nursing case study septic shock

Septic Shock (Sepsis) Case Study (45 min)

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What initial nursing assessments need to be performed for Mr. McMillan?

• Full set vital signs (T, P, RR, BP, SpO 2 )
• OLDCARTS or PQRST assessment of symptoms (urinary burning)
• LOC/orientation assessment
• Heart and lung sounds

Upon further assessment, Mr. McMillan is weak, his face is flushed, his skin is warm and dry. He is oriented to person and place, but states the year is 1952. His vital signs were as follows:

BP 99/60 mmHg Ht 170.2 cm

HR 92 bpm and regular Wt 60 kg 

RR 28 bpm SpO 2 93% on Room Air

Temp 38.9°C

What diagnostic tests should be ordered for Mr. McMillan?

•  Blood Tests – CBC, BMP, ABG, Lactic Acid, Blood Cultures x 2
• Urine Tests – Urinalysis, Urine Culture
• X-rays – Chest, Kidneys/Ureters/Bladder

What nursing actions would you take at this time for Mr. McMillan? Why?

•  Elevate the HOB to improve breathing and oxygenation
• Apply cardiac monitor
• Notify provider of elevated temp and low SpO 2  
• Apply cool washcloth to forehead and/or behind neck for comfort
• Possibly get ice packs to axillae and groin and remove any blankets to help bring the patient’s temperature closer to normal.

The ED provider orders the following:

• Bloodwork – CBC, BMP, ABG, Lactic Acid, Blood Cultures x 2
• Diagnostics – CXR (chest x-ray), KUB (x-ray of kidneys, ureters, and bladder)
• Nasal Cannula to keep SpO 2 > 92%
• Meds – 1L Normal Saline bolus IV x 1, now.  1,500 mg Vancomycin IVPB x 1 dose, now

Which order should you implement first? Why?

• Blood and urine cultures must be drawn before any antibiotics are administered.
• Blood work – urine tests – fluids – antibiotics
• IF the patient’s SpO 2 is below 92%, apply oxygen via nasal cannula – at this time, there is no indication of that, yet.

All blood and urine tests are completed and you initiate the fluid bolus for Mr. McMillan. You are still waiting for the Vancomycin to arrive from the pharmacy. You notice he is more drowsy. He is now only oriented to self and feels warmer. You take another set of vital signs to find the following:

BP 86/50 mmHg MAP 62 mmHg

HR 108 bpm Temp 39.3°C

RR 36 bpm SpO 2 88% on Room Air

Mr. McMillan’s lab results have also resulted, the following abnormal values were reported:

WBC 22,000 / mcL Lactic Acid 3.6 mmol/L

pH 7.22 pCO 2 30 mmHg

HCO 3 16 mEq/L pO 2 64 mmHg

Urine Cloudy with sediment

What action(s) should you take at this time? Why?

•  #1 – apply oxygen via nasal cannula – ensure HOB elevated for easy breathing
• Notify provider of decreasing blood pressure and elevated WBC, lactic acid ANSWER

What orders do you anticipate for Mr. McMillan? (procedures, meds, transfer, etc?)

• Mr. McMillan may need another liter of IV fluids. The guidelines are for patients to receive 30 mL/kg of body weight in the first 6 hours. That means he would need to receive at least 1,800 mL of IV fluid bonuses.
• Mr. McMillan may need vasopressors to improve his blood pressure – in which case he will also need a central line for administration of those medications as well as an arterial line to monitor his MAP.
• Mr. McMillan will need to be transferred to the ICU for close monitoring and management of his drips

Mr. McMillan responds well to the first liter of fluids, and antibiotics are initiated within an hour of arrival. The ED physicians place an arterial line and central line to initiate vasopressors. They order a Norepinephrine infusion to be titrated to keep MAP > 65 mmHg. The Critical Care team asks you to prepare the patient for transfer to the ICU.

Art. Line BP 82/48 mmHg MAP 58 mmHg

HR 122 bpm CVP 4 mmHg

RR 32 bpm SVR 640 dynes/sec/m -5 SpO 2 90% on Room Air

What, physiologically, is going on with Mr. McMillan?

• Mr. McMillan has an infection, likely urinary, and it has created a systemic inflammatory response. That inflammatory response is causing massive peripheral vasodilation so his vital organs are not receiving adequate blood flow
• He is showing signs of decreased perfusion to his brain (↓ LOC) and decreased cardiac output (↓ BP).  
• His skin is warm and flushed and his temperature is elevated because of the vasodilation in the non-vital organs.

What does it mean to titrate an infusion to keep MAP >65?

• Titration means achieving the desired result with the least amount of drug possible. Therefore we would adjust the infusion up or down to maintain the MAP above, but not too far above, 65 mmHg

After 2 days in the ICU, a norepinephrine infusion and a total of two liters of normal saline, Mr. McMillan’s blood pressure is stable, his MAP is 67 mmHg. He is becoming more alert and is now oriented to person, place, and time.  His blood and urine cultures were positive for bacterial growth. He has received multiple doses of Vancomycin as well as antibiotics targeted to his specific bacterial infection. He is being weaned off of the vasopressors, and the providers hope he can transfer out of the ICU tomorrow.

What explanation or education topics would you want to provide to the patient and his caregiver before discharge?

• Sepsis and septic shock are a result of a severe infection that has gotten into the bloodstream and affected the patient’s ability to pump blood to the body. This is what makes their blood pressure drop so low. We treat this condition by getting the infection under control and supporting the patient’s blood pressure.
• Signs and symptoms of infection – in elderly people, one of the first signs of infection is altered mental status. If the patient seems ‘off’ or ‘not themselves’, it is worth notifying a healthcare provider to prevent a worse situation. 
• The patient will need to ensure he is drinking plenty of fluids and practicing good hygiene to prevent urinary tract infections. He may also consider cranberry juice.
• If receiving a PO course of antibiotics – be sure to take the full course and notify HCP of any adverse reactions.

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Nursing Case Studies

This nursing case study course is designed to help nursing students build critical thinking.  Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process.  To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy  to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs.  If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding.  In the end, that is what nursing case studies are all about – growing in your clinical judgement.

Nursing Case Studies Introduction

Cardiac nursing case studies.

• 6 Questions
• 7 Questions
• 5 Questions
• 4 Questions

GI/GU Nursing Case Studies

• 2 Questions
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Obstetrics Nursing Case Studies

Respiratory nursing case studies.

• 10 Questions

Pediatrics Nursing Case Studies

• 3 Questions
• 12 Questions

Neuro Nursing Case Studies

Mental health nursing case studies.

• 9 Questions

Metabolic/Endocrine Nursing Case Studies

Other nursing case studies.

Sepsis and Septic Shock

Sepsis and septic shock stand as life-threatening conditions that demand swift and vigilant action from healthcare providers, with nurses playing a pivotal role in their management. As frontline caregivers , nurses are essential in recognizing early signs of sepsis, initiating prompt interventions, and providing comprehensive care to improve patient outcomes .

This article aims to highlight the critical importance of nursing in battling sepsis and septic shock, shedding light on the pathophysiology, risk factors, clinical presentations, and evidence-based interventions. By fostering a comprehensive understanding of these conditions, nurses can proactively contribute to saving lives and minimizing the burden of sepsis on patients and healthcare systems.

Table of Contents

What is sepsis and septic shock , pathophysiology, epidemiology, clinical manifestations, complications, assessment and diagnostic findings, medical management, nursing assessment, planning & goals, nursing interventions, discharge and home care guidelines, documentation guidelines.

One of the most common types of circulatory shock and the incidences of this disease continue to rise despite the technology.

• Sepsis is a systemic response to infection . It is manifested by two or more of the SIRS (Systemic Inflammatory Response Syndrome) criteria as a consequence of documented or presumed infection.
• Septic shock is associated with sepsis. It is characterized by symptoms of sepsis plus hypotension and hypoperfusion despite adequate fluid volume replacement.

The pathophysiology of sepsis involves an evolving process. The following shows the process of how sepsis works its way inside of our body.

• Microorganisms invade the body tissues and in turn, patients exhibit an immune response.
• The immune response provokes the activation of biochemical cytokines and mediators associated with an inflammatory response.
• Increased capillary permeability and vasodilation interrupt the body’s ability to provide adequate perfusion, oxygen, and nutrients to the tissues and cells.
• Proinflammatory and anti-inflammatory cytokines released during the inflammatory response and activates the coagulation system that forms clots whether or not there is bleeding .
• The imbalance of the inflammatory response and the clotting and fibrinolysis cascades are critical elements of the physiologic progression of sepsis in affected patients.

Sepsis has affected a lot of people in the United States and around the world as well. The rise in the numbers of those affected with sepsis is alarming and should be given utmost attention.

• Annually, an estimated 750, 000 people in the United States are affected by sepsis.
• By 2010, the rate may increase up to 1 million cases every year.
• Elderly patients are at most risk for developing sepsis because of decreased physiologic reserves and an aging immune system.
• Gram-positive bacteria accounts for 50% of cases of septic shock.
• It is also estimated that 20% to 30% with severe sepsis may never identify the site of infection.

There are several factors that can put the patient at risk for septic shock, and these include:

• Patients with immunosuppression have greater chances of acquiring septic shock because they have decreased immune system, making it easier for microorganisms to invade the body tissues.
• Extremes of age. Elderly people and infants are more prone to septic shock because of their weak immune system .
• Malnourishment . Malnourishment can lower the body’s defenses, making it susceptible to the invasion of pathogens.
• Chronic illness. Patients with a longstanding illness are put at risk for sepsis because the body’s immune system is already weakened by the existing pathogens.
• Invasive procedures. Invasive procedures can introduce microorganisms inside the body that could lead to sepsis.

