By

Ahmed abo elkasem M.B.BCh. ASSUIT UN.

M.S.C. GYN.& OBES. AL_AZHAR UN.

HIT & RUNIN

OBE.& GYN .

HYPEREMSIS GRAVIRUM

) وهن) علي وهنا أمه حملته بوالديه االنسان وأوصينااية لقمان سورة

14

HISTORICAL BACKGROUNDWhile vomiting in pregnancy has been

described as early as 2,000 BC

the first clear medically description of hyperemesis gravidarum was in 1852 by

Antoine Dubois.

Why this term (H.G)Hyperemesis gravidarum is from the Greek

hyper-, meaning excessive, and emesis, meaning vomiting, and the Latin gravidarum,

the feminine genitive plural form of an adjective, here used as a noun, meaning "pregnant

[woman]". Therefore, hyperemesis gravidarum means "excessive vomiting of pregnant

women."

Hyperemesis gravidarum is estimated to affect 0.3–2.0% of pregnant women.

While previously a common cause of death in pregnancy, with proper treatment this is now very rare.

Those affected have a low risk of miscarriage but a higher risk of

premature birth. Some women opt to have an abortion

because of the symptoms.

EMESIS GRAVIDARUM

Emesis gravidarum Morning sickness, also called nausea and vomiting

of pregnancy (NVP), nausea gravidarum, motion sickness, and pregnancy sickness, is a (pregnancy

discomfort) that affects more than half of all pregnant women.

Symptoms may be present early in the morning and reduce as the day progresses. However, in

spite of its common name, nausea and vomiting of pregnancy can occur at any time during the day.

For most women the sickness ends around the 12th week of pregnancy (the end of the first trimester).

Related to increased (estrogen) levels, a similar form of nausea is also seen in some women who use hormonal contraception or hormone replacement therapy. The nausea can be mild or induce actual vomiting. In more severe cases, vomiting may cause dehydration, weight loss, high blood pH, and a low level of potassium in the blood. This condition is known as hyperemesis gravidarum and occurs in about 1% of all pregnancies. Nausea and vomiting can be one of the first signs of pregnancy and usually begin around the 6th week of pregnancy (counting gestational age from 14 days before conception).

Morning sickness typically includes nausea that’s sometimes accompanied by vomiting. These two symptoms typically disappear after 12 to 14 weeks, and the vomiting doesn’t cause severe hydration.

HG typically includes nausea that doesn’t go away and severe vomiting that causes severe hydration and doesn’t allow you to keep any food or fluids down.

Morning sickness typically begins in the first month of pregnancy. It usually goes away by the third or fourth month. Pregnant women with morning sickness can get fatigue and a slight loss of appetite. They may have difficulty performing daily activities.

The symptoms of HG begin within the first six weeks of pregnancy, and nausea often doesn’t go away. HG can be extremely debilitating and cause fatigue that lasts for weeks or months. According to the HER Foundation, women with HG may experience a complete loss of appetite and may not be able to work or perform daily activities.

HG can lead to dehydration and poor weight gain during pregnancy. There’s no known way to prevent morning sickness or HG, but there are ways to manage the symptoms.

HIT & RUN???

Causes of HGAlmost all women experience some degree of morning

sickness during their pregnancy. Morning sickness is nausea and vomiting during pregnancy. Despite the

name, morning sickness isn’t confined to the morning and can occur at any time.

Morning sickness and HG seem to have a connection to human chorionic gonadotropin (hCG). This is a hormone

created during pregnancy by the placenta. Your body produces a large amount of this hormone at a rapid rate early in pregnancy. The American Pregnancy Association

states that hCG levels typically double every 48 to 72 hours. These levels can continue to rise throughout your

pregnancy.

T3,T4 IN H.G.Thyroxine LevelsIncreases in serum thyroxine levels have been

documented in 70% of pregnancies complicated by HG. Thyroid hormones are stimulated by the

increase in hCG and may result in transient hyperthyroidism. Severity of HG is sometimes

linked to the degree of hyperthyroidism. Mutations of hCG or TSH receptors have also been found to be elevated in women with HG.

