Hyperemesis Gravidarum

Etiology

The etiology of hyperemesis gravidarum is multifaceted, involving a convergence of hormonal, genetic, physiological, and possibly environmental or psychosocial influences.

Hormonal Factors

Although the precise cause is still uncertain, a strong association with hormonal changes during early pregnancy has been proposed. Human chorionic gonadotropin (hCG) is frequently implicated due to the close correlation between peak hCG levels and the timing of symptom onset, as well as its thyroid-stimulating effects, which may contribute to transient hyperthyroidism observed in some hyperemesis gravidarum patients.[5]

However, inconsistent research findings and variability in hCG subtypes suggest that hCG alone cannot account for the condition. Estrogen, particularly estradiol, has also been studied for its potential role, with some evidence pointing to elevated levels in affected individuals, though findings remain inconclusive. Additionally, gastrointestinal changes commonly seen in pregnancy, eg, delayed gastric emptying and reduced lower esophageal sphincter tone—often influenced by elevated progesterone and estrogen—may exacerbate nausea and vomiting, but these mechanisms are not exclusive to hyperemesis gravidarum.[1][5]

Genetic Factors

Recent studies have demonstrated that a genetic predisposition may contribute to hyperemesis gravidarum, as evidenced by familial clustering and a significantly elevated recurrence rate in subsequent pregnancies. Studies have indicated that specific gene variants, including GDF15, IGFBP7, and PGR, may be involved in the development of hyperemesis gravidarum due to their influence in placentation, appetite regulation, and inflammatory signaling.[1][5]

Physiological and Psychological Factors

Individuals with a personal or family history of hyperemesis gravidarum, motion sickness, or migraine-associated nausea are at greater risk, suggesting a shared biological susceptibility.[1] While psychological conditions such as depression and anxiety often coexist with hyperemesis gravidarum, these may be more likely sequelae of the illness rather than contributing causes. In a recent study, approximately 57.4% of patients with hyperemesis gravidarum also had a diagnosis of depression or anxiety. However, other studies have demonstrated that most pregnant women with hyperemesis gravidarum do not have a preexisting diagnosis of a psychological disorder.[5]

Hyperemesis Gravidarum Risk Factors

Risk factors for hyperemesis gravidarum include:

• Personal history of hyperemesis gravidarum: The most significant risk factor; recurrence risk is approximately 24%.
• Family history of hyperemesis gravidarum: Having a mother who experienced hyperemesis gravidarum increases the risk up to 3-fold.
• History of motion sickness
• History of nausea associated with migraines
• Comorbid conditions:
  • Thyroid dysfunction
  • Type 1 diabetes mellitus
  • Hypercholesterolemia
• Infection with Helicobacter pylori: Linked to increased hyperemesis gravidarum risk, though a causal relationship has not been firmly established.[1][5]

Additionally, factors that are associated with a decreased risk of developing hyperemesis gravidarum include the use of multivitamins before 6 weeks gestation and maternal cigarette smoking.[2][5]

Epidemiology

While nausea affects approximately 50% to 80% of pregnancies and vomiting occurs in about 50%, hyperemesis gravidarum occurs in roughly 0.3% to 3% of pregnancies globally, with a worldwide prevalence estimate around 1.1%.[2] This wide range in incidence is due to inconsistent diagnostic criteria and variations in study populations, including ethnic differences.[2] 

Hyperemesis gravidarum is the leading cause of hospitalization in early pregnancy and ranks second overall after preterm labor as a reason for inpatient care during gestation.[1][6] In fact, though overall pregnancy rates have decreased, a recent study found that the number of emergency department visits due to hyperemesis gravidarum has steadily increased.[6] Hyperemesis gravidarum has also been shown to affect patients younger than 24 years and of lower income levels more commonly than older pregnant patients of higher income levels.[6]

Pathophysiology

The exact cause of hyperemesis gravidarum remains unclear. However, several theories for what may contribute to the development of this disease process have been posited. (Please refer to the Etiology section for further information on hyperemesis gravidarum causes.)

