Hyperemesis gravidarum is characterized by severe and excessive nausea and vomiting during pregnancy, leading to electrolyte, metabolic, and nutritional imbalances
Hyperemesis gravidarum is linked to trophoblastic activity, gonadotropin production, and psychological factors
Possible causes of hyperemesis gravidarum include:
Pancreatitis
Biliary tract disease
Decreased secretion of free hydrochloric acid in the stomach
Decreased gastric motility
Drug toxicity
Inflammatory obstructive bowel disease
Vitamin deficiency (especially B vitamins)
Psychological factors in some cases
Transient hyperthyroidism
Assessment findings of hyperemesis gravidarum include severe nausea and vomiting, weight loss, hiccups, oliguria, vertigo, headache, electrolyte imbalance, dehydration, and metabolic alkalosis
Diagnostic test findings for hyperemesis gravidarum:
Decreased protein, sodium, and potassium levels
Increased blood urea nitrogen levels
Elevated hemoglobin levels
Elevated white blood cell count
Nursing diagnoses for hyperemesis gravidarum:
Imbalanced nutrition, less than body requirement related to frequency of excessive nausea & vomiting
Fluid volumedeficit related to excess fluid loss
Anxiety related to ineffective gravidarum coping, physiological changes of pregnancy
Activity intolerance related to weakness
Medical management of hyperemesis gravidarum includes:
Withholding oral fluids and food until there's no vomiting for 24 hours
Administering antiemetic medications
Monitoring fluid intake and output, vital signs, skin turgor, daily weight, serum electrolyte levels, and urine for ketones
Providing frequent mouth care
Recommending a diet high in dry, complex carbohydrates and suggesting eating two or three dry crackers before getting out of bed in the morning
Suggesting decreased liquid intake during meals
Ectopic Pregnancy: implantation of the fertilized ovum outside the uterine cavity
Types of Ectopic Pregnancy:
Interstitial pregnancy
Isthmic pregnancy
Ampullary pregnancy
Abdominal pregnancy
Cervical pregnancy
Ovarian pregnancy
Fimbrial pregnancy
Abdominal Pregnancy:
Product of conception is expelled into the pelvic cavity
Fetal outline is easily palpable
Sonogram or MRI is used to reveal the fetus outside the uterus
At term, the infant may be born by laparotomy
Assessment Findings/Signs and Symptoms:
Mild abdominal pain
Amenorrhea / absence of menses
Extreme pain & lower abdominal pain
Uterus is boggy & tender
Rupture of tube
Nausea & vomiting
Syncope
Shock
Causes of ectopic pregnancy:
Endosalphingitis
Diverticula
Tumors pressing on the tube
Previous surgery like tubal ligation or resection, or adhesions from previous abdominal or pelvic surgery
Transmigration of the ovum, resulting in delayed implantation
Risk for deficient fluid volume related to bleeding from a ruptured ectopic pregnancy
Powerlessness related to early loss of pregnancy secondary to ectopic pregnancy
Goal of care:
Ensure maternal blood loss is replaced and bleeding stops
Patient maintains adequate fluid volume as evidenced by normal urine output at 30-60ml/hr
Complications:
Rupture of the Tube
Infertility
Nursing Management of Ectopic Pregnancy
Salpingectomy
Salpingostomy
Oophorectomy
Administer Methotrexate
Blood transfusion
Antibiotic
High CHON diet
Emotional support
Nursing Interventions:
Date of patient’s last menses and obtain serum hCG levels
Assess vital signs and monitor vaginal bleeding for extent of fluid loss
Check amount, color, and odor of vaginal bleeding; monitor pad count
Withhold fluid/food
Assess signs and symptoms of hypovolemic shock secondary to blood loss from tubal rupture
Administer blood transfusion and analgesic
Determine if the patient is Rh – negative
Urge prompt treatment of pelvic infections to prevent recurrent ectopic pregnancy
Inform patients with fallopian tube surgery or confirmed pelvic inflammatory disease of increased risk for another ectopic pregnancy
Gestational Trophoblastic Disease, specifically Hydatidiform Mole, involves the rapid deterioration of trophoblastic villi cells, leading to grapelike clusters of vesicles due to fluid-filled cells
The embryo fails to develop past the early stages due to these cell abnormalities
Possible causes of Gestational Trophoblastic Disease include chromosomal abnormalities, hormonal imbalances, or deficiencies in protein and folic acid
Assessment findings for Gestational Trophoblastic Disease include vaginal bleeding, hyperemesis, lower abdominal cramps, an exceptionally large uterus for the gestational date, grapelike vesicles in the vagina, ovarian enlargement from cysts, and absence of fetal heart rate tones
Diagnostic tests for Gestational Trophoblastic Disease include Radioimmunoassay, Histologic examination, Ultrasonography after the 3rd month, Amniography, Doppler ultrasonography, and blood tests like WBC and urine hCG levels
