Question:

# What is it called when an infant inhales poop in the womb?

## If a baby has a bowel movement while in the womb and inhales some of the fluid it's in, they can become sick. This is called meconium aspiration. The sickness can be treated with antibiotics. In some cases, the meconium can block their airways.

Meconium aspiration syndrome (MAS, alternatively "Neonatal aspiration of meconium") is a medical condition affecting newborn infants. It occurs when meconium is present in their lungs during or before delivery. Meconium is the first stool of an infant, composed of materials ingested during the time the infant spends in the uterus. Meconium is normally stored in the infant's intestines until after birth, but sometimes (often in response to fetal distress) it is expelled into the amniotic fluid prior to birth, or during labor. If the baby then inhales the contaminated fluid, respiratory problems may occur. The most obvious sign that meconium has been passed during or before labor is the greenish or yellowish appearance of the amniotic fluid. The infant's skin, umbilical cord, or nailbeds may be stained green if the meconium was passed a considerable amount of time before birth. These symptoms alone do not necessarily indicate that the baby has inhaled in the fluid by gasping in utero or after birth. After birth, rapid or labored breathing, cyanosis, slow heartbeat, a barrel-shaped chest or low Apgar score are all signs of the syndrome. Inhalation can be confirmed by one or more tests such as using a stethoscope to listen for abnormal lung sounds (diffuse crackles and rhonchi), performing blood gas tests to confirm a severe loss of lung function, and using chest X-rays to look for patchy or streaked areas on the lungs. Infants who have inhaled meconium may develop respiratory distress syndrome often requiring ventilatory support. Complications of MAS include pneumothorax and persistent pulmonary hypertension of the newborn. Fetal distress during labor causes intestinal contractions, as well as relaxation of the anal sphincter, which allows meconium to pass into the amniotic fluid and contaminate the amniotic fluid. Meconium passage into the amniotic fluid occurs in about 5-20 percent of all births and is more common in overdue births. Of the cases where meconium is found in the amniotic fluid, meconium aspiration syndrome develops less than 5 percent of the time. Amniotic fluid is normally clear, but becomes greenish if it is tinted with meconium. The pathophysiology of MAS is due to a combination of primary surfactant deficiency and surfactant inactivation as a result of plasma proteins leaking into the airways from areas of epithelial disruption and injury. The leading three causes of MAS are If an infant inhales this mixture before, during, or after birth, it may be sucked deep into the lungs. Three main problems occur if this happens: These can lead to possibly fatal or long term health problems for the infant. High risk infants may be identified by fetal tachycardia, bradycardia or absence of fetal accelerations upon CTG in utero, at birth the infant may look cachexic and show signs of yellowish meconium staining on skin, nail and the umbillical cord, these infants usually progress onto Infant Respiratory distress syndrome within 4 hours. Investigations which can confirm the diagnosis are fetal chest x-ray, which will show hyperinflation, diaphragmatic flattening, cardiomegaly and pathy atelectasis, and ABG samples, which will show decreased oxygen levels. MAS is difficult to prevent.][ The risk of MAS increases after the 40th week of pregnancy. Amnioinfusion, a method of thinning thick meconium that has passed into the amniotic fluid through pumping of sterile fluid into the amniotic fluid, has not shown a benefit in treating MAS . Until recently it had been recommended that the throat and nose of the baby be suctioned by the delivery attendant as soon as the head is delivered. However, new studies have shown that this is not useful and the revised Neonatal Resuscitation Guidelines published by the American Academy of Pediatrics no longer recommend it.][ When meconium staining of the amniotic fluid is present and the baby is born depressed, it is recommended by the guidelines that an individual trained in neonatal intubation use a laryngoscope and endotracheal tube to suction meconium from below the vocal cords.][ If the condition worsens to a point where treatments are not affecting the newborn as they should, extracorporeal membrane oxygenation (ECMO) can be necessary to keep the infant alive. Lucinactant (Surfaxin) is used as a treatment of MAS. Albumin-lavage has not demonstrated to benefit outcomes of MAS. Steroid use has not demonstrated to benefit the outcomes of MAS. The mortality rate of meconium-stained infants is considerably higher than that of non-stained infants; meconium aspiration used to account for a significant proportion of neonatal deaths. Residual lung problems are rare but include symptomatic cough, wheezing, and persistent hyperinflation for up to 5-10 yr. The ultimate prognosis depends on the extent of CNS injury from asphyxia and the presence of associated problems such as pulmonary hypertension. In a study conducted between 1995 and 2002, MAS occurred in 1061 of 2,490,862 live births, reflecting an incidence of 0.43 of 1000. MAS requiring intubation occurs at higher rates in pregnancies beyond 40 weeks. 34% of all MAS cases born after 40 weeks required intubation compared to 16% prior to 40 weeks. M: OBS phys/devp/memb mthr/fetu/infc, epon proc, drug (2A/G2C)