During pregnancy, extensive physiological and anatomical adaptations occur that affect multiple systems, including the cardiovascular, endocrine, hematologic, renal, and gastrointestinal systems. These changes progress with increasing gestational age and contribute to the vast array of symptoms experienced during pregnancy. Notably, elevated progesterone levels reduce the motility of the gastrointestinal tract, leading to slower gastric and intestinal transit. Concurrently, increased production of placental gastrin enhances gastric acid secretion. As the pregnancy advances, the enlarging uterus exerts pressure on and shifts abdominal organs, and increases intra-abdominal pressure. This displacement also contributes to a reduction in lower esophageal sphincter tone, facilitating the occurrence of gastroesophageal reflux. These physiological shifts can result in common gastrointestinal complaints (eg, nausea, vomiting, early satiety, constipation, and reflux) during pregnancy.[3]

Despite the presence of these symptoms in normal pregnancy, they are not believed to cause hyperemesis gravidarum directly. The precise mechanisms underlying hyperemesis gravidarum remain unclear, though current understanding suggests a multifactorial etiology. Hypotheses include abnormal hormonal responses, particularly involving hCG, along with possible genetic, immunological, and gastrointestinal contributions. Although normal pregnancy involves nausea and vomiting due to physiological changes, hyperemesis gravidarum represents a more severe spectrum that likely involves additional, yet poorly understood, pathological processes beyond the standard adaptive changes of gestation.[3]

History and Physical

Clinical History

Careful history taking in women with suspected or confirmed hyperemesis gravidarum should include their pregnancy status, estimated gestational age, history of complications during prior pregnancies, the frequency and severity of nausea and vomiting, any interventions performed to treat their symptoms, and the outcomes of the attempted interventions.[7]

Clinicians should also have patients describe the onset and nature of their nausea and vomiting, as well as any associated symptoms. Hyperemesis gravidarum is characterized by continual vomiting that generally begins in the first trimester and can persist well beyond, occasionally lasting throughout the entire gestation or even into the postpartum period. The onset of symptoms most commonly occurs around 6 weeks of gestation and resolves between 16 and 20 weeks of gestation; in approximately 20% of cases, symptoms continue throughout the pregnancy.[8] When symptoms, eg, nausea and vomiting, first occur after 9 weeks of gestation, alternate diagnoses should be considered, including preexisting gastrointestinal conditions like gallstones or diabetic gastroparesis.[2][3]

Unlike the more common and milder nausea and vomiting of pregnancy, hyperemesis gravidarum severely impairs the individual's ability to maintain adequate oral intake of food and fluids, resulting in associated symptoms including significant weight loss (typically >5% of prepregnancy body weight), dry mouth, constipation, fatigue, and inability to perform daily activities.[3]  

Physical Examination Findings

In addition to persistent nausea and vomiting, hyperemesis gravidarum often leads to dehydration, electrolyte disturbances, and, less frequently, severe complications, eg, acute kidney injury, cardiac arrhythmias, and neuromuscular symptoms. Therefore, the physical exam should include fetal heart rate when at a detectable gestational age and an examination of maternal fluid status, including an examination of blood pressure, heart rate, mucous membrane dryness, capillary refill, and skin turgor. A patient's weight should be obtained for comparison to previous and future weights. If indicated, abdominal examination and pelvic examination should occur to determine the presence or absence of tenderness to palpation.

Additionally, poor nutritional intake can result in protein-energy malnutrition and a range of vitamin deficiencies. Signs of hemorrhage or abnormal bleeding can occur due to vitamin K deficiency.[9] Deficiencies in vitamin B1 (thiamine), B6, and B12 can cause signs of neurologic complications, with thiamine deficiency potentially progressing to Wernicke encephalopathy—a condition marked by confusion, eye movement abnormalities (eg, nystagmus), and impaired coordination (ataxia).[2][3]

While most cases of hyperemesis gravidarum are idiopathic, rare genetic conditions involving hormone receptor sensitivity or mitochondrial dysfunction may play a role in select patients. Physical signs that deviate from typical hyperemesis gravidarum, including fever, abnormal neurological findings, or persistent abdominal pain, warrant consideration of other underlying conditions. Additionally, though transient thyroid function abnormalities may be observed in hyperemesis gravidarum, these are usually benign, self-limited, and resolve without antithyroid treatment. Elevated free thyroxine (T4) and suppressed thyroid-stimulating hormone (TSH) levels can occur in the context of gestational transient thyrotoxicosis, which should be managed conservatively with supportive care rather than pharmacological intervention.[3]

Evaluation

The evaluation of hyperemesis gravidarum involves a thorough clinical assessment alongside laboratory and, when indicated, imaging studies to confirm the diagnosis, assess severity, and exclude other potential causes of persistent nausea and vomiting in pregnancy. A consensus on the diagnostic criteria for hyperemesis has not been established.[1] Generally, the diagnosis of hyperemesis gravidarum is based on a combination of clinical findings, including early-onset severe nausea and vomiting, substantial weight loss, signs of dehydration, and corroborating laboratory data.[3][1]

