A 34-year-old woman G1P0 at 16 weeks gestation is referred to the ED by her primary care physician as “high-risk OB” with a blood pressure of 150/100 mm Hg.
Her current exam is notable for a blood pressure of 155/100 mm Hg and trace non-pitting edema of the extremities. She has a normal BUN and creatinine. Urinalysis reveals trace proteinuria with 2 to 3 red blood cells but no ketones, leukocyte esterase, or nitrites. A bedside ultrasound shows a live intrauterine pregnancy consistent with a 16-week gestation. Her quantitative beta hCG is within the normal range for this gestational age.
1. What is the diagnosis?
2. Is a bedside ultrasound necessary given the lack of vaginal bleeding or abdominal complaints?
3. Does a quantitative hCG need to be checked?
4. How should this patient be managed?
5. At 22 weeks, the patient returns with a mild headache, 1+ pitting edema, and blood pressure of 160/110 mm Hg. Her creatinine has increased from 0.7 to 1.5 (BUN increased from 16 to 25). Urinalysis now reveals 2+ proteinuria. How should the patient be managed now?
6. The patient presents again at 32 weeks with malaise, increasing edema, and blood pressure of 175/100 mm Hg. She now has 3+ proteinuria and a creatinine of 1.7. Should she be given furosemide?
7. What is the treatment strategy at this point?
The exact diagnosis is unclear. The patient may have undiagnosed hypertension prior to being pregnant. She also may have pregnancy-induced hypertension (PIH), also known as gestational hypertension, which is usually not diagnosed before 20 weeks gestation. A third possibility is pre-existing hypertension with acute concomitant PIH. Without prior records, it is impossible to tell.
There are several important physiologic changes that occur in a normal pregnancy. Cardiac output increases and systemic vascular resistance decreases, giving a net decrease in blood pressure and increase in glomerular filtration rate (GFR). BUN and creatinine are lowered while the decreased protein reabsorption induces a mild albuminuria of pregnancy. There is also a relative anemia due to intravascular volume expansion.
In PIH, however, systemic vascular resistance often increases, causing an increase in blood pressure. Progression to pre-eclampsia then leads to a decrease in GFR, which when combined with the increased oxidative stress of pre-eclampsia, leads to increased uric acid levels. For unknown reasons, pre-eclampsia is associated with an elevation in factors such as TNF-α that cause increased capillary permeability.
Our patient warrants an ultrasound for several reasons. First, a molar pregnancy should be ruled out as the cause of hypertension. Second, the management of PIH is different when there is evidence of oligohydramnios, placental separation, or intrauterine growth restriction. Third, an assessment of fetal well-being is important. Spontaneous fetal movement and a normal fetal heart rate should be apparent at this stage. A quantitative hCG is unlikely to change management once the ultrasound is done.
There are several approaches to managing this patient. Pregnant women presenting with hypertension should have their renal function checked, as well as a urinalysis (looking for proteinuria and blood) and an ultrasound. I would probably also check a quantitative hCG (more out of habit than evidence-based practice) along with a CBC (checking her platelets) and liver function panel.
Our well-appearing patient can be discharged with no prescriptions and urgent follow-up with an obstetrician, but her proteinuria could be an early harbinger of disease, and I probably would start her on labetalol. Without it, her hypertension will likely progress. OBs tend to use nifedipine or labetalol for these cases, but I prefer the latter. This issue can be discussed with the OB on-call. In our case, the OB prefers nifedipine, and timely follow-up is arranged.
Unfortunately, our patient never receives a call for her OB appointment, and returns with worsening hypertension of 160/110 mm Hg. Based on symptoms alone, she deserves the full evaluation described above even if it was done six weeks earlier. I would also check a uric acid level at this point, and strongly consider admission given the failed outpatient treatment with worsening proteinuria and renal function. Our patient's liver function tests and uric acid level are normal, so she is actually discharged by OB after being switched to labetalol and being given clear outpatient lab and follow-up instructions.
When our patients presents yet again at 32 weeks, she has clear evidence of pre-eclampsia, which is associated with vasospasm, decreased renal flow, reduced GFR, and increased total body water. Decreased intravascular volume causes decreased uteroplacental blood flow, making diuretics contraindicated in these cases. Instead, maintenance fluids should be given to maintain urine output, while being cautious of the increased risk for pulmonary edema in pre-eclampsia.
Our patient is now admitted for magnesium therapy, IV labetalol, and steroids. Her blood pressure continues to rise, and she is also given hydralazine. Her uric acid level and liver function tests are elevated, but her platelets are normal. Her PT/PTT and fibrinogen are also normal. A bedside ultrasound shows a live intrauterine pregnancy at 31 weeks. Because there is no evidence of oligohydramnios, delivery by C-section is delayed until 33 weeks. The baby is discharged home after a brief stay in the NICU.