The signs and symptoms that are associated with septic shock and sepsis include the following:

• Since the ability of the body to provide oxygen and nutrients is interrupted, the heart compensates by pumping faster.
• Hypotension occurs because of vasodilation .
• To compensate for the decreased oxygen concentration, the patient tends to breathe faster, and also to eliminate more carbon dioxide from the body.
• The inflammatory response is activated because of the invasion of pathogens.
• Decreased urine output. The body conserves water to avoid undergoing dehydration because of the inflammatory process.
• Changes in mentation . As the body slowly becomes acidotic, the patient’s mental status also deteriorates.
• Elevated lactate level. The lactate level is elevated because there is maldistribution of blood .

Before sepsis could invade a patient’s body, it is better to prevent its occurrence here are some ways to prevent sepsis and septic shock.

• Strict infection control practices. To prevent the invasion of microorganisms inside the body, infection must be put at bay through effective aseptic techniques and interventions.
• Prevent central line infections . Hospitals must implement efficient programs to prevent central line infections, which is the most dangerous route that can be involved in sepsis.
• Early debriding of wounds. Wounds should be debrided early so that necrotic tissue would be removed.
• Equipment cleanliness. Equipment used for the patient, especially the ones involved in invasive procedures, must be properly cleaned and maintained to avoid harboring harmful microorganisms that can enter the body.

Complications could happen in a patient with sepsis if it is not properly treated or not treated at all.

• Severe sepsis. Sepsis could progress to severe sepsis with symptoms of organ dysfunction, hypotension or hypoperfusion, lactic acidosis, oliguria, altered level of consciousness, coagulation disorders, and altered hepatic functions.
• Multiple organ dysfunction syndrome . This refers to the presence of altered function of one or more organs in an acutely ill patient requiring intervention and support of organs to achieve physiologic functioning required for homeostasis .

Early assessment and diagnosis of the infection must be established to avoid its progression.

• Blood culture. To identify the microorganism responsible for the disease, a blood culture must be performed.
• Liver function test. This should be performed to detect any alteration in the function of the liver.
• Blood studies. Hematologic test must also be performed to check on the perfusion of the blood.

The current treatment of septic shock and sepsis include identification and elimination of the cause of infection.

• Fluid replacement therapy . The therapy is done to correct the tissue hypoperfusion, so aggressive fluid resuscitation must be implemented.
• Nutritional therapy . Aggressive nutritional supplementation is critical in the management of septic shock because malnutrition further impairs the patient’s resistance to infection.

Nursing Management

Nurses must keep in mind that the risks of sepsis and the high mortality rate associated with sepsis, severe sepsis, and septic shock.

Assessment is one of the nurse ’s primary responsibilities, and this must be done precisely and diligently.

• Signs and symptoms . Assess if the patient has positive blood culture, currently receiving antibiotics , had an examination or chest x-ray , or has a suspected infected wound.
• Signs of acute organ dysfunction . Assess for presence of hypotension, tachypnea , tachycardia, decreased urine output, clotting disorder, and hepatic abnormalities.

Sepsis can affect a lot of body systems and even cause their failure, so diagnosis is an important part of the process to establish the presence of sepsis.

• Risk for deficient fluid volume related to massive vasodilation.
• Risk for decreased cardiac output related to decreased preload .
• Impaired gas exchange related to interference with oxygen delivery.
• Risk for shock related to infection.

Healthcare team members should be prepared with a care plan for the patient for a more systematic and detailed achievement of the goals.

• Patient will display hemodynamic stability.
• Patient will verbalize understanding of the disease process.
• Patient will achieve timely wound healing .

Nursing interventions pertaining to sepsis should be done timely and appropriately to maximize its effectivity.

• Infection control . All invasive procedures must be carried out with aseptic technique after careful hand hygiene .
• Collaboration . The nurse must collaborate with the other members of the healthcare team to identify the site and source of sepsis and specific organisms involved.
• Management of fever . The nurse must monitor the patient closely for shivering.
• Pharmacologic therapy . The nurse should administer prescribed IV fluids and medications including antibiotic agents and vasoactive medications.
• Monitor blood levels . The nurse must monitor antibiotic toxicity, BUN, creatinine , WBC, hemoglobin , hematocrit, platelet levels, and coagulation studies.
• Assess physiologic status . The nurse should assess the patient’s hemodynamic status, fluid intake and output , and nutritional status .

After implementation of the interventions, the nurse must evaluate their effectiveness.

• Patient displayed hemodynamic stability.
• Patient verbalized understanding of the disease process.
• Patient achieved timely wound healing .

Even after discharge, the patient must still be taught how to establish home and community care regimen.

• Prevent shock episodes . The nurse should instruct the patient and the family strategies to prevent shock episodes through identifying the factors implicated in the initial episodes.
• Instructions on assessment . The patient and the family should be taught about assessments needed to identify the complications that may occur after discharge.
• Treatment modalities . The nurse must teach the patient and the family about treatment modalities such as emergency administration of medications, IV therapy , parenteral or enteral nutrition , skin care , exercise, and ambulation .

Proper documentation must be established both for legal protection and data organization.

• Document individual risk factors.
• Document assessment findings.
• Document results of the laboratory tests and diagnostic studies.
• Document plan of care and teaching plan.
• Document client’s responses to treatment, teaching, and actions performed.
• Document modifications in the plan of care.

Posts related to Sepsis and Septic Shock:

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I’m not sure if you are aware, but under “Medical Management: Pharmacologic Therapy” Drotrecogin alfa by Eli Lily & Company (pharm company) was taken off the market on Oct of 2011. Good luck with all your endeavors and keep up the good work!

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A 26-year-old female arrives with a companion to an urgent care at 0845 by personal vehicle for treatment of suspected foot infection. The patient’s companion (a female roommate) reports to the triage nurse that the patient cut her foot while wading in the ocean over the weekend. They did not initially notice the cut but discovered it while removing tar from the bottom of the right foot. Approximately 24 hours later, her foot became too painful for ambulation, and a “thick, yellowish” discharge began to drain from the cut. Vitals upon arrival at urgent care showed a temperature of 101.5F, heart rate of 130, respiratory rate of 24, and blood pressure of 86/40. Her pain was 9/10 in her right foot and described as throbbing. During a HTT assessment by the PA, the patient is reported to be arousable to voice, oriented to person and place only, and complaining of nausea. The patient reports she took Tylenol that morning to relieve pain and fever. Her skin is pale, diaphoretic, and hot.

The urgent care calls 911, and medics are dispatched to the center for transfer to the local hospital to treat the patient for suspected sepsis. Upon arrival, medics find the patient is still tachycardic, and that her blood pressure has dropped to 80/40. Her respiratory rate has increased to 30. During transport, medics insert a 20 gauge peripheral IVs in the patient’s left antecubital. They infuse a fluid bolus of 500 mL of normal saline to manage her patient’s hypotension, and administer oxygen by simple mask at 4L/min. During the primary assessment, the patient’s right foot reveals a two-inch laceration with no active bleeding that is erythematous, edematous (non-pitting), and radiating heat. Edema is covering the entire bottom of the right foot and extends to the patient’s ankle.

The patient arrives to the emergency room within 15 minutes and is admitted for treatment at 1000. On the unit, Code Sepsis is called, and the agency’s sepsis protocol based on the Surviving Sepsis campaign is implemented. The patient’s vitals are now a temperature of 102F, heart rate of 140, respiratory rate of 34, and blood pressure of 96/42. Lactate levels are immediately measured. A second 20 gauge peripheral IV is inserted into the right antecubital, blood cultures are drawn, and a swab sample is taken of the cut and submitted to the laboratory for a culture and sensitivity test. Broad spectrum antibiotic ceftriaxone (Rocephin) is administered, and patient is given Ibuprofen to manage her fever. The patient is diagnosed with septic shock, and because she is still hypotensive, 30mL/kg of normal saline is infused. The patient’s lactate levels come back as 2.4 mmol/L. Norepinephrine (Levophed) is also hung, and the patient is further monitored. With careful titration and vital monitoring, the use of vasopressors restores the patient’s blood pressure to 101/52. Although fluid resuscitation helps to bring the patient’s heart rate down to 104, Nicardipine (Cardene) was ordered in anticipation of further needs to manage tachycardia. The patient is transferred to the ICU at 1300 for further monitoring and management of her hemodynamic status.

In the ICU, the patient’s vitals stabilize. Her tachypneic state reduces, and respiratory rate is now 18. She no longer requires oxygen supplementation. Her pain is being managed with IV morphine and she rates the pain in her as 3/10. Her IV pump is running 125 mL an hour of normal saline along with piggybacked ceftriaxone (Rocephin), and labs return a lactate level of 1.5 mmol/L. The patient’s roommate arrives. She is tearful and explains to the ICU nurse that she wanted to tell the patient’s parents what happened, but the patient refused. The ICU nurse calls for the case manager and a social service consult to inquire further. The patient’s roommate explains to the interdisciplinary team that the patient does not have insurance because she is 26 and has been removed from her parents’ medical plan. The parents are also currently engaged in a divorce, do not speak to each other, and use their daughter to communicate. The patient is aware of their financial situation and her lack of medical coverage and does not want to worry her parents in spite of her critical medical state.

• What are the priority nursing interventions for this patient in the ICU setting?
• What signs and symptoms in this patient would indicate the need for mechanical ventilation?
• What is the nurse’s role in addressing the patient’s financial concerns?