Laboratory Studies

Common laboratory abnormalities in hyperemesis gravidarum reflect the effects of prolonged vomiting and reduced nutritional intake, often revealing signs of dehydration and electrolyte imbalance, eg, elevated blood urea nitrogen (BUN) or creatinine, hyponatremia, and hypokalemia. Ketonuria, an indicator of starvation due to fat metabolism, is frequently present and, while not diagnostic on its own, serves as a useful adjunctive marker of disease severity. Several professional society guidelines, including the American College of Obstetricians and Gynecologists (ACOG) and the Society of Obstetricians and Gynaecologists of Canada (SOGC), include this finding as a supportive diagnostic indicator of hyperemesis gravidarum.[1] The presence of ketonuria may guide decisions regarding the need for intravenous fluids, nutritional support, or hospitalization.[3][1]

Significant dehydration may result in acute kidney injury as evidenced by elevated serum creatinine, blood urea nitrogen, and reduced glomerular filtration. Potassium, calcium, magnesium, sodium, and bicarbonate may be affected by prolonged bouts of vomiting and reduced oral intake of fluids. In patients with fever or thyroid disease, thyroid tests, lipase, urine analysis, and liver function testing may also be completed to evaluate for alternative diagnoses.[1][2][10]

Additional laboratory findings can include a prolonged prothrombin time or international normalized ratio (INR) in cases of vitamin K deficiency, which may occur with prolonged malnutrition. An elevation in hemoglobin or hematocrit may be due to hemoconcentration in the setting of dehydration. Conversely, anemia can be noted and should be distinguished from hemolytic anemia associated with hypertensive disorders like preeclampsia. Liver enzyme elevations are observed in up to half of hyperemesis gravidarum cases; aminotransferases may rise up to 3-fold above normal, though in rare instances, levels may reach 1,000 IU/L. Mild jaundice may also occur due to transient cholestasis, with bilirubin levels generally remaining below 4 mg/dL. While hyperemesis gravidarum is not a primary hepatic condition, these liver abnormalities should be monitored and evaluated to exclude alternative hepatic pathologies if atypical features are present.[3][1]

Imaging Studies

Imaging is not essential for diagnosing hyperemesis gravidarum, but can be instrumental in ruling out other conditions. Abdominal ultrasound may be warranted in the presence of significantly elevated liver enzymes to evaluate for gallstones or vascular abnormalities. Fetal growth should be monitored in patients with prolonged symptoms or signs of malnutrition, particularly in the third trimester.[3][1]

In situations where hyperemesis gravidarum results in suspected complications, eg, internal hemorrhage or organ injury, urgent imaging with the most appropriate modality should be performed, prioritizing clinical necessity over concern for radiation exposure. In nonurgent settings, radiation-sparing techniques should be used where possible, eg, magnetic resonance imaging (MRI) to assess for possible appendicitis. Liver biopsy is rarely indicated but may be considered in unusual cases where other treatable liver diseases must be definitively ruled out.[3][1]

Treatment / Management

Outpatient Hyperemesis Gravidarum Management

Hyperemesis gravidarum management strategies depend on the severity of symptoms, hydration levels, and the patient's ability to tolerate food or fluids orally. Treatment guided by ACOG nausea and vomiting in pregnancy guidelines is recommended, in which management approaches progress in a tiered approach—starting with lifestyle modifications, escalating through pharmacologic therapy, and advancing to nutritional support in refractory cases.[1][3]

Close monitoring and individualized care plans are essential to minimize maternal complications and support healthy fetal development. While some pharmacological treatments raise occasional safety concerns, their benefits often outweigh the risks in severe cases. Early and effective intervention can reduce hospitalizations, improve quality of life, and lead to better pregnancy outcomes.[11][5](A1)

Conservative therapies

Initial intervention often involves lifestyle adjustments and nonpharmacologic treatments, including:

• Vitamin modification: Replacing standard prenatal vitamins with folic acid alone may reduce nausea.[2]

• Ginger: Commonly recommended, ginger has effectively mitigated nausea through its interaction with multiple neural pathways. Dosages of 250 mg orally 4 times daily (up to 1 g daily) are generally safe but should be avoided in patients taking blood thinners due to potential platelet inhibition.[2][12][13]

