Discussion w3 652

Discussion Replies Week 2

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Q-1

Sepsis characterized by unresponsive hypotension and lactic acidosis (serum lactate >2 mmol/L) requiring vasopressor therapy to maintain MAP> 65 mmm of Hg despite adequate fluid resuscitation. It is a condition of infection with acute organ dysfunction which is associated with high mortality, long term morbidity for those who survive. Approximately 19 million people develop sepsis every year and only 14 million survives to hospital discharge with varying prognosis (Prescott, & Angus, 2018). The survival depends on pre-sepsis health status, the severity of acute sepsis episode, quality of hospital treatments. The resuscitation and management initiated immediately within 1 hour. The interventions were measuring lactate level, re-measuring if initial lactate is >2 mmol/L, obtain cultures prior to administration of antibiotics, administer broad-spectrum antibiotics, begin rapid administration of 30 ml/kg crystalloids for hypotension or lactate >4 and apply vasopressors if the patient is hypotensive during and after fluid resuscitation to maintain MAP>65 (Levy, Evans, & Rhodes, 2018). Sequential Organ Failure Assessment (SOFA) score equal to or > 2 points are the diagnostic criteria.

SIRS-Systemic inflammatory response syndrome is a condition of the excessive inflammatory response of the body to an infectious or non-infectious process such as burns, pancreatitis, autoimmune disorders, ischemia, and trauma. The diagnostic criteria based on the presence of two out of five categories which were temperature above 100.4 or below 98.6, Heart rate over 90 beats per minute, resp. rate over 20, PaCO2 less than 32 mmHg, WBC over 12000 or less than 4000.

Severe sepsis/ septic shock- Severe sepsis is a condition of prolonged sepsis leading to multi-organ failure. The patient will be presented with positive signs and symptoms of septic shock which are persistent hypotension even after fluid resuscitation and while being on vasopressors with signs of poor perfusion such as low urinary output, cold/clammy/cyanotic extremities/digits, and altered mental status.

The sepsis protocol used in the Ascension facility (Ascension library services, 2021), is based on recognizing the signs and symptoms using the tools and automated EHR alerting the staff for screening the patients and use clinical judgments and notify MD for concern of sepsis even if the screening tool is negative. The criteria were any hypotension with MAP <65 mm of Hg, SBP <90, or decrease > 40 mm of Hg. Our hospital follows a 3-hour bundle goal which is measuring serum lactate, draw blood cultures prior to antibiotics administration, and starting of broad-spectrum antibiotics within 1 hour if possible, at least within 3 hours, and fluid replacement for any hypotension or lactate >4 with 30 ml/kg of crystalloids. 6-hour bundle includes re-measuring lactate if initial lactate elevated >2 mmol/L, starting of vasopressors for persistent hypotension, and reassess for volume status by CVP, ScvO2, and fluid challenge assessment. ICU required for patients requiring vasopressors and consider ICU placement for sepsis patients with lactate >4 mmol/L upon presentation and CVP or ScvO2 if appropriate catheter present.

The initiation of the sepsis bundle is central to the implementation of the Surviving Sepsis Campaign (SSC) 2016 guidelines are intended to be initiated within 1 hour of recognizing sepsis leads to improved sepsis survival. The new approach in the treatment of sepsis treatment is the revision of the SSC is that the 3-h and 6-h bundles have been combined into a “single hour-1 bundle” with the intention of beginning resuscitation and management immediately (Levy, Evans, & Rhodes, 2018).

References

Prescott, H. C., & Angus, D. C. (2018). Enhancing recovery from sepsis: A review. Jama, 319(1), 62-75. Retrieved from https://jamanetwork.com/journals/jama/article-abstract/2667727

Levy, M. M., Evans, L. E., & Rhodes, A. (2018). The surviving sepsis campaign bundle: 2018 update. Intensive care medicine, 44(6), 925-928. Retrieved from https://link.springer.com/article/10.1007/s00134-018-5085-0

Ascension library services. (Updated on 2/9/2021). Nursing point-of-care tools: Sepsis. Retrieved from https://ascension-wi.libguides.com/c.php?g=814937&p=6592174

Reply 1

Septic shock or sepsis-3 is an advanced stage of sepsis that presents severe symptoms. Its criteria include hypotension, organ failure, & lactic acidosis. Perfusion-related problems cause an increased level of lactate (>2 mmol/L) and decreased blood pressure instead of fluid resuscitation(Doshi et al., 2018). Hypotension can damage the organs and lead to death. So, sepsis-3 could be fatal. Vasopressors are given as first-line treatment to manage sepsis-3(Shi, Hamzaoui, De Vita, Monnet, & Teboul, 2020). The blood vessels tighten up by initiating vasopressin therapy. As a result, the blood pressure increases.

