Keywords
Gastric cancer - hyperemesis gravidarum - preeclampsia - acute renal failure
Nausea and vomiting are encountered in 75% of pregnancies and are considered part
of the “presumptive evidence” for pregnancy.[1] This morning sickness of pregnancy usually occurs during the morning but may continue during the day. The
onset is at ~6 weeks' gestation and may last up to 16 to 20 weeks.[1] In its most severe form, the patient is usually given the diagnosis of hyperemesis
gravidarum, which is defined as vomiting so severe as to produce weight loss, dehydration,
acidosis from starvation, alkalosis from loss of hydrochloric acid in vomitus, and
hypokalemia.[1] In extreme cases of volume contraction, hyperemesis gravidarum may even produce
acute renal failure (ARF).[2] Other causes of vomiting unrelated to the pregnancy are mostly gastrointestinal
or hepatobiliary in origin, but one of the rarest causes is cancer, especially gastric
cancer. It is estimated that the incidence of cancer of the digestive tract during
pregnancy is 1 in 100,000 pregnancies[3] and most are cancers of the large bowel.[4] Thus, it is not surprising that gastric cancer may be overlooked in the differential
diagnosis of a patient presenting with the symptoms of nausea and vomiting in pregnancy.
We present an unusual case of gastric cancer that may have either precipitated or
masqueraded as preeclampsia.
Case Report
A 35-year-old Hispanic woman (gravida 2, para 1) presented at 363/7 weeks' gestation complaining of uterine contractions, spotting, decreased fetal movement,
and nausea and vomiting. She was noted to have a blood pressure (BP) of 157/114 mm
Hg. The fetus was in a frank breech presentation, and the fetal heart rate tracing
revealed persistent late decelerations and absent beat-to-beat variability. The patient
was diagnosed with severe preeclampsia, started on MgSO4, and had an urgent cesarean delivery. A healthy 2595-g male with Apgar scores of
5 and 8 at 1 and 5 minutes, respectively, and with cord arterial pH of 7.23 was delivered
without incident. Observation of the liver surface at the time of surgery revealed
no abnormalities.
The patient had received prenatal care from 11 weeks with 11 total visits. Her initial
BP was 114/60 mm Hg. Her prenatal course was remarkable for persistent significant
nausea, vomiting, and poor weight gain. The patient weighed 112.5 pounds at 11 weeks,
129 pounds at 23 weeks, and 118 pounds at 34 weeks. She had been given metoclopramide,
promethazine, prochlorperazine, and simethicone without relief. An ultrasound at 213/7 weeks confirmed her dates (estimated fetal weight = 433 g, 56th percentile, and no
anomalies noted). There was no past medical or family history of gastrointestinal
or hepatobiliary disease, and a test of her stool for ova and parasites was negative.
At her initial visit at 11 weeks, her hemoglobin and hematocrit values were 8.1 mg/dL
and 27.2%, respectively, and her platelet count was533,000/mm3. An anemia workup showed a normal hemoglobin electrophoresis and a serum ferritin = 9.7
ng/mL and total iron-binding capacity = 505 μg/dL. On admission, her hemoglobin and
hematocrit values were 18.0 mg/dL and 52.8%, respectively, and her platelet count
was 194,000/mm3. Her electrolytes (mmol/L) were: Na = 135, K = 3.5, CI = 77, and CO2 = 37.0. Her blood urea nitrogen was 49 mg/dL, creatinine was 2.7 mg/dL, uric acid
was 16.9 mg/dL, aspartate aminotransferase was 49 U/L, alanine aminotransferase was
29 U/L, and albumin was 2.3 g/dL. Her prothrombin time and partial thromboplastin
time were 17.6 and 46.7 seconds, respectively, and her urinalysis showed 4(+) proteinuria.
The patient was noted to be both volume contracted and to have a hypochloremic metabolic
alkalosis. Her electrolytes were corrected with normal saline with 10 mEq KCl, and
these normalized by postoperative day 2. The patient was started on clear liquids
on the evening of postoperative day 1 but continued to have emesis and so the gastrointestinal
service was consulted. Additionally, the patient was started on hyperalimentation
with total parenteral nutrition.
A flat plate of the abdomen revealed moderate gaseous distension of the stomach ([Fig. 1]). The differential diagnosis included intermittent small bowel obstruction, gastric
outlet obstruction, or peptic ulcer disease. Contrast-enhanced axial computed tomography
imaging through the abdomen revealed a dilated stomach with thickened irregular antrum
and thickening of the posterior wall ([Fig. 2]). A nasogastric tube and famotidine were recommended. The nasogastric tube was placed
(with an initial aspiration of 1400 mL dark green fluid) and provided immediate relief.
