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Hyperemesis gravidarum--A serious complication of pregnancy. (Original Case Study).

Abstract This case study reports on a 28-year-old female who presented ten weeks gestation into her pregnancy with twins with a four-week history of nausea and vomiting. At 12 weeks gestation she had lost 14% of her prepregnancy body weight and antiemetic medications had failed. Nasogastric feeding was commenced and successfully alleviated her nausea and vomiting within 24 hours. Marginal thiamin deficiency was subsequently diagnosed and she was treated with 100 mg intramuscular thiamin and discharged on 100 mg oral thiamin daily. Nasogastric feeding continued until 16 weeks gestation at which time the tube dislodged and the patient refused to have it reinserted. She continued to vomit once per day but otherwise tolerated an oral diet. At 28 weeks gestation she was delivered by emergency caesarian due to foetal distress. Both babies died of complications of prematurity. This case highlights the need for early and aggressive nutritional intervention to prevent weight loss and nutritional deficiencies. Nasogastric feeding offers a safe and effective means of nutritional support and is able to alleviate nausea and vomiting. Furthermore it is recommended that women with hyperemesis have their thiamin concentrations monitored and in cases of severe intractable hyperemesis women may require thiamin supplements.

Key words: pregnancy, hyperemesis gravidarum, nasogastric feeding, thiamin, refeeding syndrome

Case report

A 28-year-old, previously well, primigravida was admitted to the Royal Women's Hospital, Melbourne, Victoria, at ten weeks gestation with a monochorionic, monoamnionic twin pregnancy, a four-week history of worsening hyperemesis and weight loss of 3 kg. There was no history of alcohol or drug abuse, and she was not taking any medications. Her weight prior to pregnancy was 51 kg with a BMI of 18.5 kg/[m.sup.2]. Intravenous fluids (Hartmans solution) and oral antiemetics (prochlorperazine) were administered, but vitamins were not given. Her nausea and vomiting settled and she was discharged three days later. One week after discharge she was reviewed. She had ceased her antiemetics, nausea and vomiting had returned and she had only consumed oral fluids since discharge. Her weight had dropped to 44 kg (a loss of 14% of prepregnancy weight). Nasogastric feeding was recommended but refused. Antiemetics were recommended, and nutritional drinks (Resource fruit beverage, Novartis, North Ryde NSW) were prescribed along with small, frequent meals and snacks as tolerated. Two days later she was readmitted, her nausea and vomiting had not improved. Her weight was now 43 kg. Nasogastric feeding with Osmolite (Abbott Australasia, Kurnell, NSW) was commenced at a slow rate of 40 ml per hour for 96 hours to reduce the risk of refeeding syndrome, then gradually increased over the next 48 hours to meet estimated nutritional requirements. One gram of supplemental phosphate was administered. Electrolytes were monitored daily during admission. With the exception of magnesium which steadily declined to 0.69 mmol/L at day five, all other parameters remained within the normal range.

Within 24 hours of commencing nasogastric feeding, the nausea and vomiting had settled and antiemetic medication was ceased. Eight days after this admission she was discharged on home enteral nutrition of Osmolite at a continuous rate of 80 ml per hour. This regimen provided 8800 kJ, 74 g protein, 300 g carbohydrate and 3.2 mg thiamin.

At 14 weeks gestation and five days following discharge her weight had increased to 47.4 kg, but she complained of muscle twitching down one side of her leg, and an inability to sleep. She had become very anxious and it was noted that she was repeating the same questions often. She was readmitted for further investigations. Thiamin deficiency was diagnosed: serum thiamin 34 U (normal range 50 to 100 U) red cell transketolase stimulation 17% (marginal deficiency 15 to 22%). All other parameters were within the normal range. She was administered 100 mg intramuscular thiamin and was discharged home on 100 mg oral thiamin daily and the plan of weekly outpatient visits to monitor serum electrolytes, thiamin and weight gain. Her serum thiamin concentration five days after intramuscular thiamin and daily oral thiamin administration was 99 U (normal range 50 to 100 U) and red cell transketolase was within the normal range. Her symptoms had abated.

At 16 weeks gestation the nasogastric tube was dislodged and she refused to have it reinserted. She was commenced on nutritional supplement drinks (Sustagen) to provide 2800 kJ daily and given dietary advice on increasing her energy intake. She continued to vomit at least once a day, but despite this was able to tolerate a solid diet. Her pregnancy progressed until 27 weeks gestation when she required an emergency caesarian due to foetal distress. Both babies died post delivery from complications of prematurity. Her weight at delivery was 52.5 kg.

