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Adult Nursing Skills Underpinning Complex Care 1

Adult Nursing Skills Underpinning Complex Care

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Adult Nursing Skills Underpinning Complex Care 2

Introduction

This essay examines the complications associated with the named patient after the

resection of the bladder tumour. The article discusses the pathophysiology of bladder cancer and

linking it to different types of shock. The essay will describe different types of shock to show

their relations to patient’s surgery, and perform a diagnosis for hypovolemic shock based on the

symptoms and the three stages of hypovolemic shock. The essay will explain how the patient can

be treated via an individualised approach in the form of an ABCDE assessment under nursing

management care. Adult nursing requires competence to meet the physical and mental health of

adult patients, including those that need end-of-life care (NMC 2010). The ABCDE treatment

strategy will emphasise on patient’s airways, breathing, circulation, disability, and exposure as

well as how they deliver on patient-centred care. The short-term and long-term holistic

management care will be explored in the paper. Besides, the essay will focus on pharmacology

and the different types of medication that can be used for managing hypovolemic shock and

frank haematuria. The pharmacological interventions will emphasise on treating hypovolemic

shock and frank haematuria using medication. Such consideration will entail medication doses,

side effects, and contraindications. More so, the essay will outline a plan of on-going care to

meet the individual needs of the patient. The consent of the patient will be informed in all

treatment areas alongside evidence-based practice and compliance with the NMC (2018)

standards.

Main Body

Bladder Cancer

Bladder cancer is one of the most prevalent neoplasms of the urinary system (Kim, 2018).

The urinary bladder consists of four layers, that is, the serosa, muscularis, mucosa, and
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submucosa (Kim, 2018). The mucosa comprises of five to a seven-thick layer of cells of the

stratified non-squamous epithelium. The bladder cancer initiates from the urothelium. About

90% of the histological types of bladder cancer are urothelial carcinoma. Urothelial carcinoma

involves the invasion of the underlying membrane or lamina propria by the neoplastic cells of the

urothelial origin. (Woo and Cho, 2018) The World Health Organisation (WHO) (2016)

categorise bladder cancers as low-grade or high-grader based on differentiation or

histopathology, which impacts on risk stratification and patient management. The infiltrating

urothelial carcinoma has a variable history (Casey, Catto, Cheng, Cookson, Herr, Shariat, Witjes,

and Black, 2015). The development of urothelial carcinoma occurs in two distinct pathways that

are related to papillary and flat lesions based on their morphology and pathway (Humphrey,

Moch, Cubilla, Ulbright, and Reuters, 2016). Tumour progression and poor prognosis are

associated with copy number alterations and genetic instability of the patient.

However, pathology plays a significant role in the management of bladder cancer. For

example, most patients with non-muscular invasive bladder cancer that correlated show

improved overall survival and prognosis at initial diagnosis (Babjuk, Burger, Capuon, Cohen,

Comperat, Hernadez, Kaasinen, Palou, Roupret, et al., 2017). Besides, the identification of the

level of invasion is critical to the pathologic assessment of the urothelial carcinoma for proper

staging of the condition. Bladder cancer can be multifocal or unifocal, though the majority of

patient cases present the former (Humphrey et al., 2016). The pathology report of the patient

should entail tumour local, grade and depth, presence or absence of carcinoma in situ, and

presence of the detrusor muscle in the examined specimen (Kim, 2018). For complex scenarios,

like the mentioned patient, additional pathological review by a genitourinary pathologist is


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recommended. Since the patient is more than 60 years, the common symptoms of bladder cancer

include moderate frank haematuria.

Shock

Shock can be physiological or psychological, where the latter is traumatic events or acute

stress disorder, while the former has multiple causes. According to Medlineplus (2020), the

shock is considered a life-threatening that takes place when a person’s body does not receive

sufficient blood flow. As well, physiologic shock can be triggered by an injury or condition that

interferes with the regular flow of blood in the body. In such a situation, the body cells and

organs do not receive an adequate supply of oxygen and nutrients to perform their normal

functions.