Meconium is the earliest stools of a mammalian infant. Unlike later feces, meconium is composed of materials ingested during the time the infant spends in the uterus: intestinal epithelial cells, lanugo, mucus, amniotic fluid, bile, and water. Meconium, unlike later feces, is viscous and sticky like tar, its color usually being a very dark olive green; it is almost odorless. When diluted in amniotic fluid, it may appear in various shades of green, brown, or yellow. It should be completely passed by the end of the first few days after birth, with the stools progressing toward yellow (digested milk). Meconium is normally stored in the infant's bowel until after birth, but sometimes it is expelled into the amniotic fluid (also called "amniotic liquor") prior to birth or during labor and delivery. The stained amniotic fluid (called "meconium liquor" or "meconium stained liquor") is recognised by medical staff as a sign of fetal distress, and puts the neonate at risk of meconium aspiration. Medical staff may aspirate the meconium from the nose and mouth of a newborn immediately after delivery in the event the baby shows signs of respiratory distress to decrease the risk of meconium aspiration syndrome.][ Meconium had been thought to be sterile until the team of researchers from the University of Valencia in Spain found bacterial communities in it so developed that they seemed to fall into two categories. Around half of the samples appeared to be dominated by bacteria that produce lactic acid, such as lactobacillus, while the other half mostly contained a family of so-called enteric bacteria, such as Escherichia coli. The Latin term meconium derives from the Greek μήκων, mēkōn, poppy, in reference either to its tarry appearance that may resemble some raw opium preparations, or to Aristotle's belief that it induces sleep in the fetus. A symptom of both Hirschsprung's disease and cystic fibrosis is the failure to pass meconium. Meconium can be tested for various drugs, to check for in utero exposure. Using meconium, a Canadian research group at the Hospital for Sick Children, University of Toronto, showed that by measuring a by-product of alcohol (FAEE) they could objectively detect babies exposed to excessive maternal drinking of alcohol in pregnancy. In the USA, the results of meconium testing may be used by child protective services and other law enforcement agencies to e.g. determine the eligibility of the parents to keep the newborn. Most of the time that the amniotic fluid is stained with meconium it will be homogeneously distributed throughout the fluid making it brown. This indicates that the fetus passed the meconium some time ago such that sufficient mixing occurred as to establish the homogenous mixture. Terminal meconium occurs when the fetus passes the meconium a short enough time before birth/caesarean section that the amniotic fluid remains clear, but individual clumps of meconium are in the fluid. The meconium sometimes becomes thickened and congested in the ileum, a condition known as meconium ileus. Meconium ileus is often the first sign of cystic fibrosis. In cystic fibrosis, the meconium can form a bituminous black-green mechanical obstruction in a segment of the ileum. Beyond this there may be a few separate grey-white globular pellets. Below this level, the bowel is a narrow and empty micro-colon. Above the level of the obstruction, there are several loops of hypertrophied bowel distended with fluid. No meconium is passed, and abdominal distension and vomiting appear soon after birth. About 20% of cases of cystic fibrosis present with meconium ileus, while approximately 20% of one series of cases of meconium ileus did not have cystic fibrosis. The presence of meconium ileus is not related to the severity of the cystic fibrosis. The obstruction can be relieved in a number of different ways. Meconium ileus should be distinguished from meconium plug syndrome, in which a tenacious mass of mucus prevents the meconium from passing and there is no risk of intestinal perforation. Meconium ileus has a significant risk of intestinal perforation. In barium enema, meconium plug syndrome rather shows normal or dilated colon as compared to micro-colon in meconium ileus. Meconium from 13-hour-old newborn. This image compares the appearance of meconium (from 48 hours after normal delivery at term) to the appearance of the same infant's faeces after 1 week of breastfeeding.

