Sepsis – A Guide for New Nurses and Student Nurses in Emergency Care - Critical Care Practitioner


Sepsis – A Guide for New Nurses and Student Nurses in Emergency Care

Guest Post by Tom Hreben

This is from the eyes of an ED nurse writing about sepsis for newly qualified nurses and those new to emergency care settings who may not have had much exposure to sepsis.  

This is designed to give people an overview but not to be the answer to all.

For those you need to be going to your textbooks and the primary literature.

The joy of #FOAMed and #FOANed is that it is an excellent primer for a subject which stimulates someone to seek out and evaluate the primary literature for themselves.

What is sepsis?

Sepsis is the body’s systemic response caused either by a suspected or confirmed infection from a bacterial source. To make the diagnosis of sepsis, two or more of the SIRS criteria must be found with a possible or confirmed focus or foci of infection. [Creed & Spiers, Gupta et al, Jevon & Ewens 2012]

Case Study

Here is a case study based upon the patients I have experienced thus far in my career.

This is typical of what you might see either in the Emergency Department or the Medical Assessment Unit.

This is a seventy-five-year-old male brought into the emergency department via ambulance who pre-alerted the receiving department on the suspicion of sepsis and poor vital signs.

PC – Increasing shortness of breath and productive cough

HPC – Started five days ago, seen by GP and started on oral antibiotics two days ago. Became increasingly unwell despite antibiotics.

PMHx – COPD, T2DM, venous leg ulcer and HTN

DHx – salbutamol PRN, carbocysteine 375 mg TDS, tiotropium BD, metformin 1g BD, amlodipine 5mg OD, Ramipril 2.5mg OD. No known drug allergies.

O/E – Speaking in short sentences

Accessory muscle use

Purulent sputum

No obvious deficits in chest expansion

Global wheeze and crackles mid to base on right-hand side. Dullness on percussion to mid and lower right side.

Observations: BP 90/45 HR 130 CRT 6s SpO2 82% on air, respiratory rate 32, temperature 38.6 degrees.

This patient clearly meets the SIRS criteria being pyrexic, tachycardic and tachypnoeic. The purulent green sputum suggests the chest as a focus of infection, this is reinforced by the previous treatment and diagnosis of a lower respiratory tract infection by the patient’s GP.

Assessment of the Septic Patient

As with any critically ill patient, follow the ABCDE framework.


My personal preference is to conduct two ABCDE assessments, almost in a trauma style primary and secondary survey type of thing.


My reasoning is thus, a quick hello and how are you can give you an idea of a patient’s ABCDE state. I do this to tell me is this patient going to arrest on me in the next thirty seconds and do I have enough time to go into a more detailed assessment following handover?

During my secondary assessment I can then take more time and be more thorough.

I also document my assessment in the ABCDE framework. It’s logical, allows you time to think and makes it harder for you to omit details in both examination and documentation of findings.

A – patent

B – Tachypnoeic with respiratory rate 32, SpO2 84% on air, equal chest expansion. Global wheeze and crackles mid to base on right side. Dullness on percussion to mid and lower right side.

C – BP 90/45 HR 130 CRT 6s, cold to touch.

D – Alert, blood glucose on venous blood gas 14.5 mmol/l

E – temperature 38.6 degrees

Basic investigations – blood cultures, clotting screen, full blood count, urea and electrolytes, liver function, C-reactive protein and a venous blood gas. Urinalysis and send for culture. Are they confused? Measuring of urine output is needed. Often a catheter is required for an accurate fluid balance

Management of the Septic Patient

The management of sepsis needs to be aggressive.

The need for this aggression is first recognised and then made into protocol by Rivers et al 2001. The way in which we aggressively manage septic patients has gone from the Early Goal Directed Therapy (EGDT) started by Rivers et al 2001 to bundle directed approaches advocated by Dellinger et al 2013.

ProCESS, ARISE and PROMISe have validated the need to manage sepsis aggressively, however they have cast doubts on the validity of EGDT.

That said, the principles of aggressive sepsis management established in EGDT have been validated and are still most pertinent. I do feel that some of the interventions that the Rivers et al [2001] study might make patients appear more unwell than they actually are through mandating things such as central venous access and such like. Although it has given us EGDT which forms the basis of good quality sepsis care, the reevaluation that has been provided by ProCESS and the like has been needed.

