Recognition and Management of Clinical Deterioration in Hospitalized Patients

This essay discusses the recognition and management of clinical deterioration in hospitalized patients through a case presentation of a 33-year-old male with septic and cardiogenic shock. The pathophysiology underlying the condition with relation to the clinical signs is provided. One key clinical care priority is addressed and nursing interventions for addressing the issue are discussed.

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THE DETERIORATING PATIENT
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Introduction
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
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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
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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
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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
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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).
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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.
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