Student cohort: September 2018

Module code and name: AN 623 – Adult Nursing Skills Underpinning Complex Care

Word count: 3,269

Submission date: 2nd February 2021

Seminar leader: Phil Hoddinott

Module leader: Joyce Williams

Question 2

This essay will consider the management and care of a patient that was admitted to
a ward following complications arising from a diagnosis of community acquired
pneumonia. The patients care will be administered and managed by skilled and
competent registered nurses who are appropriately IV, cannulation and
venepuncture trained and competent. All medications will be documented and
prescribed by a member of the medical team or nurse prescriber. All medications will
be administered in line with the 6 rights of medication ensuring that all IV and
controlled drugs are counter signed by another registered nurse. The patient in
question was admitted with pneumonia; this condition will be explained in depth
alongside discussing the pathophysiology of pneumonia. Using a systematic
approach, the nurse will use an A-E assessment as laid out by Resus Council
(2015), to asses and stabilise the patient through appropriate interventions and
treating the underlying cause while promoting recovery. Following the complications
resulting from pneumonia, the patient has developed sepsis leading to septic shock.
This will be explored in regards to the patient while discussing the pathophysiology
of both. Ongoing care and treatment of the patient will be planned and undertaken by
the nurse. The patient will be treated with dignity and respect in accordance with the
NMC Code (2018), consent will be gained as required by either the patient themself
or next of kin if they are unable to do so. Infection prevention and control will be
maintained throughout and the nurse will wear PPE where appropriate. All
documentation will be updated at all times to ensure accuracy in patient nursing
notes and the nurse will maintain confidentiality in accordance with the NMC Code
(2018).

Pneumonia is an acute inflammation of the lung, resulting from an infection of the

alveoli and small airways. Inflammation and oedema cause the alveoli to fill with
debris and exudate. This exudate quickly fills with neutrophils, erythrocytes, fibrin,
and a solid mass known as consolidation is formed (Pahal et al, 2020). Consolidation
in the alveoli disturbs external respiration and less oxygen defuses from the alveoli
into the pulmonary circulation as a result the patient becomes hypoxic and
tachypnoeic.

Sepsis is defined as a life-threatening organ dysfunction infection that causes the

body to attack its own tissues and organs. Sepsis can lead to multiple organ failure if
not treated and managed quickly (NICE, 2017).

Shock is a state of acute circulatory failure, which results from a number of different
physiological causes. This occurs when there is decreased tissue perfusion and
impairment of cellular metabolism, resulting in the supply and demand of nutrients
and oxygen to cells and tissues becoming imbalanced (Alexiou & Rau, 2020). This
results in inadequate tissue perfusion, caused by reduced circulatory output. The
heart fails to pump sufficiently and fails to remove waste products, therefore
increasing the risk of mortality.

When discussing shock there are five main different types to consider. The main
forms to consider are cardiogenic, hypovolaemic, anaphylactic, septic and
neurogenic. Cardiogenic and hypovolaemic result from a reduced blood flow and
loss of circulating volume. Septic, anaphylactic and neurogenic are collectively
known as distributive, which arises from redistribution of bodily fluid. Distributive
shock, and septic in particular, is the most common form (Koya & Paul, 2020), and
as it is a complication of pneumonia, this is the form that will be considered.

There are, broadly speaking, three stages of shock. Collins (2000) recognises an
initial stage in shock, when oxygen levels decrease and cellular energy production is
hindered. However, this is not universally recognised, and on assessment of a
patient, the clinical signs and symptoms can be difficult to identify at this stage,
whereas Edwards (2001) discusses three stages of shock, compensatory,
progressive and refractory. For the purposes of this essay, only these three stages
will be discussed.

The compensatory stage is where shock can be reversed if diagnosed early enough
and treated with the appropriate interventions. At this stage the body tries to maintain
homeostasis and regain tissue perfusion. In order for the body to maintain
homeostasis clinical signs and symptoms become apparent, therefore making this
stage one of shock. Chemoreceptors in the lungs are sensitive to a drop in oxygen
saturation levels, a clinical sign of this is tachypnoea as the body works harder to
both expel excess CO2 building up and get enough oxygen to the brain, as well as
maintain cell perfusion in order to neutralise the newly acidotic conditions. As there is
a rise in pH in the blood, as well changes in the blood and oxygen flow, this may lead
to an altered mental state, as well as new onset confusion or agitation.