References:

Gordon, A.C., Mason, A.J., Thirunavukkarasu, N., et al. (2016). Effect of early vasopressin vs norepinephrine on kidney failure in patient with septic shock: The VANISH randomized clinical trial. JAMA, 316 (5), 509–518. doi:10.1001/jama.2016.10485

Hinkle, J. L., & Cheever, K. H. (2014). Brunner & Suddarth’s textbook of medical-surgical nursing. Philadelphia: Lippincott Williams & Wilkins. PulmCCM. (2019, January 14). From the Surviving Sepsis Guidelines: Criteria for diagnosis of  sepsis. Retrieved from https://pulmccm.org/review-articles/surviving-sepsis-guidelines-criteria-diagnosis-sepsis/

Schmidt, G.A., & Mandel, J. (2019, March). Evaluation and management of suspected sepsis  and septic shock in adults. Retrieved from https://www.uptodate.com/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults?search=sepsis treatmentadult&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H465649907

Society of Critical Care Medicine. (2019). Hour-1 bundle: Initial resuscitation for sepsis and  septic shock. Retrieved from http://www.survivingsepsis.org/SiteCollectionDocuments/Surviving-Sepsis-Campaign-Hour-1-Bundle.pdf

Zhang, M., Zheng, Z., & Ma, Y. (2014). Albumin versus other fluids for fluid resuscitation in patients with sepsis: A meta-analysis. PloS one , 9 (12), e114666.

Nursing Case Studies by and for Student Nurses Copyright © by jaimehannans is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Current sepsis research

What nurses need to know.

Seckel, Maureen A. MSN, RN, APRN, ACNS-BC, CCNS, CCRN, FCCM, FCNS

Maureen A. Seckel is critical care clinical nurse specialist and sepsis leader at Christiana Care Health System in Newark, Del.

The author has disclosed no financial relationships related to this article.

Despite recently published definitions and guidelines that provide a framework for the care of patients with sepsis, there is no strong consensus among experts about many aspects of sepsis screening or the assessment and care of patients with sepsis. This article highlights current evidence revealed by some recent significant research studies and discusses the implications for nursing practice.

Sepsis is a major cause of mortality in the US, with a reported one out of three inpatient hospital deaths due to sepsis. 1 Despite recently published definitions and guidelines that provide a framework for the care of patients with sepsis, there is no strong consensus among healthcare providers and in the literature on all aspects of recognition and management of this deadly disease. 2,3 In addition, no one screening tool or test that is specific and sensitive to sepsis is yet available.

In order to fill the research gaps and increase the strength of evidence-based practice, an abundance of sepsis literature is published annually. It is overwhelmingly time-consuming for nurses practicing at the bedside to keep up with the rapid pace of sepsis literature, distill the research, and discern whether any given recommendation is appropriate to incorporate into practice. Although not inclusive of all sepsis literature recently published, this article highlights some of the recent significant research and discusses implications for nursing practice.

Sepsis recognition

The Sequential Organ Failure Assessment (SOFA) score is a tool used as an objective measure of organ dysfunction in critical illness, including sepsis. 4 A SOFA score of 2 or more points from the patient's baseline is abnormal and indicates an increased mortality risk. 2,4 The CDC has published an electronic SOFA tool (eSOFA) that can be used as part of a hospital toolkit for sepsis surveillance. 5 (See SOFA vs. eSOFA .)

Rhee and colleagues conducted a retrospective cohort study of adult patients in a large database of 111 hospitals. They compared SOFA scores with eSOFA scores in patients diagnosed with sepsis and validated in a four-hospital health system. 6 The results showed that the eSOFA tool had high internal consistency or correlation with the SOFA score (Cronbach's alpha, 0.81). 6 Mortality was higher in patients with eSOFA at 17.1% versus 14.4% with statistical significance ( P < .001) along with better discrimination for mortality. 6

Take-home points from this study : Neither eSOFA nor SOFA were designed to identify patients with sepsis. The eSOFA tool was designed to be a retrospective surveillance tool to track sepsis incidence and outcome monitoring for quality improvement, while SOFA is useful for predicting already-identified patients with sepsis who are at risk for higher mortality by scoring organ dysfunction. Both tools are useful to retrospectively track patients with sepsis, and eSOFA data may be easier to obtain from the electronic health record. This study showed that eSOFA scores compare favorably with SOFA scores in assessing mortality risk and may be useful to use for facility or system performance improvement opportunities. 5,6

Researchers continue to investigate drugs and other treatment strategies in a search for more effective therapies for patients with sepsis. Here is a discussion of some recent studies and their implications for clinical practice.

Vasopressors . Angiotensin II, a vasoactive peptide hormone, is a potent vasoconstrictor produced in the kidneys as part of the renin-angiotensin system. 7 In a multicenter, randomized control trial with a placebo arm, Khanna and colleagues enrolled adults with vasodilatory (distributive shock) on high-dose vasopressors after a minimum of 25 mL/kg of volume resuscitation. 8 Vasodilatory shock is the most common type of shock and is characterized by peripheral vasodilation and hypotension despite preserved cardiac output, with sepsis being the most common cause. 9 Over 80% of the patients enrolled in this study had septic shock. Patients received either an infusion of angiotensin II (n = 163) or a placebo (n = 158). 8 Results showed that patients in the angiotensin II group had statistically significant improvements in mean arterial pressure (MAP) during the first 3 hours (initiation phase) (69.9% versus 23.4% in the placebo group, P < .001). 8 Additionally, a significantly greater increase of 12.5 mm Hg in MAP was found for patients in the angiotensin II group versus 2.9 mm Hg in the placebo group ( P < .001). 8 During the first 48 hours, the angiotensin II group also had statistically significantly decreased dosing of other vasopressors, with the mean change in norepinephrine dosing (mcg/kg/min) of -0.03 ± 0.10 versus 0.03 ± 0.23, P < .001. 8 There was no change in mortality at day 7 or day 28 between the angiotensin II and placebo groups. Thromboembolic events were the most common adverse reaction in the angiotensin II group (12.9% versus 5%). 8

Take-home points for this study: Angiotensin II increased BP in patients already on a high-dose vasopressor who had vasodilatory shock, but it did not change mortality. 8 The study was sufficiently powered to show superiority in the angiotensin II group in increasing MAP and decreasing the doses of other vasopressors. 8

As an addendum, the study was published in 2017, angiotensin II received FDA approval in late 2017, and it became available on the market in 2018. 10 This is the first new vasopressor available to critical care practitioners in many years and is very specific to patients with septic shock. In the next few years, expect to see case series and other published data from centers that have added angiotensin II to their formulary.

Vitamin C, hydrocortisone, and thiamine . This combination has been suggested as synergistic adjunctive therapy for patients with sepsis and septic shock to treat decreased organ perfusion and impaired oxygen delivery and to reduce mortality. 11 In a retrospective, before/after case series at one hospital, Marik and colleagues compared 47 sepsis patients who were treated with vitamin C, hydrocortisone, and thiamine with 47 sepsis patients who were not. 12 They found no significant differences in the two patient populations regarding illness severity, meaning that they were comparable. 12 The treatment group had a statistically significant improvement in hospital mortality (8.5% versus 40.4%, P < .001), decreased duration of vasopressor administration (18.3 ± 9.8 versus 54.9 ± 28.4, P < .001), and less renal replacement therapy for acute kidney injury of 10% versus 33%, P = .02. 12

Take-home points for this study: The combination of vitamin C, hydrocortisone, and thiamine may prove effective in treating patients with sepsis, but additional stronger experimental studies such as a randomized control study need to take place. While the results were positive for this one facility, what is not known is whether the results are replicable and whether they are solely due to the combination of vitamin C, hydrocortisone, and thiamine. To investigate further, a multicenter, double-blind, placebo-controlled, randomized control trial, Vitamin C, Thiamine, and Steroids in Sepsis (VICTAS), has been registered and is in progress. 13 Data from this study should help answer the question of whether this combination of these drugs is efficacious and determine whether this combination therapy should be used to treat patients with sepsis.

Thiamine deficiency has been shown to be prevalent in patients with septic shock, but why is unknown. 14 A recent pilot study showed that thiamine administration in patients with septic shock was associated with both reduced serum lactate levels at 24 hours and possibly a mortality benefit, although not statistically significant. 15

Woolum and colleagues studied the effect of thiamine administration alone in a larger group of patients with septic shock in a retrospective, single-center, matched cohort study. 16 Patients identified for inclusion in this study had septic shock by diagnosis coding, met The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria, and had thiamine administered intravenously within 24 hours of admission. 16 A matched cohort of patients with septic shock and Sepsis-3 criteria without thiamine administration was also identified. 16 The results showed a nonstatistically significant association with improved lactate clearance and 28-day mortality in patients who received thiamine. 16

Take-home points for this study: Although the results are interesting, there was no statistical significance and, once again, stronger experimental studies need to take place before routine administration thiamine is implemented to treat patients with septic shock. 3

Prehospital antibiotics . Early antibiotic administration as soon as possible or within 1 hour of sepsis, and septic shock recognition is a strong recommendation from the recent sepsis guidelines. 3 It appears logical that giving antibiotics even earlier—for example, prehospital in the ambulance—may have a positive effect on outcomes. But what does the evidence show?

Alan and colleagues conducted a randomized controlled, open-label, multicenter trial involving adult patients with varying severity of sepsis. 17 Patients were randomized to the intervention group (1,548 patients) and a usual care control group (1,150 patients). A prehospital blood culture was obtained in the intervention group and ceftriaxone administered, along with usual care regarding fluids and oxygen. 17 Patients with a known allergy to ceftriaxone or other beta-lactam antibiotics, known pregnancy, or suspected prosthetic joint infections were excluded. 17 Results showed no statistically significant difference in mortality (28-day or 90-day), ICU admissions, or hospital length of stay between the two groups. 17

Take-home points for this study: No statistically significant benefit was found for administering an antibiotic prehospital. 17 However, the healthcare providers involved in the study did note a benefit of improved sepsis recognition and response times in general. 17

Based on this study, giving antibiotics prehospital in the ambulance cannot be recommended.

