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Discuss About The Treat Sepsis Patients Emergency Department?

A case study of a seventy-seven-year-old patient admitted to the ward through the emergency department for lower lobe pneumonia at night. She had a past history of hypertension, hypercholesterolemia and ischemic heart disease. She was on Ramipril 10mg, aspirin 100mcg, spironolactone 50mg and atorvastatin 80mg nocte.

On arrival to the emergency department, she presented with shortness of breath. She was put on oxygen and given ceftriaxone (antibiotics) which relieved this symptom. The patient had a calm night. In the morning the patient had shortness of breath and used accessory muscle to aid her in breathing. Her breathing rate was 36 breaths per minute. She was confused. Her blood pressure was 90/65 mmHg and heart rate of 120 bpm. She had a low-grade fever. Her oxygen saturation was at 91%. She complained of pain in the left lower chest on deep inspiration. The indwelling catheter that was inserted on admission has drained 30mls of urine.

The above presentations were alarming so the medical emergency team was called to intervene. The team inserted a central catheter in her subclavian vein which was secured so as to prevent her from removing it. She was started on two liters of 0.9% normal saline. She was started on azithromycin 500mg and the oxygen therapy was increased from two liters per minute to five liters.

The present paper will give, one, a detailed and structured primary assessment of Catherine. The ABCDE assessment, that is airway, breathing, cardiovascular, disability, and exposure assessment. Each assessment will be having a scientific rationale. The second part will focus on the finding obtained from the primary assessment. With this finding, a focused assessment will be done. Scientific rationale will explain the importance of each step done when assessing patient Catherine. Three, identify the type of shock that Catherine is experiencing. The pathophysiology of this shock and the clinical manifestation presented by Catherine that supports that she is experiencing the type of shock identified above. Four, explain the nursing interventions to be carried out. Prioritize the interventions giving a scientific rationale. Five, summarize the work above.

According to Olgers, Dijkstra, Drost-de Klerck, & Maaten, (2017), the ABCDE approach is the primary assessment performed on the critically ill or injured patient. This approach helps in early detection of life-threatening illnesses hence timely treatment/resuscitation. It provides life-saving modalities, breaks down the complex clinical circumstances into manageable situations. It gives a treatment guide/resuscitation guide. 

A- involves the airway assessment on Catherine. This is done so as to assess the airway patency. It should be the first one because if it gets obstructed it causes severe hypoxia which leads to cardiac arrest. The ques used when assessing the airway are as follows; the patient's voice, ability to communicate verbally, the breathing sounds, skin color, inspect the mouth for obstruction and assessment of the cervical spine injury. When there is airway obstruction there is a change in voice, the patient uses accessory muscle for breathing and they produce noisy sounds when breathing. All the above is as a result of narrowing of the airway making it had for the air to rush in or out (Thim, Krarup, Grove, & Lofgren, 2012). Catherine’s primary assessment should include, inspection of the mouth, assess the breathing sounds, inspection of the skin color, voice and communication abilities. The only significant findings on primary assessment on airway done on Catherine is that she talks in short sentences.  This indicates some aspects of airway obstruction. To treat this, the patient’s oxygen therapy is increased.

ABCDE Approach for Primary Assessment

B-breathing is assessed through oxygen saturation, auscultation of the lungs, assessment of the respiratory rate, inspection of use of axillary muscles for breathing and the chest symmetry when breathing. This is done so as to detect inadequate breathing early and intervene before any complication arises. Inadequate breathing causes inadequate tissue perfusion which can translate to cardiac arrest. Patient Catherine presents with difficulties in breathing. She uses the accessory muscle for breathing. She is hyperventilating, her respiration rate is 36 breaths per minute. Her oxygen saturation is 91%. She feels pain on deep inspiration on the right lower part of the chest. This clearly shows that she has difficulty in breathing. This means that tissue perfusion is being compromised. The immediate intervention is oxygen therapy and treating the cause. The breathing difficulty is as a result of sepsis. She has been started on broad-spectrum antibiotics to treat it. The oxygen volume she is receiving has been increased (Fein, 2014).

