Urosepsis: Pathogenesis, Nursing Strategy, and ABG Analysis

Running head: UROSEPSIS 1
UROSEPSIS
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UROSEPSIS 2
Introduction
The paper will critically analyse the case scenario of Mr Kirkman who is 75 years
older with a diagnosis of Urinary Tract Infection. He presented to the ED with complaints of
burning sensation when urinating and lower abdominal pain which radiated to his right flank.
Relating to the clinical manifestations of Mr Kirman, the paper will analyse the pathogenesis.
Secondly, the paper will discuss one nursing strategy while underpinning the evidence base.
Thirdly, the paper will analyse the results of the Arterial Blood Gas in relation the underlying
pathogenesis.
Pathogenesis of Urinary Tract Infection With Sepsis (Urosepsis)
Infection of the bladder results from the invasion and overgrowth of bacteria
(Escherichia coli (E. coli), in the urinary bladder. The bacteria take hold in the tube draining
urine to the bladder via the kidney. The condition is referred to as Urinary Tract Infection
(UTI). The UTI may affect the entire urinary system including the ureters, kidneys, urethra,
and urinary bladder. UTI is commonly caused by bacteria which enter the urethra via the
genital area and the immune system of the body tries to fight it back to prevent its
multiplication. UTI can also be caused by a fungal infection whereby the fungus enters the
urinary tract via the blood stream (Flores-Mireles, Walker, Caparon, & Hultgren, 2015).
The bacteria enter the urinary tract in multiple ways including poor personal hygiene,
sexual contact, or pre-existing condition of the urinary bladder. The spread of the bacterial
into the urinary bladder results to an infection. If the UTI stays for some time without being
treated or managed, the patient developed other complications especially sepsis. Sepsis as a
result of a UTI is known as urosepsis. Other factors which increase the risk of development
of UTI and urosepsis include diabetes, immunosuppression, age of more than 65 years, past
history of urinary tract infections, and corticosteroid treatment (Peach, Garvan, Garvan, &
Cimiotti, 2016). From the case scenario, Mr Kirman has a past history of UTI and an in-

UROSEPSIS 3
dwelling catheter which areone the key contributors to the deterioration of his condition. If it
went untreated, it resulted in the complications of urosepsis that the patient is experiencing
(Johnson, Porter, Johnston, Kuskowski, Spurbeck, Mobley, & Williamson, 2015).
In the early phase of development of the UTI, the patient develops extreme urges to
urinate, increased frequency of urination, pain, irritation, or burning sensation when voiding,
cloudy or thick urine, dark urine, and feeling of pressure in the lower back or abdomen
(Foxman, 2014). After the progression of the infection, the patient may experience nausea
and vomiting, fever, pain in the lower right flank, and fatigue. The potential complications
associated with urosepsis include pus collection near the prostate, organ failure, urinary tract
scar tissue, septic shock, and kidney damage (Lewis, Collier, & Heitkemper, 2017).
When the UTI extends to the kidneys, it results in flank pain, high fever, chills,
shaking, nausea, and vomiting. From the case study, the patient has high fever evidenced by a
temperature of 390 C. The patient also presented with lower abdominal pain which was
radiating to the right flank indicating that the infection had extended to the kidneys. The
patient has reduced urine output of 40 mls in 8 hours. This is an indication of kidney
dysfunction. When the urinary bladder is affected, the patient experiences pelvic pressure,
blood in urine, discomfort in the lower abdomen, and painful and frequent urination
(Foxman, 2014).
The presence of the UTI which extended to various body organs within the urinary
tract system stimulate an overwhelming, exaggerated, and uncontrolled systemic immune
response. The presence of infection stimulates the production of the phagocytes,
macrophages and monocytes, acting as the first line infection defence (Dreger, Degener,
Ahmad-Nejad, Wobker, & Roth, 2015). The phagocytes also release the pro-inflammatory
mediators known as cytokines to attract the neutrophils to the infection site. The cytokines
include interleukin-6, interleukin-1, and the Tumour Necrosis Factor (TNF), alpha, which