10 Things to Know About Biliary Atresia and Newborn Jaundice

Biliary atresia is a rare but serious liver condition that affects newborns and occurs when the bile ducts are blocked, damaged, or do not develop normally. Bile ducts are small tubes that carry bile from the liver to the intestine, where it helps digest fats and remove waste products. When these ducts are blocked, bile builds up in the liver, causing inflammation and progressive liver damage. Without early treatment, biliary atresia can lead to severe liver disease and may eventually require a liver transplant.

One of the earliest signs of biliary atresia is prolonged newborn jaundice, which causes yellowing of the skin and eyes due to high bilirubin levels. While jaundice is common in many newborns and often improves naturally, jaundice that continues beyond the first few weeks of life may require further evaluation. Other warning signs include pale or gray-colored stools, dark urine, poor weight gain, and an enlarged abdomen. This article explains 10 important things to know about biliary atresia and newborn jaundice, including symptoms, causes, diagnosis, treatment options, and why early medical care matters.

What is Biliary Atresia and Its Link to Newborn Jaundice?

Biliary atresia is a rare, life-threatening pediatric liver disease characterized by progressive inflammation, scarring, and complete blockage of the bile ducts shortly after birth. Because bile is an aggressive fluid containing highly corrosive bile acids meant solely for digestion, trapping it within the liver initiates a destructive cycle of cellular inflammation, cell death, and permanent liver scarring (biliary cirrhosis). If left undiagnosed, this anatomical plumbing failure leads to end-stage liver failure within the first one to two years of an infant’s life.

What Defines Biliary Atresia?

The driving mechanism behind biliary atresia is progressive obliterative cholangiopathy—a continuous, destructive immune or inflammatory response that targeting the bile ducts. These ducts act as the drainage system of the liver, funneling bile from inside the liver tissue down into the gallbladder and the small intestine.

While the exact root cause remains unknown, clinical researchers suspect a multi-hit hypothesis involving several overlapping triggers:

• Perinatal Viral Infections: Exposure to specific viruses (such as rotavirus, reovirus, or cytomegalovirus) around the time of birth can spark an aggressive, localized inflammatory response within the bile duct walls.

• Immune System Malfunctions: An autoimmune reaction where the baby’s own white blood cells (T-lymphocytes) mistakenly target and destroy the cells lining the bile ducts.

• Genetic Predispositions: Subtle structural anomalies or genetic variations that alter how the biliary tree forms during embryonic development.

• Environmental Toxins: Exposure to naturally occurring gestational toxins that selectively damage vulnerable biliary tract tissue.

Regardless of the initial trigger, the cellular chain reaction that occurs within the liver behaves like an unmanaged domino effect:

 

The Critical Difference: Physiological Jaundice vs. Biliary Atresia

Jaundice—the yellowing of an infant’s skin and sclera (the whites of the eyes)—is incredibly common in newborns, affecting a majority of infants. However, mistaking the dangerous jaundice of biliary atresia for harmless newborn yellowing is a primary reason life-saving surgeries are delayed.

To safely distinguish between them, clinicians evaluate three clear metrics: timing, persistence, and the precise chemical form of the bilirubin circulating in the blood.

1. Physiological Jaundice (The Benign Developmental Delay)

Physiological jaundice occurs as a newborn transitions to life outside the womb. Old red blood cells break down naturally, releasing a fat-soluble pigment called unconjugated (indirect) bilirubin. Because an infant’s liver is still developmentally immature, it temporarily lacks enough functional enzymes to clear this pigment quickly.

The unconjugated bilirubin backs up into the skin, typically appearing around day 2 or 3 of life, peaking by day 5, and resolving entirely on its own within 7 to 14 days as the liver matures. It represents a harmless, temporary delay rather than an active disease.

2. Biliary Atresia Jaundice (The Mechanical Obstruction)

In an infant with biliary atresia, the liver cells themselves are initially working perfectly fine. They collect raw unconjugated bilirubin from the bloodstream and successfully process it into water-soluble conjugated (direct) bilirubin, packaging it neatly into the bile fluid.