Types of Shock

The major types of shock include obstructive shock, which occurs when blood is blocked

from reaching its destination. Obstructive shock is primarily caused by the interruption of blood

flow or pulmonary embolism (Medlineplus, 2020). Also, obstructive shock can be caused by

other conditions that can trigger air or fluid build-up in the chest cavity. For instance,

haemothorax, where blood or fluids occupies the space between chest wall and lung,

pneumothorax, a condition of a collapsed lung, and cardiac tamponade, where fluids or blood

occupies the space between the heart and its muscles can lead to obstructive shock (Tintanalli,

2010).

Similarly, cardiogenic shock occurs due to damage to a person’s heart, which can be

caused by damages in the heart muscle, irregular heartbeats, or slow heart rate (Ballas and

Roberts, 2018). As well, the distributive shock is enhanced by body conditions that lead to loss

of shape of the blood vessels. By losing their tone, blood vessels might not have adequate blood
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pressure to supply the organs. Brain injuries or drug toxicities can lead to distributive shock.

Symptoms for distributive shock include low blood pressure, loss of consciousness (Gayet,

Prieto, Shakur, Ageron, Roberts, et al., 2018). Also, the anaphylactic shock is a subtype of

distributive shock caused by severe or systemic induction of Type I hypersensitivity that often

leads to degranulation of mast cells and basophils. Septic shock is a subtype of distributive shock

triggered by microbial infections (Ballas and Roberts, 2018). Neurogenic shock is considered

under the distributive type of shock caused by the reduced peripheral sympathetic nervous

system (SNS) vasomotor tone. Also, hypovolemic shock occurs when the body gets an

insufficient supply of blood due to severe blood loss or other injuries. Haemorrhagic shock is a

type of hypovolemic shock occurring due to blood loss, with traumatic injury being the leading

cause. Haemorrhagic shock can also happen because of bleeding from gastrointestinal (GI),

ectopic pregnancy, and surgical intervention.

As a result of extracellular fluid loss, hypovolemic shock can occur due to various

aetiologies. For example, gastrointestinal losses are realised when the GI tract cannot reabsorb

the fluids due to retractable vomiting, diarrhoea, or external drainage (Udwadia, 2014). As well,

renal losses of salt and fluid can trigger hypovolemic shock. Significant fluid loss from the skin

in a hot and dry climate can lead to hypovolemic shock. Also, third-spacing sequestration of

fluid in pancreatitis, intestinal obstruction, or pathological conditions with inflammatory

responses can lead to volume losses and, consequently, hypovolemic shock.

The Stages of Hypovolemic Shock

In the First Stage, which is the earliest phase of the hypovolemic shock, the patient is

likely to have lost 15% or 750 ml of their total blood volume (Weyker, Webb and Brentjens,

2017). At this point, it can be difficult to diagnose the patients since the blood pressure and
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breathing rates are still normal. However, the appearance of the skin, paleness, is the most

noticeable feature in this stage in addition to sudden anxiety feelings.

In the Second Stage, the patient is likely to have lost 30% or 1500 ml of blood volume; it

is marked by increased heart and breathing rates, which makes the diagnosis less challenging

(Weyker et al., 2017). The patients are likely to sweat more and increase anxiety and

restlessness. However, the blood pressure might be within the normal range. The diastolic

pressure might be high.

In Stage Three, the patient would have lost 30-40% or up to 2000 ml of blood volume

(Weyker et al., 2017). The systolic pressure is likely to be not more than 100 mm Hg. The heart

rate is likely to increase to above 120 beats per minute. The breathing rate will be rapid at

approximately 30 breaths per minute (Weyker et al., 2017). The patients might depict signs of

mental discomfort, including anxiety and agitation. The skill will be more pale and cold and

sweaty.

For Stage Four, the person is definitely at a critical condition because they have

experienced loss of more than 40% of total blood volume (Weyker et al., 2017). The pulse rate

will be weak but extremely rapid heart rate. At this point, the breathing is faster and difficult.

