The current essay is a discussion on recognition and management of clinical deterioration in the hospitalized patient. The discussion is focused on a case presentation of Jedda Merindah, a 33-year-old male. He was admitted via the oncology unit where he was undergoing chemotherapy for acute myeloid leukemia. He presented with hypotension. On assessment he was anxious, restless, diaphoretic, cool extremities with a tachycardia of 118 beats/min, hypotension of 90/65 mmHg, febrile (38.8oC), and a tachypnea of 28 breaths per minute. he was in respiratory distress evidenced by the use of accessory muscle with an oxygen saturation of >95%. His ECG revealed an atrial fibrillation. He had a decreased urine output reporting dark colored urine. His blood pathology results showed an anemia of 89 g/l, a leucopenia of 3.4 × 10*9/L, a thrombocytopenia of 114 × 10*9/L, a raised serum creatinine of 138 umol/L, raised urea of 11.2 umol/L, raised APTT of 47 seconds and raised INR of 2.4. the paper will discuss the signs of deterioration in this patient, providing the pathophysiology underlying the condition with relation to the clinical signs. One key clinical care priority will be addressed and nursing interventions for addressing the issue.
Shock
The patient presents with signs of shock (Angus & van der Poll, 2013). Shock is a state of circulatory insufficiency whereby the blood flow hence tissue perfusion is inadequate to meet the metabolic needs of the body. There exist several types broadly classified as; hypovolemic shock, cardiogenic shock, distributive shock and obstructive shock. Any mechanism that reduces the perfusion mechanism of tissues will cause shock. The patient meets the criteria for septic shock including hypotension with a fever of more than 38oC (Dellinger et al., 2012). Septic shock is characterized by massive vasodilation and increased endothelial permeability leading to hypotension following severe inflammation (King, Bauzá, Mella, & Remick, 2013). Coagulation is also activated in this process. Triggers of this response include lipopolysaccharide (LPS) and endotoxins of gram-negative bacteria, exotoxins and superantigens released by gram-positive bacteria (King, Bauzá, Mella, & Remick, 2013).
The patient also has atrial fibrillation on ECG, which is a cause of cardiogenic shock. Atrial fibrillation, a form of supraventricular arrhythmia causes unorganized atrial depolarization, leading to impaired ventricular filling, reducing the cardiac output and blood pressure (Arrigo, Bettex, & Rudiger, 2014). Eventually, reduction in cardiac output leads to hypoperfusion of end-organs and shock.
Shock progresses through four stages, an initial stage, a compensatory stage, progressive stage and a refractory stage. The patient is in the compensatory stage. The body releases catecholamines, epinephrine and norepinephrine as it tries to respond to the reduced perfusion There is a vasoconstriction, increased heart rate (above 100 bpm) and increased heart contractility to increase cardiac output and perfusion. Shunting of blood from non-vital organs such as skin, kidneys and the gut. Shunting of blood from the skin causes it to be cold and clammy as seen in the patient (Seymour & Rosengart, 2015). Kidney hypoperfusion leads to reduced urine output and features of acute kidney injury as present in the patient (Post, Kellum, Bellomo, & Vincent, 2017). The patient has deranged kidney functions as evidenced by a raised creatinine and urea (Zarbock, Gomez, & Kellum, 2014). Hypoperfusion causes anaerobic respiration in the cells causing a build-up of lactic acid and a metabolic acidosis. This causes hyperventilation as seen in the patient who has a tachypnea of 28 to remove excess acid (Seymour & Rosengart, 2015). A compensatory alkalosis may ensue causing a change in mentation for example confusion. The compensatory mechanisms try to keep the perfusion within normal. Blood pressure falls below 90 mmHg on a background of tachycardia. The patient is hypotensive at 90/67 mmHg. This puts a strain on the already overworked myocardium.
Clinical deterioration
Recognition of clinical deterioration is among the most life-saving intervention in critical care (Ludikhuize, Smorenburg, de Rooij, & de Jonge, 2012). According to the Australian Commission on Safety and Quality in Health Care, (2012), it is an organizations responsibility to make sure there are tools in place for the recognition of a deteriorating patient and escalation of appropriate care. It also requires for use of appropriate human indices in the assessment.
