue of the Journal of Veterinary Emergency and Critical Care.

“Evaluation of the shock index in dogs presenting as emergencies” by Porter, Rozanski, Sharp et al.

Aims of prospective study:

  • To determine a normal range for shock index (SI) in simulated patients – these healthy controls were staff and student dogs
  • To investigate whether SI is increased in dogs deemed to be in moderate to severe shock via assessment of plasma lactate – defined as venous lactate > 5 mmol/l. Exclusion criteria included:
    • Inability to obtain systolic blood pressure
    • Diagnosis of a disease condition that could result in hyperlactataemia in the absence of shock (e.g. increased oxygen demand or type-B lactic acidosis)
  • To compare SI in shock group to that of healthy dogs and dogs not judged to be in shock on presentation to the emergency room – defined as venous lactate ≤ 1.5 mmol/l on presentation.

Why did they focus on moderate to severe shock which is not something that is typically challenging to identify?
Why did they use a biochemical parameter, lactate, to define this instead of physical examination parameters?

“These data provide a pilot evaluation of SI in shock patients, but our study did not evaluate shock in occult hypoperfusion, which is an important distinction. In human studies, the proposed use and proven value of the SI is in identification of early hypovolemia or occult hypoperfusion, as well as in sustained occult shock during resuscitation…This study was designed to introduce the SI to veterinary medicine; further studies evaluating dogs with early, developing shock are warranted.”

“While defining shock solely on a biochemical marker such as lactate is not conventional nor advised in a clinical setting, shock was defined in this manner for several reasons. The first, and most relevant, is that, if selection were based upon heart rate and presence of hypotension, there would be a clear selection for dogs with a high SI. By instead selecting a biochemical marker consistently linked with shock…this study was attempting to avoid this bias. Importantly, assessment of HR and blood pressure are clinically relevant, and should be performed in a clinical setting. Secondly, classic objective parameters used to identify shock in a clinical setting vary drastically between breeds and even individuals within a breed. Setting an inclusion criteria for tachycardia (ie, 160/min) may exclude large breed dogs in shock while including small, anxious dogs that are not in shock. Clinical evaluation of shock status of an individual dog requires the synthesis of a number of parameters, but for the purpose of population analysis use of a biochemical marker of increased plasma lactate to define shock allowed for a more objective inclusion criteria.”

Blood pressure measurement:

Non-invasive oscillometric method preferred technique; used Doppler if this failed
In accordance with the American College of Veterinary Internal Medicine (ACVIM) guidelines:

  • Cuff size was chosen based on the width of the cuff approximating 40% of the circumference of the measured limb
  • Series of 3 BP measurements were taken, with the average SBP reported

Shock index:

Classified a priori as a binary variable: > 1 versus ≤ 1

“A cut off of 1 was considered clinically relevant and higher than what is used in people since dogs generally have more rapid heart rates than people, despite having similar systolic blood pressure. Thus, a normal dog would be expected to have a higher SI than a normal person. The sensitivity and specificity, along with area under the receiver operator characteristic (ROC) curve, were calculated to determine the discrimination of the shock index in healthy dogs versus shock dogs, and, separately, to determine the discrimination of the SI for [emergency] dogs not in shock versus [emergency] dogs in shock. The area under the ROC curve (AUCROC) investigates the predictive ability of shock index to predict a diagnosis of shock.”

Main results:

  • 68 healthy dogs; median shock index 0.78 (range 0.37-1.30)
  • 19 dogs assessed as not being in shock (venous lactate ≤ 1.5 mmol/l): median shock index 0.73 (range 0.56-1.20)
  • 18 dogs assessed as being in shock (venous lactate > 5.0 mmol/l): median shock index 1.37 (range 0.87-3.12). SI statistically significant difference to other two groups but the lower end of the range for these shock dogs overlaps with the ranges for the healthy and the ‘no shock’ group. 

Underlying disease conditions for shock group included pericardial effusion with cardiac tamponade (6), gastric dilatation-volvulus (3), haemoabdomen (2), and a single case of various others. Median plasma lactate 7.1 mmol/l (range 5.0-12.9 mmol/l).