The systolic blood pressure will be below 70 mm Hg. As well, heavy sweating, extremely pale

appearance, and drifting consciousness are characteristic.

Overall, based on the description, the named patient seems to be in stage three of the

hypovolemic shock.

Pathophysiology of hypovolemic shock

Apart from dehydration, trauma is considered one of the frequent causes of hypovolemia

in patients (Udwadia, 2014). Precipitating factors in a patient include that can induce
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hypovolemic shock include GI fistula, gastric tube, ileus, vomiting, fever, diarrhoea, gastric tube,

hyperglycaemia, and renal dysfunction. The loss of fluid from dehydration is primarily

comprised of plasma as opposed to whole blood, like in trauma cases. Besides, the reduction in

the volume of circulating blood leads to low venous returns regardless of its cause, and arterial

hypotension is realised in sufficiently severe hypovolemia (Webb et al., 2014). The systemic

compensatory release of catecholamines enhances peripheral vasoconstriction, cardiac

contractility, and tachycardia. In such regards, systemic blood pressure could remain stable for

the on-going hypovolemia. Myocardia failure can be increased myocardial demand for oxygen

alongside decreased tissue perfusion. The patient can also produce acidosis because of the

anaerobic metabolisms in response to reduced perfusion and myocardial dysfunction,

contributing to multiple organ failure.

A patient can lose up to 10% of blood volume without affecting their arterial pressure and

cardiac out, but more than that reduces cardiac output and oxygen delivery to the tissues and

organs (Weyker et al., 2017). Arterial pressure declines with a loss of more than 20% of total

blood volume. Hypovolemia and hypotension have differential impacts on organ functioning.

For instance, alpha-adrenergic activity is relatively higher in the splanchnic organs, making the

patient prone to hypovolemic shock and hypotension (Weyker et al., 2017). As well, ischemia is

likely to develop from the reduced GI perfusion, especially in the mucosa of the gut leading to

compromised mucosal integrity. The impaired gut barrier functioning permits the translocation

of bacteria, and endotoxins are precipitating a systemic inflammatory response because of shock.

In severe cases of hypovolemia, the pathophysiologic processes might induce sepsis (Ballas and

Roberts, 2018). In such regards, the named patient is vulnerable to multi-organ failure as a

consequence of the suspected hypovolemic shock.


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Underlying Patient Condition

Based on the case description, hypovolemic shock is the first suspected in the 70-year-old

patient triggered by the frank haematuria. Hypovolemic shock involves rapid loss of fluids

leading to multiple organ failure due to insufficient circulating volume and subsequent perfusion.

As well, the low blood pressure below 100 mm HG, drowsiness, fatigue, and faster heartbeat rate

above 120 beats per minute, among other vital signs are manifested in hypovolemic shock. The

presentation of the four-second capillary refill time and the full urinal catheter after an hour

signifies that Daniel possibly had ruptured renal arteries meaning he was having a blood loss

(Nolan and Pullinger, 2014). The moderate haematuria had probably advanced and became

gross, though the level of bleeding cannot be quickly determined. Due to urgency and adverse

effects of hypovolemic shock, immediate medical intervention is required to improve the

patient’s condition. Apart from being a life-threatening complication, hypovolemic shock can

lead to multiple organ failure (Tintinalli, 2010).

At the end of life care, gross haematuria is a more distressing complication to patients

and their families. In such consideration, nurses have to provide optimal and supportive care to

patient’s situations by combining skills between nursing and medical teams, communicating the

patient’s goals, and relieving him from symptom burden. However, since the patient’s case has

progressed to hypovolemic shock that can alter the terminal trajectory, there is a need for

intensive interventions to promote his comfort (Tintinalli, 2010).

