Keywords
pregnancy - hyperemesis - alkalosis - newborn
Metabolic alkalosis is characterized by alkalemia with an increased serum bicarbonate
and compensatory elevation of PCO2. Alkalosis begins with the loss of hydrogen ions from the body or the addition of
alkali. Protracted vomiting causes the loss of H+ and Cl− and the gain of HCO3
−. Respiratory compensation occurs through hypoventilation, resulting in an elevation
in PCO2 that buffers the rise in pH. The process is maintained by the effect of Na+, K+, and water loss on the kidney and is therefore treated by normal saline volume repletion
and correction of hypokalemia, in addition to correcting the cause of vomiting.[1] We present a case of metabolic alkalosis caused by induced and protracted vomiting
in pregnancy associated with nonreassuring fetal status, which prompted an indicated
preterm delivery. Metabolic alkalosis in both the mother and newborn was a complicating
factor managed to optimize recovery.
Case Presentation
A 21-year-old gravida 3, para 0 presented to the emergency room at 32 weeks' gestation
with lethargy, nausea, and vomiting over a 3-day period. Early in the pregnancy, the
patient had multiple admissions for hyperemesis gravidarum. The process did not resolve
with time, and her pregnancy was complicated by a total of 10 hospital admissions
for vomiting with volume depletion and electrolyte disturbances. During one of her
latter admissions, the patient was observed rapidly drinking large volumes of water,
which was subsequently followed by vomiting all the water ingested. She was under
the misconception that this action would relieve heartburn, had already trialed usual
remedies for gastroesophageal reflux, and received both gastroenterology and psychiatry
consultations. Despite this education, 2 days prior to this admission, the patient
reported that she had consumed large quantities of water resulting in vomiting.
Admission chemistry ([Table 1]) showed hyponatremia, hypokalemia, severe hypochloremia, elevated serum bicarbonate,
elevated blood urea nitrogen (BUN), and elevated creatinine, all consistent with protracted
vomiting resulting in severe electrolyte disturbance, volume contraction, and acute
kidney injury. There was hyperphosphatemia reflecting renal insufficiency and low
ionized calcium secondary to metabolic alkalosis. Fetal heart rate monitoring showed
normal rate with minimal variability and intermittent decelerations prompting a biophysical
profile that scored only two points for normal amniotic fluid. A 1,610-g male newborn
was delivered by urgent cesarean section with Apgar scores of 4 and 6 at 1 and 5 minutes,
respectively. Umbilical cord gases along with reference values[2]
[3] are provided in [Table 2] and showed a metabolic alkalosis with elevated serum bicarbonate levels, hypercapnia,
and base excess. The mother remained somnolent after delivery under spinal anesthesia,
was transferred to the intensive care unit, and her venous blood gas ([Table 2]) in conjunction with her serum electrolytes showed a hypochloremic metabolic alkalosis
with compensatory hypoventilation as the cause of fetal/newborn metabolic disturbance.
Table 1
Maternal and newborn chemistry with reference values in parentheses
|
Analyte
|
Maternal value
|
Newborn value
|
|
Na+ (mmol/L)
|
129 (136–145)
|
123[a] (138–146)
|
|
K+ (mmol/L)
|
2.8 (3.5–5.1)
|
3.0 (3.5–5.1)
|
|
Cl− (mmol/L)
|
< 60 (98–107)
|
62 (98–107)
|
|
BUN (mmol/L)
|
12.49 (2.14–8.21)
|
12.85 (2.14–8.21)
|
|
Creatinine (μmol/L)
|
280.60 (45.75–76.25)
|
268.40 (22.88–76.25)
|
|
HCO3
− (mmol/L)
|
43 (22–29)
|
38 (22–29)
|
|
Ca2+ (mmol/L)
|
2.10[b] (2.10–2.55)
|
1.70 (1.90–2.60)
|
|
Ionized calcium (mmol/L)
|
0.20 (0.29–0.32)
|
0.17[a] (0.28–0.33)
|
|
PO4
3− (mmol/L)
|
2.39 (0.94–1.45)
|
1.97 (1.45–2.91)
|
Abbreviation: BUN, blood urea nitrogen.
a Whole blood.
b Corrected for albumin.