“sensitivity (Sn), specificity (Sp) and ROC area were calculated using a cut off of SI > 1 defined a priori as a clinically relevant cutpoint:

  • In healthy dogs compared to those dogs in shock, an area under the receiver operator characteristic (AUROC) of 0.89 (CI 0.81–0.98) was seen, with a Sn of 89% and Sp of 90%.
  • In [emergency] dogs not deemed in shock compared to those deemed in shock, an AUROC of 0.92 (CI 0.83–1.00) was seen, with a Sn of 89% and Sp of 95%.”

[Area under an ROC curve (AUROC) approaching 1.0 would be considered excellent.]

Authors’ conclusions:

  • This study documented that the SI may be determined in dogs and that SI is significantly higher in dogs with shock compared to both healthy dogs and dogs presenting to the emergency room but not deemed to be in shock.
  • Specifically, an SI of > 1.0 is a highly sensitive and specific indicator to distinguish ER dogs not in shock and healthy dogs from dogs with biochemical evidence of moderate to severe shock.
  • Our findings support that SI has value as an indicator of shock in sick dogs presenting to the ER, and may serve as part of an initial evaluation.
  • In addition, the SI has not previously been evaluated in a veterinary population, so this study serves to introduce the SI and establish a reference interval for shock index in dogs (0.37–1.30).

Remember, did not look at dogs with lactate between 1.5-5.0 mmol/l so potentially that category in which the shock index could have the most value.

“Assessment of shock index in healthy dogs and dogs in hemorrhagic shock” by Peterson, Hardy and Hall.

Aims of retrospective study:

  • To establish a normal reference interval for canine SI
  • To compare SI in normal healthy dogs to dogs with known haemorrhage

Hypothesis: SI would differentiate a population of dogs with haemorrhagic shock from healthy controls.

Retrospectively analysed data collected prospectively for two previous studies
Blood pressur measurement: either non-invasive oscillometric or Doppler techniques

Control group (healthy dogs): 78 client-, student-, and staff-owned dogs
Haemorrhage group consisted: 38 dogs diagnosed with acute haemorrhagic shock, which presented to the Emergency Service. Variety of causes; bleeding intra-abdominal mass most common.

Bleeding dogs retrospectively classified by three board-certified ECC clinicians into 1 of 4 categories of shock based on heart rate, blood pressure, base excess and comorbidities:

  • All classified as having at least mild haemorrhagic shock
  • Used a combination of physical examination, base excess instead and comorbidities

Statistically significant difference in shock index between haemorrhage group and healthy group:

  • Haemorrhage group: median SI 1.37 (range 0.78–4.35)
  • Healthy group: median SI 0.91 (range 0.57–1.53)
  • Noteworthy overlap in ranges

Other results:

  • Statistical correlation between shock index and lactate
  • No correlation between SI and length of hospital stay in haemorrhage group
  • No increased risk of mortality (death or euthanasia) with increasing SI in dogs with haemorrhage

Evaluated sensitivity and specificity for different shock index cut-offs
Using a shock index cut-off of 1.0 (as was used a priori in the other canine study) performed more poorly here
Also analysed how well heart rate and systolic blood pressure performed in differentiating haemorrhagic shock dogs from healthy dogs

“Our study does not suggest that SI is a superior tool to SBP or HR, but the data support its ability to differentiate between a normal population of dogs from a population of dogs with hemorrhagic shock. Although there is some overlap of SI between normal dogs and dogs in hemorrhagic shock, the calculation could be used along with clinical assessment as an additional triage tool for emergency clinicians and may prompt further investigation for hemorrhage if the value is above 0.9.”

Other Considerations/Implications

Practical implications of using the shock index?

•    Is it quick and easy to do?
•    Does it require any equipment or additional training or resources?
•    And does it end up costing the pet’s carers any extra money?

Heart rate typically quick and easy to do; ensure no pulse deficits if using pulse rate.