( Thyroid function in patients with hyperemesis gravidarum)Bouillon R, Naesens M, Van Assche FA, De Keyser L, De Moor P, Renaer M, De

Vos P, De Roo M .Am J Obstet Gynecol 1982 Aug 15;143(8):922-6

An increased free thyroxine (T4) index was observed in 73% of 33 consecutive pregnancies complicated by severe hyperemesis gravidarum. The free triiodothyronine (T3) index was increased in only four of 11 hyperthyroxinemic patients. In five hyperthyroxinemic patients tested, no increase in serum thyrotropin was observed after the injection of thyrotropin-releasing hormone (THR). Goiter, exophthalmos, or previous history of hyperthyroidism was absent in all patients.!!! The thyroxinemia returned to normal in one to several weeks, whether or not it was treated with antithyroid drugs. The thyroid function during the period of hyperemesis had no influence on the subsequent rate of abortion or duration of pregnancy.!! A lower birth weight, however, was observed in children born to hyperthyroxinemic mothers. Hyperemesis gravidarum should be included in the differential diagnosis of elevations in free T4 index during pregnancy and included in the differential diagnosis of hyperthyroidism.

Source Etiology Pathophysiology

•Placenta• Corpus luteum hCG

•Distention of gastrointestinal tract

•Crossover with TSH, causing gestational

thyrotoxicosis[5]

Placenta •Estrogen•Progesterone

•Decreased gut mobility

•Elevated liver enzymes

•Decreased lower esophageal sphincter

pressure•Increased levels of

sex steroids in hepatic portal system

[21]

Gastrointestinal tract Helicobacter pylori Increased steroid levels in circulation[22]

Pathophysiology Morning sicknessAlthough the pathophysiology of HG is poorly understood, the most commonly accepted theory suggests that levels of hCG are associated with it.[5] Leptin may also play a role.[19]

Possible pathophysiological processes involved are summarized in the following table:

RISK FACTORS Some factors that could increase your risk of getting HG are:BAD Pshycological status.Family history .having a history of HGbeing pregnant with more than one babybeing overweightbeing a first-time motherTrophoblastic disease can also cause HG. Trophoblastic disease occurs when there’s an abnormal growth of cells inside the uterus.

HIT & RUN???

H.G. IS AN IDIOPATHIC DIEASES

DIAGNOSIS OF H.G

•Severe nausea and vomiting •Food aversions •Weight loss of 5% or more of pre-pregnancy weight •Decrease in urination •Dehydration •Headaches •Confusion •Fainting •Jaundice •Extreme fatigue •Low blood pressure •Rapid heart rate •Loss of skin elasticity •Secondary anxiety/depression

Investigations

Common investigations include :blood urea nitrogen (BUN) and electrolytes, liver function tests, urinalysis,[

thyroid function tests.Blood sugar Hematological investigations include: hematocrit levels, which are usually raised in HG. ultrasound scan may be needed to know gestational status and to exclude molar or partial molar pregnancy.

What are the treatments for hyperemesis gravidarum?In some cases hyperemesis gravidarum is so severe that hospitalization may be required.Hospital treatment may include some or all of the following:Intravenous fluids (IV)– to restore hydration, electrolytes, vitamins, and nutrientsTube feeding:

Nasogastric – restores nutrients through a tube passing through the nose and to the stomachPercutaneous endoscopic gastrostomy – restores nutrients through a tube passing through the abdomen and to the stomach; requires a surgical procedure

dose.

Medications – metoclopramide, antihistamines, and antireflux medication.A number of antiemetics are effective and safe in pregnancy including: pyridoxine/doxylamine, antihistamines (such as diphenhydramine), and phenothiazines (such as promethazine). With respect to effectiveness, it is unknown if one is superior to another,[ and there is even limited evidence of significant effect at all of pharmacological therapy in hyperemesis gravidarum.

While pyridoxine/doxylamine, a combination of vitamin B6 and doxylamine, is effective in nausea and vomiting of pregnancy, some have questioned its effectiveness in HG.

Ondansetron(zovran ) may be beneficial, however, there are some concerns regarding an association with cleft palate,and there is little high-quality data. Metoclopramide is also used and relatively well tolerated.Evidence for the use of corticosteroids is weak; there is some evidence that corticosteroid use in pregnant women may slightly increase the risk of oral facial clefts in the infant and may suppress fetal adrenal activity Ho hydrocortisone and prednisolone are inactivated in the placenta and may be used in the treatment of hyperemesis gravidarum after 12 weeks

Nutritional supportWomen not responding to IV rehydration and medication may require nutritional support. Patients might receive parenteral nutrition (intravenous feeding via a PICC line) or enteral nutrition (via a nasogastric tube or a nasojejunal tube). There is only limited evidence from trials to support the use of vitamin B6 to improve outcum.