Steroids . Many studies have been conducted to evaluate the use of steroids in patients with sepsis, with conflicting results. Based on weak evidence, the most recent sepsis guidelines recommended against routinely using I.V. glucocorticoid therapy as part of initial therapy. Glucocorticoid therapy may be considered in select patients with refractory septic shock (systolic BP less than 90 mm Hg) for more than 1 hour following both adequate fluid resuscitation and vasopressor administration. 3

One recent study found that continuous infusions of hydrocortisone in patients with septic shock requiring mechanical ventilation did not improve 90-day mortality. 18 However, another study showed a decrease in 90-day mortality in ICU patients with septic shock who received both intermittent hydrocortisone and fludrocortisone. 19

In a systematic review and meta-analysis, Fang and colleagues looked at whether corticosteroids were associated with a decrease in 28-day mortality in adult patients with sepsis, severe sepsis, or septic shock. The review included 37 randomized control studies with 9,564 patients meeting inclusion criteria. 20 The results showed an association between improved 28-day mortality and corticosteroid use with a relative risk, 0.90; 95% CI, 0.82-0.98. 20 However, no statistically significant improvement was found in 90-day mortality (relative risk, 0.94; 95% CI, 0.85-1.03). 20 In other words, corticosteroids were associated with significant benefit for both ICU and in-hospital 28-day mortality. Other findings that may be associated with corticosteroid use include shock reversal and vasopressor-free days, decreased ICU length of stay, time to resolution of shock, and SOFA score. 20

Take-home points for this study : Corticosteroids were associated with a reduced 28-day mortality in adults with sepsis, severe sepsis, and septic shock. 20 There is some suggestion from this analysis that low-dose corticosteroids and a longer course of therapy may be better. 20 What we still do not know is the optimal strategy for administering corticosteroids, including optimal dosing for patients with sepsis. Additional research is needed to find the correct risk-benefit ratio.

Fluids . There is tremendous debate about whether resuscitation with 30 mL/kg of crystalloid fluids is appropriate for all patients with sepsis based on recent sepsis guidelines who are hypotensive or who have an elevated serum lactate level (4 mmol/L or greater; normal, 0.5-1 mmol/L). 3,21-23 Many clinicians cite safety concerns for patients with heart failure or renal failure. 21

Corl and colleagues designed a randomized control pilot study in two hospitals to compare outcomes in patients treated with a restrictive fluid resuscitation strategy (60 mL/kg or less of I.V. fluid) versus those receiving higher-volume resuscitation. 24 Patients with severe sepsis or septic shock were randomized in ED triage after an initial 1,000 mL of I.V. fluid to either a restrictive fluid strategy (55 patients) or usual care (54 patients) for the first 72 hours of treatment. 24 The results showed no difference in 30-day mortality outcomes between the two groups (21.8% versus 22.2%). 24 The restrictive fluid group received statistically significantly less fluid in the first 72 hours than the usual care group (3,785 ± 1,167 versus 5,150 ± 2,421, P < .0001). 24 No differences were found between the two groups in development of new organ failure, hospital or ICU length of stay, or serious adverse events. 24

Take-home points for this study: A restrictive fluid strategy in this small pilot study reduced the volume of fluid administered in patients with severe sepsis and septic shock without increase in mortality, organ failure, length of stay, or adverse events. This was a pilot study and was not intended to be conclusive but to test the concept in a small group. A larger study is planned to address the question of restrictive fluids. 24 In addition, the Crystalloid Liberal or Vasopressors Early Resuscitation in Sepsis (CLOVERS) study is currently underway. This study is designed to add to the body of evidence regarding fluid resucitation. 25

Another study also looked at fluid resuscitation and outcomes to identify predictors of reaching the sepsis guideline goals for fluid resuscitation and examined the effects on clinical outcomes, including at-risk populations. 26 In a retrospective cohort study conducted in one ED, Kuttab and colleagues compared patients with severe sepsis or septic shock who had received 30 mL/kg of fluid resuscitation in the first 3 hours (509 patients) versus patients (523 patients) who never received resuscitation fluids or for whom fluids were delayed. 26 The results showed that certain patients were less likely to receive 30 mL/kg crystalloid bolus within 3 hours (30by3) sepsis onset: those who were older adults (odds ratio [OR], 0.62; 95%, 0.46-0.83), male (OR, 0.66; 95%, 0.49-0.87), obese (OR, 0.18; 95%, 0.13-0.25), had end-stage renal failure (OR, 0.23; 95%, 0.13-0.40), had heart failure (OR, 0.42; 95%, 0.29-0.60), or documented fluid overload (OR, 0.30; 95%, 0.20-0.45). Patients who did not meet 30by3 had increased odds of mortality (OR, 1.52; 95%, 1.03-2.24), delayed hypotension (OR, 1.42; 95%, 1.02-1.99), and increased ICU length of stay (regression coefficient, 2; 0.5-3.6).

Take-home points for this study: Patients with severe sepsis or septic shock who failed to meet a 30by3 fluid resuscitation strategy had increased odds of in-hospital mortality regardless of associated comorbidities such as end-stage renal failure and heart failure. Because this study was retrospective and homogeneous (limited to the population of one ED), additional prospective studies are needed to confirm the association. It does add knowledge to the discussion whether 30 mL/kg is safe for all patient populations with sepsis who meet criteria for fluid resuscitation.

Restoration of perfusion

Serum lactate levels have been used as a surrogate for tissue perfusion to assess sepsis resuscitation; however, persistent elevated levels may be associated with not only decreased mortality in sepsis but also with other nonsepsis causes. 27 In addition, lactate levels may not be readily available in nonresourced countries. 3 Capillary refill time, which nurses can easily assess, may reflect serum lactate levels. To investigate whether this simple assessment skill could be used instead of serum lactate levels to guide resuscitation, Hernandez and colleagues conducted a study comparing assessment of capillary refill time versus serum lactate levels and the effect on mortality in patients with septic shock. In a randomized, nonblinded, multicenter study, adult patients with septic shock were recruited within 4 hours of septic shock diagnosis and randomized to one of two groups. 28 For the intervention group, capillary refill time was documented every 30 minutes (see Capillary refill time study procedure for the control group), and serum lactate levels were obtained every 2 hours. 28 In each group, 212 patients were included in the analysis. 28 The primary outcome of 28-day mortality, although not statistically significant, was lower in the capillary refill time group (34.9%) versus the lactate group (43.3%). 28 The capillary refill time group was associated with less organ dysfunction at 72 hours as measured by the SOFA score. 4,28 No statistical differences in other outcomes were found. 28

Take-home points for this study: Guiding resuscitation by measuring capillary refill time was associated with decreased 28-day mortality and organ dysfunction at 72 hours in this study. But because these findings were not statistically significant, the evidence is not strong enough to move this strategy into practice. 28

Recently the authors repeated the data analysis using a different statistical model, the Bayesian model. 29 The Bayesian model provides a probability or likelihood of the effect. In the reanalysis, they found a high probability that capillary refill time was associated with lower mortality at both 28 and 90 days and a lower SOFA score (less organ dysfunction) at 72 hours when compared with the lactate group. 29 This provides more evidence that a capillary refill time strategy for targeted resuscitation may be a reasonable alternative and associated with lower mortality and faster resolution of organ dysfunction. 29 Expect to see more discussion in the literature about this promising use of a simple bedside assessment skill that every nurse could use in the future to guide sepsis resuscitation strategies.

Phenotypes and biomarkers

Ongoing investigation of phenotypes and biomarkers is likely to yield more treatment breakthroughs in the future. Part of the sepsis definition includes the terminology of dysregulated host response (see Sepsis terms ). 2 What is not known is how to identify individual clinical features that make patients more susceptible to developing sepsis. What if in the future, the healthcare team could more easily identify these patients and use this information to prescribe patient-specific therapy?

In a retrospective analysis, Seymour and colleagues used machine learning to determine phenotypes in patients identified with sepsis in databases from three clinical observational cohorts and three randomized control trials. 30 A phenotype is a specific collection of clinical variables in patients who respond differently to treatment and have different risks for poorer outcomes. 30,31 Four phenotypes were identified in this analysis based on 29 variables located in the electronic health record associated with sepsis onset or outcomes: alpha, beta, gamma, and delta. 30 The four phenotypes were correlated with host immune response, mortality, and other clinical outcomes. 30

Take-home points for this study: Further research would need to be done both retrospectively and prospectively to determine reproducibility and clinical utility in all sepsis patient populations, but the concept itself is intriguing and may be the beginning of future steps toward understanding sepsis. The ability to identify phenotypes would help clinicians individualize patient care, identify associations with biomarkers, and determine which patients are more likely to have better clinical response and outcomes related to treatment.

Looking to the future

We know that research is continually evolving to find the best evidence-based care that will provide optimal outcomes for our patients. The future for sepsis recognition and management relies on continued research and distillation of that research into guidelines and recommended strategies. While this brief review of recent sepsis literature is not all-inclusive, it gives nurses insight into the current evidence and highlights questions that still need to be answered.

Capillary refill time study procedure 28

• Apply firm pressure to ventral surface of the right index finger distal phalanx with glass microscope slide.
• Increase pressure until skin blanches and maintain for 10 seconds.
• Measure time for return of normal skin color with chronometer.
• Abnormal ≥3 seconds.