C-circulation is assessed through capillary refill time, systolic and diastolic blood pressure, the pulse rate, mucosal membrane and the temperature feel of the extremities. This assessment is important as it focusses on circulation. It allows early detection of circulation issues so as to remedy early. Patient’s Catherine blood pressure is 90/65mmHg with a heart rate of 120beats per minutes. This pulse is weak and thready. Her skin is flushed and sweaty. Her capillary refill is three seconds. All this indicates that there is inadequate tissue perfusion. This is life-threatening as can cause cell death and organ dysfunction. To avoid this the patient is to be infused with blood expanders, 0.9% normal saline. The patient is on broad-spectrum antibiotics to treat the sepsis which is causing hypotension. The patient also needs to lie in the supine position with her legs propped to ease venous return (Kumar et al., 2013).

D-disability is assessed through the level of consciousness. This is achieved through AVPU method, Glasgow Coma Score, the limb movement, the pupil reflexes to light and the blood glucose level. This assessment is important as the unconsciousness has effects on breathing and airway patency. Patient Catherine has a GCS of 14/15 and she is confused. Her pupils react on light and dilate at 3mm. This indicates that the patients’ needs close monitoring of the airway and breathing can be compromised (Barrett, Barman, & Boitano, 2017). 

E-exposure is assessed through body temperature and then a head to toe physical assessment examining signs of skin reactions, trauma, and deep venous thrombosis. This is important as it allows early detection of hypothermia, hyperthermia, trauma, or/and allergic reaction. Patient Catherine has a low-grade fever; exposure will help in reversing. While exposing the patient, her dignity should be observed (Hinkle & Cheever, 2013).

This is the nursing assessment of specific body systems as pertaining to the presenting complaints. Since it is a case of circulatory shock, it is the cardivascular system that will be thoroughly assessed. The presenting complaints in the cardiovascular system include palpitations, difficulty breathing, chest pain, dysponea and syncope (Glynn & Drake, 2014).

Findings from Primary Assessment

On inspection, the overall appearance of the patient is noted. The patient could be confused, sick looking or in obvious pain. Look at the chest to assess symmetry and movement with respiration. Palor and obvious cyanosis are observed as in septic shock hypoperfuion and hypoxia could lead to this. The hands are inspected for stigmata of cardiovascular disease such as finger clubbing, splinter hemorrhages, nicotine stains, cyanosis, anemia, coldness or hotness of the skin and oedema. The pulses are then measured as in septic shock the circulating volume is relatively reduced due to vasodilation. It is measured in relation to rate, rhythm, volume, and character. Thee jugular venous pressure is also measured to have an indication of cardiac function and any volume or pressure defects.The blood pressure is also measured as hypotension is a hallmark of septic shock and also the patient was a known hypertensive.

Palpation involves location and decription of the apex beat of the heart. It is described as displaced or not displaced from its normal position in an adult at fifth intercoastal space, mid-clavicular line. The patient is palpated to also note any masses and skin. The apex is displaced in heart enlargement. Also heaves and taps can be felt by the palm in heart enlargement. Catherine might have an enlarged heart due to hypertension.

Auscultation is the final step in the examination whereby a stethoscope is used to listen to heart sounds and over the aorta. Since the patient has suspected myocardial depression as expected in septic shock, the quality of the heart sounds should be noted and the heart rate charted Any added heart sounds and murmers can be described as thay point to a specific cardiac pathology (Colledge, Walker & Ralston, 2013). One should also listen for friction rubs as this is a common phenomena in pericarditis.

In order to develop septic shock, one has to develop sepsis. Sepsis is multisystem organ dysfunction due to a response to infection in the host. it is in itself life-threatening. Septic shock occurs in a division of those with sepsis as the infection causes circulatory insufficiency with underlying metabolic and cellular derangements. The risk of sepsis and therefore septic is increases in pneumonia and bacteremia but can occur following most infections including intraabdominal infections, infections involving indwelling catheters, skin, and wound infections.