After a hypovolemic shock, functions of the endothelium are highly altered because of

ischemia of the endothelial cells and reperfusion of the resuscitation with fluids. Besides, the

cause of the hypovolemic shock is first determined since it informs on the treatment modality to

be undertaken. The aetiology of hypovolemic shock requires immediate replacement of blood or


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fluids to be performed to minimize tissue ischemia. Hypovolemic shock occurs from either blood

or extracellular fluid loss (Yunos, Bellomo, Glassford, Sutcliffe, Lam, et al., 2015). The type of

fluid and rate of replacement is considered when replacing fluid for the hypovolemic shock

patient.

Relevant tests, investigations and interventions for the patient

Both history and physical examination of the patient is vital in testing for hypovolemic

shock. For instance, the mentioned patient has a history of recent surgery. The full urinary

catheter signifies fluid loss. Some non-specific physical evaluation can be useful in determining

the presence of hypovolemic shock, like pale skin, reduced jugular venous distension, and

dryness in the mucous membranes (Udwadia, 2014). The patient can also appear sweaty,

cyanotic and cold.

For investigations, hypovolemic shock can translate to various abnormal laboratory

values. For instance, increased blood-urea-nitrogen (BUN) level and serum creatinine are

realised due to prerenal kidney failure (Binhas et al., 2011). Even though the effects of the acid-

base balance vary among individuals with significant GI losses, the patient is likely to

demonstrate lactic acidosis from increased anaerobic metabolism. For cases of haemorrhagic

shock, the patient will have severely decreased amounts of haemoglobin and haematocrit.

Hypovolemic patients are also likely to experience low-urinary sodium because of the kidneys

attempt to convert sodium into water to increase the volume of extracellular fluid. Blood volume

depletion can be suggested by fractional excretion of less than 1% sodium. Besides, increased

urine osmolality is typical of hypovolemic patients.

Similarly, the central venous pressure (CVP) can be used to assess the blood volume

status (Weyker et al., 2017). However, CVP’s sensitivity has been questioned due to possible
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compromise of the outcomes as a measure of volume following failure of the right-sided heart,

chest-wall compliance and ventilator settings. The measurement of variations in pulse pressure

through different commercial devices has been considered as a measure of volume

responsiveness. As well, respiratory variations can be measured in inferior vena cava by taking

the diameter as a measure of volume responsiveness (Udwadia, 2014). However, such

evaluations have only been validated among hypovolemic patients with irregular breaths or

arrhythmias. Though it has limits, volume responsiveness can be determined by echo on passive

leg raises on cardiac contractility.

For management, hypovolemic patients with haemorrhagic shock at early stages can be

subjected to the use of blood products over crystalloid resuscitation for better outcomes. As well,

balanced transfusion of plasma to platelets to packed red blood cells in the ration of 1:1:1 or

1:1:2 is useful in enhancing haemostasis (Annane, Siami, Jaber, Martin, Elastrous, et al., 2013).

Besides, for a patient with severe bleeding following surgery or trauma, anti-fibrinolytic

administration can be considered to minimise chances of death or major bleed. For a patient with

hypovolemic induced by fluid loses, rapid infusion of isotonic crystalloid solution is considered

at the earlier phase since the exact fluid deficit cannot be determined. Such consideration allows

for quick restoration of tissue perfusion. As well, fluid repletion can be examined through

measurements of blood pressure, urine output, mental status, and peripheral oedema. Various

techniques have been availed for measuring fluid responsiveness, like ultrasound, CVP

monitoring, and pulse rate variations (Annane et al., 2013). Unfortunately, vasopressors should

not be used for hypovolemic shock because they worsen tissue perfusion.

Moreover, crystalloid fluid resuscitation has been preferred for severe volume depletion

that is not related to bleeding. However, the chemistry of the patient, predetermined resuscitation
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volume, acid-base status, and physician preferences guides the types of crystalloid to be used

(Annane et al., 2013). Several isotonic fluids with low-chloride concentrations are commercially

available, like Ringer’s solutions and PlasmaLyte that considered balanced crystalloids (Gatey-

Sgeron et al., 2018). More importantly, the aetiology of extracellular fluid loss must be identified

and treated in the hypovolemic shock patient.