A) Endotracheal tube which sits in the trachea. B) Inflatable Cuff which facilitates the inflation of the balloon at the end of the tube to allow it to sit securely in the airway. The balloon can also be deflated via this cuff upon extubation. C) Trachea In medicine, mechanical ventilation is a method to mechanically assist or replace spontaneous breathing. This may involve a machine called a ventilator or the breathing may be assisted by a registered nurse, physician, respiratory therapist, or other suitable person compressing a bag or set of bellows. There are two main divisions of mechanical ventilation: invasive ventilation and non-invasive ventilation. There are two main modes of mechanical ventilation within the two divisions: positive pressure ventilation, where air (or another gas mix) is pushed into the trachea, and negative pressure ventilation, where air is essentially sucked into the lungs. Mechanical ventilation is indicated when the patient's spontaneous ventilation is inadequate to maintain life. It is also indicated as prophylaxis for imminent collapse of other physiologic functions, or ineffective gas exchange in the lungs. Because mechanical ventilation only serves to provide assistance for breathing and does not cure a disease, the patient's underlying condition should be correctable and should resolve over time. In addition, other factors must be taken into consideration because mechanical ventilation is not without its complications (see below) Common medical indications for use include: Barotrauma — Pulmonary barotrauma is a well-known complication of positive pressure mechanical ventilation. This includes pneumothorax, subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum. Ventilator-associated lung injury — Ventilator-associated lung injury (VALI) refers to acute lung injury that occurs during mechanical ventilation. It is clinically indistinguishable from acute lung injury or acute respiratory distress syndrome (ALI/ARDS). Diaphragm — Controlled mechanical ventilation may lead to a rapid type of disuse atrophyinvolving the diaphragmatic muscle fibers, which can develop within the first day of mechanical ventilation. This cause of atrophy in the diaphragm is also a cause of atrophy in all respiratory related muscles during controlled mechanical ventilation. Motility of mucocilia in the airways — Positive pressure ventilation appears to impair mucociliary motility in the airways. Bronchial mucus transport was frequently impaired and associated with retention of secretions and pneumonia.
Mechanical ventilation is often a life-saving intervention, but carries many potential complications including pneumothorax, airway injury, alveolar damage, and ventilator-associated pneumonia. Other complications include diaphragm atrophy, decreased cardiac output, and oxygen toxicity. One of the primary complications that presents in patients who are mechanically ventilated is acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). ALI/ARDS are recognized as significant contributors to patient morbidity and mortality. In many healthcare systems prolonged ventilation as part of intensive care is a limited resource (in that there are only so many patients that can receive care at any given moment). It is used to support a single failing organ system (the lungs) and cannot reverse any underlying disease process (such as terminal cancer). For this reason there can be (occasionally difficult) decisions to be made about whether it is suitable to commence someone on mechanical ventilation. Equally many ethical issues surround the decision to discontinue mechanical ventilation. It can be used as a short term measure, for example during an operation or critical illness (often in the setting of an intensive care unit). It may be used at home or in a nursing or rehabilitation institution if patients have chronic illnesses that require long-term ventilatory assistance. Due to the anatomy of the human pharynx, larynx, and esophagus and the circumstances for which ventilation is needed, additional measures are often required to secure the airway during positive pressure ventilation in order to allow unimpeded passage of air into the trachea and avoid air passing into the esophagus and stomach. Commonly this is by insertion of a tube into the trachea which provides a clear route for the air. This can be either an endotracheal tube, inserted through the natural openings of mouth or nose or a tracheostomy inserted through an artificial opening in the neck. In other circumstances simple airway maneuvres, an oropharyngeal airway or laryngeal mask airway may be employed. If the patient is able to protect their own airway and non-invasive ventilation or negative-pressure ventilation is used then an airway adjunct may not be needed. The iron lung, also known as the Drinker and Shaw tank, was developed in 1929 and was one of the first negative-pressure machines used for long-term ventilation. It was refined and used in the 20th century largely as a result of the polio epidemic that struck the world in the 1940s. The machine is effectively a large elongated tank, which encases the patient up to the neck. The neck is sealed with a rubber gasket so that the patient's face (and airway) are exposed to the room air. While the exchange of oxygen and carbon dioxide between the bloodstream