Blood pressure:

Not all practices have blood pressure devices
Doppler-based devices are fine as they approximate systolic blood pressure (some literature discussion about this, including cats vs. dogs and conscious vs. under anaesthesia, but this is the consensus position)
Important to adhere to best practice guidelines for measurement and to ensure readings are repeatable, reliable and trendable

Depending on how blood pressure measurement is charged in your practice, could using the shock index end up costing your clients more and if so, do you think it is worth it?

“I think after learning what I have through researching this episode I will in the future start to pay attention to what the shock index is in individual canine patients and just get a personal anecdotal sense of what I feel about it, how it performs. But of course we have to remember that if you use the shock index you don’t just forget about everything else. You should be seeing it as another tool to enhance your identification, assessment and management of dogs in shock rather than replacing what you currently do. So we use our physical perfusion parameters, of which heart rate is just one, and assess them together looking at the whole picture…We use lactate and blood pressure in addition and put all these findings together to assess and manage these patients. And as long as you do that then I can certainly see it doing no harm and potentially being helpful. So I am interested to see how it performs and especially to tease out how it performs in patients in which pain for example is a component of their initial tachycardia.

What we definitely can’t do at the moment in my opinion is to use the shock index in an overt way to predict progression or prognosis. We most definitely do not have anything like the evidence base we would need to start trying to use the shock index in this way and I am not sure if we ever will. So as a supplementary assessment and monitoring tool, sure, as anything more than that, then I would say no, at least not in 2015.”

If you would like a copy of any of the papers mentioned below then do get in touch

Do you use the shock index? If so, how do you find it?
Would you consider using the shock index after listening to this episode?

PAPERS THAT INFORMED OR WERE MENTIONED IN THIS EPISODE:

Veterinary literature:

Peterson KL, Hardy BT, Hall K. Assessment of shock index in healthy dogs and dogs in hemorrhagic shock. J Vet Emerg Crit Care 2013. 23(5):545-550.

Porter A, Rozanski E, Sharp C, et al. Evaluation of the shock index in dogs presenting as emergencies. J Vet Emerg Crit Care 2013. 23(5):538–544.

Human Medicine literature:

Allgöwer M, Burri C. Shock index. Dtsch Med Wochenschr 1967. 92:1947–1950.

Kristensen A, Holler J, Hallas J, Lassen A, Shapiro N. Is the shock index a universal predictor in the emergency department? A cohort study. Critical Care 2015, 19(Suppl 1):P148. Poster presentation.

Mutschler M, Nienaber U, Münzberg M, et al. The Shock Index revisited – a fast guide to transfusion requirement? A retrospective analysis on 21,853 patients derived from the TraumaRegister DGU®. Crit Care 2013. 17(4):R172.

Olaussen A, Blackburn T, Mitra B, Fitzgerald M. Review article: Shock Index for prediction of critical bleeding post-trauma: A systematic review. Emerg Med Austral 2014. 26(3):223-228.

Pandit V, Rhee P, Hashmi A, et al. Shock index predicts mortality in geriatric trauma patients: an analysis of the National Trauma Data Bank.  J Trauma Acute Care Surg 2014. 76(4):1111-1115.

Rady MY, Nightingale P, Little RA, et al. Shock index: a re-evaluation in circulatory failure. Resuscitation 1992. 23(3):237–234.

Singh A, Ali S, Agarwal A, Nath Srivastava R. Correlation of Shock Index and Modified Shock Index with the Outcome of Adult Trauma Patients: A Prospective Study of 9860 Patients. N Am J Med Sci 2014. 6(9):450–452.

Tseng J, Nugent K. Utility of the shock index in patients with sepsis. Am J Med Sci 2015. 349(6):531-5.

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

Steroids and Shock!

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

Listen to Stitcher

Exogenous therapeutic steroids include hydrocortisone, dexamethasone, betamethasone, methylprednisolone etc. All have glucocorticoid activity but vary with respect to mineralocorticoid activity.