Esophagogastroduodenoscopy revealed antral/prepyloric distortion secondary to a submucosal
mass consistent with either neoplasm or infectious cause. No ulcer was seen. A biopsy
showed poorly differentiated adenocarcinoma, and a computerized tomography scan of
the abdomen revealed a 3 × 4-cm mass in the pylorus and no perigastric lymphadenopathy
or liver metastases. The patient underwent a total gastrectomy, Roux-en-Y esophagojejunostomy,
feeding jejunostomy, and omentectomy with node sampling 11 days after her cesarean
delivery. She had a 12.0 × 9.5-cm gastric carcinoma, and 8 of 15 lymph nodes were
positive (stage IIIA [T3, N1, MX]); distant metastasis was not assessed at the time
of surgery.
Figure 1 A flat plate of the abdomen reveals moderate gaseous distension of the stomach.
Figure 2 Contrast-enhanced axial computed tomography image through the abdomen revealing a
dilated stomach with thickened irregular antrum and thickening of the posterior wall.
The patient was discharged home 23 days after her initial admission. The baby was
discharged home on day of life 7. The patient was alive 15 months after surgery but
has since been lost to follow-up.
Discussion
This was an unusual case presentation of gastric cancer in pregnancy. Because of hyperemesis
gravidarum, the patient was volume contracted and had hypochloremic metabolic alkalosis.
This volume contraction may have been the cause of her prerenal ARF, with resultant
proteinuria and hypertension. Whether she had preeclampsia in addition to the cancer
or whether the signs and symptoms were all due to her gastric cancer is unclear. It
is also unknown, if she did in fact have preeclampsia and whether the ARF precipitated
the preeclampsia or was the result of preeclampsia. ARF is a known complication of
preeclampsia. Although hyperemesis gravidarum has been described as a cause of ARF,[2] a review of the literature on gastric cancer in pregnancy shows this to be a very
rare cause of hyperemesis.
Preeclampsia has been mistaken for hepatitis, cholangitis, systemic lupus erythematosus,
immune thrombocytopenic purpura (ITP), gastric ulcer, detached retina, and acute appendicitis.[5] Because of this, it was dubbed the “great imitator” at the 1975 Pacific Coast Obstetrical
and Gynecological Society.[5] Goodlin suggested that the diagnosis of preeclampsia or hemolysis, elevated liver
enzymes, and low platelet count (HELLP syndrome) has also been applied to processes
unrelated to pregnancy.[5] These diseases include cardiomyopathy, dissecting aortic aneurysm, cocaine abuse,
essential hypertension and chronic renal disease, acute fatty liver of pregnancy,
gangrenous or ruptured gall bladder, glomerulonephritis, ITP, lupus erythematosus,
malignant pheochromocytoma, and a ruptured bile duct.[5] To this list we may now add gastric cancer.
Cancer of the stomach is a very rare condition and rarer in pregnancy.[3] This low incidence is obviously influenced by the fact that the peak incidence of
pregnancy is below 35 years of age.[1] The peak incidence of gastric cancer is in the sixth decade, and men are affected
twice as frequently as women.[6] In a review of the German National Cancer Registry, Haas[7] demonstrated a lower incidence than expected of all cancers, including stomach cancer,
in pregnant women and speculated that women with subclinical cancers do not usually
become pregnant, presumably due to decreased libido resulting from constitutional
symptoms. Alternatively, it was suggested that “conception, implantation, or early
embryonic development could be disrupted by hormonal or immunologic concomitants of
malignant disease.”[7] Most of the cases are diagnosed in advanced stages either because the patient's
symptoms are attributed to her pregnancy or because of a reluctance to pursue diagnostic
studies during pregnancy.[8] This delay may explain the poor prognosis of this malignancy. It has been suggested
that persistent gastrointestinal symptoms during pregnancy should be evaluated by
gastroendoscopy,[1] and we endorse this recommendation. In those cases where there is persistent vomiting,
electrolyte analysis and blood gas evaluation may be indicated to rule out serious
disturbances and to guide therapy.
Our case suggests that gastric cancer may be a rare cause of hyperemesis in pregnancy,
with ultimate renal failure and/or preeclampsia as the presenting diagnosis. Early
diagnosis of this malignancy is important in improving the patient's prognosis.
