Recognition and Management of Clinical Deterioration in Hospitalized Patients

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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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