The clinical emergency is a mechanical plumbing failure. Because the bile ducts are scarred and completely blocked, the processed bile cannot exit into the intestine. With the drainage pathways sealed off, the corrosive, conjugated fluid overflows out of the liver cells and leaks backward into the infant’s bloodstream, staining tissues throughout the body.

Core Laboratory & Diagnostic Comparison

Clinical Feature	Physiological Jaundice	Biliary Atresia Jaundice
Primary Blood Marker	Elevated Unconjugated (Indirect) Bilirubin.	Elevated Conjugated (Direct) Bilirubin.
Critical Lab Threshold	Direct bilirubin stays completely normal (well below 1.0 mg/dL).	Direct bilirubin accounts for more than 20% of the total bilirubin (or is greater than 1.0 mg/dL).
Onset Profile	Appears within the first 48 to 72 hours of life.	Often masked early on by normal newborn jaundice, but becomes distinct after 14 days of life.
Persistence	Steadily improves and vanishes entirely within 1 to 2 weeks.	Persists, deepens, and darkens over time; it does not fade away.
Organ Health Impact	Harmless to the liver; resolves cleanly without tissue damage.	Highly toxic; causes ongoing destruction to liver cells every day it remains uncorrected.

Early Physical Warning Signs Beyond Jaundice

Because infants with biliary atresia are initially born looking healthy, parents and healthcare providers must look for specific physical indicators that point directly to a drainage obstruction.

1. Acholic (Pale, Clay-Colored) Stools

In a healthy infant, the signature yellow, gold, or green color of stool is caused directly by bile pigments being dumped into the intestines. When an infant has biliary atresia, the physical blockage prevents bile from ever reaching the digestive tract.

As a result, the stool loses all its normal pigment, presenting as pale yellow, light ivory, gray, or completely white (acholic stools). Utilizing an infant stool color card is one of the most effective ways parents can screen for this condition at home.

2. Dark, Tea-Colored Urine

A healthy newborn’s urine should be completely clear or light straw-colored. In biliary atresia, because the conjugated bilirubin cannot escape through the stool, the body attempts to filter the massive backlog out through the kidneys. Because conjugated bilirubin is water-soluble, it passes into the urine, staining it a deep, dark amber or tea-like color.

🛑 The 14-Day Diagnostic Deadline

Because breastfed infants can sometimes experience prolonged, benign jaundice, it is alarmingly easy for families to assume a yellow tint at 3 weeks of life is just “normal breastfeeding jaundice.”

To prevent missed diagnoses, strict medical protocols dictate that any infant who remains visibly jaundiced past 14 days of life MUST immediately receive a fractionated bilirubin blood test to evaluate the exact direct and indirect counts. If the direct portion crosses the 20% threshold, it is treated as a highly time-sensitive diagnostic emergency.

10 Warning Signs of Biliary Atresia in a Jaundiced Newborn

When evaluating an infant with lingering newborn jaundice, identifying Biliary Atresia early is a race against time. Because the condition triggers rapid, irreversible liver scarring (biliary cirrhosis), recognizing the full clinical picture within the first few weeks of life can fundamentally alter an infant’s long-term survival.

Beyond the persistence of yellow skin, clinicians and parents must monitor a distinct cluster of 10 critical warning signs that point to a progressive biliary blockage.

The Primary Red Flags: Stool and Urine Anomalies

The most specific and immediate warnings of a physical plumbing failure in the liver are found in the diaper. These two signs are the direct result of bile flow being completely blocked (cholestasis).

1. Pale, Chalky-White Stools (Acholic Stools)

In a healthy infant, the normal shades of mustard yellow, gold, or green are caused by bile pigments being dumped into the intestines. In biliary atresia, the physical blockage prevents bile from ever reaching the digestive tract. Lacking this pigment, the stool takes on an abnormally pale, ivory, gray, clay-colored, or chalky-white appearance. Many pediatric health systems utilize an infant stool color card to help caregivers cross-reference and screen for these abnormal shades at home.

