From Injury to Sepsis: A Comprehensive Analysis of Julia's Medical Journey

Introduction

Julia is 68 and has a history of type 2 diabetes (T2DM) hypertension (HTN). She cut her finger whilst weeding her garden. However, whilst in Accident and Emergency (A&E), she felt of pain and tenderness within her lower injured arm. It was discovered that, Julia had cellulites, which led to a significant drop in her vital signs. This suggests that, she is suffering from sepsis. According to Singer et al. (2016), sepsis is a life threatening organ dysfunction initiated by a dysregulated host response to the specific infection. The common cause of sepsis is bacteria either Gram-positive or Gram-negative and sometimes could also be caused by fungal infections (Ashelford et al., 2019). This essay will discuss Julia’s signs and symptoms using ABCDE, NEWS 2, pathophysiology and compensatory mechanism of acute illness attempting to maintain homeostasis. It will then discuss medical and nursing management using evidence based care and SBAR (situation, background, assessment and recommendation). Finally, it will explore the psychosocial care needs involving patient and multidisciplinary team.

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Analysis of signs and symptoms:

Consent would be gained before proceeding to assessment (Royal College of Physicians (RCP), 2017). The ABCDE (airway, breathing, circulation, disability and Exposure) approach will be used by following the look, listen and feel structure (Resuscitation Council, 2015). In addition to this, News 2 will be used to score Julia’s vital signs and finally SBAR to effectively communicate within the team and improve her health (RCP, 2017).

Airway:

Julia’s airway is patent. The evidence is because she is able to talk in full sentences during assessment (Resuscitation Council, 2015).

Breathing:

Julia has an increased RR, which is 28 and News=3. The normal range is from 12-20 as per the RCP (2017).This suggest that she is tachypneic. Tachypnoea is a compensatory mechanism triggered by chemoreceptors that detects changes in the blood potential of hydrogens (pH) and Carbone dioxide (CO2). Then the respiratory centre situated in the brain stem simulateshypercapnia drive increasing RR in order to remove CO2 and improve tissue perfusion (Ashelford et al., 2019).

Julia is also hypoxic because her SpO2 is 91%, News=3. According to RCP, (2017) a normal range for oxygen saturation is 94-98 for non COPD patients.This clearly suggest that she is going into an acute respiratory distress syndrome (ARDS) due to increased capillary permeability filling the alveoli with fluid and loss of compliance, this further causes ventilation and perfusion mismatch (Tortora and Derrickson, 2015).

Circulation:

Julia is tachycardic with a HR of 112 bpm, News=2. The normal range is 60-90 as per RCN, (2017). Tachycardia is a compensatory mechanism due to low BP and this happens when the baroreceptors detects a decrease in stroke volume. This further stimulates the sympathetic nervous system (SNS) to release adrenaline that causes an increase in heart rate, vasoconstriction, heart contractility and cardiac output in order to increase blood pressure (Tortora and Derrickson, 2015).

Julia is hypotensive as her BP is 89/45, News=3 (RCP, 2017). This is due to a major vasodilation and capillary leak caused by the sepsis (Ashelford, et al. 2019).

Julia has hyperpyrexia, because her temperature is 39.2 degrees Celsius, News=2, a normal range is 36.1-38as per the RCP, (2017). This is her body’s response to the infection, caused by pyrogens, which are fever producing proteins stimulated by monocytes and macrophages that work as the body’s defence system by acting upon the thermoregulation centre in the hypothalamus in this process, the cells work hard to fight the infection by product is heat which is released through vasodilation (Jevon, et al. 2020).

Her capillary refill time is 2 seconds that suggests that she has not peripherally shut down. However looking at her vital signs it is very likely to change, because the body will try to compensate for the low blood pressure and will shut down blood from the peripheries to the vital organs by vasoconstriction. The ideal parameter is below 2seconds (Resuscitation Council, 2015). She has already reached the borderline, despite being within normal range.

Her C-reactive protein is above 285mg/l, which clearly suggests that, there is an infection happening and this is useful while monitoring treatment response (Jevon, et al. 2020).

Julia has oliguria because her urine output is 10 mls for the past three hours, whereas she should be voiding more according to her body weight which is 75 kg. As per the Resuscitation Council, (2015), a healthy person should be voiding 0.5ml/kg/h.

