Pathophysiology of UTI and Sepsis

This document discusses the pathophysiology of urinary tract infection (UTI) and sepsis, including the interaction between uropathogens and the host, the development of pyelonephritis and urosepsis, and the clinical manifestations of these conditions. It also provides information on the nursing strategies and interventions for managing UTI and sepsis. The document includes references for further reading.

Running head: NURSING
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UTI is a type of urinary infection occurring in the urinary system such as kidneys, ureters
and bladders that occurs because of interaction between uropathogen and the host. The
uropathogen attach to the epithelial surface, colonizes and ascend to the urinary bladed resulting
in symptomatic and symptomatic bacteria (Dreger et al., 2015). Once the bacterium has ascended
to the bladder, they increase in number and cause inflammation of the bladder. The bacteria
affects the epithelium cells and the bacteria replicates and produces biofilms. This replication of
pathogenic bacteria leads to urinary tract irritation and infection and also result in the impairment
of bladder emptying. Bladder outlet obstruction may lead to ascending of urine into the ureters
and lastly to the kidney leading to a condition called pyelonephritis. Pathogenesis of
pyelonephritis takes two steps (McLellan & Hunstad, 2016). First, the Bacteria attaches to the
epithelium activating an inflammatory response which involves toll-like receptor 4 (TLR4) and
glycosphingolipid (GSL) receptors. Second, the receptors release chemokine’s that causes
increased blood flow to the infected area and stimulation of nerves which causes right abdominal
pain, radiating into the right flank (Biroga, Bosner, & Becker, 2016). Abdominal pain affects the
diaphragm and the outer intercostal muscles making it not possible to move air in and out of the
lungs. This causes the activation of additional muscles known as the accessory muscles. In case
of the patient, Mr Kirkman, it was observed from his vital symptoms that he was suffering from
urinary tract infection associated with severe sepsis. The blood pressure was very low as
compared to the normal range. The pyelonephritis results in tubular injury and impediment,
which further results in the development of interstitial nephritis (Artero et al., 2016). The
development of interstitial nephritis increases the potential risk of pathogenic bacteria to escalate
from the kidney and affect the blood resulting in the condition of urosepsis. The development of
urosepsis condition leads to septic shock that disturbs the systemic reaction by releasing

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cytokines to dilate the blood vessels, hence permitting extra blood to flow from the infected area.
The dilation of blood vessels (vasodilation) in this condition results in low blood pressure in the
patient as the renin-angiotensin system is altered.
The heart rate of the patient was very high as compared to the usual range due to
infection of pathogenic bacteria that invades the urinary bladder and results in high heart rate.
The individual who is suffering from urinary tract infection (UTI) associated with severe sepsis
exhibited the symptom of high heart rate and high respiratory rate (Gupta, Grigoryan & Trautner,
2017). Tachypnea is a condition that develops in the patient with UTI as the invading pathogen
reduces the body’s immune system or capability to fight, which in turn decreases the blood flow
rate thus making the immune system very weak and ineffective. The pathogenic bacteria
decreases the flow of pure oxygenated blood throughout the body that increases the body’s
demand to breathe as the oxygenated blood cannot reach the brain. Hence, the respiratory and
heart rate is more in case of the patient (Reinhart et al., 2017). The examination of full blood
count of patient shows normal value for haemoglobin, red cell count and platelet. However, the
WBC count has increase. The increase in WBC count for Mr. Kirkman in full blood count is also
explained by activation of the rennin angiotensin system due to inflammatory response during
sepsis. Systematic inflammatory response syndrome in patient with sepsis is manifested by high
heart rate, high WBC count and high respiratory rate (Bellomo et al., 2017)). For this reason,
WBC count and respiratory rate of Mr. Kirkman was high. The haemoglobin level and of patient
is within normal range.
Urosepsis is caused by pathogens like E. coli, Proteus spp and Enterobacter spp and this
result in bacterimia in patient. Mr. Kirkman also experienced burning sensation during urination
because of bacterial infection of the urinary tract. For this reason, urine testing is done for