Sepsis terms 2

Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection

Organ dysfunction: an acute change in a patient's total SOFA score 2 points consequent to the infection, based on a baseline SOFA score of zero in patients without preexisting organ dysfunction. A score of 2 indicates an overall mortality risk of approximately 10% in patients with suspected infection.

Septic shock: a subset of sepsis where underlying circulatory and cellular/metabolic abnormalities increase mortality. Patients in septic shock have persisting hypotension that requires vasopressors to maintain a MAP of 65 mm Hg and a serum lactate level over 2 mmol/L (18mg/dL) despite adequate volume resuscitation.

evidence-based practice; organ dysfunction; sepsis; septic shock; SOFA score

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Case Study: A Systematic Approach to Early Recognition and Treatment of Sepsis

Submitted by Madeleine Augier RN BSN

Tags: assessment Case Study emergency department guidelines mortality prevention risk factors sepsis standard of care treatment

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Sepsis is a serious medical condition that affects 30 million people annually, with a mortality rate of approximately 16 percent worldwide (Reinhart, 2017). The severity of this disease process is not well known to the public or health care workers. Often, health care providers find sepsis difficult to diagnose with certainty. Deaths related to sepsis can be prevented with accurate assessments and timely treatment. Sepsis must be considered an immediate life-threatening condition and needs to be treated as a true emergency.

Relevance and Significance

Sepsis is defined as “the life-threatening organ dysfunction resulting from a dysregulated host response to infection” (Kleinpell, Schorr, & Balk, 2016, p. 459). Jones (2017) study of managing sepsis affirms that the presence of sepsis requires a suspected source of infection plus two or more of the following: hyperthermia (>38.1 degrees Celsius) or hypothermia (<36 degrees Celsius), tachycardia (>91 beats per minute), leukocytosis or leukopenia, altered mental status, tachypnea (>21 breaths per minute), or no urine output for 12 hours. If the infection persists, acute organ dysfunction or failure occurs from widespread inflammation, eventually leading to septic shock (Palleschi, Sirianni, O’Connor, Dunn, & Hasenau, 2013).  Palleschi et al.  (2013) states that during septic shock, “the cardiovascular system fails, resulting in hypotension, depriving vitals organs of an adequate supply of oxygenated blood” (p. 23). Ultimately the body can go into multiple organ dysfunction syndrome (MODS), leading to death if there is inaccurate assessment and inadequate treatment.

The purpose of this case study is to make the nurse practitioner aware of the severity sepsis, and how to accurately diagnose and treat using evidence-based data. Sepsis can affect everyone, despite his or her age or comorbidity.  Center for Medicare and Medicaid Services (CMS) has diagnosed this problem as a priority and uses sepsis management in determining payment to providers (Tedesco, Whiteman, Heuston, Swanson-Biearman, & Stephens, 2017). This medical diagnosis is unpredictable and presents a challenge to nurse practitioners worldwide. Early recognition and treatment of sepsis by the nurse practitioner is critical to decrease morbidity and mortality.

After completing this case study, the reader should be able to:

• Identify the risk factors of sepsis
• Identify the signs and symptoms of sepsis
• Identify the treatment course of sepsis

Case Presentation

A 65-year-old Asian female presented to the emergency department accompanied by her husband with a chief complaint of altered mental status. Upon assessment, the patient was lethargic, and alert and oriented to person only. The patient’s heart rate was 136, blood pressure 104/50, oral temperature 99 degrees Fahrenheit, oxygen saturation 97% on 4 liters nasal cannula, and respirations 26 per minute. The patient’s blood glucose was obtained with a result 454.

Further orders, such as labs and imaging were made by the provider to rule out potential diagnoses. A rectal temperature was obtained revealing a fever of 103.7 degrees Fahrenheit. The patient remained restless on the stretcher. After one hour in the emergency department, her heart rate spiked to 203 beats per minute, respirations became more rapid and shallow, and she became more lethargic. The patient’s altered mental status, increasing heart rate and respirations caused the providers to act rapidly.

Medical History

The patient’s husband reports that she is a type one diabetic, he denies any other medical conditions. In addition, the patient’s husband states that she has not been exposed to any sick individuals in the past few weeks. The husband reports a family history of diabetes, other wise no significant familial history. No history of smoking, drinking, or illicit drug use was to be noted.

Physical Assessment Findings

The patient appeared lethargic and confused with a Glasgow Coma Scale of 12. She appeared tachypnic, with shallow respirations, and a rate of 28 breaths per minute. Upon auscultation, breath sounds were coarse. Her abdomen was soft and non-tender, no nausea or vomiting noted. The patient appeared diaphoretic, and her legs were mottled.

Laboratory and Diagnostic Testing and Results

During the initial assessment, a complete blood count (CBC), basic metabolic panel (BMP), and lactic acid level were ordered for blood work. A STAT electrocardiogram (EKG), urinalysis, and a chest X-ray were ordered to differentiate possible diagnoses. The CBC revealed leukocytosis with a white blood cell count of 23,000 and an increased lactic acid level of 4.3. The anion gap and potassium level remained within a normal limit, ruling out the possibility of diabetic ketoacidosis (DKA). The patient’s EKG showed supraventricular tachycardia (SVT). The chest X-ray revealed infiltrates to the right lung. The urinalysis was free from leukocytes or nitrites. Blood cultures were ordered to confirm their hypothesized diagnosis, septicemia.

Pharmacology

The provider initiated intravenous (IV) fluid treatment with Lactated Ringers at a bolus of 30 mL/kg. Because the patient’s heart rate was elevated, 6 mg of adenosine was ordered to combat the SVT. Additionally, broad-spectrum IV antibiotics were initiated. One gram of vancomycin and 3.375 grams of piperacillin-tazobactam were the preferred antibiotics of choice.

Final Diagnosis

Upon arrival, the providers were ruling out DKA and sepsis, given the patient’s history.

The patient’s elevated white blood cell counts, temperature, lactic acid level, heart/respiratory rate, and altered mental status were all clinical indicators of sepsis. The chest X-ray revealed a right lung infiltrate, persuading the providers to diagnose the patient with sepsis secondary to pneumonia.

Patient Management

After sepsis was ruled as the patient’s diagnosis, rapid antibiotic administration and IV fluid treatment became priority after the patient’s heart rate was controlled. A cooling blanket and a temperature sensing urinary catheter was placed to continuously monitor and control the patient’s fever. Later, the patient was transferred to a critical care unit for further treatment. Shortly after being transferred, the patient went into respiratory failure and was placed on a ventilator. After two days in the ICU, the patient remained in septic shock, and died from multisystem organ failure.

When the patient initially presented to the emergency department, accurate and rapid diagnosis of sepsis was critical in order to stabilize the patient and prevent mortality. A challenge was presented to the provider regarding a rapid diagnosis due to the patient’s history and her presenting signs and symptoms. Increased awareness and interprofessional education regarding sepsis and its’ treatment is vital to decrease mortality. Health care providers need to be competent in recognizing and accurately treating sepsis in a rapid manner.

Research shows that outcomes in sepsis are improved with timely recognition and early resuscitation (Javed et al., 2017). It is important for the provider to identify certain risk factors and symptoms to easily diagnose sepsis. A research study by Henriksen et al. (2015) proved that age, and comorbidities including psychotic disorders, immunosuppression, diabetes, and alcohol abuse served as top risk factors for sepsis.

Once the diagnosis of sepsis is determined, rapid treatment must be initiated. The golden standard of treatment consists of a bundle of care that includes blood cultures, broad-spectrum antibiotic agents, and lactate measurement completed within 3 hours as described by Henriksen et al. (2015). A study by Seymour et al. (2017) showed that the more rapid administration of the bundle of care is correlated with a decreased mortality rate. In addition, The Survival of Sepsis Campaign formed a guideline to sepsis treatment; Rhodes et al. (2016) suggests giving a 30 mL/kg of IV crystalloid fluid for hypoperfusion. If hypotension persists (mean arterial pressure <65), vasopressors, preferably norepinephrine, should be initiated (Rhodes et al., 2016). Prompt recognition of sepsis and implementation of the bundle of care can help reduce avoidable deaths.

To increase awareness, interprofessional education regarding sepsis and its’ common signs and symptoms needs to be established. Evidence-based protocols should be utilized in hospital care settings that provide nurse practitioners with a guideline to follow to ensure rapid and accurate treatment is given. Increased awareness and education helps providers and other healthcare workers to properly identify and accurately treat sepsis.

The public and health care providers must become more aware and educated on the severity of sepsis. It is crucial to be able to recognize signs and symptoms of sepsis to prevent further complications such as septic shock and multi-organ failure. Increased awareness, interprofessional education, accurate assessment, and rapid treatment can help reduce incidence and mortality. Sepsis management must focus upon early goal-directed therapy (antibiotic administration, fluid resuscitation, blood cultures, lactate level) and individualized management pertaining to the patient’s history and assessment (Head & Coopersmith, 2016). Misdiagnosis and delay in emergency treatment can result in missed opportunities to save lives.