She also has a raised lactate level of 6mmol/l, which should have been less than 2mmol/l this clearly suggest that she as a metabolic acidosis as perThe UK Sepsis Trust, (2017).She is likely to be having acute kidney injury due to both oliguria and metabolic acidosis (Ashelford, et al., 2019)

Cellulitis:

Cellulitis is an infection of the subcutaneous layer of the skin caused by bacteria, resulting into: swelling, redness and pain around the affect area and could also spread to other parts such as the blood leading to sepsis as in Julia’s case (NHS, 2018). The cut has led to cellulitis and eventually to sepsis, which will be discussed in the following paragraphs.

Sepsis is when a bacteria enters the body, mast cells detects this and stimulates the production histamine. White blood cells and histamine stimulates more white blood cells to travel to wound area in an attempt to stop the infection. Then neutrophils and monocytes are stimulated to produce cytokines by the endotoxins present on the bacteria cell wall. The cytokines along with the histamine cause a major vasodilation and subsequently reducing the systemic vascular resistance and a drop in BP. Furthermore, leukocytes adhere to the walls of the capillaries to try and eliminate the infection but damage the walls causing endothelial dysfunction then increased permeability. This causes plasma shift from intravascular space to the interstitial space, resulting in a major decrease in circulating blood volume, preload, cardiac output and difficulty in oxygen delivery to the cell from the blood. On the other hand the clothing cascade is triggered by endotoxins in an attempt to block off the gaps in the capillary wall with clots. Along with coagulation activation, fibrinolysis is also is stimulated, which means clots formed within the vessels will not be broken down and can travel in the blood stream as micro thrombi, which obstruct blood flow and eventually leads to tissue hypoxia in vital organs (Ashelford, et al. 2019).Therefore, cells switch from aerobic to anaerobic metabolism which produce lactate, which combines with water to form lactic acidresulting into metabolic acidosis (Tortora and Derrickson, 2015).

This makes Julia at a very high risk of developing acute kidney injury (AKI), not only being at a high risk because of her PMH (if on medication to manage her comorbidities, which might be ace inhibitor for HTN and metformin/ insulin are nephrotoxic), metabolic acidosis (leads to waste build up), oliguria and drop in BP. All this suggest that Julia is having intrinsic kidney injury due to low glomerular filtration rate (GFR) (NICE, 2019). Lewington and kanagasumdra (2011), further stated that, a decreased in circulating blood volume leads to poor renal perfusion and oliguria eventually to kidney tissue damage, as the kidneys are very vascular and also regulates blood pressure. It is also important to know that inflammatory response from cytokines and mediators could directly affect lung function due to fluid build-up into the alveoli resulting into hypoxia, then ventilation and perfusion mismatch, because the oxygen is not able to perfuse through the alveoli into the blood stream leading to hypoxemia and decreased oxygen delivery to cells and tissues (Tortora and Derrickson, 2015).

Compensatory mechanism:

The body responds to a drop in BP in many ways by activating the renin-angiotensin-aldosterone-system (RAAS). The kidneys sense a decreased in GFR, then activates the RAAS. The juxtaglomerular cells in the kidneys detect a decrease in tissue perfusion, then releases renin. The liver on the other hand releases angiotensinogen which combines with renin in order to form angiotensin 1. Angiotensin 1 travels to the lungs where angiotensin converting enzyme (ACE) is released, this then convert angiotensin1 into angiotensin 2. Angiotensin 2 is a powerful vasoconstrictor; therefore it increases systemic vascular resistance. It also stimulates the adrenal gland to release the hormone aldosterone, which retains water and sodium to increase circulating blood volume eventually BP. Then finally the pituitary gland to the release a hormone called ADH (anti diuretic hormone), by stimulating the kidneys to hold on to more water in order to increase circulation volume in an attempt to increase the BP (Ashelford, et al. 2019).

Another response of the body to low BP is the baroreceptors located in the carotid sinus and aortic arch detect a drop BP due to reduced tension from stretch of the vessels then stimulate the SNS to release adrenaline and noradrenaline causing vasoconstriction, increased heart rate by increasing the nerve activity to the Sino-atrial node in the heart causing it to fire more increasing cardiac output with cardiac contractility and this helps to increase the BP. Adrenaline on the other hand causes the smooth muscle cells in the vessels to constrict in order to increase vascular resistance eventually BP(Tortora and Derrickson, 2015).

Disability:

Julia’s blood glucose is slightly elevated with 9 mmol/l. According to Diabetes UK (2019), the aim forglycaemia level of a diabetic individual is between 4 and 8 mmol/l.I would get concerned at this point duesepsis element along with her diabetes, because hyperglycaemia could hinder healing process. Ashelford, et al., (2019) stated that, diabetes can weaken the immune system and makes the individual more susceptible to infection.