The pathophysiology of septic shock is a complex interplay of immune responsiveness, inflammation, and end-organ involvement. The hallmarks of septic shock include hypotension, vasodilation and increased endothelial permeability on a background of severe inflammation. There is also an activation of the coagulation cascades (McConnell & Coopersmith, 2016). Powerful initiators of this inflammatory response include lipopolysaccharide (LPS) and endotoxins of gram-negative bacteria including E. coli, shigella etc. Another initiator is exotoxins and superantigens released by gram-positive bacteria including S. aureus, S. pneumonia, and H. influenza. The patient has lobar pneumonia which is commonly caused by gram-positive bacteria hence septic shock is feasible.  Lipopolysaccharide of gram-negative bacteria binds to a binding site on macrophages as the initial stage of the inflammatory response. The binding initiates a signal pathway that activates a proinflammatory state with the release of powerful inflammatory mediators. Cytokines releases include interleukins-1, interleukin-2, interleukin-6, interleukin-8, interleukin-12, tumor necrosis factor and platelet activating factor. The interplay of this cytokines with the vessel walls and endothelium at a massive multiorgan level causes the dramatic manifestations of sepsis. The cytokines interact with the hypothalamus resetting the body’s thermoregulatory setting giving the patient fever. This is an important clinical presentation as it helps differentiate septic shock from other forms of shock like hypovolemic shock where the skin is cold and clammy unlike the hot skin of a septic shock patient. On the endothelium, the cytokines induce nitric oxide synthesis through endothelial damage. Nitric oxide is a powerful vasodilator hence it leads to profound vasodilation. The endothelial regulatory mechanisms are also dysfunction so, despite high levels of circulating catecholamines to try and offset the vasodilation, it persists hence the reduced peripheral resistance. Vasodilation has an important role in the pathogenesis of shock. Due to vasodilation, the intravascular space is increased leading to a relative hypovolemia. Endothelial damage also causes increased capillary permeability and further extravasation of fluid from the intravascular space (Kalil, 2018).

Type of Shock Experienced

Damage to the endothelial cell causes activation of the coagulation cascade. Damaged endothelial cells cause neutrophil margination and platelet aggregation and by releasing tissue factor (TF) also activate the complement pathway. Endothelial cells also express immune receptors explaining their role in activation of coagulation. There is defective fibrinolysis coupled with inflammation and pro coagulation leads to hemostatic derangements including clot and end-organ damage due to ischemia. The procoagulant state leads to disseminated intravascular coagulation (DIC) (Kalil, 2018).

The clinical manifestations can be largely divided into three sections: signs and symptoms of sepsis, signs, and symptoms of the specific infection and signs of specific end-organ dysfunction.

  1. Signs and symptoms of sepsis

Signs of sepsis are usually nonspecific. They include fever, fatigue, anxiety, confusion, nausea, and vomiting. Fever is due to cytokines produced by macrophages in response to the infection resetting the thermoregulatory control of the hypothalamus. Catherine had a fever of 38.90 C. mental status is usually altered with anxiety, confusion, and agitation. Catherine was confused and removed her IV line necessitating the team to suture the central line in place.

  1. Signs and symptoms of the specific infection.

With a diagnosis of lobar pneumonia on treatment, Catherine still has signs and symptoms of pneumonia. She has a fever, difficulty in breathing as shown by the use of accessory muscles and the high respiratory rate and chest pain which is worse on breathing meaning it is most likely a pleuritic chest pain due to the setting of pleuritis. These symptoms can be explained by the disease process in pneumonia that causes lung consolidation and impaired respiratory function (Colledge, Walker & Ralston, 2013)

  1. Signs and symptoms of end-organ dysfunction

Septic shock will affect virtually all organ systems as hypoperfusion is global. In the cardiovascular system, the main sign is hypotension (Russell, Rush, & Boyd, 2018). This is due to the massive vasodilation that increases the intravascular compartment leading to a relative hypovolemia. The capillary endothelium is damaged losing some local regulation of peripheral resistance, one of the determinants of blood pressure together with cardiac output. Myocardial depression also contributes to hypotension (Bridges & Dukes 2015). It is postulated that several factors cause myocardial depression in septic shock including ischemia due to hypoperfusion, inflammatory cytokines, and coronary vessel dysfunction e.g. due to clots from a procoagulant state and any underlying heart disease. Catherine developed hypotension as on presentation her blood pressure was 140/90 mmHg but at review 6 hours later was at 90/55 mmHg. She has a history of ischemic heart disease and is hypertensive. These are risk factors for her as she can easily develop heart failure, myocardial infarction, and hypertension can mask the hypotensive state of shock hence giving a false impression of severity. She also has a tachycardia of 120bpm due to compensation as the heart tries to maintain perfusion in the setting of low intravascular volume. Catecholamines are responsible for this reflex.

In the respiratory system, tachypnea and hyperventilation arise. These set in as the alveoli become hypoperfused and reduce the production of surfactant which is important in keeping them open leading to a fall in oxygen saturation. Pulmonary capillaries leak due to direct injury to the capillary endothelium leading to pulmonary edema and alveoli collapse (Russell, Rush, & Boyd, 2018). This is denoted as acute lung injury or acute respiratory distress syndrome. Breathing difficulty becomes a concern as the patient becomes unable to maintain oxygen saturation. Catherine had a respiratory rate of 26 at presentation and 36 6 hours later both showing higher than normal rates. She was also using accessory muscles and was short of breath.