Medication

When fluid administration, among other interventions, fails to reverse the hypovolemic

shock, pharmacological therapy is applied to treat the hypovolemic patient. The medications will

be prescribed based on the patient situation and cause of fluid loss. Vasoactive drugs, such as

norepinephrine, vasopressin, phenylephrine and arginine, are given to prevent the patient from

cardiac failure. Even though they can be prescribed in different situations, early use of the

vasopressors has been associated with poor health outcomes in hypovolemic shock and higher

mortality rates (Plurad, Talving, Lam, et al., 2011). No dosage of the vasopressors has been

universally recommended in hypovolemic patients (Djogovic, MacDonald, Wensel, et al., 2015).

However, dopamine is dose-dependent and can be used at low doses of five to 15 micrograms

per kilograms per minute in adrenergic activation to increase renal blood flow, heart rate, and

contractility (Cardenas et al., 2015). Vasopressors all administered intravenously, often through

continuous infusion to allowed for fast and desired outcomes. As well, since dehydration can be

secondary to hyperglycaemia, insulin is administered. For diarrhoeal cases, the patient will

receive antidiarrheal medication. In the case of vomiting, antiemetic drugs are provided.

On the other hand, adverse effects on the use of vasoactive drugs rest on the mechanism

of action. For instance, arrhythmias are one of the common adverse effects. Vasopressin can lead

to coronary artery constriction, myocardial ischemia, bronchial constriction, hyponatremia, and


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chest pain, among others (Cardenas et al., 2015). As well, dopamine and epinephrine have been

associated with local tissue necrosis, pulmonary oedema, and tachycardia (Cardenas et al., 2015).

Phenylephrine induces myocardial, renal, peripheral, or mesenteric ischemia, local tissue

necrosis and reflex bradycardia. Norepinephrine has similar effects to epinephrine in addition to

dysrhythmia and bradycardia.

Vasoactive medications are contraindicated for anaphylactic hypersensitivity reactions

(Cardenas et al., 2015). Adrenergic vasopressors are contraindicated for patients with

uncorrected tachyarrhythmia, or combined use with halogenated hydrocarbons during

anaesthesia.

On-going nursing management

The primary prevention of hypovolemic shock is the focus of adult nursing care. The

preventive mechanisms are determined based on the possible causes guided by the vital signs,

like high pulse beats per minute, low blood pressure, or any post-surgery injury (Myburgh,

2018). The nursing assessment data encompasses ineffective tissue perfusion, deficit fluid

volume, risks of metabolic acidosis, and positive anxiety in the patient. Based on such

evaluation, the nursing care unit will have to maintain the patient’s fluid volume, pressure and

pulse at functional levels. The team must demonstrate an understanding of the causative factors

to the fluid volume deficit in the patient.

For evidence of intra-professionalism, an adult nurse needs to show their knowledge and

competence, consult with the working team, and effectively communicate (NMC, 2010). As

well, the nurses must demonstrate positive interpersonal attributes in practice and decision-

making to immediately improve the status of the hypovolemic patient. Through collaboration,

the nursing team will deliver high-quality care to the patient, address complex care issues,
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responsible for safe, person-centred, and evidence-based nursing. The adult nurses should be

compassionate, respectful, and dignified since the environment has significant impacts on their

mental health and wellbeing of hypovolemic patients. Partnership with other care professionals is

vital in understanding the underlying conditions of the patients and the situation at hand,

especially in elderly patients.

Conclusion

Overall, the mentioned patient suffers from the risk of hypovolemic shock due to

significant loss of the total blood volume. Based on the case presentation, the patient is in stage

three of hypovolemic shock. Due to the underlying conditions of bladder cancer and frank

haematuria, immediate medical and nursing intervention is appropriate for the patient to manage

the shock. History and physical examination assist in examining hypovolemic shock. Isotonic

crystalloid fluids can be used in the interventions. By observing the adverse effects and

contraindications, vasoactive drugs may be used as deemed appropriate. The complexity and

urgency of the case require collaboration and evidence-based nursing practice to deliver on high-

quality care and better patient outcomes.


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