Case Study Analysis: Uterine Fibroids, Post-Hysterectomy Deterioration

This case study examines a 49-year-old woman, Cynthia Jones, diagnosed with uterine fibroids. The study explores the etiology and pathophysiology of uterine fibroids, including risk factors such as menarche, parity, age, obesity, and hormonal influences. It details Cynthia's post-operative deterioration after a total hysterectomy, identifying hypovolemic shock as a critical complication. The analysis highlights the vital roles of multidisciplinary teams, including medical doctors, nursing staff, dialysis teams, family members, and pharmacists, in ensuring effective patient care and recovery. The study emphasizes the importance of collaborative approaches to address the patient's needs and improve outcomes. The paper concludes with a summary of the key findings, underscoring the complexity of uterine fibroids and the significance of comprehensive medical interventions.

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Introduction
Uterine leiomyoma (uterine fibroids) are benign tumors of the uterus whose etiology is
unknown. These lesions arise from the myometrium transformation which results from specific
pathological and physiological conditions. They are the most common tumors of women globally
and most of them affect women during their reproductive ages. Among this population, 80% of
them suffer for their whole lifetime. They can be large leiomyomas that are palpable while others
are very small. They, however, rarely transform into sarcomas. Clinically, they present with;
excessive menstrual bleeding, intermenstrual bleeding, dysmenorrhea, chronic pelvic pain,
pressure symptoms, for example; feeling bloated, an increase in the urinary frequency, and
disturbance to the bowel. In addition to this, they cause subfertility as they have been linked to
early loss of pregnancy and third-trimester complications (Hinkle &Cheever, 2013). This essay
will focus on a case study of a patient whose presentation points to uterine fibroids. Firstly, the
etiology and the pathogenesis of the uterine fibroids will be outlined. Secondly, the cause of her
deterioration postoperatively after she underwent a total hysterectomy. Thirdly, three
multidisciplinary teams caring for her and their role in the patient’s care will be discussed.
Lastly, a conclusion summarizing the study/paper.
The etiology and pathophysiology of uterine fibroids.
As earlier explained it is unknown what causes uterine fibroids although they have been
linked to genetic makeup, hormonal aspects, epidemiology and the molecular biology. During
the embryonic development, the undifferentiated cells of the endoderm proliferate to form the
uterine muscles (Chabbert-Buffet, Esber & Bouchard, 2014). It is believed that these cells have a
longer period of instability and that they are the progenitor cells of the fibroids. These cells
reside in the myometrium and they start to proliferate at menarche due to different triggers. For

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example; hormonal changes, menopause, and steroids. For a clear explanation these
factors/triggers have been divided into four; the effectors, the risk factors, the promoters, and the
initiators. The risk factors/predisposing factors give a clue of the etiology of the uterine tumors
and in coming up with prevention strategies. Secondly, the specific initiators are unknown
although theories have been formulated to explain it. Thirdly, the growth promoters, which are
the ovarian hormones progesterone and estrogen. Lastly, growth factors have also been linked
with the effectors (Hinkle &Cheever, 2013).
Risk factors associated with uterine fibroids.
Menarche
It has been reported that there is a slight increase in risk of getting leiomyoma when one
experiences their menarche early. Hall, (2018) study reported that women who experienced
menarche at 10 years and below had a higher risk of developing uterine fibroids compared to
women who experienced their menarche at 16 years and above. The explanation given was that
early menstrual cycles increase the number of the cell division that the myometrium undergoes in
the reproductive years which results in an increased chance of gene mutation that controls the
myometrium proliferation.
Parity
It has been reported that nulliparous have a high risk of developing uterine fibroids
compared to multiparous. In addition to this, the more children one bears the lower the risks. It
was reported that pregnancy tends to reduce exposure to estrogen that is unopposed whereas in
cases of reduced fertility or nulliparity, they are associated with anovulatory cycles that exposes
them to long durations of unopposed estrogen (Donnez et al., 2016).

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Age
Studies have shown an increase in fibroids diagnosis in women at the age of forties. The
reasons for this observation are not known although it may be as a result of the increased growth
of the fibroids or increased symptomatology of already existing fibroids. Therefore, if the growth
of the uterine fibroids accelerates at the late reproductive ages this means that the hormonal
factors that are associated with peri-menopause are modulators and this acceleration in growth is
simply as a result of a cumulative culmination of the 20-30 years of estrogen and progesterone
stimulation (Donnez et al., 2014).
Menopause
It has been found out that at post-menopause, there is a reduction of risk of the fibroids
requiring surgical interventions. This has been linked to tumor shrinking as a result of the
absences of the hormones stimulus due to the menopause (Khan, Shehmar, & Gupta, 2014).
Obesity
The likelihood of uterine fibroids has been associated with obesity. A study by Rose et
al., (2016) showed that for every 10kgs gained it increases one’s likelihood of developing uterine
fibroids by 21%. In addition to this, every increase in the Basal Metabolic Index (BMI) there was
a 6% increase in the risk. A study by Sato et al., 2018 showed that women with a BMI of less
than 24 and a body fat percentage of more than 30% or those with upper body fat distribution
have a significantly high risk of getting uterine fibroids. This is explained by the increased
conversation of the circulating adrenal androgens to estrone by the excess fat tissue. There is also
a decrease in the hepatic production of the sex hormone-binding globulin which causes an
increase in the unbound estrogen that is physiologically active (Morr et al., 2016).

