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Diagnosis of a G1PO Patient With Vomiting and Nausea Symptoms
Introduction
This diagnosis is especially essential for women whom it is on their first time getting pregnant and have never delivered before (G1PO). In this population of patients, there are multiple genitourinary, gastrointestinal, metabolic, and neurologic factors to consider. When vomiting occurs, the first thing that comes into mind is gastrointestinal conditions, including peptic ulcer, small bowel blockage, cholecystitis, and appendicitis. There are also pathologies connected to pregnancy to consider, including hemolysis or cholestasis, an increase in liver enzymes, or low platelet count (HELLP) syndrome. The abnormalities of the patients liver and abdominal soreness make these diagnoses.
Subjective Data
This clinicopathological case concerns a twenty-five-year-old woman (G1P0) who was approximately ten weeks pregnant with a chief complaint of nausea and vomiting during her first prenatal visit. In particular, pancreatitis and cholecystitis are more appropriate to take into account. In addition, the right upper quadrant ultrasonography is rarely described as diagnostic, and the pain is merely localized. HELLP and pregnancy cholecystitis might initially be on the differential due to the lab abnormalities from the patients lab results. However, since the patient is in her first trimester, neither of these diagnoses is appropriate at this time of pregnancy. In addition, biliary pathology and cholecystitis can still be included in the list despite the lack of ultrasound data from the patient. In addition, it takes the reader through the different diagnoses and evaluations of the patient. Moreover, this case includes the patients tachycardia and agitation, which lead to the correct diagnosis. The keywords presented in this case are; pregnancy, CPC, and hyperemesis gravidarum.
The patient believed she was approximately ten weeks pregnant but was unsure about her last period. According to a review of her medical records, she failed to visit an obstetrician immediately after her pregnancy. The patient was given an informal diagnosis of hyperemesis gravidarum based on a previous non-prenatal visit when she had come with emesis and was started on metoclopramide. She had also been experiencing six to eight episodes of emesis daily but denied having emesis on her first prenatal visit. However, she stated that she experienced minor spotting but denied any tissue passing. Moreover, she claimed that she had used one pad per day for the past three days. Lastly, the patients medical records showed no history of surgery since birth.
Objective Data
The review of symptoms revealed that exhaustion, nausea, vomiting, and vaginal bleeding were positive. In addition, the patient had no family or social history or ongoing medical issues. She took prescribed prenatal vitamins daily and ten mg of metoclopramide as needed for motion sickness. The patient arrived at the prenatal appointment with a temperature of 98.7 degrees Fahrenheit, a heartbeat of 86, breathing at 18 breaths per minute, 86% saturation on room air, and a blood pressure of 110/80 mercury millimeters (mm Hg). When examined, she experienced diffuse stomach discomfort, tachycardia, and a flattened affect. She would respond to inquiries politely but briefly with a single word. The pelvic exam revealed the absence of adnexal soreness, a closed cervical OS with white vaginal discharge, and a friable erythematous cervix that was painful to touch. Another possible cause of vomiting and nausea was suggested to be genitourinary, including ectopic pregnancy, ovarian torsion, or pyelonephritis. However, the workup of the patient ruled out these causes, but the physician still entertained the possibility of other infectious causes.
Assessment
Other test results from the lab included the quantitative human chronic gonadotropin HCG): > 208,656 milli-international units per milliliter (m [IU]/Ml) and a high sensitivity troponin of 14(0-12 picograms per milliliter (pg/ml). In addition, her urinalysis revealed significant blood [negative), a high count of red blood cells (3-5), eighty ketones [0 mg/deciliter), and moderate bacteria. Both a formal ultrasound of the pregnancy and an electrocardiogram were also done. The ultrasound showed a live, intrauterine pregnancy with a gestational age of ten weeks, four days, based on the measurement of the crown-rump distance.