This is the evolution of sepsis care, we needed to make interventions and create EGDT but now we are looking at can it be done better or to look at the individual aspects of care that was advocated by Rivers et al [2001].

One thing I feel strongly about in regards to monitoring is the use of central venous pressure to guide fluid resuscitation.

It isn’t useful or really an accurate reflection of a patient’s fluid status as it is dependent on so many variables. Further to that it’s been shown that it isn’t suitable to monitor fluid status. Following that, when we have adequately fluid resuscitated patients but without desired effect, the decision to then use vasoactive drugs is made based on MAP as opposed to CVP.

CVCs however, are not without their place. They are very useful for administering drugs, especially vasoactive drugs as there is no research to suggest that vasoactive drugs can be administered peripherally for any significant period of time (a subject debated by REBELEM and EmCrit, well worth looking at) [Rezaie 2015, Weingart 2013]; a multiple lumen line offers the chance to have one access point but being able to infuse many things through it.

Sepsis management ultimately boils down to the aggressive control of the source of infection with the early administration of IV antibiotics (initially broad spectrum then more specific to source and causative organism). Adequate fluid resuscitation is vital, the rest of care involves supporting the patient’s systems.

High-quality nursing care is essential to ensuring the best possible outcome for these patients. This type of patient can be very resource intense in terms of nursing based around time consuming and complex interventions that can be required.

Management Tips

Big cannulas and lots of them. I get my first set of bloods when I’m cannulating patients. I also get a venous blood gas so I can ascertain lactate levels.

The reason I choose big cannulas is these patients need large volumes of fluid, this is best administered through large bore cannulas.

Ideally I have one or two big bore lines for my volume resuscitation and then a further smaller line which I can dedicate to drugs such as antibiotics and paracetamol for fever control. Given some drugs such as gentamicin are unsuitable for administering as a bolus having a line purely for drugs seems prudent because you are not then using your sole access for one infusion which may or may not be compatible with other infusions.

By large bore lines I mean eighteen gauge (green) or bigger.

Cardiac monitoring is helpful to show rate and rhythm. This can show electrolyte imbalances as well and suggesting that someone is responding to fluid resuscitation. Also these monitors can calculate mean arterial pressure.

This is essential as it helps determine if vasopressors are going to be required [Gupta et al 2015, Rivers et al 2001, ProCESS 2014, Cutler & Cutler 2010] Additionally I would throw in a caveat of be wary of an apparently normal blood pressure.

Take the context of the case study above, a person who is hypertensive normally and runs with a systolic blood pressure around 160 mmHg yet presents with a blood pressure of 110/60 mmHg suggests profound hypotension. A trial from France shows that fluid resuscitating patients known to be hypertensive to a higher MAP than non hypertensive patients made no difference to outcome [Asfar et al 2014].

Additionally don’t be fooled by a normotensive and apparently well looking patients until you’ve seen what their lactate is doing, more on lactate shortly [RCEM 2015].

Many sources advocate high flow oxygen for septic patients, regardless of if they have COPD or not. I would be more cautious, putting someone with COPD into type two respiratory failure is a problem that they do not need.

Titrate your oxygen therapy. I can understand that there is an increased need for oxygen driven by increased metabolic demand, however, there are some patients to whom applying high flow oxygen to requires a little more thought and consideration of the risks versus the benefits of this.

Potentially, in those known to retain their carbon dioxide I would say aim for saturations as you would following BTS emergency oxygen use but aim for the upper end of 88 – 92% using Venturi masks. Nasal cannulae are the things of the devil as far as I am concerned.

My rationale for that is that these things deliver such a varied FiO2, this is due to the ventilatory volumes of a patient, how they breath and their breathing patterns. I cannot closely control the FiO2 in the same way I can if I were using a Venturi type system.

Ten percent of COPD sufferers will have type two respiratory failure. Forty to fifty percent of COPD patients are at risk of going into type two respiratory failure [Leach 2014]. As you can see this is strong ground to be very vigilant in regards to administering oxygen.