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patients with urosepsis to identify level of infectious load in the urine. The clinical symptoms
like fever, high heart rate, edema and hyperglycaemia is seen in patient because of pro-
inflammatory and anti-inflammatory host response to infection (Walter et al., 2017). Fever
occurs because of defensive response of the body to the infection and release of pyrogens which
impairs the function of hypothalamus, the brain part that regulates body temperature. Clinical
manifestation of fever is seen as pyrogen disrupts the function of hypothalamus. In addition,
heart rate increases because of hypotension and activation of the sympathetic nervous system
(Baygin & Kararmaz, 2018). This explains the reason behind high body temperature and heart
rate of 135 for Mr. Kirkman. The clinical manifestation of patient also revealed low urine output
indicated by passing of only 40 mls urine in last 8 hours. As severe sepsis affects the renal
system, it leads to severe damage to the kidney. For this reason, oliguria or low urine output is
seen in Mr. Kirkman. Renal failure is associated with acute oliguria (Dreger et al., 2015).
The review of the pathophysiology behind sepsis in Mr. Kirkman revealed that there is
relation between sepsis and UTI as both the condition is associated with inflammatory reacton
and release of cytokines and interleukins. Sepsis results in dysfunction of one major organ in
UTI patient which is the kidney (Gotts & Matthay, 2016). Low oxygen is seen because of
inflammatory response to infection and reduce tissue oxygenation because of hemodynamic
changes and respiratory failure. For this reason, there is a need to consider supplementary
oxygen use for sepsis management (NIfHaC, 2016). From the above intervention it clear that the
patient required effective nursing strategy to assist in recovering as soon as possible. The most
crucial nursing strategy will be to evaluate the symptoms of urinary tract infection such as fever,
chills, burning sensation in urine and cloudy urine. This symptoms will help the specialist to
better understand the complexity of his health condition and to access the symptoms of urinary

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tract infection associated with severe sepsis. The patient should be encouraged to consume more
amount of fluid to keep them hydrated and help the body to flush out harmful bacteria and toxins
through urine that results in urinary tract infection (Nicolle, 2016).
Airway: The patient’s ability to speak in full sentence was evaluated. Mr. Kirkman was found to
speak in single words indicating signs of airway difficulty.
Breathing: The patient was found to use access muscle indicating sign of respiratory distress.
The respiratory rate was 35 bpm and SPO2 values was 82%. According to the diagnostic criteria
for sepsis, the two vital signs comes under yellow zone observation as RR was greater than 25
breaths per minute and SPO2 was less than 95%. This confirms that patient has a sepsis.
The lactate value of Mr. Kirkman is very high indicating risk of severe sepsis. This
occurs because of inadequate tissue perfusion occurring due to organ dysfunction. For this
reason, serum lactate is a sensitive marker for septic shock and it is used as one of the diagnostic
criteria for severe sepsis (Lee & An, 2016). The low Ph value is seen because of alterations in
acid-base balance due to sepsis and occurrence of metabolic acidosis because of renal failure,
hemodynamic changes and reduced tissue oxygenation (NIfHaC, 2016). Reduce partial oxygen
pressure was seen because of sub-optimal oxygen delivery because of hypotension. This is again
seen due to the pathophysiology of sepsis and activation of the rennin angiotensin system. The
reduction in bicarbonate concentration is seen due to inadequate oxygen delivery following
sepsis and progression of inflammation (Suetrong & Walley, 2016).

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References:
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Effect of bacteremia in elderly patients with urinary tract infection. The American journal
of the medical sciences, 352(3), 267-271.
Baygin, O., & Kararmaz, A. (2018). Sepsis and Tachycardia: Etiologic Factors and Effects on
Prognosis. J Anaesth Ther 1: 103 Abstract RESEARCH ARTICLE Introduction, 1(1).
Bellomo, R., Kellum, J. A., Ronco, C., Wald, R., Martensson, J., Maiden, M., ... & Schneider, A.
(2017). Acute kidney injury in sepsis. Intensive Care Medicine, 43(6), 816-828.
Biroga, T., Bosner, K., & Becker, J. (2016). Studies of the symptom abdominal pain--a
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emerging vital sign. Journal of thoracic disease, 8(7), 1388.

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