A 27-year-old pregnant woman presented to the ED with a chief complaint of abdominal pain and vomiting.
The patient was 2 months pregnant and had received no prenatal care. Her pain was located in the epigastric region and had been ongoing for 3 days without radiation to the back, chest, or lower abdomen. The patient described her pain as sharp, and a 7 on a 0-to-10 pain intensity rating scale. She had started vomiting several hours before arriving at the ED. She denied any vaginal bleeding, diarrhea, melena, dysuria, hematuria, or hematemesis. She had a past medical history of Bell palsy and a transverse and sagittal sinus thrombosis during her only previous pregnancy, which was delivered via a cesarean section due to prolonged and difficult labor. She was not taking any prescription or over-the-counter medications, and denied tobacco, alcohol, or illicit drug use.
The patient was afebrile, well-nourished and well-developed. She was not in any acute distress. Her mucous membranes were slightly dry. Her lungs were clear to auscultation and she did not have accessory muscle use with respiration. Cardiac auscultation revealed normal heart sounds and regular rate and rhythm. Her abdomen was soft, nondistended, and tender to palpation in the epigastric region without guarding, rebound, or rigidity. She had no costovertebral angle tenderness.
Treatment during this visit consisted of an IV infusion of 1 L of 0.9% sodium chloride solution for hypovolemia and 12.5 mg IV promethazine for nausea. Laboratory evaluation revealed beta-HCG of 92,961 mIU/mL and urinalysis demonstrated 11,000 to 15,000 cells/mm3 of white blood cells (WBCs), but was otherwise unremarkable. A complete metabolic panel was ordered and the serum bicarbonate measured at 21 mmol/L. Liver function tests, lipase, and glucose were within normal limits. A transvaginal ultrasound confirmed her pregnancy at 7 weeks, 5 days with active fetal heartbeat. Before discharge, she was given 1 g IV ceftriaxone for a presumed urinary tract infection (UTI). She also was prescribed promethazine 25 mg tablets for nausea during pregnancy, and a 10-day course of nitrofurantoin 100 mg twice daily for treatment of the UTI. She was instructed to return to the ED if symptoms became worse and to follow up with her obstetrician in 1 week.
On the following day, the patient returned to the ED with a chief complaint of hematemesis. She denied any chest pain, shortness of breath, diarrhea, melena, fevers, neck pain, palpitations, or syncope. She had taken one 25 mg tablet of promethazine, but continued vomiting, so she returned to the ED. Physical examination was unchanged from the previous ED visit. Another urinalysis, urine culture, and comprehensive metabolic panel were ordered. Urinalysis showed WBCs of zero to 2,000 cells/mm3, but was otherwise unremarkable. The comprehensive metabolic panel showed serum bicarbonate was 20 mmol/L with an anion gap of 16 mEq/L.
She was given a 2 L IV infusion of 0.9% sodium chloride solution. She was discharged with a prescription for ondansetron 4 mg oral dissolving tablet as needed for nausea and was instructed to follow up with her obstetrician or return to the ED if symptoms worsened.
Ten hours later, the patient returned for a third time to the ED with a chief complaint of increasing abdominal pain that had now persisted for 4 days. She reported that her epigastric pain was now radiating to her lower abdomen, and the hematemesis had persisted. On examination, her vital signs were BP, 100/70 mm Hg; heart rate, 159 beats/minute; respirations, 18 breaths/minute; and temperature, 97.6° F (36.4° C) oral. Her mucous membranes were dry. Her abdomen was tender in the epigastric and right upper quadrant region with guarding.
An ECG showed a tachycardic rhythm at a rate of 159 beats/minute with nonspecific ST-segment and T wave changes. A complete blood cell (CBC) count, comprehensive metabolic panel, lipase, urinalysis, urine culture, blood cultures, and lactic acid level were ordered, as well as pelvic and right upper quadrant ultrasounds. The CBC count showed an elevated WBC count of 25,700 cells/mm3 with a left shift. She was anemic with a hemoglobin of 10.1 g/dL. Her last CBC count was in 2008, and reported a hemoglobin of 11 g/dL. Lactic acid was grossly elevated at 12.4 mmol/L, indicating a significant underlying cause of possible peritonitis, bacteremia, or sepsis.1 Liver function tests, lipase, and urinalysis were unremarkable. Right upper quadrant ultrasound demonstrated some gallbladder sludge, but was otherwise unremarkable.