and the pulmonary airspace works by diffusion and requires no external work, air must be moved into and out of the lungs to make it available to the gas exchange process. In spontaneous breathing, a negative pressure is created in the pleural cavity by the muscles of respiration, and the resulting gradient between the atmospheric pressure and the pressure inside the thorax generates a flow of air. In the iron lung by means of a pump, the air is withdrawn mechanically to produce a vacuum inside the tank, thus creating negative pressure. This negative pressure leads to expansion of the chest, which causes a decrease in intrapulmonary pressure, and increases flow of ambient air into the lungs. As the vacuum is released, the pressure inside the tank equalizes to that of the ambient pressure, and the elastic coil of the chest and lungs leads to passive exhalation. However, when the vacuum is created, the abdomen also expands along with the lung, cutting off venous flow back to the heart, leading to pooling of venous blood in the lower extremities. There are large portholes for nurse or home assistant access. The patients can talk and eat normally, and can see the world through a well-placed series of mirrors. Some could remain in these iron lungs for years at a time quite successfully. Today, negative pressure mechanical ventilators are still in use, notably with the polio wing hospitals in England such as St Thomas' Hospital in London and the John Radcliffe in Oxford. The prominent device used is a smaller device known as the cuirass. The cuirass is a shell-like unit, creating negative pressure only to the chest using a combination of a fitting shell and a soft bladder. Its main use is in patients with neuromuscular disorders who have some residual muscular function. However, it was prone to falling off and caused severe chafing and skin damage and was not used as a long term device. In recent years this device has re-surfaced as a modern polycarbonate shell with multiple seals and a high pressure oscillation pump in order to carry out biphasic cuirass ventilation. The design of the modern positive-pressure ventilators were mainly based on technical developments by the military during World War II to supply oxygen to fighter pilots in high altitude. Such ventilators replaced the iron lungs as safe endotracheal tubes with high volume/low pressure cuffs were developed. The popularity of positive-pressure ventilators rose during the polio epidemic in the 1950s in Scandinavia and the United States and was the beginning of modern ventilation therapy. Positive pressure through manual supply of 50% oxygen through a tracheostomy tube led to a reduced mortality rate among patients with polio and respiratory paralysis. However, because of the sheer amount of man-power required for such manual intervention, mechanical positive-pressure ventilators became increasingly popular. Positive-pressure ventilators work by increasing the patient's airway pressure through an endotracheal or tracheostomy tube. The positive pressure allows air to flow into the airway until the ventilator breath is terminated. Subsequently, the airway pressure drops to zero, and the elastic recoil of the chest wall and lungs push the tidal volume — the breath—out through passive exhalation. Ventilators come in many different styles and method of giving a breath to sustain life. There are manual ventilators such as Bag valve masks and anesthesia bags require the user to hold the ventilator to the face or to an artificial airway and maintain breaths with their hands. Mechanical ventilators are ventilators not requiring operator effort and are typically computer controlled or pneumatic controlled. Mechanical ventilators typically require power by a battery or a wall outlet (DC or AC) though some ventilators work on a pneumatic system not requiring power. The trigger is what causes a breath to be delivered by a mechanical ventilator. Breaths may be triggered by a patient taking their own breath, a ventilator operator pressing a manual breath button, or by the ventilator based on the set breath rate and mode of ventilation. The cycle is what causes the breath to transition from the inspiratory phase to the exhalation phase. Breaths may be cycled by a mechanical ventilator when a set time has been reached, or when a preset flow or percentage of the maximum flow delivered during a breath is reached depending on the breath type and the settings. Breaths can also be cycled when an alarm condition such as a high pressure limit has been reached, which is a primary strategy in pressure regulated volume control. Limit is how the breath is controlled. Breaths may be limited to a set maximum circuit pressure or a set maximum flow. Exhalation in mechanical ventilation is almost always completely passive. The ventilator's expiratory valve is opened, and expiratory flow is allowed until the baseline pressure (PEEP) is reached. Expiratory flow is determined by patient factors such as compliance and resistance. Mechanical dead space is defined as the volume of gas re-breathed as the result of use in a mechanical device. $V_{Dmech} = V_T - V_{Dphys} - \frac{PaCO2(V_T - V_D - V_{Dmech})}{P_{ACO_{2}}}$ $\frac{V_D}{V_T} = \frac{PaCO_2 - P\bar{E}CO_2}{PaCO_2}$ Mechanical ventilation utilizes several separate systems for ventilation