Discussion

Approximately two percent of all pregnancies are complicated by hyperemesis gravidarum, a condition characterised by intractable nausea and vomiting, fluid and electrolyte imbalances, ketonuria, weight loss, nutritional deficiencies and in some instances neurologic disturbances and liver or renal abnormalities (1-3). If untreated and symptoms persist, foetal viability and the mother's life may be threatened. Women with hyperemesis gravidarum are at high risk of malnutrition (4,5). They often experience weeks of diminished oral intake complicated by nausea, vomiting and weight loss before hospitalisation. Losses of up to ten percent of body weight are not uncommon (5). Weight loss of more than five percent of prepregnancy weight has been associated with retarded foetal growth (6). The patient in our case study exhibited seven weeks of intractable nausea and vomiting, and was suffering from dehydration and ketonuria on admission to hospital, and had lost 14% of her body weight at 12 weeks gestation.

Women with hyperemesis gravidarum usually require frequent hospital admissions and treatment with antiemetics, correction of fluid and electrolyte imbalances and gradual introduction of fluids and food (5). Nutritional support is vital to both prevent significant weight loss and to ensure good perinatal outcome (7). Women who fail to respond to conservative measures such as antiemetic medication, intravenous hydration and dietary manipulation and in whom oral feeding fails, pose special problems. Nasogastric feeding offers an effective and safe means of nutritional support, relieves intractable nausea and vomiting within 24 hours of initiation, and achieves positive foetal and maternal outcomes (1,5,7,8). The mechanisms by which enteral feeding alleviates hyperemesis remain unclear (8). In our patient both nausea and vomiting settled within 24 hours of commencement of nasogastric feeding leading to cessation of all antiemetic medication.

Any condition in which protracted vomiting is a feature, such as hyperemesis, may lead to thiamin deficiency. Thiamin deficiency can result in serious maternal and foetal sequelae. Cases of acute berri berri with acute cardiac failure have been reported in offspring of asymptomatic mothers with low thiamin intakes two to four days after birth (9). Wernicke's encephalopathy, a potentially fatal neurological disorder resulting from thiamin deficiency, is associated with hyperemesis, but remains an under recognised problem in obstetric practice (10). It was first reported in 1914, and some 25 cases have since appeared in the literature. Only half of these pregnancies resulted in the births of normal children. A number of recent cases (10-14) describing Wernicke's encephalopathy from hyperemesis have reported complications including blindness, convulsions and coma in the mother. The patient in this case study was only marginally thiamin deficient as indicated by her red blood cell transketolase. The effects of ma rginal deficiency are unclear, therefore treatment was instigated.

In order to prevent thiamin deficiency it has been recommended that women with hyperemesis in whom vomiting is severe or prolonged receive oral thiamin supplements (10-14). Oral medication is the preferred method of supplementation but may not always be tolerated. Monitoring of thiamin status is essential in these women. In addition, patients should not be given prolonged intravenous treatment consisting of only saline or dextrose as nutritional deficiencies may develop. Lavin et al. (2) reported on two women with hyperemesis who developed Wernicke's encepalopathy after being treated with glucose-containing intravenous fluids without vitamins. The report on confidential enquiries into maternal deaths in the UK (15) recommends that 'in all cases where an intravenous infusion is required, thiamin should also be administered'.

Carbohydrate-rich regimes such as intravenous administration of glucose, nasogastric feeding and hyperalimentation solutions given to malnourished patients, have been recognised in precipitating the 'refeeding syndrome'. The refeeding syndrome has been well described (16-19) and is associated with considerable morbidity and mortality. The most widely reported clinical features are fluid balance abnormalities, abnormal glucose metabolism, hypophosphataemia, hypomagnesaemia, hypokalaemia and thiamin deficiency (16,18).

Due to an increased risk of refeeding syndrome in women with hyperemesis, initiation of nutritional support should be slow, particularly during the first week, to prevent dramatic changes in fluid and electrolyte status. Daily monitoring of serum electrolyte concentrations including magnesium, phosphate, potassium and fluid balance and appropriate supplementation to correct electrolyte disorders are important to prevent refeeding syndrome and its associated complications. Hypophosphataemia, a predominant feature of refeeding syndrome, can develop rapidly and result in death, hence the phosphate supplementation of this patient. This case also highlighted the need to monitor and supplement with thiamin.

The patient in this case study was delivered at 27 weeks gestation due to foetal distress. Monochorionic, monoamniotic twin pregnancies have the highest perinatal mortality rate of all twin pregnancies and the rate of foetal demise is as high as 50% (20). Demise is caused by entanglement of the umbilical cords due to foetal movement. Foetal distress indicated that this was likely in this pregnancy and hence the emergency caesarean. An additional factor that may have influenced outcome status is overall weight gain. Weight gains of 16 to 18 kg at greater than or equal to 37 weeks gestation have been recommended for optimal foetal outcomes in twin pregnancies (21-23).