• Head, L. W., & Coopersmith, C. M. (2016). Evolution of sepsis management:from early goal-directed therapy personalized care. Advances in Surgery, 50 (1), 221-234. doi:10.1016/j.yasu.2016.04.002
• Henriksen, D. P., Pottegard, A., Laursen, C. B., Jensen, T. G., Hallas, J., Pedersen, C., & Lassen, A. T. (2015). Risk factors for hospitalization due to community-acquired sepsis-a population-based case-control study. PLOS ONE, 10 (4), 1-12. doi:10.1371/journal.pone.0124838
• Javed, A., Guirgis, F. W., Sterling, S. A., Puskarich, M. A., Bowman, J., Robinson, T., & Jones, A. E. (2017). Clinical predictors of early death from sepsis. Journal of Critical Care, 42 , 30-34. doi:10.1016/j.jcrc.2017.06.024
• Jones, J. (2017). Managing sepsis effectively with national early warning scores and screening tools. British Journal of Community Nursing, 22 (6), 278-281. doi:10.12968/bjcn.2017.22.6.278
• Kleinpell, R. M., Schorr, C. A., & Balk, R. A. (2016). The new sepsis definitions: Implications for critical care. American Journal of Critical Care, 25 (5), 457-464. doi:10.4037/ajcc2016574
• Palleschi, M. T., Sirianni, S., O'Connor, N., Dunn, D., & Hasenau, S. M. (2013). An interprofessioal process to improve early identification and treatment for sepsis. Journal for Healthcare quality, 36 (4), 23-31. doi:10.1111/jhq.12006
• Reinhart, K., Daniels, R., Kissoon, N., Machado, F. R., Schachter, R. D., & Finfer, S. (2017). Recognizing sepsis as a global health priority-A WHO resolution. The New England Journal of Medicine, 377 (5), 414-417. doi:10.1056/NEJMp1707170
• Rhodes, A., Evans, L. E., Alhazzani, W., Levy, M. M., Anotnelli, M., Ferrer, R.,...Beale, R. (2017). Surviving sepsis campaign: International guidelines for management of sepsis and septic shock: 2016. Intensive Care Medicine, 43 (3), 304-377. doi:10.1007/s00134-017-4683-6
• Seymour, C. W., Gesten, F., Prescott, H. C., Friedrich, M. E., Iwashyna, T. J., Phillips, G. S.,...Levy, M. M. (2017). Time to treatment and mortality during mandated emergency care for sepsis. The New England Journal of Medicine, 376 (23), 2235-2244. doi:10.1056/NEJMoal1703058
• Tedesco, E. R., Whiteman, K., Heuston, M., Swanson-Biearman, B., & Stephens, K. (2017). Interprofessional collaboration to improve sepsis care and survival within a tertiary care emergency department. Journal of Emergency Nursing, 43 (6), 532-538. doi:10.1016/j.jen.2017.04.014

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Septic Shock Nursing Diagnosis and Nursing Care Plan

Last updated on May 15th, 2022 at 11:41 am

Septic Shock Nursing Care Plans Diagnosis and Interventions

Septic shock is a fatal condition that develops once sepsis becomes severe. It is characterized by a drop in blood pressure following infection, changes in mentation, and organ failure.

Signs and Symptoms of Septic Shock

Common symptoms of septic shock include:

Types of Septic Shock

Causes of septic shock.

Septic shock can be caused by a variety of infections, including, but not limited to:

Risk Factors of Septic Shock

Diagnosis of septic shock, treatment of septic shock, septic shock nursing diagnosis, nursing care plan for septic shock 1.

Nursing Diagnosis : Risk for infection related to a compromised immune system, secondary to septic shock.

Nursing Care Plan for Septic Shock 2

Nursing Diagnosis: Risk for Impaired Gas Exchange related to regulatory dysfunction, secondary to septic shock.

Nursing Care Plan for Septic Shock 3

Nursing Diagnosis: Deficient Fluid Volume related to increased urinary output, as evidenced by weight loss, dry skin, insufficient fluid intake, and imbalance in intake and output ratio

Nursing Care Plan for Septic Shock 4

Nursing Diagnosis: Hyperthermia related to a compromised compensatory system, secondary to septic shock, as evidenced by flushed skin, malaise, fatigue, headache, pain, loss of appetite, tachypnea, and tachycardia.

Nursing Care Plan for Septic Shock 5

Nursing Diagnosis: Deficient Knowledge related to a lack of information on the condition, secondary to septic shock, as evidenced by verbalized concerns about disease, frequent requests for information, information misinterpretation, difficulty following guidelines, and difficulty performing tests

Nursing References

Gulanick, M., & Myers, J. L. (2022).  Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon

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Septic shock: a case study

• PMID: 8696026
• DOI: 10.1016/s0964-3397(96)81713-7

Septic shock is a pathological process that is common to most intensive care units; however, despite major developments in intensive care and medicine, it continues to be one of the commonest causes of morbidity and mortality. This article describes the management of a patient admitted to intensive care with septic shock. Some of the principles regarding septic shock, including the pathophysiology, management and nursing care, are explored. Also included are some of the current theories and research into the sepsis syndrome.

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• Clinical management for patients admitted to a critical care unit with severe sepsis or septic shock. Cheung WK, Chau LS, Mak II, Wong MY, Wong SL, Tiwari AF. Cheung WK, et al. Intensive Crit Care Nurs. 2015 Dec;31(6):359-65. doi: 10.1016/j.iccn.2015.04.005. Epub 2015 Aug 17. Intensive Crit Care Nurs. 2015. PMID: 26292920
• [Consensus recommendations from Australia for nursing measures in sepsis and septic shock with a commentary from the German perspective]. Panknin HT; Kompetenznetzwerk Sepsis. Panknin HT, et al. Kinderkrankenschwester. 2012 Oct;31(10):422-7. Kinderkrankenschwester. 2012. PMID: 23130412 German. No abstract available.
• Septic shock in the oncology patient. Hartnett S. Hartnett S. Cancer Nurs. 1989 Aug;12(4):191-201. Cancer Nurs. 1989. PMID: 2670198 Review.
• Pathophysiology and assessment of sepsis and septic shock. Littleton MT. Littleton MT. Crit Care Nurs Q. 1988 Jun;11(1):30-47. doi: 10.1097/00002727-198806000-00006. Crit Care Nurs Q. 1988. PMID: 3292022 Review. No abstract available.
• Septic shock with no diagnosis at 24 hours: a pragmatic multicenter prospective cohort study. Contou D, Roux D, Jochmans S, Coudroy R, Guérot E, Grimaldi D, Ricome S, Maury E, Plantefève G, Mayaux J, Mekontso Dessap A, Brun-Buisson C, de Prost N. Contou D, et al. Crit Care. 2016 Nov 6;20(1):360. doi: 10.1186/s13054-016-1537-5. Crit Care. 2016. PMID: 27816060 Free PMC article. Clinical Trial.

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Pathophysiology

Septic shock.

Septic shock is

“A life-threatening organ dysfunction caused by a dysregulated host response to infection” (McCance & Huether, 2019, p. 1550).

T he infectious process starts with an infectious agent entering the bloodstream and causing bacteremia either d irectly from the site of infection or i ndirectly by releasing toxic substances into the bloodstream. Some of the m ost common causes of septic shock are g ram-negative or gram-positive bacteria, viruses, and fungi. The m ost common sites of infection are the lungs, bloodstream, intravascular catheters, intra-abdominal, urinary tract, and surgical wounds (McCance & Huether, 2019).

Normal Physiology

In normal physiology, when a pathogen invades the body, the body will react with local and systemic responses.

• O ur f irst line of defense is the body’s natural physical, mechanical, and biochemical barriers such as the epithelial cells and surfaces of the skin. These defenses prevent microorganisms from getting into tissues and also have the ability to remove infectious microorganisms. The surfaces of the skin and mucous membranes of the body also contain normal microbiomes (“normal flora”) that also protects the body by releasing chemicals to prevent pathogens from being colonized (McCance & Huether, 2019).
• The body’s s econd line of defense is the inflammatory response. Inflammation causes a vascular response that makes vessel walls become leaky and more permeable and makes white blood cells adhere to vessel walls and migrate out into the tissues. Symptoms usually produced by inflammation are the heat, redness, edema and pain. The goal of inflammation is to prevent and limit infection and interact with components of the adaptive immune system as well as prepare the body for healing (McCance & Huether, 2019). 

There are three important plasma protein systems involved to provide an active barrier against invading pathogens in the inflammatory response.

• One is c omplement system which destroys pathogens directly and work with other components of the immune responses by three pathways: (1) classic, (2) lectin and (3) alternative. The main functions of these are to induce rapid mast cell degranulation, attract white blood cells to pathogens, and “tag” pathogens for destruction (McCance & Huether, 2019).
• Second is the c lotting or coagulation system which forms blood clots that include a meshwork of protein strands at the injured or inflamed site to stop bleeding, trap pathogens to prevent the spread of infection, and provide a framework for repair and healing (McCance & Huether, 2019).
• The last important inflammatory response is from the k inin system which activates and assists inflammatory cells by the release of mainly bradykinin which causes dilation of blood vessels, pain, smooth muscle contraction, increase vascular permeability and leukocyte chemotaxis (McCance & Huether, 2019). 

There are also many biochemical mediators of the innate immune system that secrete cytokines responsible for activating other cells such as interleukins, chemokines, interferons, and other molecules. These chemicals are important to the vascular changes that occur during the inflammatory process (McCance & Huether, 2019).

Along with the cellular mediators are the cellular components such as platelets, phagocytes (neutrophils, eosinophils, monocytes, macrophages and dendritic cells), natural killer cells, and lymphocytes. The components respond to the site of the injury together to limit the tissue injury, kill pathogens, remove the debris, and prepare for healing and tissue repair (McCance & Huether, 2019). 

Figure 5: Summary of Sepsis Pathology Source: McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biological basis for disease in adults and children (8th ed.). St. Louise, MO: Mosby.