Medical management of Gestational Trophoblastic Disease involves dilatation and suction curettage, postoperative treatment based on blood loss and complications, monitoring hCG levels, prophylactic chemotherapy, and chemotherapy and radiation for metastatic choriocarcinoma
Nursing management includes assessing vital signs, monitoring for complications like hemorrhage and uterine infection, saving expelled tissue for analysis, explaining contraceptive use, and dietary recommendations
Two types of Gestational Trophoblastic Disease are Complete Moles, characterized by swelling and cystic formation of all trophoblastic cells, and Partial Moles, with edema of some trophoblastic villi and some normal villi
Complete Moles are genetically diploid, paternal-derived, associated with choriocarcinoma, and have no fetal blood present
Partial Moles may have fetal blood present, an embryo up to 9 weeks gestation, are genetically triploid, derived from both parents, and have 69 chromosomes with 3 chromosomes for every pair
Invasive types of Gestational Trophoblastic Neoplasia include Invasive mole (limited to the uterus), Choriocarcinoma (can metastasize to the lungs), and Placental site tumor (rare, arising from trophoblastic cells)
Incompetent cervix, also known as premature cervical dilation, typically occurs around week 20 of pregnancy
Pathophysiology of incompetent cervix:
Associated with congenital structural defects or previous cervical trauma
Also linked to increasing maternal age
Connective tissue structure of the cervix is not strong enough to maintain closure of the cervical OS during pregnancy
Assessment findings of incompetent cervix include:
History of repeated 2nd trimester spontaneous abortions
Cervical dilation
Pink-stained vaginal discharge
Increased pressure with possible ruptured membranes
Nursing diagnosis of incompetent cervix: Anxiety related to impending loss of pregnancy as evidenced by premature dilation of the cervix
Diagnostic test findings of incompetent cervix:
Ultrasound
Nitrazine test (on amniotic fluid)
Medical management of incompetent cervix includes:
McDonald’s procedure: using a nylon suture horizontally and vertically
CERCLAGE: Placement of a purse-string suture in the cervix
Shirodkar procedure: using sterile tape in a purse-string suture
Nursing Interventions of incompetent cervix:
Bed rest after surgery
Prepare the woman for cervical cerclage under regional anesthesia as indicated
Sutures will be removed around the 37th-39th week of pregnancy
Possible complications of incompetent cervix: spontaneous abortion and preterm birth
Spontaneous Abortion: pregnancy loss at less than 20 weeks gestation in the absence of medical or surgical measures
Types of Spontaneous Abortion:
Complete Abortion: Entire products of conception are expelled spontaneously without any assistance
Habitual Abortion/Recurrent: Spontaneous loss of 3 or more consecutive pregnancies at the same gestation age
Incomplete abortion: Uterus retains part or all of the membranes/placenta
Inevitable/Imminent Abortion: Membranes rupture and the cervix dilates
Missed abortion: fetus dies in utero but is not expelled
Threatened abortion: Bloody vaginal discharge occurs during the 1st half of pregnancy
Septic abortion: Infection accompanies abortion
Causes of Spontaneous Abortion (Fetal Factors):
Defective embryologic development from abnormal chromosome
Faulty implantation of fertilized ovum
Failure of the endometrium to accept the fertilized ovum
Causes of Spontaneous Abortion (Maternal Factors):
Maternal infections
Severe malnutrition
Abnormalities of the reproductive organs
Causes of Spontaneous Abortion (Placental Factors):
Premature separation of the normally implanted placenta
Abnormal placental implantation
Abnormal platelet function
Diagnostic test findings:
Evidence of expulsion of uterine contents, pelvic examination, laboratory studies and Ultrasonography
Assessment Findings:
Pink discharge for several days
Scant brown discharge for several weeks before the onset of cramps and increased vaginal bleeding
Complications of spontaneous abortion:
Hemorrhage: Position the woman flat, massage the uterine fundus, Dilatation and curettage, Direct replacement of fibrinogen, Methergine (methylergonovine maleate)
Infection: E. Coli (spread from the rectum forward into the vagina), Endometritis
Sepsis: complicated by infection
Isoimmunization: Production by the mother’s immunologic system of antibodies against Rh-positive blood
Powerlessness
Procedures Used in Pregnancy Termination:
Vacuum Curettage: Used for 1st tri abortions to remove remaining products of conception
Dilatation & Curettage: Dilatation of the cervix followed by gentle scraping of the uterine walls to remove products of conception, local or general anesthesia is needed