Nursing Interventions

The metabolic manifestations of hyperventilation and confusion are due to metabolic acidosis. Due to hypoperfusion and hypoxia, tissues revert to anaerobic respiration producing lactic acid that accumulates due to impaired renal function causing lactic acidosis. The body tries to compensate by more excretion of carbon dioxide through hyperventilation. However, hyperventilation can lead to overcompensation with the development of respiratory alkalosis that gives the patient confusion (Vincent & Ferreira, 2016).

Central nervous system manifestations include altered mental status as shown by agitation, confusion, and anxiety and ischemic events e.g. stroke. This is due to brain hypoperfusion and hypoxia in the setting of relative low intravascular volume. Catherine was confused and agitated, removing her IV line. Her GCS score deteriorated from 15/15 at 0130 to 14/15 six hours later.

Renal system manifestations include a low urine output. This is due to hypoperfusion and hypotension. An acute renal failure may ensue due to severe hypoxia leading to renal ischemia. Other mechanisms include activation of neutrophils and cytokines that have an effect on tubular injury. Catherine has renal injury as shown by low urine output of the only 30ml in the last six hours.

Hematologic manifestations include bleeding tendencies and thrombosis. The procoagulant state in sepsis leads to disseminated intravascular coagulation a complication of the deranged coagulation system. Impaired fibrinolysis predisposes the patient to thrombus formation leading to end organ damage including pulmonary emboli, myocardial infarction, gut ischemia, deep venous thrombosis, and stroke.

A patient in shock regardless the specific type, the major nursing diagnosis include one, the risk for metabolic acidosis as a result of inadequate perfusion which makes the cells to respire anaerobically. Two, fluid volume deficit. Three, tissue perfusion inadequacy. Four, self-care inadequacy and anxiety (Hinkle & Cheever, 2013).

The nursing care interventions aim at restoring effective tissue perfusion, maintaining the fluid volume within the normal range, stabilizing the patient’s vitals, and keeping the patient conscious and alert. This is achieved through, one, ensuring safe infusion of the intravenous fluids. Two, proper drug administration. Three, increasing the oxygen volume received by the patient per minute. Four, close monitoring of the patient’s vitals. Five, the nurse should monitor the patient’s weight and intake and output regularly.

The nurse should ensure that patient’s safety is observed during intravenous infusion. The medical team ordered the patient to be infused 2 liters of 0.9% normal saline. This is a volume expander as it increases the osmotic pressure in the intravascular drawing water from the extracellular compartment. This helps in tissue perfusion by increasing blood volume which increases blood pressure (Choi, Yip, Quinonez, & Cook, 2014). While infusing patient Catherine, the signs and symptoms of cardiovascular overload should be monitored regularly. These signs and symptoms include coughing, shortness of breath, generalized body swelling and rapid weight gain. Early detection gives room for resuscitations (Kreimeirer, 2016).

Proper drug administration. Patient Catherine has been prescribed azithromycin 500mg. The nurse should ensure that the ten rights of medication administration are followed. The right medication, right dosage, right time, right route, and the right patient should be observed. When this is observed, the drug efficiency is increased. The patient is having septic shock. Azithromycin will help in treating the sepsis which will, in turn, reverse shock. It is therefore important for the nurse to observe the medication rights (Rauen & Munro, 2015).

Summary

Increase oxygen therapy dosage. Initially, Catherine was receiving 2 liters of oxygen per minute. The medical ordered the oxygen level to be increased. The aim of the nursing interventions as mentioned earlier is to restore adequate tissue perfusion. The nurse should increase oxygen volume being received by the patient to about 5litres per minute. This will increase tissue perfusion as more oxygen will reach the cells (Gotts & Matthay, 2015).

The nurse should monitor the patient’s vitals regularly. This is so as to detect when the patient condition is deteriorating. Patient Catherine is critically ill; her vitals should be monitored every fifteen minutes. This will help in detecting changes in her condition which will allow timely intervention. The vitals include the respiration rate, blood pressure, pulse rate, temperature, and pain.