Nasal cannulae are the things of the devil as far as I am concerned. My rationale for that is that these things deliver such a varied FiO2, this is due to the ventilatory volumes of a patient, how they breathe and their breathing patterns. I cannot closely control the FiO2 in the same way I can if I were using a Venturi type system.

Ten percent of COPD sufferers will have type two respiratory failure. Forty to fifty percent of COPD patients are at risk of going into type two respiratory failure [Leach 2014]. As you can see this is strong ground to be very vigilant in regards to administering oxygen.

Fluid balance – maintain an accurate fluid balance. The Survive Sepsis campaign recommends catheterising patients to monitor urine output, a surrogate marker for renal perfusion and volume status. That said, I’m no fan of a surrogate marker.

The reason being is that if you can monitor something directly and accurately then why not do so directly as opposed to monitoring it via a proxy which may or may not be flawed. In regards to volume status I’d be more interested in looking at arterial blood pressure, pulse pressures and importantly the mean arterial pressure following interventions such as aggressive fluid resuscitation.

I’d be most interested in MAP as this is used to help determine if a patient requires vasoactive medications following fluid resuscitation.

Lactate. The measurement of this is fundamental. It forms part of the sepsis six. It can also act as a tool to help predict mortality. Essentially, the crux of this is, the higher the lactate, the greater the mortality.

However, more important than that it can help class how severe someone’s sepsis is but it can also reveal a cryptic septic shock in a patient who is apparently unwell, normotensive and not tachycardic. [RCEM 2015, Dellinger et al 2013, NCEPOD 2015]

At the end of the day, you cannot go far wrong if you follow the sepsis six care bundle. So ultimately this initially boils down to giving three things and taking three things. Give oxygen, give broad spectrum antibiotics and fluids. Take blood cultures, measure lactate and monitor urine output. [Dellinger 2013]


I need not reiterate the haste with which sepsis needs to be recognised and managed. Mortality equates to more than forty percent. You are seven times more likely to die as a result of sepsis than you are of an acute coronary syndrome.

We have improved a lot of sepsis care, however as NCEPOD shows, we still have a way to go. [Leach 2014, NCEPOD 2015, RCEM 2015] Sepsis is a condition where you can make a palpable difference and a meaningful intervention within a very short space of time.


Leach R (2014) Critical Care Medicine at a Glance. Third edition. Wiley & Sons; Chichester

Rivers E et al (2001) Early goal directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine 345, 1368 – 1377

Dellinger RP et al (2013) Surviving Sepsis Campaign: international guidelines for the management of severe sepsis and septic shock: 2012. Critical Care Medicine 41 (2) 580 – 637

ProCESS Investigators (2014) A randomised trial of protocol based care for early septic shock. New England Journal of Medicine 380 (18) 1683 – 1693

NCEPOD (2015) National Confidential Enquiry into Patient Outcome and Death: Sepsis: Just say sepsis! Available online at Accessed on 16/12/15

Royal College of Emergency Medicine (RCEM) (2015) A clinical toolkit for Emergency Departments. Available online at Accessed on 16/12/15

Asfar P et al (2014) High versus low blood pressure target in patients with septic shock. New England Journal of Medicine

Cutler L & Cutler J (2010) Critical Care Nursing Made Incredibly Easy. Lippincott Wilkins & Williams; London

Jevon P & Ewens B (2012) Monitoring the critically ill patient. Wiley – Blackwell; Chichester.

Creed F, Spiers C (2010) Care of the acutely ill adult: an essential guide for nurses. Oxford University Press; Oxford

Rezaie S (2015) Mythbuster: administration of vasopressors through peripheral intravenous access. Available online at Accessed on 16/12/15

Weingart S (2013) Podcast 107 – Peripheral vasopressor infusions and extravasation. Available online

at Accessed on 16/12/15

Tom is a registered nurse working in emergency care settings splitting his time between ED and EAU. His passions involve furthering nurse education in regards to physical assessment combined with the assessment and care of the rapidly deteriorating patient.

He also has a keen interest in simulation learning. Tom has an interest in massive transfusion in trauma, having written his undergraduate dissertation on the subject.

Stereotypically lacking in attention span, usually well natured when adequately caffeinated.

Tom studied and now works in Oxfordshire

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