The use of vital signs; blood pressure, heart rate, temperature and level of consciousness (GCS), are the most commonly used parameters for the monitoring of deterioration (Barfod et al., 2012). Mortality and other events such as cardiac events are usually preceded by abnormal vitals (Jones, Mitchell, Hillman, & Story, 2013). The patient presents with signs of deterioration including a hypotension of 90/67 mmHg and a tachycardia of 118 beats/min.
One of the systems that used vital data is the modified early warning system (MEWS). It uses temperature, blood pressure, heart rate and level of consciousness to calculate a score which initiates a response with each progressive rise in the score (Kyriacos, Jelsma, & Jordan, 2011). According to the MEWS, the patient scores at 5 which is past the trigger point for action. The response involves notifying the nursing team leader, increasing the frequency of observations to at least half-hourly, assigning an escort and requesting a medical officer clinical review (Kyriacos, Jelsma, & Jordan, 2011).
Clinical care priority and care planning
Shock is a progressive clinical entity with a propensity for rapid deterioration. The patient has a real risk of progression into progressive shock with further worsening of perfusion, with blood pressure less than 90 and tachycardia of more than 150 beats per minute. If the patient progress, it carries a worse prognosis with increased mortality. Progression to refractory stage causes irreversible cellular damage and multi-system organ failure. Prevention of this catastrophic eventuality through recognition of clinical care priorities is important.
At this stage, the clinical care priority is fluid management (Malbrain et al., 2018). The nursing diagnosis is deficient fluid volume related to septic shock and cardiogenic shock, evidenced by hypotension, tachycardia, altered mental status and reduced urine output.
Goals of interventions
Planning goals of therapy are done following the SMART approach. The goals need to be specific, measurable, attainable, relevant and timely . The goals of therapy in this patient is: maintaining the patients circulating volume evidenced by normalization of vital signs including blood pressure and pulse rate, normalization of urine output, return to normal mental status, normal bowel sounds and skin warm and dry (Malbrain et al., 2018).
Nursing interventions
The first intervention is monitoring trends in blood pressure, pulse rate, temperature, and level of consciousness. Monitoring these signs gives clues on the progression of shock and response to therapy (Kyriacos, Jelsma, & Jordan, 2011). Hypotension is as a result of massive vasodilation leading to a relative hypovolemia. Worsening hypovolemia and hypoperfusion can be picked on monitoring of blood pressure. Tachycardia is due to the sympathetic response to shock states and worsening tachycardia is a poor prognostic factor due to increased myocardial strain, development of arrhythmias and cardiac collapse (King, Bauzá, Mella, & Remick, 2013). Worsening fever is an indicator of worsening sepsis and need for intervention. It is due to release of inflammatory cytokines from the infection causing a central thermoregulation center reset of the basal body temperature. It is an important sign of sepsis and should be looked out for.
Administration of fluids as indicated is the next recommended action. In septic shock, hypoperfusion and hypotension lead to impaired cellular function. Correction of hypoperfusion and hypotension requires aggressive fluid administration (Malbrain et al., 2018). The fluid administration progresses in four phases including a resuscitation phase (within minutes), the optimization phase (within hours), a stabilization phase (within days) and evacuation (days to weeks). During resuscitation, early fluid boluses are indicated with crystalloids (Macdonald et al.,2017). The Surviving Sepsis Campaign recommends a dose of 30ml/ kg of crystalloids, which should be given within the first 3 hours (Malbrain et al., 2018; Perel, Roberts, & Ker, 2013). Optimization phase also involved directed fluid boluses with the aim of optimizing organ support and tissue perfusion. This phase is directed by indices of fluid responsiveness and is aimed at preventing fluid overload. The stabilization phase involves giving of maintenance fluids for normal maintenance and replacement of losses. This phase follows recovery from shock as it assumes a hemodynamically stable patient. The final phase is a de-resuscitation phase following recovery or a third hit where there is increased permeability leading to capillary leaks and edema (Malbrain et al., 2018).
The third nursing intervention is the administration of drugs as indicated. According to Surviving Sepsis Campaign, drugs used in the treatment of septic shock include broad-spectrum antibiotics for the infection, norepinephrine to provide ionotropic support, epinephrine when needed, and vasopressin as a combination with epinephrine (Malbrain et al., 2018).