I support your opinion; SOFA score = or > 2 diagnoses is sepsis-3. I strongly agree the increased heart rate, respiration rate, hypothermia, and leukocytosis are the diagnostic criteria for SIRS. The patients presenting symptoms of sepsis-3, like low urinary output (due to low BP) and mental retardation, may follow the diagnostic procedures. Blood cultured test with antibiotic administration & the serum lactate levels is checked. High lactate levels (>4 mmol/L) shifts the patient to ICU. Timely management of sepsis-3 may save lives, according to Surviving Sepsis Campaign (SSC). Additionally, if vasopressin therapy remains ineffective, epinephrine is given with it as a second-line treatment in sepsis-3.

References

Doshi, P. B., Park, A. Y., Banuelos, R. C., Akkanti, B. H., Darger, B. F., Macaluso, A., . . . Chambers, K. A. (2018). The Incidence and Outcome Differences in Severe Sepsis with and without Lactic Acidosis. Journal of emergencies, trauma, and shock, 11(3), 165-169. doi:10.4103/JETS.JETS_102_17

Shi, R., Hamzaoui, O., De Vita, N., Monnet, X., & Teboul, J.-L. (2020). Vasopressors in septic shock: which, when, and how much? Annals of translational medicine, 8(12), 794-794. doi:10.21037/atm.2020.04.24

Q-2

Sepsis

This is a condition that is potentially life-threatening that usual occurs when the body or the immune system declines or fails to act on the invading pathogen. The body is overwhelmed by the invading agent and is unable to mount an adequate response therefore leading to disseminated spread of the infection throughout the body. The criteria for diagnosing sepsis required the presence of an ongoing infection plus 2 or more of the following:

Hypotension

Defined as SBP <90mmHG

<70mmHg MAP

Increased lactate levels

Defined as > 1 mmol/L

Mottled skin

Decreased capillary refill

Febrile of >38 degrees C

And Tachypnea

Increased in heart rate and respiratory rate

Alterations in mental status

Increased WBC count

Increased in CRP levels

Increased procalcitonin levels

Decreased paO2

With significant hypoxemia

Decreased in urine output

Defined as <0.5ml/kg/hr. for at least 2 hours despite administration of fluid resuscitation

Decreased platelet count (Evans, 2018)

Severe sepsis

This is a continuation of sepsis that is complicated by the onset of an organ failure. Criteria for diagnosing severe sepsis requires the following criteria:

Hypoperfusion exemplified by renal failure

Organ dysfunction

At least one organ involved

Fever

Decreased mean arterial pressure (MAP)

Defined as <60mmHg

Increased in creatinine levels

Alterations in mental status

Abnormal coagulation studies

Abnormal PT/APTT or thrombin time results

Increased bilirubin (>2.0mg/dl) (Evans, 2018)

SIRS

Defined as systemic inflammatory response to infection may it be suspected or confirmed by clinical evaluation. Criteria of SIRS are the presence of at least 2 of the following:

Fever of >38 degrees Celsius

Hypothermia of <36 degrees Celsius

Tachycardia

Tachypnea

Increased WBC count (Evan, 2018)

Septic shock

This is the consequence of an untreated or unsuccessfully treated sepsis that leads to circulatory collapse exemplified by a significant drop in blood pressure levels. Criteria for diagnosis include the persistence of the following despite adequate fluid resuscitation:

Hypotension

Decreased MAP

Increased lactate levels (Evans, 2018)

For the current hospital protocol regarding positive severe sepsis and/or septic shock assessments, the RN will immediately initiate an electronic order for lactate level and the RN will administer antibiotic(s) and/or IV fluids as ordered by the physician. Administration of the antibiotic(s) and fluids must be documented in the patient’s medication administration record. Blood cultures should be drawn prior to administration of antibiotics and documentation should reflect blood culture collection (Dellinger & Levy, 2018).