The nurse should monitor Catherine’s input and output closely. The patient has shock, which interferes with tissue perfusion to the kidneys. This causes renal insufficiency hence fluid and wastes retention. So as to detect when renal failure sets in the nurse should monitor the input/output of the patient. The nurse should weigh the patient regularly so as to detect fluid retention. When renal failure is detected early, hemodialysis and reduction or halt fluid intake can reverse this condition (Hinkle & Cheever, 2013).

Conclusion

The paper focusses on patient Catherine who has septic shock. Primary assessment and focused assessment was done on the patient. The ABCDE approach which assesses the patient condition in a glimpse allowing timely detection and management was done. The focused assessment of the respiratory system was done. Details and rationales on how and why the assessment was done have been explained above. The pathophysiology of shock and to be specific septic shock has been explained. The manifestation of shock has been explained and lastly, the nursing interventions have been discussed.

References

Barrett, E., Barman, M., Boitano, S. (2017). Ganong’s Review of Medical Physiology. (24th ed). New York, N.Y: McGraw Hill Medical.

Bridges, J. & Dukes, S. (2015). Cardiovascular aspects of septic shock: pathophysiology, monitoring, and treatment. Critical Care Nurse, 25(2), 14-40.

Choi, P., Yip, G., Quinonez, L., & Cook, D. (2014). Crystalloids vs. colloids in fluid resuscitation: A systematic review. Critical Care Medicine. 27(1), 200–209.

Colledge, N., Walker, R, & Ralston, S. (2013). Davidson’s Principles and Practice of Medicine. (21st ed). New York, N.Y: ‎Edinburgh.

Fein, A. M., (2014). Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock. Critical Care Clinics, 16(2), 289–313.

Glynn, M. & Drake, W. (2014). Hutchinson’s Clinical Methods: an integrated approach to clinical practice. London: Elsevier.

Gotts, J. & Matthay, M. (2016). Sepsis: pathophysiology and clinical management. The British Medical Journal. 353(1). 1585.

Guyton, A. C. (2015). Textbook of Medical Physiology. (13th ed.). Philadelphia: W. B. Saunders

Hinkle, J.L, Cheever, K.H. (2013). Brunner and Saddarth’s Textbook of Medical and Surgical Nursing, (13th ed) Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Kalil, A. (2018). Septic shock treatment and management. Medscape. Retrieved 19 March 2018, from https://emedicine.medscape.com/article/168402-treatment

Kreimeier, U. (2016). Pathophysiology of fluid imbalance. Critical Care, 4(2): S3–S7.

Kumar, A., Roberts, D., Wood, E., Light B., Parrillo E., Sharma, S., …, Cheang, M. (2013). Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Critical Care Medicine. 34(6):1589-96.

McConnell, W. & Coopersmith, M. (2016). Pathophysiology of septic shock: from bench to bedside. PubMed. Retrieved 19 March 2018, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4868872/

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Olgers, T., Dijkstra, M., Drost-de Klerck, M., & Maaten, J. (2017). The ABCDE primary assessment in the emergency department in medically ill patients; an observational pilot study. The Netherlands Journal of Medicine, 2017(3).

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Rivers, E., Nguyen, B., Havstad, S., Ressler, J., Muzzin, A., Knoblich, B., …. Tomlanovich, M. (2001) Early goal-directed therapy in the treatment of severe sepsis and septic shock. The New England Journal of Medicine,345(19), 1368–1377.

Russell, J., Rush, B. & Boyd, J. (2018). Pathophysiology of shock. Critical care clinics. 34(1). Pg. 43-61.

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Thim T., Krarup, N., Grove, L. & Lofgren B. (2012). ABCDE – a systematic approach to critically ill patients. International Journal of General Medicine.2010;172(47):3264–3266.

Van der Vegt, A., Holman, M. & ter Maaten, J. (2012). The value of the clinical impression in recognizing and treating sepsis patients in the emergency department. European Journal of Emergency Medicine.19:373-8.

Vaughan, J. & Parry, A. (2016). Assessment and management of the septic patient: part 1. British Journal of Nursing. 25(17). Retrieved 19 March 2018, from https://doi.org/10.12968/bjon.2016.25.17.958

Vaughan, J. & Parry, A. (2016). Assessment and management of the septic patient: part 2. British Journal of Nursing. 25(21). Retrieved 19 March 2018, from https://doi.org/10.12968/bjon.2016.25.21.1196.

Vincent, L., Ferreira, L., (2016). Evaluation of organ failure: We are making progress. Intensive Care Medicine, 26(6), 1023– 1024

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