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“Pregnant and Starving to Death”: A Case of Starvation Ketoacidosis
Abstract Number: RF4BD-440
Abstract Type: Case Report Case Series
A 22 yo AA G1P0 at 32w6d with twin gestation presents with 3 days’ refractory abdominal pain, n/v, and PO intolerance. HR was 114 and BP was 160/89. Labs were notable for Cr 1.11, anion gap 27, glucose 52, and UA with large ketones. She was admitted for pre-eclampsia with severe features. Hypoglycemia was treated with dextrose without improvement. Starvation ketoacidosis of pregnancy was suspected. Her BP normalized after labetalol, but later that day fetal distress was noted on monitors and she was taken emergently to OR for cesarean delivery under GA-ETT with post-induction A-line. Neonates’ APGARs were 5, then 6. Initial ABG was: pH 7.13/bicarb 14.3/base deficit 14/lactate 3.06. She received 150 mEq bicarb and 4L crystalloid during the case. EBL was 1L. She remained intubated and was admitted to SICU postoperatively. After 24h of fluid and electrolyte resuscitation, metabolic derangements resolved. She discharged on POD5.
Discussion: Starvation ketoacidosis of pregnancy (SKP) is an uncommon complication, most often seen in the 3rd trimester. Data from DKA patients show that metabolic acidosis is strongly associated with IUFD; mortality rates estimated at 9-35%. The pathogenesis involves ketoacids crossing the placenta, volume depletion, and electrolyte derangement(1).
In ketoacidosis, a state of low glucose utilization (eg: starvation or insulin deficiency) forces the body to generate acetyl CoA from beta-oxidation of fatty acids to use in the citric acid cycle. Excess acetyl CoA is converted to ketone bodies, which accumulate to induce acidosis. Hormonal changes of pregnancy are implicated in the pathogenesis. Glucagon and human placental lactogen secreted by the placenta lead to a relative state of insulin resistance during pregnancy, making parturients susceptible to ketosis. 12-24 hrs of starvation (most often related to a period of severe vomiting, as in our patient) may be sufficient to induce ketoacidosis in otherwise healthy pregnant patients, compared to 14 or more days in the general population(1).
The differential for metabolic acidosis in pregnancy is broad, and SKP is a relative diagnosis of exclusion. Most cases are managed by emergent delivery as acidosis begins to induce fetal distress(2). However, some case reports suggest that aggressive early treatment with dextrose and fluid may reverse the acidosis and allow normal progression of pregnancy(3). Having high clinical suspicion may reduce the number of cases requiring emergent delivery. Working with OB colleagues to develop a protocol facilitating early recognition of acidosis is the next step in reducing maternal and fetal morbidity from SKP.
1. Eur J Obstet Gynecol Reprod Biol. 167 (2013) 1-7
2. Int J Obstet Anesth. 2011 Jul;20(3):253-6
3. S Afr Med J 2018; 108(8):636-639