SHOCK:

Essentially, critically low systemic tissue oxygen delivery
Typically due to systemic hypoperfusion:

  • Four types of ‘hypoperfusion’ shock: hypovolaemic, (mal)distributive, cardiogenic, obstructive
  • May be present concurrently
  • Some include septic shock and/or anaphylactic shock as separate types

Some older resources recommended (often high dose) steroid use in shock but things have changed, e.g.

“High dose fast-acting corticosteroids are no longer recommended for use in shock…recent studies have not demonstrated significant benefit and it actually may cause increased deleterious effects.” (Dexamethasone entry, Plumb’s Veterinary Drugs online, 2015).

LITERATURE

Unable to identify any recent reviews of steroid use in shock in general
Vast majority is on use of steroids in septic shock in people, either clinical studies or review articles citing experimental animal studies and clinical human trials.

STEROID USE IN SHOCK

On-going debate for many years, e.g.

  • “Role of corticosteroids in the treatment of circulatory collapse states” from Clinical Pharmacology and Therapeutics in 1970
  • “Should corticosteroids be used in shock?” from Medical Clinics of North America in 1973
  • “Steroids and severe hemorrhagic shock” from Surgery 1977.

“Should corticosteroids be given in shock?” from Drugs and Therapeutics Bulletin in 1976, Volume 14, Issue 4:

“The adrenals respond to shock by increased cortisol secretion…Any beneficial effect of corticosteroids is therefore not due to the correction of adrenal insufficiency.” See more on this later.

“The effects of corticosteroids in shock are difficult to study because of the variety of causes and the lack of animal models which mimic the conditions found in man.”

“There is insufficient evidence to support the use of corticosteroids in traumatic, haemorrhagic, neurogenic or cardiogenic shock. In patients with endotoxin shock it seems reasonable to give a glucocorticoid if there has been no improvement in response to adequate fluid replacement and ventilation together with an appropriate antibiotic regime…Endotoxaemia is the only form of shock in which corticosteroids may be helpful. Very large doses are needed. An adequate prospective trial of this therapy is, however, badly needed.”

Using references from the 1950s, 1960s and early 1970s!

Some animal experimental studies of high dose methylprednisolone use in haemorrhagic shock models.

Steroids in Septic Shock

Sepsis’: systemic inflammatory response syndrome (SIRS) that is due to a confirmed or suspected infectious cause.
Severe sepsis’: sepsis in which there is evidence of organ dysfunction; organ dysfunction may also include hypotension or tissue hypoperfusion which is essentially seen as dysfunction of the cardiovascular system.
Septic shock’: sepsis-induced hypotension or tissue hypoperfusion which persists despite adequate fluid resuscitation.

Sepsis-induced hypotension or tissue hypoperfusion:

  • Distributive shock with generalised vasodilation which increases the capacity of the intravascular space and causes a relative hypovolaemia
  • Also some absolute hypovolaemia with fluid being lost from the circulation through the leaky inflamed blood vessels
  • +/- Some degree of myocardial dysfunction
  • +/- Impaired cellular ability to take up and utilise oxygen

Proposed pathophysiology of sepsis is complex!

HUMAN LITERATURE

Experimental and clinical papers from as far back as the 1940s
E.g. “Effect of cortisone on acute streptococcal infections and post-streptococcal complications” (Journal of Clinical Investigation, 1951)

Lot of further work published since then on steroid use in septic shock:

  • Non-human and human experimental work
  • Clinical studies including prospective RCTs – mostly adults but also some paediatric

BENEFIT-RISK

Potential benefits of steroid in septic shock:

In septic shock pro-inflammatory pathways may have overwhelmed anti-inflammatory pathways and endogenous glucocorticoids so supplementing glucocorticoids may be helpful?
Various suggested molecular and cellular pathophysiological mechanisms by which glucocorticoids may further help to augment compensatory anti-inflammatory response.

Through various (often not definitively proven) mechanisms steroids may help to restore both cardiovascular system dysfunction and indeed organ dysfunction in other sites.