Conclusions

Women with hyperemesis require careful management. It is recommended that any pregnant woman who develops hyperemesis should have her thiamin concentrations monitored. Cases of severe intractable hyperemesis may require oral thiamin supplements daily until vomiting ceases. Nutritional intervention should be provided early and aggressively to prevent significant weight loss and to allow good perinatal outcome. In women who have lost substantial weight (more than ten percent of body weight) and who do not tolerate oral diet, nasogastric feeding should be considered as part of their management. The feeding should be commenced at a slow rate and gradually increased to meet nutritional requirements in order to avoid refeeding syndrome. Prolonged intravenous infusion of dextrose and saline solutions may precipitate refeeding syndrome and/or exacerbate malnutrition. Vitamins and minerals also need to be administered intravenously in appropriate dosage. Careful attention must be given to the rapid correction of elect rolyte and fluid abnormalities and thiamin concentrations.

Acknowledgments

The contribution of Mary Anne Silvers and David Howells for advice and review of the manuscript is gratefully acknowledged.

References

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(2.) Lavin PJ, Smith D, Kori SH, Ellenberger C. Wernicke's encephalopathy: A predictable complication of hyperemesis gravidarum. Obstet Gynecol 1983;62(3)Suppl:13-5.

(3.) Chatwani A, Schwartz R. A severe case of hyperemesis gravidarum. Am J Obstet Gynecol 1982;143:964-5.

(4.) Schulman PK. Hyperemesis gravidarum: An approach to the nutritional aspects of care. J Am Diet Assoc 1982;80:577-8.

(5.) Boyce R. Enteral nutrition in hyperemesis gravidarum: A new development. J Am Diet Assoc 1992;92:733-6.

(6.) Gross S, Librach C, Cecutti A. Maternal weight loss associated with hyperemesis gravidarum: A predictor of foetal outcome. Am J Obstet Gynecol 1989;160:906-9.

(7.) Barclay BA. Experience with enteral nutrition in the treatment of hyperemesis gravidarum. Nutr Clin Pract 1990;5:153-5.

(8.) Hsu JJ, Clark-Glena R, Nelson DK, Kim CH. Nasogastric enteral feeding in the management of hyperemesis. Enteral Nutrition 1996;88:343-6.

(9.) King EQ. Acute cardiac failure in the newborn due to thiamin deficiency. Exp Med Surg 1967;25:173-7.

(10.) Rees J, Ginsberg L, Schapira A. Two pregnant women with vomiting and fits, Am J Obstet Gynecol 1997:177:1539-40.

(11.) Gardian G, Voros E, Jardanhazy T, Ungurean A, Vescoi L. Wernicke's encephalopathy induced by hyperemesis gravidarum. Acta Neurol Scand 1999;99:196-8.

(12.) Tesfaye S, Achari V, Yang YC, Harding S, Bowden A, Vora J. Pregnant, vomiting, and going blind. Lancet 1998;352:1594.

(13.) Hillbom M, Pyhtinen J, Pylvanen V, SotanIemi K. Pregnant, vomiting, and coma. Lancet 1999;353:1584.

(14.) Bergin P. Harvey P. Wernicke's encephalopathy and central pontine myelinolysis associated with hyperemesis gravidarum. BMJ 1992;305:517-8.

(15.) Report on confidential enquiries into maternal deaths in the United Kingdom 1991-1993. London: Stationery Office; 1996.

(16.) Stubbs C. Case study: refeeding syndrome and thiamin deficiency after extended starvation. Aust J Nutr Diet 1999;56:221-3.

(17.) Brooks M, Melnik G. The refeeding syndrome: An approach to understanding its complications and its occurrence. Pharmacotherapy 1995;15:713-26.

(18.) Crook M, Hally V, Panteli J. The importance of the refeeding syndrome. Nutrition 2001;17:632-7.

(19.) Solomon S, Kirby D. The refeeding syndrome. JPEN 1990;14:90-7.

(20.) Newman R, Luke B. Multifetal pregnancy--a handbook for care of the pregnant patient. Philadelphia: Lippincott Williams and Wilkins; 2000.

(21.) Luke B, Minogue J, Abbey H, Keith L, Witter F, Feng T, et al. The association between maternal weight gain and the birthweight of twins. Journal Maternal-Fetal Medicine 1992;1:267-76.

(22.) Luke B, Leurgans S. Maternal weight gains in ideal twin outcomes. J Am Diet Assoc 1996;96:178-81.

(23.) Luke B. What is the influence of maternal weight gain on the fetal growth of twins? Clin Obstet Gynecol 1998;41:57-64.

Royal Women's Hospital, Carlton, Victoria

K. Roem, BSc, GradDipDiet, Dietitian, Department of Nutrition and Dietetics

Correspondence: K. Roem, Department of Nutrition and Dietetics, Royal Women's Hospital, Grattan Street, Carlton, Vic 3053
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Author:Roem, Kerryn
Publication:Nutrition & Dietetics: The Journal of the Dietitians Association of Australia
Geographic Code:8AUVI
Date:Jun 1, 2002
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