Hyperemesis: When Nutrition is Compromised for Mom and Baby

Emily Moots

Hyperemesis gravidarum: Definition

• Intractable nausea and vomiting leading to fluid, electrolyte, and acid–base imbalance, nutrition deficiency, and weight loss during early pregnancy

• Characterized by persistent vomiting, weight loss of more than 5%, ketonuria, electrolyte abnormalities (hypokalemia), and dehydration (high urine specific gravity

Occurrence of more than three episodes of vomiting per day with ketonuria and more than 3 kg or 5% weight loss

Facts

The onset of the nausea is within 4 weeks after the last menstrual period in a majority of patients. The problem peaks at about 9 weeks of gestation.

60% of cases resolve by the end of the first trimester, and 91% resolve by 20 weeks of gestation

Causes

Exact mechanism is unclear HCG is the most likely endocrine factor which

accounts for the development of HG. This conclusion is based on observed associations between increased production of HCG (as in molar or in multiple pregnancies) and the fact that the incidence of hyperemesis is highest at the time when HCG production reaches its peak during pregnancy (around 9 weeks gestation). However, there is no evidence to support this hypothesis and some pregnant women do not experience nausea and vomiting despite elevated HCG-levels.

Assessment

40 y.o. Hispanic female, G4P4, 10 weeks pregnant with a PMH of DM, CAP-symptoms and complaints include vomiting and back pain

EGD done showing no obstruction and a cholecystectomy was done in the past

Anthropometric Data

Height: 5’2”-slightly short stature Weight: 110#, 100% of IBW-meeting perfectly BMI: 20.3-normal NKA, no chewing/dental problems, no bowel

problems, no known changes in eating habits, good appetite

Vomiting-not absorbing needed nutrients Past Diet Prescriptions: Clear Liquid 24-Hour Recall not Applicable since patient is on

TPN and discussing food is not appropriate

Nutrition Focused Physical Assessment

Appearance: pale, normal sized, muscle wasting not visibly present, appetite good since patient noted hunger, patient is active, compliant, family present

Lab Data

(11/23) Total Protein (5.6 g/dL) is low most likely from a reduced intake of protein or malabsorption, calcium is low but when corrected for low albumin is normal (~ 9.34 mg/dL). Albumin is low (2.7 mg/dL) either due to pregnancy, excess hydration, or inadequate protein intake. The A/G ratio may be low (.9) since Albumin is low.

Krause’s Food & Nutrition Therapy (2008)

Lab Data Cont.

Glucose (142 mg/dL) and AccuChecks (165, 181, 190 (mg/dL) are occaisionally high which is related to poor glucose control due to the pt’s DM. Na (131 mEq/L) and Cl (98 mEq/L) may be low due to fluid retention with pregnancy, excess free water intake, or malabsorption from vomiting. Low Hgb (11/22-9.9 g/dL), Hct (11/22-27.8%), and RBC (11/22-3.09 x 10^6/mm3) is most likely related to inadequate intake of iron and can also be lower due to pregnancy.

Krause’s Food & Nutrition Therapy (2008)

Medications

Pepcid- Inj. 20 mg Q12H- Anti-GERD- reduces Iron and Vit B12 absorption, N/V/D/C

Zofran-Inj. 8 mg Q4H-Antiemetic, Antinausea-Dry mouth, C/D, fatigue, abdominal pain

Promethazine HCl- IV with Saline 25 mg Q4H/PRN- Antiemetic-increase need for Riboflavin, Dry Mouth, N/V/C

Pronsky, Zaneta M. & Crowe, SR Jeanne P. (2010) Food Medication Interactions. 16th Ed. Food-Medicationi Interactions. Birchrunville, PA

Meds Cont.

Insulin Aspart.-TID-Antidiabetic- weight gain Acetaminophen- PO 325 mg Q4H/PRN-

Analgesic- caffeine increases rate of absorption and effect, increased Vit C may decrease excretion and increase risk for toxicity

Drug Interactions and Side Effects

Although vomiting is a possible side effect of some of the medications she is receiving, vomiting is related to the condition and not side effects

Medication could exacerbate vomiting but there is no way to tell and the side effects are not main concern at this time

If the vomiting does not stop after the patient has been on anti-emetics for a period of time it seems that these medications could be discontinued since they are not working.