While in the ED, the patient was administered a 5 L infusion of 0.9% sodium chloride solution IV, hydromorphone 1 mg IV for pain, ondansetron 4 mg IV for nausea, and 3.375 mg IV piperacillin-tazobactam. She also received two doses of metoprolol 2.5 mg IV. A surgery consult was obtained in the ED. After surgical consultation, an MRI of the abdomen and pelvis was ordered; however, before the MRI could be performed the patient's condition deteriorated. The patient become increasingly tachycardic, and hypotensive with worsening pain. Because she now had signs and symptoms of acute abdomen and had significantly abnormal laboratory values, emergency exploratory laparotomy was recommended. The patient was advised on the risks of surgery including fetal loss and agreed to the plan.
The surgery team found necrosis of the small bowel and cecum. They resected 200 cm of the small bowel and 8 cm of the cecum. An anastomosis was created joining about 12 cm of proximal jejunum to the ascending colon. The patient began lifelong total parenteral nutrition. Hematology/oncology was consulted for evaluation of hypercoagulable disorders. Orders included anticardiolipin antibody, lupus anticoagulant, antithrombin 3, Leiden factor V, protein S, protein C, antinuclear antibodies, and erythrocyte sedimentation rate. The patient was ultimately diagnosed with protein S and protein C deficiency and placed on lifelong enoxaparin anticoagulant therapy. It was determined that this was the cause of the patient's current thrombosis, and very likely, the cause of her previous transverse and sagittal sinus thrombosis. The patient ultimately went on to deliver a healthy baby at 38 weeks by cesarean section.
This case demonstrates the challenges of diagnosing and treating pregnant patients with non-pregnancy-related pathology. Because the patient presented with abdominal pain in pregnancy, her workups initially began with evaluation of the fetus and common pathologies of pregnancy. In her first visit to the ED, the clinician ordered a transvaginal ultrasound, which showed good fetal heart rate, and it was assumed the patient was stable enough to be followed outpatient with her obstetrician. Her urinalysis reported WBCs to be 11,000 to 15,000 cells/mm3, which led to the patient being diagnosed with a UTI and discharged. Acute pyelonephritis was excluded as the patient was afebrile with no costovertebral angle tenderness.
Gangrenous cholecystitis, another possible diagnosis, was excluded on the patient's first and second ED visits because her liver function tests and lipase level were normal.2 Perforated viscus also was on the differential diagnosis. On her first ED visit, the only imaging she had focused on her pregnancy. No imaging was performed on the second ED visit, and a perforated viscus was only ruled out during the emergency exploratory laparotomy.
Appendicitis, the most common surgical emergency in pregnancy, should be considered when evaluating abdominal pain in pregnant patients.3 If performed during the first or second visit and found to be abnormal, a CBC count could have given clinicians a clue that the patient's pain was not solely caused by her pregnancy. A ruptured appendix can result in peritonitis, bacteremia, sepsis with ensuing lactic acidosis, and hemodynamic shock.3
The patient's high lactic acid level, high WBC count, and severe abdominal tenderness made mesenteric ischemia a likely diagnosis.4 Venous embolism or thrombosis can form and compromise blood flow to the intestines.4 This is a surgical emergency and if not addressed can lead to bowel ischemia and necrosis.4 Because the patient was pregnant and her vascular compromise was venous rather than arterial, a magnetic resonance venography would have been the test of choice for the diagnosis.4
After the patient's transverse and sagittal sinus thrombosis 4 years earlier, no clinician evaluated her for any hypercoagulable disorders. Pregnancy left her more susceptible to developing a thrombosis.5 Pregnancy induces a state of hypercoagulation by affecting multiple clotting mechanisms to protect against hemorrhage before and after delivery.5 The patient was already in a hypercoagulable state prepregnancy by being protein S and protein C deficient. The pregnancy exacerbated this by further reducing her already low protein S and C.5
This case highlights the need for clinicians to be aware that pregnant patients can present with intra-abdominal pathology that can mimic common pregnancy complaints. Through the course of their pregnancy, women will experience displacement of their organs; therefore, the clinical presentation may be atypical from the nonpregnant patient. Clinicians should not assume that all abdominal pain is pregnancy-related and must always be ready to intervene if pathology requires surgical intervention.
1. Gauer R, Forbes D, Boyer N. Sepsis: diagnosis and management. Am Fam Physician
2. Ønder A, Kapan M, Ülger BV, et al. Gangrenous cholecystitis: mortality and risk factors. Int Surg
3. Abbasi N, Patenaude V, Abenhaim HA. Management and outcomes of acute appendicitis in pregnancy
—population-based study of over 7000 cases. BJOG
4. Guan X, Huang L, Li L. Acute mesenteric venous thrombosis in a pregnant woman at 35 weeks of gestation: a case report and review of the literature. BMC Pregnancy Childbirth
5. Uchikova EH, Ledjev II. Changes in haemostasis during normal pregnancy
. Eur J Obstet Gynecol Reprod Biol