As cardiac volume output falls, circulating volume decreases and the patient’s blood
vessels vasodilate. The body, in making an effort to increase blood volume,
increases heart rate, resulting in the patient becoming tachycardic. A large reduction
in circulatory volume results in hypotension. Here the sympathetic nervous system is
trying to regulate blood flow and pressure through increase the heart rate, so that
there is greater cardiac output. The patient being tachycardic and hypotensive
triggers the sympathetic nervous systems response, known as “fight or flight,” in
order to maintain homeostasis within the body.

The baroreceptors found in the aortic arch and carotid artery detect the blood
pressure reduction, triggering the adrenal glands, located on the top of kidneys, to
release catecholamines. These combine with adrenaline and noradrenaline to cause
vasoconstriction within the vessels and increase myocardial contractions and cardiac
output as a compensatory mechanism. Adrenaline acts on the beta-receptors found
in the lungs and assists with bronchodilation. Noradrenaline also acts as a
vasoconstrictor.
As a result of the fall in cardiac output, the renal system will also be impacted. The
baroreceptors detect the hypotension and poor perfusion to the kidneys, which
triggers the Renin Angiotensin Aldosterone System (RAAS) in an attempt to restore
fluid volume and maintain blood pressure (Atlas, 2007). This causes the kidney to
release renin which converts angiotensinogen into angiotensin 1, which is then
metabolised into angiotensin 2, a vasoconstrictive hormone, that increases both
systemic blood pressure and renal perfusion. The resultant angiotensin 2 stimulates
the adrenal glands in order to produce the hormone aldosterone which will prompt
reabsorption of sodium. Therefore, more water is drawn back into the blood helping
to maintain and increase circulating volume, and as a result urine production
decreases. Angiotensin 2 also stimulates the pituitary gland and the anti-diuretic
hormone (ADH) is released which also increases thirst (Edwards, 2001).

The Progressive stage commences when compensatory mechanisms have failed to

maintain tissue perfusion. Early intervention at this point can reverse the shock,
however if treated incorrectly, there will be additional loss of cardiac output leading to
multiple organ failure due to poor perfusion.

As a result of increased capillary permeability, fluids cross from intravascular to

interstitial space, leading to an increase in both concentration and viscosity of the
blood. The increase in permeability of the pulmonary capillaries causes pulmonary
oedema, meaning the patient will develop cool and clammy skin at the extremities.
The body is no longer able to respond to catecholamines, adrenaline and
noradrenaline, causing a reduction in systemic vascular resistance, leading to
hypotension. This leads to the body functioning in anaerobic metabolism, resulting in
metabolic acidosis, a consequence of production of lactic acid. This causes the body
to become acidotic. If metabolic acidosis is prolonged, adenosine triphosphate levels
reduce, leading to concentration of sodium in the cells resulting in poor functioning
as the cells deteriorate. Gradually the body is no longer able to maintain balance to
protect the vital organs.
As shock progresses, histamine and prostaglandin are released causing
vasodilation, and further decrease peripheral vascular resistance, causing reduced
blood flow to the heart. This leads to additional decreases in cardiac output and
blood pressure, resulting in cellular hypoxia. Hypoxia can impact on the vasomotor
centre of the brain, causing an alteration to mental state and decrease in
consciousness level. As the heart becomes ischemic it also becomes irregular and
tachycardic. Multi organ failure will begin due to limited perfusion. This leads to the
next stage.

The refractory stage sees continued falls in blood pressure and pulse, resulting in
inadequate tissue perfusion, causing the failure of the body to respond to any further
treatments or therapy. Severe tissue hypoxia, ischemia and necrosis to the organs,
alongside respiratory failure, acute kidney injury and acidosis combine to cause
multiple organ failure. The body becomes ultimately unresponsive to
pharmacological intervention and death occurs. This stage is irreversible.

In order to prevent further deterioration in the patient, there are a number of tools
clinicians can use to asses patient. Nurses can utilise the quick Sepsis Organ Failure
Assessment (QSOFA, no date). This tool uses three criteria to judge when a patient
is at risk of sepsis, scoring from zero to three. One point is assigned for each of:
tachypnoea greater than 22 resps per minute; hypotension, or systolic blood
pressure below 100mmHg; and a reduction in consciousness, indicated by change in
GCS.