• Acupressure/acupuncture: Stimulating traditional Chinese acupoints on the wrist, either manually or with pressure bands, has been demonstrated in limited studies to alleviate nausea. Other studies have shown this treatment modality to be ineffective. However, though evidence is mixed, the technique is considered safe and noninvasive, but more rigorous trials are needed to validate its routine use.[5][2]

(A1)

Pharmacologic therapies

When conservative strategies fail, the following stepped medication regimen is recommended by ACOG:

• First-line agents
  • Pyridoxine (vitamin B6): The typical dosages are 10 to 25 mg up to 4 times daily, administered alone or combined with doxylamine, to help with mild to moderate symptoms. High doses (>500 mg/d) may lead to neuropathy.[2][3]
  • Pyridoxine and doxylamine: Doxylamine is an antihistamine frequently combined with pyridoxine, administered as a combination tablet with either of the following regimens:
    • Pyridoxine 10 mg/doxylamine 10 mg: 2 tablets at night initially; may increase to 1 tablet in the morning, 1 tablet in the afternoon, and 2 tablets at bedtime
    • Pyridoxine) 20 mg/doxylamine 20 mg: 1 tablet orally at bedtime initially, may increase to 1 tablet in the morning and 1 tablet at bedtime [2]
•  Second-line agents (added to first-line therapy if insufficient)
  • Second-line agents can be added to first-line therapy if first-line agents are insufficient to control symptoms.
  • Dimenhydrinate and diphenhydramine: These are antihistamines that may offer symptom relief but can cause drowsiness.
    • Dimenhydrinate 25 to 50 mg by mouth every 4 to 6 hours, as needed 
    • Diphenhydramine 25 to 50 mg by mouth every 4 to 6 hours
• • Dopamine antagonists: These medications are often effective but may cause adverse effects like sedation or dystonia.[2] 
    • Prochlorperazine 25 mg every 12 hours rectally
    • Promethazine 12.5 to 25 mg every 4 to 6 hours, orally or rectally
• Third-line agents
  • Oral antiemetics should be added to first- and second-line therapies for persistent vomiting in patients without dehydration.
  • Metoclopramide: Offers prokinetic and antiemetic effects with a typical dosage of 5 to 10 mg every 6 to 8 hours, orally or intramuscularly (IM)
  • Ondansetron: Found to be more effective than other agents and generally considered safe, though some studies raise concerns about potential birth defects, including heart defects and cleft palate; recommended dosage is 4 mg orally every 8 hours
  • Trimethobenzamide: Typical dosage 200 mg every 6 to 8 hours IM [2]

Inpatient Hyperemesis Gravidarum Management

Although hyperemesis gravidarum has no universal standard for admitting patients for inpatient care, most experts recommend admission for persistent vomiting despite oral antiemetics, patients who require IV fluids, who have conditions necessitating close monitoring, or abnormal evaluation findings. Hospitalization allows for IV treatment and gastrointestinal rest, which can help avert complications of hyperemesis gravidarum and an increased likelihood that an outpatient treatment plan can be continued after discharge.[1]

When dehydration is present, the following IV therapies are introduced:

• Fluid resuscitation with up to 2 L of IV crystalloid or Lactated Ringer's over 2 hours is initially used to rehydrate and correct electrolyte imbalances; IV fluids should then be titrated to maintain urine output of at least 100 mL/h. Glucose-saline solutions may offer additional benefits. Potassium, calcium, magnesium, and sodium levels should also be monitored and replaced with IV supplementation as needed.

• Thiamine 200 to 500 mg IV every 8 hours, and an IV multivitamin solution should also be initiated in the first few days after admission or until the patient tolerates oral intake to prevent Wernicke encephalopathy and other nutritional deficiencies.

• IV antiemetics, including ondansetron, metoclopramide, dimenhydrinate, and promethazine, are typically delivered in the same dosages as their oral formulations, as well as acid-reducing medications (eg, pantoprazole) should be administered. Caution should be used when patients are placed on multiple medications, as drug interactions can occur. For instance, serotonin antagonists (eg, ondansetron) may have the adverse effect of QT prolongation, especially when combined with other medications (eg, antihistamines), and metoclopramide with phenothiazine increases the risk of extrapyramidal effects.[1][2]

Inpatient nutritional management

When oral intake remains poor despite other interventions, additional nutritional therapy is critical to avoid maternal malnutrition, maintain maternal weight gain, and ensure appropriate fetal growth. The following management strategies may be utilized:

Enteral nutrition

Enteral nutrition is typically the preferred method for nutritional support, with nasogastric feeding often used first due to its effectiveness and relatively low risk of complications. In cases where nasogastric feeding is poorly tolerated or prolonged support is required, alternative methods such as nasojejunal or percutaneous endoscopic gastrojejunostomy (PEG-J) feeding may be considered. Although enteral nutrition can present challenges, including tube dislodgement, vomiting, and patient discomfort, this alternative feeding modality is generally associated with faster symptom relief and improved maternal weight outcomes.[3]

Parenteral nutrition

If enteral feeding is not a viable option, parenteral nutrition may be necessary. Peripheral parenteral nutrition can be used for short-term nutritional support, but has limited concentration capacity. Central parenteral nutrition, administered through central venous access like peripherally inserted central catheters (PICCs), allows for more comprehensive nutrient delivery but carries increased risks, including infection and thrombosis, particularly significant risks during pregnancy.[3]

Additional dietary supplementation

Proper monitoring is essential when using nutrition therapies. Caloric needs should be calculated using predictive formulas, adjusted for stress and nutritional deficits. Protein requirements range from 1.1 to 1.52 g per kg of body weight per day, while carbohydrate intake should meet a minimum of 175 g daily to prevent ketosis. Fats should constitute 20% to 35% of total caloric intake, and supplementation with DHA (300 mg/day) is recommended.[3]

Hydration is also vital, with at least 3 L of fluid intake daily, including fluids from food sources. Due to poor dietary intake, many hyperemesis patients require micronutrient supplementation. Key nutrients include thiamine (vitamin B1), iron, calcium, magnesium, vitamin D, and iodine, as most affected individuals consume less than half of the daily recommended amounts. Routine laboratory assessments of these micronutrients and electrolytes should be performed daily until appropriate levels are maintained, then repeated weekly on an outpatient basis.[3]

Alternative Treatments

For patients with refractory hyperemesis gravidarum, alternative medications such as mirtazapine, a noradrenergic and specific serotonergic antidepressant, olanzapine, an antipsychotic, or short-term methylprednisolone may be considered. Prolonged administration or use of corticosteroids before 10 weeks gestation is discouraged due to possible risks of fetal abnormalities. A common dosage used for methylprednisolone is 16 mg every 8 hours, orally or intravenously, for 3 days initially, tapered over 2 weeks to the lowest effective dose for a maximum total duration of use of 6 weeks.[1]

Emerging therapies that have demonstrated some effectiveness in clinical trials include:

• Gabapentin: Has shown promise in reducing nausea severity and improving nutritional intake
• Clonidine (transdermal): Demonstrated symptom relief for patients unable to tolerate oral medication [5]
• Diazepam: May reduce rehospitalization when added to IV fluid therapy
• Droperidol and diphenhydramine: Effective in reducing inpatient stay duration, although droperidol is associated with QT prolongation
(B2)

Psychological Support

Recent studies have also found that patients with severe hyperemesis gravidarum have increased rates of anxiety, depression, and posttraumatic stress disorder. Therefore, psychological interventions should be implemented alongside other treatment approaches to manage this condition effectively.[14](B3)

Differential Diagnosis

Evaluating women presenting with hyperemesis for gestational trophoblastic disease (GTD) and multiple gestations, as they may also present with severe nausea and vomiting in the first trimester of pregnancy. The workup may begin with an obstetric ultrasound scan, which will confirm the diagnosis in most cases. Nonobstetrical causes for nausea and vomiting can also occur during pregnancy and should always remain on the differential.

The diagnosis of hyperemesis gravidarum is clinical and largely a diagnosis of exclusion. The list of potential differential diagnoses for patients with similar symptoms is quite extensive, including:

• Gastrointestinal conditions
  • Gastroenteritis
  • Gastroparesis
  • Achalasia
  • Biliary tract disease
  • Hepatitis
  • Intestinal obstruction
  • Peptic ulcer disease
  • Pancreatitis
  • Appendicitis
• Genitourinary conditions
  • Pyelonephritis
  • Uremia
  • Ovarian torsion
  • Kidney stones
  • Degenerating uterine leiomyoma
• Metabolic conditions
  • Diabetic ketoacidosis
  • Porphyria
  • Addison disease
  • Hyperthyroidism
  • Hyperparathyroidism
• Neurologic disorders
  • Pseudotumor cerebri
  • Vestibular lesions
  • Migraine headaches
  • Tumors of the central nervous system
  • Lymphocytic hypophysitis
• Miscellaneous conditions (eg, drug toxicity or intolerance)
• Psychological conditions (eg, anxiety and depression)
• Pregnancy-related conditions (eg, acute fatty liver of pregnancy, preeclampsia) [2][3]