Potential risks:

Steroid-induced immunosuppression may impair ability to resolve primary infection and also predispose to new onset hospital-acquired (potentially multidrug resistant) superinfections.
Gastrointestinal ulceration and bleeding, muscle weakness

If we are saying that steroids can theoretically play a beneficial role in septic patients and in particular septic shock, then should the aim be to give all septic patients steroids on the basis that if some is helpful, more is even better? Or put another way is there a rationale for supraphysiological steroid use?

If using steroids in this supraphysiological way does not make sense or is not supported by the evidence, then is there a role for physiological steroid use to top up glucocorticoid activity in the face of potentially overwhelmed/depleted/inadequate endogenous reserves?

CURRENT HUMAN (and VETERINARY?) RECOMMENDATIONS

Do not use steroids in all patients with septic shock
Use steroids at appropriate doses for (rare) patients known to have a specific infection for which steroids are indicated
On-going debate about use of ‘low dose’ ‘physiological’ steroids in patients with possible ‘relative adrenal insufficiency’ or ‘critical illness-induced corticosteroid insufficiency’…

Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012

Adults:

“We suggest not using intravenous hydrocortisone as a treatment of adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability…If this is not achievable, we suggest intravenous hydrocortisone alone at a dose of 200mg per day.”

Grade 2C = weak recommendation based on low quality evidence.

Paediatrics:

“We suggest timely hydrocortisone therapy in children with fluid-refractory, catecholamine-resistant shock and suspected or proven absolute (classic) adrenal insufficiency.”

Grade 1A = strong recommendation with high quality evidence.

“Timing of Corticosteroids in Refractory Septic Shock: A Key or Wishful Thinking?” (Editorial, Critical Care Medicine 2014): 

“Corticosteroid administration in the refractory critically ill patient with presumed sepsis has shadowed our practices almost since the clinical development of these hormones and the inception of modern critical care. Most, if not all of us, have witnessed a near miraculous stabilization of a patient hovering near death’s door when a bolus of hydrocortisone, methylprednisolone, or dexamethasone has been administered to that patient. Clearly, for the rare individual with primary adrenal failure (Addison’s disease), this would be mandatory therapy, but for the wide spectrum of septic patients with suspected adrenal insufficiency, corticosteroid resistance, or other, there is insufficient compelling data to show benefit to a broader use of corticosteroids in septic patients.”
“Mysteries related to the use of steroids in septic shock remain unsolved. The first and foremost is identifying a test that will help clinicians decide whether to initiate steroids in the first place. Creating such a test is largely complicated by intrinsic changes that occur during septic shock…As the inherent difficulties in developing such a test continue to be investigated, practitioners who use steroids in patients with refractory septic shock may consider using them earlier on after diagnosis.”

American Journal of Respiratory and Critical Care Medicine, 2012:

“This concise evidence-based review highlights the strengths and weaknesses of the current data to inform the practicing clinician as to which patients are likely to derive significant benefit from corticosteroid treatment, while we await more definitive guidance from future multicenter, prospective, randomized, controlled trials designed to better answer these important therapeutic questions.”

Paediatric Critical Care Medicine, 2013:

“The literature on the use of steroids in pediatric shock is limited in amount and methodological quality and demonstrates conflicting results. The limited evidence on which current guidelines are based strongly supports the need for a well-designed, pragmatic randomized controlled trial on the use of steroids in pediatric shock to inform future guidelines.” 

Burkitt Creedon JM. Controversies surrounding critical illness-related corticosteroid insufficiency in animals. J Vet Emerg Crit Care 2015. 25(1):107-112.

**Please feel free to contact me if you would like a copy of this paper**

“…continued controversy over adrenal function testing and the use of glucocorticoids in [human] patients with severe sepsis and septic shock.

Unfortunately, even less is known and understood about normal and abnormal corticosteroid metabolism and the possible benefit of corticosteroid therapy in critically ill veterinary patients. The purposes of this review are to describe the controversies surrounding CIRCI and the use of hydrocortisone in critically ill patients and to present published diagnostic and therapeutic strategies in companion veterinary species.”