Following the initial lab abnormalities, a right upper quadrant ultrasound was performed, which revealed gallbladder sludge and no wall thickening, pericholecystic fluid, or common bile duct dilation. Additionally, there was a negative sonographic Murphys sign. The levels of alcohol, Thyroid Stimulating Hormone (TSH), prothrombin time, serum lipase, and acetaminophen were also measured. These measurements showed that acetaminophen, lipase levels, and alcohol were abnormally low. As a result, repeat vitals were taken, showing the patients heart rate to be 132 beats per minute, oxygen saturation to be ninety-eight percent room air, and blood pressure to be 127/77 mm Hg. The patient was then provided with two liters of normal saline and moved to tertiary care for a greater level of treatment. This movement was initiated following consultation with gynecology obstetrics, and Intensive care.
Before being sent from the ED to a tertiary care facility, the TSH test of the patient, which ranged from 0.27 to 4.20 milli-international units per liter (MIU/L), indicated that the patient was experiencing a thyroid storm. The patient scores forty-five points on the Burch-Wartofsky point scale (BWPS) for thyrotoxicosis. The amounts of triiodothyronine (T3) and free thyroxine (T4) were also measured based on the diagnosis. The patient was administered hydrocortisone and one hundred mg IV [intravenous). However, she was denied a propylthiouracil prescription due to her liver dysfunction after consultation with the tertiary care facility. Following her exit from the ED, the patient had additional blood work performed. The results after measurement were as follows; T3, free (FT3): 5.54 (2.52-4.33 pg/mL), PT> 1330 (11.2-12.1s), and INR: >10.8 (INR: 1.0). Overall, the final diagnosis of this patient was thyroid storm during her first trimester with acute liver failure as well as severe deficiency in vitamin K both caused by hyperemesis gravidarum.
Plan
The patient was referred to the medical critical care unit at the tertiary care facility for four days. A four-day visit was to manage and treat her thyroid storm while she was still in her first trimester of pregnancy. In this facility, hyperemesis gravidarum was identified as the primary cause of the thyroid storm, vitamin K insufficiency, and liver failure. Immediately her transaminitis began to improve; the endocrine consultant advised the beginning of hydrocortisone 50 mg IV thrice a day. In addition, 10mg of propranolol and methimazole were administered to the patient after every six hours. After a thyroid ultrasound and thyroid-stimulating immunoglobulin tests, the results showed they were within normal ranges. The patient was cleared from the tertiary facility with a seven-day course of twenty mg of prednisone because her daily T4/T3 levels were downward. In addition, she had reached her baseline when she was discharged.
Conclusion
In conclusion, consideration should always be given to metabolic reasons for vomiting because they might range from something as straightforward as hyperemesis gravidarum to something more complicated, like a thyroid condition. Although an earlier diagnosis of hyperemesis gravidarum might have contributed to the patients illness, thyroid issues must also be considered in such a situation. If the patient has tachycardia and agitation, her presentation will probably increase the likelihood of a thyroid condition. In addition, the only diagnosis capable of linking all her concerns in the discussion of potential causes is a thyroid diagnosis. Moreover, although hyperemesis gravidarum is frequently seen in the ED, emergency personnel are less aware of how it affects thyroid function. Thyroid hormone levels can rise in these people. This notion is based on the fact that HCG and TSH share a structural resemblance causing thyroid stimulation and a rise in HCG levels during pregnancy.
When considering hyperthyroidism during pregnancy, medical practitioners must decide if the thyroid anomaly is caused by gestational transitory thyrotoxicosis or the main illness such as thyroiditis or Graves disease. One of the most frequent causes of hyperthyroidism in pregnant women is associated with Graves disease (Alexander et al., 2017). However, these people frequently have a history of the condition and show other symptoms, such as goiter or exophthalmos, indicative of the disease. In the case of our patient, her physical examination revealed no abnormalities suggestive of thyrotoxicosis. In addition, apart from hyperemesis, there was no significant past medical history. As a result, although not completely impossible, it was less likely for the patient to be connected to hyperthyroidism.
Reference
Alexander, E. K., Pearce, E. N., Brent, G. A., Brown, R. S., Chen, H., Dosiou, C., Grobman, W. A., Laurberg, P., Lazarus, J. H., Mandel, S. J., Peeters, R. P., & Sullivan, S. (2017). 2017 guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid, 27(3), 315389. Web.
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