Coda Change

Michael Perlmutter guides you through the prehospital diagnosis and treatment of sepsis.

Sepsis is a difficult diagnosis to make. Even in the hospital, where a plethora of tests are available to assist the clinician.

The diagnosis remains a challenging one, due to the very nature of sepsis. A shadowy shape-shifter notorious for its ability to hide in plain sight.

For now, even in-hospital, there is no test with perfect sensitivity or specificity for sepsis.

This is especially true in the prehospital environment, where we must rely on tools we can bring into the field: physical exam, point of care tests (lactate/venous gas), assessment of end-tidal CO2, and ultrasound.

First, early diagnosis of cases ranging from early sepsis to septic shock. Point of care testing is essential.

Measurement of EtCO2 serves two purposes: as a reasonable surrogate for lactate and providing an accurate respiratory rate. A vital sign that is notoriously poorly assessed.

Respiratory rate plays a key role in both SIRS and SOFA/qSOFA criteria for sepsis, making an accurate count essential. Ultrasound should also play a pivotal role in prehospital sepsis management.

Much has been made of the prehospital FAST exam, however, the ability of POCUS to gauge fluid responsiveness and cardiac function is far more useful.

Assessment of the IVC may aid in determining the value of volume resuscitation by helping to identify patients who are responsive to volume and those who would be better served by early initiation of vasopressors.

Similarly, assessment of cardiac function may prove extremely useful in selecting a pressor. POCUS may also assist in differentiating sepsis from other aetiologies by identifying a source, such as pneumonia. The second fundamental aim is treatment equivalent to that available in-hospital. This includes judicious administration of balanced IV fluids guided by POCUS and clinical assessment of fluid responsiveness, early pressors, and early antibiotics, particularly where transport times are significant.

When sepsis is diagnosed by EMS, a "sepsis alert" should be communicated to the receiving hospital, to facilitate ongoing early, aggressive care upon arrival of the retrieval team.

Advanced prehospital diagnosis and treatment can produce dramatic reductions in mortality from sepsis.

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Endothelium was once thought to be an inert organ. However, it plays an important role in multiple functions. These include coagulation, inflammation and determination of vascular permeability.

He then gives a brief overview of the endothelial arrangement, function of the glycocalyx layer and how an injury causing a loss of the protective layer results in holes in the endothelium. The inflammatory cells enter via these holes and causes oedema in the affected organs leading to multiple pathologies.

Activation of cortactin protein and the myosin light-chain kinase (MLCK) enzymes activate stress fibres resulting in pulling of endothelial cells thereby increasing its permeability.

Danny discusses the role of endothelial dysfunction in acute respiratory distress syndrome (ARDS) at macrovascular, microvascular and molecular levels. Macrovascular thrombosis is related to an increase in severity of ARDS, pulmonary hypertension, and mortality.

At a microvascular level there is a loss of vascularity and increased blood vessel thickness. At a microscopic level, endothelial cells appear swollen and damaged in ARDS. Endothelial dysfunction drives organ dysfunction and mortality. Changes in various endothelial markers like increased von Willebrand factor (vWF), decreased protein C and increased pulmonary dead space correlate with increased mortality.

Studies show that endothelial dysfunction is a more specific and sensitive method to predict mortality of critically ill patients when compared to SOFA score, SAPS 2 score and WCC. Danny discusses ventilator strategies for endothelial cells in ARDS patients. Lowering the tidal volume of ventilators and employing recruitment manoeuvres are such strategies.

Both of these cause a decrease in oedema by reducing endothelial permeability. He then shares the various potential pharmacological treatments for treating endothelial damage. These include statins and spingosine-1-phosphate (S1P). Different studies on the effect of statins in ARDS show contradicting result.

However, targeted therapies can be designed by studying the phenotypes and molecular basis of ARDS in each patient.

The role of the endothelium as a mediator of critical illness by Danny McAuley

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Bill Knight explains the concept of death by neurological criteria and the complexities surrounding organ donation in such situations.

Bill discusses the process of dying, the definition of death, how to approach the neurologically dead patient and how to consider organ donation.

Due to advancements in medical technology and processes, the definition of death is a challenging one.

Bill talks at length about the definition of death by the neurological criteria. Dying is an active process, whereas death is an event.