Pathophysiology of Hyperemesis Gravidarum

Exact mechanism is unclear Produced by the placenta

Hyperemesis Gravidarum Cont.

Correlates closely with the level of human chorionic gonadotropin (hCG), theorized that hCG may stimulate estrogen production from the ovary and increased estrogen is known to cause nausea and vomiting

Mean plasma adenosine concentration in women with hyperemesis gravidarum was significantly higher than those in nonpregnant women and women with normal pregnancies

Vitamin B deficiency may contribute to hyperemesis gravidarum, since the use of multivitamins containing vitamin B reduces the incidence of nausea and vomiting

Nutrition Needs

Calories: 32 kcal/kg = 1600 kcal/day– Fits with ASPEN recommendations based off of EER for

pregnancy

Protein: 1.5 g/kg = 75 g/day– Up to 2g/kg recommended for patient’s under stress

Iron: 3-6 mg/day Calcium and Iodine: Recommended to increase if

remain on TPN for longer period of time Fluid: 1300 ml/day (750 mL for 10% AA , 379 mL for

70% Dext )

The ASPEN Nutrition Support Curriculum, 2007

PES Statements

Inadequate energy intake R/T hyperemesis gravidarum AEB multiple episodes of emesis/day.

Food and nutrition related knowledge deficit R/T diagnosis of DM AEB poor glucose control and pt report of lack of DM education.

Diet Orders

11/16-Dinner: Clear Liquid 11/18-Dinner: NPO/Enteral 11/22-Breakfast: NPO/TPN 11/24-Dinner: Clear Liquid and TPN

11/26-Lunch: GI Soft 11/28-Breakfast: Diabetic Diet 2000 kcal

Discussion of Diet Orders

Hyperemesis gravidarum can be indication for TPN- severe and weight loss

Need nutrients to sustain life and if vomiting continues after trying PO and enteral nutrition then TPN

I would have liked enteral nutrition via the NG tube to be continued longer to see if progress was made before initiating TPN.

Interventions

Intervention #1: Work with medical team to reduce vomiting and advance diet as medically appropriate

Intervention #2: prior to discharge be sure patient understands nutrition being discharged home with or ways to combat vomiting and eat a balanced diet during pregnancy if a normal PO diet is appropriate at time of discharge

Intervention #3: have pt be able to spread out CHO intake, begin learning CHO at meals and snacks, and achieve normal glucose levels

Barriers

Being preoccupied with vomiting at this time, language barriers, and also being preoccupied with pregnancy could affect her level of compliance at this time

Monitor/Evaluate

Weight, labs, pt report of symptoms, consulting MD or RN on pt’s status

Monitoring for success: Assessing whether the pt stops vomiting and tolerates a clear liquid diet or is ready for diet advancement

References

Jueckstock, J. K., Kaestner, R. R., & Mylonas, I. I. (2010). Managing hyperemesis gravidarum: a multimodal challenge. BMC Medicine, 846-57. doi:10.1186/1741-7015-8-46

Mahan, Kathleen L. & Escott-Stump, Sylvia (2008). Krause’s Food & Nutrition Therapy. Elsevier. Philidelphia.

McCulloch, David K. (2008) Pathogenesis of Type 2 diabetes mellitus. UpToDate. Available from http://www.uptodate.com/online/content/. Assessed November 18, 2010.

Niebyl, Jennifer R. (2010). Nausea and Vomiting in Pregnancy. New England Journal of Medicine [serial online]. November 18, 2010;363(21):2078. Available from: Academic Search Premier, Ipswich, MA. Accessed November 26, 2010.

Pronsky, Zaneta M. & Crowe, SR Jeanne P. (2010) Food Medication Interactions. 16th Ed. Food-Medicationi Interactions. Birchrunville, PA

Schmitt, Steven (2009). Community-Acquired Pneumonia. Cleveland Clinic. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/infectious-disease/community-acquired-pneumonia/#s0025 Accessed November 26, 2010

The A.S.P.E.N. Nutrition Support Core Curriculum (2007). Pregnancy and Lactation. 384-396. www.nutrition care.org

Yoneyama, Y., Suzuki, S., Sawa, R., & Araki, T. (2005). Plasma adenosine concentrations increase in women with hyperemesis gravidarum. Clinica Chimica Acta, 352(1/2), 75-79. doi:10.1016/j.cccn.2003.12.026

Questions?