Urinary Tract Infection with Severe Sepsis

Running header: URINARY TRACT INFECTION WITH SEVERE SEPSIS 1
Urinary tract infection with severe sepsis
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Urinary tract infection with severe sepsis
Pathogenesis of UTI and Sepsis
Urinary tract infection involves the lower urinary tract infection or the upper urinary tract
infection. In lower urinary tract infection the bacteria colonize the periurethral area where it
accumulates and ascends to the bladder. The bacteria continue to replicate in the bladder, after
sufficient increase it ascends to the ureter towards the kidney (Woodford & George, 2017). It
uses it fimbria in the ascension process. The infection damages the renal parenchyma leading to a
condition called pyelonephritis. Severe infection may result in acute kidney injury where there
are tubular obstruction and damage. If the inflammation continues, inflammatory cells infiltrate
the renal parenchyma leading to activation of the innate immune system. This results in
cytokines which cause the development of sepsis (Woodford & George, 2017).
Painful urination mostly indicates a lower urinary tract infection. The burning sensation is
mostly felt at the opening of the urethra and less frequently over the bladder. Painful urination is
also known as dysuria. Dysuria is usually caused by urethral or bladder inflammation. The major
causes are urethritis and cystitis. Urethritis involves invasion by an infectious agent which
damages the local mucous membrane of epithelial cells (Nichole, 2017). This causes
inflammatory changes which involve the collection of leukocytes and chemical mediators such
as cytokines and antibodies. Accumulation of this mediators result in pain and swelling.
Inflammation can also cause continuous scarring which constricts the urethra. The swelling and
accumulation of fibrous tissue can make micturition painful and difficult (Nichole, 2017). The
obstruction of the urethra makes it impossible for one to void leading to a collection of stagnant
urine in the bladder, generally called urine stasis. Urine stasis brings about severe infection if not

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managed earlier; the back pressure of urine results to a kidney infection which is manifested with
lower abdominal pain which radiates to the right flank (Nichole, 2017).
Mr. Kirmann had a heart rate of 135, blood pressure 80/42, temperature 39, oxygen saturation
of 82% and respiratory rate of 32. The abnormally high temperatures of 39C was a result of
bacterial infection in the blood. Pyrogens are released by white blood cells and macrophages.
This chemicals flow in the bloodstream to the hypothalamus in the brain which controls body
temperature. Pyrogens raise the set point of the hypothalamus through the action of prostaglandin
E2 (Rodgers, 2014). This causes the hypothalamus to increases the core body temperature to a
new set point causing fever. High temperatures cause an increase in breathing rate, heart rate and
blood circulation to the skin. An increased core body temperature causes the blood vessels to
dilate which decrease blood pressure. The dilation of blood vessels due to fever will result in an
increased heart rate so as to maintain the blood pressure. High temperatures also denature the
bond between iron in hemoglobin and O2 resulting in a decreased oxygen saturation (Rodgers,
2014).
Ideally, normal urine color should be pale yellow and a normal urine volume of 800-2000
milliliters in 24 hours which indicates that an individual is hydrated. Mr. Kirmann had a dark
urine output passed in small amounts of approximately 40ml in the last 8 hours. Dark urine is
usually a sign of dehydration which mostly occurs when there is less water in the body. Fever
causes increased sweating, fluid, and electrolyte loss. There is also a possibility of drinking less
water due to feeling unwell. Too much loss of water will cause a decreased urine output which
appears darker in color (Walker, Caparon, & Hultegren, 2015).