The acceptance of death by the neurological criteria is often challenging as Bill will highlight. Bill talks about the care of the dying or dead patient.

There is an alignment of parallel intentions – first and foremost resuscitation of patients and then failing that, proceeding to considering and actioning organ donation. This is important due to the shortage of viable donor organ worldwide.

The donation process itself is complex. Bill provides his thoughts. He insists that an intensivist be involved as this has been shown to increase the number of viable and healthy organs made available.

The timing is also important. Available evidence does not support the need for immediate procurement after brain death. Taking time to optimise perfusion and allow recovery and cardiac function is appropriate and should be done.

Bill also discusses other treatment options at the time of death such as optimising endocrine function.

Finally, Bill will provide some practical considerations when communicating with the dead patient's family. This involves being clear on your messaging. You are supporting organs, not life.

To reinforce this point, Bill suggests not examining or talking to the patient. He also recommends using all of the available hospital support services.

Similarly, it is best to not introduce the topic of organ donation to the family yourself as the treating clinician. Utilise the Organ Procurement Organisations (or similar services) and get them involved early to speak with the family.

Join Bill Knight in his talk on the North American perspective on Organ Donation, brain death and management of the brain dead donor prior to organ donation.

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Greg Kelly focuses on transferable skills from adult practice applicable to the collapsed neonate, taking us first through a systematic approach to the common underlying causes and the physiology behind them. He outlines a comprehensive approach to the clapped out baby even when the underlying cause isn't immediately clear and reassures us that there are plenty of simple interventions we can undertake.

Allow me to introduce to you this extraordinarily talented doctor. John Hinds became involved in our motorcycle racing medical team as a medical student and progressed to inspirational teacher and natural leader. He had a burning passion for improving the care of the injured and on qualification it was evident he was destined for greatness within the world of critical care. In his role as Delta 7 for the Northern Ireland Ambulance Service and as a travelling doctor at motorcycle races in Ireland Doc John brought the highest standards of care and compassion to the most unfortunate at their hour of greatest need. I took this young man as my pupil teaching him the role of motorcycle doctor and quickly realised this exceptional doctor was truly special. In truth the pupil quickly became the master and I had the privilege of 15 years of working alongside him as his wingman.

Where does the abdominal assessment occur when you manage a paediatric trauma patient? Warwick Teague challenges us to stop just leaving it to the paediatric surgeon as he talks us through his approach to the abdomen in a paediatric trauma, including the key aspects of assessment and treatment - so simple, he says, even a surgeon can do it.

Trish Woods guides you through some clinical pearls in the intensive care management of neonates.

The complex physiology of the transitioning required in the journey from foetal life to neonatal presents many challenges and scary moments.

Many things can go wrong in the neonatal period as babies transition to life in the real world. Trish highlights her thoughts on the use of positive end expiratory pressure (PEEP), how deep to intubate, when to clamp the cord and the use of ultrasound.

When babies arrive early their lungs can be full of meconium or fluid. Due to this, Trish recommends using PEEP – without which there is distal airway collapse and fluid accumulation.

Aeration of the lungs is vital. To this end, how deep should intubation be aimed? The depth may not be overly important. This is because regional lung aeration triggers widespread, global increase in pulmonary blood flow.

There is little definitive evidence to guide clinicians on when to clamp the cord – early or late. Trish recommends considering the physiology of clamping the cord.

After clamping the cord there is a massive drop in cardiac output. Ventilatory support will turn this around – something to remember.

In a compromised baby, perhaps we should aim to clamp the cord sooner and then initiate ventilation.

Finally, Trish highlights the utility of ultrasound. Viewing the heart and lungs provides crucial information for the clinician.

Furthermore, Trish discusses actively looking for aeration, collapse, consolidation and pneumothorax in the lungs and thorax.

Overall, don't forget the essentials. Trish reminds you to keep life sweet, warm, and tempting and help neonates to transition into the big world.