Aetiology of CIRCI is unknown and “There is almost certainly interindividual variation in its pathophysiology…and more than one mechanism may be present concurrently in the same patient. It is also unknown whether different mechanisms may be at play in different species, as very limited to no data regarding appropriate corticosteroid metabolism are available in veterinary species”.

Diagnosis of CIRCI:

“The complicated and likely multifactorial nature of CIRCI's pathogenesis…has led to significant controversy regarding the best way to identify patients with the syndrome. Baseline cortisol concentration, delta cortisol concentration using standard vs low-dose ACTH stimulation test protocols, endogenous hormone ratios, measurement of total vs free cortisol, response to treatment, and other methods have been advocated by various authors as appropriate method(s) for detecting cortisol insufficiency or resistance in critical illness in people.

It is probably most accurate to say that due to disparate data from different studies and resultant clinical equipoise, the human critical care community does not advocate any method of diagnosis for CIRCI at present. In a practical sense, the “diagnosis” of CIRCI in people is currently made by evaluating response to treatment with low-dose hydrocortisone, because current guidelines recommend treating pressor-resistant septic shock patients with hydrocortisone without or with no regard to HPA axis assessment.”

Of course less is known about the best way to identify CIRCI in critically ill dogs and even less in critically ill cats. The author also mentions some studies relating to foals.

Treatment:

“The dose is referred to as “low,” “physiologic,” “stress,” or “replacement,” depending on author…Whether this approach is appropriate in horses, dogs, and cats is unknown. The required dose for any individual patient (human or veterinary) is unknown, as the precise glucocorticoid deficiency or responsiveness in any critically ill individual cannot be determined. Meta-analyses confirm that while these lower doses of corticosteroids may confer benefit in people with septic shock, higher doses are not beneficial and may be detrimental.”

Lack of consensus about treatment of CIRCI in human medicine
Decision to treat is murkier and treatment methods more variable in veterinary medicine

Treatment regimens have been published primarily in case reports, reviews, and book chapters, with no reliable clinical trial data available in veterinary species

Review article ends with:

“Considering the substantial controversy and uncertainty that still surround the syndrome of CIRCI, it is fortunate that another large-scale, multicenter trial investigating the use of hydrocortisone in septic shock is currently underway…This trial began enrollment in February 2013, and aims to include 3800 people with septic shock. Results of this investigation may significantly influence CIRCI identification and management in people. However, because of species differences in endogenous cortisol metabolism and in responsiveness to exogenous steroids, studies in individual veterinary species will be required to make specific recommendations in companion animals. Until further data become available, practitioners will continue to make clinical judgments regarding the diagnosis and treatment of corticosteroid insufficiency in critically ill patients.”

EPISODE SUMMARY:

Use of steroids in shock in general is not recommended unless that patient happens to have a steroid-responsive disease as the cause of their shock; this is rare.
‘Low dose’ or ‘physiological’ steroids can be used in patients with septic shock – or other critical illness – that is refractory to fluid resuscitation and exogenous catecholamine use; many veterinary practitioners may not have access to vasopressor/inotropic agents.

  •  A positive response to low dose steroid use suggests the presence of CIRCI
  • Hydrocortisone is typically suggested; dexamethasone may be less preferable but can still be used
  • ***Much remains to be clarified about this in human and especially veterinary medicine in terms of which patients are the best candidates, when to start steroids, what protocol to use and so on.***

Please feel free to contact me if you would like a copy of Dr. Burkitt’s paper for educational purposes.

I would also love to hear any thoughts or comments about this episode and about your practice. 

PAPERS THAT INFORMED OR ARE MENTIONED IN THIS EPISODE:

Annane D. Corticosteroids for severe sepsis: an evidence-based guide for physicians. Ann Int Care 2011.
http://link.springer.com/article/10.1186/2110-5820-1-7/fulltext.html 

Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids for severe sepsis and septic shock: a systematic review and meta-analysis. BMJ 2004; 329:480–484.

Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids for treating severe sepsis and septic shock. Cochrane Database Syst Rev 2004; (1):CD002243.

Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids in the treatment of severe sepsis and septic shock in adults: a systematic review. JAMA 2009. 301:2362–2375.

Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002. 288:862–871.

Burkitt JM, Haskins SC, Nelson RW, et al. Relative adrenal insufficiency in dogs with sepsis. J Vet Intern Med 2007. 21:226–231.

Burkitt Creedon JM. Controversies surrounding critical illness-related corticosteroid insufficiency in animals. J Vet Emerg Crit Care 2015. 25(1):107-112.

Couetil LL, Hoffman AM. Adrenal insufficiency in a neonatal foal. J Am Vet Med Assoc 1998. 212:1594–1596. 

Durkan S, de Laforcade A, Rozanski E, et al. Suspected relative adrenal insufficiency in a critically ill cat. J Vet Emerg Crit Care 2007. 17:197–201.

Greenberg SB; Coursin DB. Timing of Corticosteroids in Refractory Septic Shock: A Key or Wishful Thinking? Crit Care Med 2014. 42(7):1733–1735.

Hahn EO, Houser HB, Rammelkamp CH, et al. Effect of cortisone on acute streptococcal infections and post-streptococcal complications. J Clin Invest 1951. 30(3):274–281.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC436257/ 

Hardaway RM, Williams CH. Influence of steroids on hemorrhagic and traumatic shock. J Trauma 1987. 27(6):667-670.

Hart KA, Barton MH. Adrenocortical insufficiency in horses and foals. Vet Clin North Am Equine Pract 2011. 27:19–34.

Marik PE, Pastores SM, Annane D, et al. Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine. Crit Care Med 2008. 36:1937–1949.

Martin LG, Groman RP, Fletcher DJ, et al. Pituitary-adrenal function in dogs with acute critical illness. J Am Vet Med Assoc 2008. 233:87–95.

Martin LG. Critical illness-related corticosteroid insufficiency in small animals. Vet Clin North Am Small Anim Pract 2011; 41:767–782, vi.

Menon K, McNally D, Choong K, Sampson M. A Systematic Review and Meta-Analysis on the Effect of Steroids in Pediatric Shock. Ped Crit Care Med 2013. 14(5):474-480.

Moran JL, Graham PL, Rockliff S, et al. Updating the evidence for the role of corticosteroids in severe sepsis and septic shock: a Bayesian meta-analytic perspective. Crit Care 2010; 14:R134.

Patel GP, Balk RA. Systemic Steroids in Severe Sepsis and Septic Shock. Am J Resp Crit Care Med 2012. 185(2):133-139.
http://www.atsjournals.org/doi/full/10.1164/rccm.201011-1897CI

Peyton JL, Burkitt JM. Critical illness-related corticosteroid insufficiency in a dog with septic shock. J Vet Emerg Crit Care 2009. 19:262–268.

Prittie JE, Barton LJ, Peterson ME, et al. Hypothalamo-pituitary-adrenal (HPA) axis function in critically ill cats. J Vet Emerg Crit Care 2003; 13:165.

Raflo GT, Jones RC Jr, Wangensteen SL. Inadequacy of steroids in the treatment of severe hemorrhagic shock. Am J Surg 1975. 130(3):321-327.

Schoeman JP, Herrtage ME. Adrenal response to the low dose ACTH stimulation test and the cortisol-to-adrenocorticotrophic hormone ratio in canine babesiosis. Vet Parasitol 2008. 154:205–213.

Should corticosteroids be given in shock? Drug Ther Bull 1976. 14(4):14-16. (no authors listed)

Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008. 358:111–124.

Sullivan L, Burkitt Creedon JM. Critical illness-related corticosteroid insufficiency. In: Bonagura JD, Twedt DC. eds. Kirk's Current Veterinary Therapy XV. St. Louis: Elsevier Saunders; 2014, pp. 78–79.

Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
http://www.sccm.org/Documents/SSC-Guidelines.pdf 

Venkatesh B, Myburgh J, Finfer S, et al. The ADRENAL study protocol: adjunctive corticosteroid treatment in critically ill patients with septic shock. Crit Care Resusc 2013. 15:83–88.

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***