NRSG258 Acute Care Nursing 1 | Uterine Leiomyoma are Benign Tumors

Cynthia Jones is a 49 year old woman who lives on a rural property with her 13yr old son. She is now widowed following a farm accident where her husband was killed. Cynthia has two other children who both live some distance away. She has been experiencing symptoms of dysmenorrhea which has led to a diagnosis of uterine fibroids (leiomyomas). Cynthia has a history mild depression.

Cynthia was admitted to hospital for a Total Abdominal Hysterectomy via general anaesthesia.

After 1 hour in the post-anaesthetic recovery room (PARU) and an uneventful recovery, she was transferred to the ward, where you have been allocated to her care.

In relation to Cynthia Jones:

Answer:

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 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).

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).

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)

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 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).

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.

References

Barrett, E., Barman, M., Boitano, S. (2017). Uterine Fibroids. Ganong’s Review of Medical Physiology. (24th ed). New York, N.Y: McGraw Hill Medical.

Bulun, S. E. (2013). Uterine fibroids. New England Journal of Medicine, 369(14), 1344-1355.

Chabbert-Buffet, N., Esber, N., & Bouchard, P. (2014). Fibroid growth and medical options for treatment. Fertility and sterility, 102(3), 630-639.

Colledge, N., Walker, R, & Ralston, S. (2013). Uterine Fibroids. Davidson’s Principles and Practice of Medicine. (21st ed). New York, N.Y: ‎Edinburgh.

Donnez, J., Donnez, O., Matule, D., Ahrendt, H. J., Hudecek, R., Zatik, J., ... & Bouchard, P. (2016). Long-term medical management of uterine fibroids with ulipristal acetate. Fertility and sterility, 105(1), 165-173.

Donnez, J., Hudecek, R., Donnez, O., Matule, D., Arhendt, H. J., Zatik, J., ... & Bouchard, P. (2015). Efficacy and safety of repeated use of ulipristal acetate in uterine fibroids. Fertility and sterility, 103(2), 519-527.

Donnez, J., Vázquez, F., Tomaszewski, J., Nouri, K., Bouchard, P., Fauser, B. C., ... & Osterloh, I. (2014). Long-term treatment of uterine fibroids with ulipristal acetate?. Fertility and sterility, 101(6), 1565-1573.

Glynn, M. & Drake, W. (2014). Uterine Fibroids. Hutchinson’s Clinical Methods: an integrated approach to clinical practice. London: Elsevier.

Hall, M. (2018). The theory of groups. Courier Dover Publications.

Hinkle, J.L, Cheever, K.H. (2013). Uterine Fibroids. Brunner and Saddarth’s Textbook of Medical and Surgical Nursing, (13th ed) Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Khan, A. T., Shehmar, M., & Gupta, J. K. (2014). Uterine fibroids: current perspectives. International journal of women's health, 6, 95.

Morr, M., Lukasz, A., Rübig, E., Pavenstädt, H., & Kümpers, P. (2016). Sepsis recognition in the emergency department–impact on quality of care and outcome?. BMC emergency medicine, 17(1), 11.

Shah, M. K., Workeneh, B., & Taffet, G. E. (2014). Hypernatremia in the geriatric population. Clinical interventions in aging, 9, 1987.

Sparic, R., Mirkovic, L., Malvasi, A., & Tinelli, A. (2016). Epidemiology of uterine myomas: a review. International journal of fertility & sterility, 9(4), 424.

Stewart, E. A. (2015). Uterine fibroids. New England Journal of Medicine, 372(17), 1646-1655.

Williams, A. R., Bergeron, C., Barlow, D. H., & Ferenczy, A. (2012). Endometrial morphology after treatment of uterine fibroids with the selective progesterone receptor modulator, ulipristal acetate. International journal of gynecological pathology, 31(6), 556-569.

Wise, L. A., & Laughlin-Tommaso, S. K. (2016). Epidemiology of Uterine Fibroids–From Menarche to Menopause. Clinical obstetrics and gynecology, 59(1), 2.

Wolfsdorf, J. I., Glaser, N., Agus, M., Fritsch, M., Hanas, R., Rewers, A., ... & Codner, E. (2018). Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State: A Consensus Statement from the International Society for Pediatric and Adolescent Diabetes. Pediatric diabetes.