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Deirdre talks 'bad blood' – the complex world of critical care haematology. Critically ill patients frequently have activation of inflammatory and clotting pathways. These are likely adaptive responses in the human. When they run riot, or the fine balance between pro- and anti-inflammatory states is shifted, there can be significant morbidity and mortality. Deirdre presents three patients to highlight these issues and what you can do about it. This acronym-busting talk will focus on some acquired haematological disorders in critically ill patients. Platelets make up a tiny percentage of blood – just 0.01%. However, they have a crucial role to play. A low platelet count can be due to reduced production or increased destruction. Disseminated Intravascular Coagulation (DIC) is a clinical and laboratory diagnosis that affects about 1% of hospitalised patients. At the most severe end it is associated with bleeding and/or thrombotic complications. Disorders such as thrombotic thrombocytopenia purpura (TTP) and other forms of micro-angiopathic haemolytic anaemia (MAHA) will also be described including the role of ADAMST13. The knowledge of what is what, is critical, as it will dictate treatment. Heparin-Induced Thrombocytopaenia (HIT) is an uncommon but important condition which is difficult to diagnose in a critically ill patient. It is a heparin dependent pro-thrombotic disorder. There is no good test for HIT. Have you always wondered about NETs (neutrophil extracellular traps) and their importance? If so this whistle-stop tour of non-malignant hematology in the ICU is for you! Deirdre drives home the message that low platelets are common in the critically ill and the causes are multifactorial.

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Mervyn Singer discusses the use of biomarkers in critical care. Multiple biomarkers - physiological, biochemical, biological - can prognosticate early in critical illness, even in the ED. These biomarkers are numerous - lipids, progesterone, troponin, thyroid stimulating hormone, inflammatory cytokines, mitochondrial dysfunction… so on and so forth! Prognostication can happen as early as the Emergency Department. Studies from the States have found high levels of inflammatory cytokines can predict death, separately from clinical presentation. Therefore, we can predict when critically ill patients are destined to die. So, does this mean that we are just prolonging the life of those destined to die in critical care? Perhaps. Mervyn discusses this being the possible reason for many failed ICU studies. Concurrently, the only progress in critical care in the past 20 years may be due only to less iatrogenic harm. Furthermore, he explains his experiments with rats demonstrating the use of cardiovascular parameters, cytokines, troponins and even cholesterol being accurate prognostic biomarkers. Then, Mervyn goes on to identify the use of steroids in sepsis. He talks about research that demonstrates a benefit to steroid use, but only in those patients predicted to die using the aforementioned biomarkers. This could be a key to selecting an appropriate patient group to allocate a specific treatment too. Furthermore, we examine treating sepsis with beta blockers. Giving beta blockers to everyone has no effect at best and a harmful effect at worst. However, giving beta-blockers to those who were predicted to die conferred benefit! In conclusion, we can predict outcome early in disease. This may allow better selection of patients for certain treatments! We thus need to adopt a completely different strategy for such patients predetermined to die. This also applies to trial design, especially where survival is the endpoint.

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Jim Manning presents the how and why of adrenaline in cardiac arrest. The use of adrenaline in cardiac arrest resuscitation has been popular since the 1960s. Laboratory studies and anecdotal experience showed improved rates of return of spontaneous circulation (ROSC) with the use of adrenaline at small dosages. This led to the widespread adoption of adrenaline administration during cardiac arrest into every resuscitation guideline for decades to come. Extensive laboratory studies characterised the beneficial physiological effects of adrenaline during cardiac arrest and closed-chest cardiopulmonary resuscitation (CC-CPR). Adrenaline administered during CC-CPR results in peripheral arterial vasoconstriction that raises the aortic pressure. Particularly during the relaxation phase of CC-CPR. This increase in aortic pressure results in an increased aortic to right atrial pressure gradient that drives blood flow to the myocardium during CC-CPR. This pressure gradient is known as the coronary perfusion pressure (CPP) and this correlates with ROSC in laboratory investigations and clinical studies. During the 1990s, the use of "high-dose" adrenaline showed increased rates of ROSC compared to "standard-dose" adrenaline. However, larger doses of adrenaline did not result in improved survival. Recent meta-analyses have raised serious questions about the value of adrenaline. Notably, showing a benefit for achieving ROSC but no clear evidence of improved long-term survival. Controlled clinical trials to address this question are now underway. However, there is another important issue that needs to be addressed: the "route" of administration. With the growing interest in endovascular resuscitation, the use of intra-aortic adrenaline titration offers a means of rapidly and effectively delivering adrenaline to peripheral arterial effector sites while providing arterial pressure and CPP monitoring to guide titration of adrenaline doses to achieve an optimal hemodynamic effect while avoiding excessive adrenaline doses.

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