referred to as the mode. Modes come in many different delivery concepts but all modes fall into one of three categories; volume cycled, pressure cycled, spontaneously cycled. The selection of which mode of mechanical ventilation to use for a given patient is generally based on the familiarity of clinicians with modes and the equipment availability at a particular institution. In adults when 100% Fi is used initially, it is easy to calculate the next Fi to be used and easy to estimate the shunt fraction. The estimated shunt fraction refers to the amount of oxygen not being absorbed into the circulation. In normal physiology, gas exchange (oxygen/carbon dioxide) occurs at the level of the alveoli in the lungs. The existence of a shunt refers to any process that hinders this gas exchange, leading to wasted oxygen inspired and the flow of un-oxygenated blood back to the left heart (which ultimately supplies the rest of the body with unoxygenated blood). When using 100% Fi, the degree of shunting is estimated by subtracting the measured Pa (from an arterial blood gas) from 700 mmHg. For each difference of 100 mmHg, the shunt is 5%. A shunt of more than 25% should prompt a search for the cause of this hypoxemia, such as mainstem intubation or pneumothorax, and should be treated accordingly. If such complications are not present, other causes must be sought after, and PEEP should be used to treat this intrapulmonary shunt. Other such causes of a shunt include: Withdrawal from mechanical ventilation—also known as weaning—should not be delayed unnecessarily, nor should it be done prematurely. Patients should have their ventilation considered for withdrawal if they are able to support their own ventilation and oxygenation, and this should be assessed continuously. There are several objective parameters to look for when considering withdrawal, but there is no specific criteria that generalizes to all patients. Trials of spontaneous breathing have been shown to accurately predict the success of spontaneous breathing. See main article respiratory monitoring. One of the main reasons why a patient is admitted to an ICU is for delivery of mechanical ventilation. Monitoring a patient in mechanical ventilation has many clinical applications: Enhance understanding of pathophysiology, aid with diagnosis, guide patient management, avoid complications and assessment of trends. Most of modern ventilators have basic monitoring tools. There are also monitors that work independently of the ventilator, which allow to measure patients after the ventilator has been removed, such as a T tube test. There are various procedures and mechanical devices that provide protection against airway collapse, air leakage, and aspiration: $\dot{V}_A = \ V_T - V_{DSphys} * f$ $PaCO_2 = \frac{0.863 * \dot{V}_{CO_2}}{\dot{V}_A}$ $V_A = V_T - V_f$ $\frac{Q_{SP}}{Q_T} = \frac{CcO_2 - CaO_2}{5+(CcO_2 - CaO_2)}$ The Roman physician Galen may have been the first to describe mechanical ventilation: "If you take a dead animal and blow air through its larynx [through a reed], you will fill its bronchi and watch its lungs attain the greatest distention." Vesalius too describes ventilation by inserting a reed or cane into the trachea of animals. In 1908 George Poe demonstrated his mechanical respirator by asphyxiating dogs and seemingly bringing them back to life. M: RES anat (n, x, l, c)/phys/devp noco (c, p)/cong/tumr, sysi/epon, injr proc, drug (R1/2/3/5/6/7)

Blood gas is a laboratory test of blood where the purpose is primarily to measure ventilation and oxygenation. The source is generally noted by an added word to the beginning; arterial blood gases come from arteries, venous blood gases come from veins and capillary blood gases come from capillaries. Abnormal results may be due to lung, kidney, or metabolic diseases. Head or neck injuries or other injuries that affect breathing can also lead to abnormal results.

In medicine (obstetrics), the term fetal distress refers to the presence of signs in a pregnant woman—before or during childbirth—that suggest that the fetus may not be well. Because of its lack of precision, the term is eschewed in modern American obstetrics. Generally it is preferable to describe specific signs in lieu of declaring fetal distress that include: Some of these signs are more reliable predictors of fetal compromise than others. For example, cardiotocography can give high false positive rates, even when interpreted by highly experienced medical personnel. Metabolic acidosis is a more reliable predictor, but is not always available. There are many causes of "fetal distress" including: Instead of referring to "fetal distress" current recommendations hold to look for more specific signs and symptoms, assess them, and take the appropriate steps to remedy the situation. Traditionally the diagnosis of "fetal distress" led the obstetrician to recommend rapid delivery by instrumental delivery or by caesarean section if vaginal delivery is not advised. M: OBS phys/devp/memb mthr/fetu/infc, epon proc, drug (2A/G2C)