Approaches to severe sepsis and septic shock continue to evolve with strategies put forward and discarded regularly. The focus for sepsis shock is now on timely fluid resuscitation, antibiotics, and, if necessary, vasopressor agents. However, the Holy Grail seems to have always been to intervene in the inflammatory cascade, shutting down what is often a deleterious set of forces that contribute to death. Complicating factors have been that sepsis is such a heterogeneous condition, not only in the infectious causes but in the host immune responses. However, despite some initial successes, there was never enough convincing data to suggest sufficient bang for the buck with respect to mortality reduction. Nevertheless, trial continue including high-dose vitamin C, employed with corticosteroids and thiamine in sepsis, and it appears preliminarily to show benefit (Singer & Sepsis Definitions Task Force, 2016).

References

Dellinger, R.P. & Levy M., (2018). Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: Critical Care Medicine (36) 1394-1396. Retrieved from http//:CritCareMed2018.org/39874

Evans T. (2018). Diagnosis and management of sepsis. Clinical medicine (London, England), 18(2), 146–149. https://doi.org/10.7861/clinmedicine.18-2-146

Singer, M., & Sepsis Definitions Task Force (2016). Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 315(8), 775–787. https://doi.org/10.1001/jama.2016.0289

Reply 2

The presence of an infection within the body initiates a cascade of reactions. The body does not show a potent immune response because of pathogens. This is the first stage of sepsis. This leads to a life-threatening state. I strongly agree with sepsis's diagnostic criteria as hypotension, elevated heart and respiratory rate, lactic acidosis, and tachypnea. Some conditions are secondary to these conditions, such as hypotension cause low urinary output. Like other organs, hypotension cause dysfunction of the CNS. The deterioration in CNS results in mental retardation (Czempik, Pluta, & Krzych, 2020). Platelet count is decreased due to invading pathogens. Organ damage may cause hypoxemia. Organ damage is the characterization of second-stage (or severe) sepsis. The diagnostic criteria are different in this stage.

I support your criteria; organ damage results in perfusion abnormality and high creatinine levels in case of kidney failure (Peerapornratana, Manrique-Caballero, Gómez, & Kellum, 2019) abnormal PT/APTT, coagulation, and anti-coagulation (thrombin) studies.

In my opinion, liver damage causes hyperbilirubinemia. The body shows a systematic inflammatory response to infection. The criteria to assess SIRS are hypothermia, tachycardia, and high WBCs count. If sepsis is not treated, it develops an acute stage septic shock. The diagnosis is made by blood cultures, clinical presentation, and blood tests. Studies are conducted to reduce septic mortality.

References

Czempik, P. F., Pluta, M. P., & Krzych, Ł. J. (2020). Sepsis-Associated Brain Dysfunction: A Review of Current Literature. International journal of environmental research and public health, 17(16), 5852. doi:10.3390/ijerph17165852

Peerapornratana, S., Manrique-Caballero, C. L., Gómez, H., & Kellum, J. A. (2019). Acute kidney injury from sepsis: current concepts, epidemiology, pathophysiology, prevention and treatment. Kidney international, 96(5), 1083-1099. doi:10.1016/j.kint.2019.05.026

Q-3

Sepsis, SIRS, Severe Sepsis, and Septic Shock are all related to one another and can appear in a patient at any stage. The first, SIRS, or systemic inflammatory response syndrome (SIRS) which is defined as an exaggerated defense response of the body to an external stressor like infection by dysregulation of pro and anti-inflammatory pathway occurring at the same time (Chakraborty, & Burns, 2020). In this scenario, we can say that an infection has triggered SIRS, and then it's a ladder approach into the subsequent definitions. Sepsis has been defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection (Vucelic et al., 2020). Severe sepsis builds on the sepsis definition and adds that it has now gotten to the point where there is now tissue or organ hypoperfusion and subsequent ischemic damage (Vucelic et al., 2020). The final step, septic shock, is the most severe form of sepsis and occurs when hypoperfusion and ischemic damage is so great that it causes systemic hypotension by compromising the circulatory and metabolic homeostatic processes (Mahapatra& Heffner, 2020).