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Oral contraceptives
This is a factor that has conflicting results as some studies indicate that use of oral
contraceptives reduces the risk by 17% every 5 years they are used (Stewart, 2015). They also
state that the higher the progesterone in the pills the lower the risks as it reduces the levels of the
unbound estrogen. In contrast, has been reported that oral contraceptives influence the
development and the growth of the uterine fibroids. However, this has been seen in those women
that used them in their teenage years (Sparic, Mirkovic, Malvasi, & Tinelli, 2016).
Others
Lack of exercising, smoking, hormonal replacement therapy, geographical differences,
diet, racial differences, use of tamoxifen, and use of xenoestrogen. This is other risks associated
with uterine fibroids growth or/and development (Colledge, Walker & Ralston, 2013).
Initiators of tumorigenesis
The etiology of the tumor is unknown therefore, theories are used to explain its initiation.
For example, some theories hypothesis states that increase in estrogen and progesterone levels
leads to an increased mitotic rate that leads to the formation of the myoma by having an
increased likelihood of the somatic mutation (Bulun, 2013). Another theory hypothesis that the
pathogenesis of the uterine fibroids is a response to an injury that mimics surgical scars after
healing. In addition to this, on the genetic heredity, the findings show that African American
women have a higher chance of developing uterine fibroids. It was also found out that fibroids
development and growth is 4.2 times in women whose relatives has that history (Glynn & Drake,
2014)

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The promoters; the role of progesterone and estrogen.
Estrogen is the primary proposed promoter of the uterine fibroids. This can be supported
by the following risk factors; it develops during the reproductive years, its likelihood is increased
by early menarche, higher risks in nulliparous as they experience long anovulatory cycle, higher
in obese women as a result of increased conversation of estrogen and it regresses in menopause.
Progesterone as estrogen is associated with the above and also when anti-progesterone therapy is
done the tumors reduces (Bulun, 2013)).
Deterioration of the patient post total hysterectomy.
Patient Cynthia Jone who is 49 years old just underwent through a total hysterectomy via
general anesthesia due to uterine fibroids. After surgery, she was taken to the post-anesthetic
recovery room (PARU) for an hour where she recovered uneventfully. She was later transferred
to the wards. In the wards her vital signs are as follows; 30 breaths per minute, systolic pressure
of 90mmhg and diastolic of 50mmhg, 130 heartbeats per minute, temperatures of 36’c, she has
no pain, she is on morphine 1mg bolus, her in situ urinary catheters has drained 10mls of urine
for the last one hour and on the surgical site the dressing is transparent although there is
moderate haemoserous ooze that is noted.
The patient seems to be in shock and to be a specific hypovolemic shock as a result of
hypovolemia which probably developed during surgery due to blood loss. Shock is a medical
emergency in which there is inadequate perfusion of tissues. There is reduced oxygen and
nutrients supply to the vital organs and for cellular functioning. This causes cells to convert to
anaerobic respiration, build-up waste leading to cell death. Inadequate perfusion to end organs

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leads to dysfunction that translates to organ failure and eventually death (Shah, Workeneh &
Taffet 2014).
Hypovolemic shock has four phases; the initial, compensatory, progressive and
irreversible. At the compensatory phase, the blood pressure is relatively normal, the heart rate is
above 100beats per minute, her breath rate is more than 20 breaths in a minute, the skin is cold
and clammy, a decreased urinary output, mental confusion and clinical manifestation of
respiratory alkalosis. Secondly, the progressive phase manifests as follows; systolic pressure that
is less than 80-90mmHg, a heart rate that is more than 150 beats per minute, rapid and shallow
breaths characterized by crackles, skin that has petechial and is mottled, urinary production of
0.5ml/kg/hr, patients exhibit signs of lethargy and metabolic acidosis (Wise & Laughlin-
Tommaso, 2016). Lastly, irreversible phase, the patient required mechanical ventilation, the
patient is asystole, on respiration the patient requires intubation, the skin is jaundiced, on the
urinary out the patient requires dialysis, the patient is unconscious and has profound symptoms
of acidosis (Barrett, Barman & Boitano, 2017).
It is clear from the above that patient Cynthia is at the progressive phase of shock. Her
systolic blood pressure is at 90mmHg and her heart rate is at 130bpm which is as a result of
myocardial depression as the heart overworked in the compensatory phase so as to meet the
oxygen requirement. Her urine output is 10ml for the last one hour, this is as a result of the blood
shunting so as to supply blood to the vital organs. This applies to the skin temperatures although
the cool temperature is further worsened by the vasoconstrictions. Lastly, she is hyperventilating
to increase oxygen supply (Williams, Bergeron, Barlow & Ferenczy, 2012).

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Multi-disciplinary team.
As explained earlier shock is a medical emergency that requires immediate intervention
so as not to lose a patient. Effective patient care requires collaborative care. The patient care
should involve the medical doctors and the nursing team. In addition to this, the patient requires
a dialysis team, family members, and pharmacists. Firstly, the dialysis team is important as the
patient is heading to renal failure as a result of shunting due to the shock (Wolfsdorf et al., 2018).
Secondly, family members need to be involved in the patient’s care. they need to be informed of
the care given to the patient and the status of the patient so as not to feel neglected (Donnez et
al., 2015). They also need advice from the health care providers so as to be comfortable and get
some rest. Lastly, they need a pharmacist as they need pharmacological support to aid in cardiac
contraction, respiration and renal functioning (Glynn & Drake, 2014).
Conclusion
It is clear that uterine fibroids have no specific etiologies although the risk factors give
cues on the etiology and the pathophysiology. The risk factors identified included; smoking,
menopause, menarche, age, obesity, genetic predisposition, geographical location and racial
differences. Secondly, from the manifestation of the patient shows that the patient is at the
progressive phase of hypovolemic shock. Lastly, the patient care should be collaborative so as to
achieve the best care.

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