While this is a valuable tool, it is important to consider the full range of clinical
presentations to ensure an accurate assessment as these could be the results of
other conditions. Churpek et al (2017) state that other tools, such as NEWS2 (NHS
England, 2017) provide a more complete picture of the patient’s clinical state and
make for better outcomes. NICE (2017) recognises increased oxygen therapy to
maintain saturation above 92% in non-COPD patients, cyanosis of lips, skin or
tongue, and failure to pass urine in previous 18 hours as high-risk signs of sepsis.

According to the Sepsis Trust UK (No date), there are five sepsis related deaths
every hour in the UK. It is therefore of critical importance for nurses and other
clinicians to recognise sepsis early to reduce this rate.

Following the initial assessment, the nurse would gain consent to carry out an A-E
assessment, ensuring dignity and respect for the patient throughout (NMC, 2018).
This is a systematic approach to provide a baseline for the nurse and aids planning
of ongoing care and establish changes to the patient’s condition. It also highlights if
emergency interventions are needed (Resuscitation Council, 2015). Where possible,
the nurse communicates the findings and interventions with the patient. From looking
at recent observations the nurse at this point should inform senior staff/ Nurse in
charge as there is sepsis red flags that are identified and to get them to review.

The assessment will begin with the airway. As there is no sign of obstruction and the
patient is communicating clearly, the airway is patient (Dougherty et al, 2015).
Obstruction of the upper airway is a medical emergency, if the nurse believes that
the patients airway is obstructed then urgent expert help is needed immediately, in
order to prevent further deterioration.

Once the airway is patent, breathing will then be assessed. The nurse will assess the
patient by using the look, listen and feel approach for no more than ten seconds. The
nurse would also assess the patients position in the bed and ensure that they are
sitting at a 45–90-degree angle to inspire lung expansion (Dougherty et al 2015).
The patient has a respiratory rate of 27 resps per minute, considered tachypnoeic.
Oxygen saturation will be measured using a pulse oximeter, currently reading 89%
on room air. Therefore, as an emergency intervention the nurse will give 15l of
oxygen via a reservoir mask (O’Driscoll et al, 2017). This will be prescribed on the
drug chart along with the target oxygen saturation, for a sepsis patient this is 94-
98%. The nurse will auscultate the chest, possibly hearing cracking. Chest
expansion will be examined and the patient should show equal depth and pattern
across the chest cavity. The nurse should reassess airways to ensure it is still patent
and reassess SpO2 levels aiming between 94-98%. The nurse will then move on to
circulation.

At this point the nurse will insert a cannula for IV access using the Aseptic Non-
Touch Technique, using a size 14 or 16 gauge for emergency accesses. The blood
pressure reading is 87/40mmHg, therefore hypotensive, most likely due to arterial
vasodilation. In this case, a stat dose of 500ml of sodium chloride over 10-15
minutes will be prescribed and administered by the nurse. After reassessing the
patient, if blood pressure still has not risen, then another 500ml can be prescribed
and given stat. This will be repeated if systolic blood pressure does not increase to at
least 90mmHg.

Next, the nurse will access the heart rate by feeling the carotid pulse to assess its
quality, if it is regular or irregular, strong or weak. The patient's heart rate is currently
120 beats per minute. This referred to as tachycardia due to the heart compensating.
After the fluid challenge is given, the heart rate will need to be assessed. Capillary
refill time can be assessed to indicate the state of blood flow in the body. Currently,
the patient’s refill time is 5 seconds, indicating a significant reduction in blood flow.
The nurse can visually assess for peripheral cyanosis, as inadequate perfusion
permits oxygen extraction by the tissues resulting in a blue tint to the extremities. To
measure urine output, a catheter will be inserted to monitor the patient's hourly
output rate, which should equal 0.5ml/kg/hr. This provides an accurate means of
monitoring output of the patient, and along with a fluid balance chart is the most
effective way to measure accordingly.

Assessing disability will involve a rapid assessment of the patient’s neurological

status, this includes ACVPU- this will measure the patient’s level of consciousness,
along with Glasgow Coma Scale. If the patient is not fully alert or is below 15 on the
GCS an SBAR should be carried out by the nurse explaining the situation,
background, assessment and recommendation to the medical team. The pupils
should be checked to ensure that the patient’s pupils are equal and reacting to light.
Additionally, capillary blood glucose levels should be checked by the nurse or a
trained HCA. NICE (2020) recommends 5-7 mmol/l before breakfast, 4-7 mmol/l
before other meals, and between 5-9 mmol/l up to 90 minutes after a meal. Finally,
an initial pain assessment will be taken by the nurse and shared with the doctor to
know what analgesia needs to be prescribed