Table 2
Umbilical cord and maternal blood gas results with reference values in parentheses
|
Umbilical cord blood gas
|
Maternal blood gas[a]
|
|
Venous
|
Arterial
|
Venous
|
|
pH
|
7.36 (7.35 ± 0.05)
|
7.36 (7.28 ± 0.05)
|
7.45 (7.33–7.43)
|
|
pCO2 (kPa)
|
11.84 (5.08 ± 0.67)
|
12.64 (5.35 ± 1.12)
|
9.71 (5.45–6.78)
|
|
pO2 (kPa)
|
0.93 (3.88 ± 0.52)
|
0.93 (2.39 ± 0.82)
|
5.19
|
|
HCO3
− (mmol/L)
|
50.3 (20.4 ± 4.1)
|
53.7 (22.3 ± 2.5)
|
50.7 (24–28)
|
|
Base excess (mmol/L)
|
19.9 (−4.0 ± 2.0)
|
23.0 (−4.0 ± 2.0)
|
23.1
|
a Collected 2 hours postpartum.
The mother was treated with normal saline replacement, intravenous potassium chloride
and calcium gluconate as her acute kidney injury was secondary to hypovolemia. Bilevel
positive airway pressure (BiPap) ventilation was used to correct her hypercapnia and
improve her mental status. The BiPap was discontinued after 24 hours with return to
normal consciousness. Adequate urine output was maintained, and by postoperative day
3, serum sodium, potassium, chloride, bicarbonate, ionized calcium, phosphate, BUN,
and creatinine all returned to normal limits. The patient was discharged on postoperative
day 4.
The newborn's course began with poor respiratory effort requiring continuous positive
airway pressure (CPAP) and 40% fraction of inspired oxygen (FiO2). The newborn's electrolyte, acid–base, and serum chemistry pattern mirrored the
mother's hypochloremic metabolic alkalosis ([Table 1]). He received surfactant but required intubation for persistent oxygen requirement
and hypercapnia. In addition, 3% saline was used to correct hyponatremia; potassium
chloride and calcium gluconate boluses were used to correct hypokalemia and hypocalcemia.
He maintained good urine output, and by day 4 of life, metabolic abnormalities corrected
to normal, and he was extubated and maintained on CPAP. He was eventually discharged
on day 78 of life with bronchopulmonary dysplasia that required 0.5 L/min 100% FiO2 via nasal cannula.
Discussion
This case demonstrates the development of metabolic alkalosis in a pregnant woman
caused by protracted vomiting with volume depletion and loss of sodium, hydrogen,
and chloride severe enough to prompt preterm delivery for nonreassuring fetal status.
It also demonstrates the dependence of the fetus on both the placenta and mother to
maintain physiologic acid–base and electrolyte balance. The fetal kidney primarily
maintains amniotic fluid volume and blood pressure.[4] Creatinine levels in newborns likewise reflect that of the mother.[5] Since the mother had metabolic alkalosis that was not corrected and the fetus required
urgent delivery, it became a problem for the newborn as well. In both the mother and
newborn, the process was managed by fluid and electrolyte restoration with appropriate
ventilation to counteract the maladaptive compensatory hypoventilation, allowing gradual
renal correction of the alkalosis in mother and newborn.
Conclusion
Metabolic alkalosis of the newborn resulting from maternal metabolic alkalosis has
been described in a handful of cases in the literature.[6]
[7]
[8] These cases were believed to occur in mothers with a known or suspected eating disorder.
Metabolic alkalosis appears to come to clinical attention in infants because the compensatory
respiratory acidosis leads to hypoventilation and oxygen desaturation. In our case,
the indication for delivery at 32 weeks' gestation was the nonreassuring fetal status,
likely related to maternal hypovolemia and hypercapnia. The metabolic alkalosis of
both the mother and fetus was apparent on the umbilical cord blood gases and treated
similarly with assisted ventilation, replacement of serum sodium, potassium, and chloride
resulting in resolution of metabolic abnormalities within 3 days. Whether or not vomiting
in pregnancy is related to an eating disorder, vomiting in pregnancy is common, and
the potential for metabolic alkalosis may adversely affect the fetus or newborn. Metabolic
alkalosis in a newborn should be considered in newborns with oxygen desaturation and
hypoventilation. Schimert et al used the term “transplacental metabolic alkalosis”
to describe their case report of a newborn with metabolic alkalosis, and this term
succinctly describes our case as well.[6]
