Hyperemesis gravidarum - A Brief Discussion

Hyperemesis gravidarum: This is defined as persisting vomiting in pregnancy which causes weight loss (>5% of pre-pregnancy weight) and ketosis.

Incidence: It affects 1% of pregnant women.

Risk factors; Risk is increased in

• Very young, 
• primigravida, 
• working outside home, 
• preexisting diabetes, 
• hyperthyroidism, 
• psychiatric illness, 
• family history, 
• those with previous eating disorders and 
• multiple or molar pregnancy 

Clinical Presentation

• Inability to keep food or fluids down; 
• weight loss (2–5 kg)with or without nutritional deficiency, 
• dehydration, 
• hypovolaemia, 
• tachycardia, 
• postural hypotension,
• electrolyte disturbance with hypokalaemia and hyponatraemic shock,
• polyneuritis (B vitamins defeciency), 
• behaviour disorders, 
• liver and renal failure in severe cases.  
• There may be ptyalism (inability to swallow saliva) and spitting.

Workup

• Do PCV and U&E to help guide IV fluid regimen. 
• 50% of patients have abnormal LFTs (usually raised aminotransferase and bilirubin). 
• Thyroid function tests are abnormal in 60% of those with hyperemesis. This is biochemical hyperthyroidism with raised free thyroxine and suppressed TSH. In women with hyperemesis thyroxine is converted to reverse tri-iodothyronine in the tissues which is physiologically inactive so stimulating metabolic rate less and conserving energy stores. The severity of hyperemesis correlates with the degree of biochemical hyperthyroidism, and those with abnormal Thyroid function testsrequire longer hospitalization to prevent readmission. The biochemical hyperthyroidism settles as vomiting settles so does not require treatment in its own right. 
• Chart losses, weigh, record pulse and standing and lying blood pressure. 
• Exclude UTI.
• Do ultrasound scan to exclude twins or hydatidiform mole.

Treatment 

• Admit to hospital. 
• Give thromboprophylaxis (eg enoxaparin 40mg/24h SC) and anti-embolic stockings. 
• Spend time optimizing psychological well being. Most patients improve with due care and attention. 
• If not too severe it may settle with rest, ginger, pyridoxine, dry bland food, and carbonated drinks. 
• Routine thiamine supplementation is wise for all women admitted (eg thiamine 25–50mg/8h PO) or if IV required 100mg diluted in 100mL normal saline given over 60min, repeated at weekly intervals. This is to prevent development of Wernicke’s encephalopathy —which is then associated with 40% fetal loss. 
• Correct dehydration with IV infusion (eg with normal saline infusion with potassium added to each bag as guided by U&E). 
• Beware rapid reversal of hyponatraemia which can cause fatal central pontine myelinosis. 
• If condition does not improve after rehydration anti-emetics may be needed eg cyclizine 50mg/8h PO/IM or IV. 
• Other recognized anti-emetics used: metoclopramide, prochloperazine, chlorpromazine, domperidone, ondansetron. 
• Phenothiazines can cause drowsiness, extrapyramidal side effects, and oculogyric crisis. 
• Those resistant to conventional treatments may respond to steroid treatment, eg hydrocortisone 100mg twice daily followed by 40mg prednisolone/24h tapering down. Prednisolone can then usually be reduced to 2.5–10mg/24h by 20 weeks' gestation. If it is needed long-term screen for UTI and gestational diabetes. Prednisolone is metabolized by the placenta, fetal blood levels are low and adverse fetal effects have not been reported.
• Parenteral nutrition may, very rarely, be needed. 
• If nutritional support is required both nasojejunal tube feeding and percutaneous endoscopic gastrostomy have been successfully used.  Parenteral nutrition has been found to be associated with serious complications (eg line sepsis). 
• Get a dietician’s help.