Neurological Complications

Some of the most serious complications are Neurological Complications caused by nutrient and electrolyte deficiencies.

Prevention is best achieved by:

  • Effective antiemetic care
  • Laboratory monitoring
  • IV nutrient supplementation
  • Careful rehydration


It is usually caused by vitamin deficiencies, most notably thiamin (B1) deficiency, and precipitated by administration of glucose-containing fluids before deficiencies are corrected. Lab values of hormones, other electrolytes, and nutrients can vary as is shown in the research; thus, lab results should not be used solely to determine a diagnosis.

Further, it should not be assumed that women on TPN will not have Wernicke’s Encephalopathy. TPN often does not include a complete vitamin profile and these women are still at risk. Even MVI infusion only has 6 mg of thiamine and much higher doses are recommended for HG mothers, specifically a minimum of 100 mg of thiamine in their IV fluids daily.


If symptomatic of WE, much higher doses are crucial to prevent severe complications. Doses of thiamin up to 1500 mg per day for 5 days to 3 weeks are suggested as treatment for WE, followed by oral dosing of 100-500 mg per day for at least 6 weeks, longer if the patient continues to have restricted intake and refractory HG.


See our published Case Study on HG and WE/CPM/EPM for recommendations on identification, prevention and treatment.

Neurological Complications

Central & Extra Pontine Myelinolysis (Osmotic Demyelination Syndrome, ODS)

Classic Signs: Confusion, loss of consciousness, horizontal gaze paralysis, and spastic quadriplegia. Delirium is also very common. 

ODS is nerve damage caused by the destruction of the covering layer (myelin sheath) of nerve cells in the brainstem (pons). Women with HG may exhibit signs of extra and central pontine myelinolysis, neurological disorders caused by electrolyte shifts, most commonly when low sodium or potassium levels are corrected too quickly. ODS also has a high rate of irreversible neurological damage.

Comorbid Diagnosis

It is not uncommon for pontine myelinolysis and Wernicke’s Encephalopathy (WE) to occur simultaneously with other disorders related to malnutrition and electrolyte disturbances. Women with HG should be monitored closely and given nutritional support and methodical electrolyte replacement to prevent maternal and/or fetal morbidity and mortality.

See our published Case Study on HG and WE/CPM/EPM for recommendations on identification, prevention and treatment. 

Wernicke's Encephalopathy

Signs: Vision and mental status changes, gait abnormalities, weakness, dysarthria, confabulation, and coma.

Persistent thiamin deficiency during HG is very common and can be exacerbated by many factors including infections (e.g., UTI), high carbohydrate diet, vitamin deficiencies (e.g., Mg), protein deficiency, antacids, and diuretics. Chronic vague symptoms (e.g., fatigue, weakness, muscle wasting, nausea, vomiting) attributed to HG or pregnancy are also a manifestation of thiamin deficiency.

Without proactive and aggressive management, deficiency can become severe and trigger life-threatening complications like Wernicke’s Encephalopathy. 

Unfortunately, Wernicke’s Encephalopathy (WE) is too common in hyperemesis gravidarum due to malnutrition yet very often goes unrecognized until significant and potentially permanent morbidity occurs. It can be fatal in up to 20% of cases and causes fetal loss in about half of patients. 


Presentation in HG

Women may or may not present with the classic triad of symptoms, visual disturbances, confusion and muscular weakness. Early intervention with thiamine replacement is typically all that is needed to prevent this complication.  

Wernicke’s Encephalopathy (WE) can develop after just a few weeks of vomiting. Women vomiting more than one week should be routinely given oral thiamine replacement, along with a parenteral multivitamin and thiamin prior to IV fluids with glucose. 

Always give 200 mg IV thiamin (vitamin B1) with IV glucose or parenteral/enteral nutrition.