Julia is alert and oriented, which suggest there is good brain perfusion, News=0on AVPU (RCP, 2017).

Exposure:

Julia is inpain due to the red, hot and swollen skin in her left arm caused by inflammatory response of the infection (Ashelford, et al., 2019).

NEWS 2 Score:

Aggregated score is 13 andthis is a medical emergency, suggesting that Julia is at very high risk of airway occlusion and multi organ dysfunction which might lead to death if not treated immediately. Therefore, I am going to be confident under the 6cs, use SBAR system to communicate, track, trigger and make sure that my patient is seen by a specialist as soon as possible.Julia requires constant monitoring, an emergency assessment by the critical care outreach team(CCOT) and a referral to high dependency care unit(RCP, 2017). I will also make sure that the consultant has prescribed the required medication to enable me to start the sepsis six care bundle as soon as possible following my trust protocol and make sure that it is completed within 60 minutes (The UK Sepsis Trust, 2014). The way I am going to do this is SBAR as per RCP, (2017).

Situation: Call the medical team, introduce myself then let them know that it is an SBAR call and where I am calling from before discussing the situation, which is: I have a patient that is scoring 13 on news 2, has deteriorated and requires an urgent medical review.

Background: Julia is a 68 year old female admitted with sepsis today. Her PMH is T2DM and HTN. The plan is to start anticipatory medication given such as administering oxygen and start sepsis 6 bundles as per trust guidelines.

Assessment:

Airway: is patent, clear andshe is talking in full sentence. Breathing: RR is 28, SpO2 91% on air. Circulation: HR is 112, BP 89/45, skin is pink and CRT is 2 secs. Disability: she is alert with a BM of 9 mmol/l and in pain. Exposure: temperature is 39.2 degrees Celsius and I amalso concerned about her swollen arm and high score.

Recommendation: I need you to come and see my patient now please. I will also ask the doctor if there is any intervention he/she wants me to do in the meantime such as: Bloods, Venous access, ECG, Monitor or oxygen.

Airway: Julia’s airway is patent but at risk with the high news 2 score. However I wouldconstantly monitor and reassess.

Breathing:

I would sit Julia up right at 45 degrees to optimise oxygenation and ventilation. Administer high flow oxygen therapy 15l in non rebreathe mask to corrected hypoxia and aim saturations between 94-98% for non COPD patients (BTS, 2017). Constantly monitor SpO2, also make sure that the oxygen is humidified because she is on high concentration oxygen to reduce dryness of the airways and count respiration rate (BTS, 2017).

Circulation:

I would secure two large bore intravenous grey catheters (IV) access, then take blood cultures to help identify the pathogen causing the infection so that antibiotics (ATB) can be adjusted accordingly. The best practice is to take blood cultures for sepsis screening before administering any antibiotic (The UK Sepsis Trust, 2014).

I would administer a broad spectrum IV ATB as per the trust guidelines because sepsis is caused by bacterial infection and broad spectrum ATB is designed to kill a wide variety of bacteriaissue (The UK Sepsis Trust, 2014). For example, erythromycin, ciprofloxacin and doxycycline. Therefore this might promptly reverse the systemic inflammation response; meanwhile the blood results are backing (NICE, 2016).

To treat both the sepsis and AKI, I will administerIV fluids to replace the blood volume as in sepsis the patients goes into hypovolaemia, low GFR and hypotension due to increase capillary permeability and vasodilation. Increasing Julia’s fluid replacement causes an increase in her circulation, GFR and BP. This is done following the NICE guidelines, (2013)on fluid resuscitation, by giving 500 mls of fluid bolus over 15 minutes, then repeat and monitor for any improvement, also consider age and type of fluid to administer. I would personally go for crystalloids, 0.9% normal saline, although it might lead to hyperchloremia and increases acidosis. However Hartmann’s solution has electrolytes such as potassium and Julia has oliguria with a raised lactate level, classic signs of AKI. Meaning that there might have a build-up in potassium level (hyperkalaemia) because she is not voiding the waste. This puts heart risk cardiac arrest such as ventricular fibrillation (VF) and arrhythmia.Therefore in Julia’s case 0.9%saline and constant arterial blood gas (ABG) monitoring for lactate is safer. Then observe fluid response and monitor (The UK Sepsis Trust, 2014).