Septic shock begins when the pathogen enters the bloodstream. This stimulates the release toxic substances called the triggering molecules, which triggers the body to activate the proinflammatory responses and release proinflammatory cells such as leukocytes, macrophages, monocytes and platelets as well as proinflammatory mediators such as cytokines (interleukins, tumor necrosis factor alpha and other mediators). Cytokines along with the vasoactive peptides cause vasodilation causing hypotension, relative hypovolemia, and decreased in oxygen delivery to the tissues. The release of proinflammatory cytokines also activate plasma protein systems of the complement, coagulation and kinin systems (McCance & Huether, 2019).

Dysfunction of epithelial cells cause further capillary leaking and microvascular thrombus, tissue hypoxia and apoptosis. Due to tissue hypoxia, the body will start breaking down carbohydrates to make ATP or energy for the body. As more anaerobic cells are being used for energy, the more lactic acid is produced. Without correction, the accumulation will lead to metabolic acidosis causing further damage to the tissues (McCance & Huether, 2019).  

As the responses of proinflammatory and antiinflammatory mediators intensify the body experiences persistent low arterial pressure, low tissue perfusion, low systemic vascular resistance which will profoundly affect the circulatory, cellular and metabolic systems. These responses will lead to multiple organ dysfunction syndrome (MODS) due to dysfunction of the kidneys, liver, intestines, lungs and brain as a result of tissue hypoxia and lack of tissue perfusion (McCance & Huether, 2019). 

Septic shock is measured by the SOFA score and assessing different systems in relation to the severity of the organ failure. The quick SOFA criteria include a respiratory rate equal or greater than 22 per minutes, altered mentation and systolic blood pressure less than 100 mmHg. The standard SOFA scoring includes respiration, coagulation of platelets, bilirubin level of the liver, mean arterial pressure, glasgow coma scale score, creatinine level, and urine output.

Figure 6. The Sequential Organ Failure Assessment (SOFA) Score Source: Marik, P. E., & Taeb, A. M. (2017). SIRS, qSOFA and new sepsis definition. Journal of thoracic disease , 9(4), 943-945.

Clinical manifestations

Clinical manifestations of septic shock usually include f ever, chills, sweating, w arm progressing to cool skin, r espiratory distress, altered mentation, decreased urine output, hypotension, elevated liver enzymes, and decreased platelet counts (McCance & Huether, 2019). 

Surviving Sepsis: What Every Nurse NEEDS to Know to Be SAFE in Practice

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A case report of septic shock syndrome caused by S. pneumoniae in an immunocompromised patient despite of vaccination

Josef singer.

1 Division of Infectious Diseases and Tropical Medicine, Department of Internal Medicine I, Medical University of Vienna, 1090 Vienna, Austria

Christoph Testori

2 Department of Emergency Medicine, Medical University of Vienna, 1090 Vienna, Austria

Peter Schellongowski

3 Intensive Care Unit 13i2, Department of Internal Medicine I, Medical University of Vienna, 1090 Vienna, Austria

Ammon Handisurya

4 Clinical Department for Nephrology and Dialysis, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria

Catharina Müller

Eva-maria reitter, wolfgang graninger, paul knöbl.

5 Clinical Department of Hematology and Hemostaseology, Department of Internal Medicine I, Medical University of Vienna, 1090 Vienna, Austria

Thomas Staudinger

Stefan winkler, florian thalhammer, associated data.

The dataset supporting the conclusions of this article is included within this article.

Background and case presentation

We report a case of septic shock syndrome caused by Streptococcus pneumoniae in a patient who had undergone splenectomy due to an autoimmune lymphoproliferative syndrome (ALPS), which is characterized as a dysfunction of immunoregulation. Although the patient was vaccinated with a conjugated polysaccharide vaccine after the splenectomy, he was still susceptible to S. pneumoniae infection, because the isolated serovar (24F), a serovar long thought to be apathogenic, is not covered by any vaccine currently approved, neither a conjugated nor an unconjugated polysaccharide one.

Conclusions

This case demonstrates that, due to presence of different serovars, also infections with bacteria against which patients are vaccinated have to be considered as differential diagnosis. Although vaccine development has extended the coverage of S. pneumoniae from 7 to 23 serovars within recent years, there is still demand for novel vaccines which can provide broader protection also against so-thought “apathogenic” strains, especially for groups at high risk.

Streptococcus pneumoniae is a grampositive diplococcus, which asymptomatically colonizes the upper respiratory tract [ 1 ], but can also cause diseases like rhinosinusitis [ 2 ], pneumonia [ 3 ], otitis media [ 4 ] or meningitis [ 5 ]. In severe cases S. pneumoniae (or “Pneumococci” as they are also termed) can induce septic shock syndrome, a life-threatening event [ 6 ]. Thus, specific prophylaxis has been developed and vaccination against the most common strains of S. pneumoniae is recommended for children, patients over 51 years of age and populations at risk, e.g. patients receiving immunosuppression after organ transplantation or persons with immune defects [ 7 , 8 ].

As more than 90 different serovars of S. pneumoniae could be identified so far [ 9 ], research aims at developing vaccines that deliver broad immunity. So far, four different vaccines have been licensed and are in clinical use: Prevnar® (Wyeth/Pfizer), Synflorix® (GlaxoSmithKline), Prevnar13® (Pfizer) and Pneumovax23® (Merck) [ 10 , 11 ].

Prevnar® (or Prevenar®, as it is marketed in Austria) is a heptavalent conjugated polysaccharide vaccine consisting of polysaccharides from pneumococcal serotypes 4, 6B, 9 V, 14, 18C, 19F, and 23F, individually conjugated to CRM 197 , a non-toxic diphtheria toxin mutant [ 12 ]. Synflorix® covers the same serovars as Prevnar® plus serotypes 1, 5, and 7F. It is also a conjugated polysaccharide vaccine, using nonlipidated cell-surface liporotein (protein D) of Non-Typeable Haemophilus influenzae (NTHi) as well as tetanus and diphtheria toxoid as carriers [ 13 ]. Prevnar13® (Prevenar13® in Austria), also a conjugated polysaccharide vaccine (to CRM 197 ), delivers immunity against serovars 1, 3, 4, 5, 6A, 7F, 9 V, 14, 18C, 19A, 19F, 23F [ 14 ].

Pneumovax23®, the non-conjugated, 23-valent vaccine, however, consists of polysaccharides from serovars 1, 2, 3, 4, 5, 6B, 7F, 8, 9 N, 9 V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19F, 19A, 20, 22F, 23F & 33F and covers theoretically 85–90% of all circulating strains [ 15 ].

In Austria, the recommended vaccination scheme for infants is a conjugated vaccine at months 3, 5 and 12. This early start of vaccination is advised as the peak of meningitis manifestations caused by S. pneumoniae is within the 2nd year of life. Moreover, people over 51 years of age are advised in Austria to undergo vaccination, too. This population is not primarily affected by invasive pneumococcal diseases (meningitis or sepsis), but at risk to develop severe pneumonia. Thus, the Austrian Ministry of Health recommends a two-step immunization procedure, starting with the conjugated polysaccharide vaccine Prevenar13® followed by Pneumovax23® after 8 weeks. This serial immunization regimen has been established due to the better initial response in antibody titres to Prevenar13®, which is effectively boostered by immunization with Pneumovax23®, but also extends immunity to the 11 serovars that are not covered by Prevenar13®. It is not fully clear yet, how long these protective effects last; therefore people in Austria are advised to refresh their immunization protection. Preliminary data suggest that the protection lasts at least 3.5 years [ 8 ].

In Austria, populations at extended risk, such as patients with immune defects, HIV-positive, organ-transplanted or splenectomized patients, but also persons with cochlea implants or liquor-fistulas are advised to receive vaccinations between the age of 18 and 50 as well, depending on their pre-immunization status with either a conjugated or the non-conjugated 23-valent vaccine [ 8 ]. When and to which extent booster injections are necessary is still under investigation.

However, even an optimal vaccination status cannot fully prevent pneumococcal disease as our case report demonstrates.

Case presentation

The 25-year old male caucasian patient suffered from an autoimmune lymphoproliferative disorder (ALPS) that was treated by splenectomy 24 months before this event. He had no previous episodes of severe infections. In March 2014, he developed malaise, chills and abdominal pain of sudden onset after heavy exercise, and contacted his nearest outpatient clinic. A routine check-up involving ECG, chest X-ray, blood pressure measurement and determination of O 2 -saturation showed no significant abnormalities. Blood results showed slightly elevated leukocyte counts with 11.3 G/L, normal red blood cell counts (4.78 T/L) and normal platelets with 294 G/L (see Table ​ Table1). 1 ). The patient was sent home after transfusion of 1 L isotonic infusion solution and symptomatic therapy with metamizol and paracetamol.

Blood parameters from initial presentation at the outpatient clinic of the peripheral hospital until day 5 upon admission on our intensive care unit

Eight hours later, the general condition of the patient worsened rapidly and he had to be hospitalized because at that time he had already developed leukopenia (2.8 G/L), his platelet levels were low (108 G/L) and the serum creatinine was elevated (2.0 mg/dl). Hemostasis parameters were also altered (again depicted in Table ​ Table1). 1 ). A rapid test for S. pneumoniae -antigen was positive and although antimicrobial therapy was started immediately, the patient developed hemodynamic problems (systolic RR: 50 mmHg) and had to be transferred to an intensive care unit (ICU). In spite of catecholaminergic therapy, fluid resuscitation and intubation, the organ dysfunction of the patient deteriorated and he developed severe septic shock with metabolic acidosis (lactate 15 mmol/L), anuric renal failure, overt disseminated intravascular coagulation (DIC) and fast spreading necrotic skin lesions, resembling purpura fulminans.