My current clinical sepsis protocol is pretty standard, it starts with recognizing and identifying a possible sepsis patient, and then it moves to determine what stage they are in. Is it SIRS, Sepsis, Septic Shock, or Severe Sepsis? We begin by assessing the patient's vital signs, and most of the time they are hypotensive at this point. We then start with fluid resuscitation with 0.9% NS, a full blood panel including blood cultures, and then subsequent broad-spectrum antibiotics to cover a wide variety of possible infectious diseases. Then depending on if the patient needs vasopressors or even a ventilator, will eventually determine where the patient will be admitted to.

One new approach to sepsis management is based on the question how much fluid do we give, or is the patient even a fluid responder? This brings about new light to the subject as there are people who can be fluid responders or non-fluid responders which can only be aided by vasopressors (Krige, Bland, &Fanshawe, 2016). While this idea has been around for a little while, how to measure it has been in the spotlight more recently, with devices such as utilizing ECHOs or TEEs (Krige, Bland, &Fanshawe, 2016). While the passive leg raise can provide 150-300 mL of blood to the thoracic component of the body, it will also show an increase in cardiac output due to an increase in preload, subsequently raising afterload and overall blood pressure (Krige, Bland, &Fanshawe, 2016). While measuring this with an ECHO or TEEs we are looking for ventricular variability, whereas greater than 4% indicates dehydration and the ability to accept more fluid, and up to greater than 12% which indicates the need for massive fluid resuscitation (Krige, Bland, &Fanshawe, 2016). In addition to maintaining blood pressure and blood flow, we also want to make sure that the output is balanced as well, in order to prevent fluid volume overload, but this is unlikely if a patient is in full-blown septic shock (Krige, Bland, &Fanshawe, 2016).

References

Chakraborty, R.K., Burns B. (2020). Systemic Inflammatory Response Syndrome. StatPearls Treasure Island StatPearls Publishing. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK547669/

Krige, A., Bland, M., &Fanshawe, T. (2016). Fluid responsiveness prediction using VigileoFloTrac measured cardiac output changes during passive leg raise test. Journal of Intensive Care, 4(1). https://doi-org.lopes.idm.oclc.org/10.1186/s40560-016-0188-6

Mahapatra, S., Heffner, A.C. (2020) Septic Shock. StatPearls Treasure Island StatPearls Publishing. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK430939/

Vucelić, V., Klobučar, I., Đuras-Cuculić, B., GverićGrginić, A., Prohaska-Potočnik, C., Jajić, I., Vučičević, Ž., &Degoricija, V. (2020). Sepsis and septic shock - an observational study of the incidence, management, and mortality predictors in a medical intensive care unit. Croatian Medical Journal, 61(5), 429–439.

Reply 3

Patients are immunocompromised; they can develop sepsis at any stage. The sepsis, if remains untreated, leads to severe sepsis and septic shock. An inflammatory response elicited by the body against pathogens causes systematic inflammatory response syndrome (SIRS). I agree with your point, the immune system first induces a pro-inflammatory response, an anti-inflammatory response then follows it. It is correct to say that infections lead to SIRS(Ye-Ting & Dao-Ming, 2018). The impaired immune response is the major cause of sepsis that results in organ dysfunction. The organ dysfunctioning contributes to organ hypoperfusion in the next stage of sepsis i.e. severe sepsis.

In my opinion, sepsis becomes severe sepsis if treatment is not initiated at the time. The third stage, sepsis, is the advanced and most severe stage. It is called septic shock. The severity of sepsis leads to metabolic and homeostatic fluctuations resulting in hypotension and accumulation of lactic acid. You are right sepsis diagnostic protocol begins with assessing the possible etiology of infection. Vital signs like hypotension help in the evaluation of the stage of sepsis(Hébert, Boucher, Guimont, & Weiss, 2017). Broad-spectrum antibiotics are helpful in blood culturing. The measurement of fluid is a novel approach.The cardiac output increased in fluid-responders measured with ECHO. Balance cardiac output indicates optimal blood pressure & blood flow.

References

Hébert, A., Boucher, M.-P., Guimont, C., & Weiss, M. (2017). Effect of measuring vital signs on recognition and treatment of septic children. Paediatrics & child health, 22(1), 13-16. doi:10.1093/pch/pxw003

Ye-Ting, Z., & Dao-Ming, T. (2018). Systemic Inflammatory Response Syndrome (SIRS) and the Pattern and Risk of Sepsis Following Gastrointestinal Perforation. Medical science monitor : international medical journal of experimental and clinical research, 24, 3888-3894. doi:10.12659/MSM.907922