Check her lactate levels: this is a sign of metabolic acidosis as cells have switched to anaerobic metabolism in response to reduced tissue perfusion, which suggest that the patient is in shock due to cellular and metabolic abnormalities. Monitoring lactate will enable me to know if the oxygen and fluid therapy is working effectively (The UK Sepsis Trust, 2014).

Monitor Julia’shourly urine output in an urometer catheter bag: this will show if her kidneys are being perfused well and she is not in fluid retention, which might lead to oedema causing another issue (The UK Sepsis Trust, 2014).

I would constantly monitor BP and HR to monitor improvement, if not despite adequate volume resuscitation. I would use SBAR to get the same doctor to review Julia promptly and refer to CCOT and renal unit. I would check for any HTN medication she is on and stop them as they might be nephrotoxic because it is vital to the kidneys working effectively in order to maintain homeostasis (The UK Sepsis Trust, 2014). To investigate for risk of arrhythmias, I will use a 12 leadelectrocardiogram (ECG) monitor to check for the heart electrical conduction. Order ABG to check for chemical imbalances this would enables me to know if my treatments are effective. I would also check Julia’s urea, creatinine level and do a urinalysisfor the AKI element as there might be electrolytes imbalances. Then order a chest X-ray to know the lung function. Finally a clothing screen to check the clothing factors.

Disability:

I am concerned about Julia’s comorbidities, when she is more stable and comfortable, I will take history from her to know how she is managing her diabetes: if with diet, tablets or insulin. This will enable me to provide the right care. Her HTN, smoking and drinking status then make every contact count by giving health advice which will prevent further illness and reduce future hospital admission as per the Kings fund, (2019). I would also offer her some food to avoid hypoglycaemia and closely monitor her glucose levels. Finally perform a regular Glasgow comma scale (GCS) monitoring.

Exposure:

I would assessJulia’s skin changes by providing dignity and minimising heat loss as per the ABCDE using look, listen and feel approach. Any skin changes for oedema, rashes due to build up toxins in oliguriastate (resuscitation council, 2015). I would have a close look at the swollen arm and aim to reduce swelling by raising the arm and protecting from breaking down. I would also asses her pain using the 0-3 numeric scale and manage using the WHO (2010) pain management ladder,this will help determine the amount of analgesiato provide. Then administer IV paracetamol to relieve pain and reduce temperature. I would then check the wound site (size, colour, smell) then swab. I would use the malnutrition universal screening tool (MUST) score to check her nutritional status. I will also use the pressure area risk assessment chart (Waterlow) score to known her risk of skin breakdown and provide the appropriate care to avoid pressure sores and moisture lesions, by ordering a pressure relieving mattress and keeping frequent turns. I would consider referral to the podiatrist using my inter-professional skills for appropriate wound management. I would reassess Julia by using ABCDE assessment to known if she is improving.

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Psychosocial care:

I would to reassure Julia under the 6cs, by being compassionate and provide reassurance (NHS England, 2015). The way in which I would do this, is to let her known that, we are doing our best to make her feel better, not to worry she is in safe hands and a doctor is on the way to review her. I would also provide emotional and psychological support by adhering to my profession code of conduct by providing clear and honest information. I would ask Julia about her family history, who she lives with and if she has a next of kin and finally check if she has any advanced directives in place, which must be respected as per the NHS constitution, (2015), patients have the right to either accept or refuse treatment. I would protect Julia’s information as per the NMC, code (2018) section 5.2. All the healthcare staff must comply with confidentiality as a duty to protect patients’ information. I would make sure that, I practice with outmost professionalism by adhering to the NMC code of professional conduct and know what the NHS constitution stands for, provide respect and dignity at all times.I would consider referral to diabetes specialist, dietitian, nephrologist and social worker if she requires any care package after discharge. I would finally refer Julia to support group, because some sepsis survivors are likely to experience psychological, physical and emotional difficulties, which might last for months as a result of fear of having sepsis again (The UK Sepsis Trust, 2019).

Conclusion:

In order to summarise, the overall effect of Julia’s condition is low circulating blood volume, lack of oxygen, low tissue perfusion and oxygen delivery to the tissues and organs. It makes it key for early recognition, adequate interventionand response to sepsis in order to prevent deterioration and death. This is achieved through the competence of the professional, knowing the patient’s risk factors as per the nice guidelines (2016), ‘Think “Could this be sepsis?” such as altered vital signs scoring the patient on sequential organ failure assessment (SOFA) score such as Julia’s case, increased RR, HR, low BP and SpO2 suggesting red flags of sepsis and manage according to sepsis six guidelines in a timely manner (The UK Sepsis Trust, 2014).


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