Conclusion
Clinical deterioration is aa manageable critical care phenomena with adequate evaluation and monitoring of vital signs. The case study patient presented with features of septic shock leading to circulatory and multisystem manifestations. The clinical priority in this patient was a fluid deficiency due to massive vasodilatation and relative hypovolemia. Nursing intervention to remedy this included monitoring of vitals to assess deterioration or response to therapy, administration of fluids as indicated and administration of drugs as indicated.
References
Angus, D. C., & van der Poll, T. (2013). Severe Sepsis and Septic Shock. New England Journal of Medicine, 369(9), 840-851. doi:10.1056/NEJMra1208623
Arrigo, M., Bettex, D., & Rudiger, A. (2014). Management of Atrial Fibrillation in Critically Ill Patients. Critical Care Research and Practice, 2014, 10. doi:10.1155/2014/840615
Australian Commission on Safety and Quality in Health Care. (2012). National safety and quality health service standards. Australian Commission on Safety and Quality in Health Care. Retrieved 20, August 2018 from https://www.safetyandquality.gov.au/
Barfod, C., Lauritzen, M. M. P., Danker, J. K., Sölétormos, G., Forberg, J. L., Berlac, P. A., . . . Lange, K. H. W. (2012). Abnormal vital signs are strong predictors for intensive care unit admission and in-hospital mortality in adults triaged in the emergency department – a prospective cohort study. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 20(1), 28. doi:10.1186/1757-7241-20-28
Dellinger, R. P., Levy, M. M., Rhodes, A., Annane, D., Gerlach, H., Opal, S. M., . . . Moreno, R. (2013). Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012. Intensive Care Med, 39(2), 165-228. doi:10.1007/s00134-012-2769-8
Jones, D., Mitchell, I., Hillman, K., & Story, D. (2013). Defining clinical deterioration. Resuscitation, 84(8), 1029-1034. doi:https://doi.org/10.1016/j.resuscitation.2013.01.013
King, E. G., Bauzá, G. J., Mella, J. R., & Remick, D. G. (2013). Pathophysiologic mechanisms in septic shock. Laboratory Investigation, 94, 4. doi:10.1038/labinvest.2013.110
Kyriacos, U., Jelsma, J., & Jordan, S. (2011). Monitoring vital signs using early warning scoring systems: a review of the literature. Journal of Nursing Management, 19(3), 311-330. doi:10.1111/j.1365-2834.2011. 01246.x
Ludikhuize, J., Smorenburg, S. M., de Rooij, S. E., & de Jonge, E. (2012). Identification of deteriorating patients on general wards; measurement of vital parameters and potential effectiveness of the Modified Early Warning Score. Journal of Critical Care, 27(4), 424.e427-424.e413. doi: https://doi.org/10.1016/j.jcrc.2012.01.003
Macdonald, S. P. J., Taylor, D. M., Keijzers, G., Arendts, G., Fatovich, D. M., Kinnear, F. B., . . . Wibrow, B. (2017). REstricted Fluid REsuscitation in Sepsis-associated Hypotension (REFRESH): study protocol for a pilot randomised controlled trial. Trials, 18(1), 399. doi:10.1186/s13063-017-2137-7
Malbrain, M. L. N. G., Van Regenmortel, N., Saugel, B., De Tavernier, B., Van Gaal, P.-J., Joannes-Boyau, O., . . . Monnet, X. (2018). Principles of fluid management and stewardship in septic shock: it is time to consider the four D’s and the four phases of fluid therapy. Annals of Intensive Care, 8(1), 66. doi:10.1186/s13613-018-0402-x
Perel, P., Roberts, I., & Ker, K. (2013). Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database of Systematic Reviews (2). doi: 10.1002/14651858.CD000567.pub6
Post, E. H., Kellum, J. A., Bellomo, R., & Vincent, J. L. (2017). Renal perfusion in sepsis: from macro- to microcirculation. Kidney Int, 91(1), 45-60. doi: 10.1016/j.kint.2016.07.032
Seymour, C. W., & Rosengart, M. R. (2015). Septic shock: Advances in diagnosis and treatment. JAMA, 314(7), 708-717. doi:10.1001/jama.2015.7885
Zarbock, A., Gomez, H., & Kellum, J. A. (2014). Sepsis-induced AKI revisited: pathophysiology, prevention and future therapies. Current Opinion in Critical Care, 20(6), 588–595. https://doi.org/10.1097/MCC.0000000000000153
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