Staging

Modified Pregnancy-Unique Quantification of Emesis and Nausea Score 

No single measure can easily define, quantify, or evaluate the treatment of hyperemesis. Still, an English pregnancy-specific questionnaire, PUQE (Pregnancy-Unique Quantification of Emesis), has been developed to assess the severity of emesis in pregnancy. This questionnaire contains 3 questions regarding the time span of nausea, vomiting, and retching, respectively, as well as 1 question assessing the global psychological and physical quality of life (QOL).

Initially, the questionnaire evaluated symptoms during the last 12 hours, but has been modified to encompass 24 hours and the whole of the first trimester of pregnancy.[15] The PUQE-score has been validated to correlate with the inability to take iron supplementation during pregnancy, the risk of hospitalization due to hyperemesis gravidarum or severe NVP, increased health care costs due to NVP, reduced well-being, and QOL.

Prognosis

As hyperemesis gravidarum involves the mother and the fetus, both patients must be considered when discussing long-term prognosis.

Maternal  Prognosis

The maternal prognosis in cases of hyperemesis gravidarum is generally favorable with timely and appropriate intervention, although the condition can pose significant challenges if left untreated. With effective management—including nutritional support, pharmacologic therapy, and careful monitoring—most women recover without long-term complications. Enteral nutrition often improves maternal weight gain and symptom control, while parenteral nutrition can provide essential support when enteral methods are not feasible.[2][3][1]

Close monitoring for complications, eg, refeeding syndrome and nutrient deficiencies, is necessary to prevent serious outcomes like Wernicke encephalopathy. Despite the physical and emotional burden hyperemesis gravidarum can place on affected individuals, proactive treatment and nutritional repletion greatly improve maternal outcomes and reduce the risk of lasting health consequences.[2][3][1]

Fetal Prognosis

The long-term prognosis of pregnancies affected by hyperemesis gravidarum includes potential risks to offspring, with emerging evidence suggesting a modest increase in adverse health outcomes. A systematic review encompassing nearly 1.8 million offspring found associations between in utero exposure to hyperemesis gravidarum and elevated rates of neurodevelopmental and psychological disorders. Furthermore, recent studies demonstrated a higher risk of anxiety disorders and sleep disturbances in children born to mothers with hyperemesis gravidarum, as well as a potentially heightened risk of testicular cancer in male offspring up to the age of 40.[16]

Studies examining children exposed to hyperemesis gravidarum indicated a higher incidence of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), cognitive and motor development issues, and one neuroimaging study found reduced cortical brain volume. Consequently, the evidence suggests that hyperemesis gravidarum may confer a small but notable risk of long-term health consequences in offspring. However, this is based on a limited number of studies.[16]

Complications

In severe or untreated cases, hyperemesis gravidarum can lead to significant complications, eg, dehydration, electrolyte imbalances, urinary tract infections, and esophageal damage from persistent vomiting. These imbalances may progress to cardiac arrhythmias, rhabdomyolysis, and severe nutritional deficiencies. One of the most serious consequences is Wernicke encephalopathy, caused by thiamine deficiency, presenting with confusion, eye movement abnormalities, and gait disturbances, with other manifestations including nystagmus and memory impairment.[1] 

Lack of vitamin K may result in coagulopathy and increased bleeding risk. Other serious, though less common, complications of hyperemesis gravidarum include gastrointestinal trauma, eg, Mallory-Weiss tears, esophageal rupture (Boerhaave syndrome), liver dysfunction, pneumothorax, retinal hemorrhages, splenic injury, and placental complications including abruption or hemorrhage.[2]

Beyond its physical toll, hyperemesis gravidarum is associated with substantial psychological distress, including increased rates of depression, posttraumatic stress, and suicidal ideation. In extreme cases, the condition has led to the termination of wanted pregnancies. Furthermore, hyperemesis gravidarum has been linked to adverse pregnancy outcomes, including fetal growth restriction, placental abruption, and preeclampsia, especially in the second trimester. According to some studies, hyperemesis gravidarum may have long-term effects on offspring, including developmental and behavioral challenges; however, further research is needed to find clear evidence of a link.[1]