Hyperalimentation may be necessary in certain cases to help maintain volume requirements and allow weight gain.[25] A physician might also prescribe Vitamin B1 (to prevent Wernicke's encephalopathy) and folic acid supplem

Other treatments may include:Bed Rest –This may provide comfort, but be cautious and aware of the effects of muscle and weight loss due to too much bed rest.Acupressure – The pressure point to reduce nausea is located at the middle of the inner wrist, three finger lengths away from the crease of the wrist, and between the two tendons. Locate and press firmly, one wrist at a time for three minutes. Sea bands also help with acupressure and can be found at your local drug store.Herbs – ginger or peppermintHomeopathic remedies are a non-toxic system of medicines. Do not try to self medicate with homeopathic methods; have a doctor prescribe the proper remedy and

accupressure

Complications Pregnant woman( indictions of i.c.u.)If HG is inadequately treated, anemia, hyponatremia,Wernicke's encephalopathy, kidney failure, central pontine myelinolysis, coagulopathy, atrophy, Mallory-Weiss tears, hypoglycemia, jaundice, malnutrition, pneumomediastinum, rhabdomyolysis, deconditioning, deep vein thrombosis, pulmonary embolism, splenic avulsion, or vasospasms of cerebral arteries are possible consequences. Depression and PTSD are common secondary complications of HG and emotional support can be beneficial

InfantThe effects of HG on the fetus are mainly due to electrolyte imbalances caused by HG in the mother.[20] Infants of women with severe hyperemesis who gain less than 7 kg (15.4 lb) during pregnancy tend to be of lower birth weight, small for gestational age, and born before 37 weeks gestation.In contrast, infants of women with hyperemesis who have a pregnancy weight gain of more than 7 kg appear similar to infants from uncomplicated pregnancies.There is no significant difference in the neonatal death rate in infants born to mothers with HG compared to infants born to mothers who do not have HG. Children born to mothers with undertreated Hyperemesis have a fourfold increase in neurobehavioral diagnoses.

DM & HG Factors precipitating ketoacidosis in diabetic pregnanciesEmesis.(starvation )>Infection.Non-compliance.Insulin pump failure.β-Sympathetomimetic drugs.Corticosteroids.Poor management.

Case reportA 28 year old woman with type 1 diabetes of five years’ duration, and with no evidence of diabetic microvascular or macrovascular complications, presented at 36 weeks’ gestation in her fifth pregnancy with a two day history of persistent vomiting and decreased fetal movements. On direct questioning she admitted to have skipped her last two doses of insulin because of persistent vomiting. She had previous admissions for diabetes and had, in general, been an infrequent attendee at the diabetes clinic and took poor care of her diabetes. During this unplanned pregnancy, she had defaulted on the majority of her diabetes specialist nurse clinic appointments and her glycaemic control as measured by glycated haemoglobin (HbA1c) had been poor throughout with readings of 11.5%, 6.4%, and 7.5% (upper reference range 5.5%) in the first, second, and third trimesters respectively. On examination she was tachypnoeic, hyperventilating, tachycardic, and dehydrated. Systemic examination was normal and there were no foci of infection. Fetal heart sounds were absent.

Investigations Biochemistry: venous plasma glucose 13 mmol/l, sodium 142 mmol/l, potassium 3.3 mmol/l, bicarbonate 10 mmol/l, chloride 100 mmol/l, urea 8 mmol/l, and creatinine 136 μmol/l. Arterial blood gas: pH 7.10, oxygen tension 13 kPa, carbon dioxide tension 2.3 kPa. Urine dipstick showed 4+ ketones, 4+glucose. The chest radiograph was normal; urine and blood cultures were negative. Management She was admitted to the high dependency unit and resuscitated with supplemental oxygen, intravenous fluids, and insulin infusion as per the protocol for diabetic ketoacidosis. She was placed in left lateral position to decrease aortocaval compression. Ultrasound and cardiotocogram confirmed intrauterine death of the fetus. After maternal stabilisation and reversal of acidosis, delivery was induced. Postmortem examination of the fetus confirmed stillbirth with no congenital anomalies.

THANK YOU