Finally, exposure can be safely assessed once airways, breathing, circulation and
disability have been completed. The nurse undertakes a full head-to-toe assessment
of the patient, checking for obvious wounds or bleeding as well as confirming
integrity of pressure areas. Swelling of the legs should also be checked for, as well
as signs of deep vein thrombosis. The temperature of the patient will be checked and
recorded, in this case a reading of 39 degrees is obtained. Pyrexia has been
identified as a key indicator of sepsis in a patient (Gao et al, 2017). IV paracetamol
can be administered to lower the temperature and assist with pain. The nurse should
investigate for allergies in the patient, particularly penicillin, when administering a
prescribed antibiotic.

Based on the patients NEWS2 (2017) score of 12, the nurse will initiate an SBAR
(Smith et al, 2020) as an escalation recommending that a member of the respiratory
team come and review the patient alongside the critical care team as serious
interventions and recommendations are needed by the nursing team. The nurse will
have to focus on ongoing care for this patient by initiating continuous monitoring of
the patient’s condition, watching for any changes that might arise.

Following the assessment, the team can plan and undertake interventions as
required, and manage the care of the patient further. The Sepsis 6 bundle was
introduced to the NHS in 2006 (The UK Sepsis Trust, no date). This tool is based on
the principle of three in and three out for the patient. The nurse should take blood
cultures to find out the source of infection and provide a guide to treatment. A broad-
spectrum antibiotic should be administered IV as the patient has pneumonia.
Ciprofloxacin is commonly used in the diagnoses of pneumonia, primarily because it
is safe to administer since it is unrelated to penicillin and therefore is appropriate to
use in patients allergic to penicillin.

Lactate levels should be measure by a competent professional, a level above 2mmol

is a red flag for sepsis (Fan et al, 2016). This is an indication of poor tissue perfusion
and anaerobic metabolism; therefore, high flow oxygen should be administered and
oxygen levels monitored via the oximeter. This is due to the patient most likely being
at the compensatory stage and tissues are beginning to lose oxygen and tissue
perfusion and struggling to maintain adequate oxygenation in the blood.

The next step is to give fluid challenge. This was initially commenced during the A-E
assessment, and as it goes on blood pressure and urine output should be monitored
continuously. The catheter already inserted and proper maintenance of a fluid
balance chart will assist with this.

Finally, blood cultures should be taken. Additionally, an arterial blood gas should be
taken by a trained member of staff to determine the current pH of the blood along
with the current O2 and CO2 levels. Further blood tests such as full blood count,
creatinine-reactive protein and white blood cell will display infection markers (Fan et
al, 2016). This will assist the medical team in determining the most appropriate
antibiotic to administer in preference to the broad-spectrum being delivered initially.
Further, a group and save, liver function test, clotting screen and urea can indicate
the quality of current renal function.

Reviews by the respiratory team and critical outreach team may be required to plan
an appropriate care plan for the patient. The nurse will implement this and provide
input and suggestions where appropriate. This may include a patient transfer to HDU
or ICU bed in order to carry enhanced treatment or care. The nurse should ensure to
communicate effectively with the family members and next of kin of the patient and
ensure they are fully updated on the care plan without any medical jargon being
used so they are fully aware of the situation.

It may be necessary for the patient to be provide anti-coagulant therapy, such as

apixaban or dalteparin, as the patient may not be able to mobilise effectively
unaided. It may also be necessary to implement an acute kidney infection care plan,
as septic shock puts the patient at high risk developing this (Peerapornratana et al,
2019). The patient should also be screened for MRSA as part of the admission
process, as this will minimise the possibility of the patient acquiring or passing on a
hospital required infection. A chest x-ray may also be required once the patient
begins to stabilise in order to assess the progression of the pneumonia.