Amniotic fluid or liquor amnii is the protective liquid contained by the amniotic sac of a pregnant female. From the very beginning of the formation of the extracoelomal cavity, amniotic fluid [AF] can be detected. This firstly water-like fluid originates from the maternal plasma, and passes through the fetal membranes by osmotic and hydrostatic forces. As the placental and fetal vessels develop, the fluid passes through the fetal tissue, as the exsudatum of the skin. After the 20th-25th week of pregnancy when the keratinization of skin occurs, the quantity of amniotic fluid begins to depend on the factors that comprise the circulation of AF. At first it is mainly water with electrolytes, but by about the 12-14th week the liquid also contains proteins, carbohydrates, lipids and phospholipids, and urea, all of which aid in the growth of the fetus. The volume of amniotic fluid is positively correlated with the growth of fetus. From the 10th to the 20th week it increases from 25ml to 400ml approximately. From the 8th week, when the fetal kidneys begin to function, fetal urine is also present in the AF. Approximately in the 10th week the breathing and swallowing of the fetus slightly decrease the amount of AF, but neither urination nor swallowing contributes significantly to AF quantity changes, until the 25 week, when keratinization of skin is complete. Then the relationship between AF and fetal growth stops. It reaches the plateau of 800ml at the 28 week (gestational age). The amount of fluid declines to roughly 400 ml at 42 weeks ga. The forewaters are released when the amnion ruptures. This is commonly known as the time when a woman's "water breaks". When this occurs during labour at term, it is known as "spontaneous rupture of membranes" (SROM). If the rupture precedes labour at term, however, it is referred to as "premature rupture of membranes" (PROM). The majority of the hindwaters remain inside the womb until the baby is born. Artificial rupture of membrane (ARM), a manual rupture of the amniotic sac, can also be performed to release the fluid if the amnion has not spontaneously ruptured. Amniotic fluid is "inhaled" and "exhaled" by the fetus. It is essential that fluid be breathed into the lungs in order for them to develop normally. Swallowed amniotic fluid also creates urine and contributes to the formation of meconium. Amniotic fluid protects the developing baby by cushioning against blows to the mother's abdomen, allowing for easier fetal movement and promoting muscular/skeletal development. Analysis of amniotic fluid, drawn out of the mother's abdomen in an amniocentesis procedure, can reveal many aspects of the baby's genetic health. This is because the fluid also contains fetal cells, which can be examined for genetic defects. Amniotic fluid normally has a pH of 7.0 to 7.5. Because pH in the upper vagina is normally acidic (pH 3.8-4.5), a vaginal pH test showing a pH of more than 4.5 strengthens a suspicion of rupture of membranes in case of clear vaginal discharge in pregnancy. Other tests for detecting amniotic fluid mainly include nitrazine paper test and fern test. Recent studies show that amniotic fluid contains a considerable quantity of stem cells. These amniotic stem cells are pluripotent and able to differentiate into various tissues, which may be useful for future human application. Some researchers have found that amniotic fluid is also a plentiful source of non-embryonic stem cells. These cells have demonstrated the ability to differentiate into a number of different cell-types, including brain, liver and bone. It is possible to conserve the stem cells extracted from amniotic fluid in private stem cells banks. Some private companies offer this service for a fee. Too little amniotic fluid (oligohydramnios) can be a cause or an indicator of problems for the mother and baby. The majority of pregnancies proceed normally and the baby is born healthy, but this isn't always the case. Babies with too little amniotic fluid can develop contractures of the limbs, clubbing of the feet and hands, and also develop a life threatening condition called hypoplastic lungs. If a baby is born with hypoplastic lungs, which are small underdeveloped lungs, this condition is potentially fatal and the baby can die shortly after birth due to inadequate oxygenation. Potter sequence refers to a constellation of findings related to insufficient amniotic fluid and includes shortened and malformed limbs with clubbed feet and the underdeveloped lungs that can lead to perinatal death. On every prenatal visit, the obstetrician/gynaecologist or midwife should measure the patient's fundal height with a tape measure. It is important that the fundal height be measured and properly recorded to track proper fetal growth and the increasing development of amniotic fluid. The obstetrician/gynaecologist should also routinely ultrasound the patient—this procedure will also give an indication of proper fetal growth and amniotic fluid development. Oligohydramnios can be caused by infection, kidney dysfunction or malformation (since much of the late amniotic fluid volume is urine), procedures such as chorionic villus sampling (CVS), and preterm premature rupture of membranes (PPROM). Oligohydramnios can sometimes be treated with bed rest, oral and intravenous hydration, antibiotics, steroids, and amnioinfusion.][ It is also important to keep the baby warm and moist. The opposite of oligohydramnios is polyhydramnios, an excess volume of amniotic fluid in the amniotic sac. M: OBS phys/devp/memb mthr/fetu/infc, epon proc, drug (2A/G2C)
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