Thus, the patient received fibrinogen (Haemocomplettan®, CSL Behring) and prothrombincomplex (Beriplex®, CSL Behring) alongside clindamycin, linezolid and intravenous immunoglobulins (Pentaglobin®, Biotest Pharma GmbH) and was transferred to our intensive care unit at the Medical University of Vienna.

Upon admission, his hemodynamic and respiratory situation was stable. The metabolic acidosis, however, worsened: lactate levels increased to 18 mmol/L and signs of hepatic impairment were detectable with elevated transaminases and hypoglycemia. Moreover, creatine kinase (CK) levels were massively increased at 6678 U/L and myoglobin values were at 11,500 ng/mL. The skin lesions progressed, and confluent lesions spread over the whole face, both hands and both feet. Hemostasis parameters showed thrombocytopenia (33 G/L), a PT of 31%, an aPTT of >180 s, fibrinogen values of 72 mg/dl and massively elevated D-Dimer levels (72.19 μg/ml), resembling septic coagulopathy with purpura fulminans. According to local and international recommendations, coagulation therapy with a plasma-derived protein C concentrate (Ceprotin®, Baxalta), was initiated. An initial bolus dose of 100 U/kg body weight was given, followed by 10 U/kg/h, aiming for plasma protein C activity values of 100 U/dL. Additional hemostatic therapy consisted of fibrinogen and platelet concentrates, antithrombin replacement (aiming for antithrombin levels of 100 U/dL), and low dose heparin infusion (250 U/kg BW/h). Moreover, extracorporeal renal replacement therapy had to be started because of acute renal failure.

Table ​ Table1 1 summarizes the blood parameters as well as clinical scores from the initial presentation at the outpatient clinic of the peripheral hospital until day 5 upon admission on our intensive care unit.

Under this treatment the patient could be successfully stabilized. Although CK and myoglobin values continued to increase during the next 3 days and the face and the limbs of the patient were impressively hypoperfused, there were no signs for a compartment syndrome, and no surgical intervention was necessary. After peaking at day 3 upon admission, CK values decreased within the next weeks until returning into the normal range after 4 weeks. In parallel, also the hemostaseologic parameters improved and the skin situation ameliorated.

The renal situation, however, remained unchanged and until week 4 no sufficient renal function could be established. Therefore, the patient was changed from continuous hemofiltration to intermittent hemodialysis, which was well tolerated. Creatinine levels were constantly high, peaking with 7.95 mg/dl.

After 27 days, the patient could be transferred from the intensive care unit to our infectiological ward, where he stayed for another 26 days. Within this stay and under forced fluid substitution, his creatinine levels returned almost into normal range (1.27 mg/dl); also the urine output increased, so renal replacement therapy could be stopped after 4 weeks upon admission. In following, renal function returned to normal. The local skin situation improved constantly, necrotic areas were surgically removed and healed decently.

The patient could be finally transferred to a rehabilitation center, from which he was discharged fully recovered.

Thorough examination of initial blood cultures showed that the patient had an infection with S. pneumoniae serovar 24F, a serovar, which has been long thought to be apathogenic.

A recent study of the “National Reference Center for Pneumococci” at the Austrian Agency for Health and Food Safety (AGES) depicting infections with S. pneumoniae in 2009 revealed that 303 invasive illnesses and 19 deaths occurred due to S. pneumoniae in Austria. Extrapolated to the population, Austria had 3.62 invasive diseases/100,000 inhabitants and a mortality of 0.23/100,000 resulting in a lethality of 6.3% in 2009. Scaled by diagnosis 43 Meningitis- (incidence 0.52/100,000), 82 Sepsis- (0.98/100,000) and 118 pneumonia/bacteremia-diseases (1.42/100,000) were detected [ 16 ].

Scaled by serovars, the most frequent infections were caused by serovar 3 (18.66%), followed by 1 (7.84%), 14 (7.09%) 7F (7.09%), 6A (6.72%) and 4 (5.97%). All others of the 39 different identified serovars (serovars could be isolated in total in 268 cases) occurred in less than 5%. Serovar 24F, the serovar infecting our patient was identified in only 3 cases [ 16 ]. In 2011 Serovar 24F was detected in 2 cases [ 17 ] and 2012 only once [ 18 ] in Austria.

This is in line with international data, e.g. in a meta-analysis of Hausdorff et al., who surveyed articles published in MEDLINE identifying pneumococcal isolates from patients. This study revealed that serovars 1 and 14 were most frequently isolated from blood, whereas 6, 10 and 23 could be isolated most frequently from cerebrospinal fluid samples [ 19 ]. A recent study investigating pneumococcal meningitis cases in France between 2001 and 2014 revealed that among the non-vaccine covered serotypes, serovars 12F and 24F emerged after the introduction of Prevnar® and Prevnar13® [ 20 ].

Also our case clearly shows that unusual strains of S. pneumoniae can cause severe courses of infections, especially in immunocompromised patients. Our 25-year old patient suffers from an autoimmune lymphoproliferative disorder (ALPS), which is characterized as a dysfunction of immunoregulation [ 21 ]. In most cases, ALPS is caused by a defect of the extrinsic apoptosis pathway, which signals via the FAS-receptor [ 22 ], resulting in lymphoproliferation with clinical manifestations such as lymphadenopathy and splenomegaly [ 23 , 24 ]. Our patient had to undergo repetitive extirpations of lymph nodes and was also splenectomized two years prior to the reported event, making him highly susceptible to infections by encapsuled bacteria, such as S. pneumoniae [ 25 ]. Especially within the first years after splenectomy, overwhelming post-splenectomy infection (OPSI) syndromes can be seen [ 21 , 26 ]. As in our case, this syndrome can be associated with disseminated intravascular coagulation (DIC) and subsequent protein C deficiency. Thus, replacement therapy with plasma-derived protein C concentrates is beneficial to overcome purpura fulminans and DIC [ 27 , 28 ], as it could be experimentally demonstrated that protein C is able to limit hemostatic system activation, halt DIC, and can contribute to normalization of organ microcirculation [ 29 ].

In order to prevent OPSI, our patient had been vaccinated against S. pneumoniae , Haemophilus influenzae , and Neisseria meningitidis . He was vaccinated with Prevenar13®, but as none of the licensed vaccines provides protection to the serovar 24F, he was still susceptible to pneumococcal infection, which thus had to be considered as differential diagnosis.

Summarizing, our case demonstrates the need for continuous vaccine development. In case of S. pneumoniae , in recent years, novel vaccines have extended the coverage from 7 to 23 serovars, for which immunity can be delivered, but still broader protection against also so-thought “apathogenic” strains would be needed, especially for groups at high risk.

Acknowledgements

The authors thank Judit Fazekas, MSc, for critical reading of the manuscript.

The authors declare that funding was not utilized for the preparation of this manuscript.

Availability of data and materials

Authors’ contributions.

JS cared for the patient, performed the literature review and wrote the manuscript; CT, PS, AH, CM, EMR, WG, PK, TS, SW and FT cared for the patient. All authors reviewed the manuscript and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report.

Ethics approval and consent to participate

Not applicable.

Abbreviations

Contributor Information

Josef Singer, Email: [email protected] .

Christoph Testori, Email: [email protected] .

Peter Schellongowski, Email: [email protected] .

Ammon Handisurya, Email: [email protected] .

Catharina Müller, Email: ta.relleumrd@ihtaC .

Eva-Maria Reitter, Email: [email protected] .

Wolfgang Graninger, Email: [email protected] .

Paul Knöbl, Email: [email protected] .

Thomas Staudinger, Email: [email protected] .

Stefan Winkler, Email: [email protected] .

Florian Thalhammer, Email: [email protected] .

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Doctors Saved Her Life. She Didn’t Want Them To.

When her “do not resuscitate” order was ignored, Marie Cooper found herself in a painful situation she had hoped to avoid.

Supported by

By Kate Raphael

Photographs by Kristian Thacker

• Aug. 26, 2024

Marie Cooper led her life according to her Christian faith. She baked pies for her neighbors in northern West Virginia, and said grace before even a bite of food. She watched Jimmy Swaggart, a televangelist preacher — a little too loudly, in her daughter Sherry Uphold’s opinion. And she always said that at the end of her life, she did not want to be resuscitated.

“My mother’s religious belief is when it is her time to go, that’s God’s choosing, not hers,” Ms. Uphold said. “She was very adamant about that.”

Last winter, doctors found cancer cells in her stomach. She’d had “do not resuscitate” and “do not intubate” orders on file for decades and had just filled out new copies, instructing medical staff to withhold measures to restart her heart if it stopped, and to never give her a breathing tube.

In February, Ms. Cooper walked into the hospital for a routine stomach scope to determine the severity of the cancer. After the procedure, Ms. Uphold visited her mother in the recovery room and saw her in a panic. Despite having an oxygen tube in her nose, Ms. Cooper was gesturing as if she could not breathe. She was able to force out just one word at a time.

Ms. Uphold called for help and was ushered to a waiting room while the medical team called an emergency code. Ms. Cooper grew even more distressed and “uncooperative,” according to medical records. Doctors restrained her and inserted a breathing tube down her throat, violating the wishes outlined in her medical chart.

Ms. Uphold, livid, confronted the doctors, who could not explain why Ms. Cooper had been intubated. When Ms. Cooper awoke, she tried to pull at the tubes and IV lines protruding from her body. She motioned to her daughter and the doctors that she desperately wanted her breathing tube removed. “They had me tied down,” Ms. Cooper said. “I was scared to death.” Ms. Uphold found herself in a situation she and her mother had always wanted to avoid.

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