To conclude, it is essential for the nurse to act quickly, confidently and competently
in using their skills when managing a deteriorating patient. Escalating appropriately
by informing senior staff, carrying out an SBAR and contacting the critical outreach
team are essential progressions to maximise the patient's chances of recovery. If
these assessments and treatments are initiated with adequate rapidity, the patient's
blood pressure should rise to at least above 90 mmHg. Heart rate, temperature and
capillary refill time should return to normal parameters as the medications and
therapies take effect. It should be possible to gradually titrate the oxygen flow down
as resp rate and oxygen saturation levels return to normal. As such, the patient
should stabilize and will be transferred to a HDU bed for closer monitoring with the
appropriate documentation. Due to effective inter-professional collaboration the
patient should eventually make a full recovery.
References

Alexiou, A., Rau, C., (2020) ‘Shock,’ BMJ Best Practice. Available at:
https://bestpractice.bmj.com/topics/en-gb/3000121

Atlas, S. A. (2007). The Renin-Angiotensin Aldosterone System: Pathophysiological

Role and Pharmacologic Inhibition. Journal of Managed Care Pharmacy, 13(8 Supp
B), 9–20. Available at: doi:10.18553/jmcp.2007.13.s8-b.9

Churpek, M. M., Snyder, A., Han, X., Sokol, S., Pettit, N., Howell, M. D., & Edelson,
D. P. (2017). Quick Sepsis-related Organ Failure Assessment, Systemic
Inflammatory Response Syndrome, and Early Warning Scores for Detecting Clinical
Deterioration in Infected Patients outside the Intensive Care Unit. American journal
of respiratory and critical care medicine, 195(7), 906–911.
https://doi.org/10.1164/rccm.201604-0854OC
Dougherty, L., Lister, S., West-Oram, A., (ed) (2015), Royal Marsden Manual of
Clinical Nursing Procedures 9th ed, Chichester, The Royal Marsden NHS Trust

Edwards, S. (2001). Shock: types, classifications and explorations of their

physiological effects. Emergency Nurse, 9(2), 29-38. Available at:
doi:10.7748/en2001.05.9.2.29.c1359

Fan, S. L., Miller, N. S., Lee, J., & Remick, D. G. (2016). Diagnosing sepsis - The
role of laboratory medicine. Clinica chimica acta; international journal of clinical
chemistry, 460, 203–210. Available at: https://doi.org/10.1016/j.cca.2016.07.002

Koya, H. H., Paul M. Shock. [Updated 2020 Nov 21]. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK531492/

NICE (2017), Sepsis: Risk Stratification Tools. Available at:

https://www.nice.org.uk/guidance/ng51/resources/algorithm-for-managing-
suspected-sepsis-in-adults-and-young-people-aged-18-years-and-over-in-an-acute-
hospital-setting-2551485715 (NICE 2017)

NICE (2020), Testing Your Own Blood Glucose, and Target Levels. Available at:
https://www.nice.org.uk/guidance/ng17/ifp/chapter/testing-your-own-blood-glucose-
and-target-levels#:~:text=Target%20blood%20glucose%20levels,-Blood%20glucose
%20levels&text=To%20minimise%20your%20risk%20of,other%20times%20of
%20the%20day.

Nursing and Midwifery Council (2018), The Code page 8, section 5. Available at:
https://www.nmc.org.uk/standards/code/read-the-code-online/#third
O’Driscoll, B.R., Howard, L.S., Earis, J., Mak, V., (2017) British Thoracic Society
Guideline for oxygen use in adults in healthcare and emergency settings. BMJ Open
Resp Res Available at: doi:10.1136/ bmjresp-2016-000170

Pahal P, Rajasurya V, Sharma S. Typical Bacterial Pneumonia. [Updated 2020 Aug

15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK534295/

Peerapornratana, S., Manrique-Caballero, C. L., Gómez, H., & Kellum, J. A. (2019).

Acute kidney injury from sepsis: current concepts, epidemiology, pathophysiology,
prevention and treatment. Kidney international, 96(5), 1083–1099.
https://doi.org/10.1016/j.kint.2019.05.026

Quick Sepsis Organ Failure Assessment (No date), What is qSOFA?. Available at:
https://qsofa.org/what.php

Resuscitation Council (2020), The ABCDE Approach. Available at:

https://www.resus.org.uk/resuscitation-guidelines/abcde-approach/

Smith, G., Allan, A., Gordon, P. A. L., Peet, H., Quint, M., Sadler, P., Sayer, N.,
Sced, A., Thomas, R., Brennan, P. A., Blakely, S., Davies, P., Robson, J., Austin, R.,
Stockwell, B., Wood, L., Smale, M., (2020), Acute Life-Threatening Events
Recognition and Treatment. 5th ed, Cosham, Portsmouth Hospitals NHS Trust.

The UK Sepsis Trust (No date), How Did the Sepsis 6 Come About? Available at:
https://sepsistrust.org/professional-resources/clinical/
The UK Sepsis Trust (No Date) About Sepsis. Available at:
https://sepsistrust.org/about/about-sepsis/