2. Dark, Tea-Colored Urine

A healthy, well-hydrated newborn passes clear or very light straw-colored urine. Because an infant with biliary atresia has blocked ducts, the water-soluble conjugated (direct) bilirubin backs up into the blood. The body tries to compensate by filtering this massive backlog out through the kidneys. This high concentration of pigment permanently stains the urine a deep amber, tea, or cola color—even when the baby is perfectly hydrated.

8 Secondary Physical Symptoms to Monitor

As the disease progresses and bile acids accumulate in the body, the infant will develop a series of systemic, structural, and behavioral symptoms:

3. Persistent Jaundice

While standard physiological newborn jaundice cleanly resolves within 10 to 14 days, the jaundice of biliary atresia persists and deepens past 2 to 3 weeks of life. The yellowing of the skin and the whites of the eyes (scleral icterus) will darken or take on a slightly greenish-bronze tint as bilirubin levels climb.

4. Poor Weight Gain (Failure to Thrive)

Bile is biologically required to break down dietary fats and absorb fat-soluble vitamins ($A$, $D$, $E$, and $K$). Because bile cannot reach the small intestine, the infant cannot process nutrients from breast milk or formula. This creates profound malnutrition, causing the baby to experience poor weight gain or weight loss despite eating.

5. Swollen, Firm Abdomen (Hepatomegaly)

The corrosive backup of bile fluid causes rapid inflammation and swelling of the liver tissue itself. The baby’s abdomen will look visibly distended, and the upper right side of the belly will feel unusually firm or hard to the touch. As tissue scarring increases, the spleen may enlarge as well (splenomegaly).

6. Systemic Itching (Pruritus)

When toxic bile acids have nowhere to go, they overflow into the bloodstream and deposit directly into the skin. This triggers intense, constant itching from the inside out. The infant will appear highly restless, constantly rubbing their face against sheets, or scratching at their limbs to find relief.

7. Visible Abdominal Veins

As extensive liver scarring (cirrhosis) sets in, it compresses the blood vessels inside the organ. This creates a dangerous backup of blood pressure in the abdominal vascular system, known as portal hypertension. To bypass the scarred liver, blood forces its way into superficial vessels, making the veins across the surface of the baby’s stomach look swollen, blue, and highly visible.

8. Excessive Irritability and Fussiness

Infants with biliary atresia are often deeply uncomfortable, unusually fussy, and incredibly difficult to console. This persistent irritability stems from a combination of localized abdominal pain, stretching of the liver capsule, and the systemic distress caused by circulating toxins.

9. Poor Feeding and Lethargy

As the liver’s metabolic functions decline, the infant will display a progressively weak suck, a lack of interest in feeding, or excessive sleepiness during normal waking hours. This lethargy compounds the child’s nutritional deficiencies.

10. Shrill, High-Pitched Cry

A distinct, high-pitched, or piercing cry is a non-specific indicator of neurological irritation, intense physical discomfort, or severe systemic illness in newborns. It reflects the overall toll the unmanaged disease is taking on the baby’s central nervous system and body.

🛑 The 14-Day fractionated Bilirubin Directive

It is dangerously easy to mistake biliary atresia for benign “breastmilk jaundice” during the third week of life.

To eliminate any ambiguity, international pediatric guidelines state that any infant who remains visibly jaundiced past 14 days of life MUST immediately undergo a fractionated bilirubin blood test. If the direct (conjugated) portion accounts for more than 20% of the total bilirubin, the baby requires an immediate, aggressive diagnostic workup to prepare for surgical intervention.

Immediate Actions to Take if Biliary Atresia is Suspected

If Biliary Atresia is suspected due to the presence of warning signs like persistent jaundice, pale stools, or dark urine, the immediate and most critical action is to contact a pediatrician for an urgent medical evaluation. Time is of the essence, as the prognosis for Biliary Atresia is directly linked to how early it is diagnosed and treated.

To facilitate a swift and accurate diagnosis, parents should prepare specific information for the medical appointment. This preparation allows the physician to quickly assess the situation and order the necessary diagnostic tests, such as a fractionated bilirubin blood test, which can confirm the presence of cholestatic jaundice. Do not adopt a “wait and see” approach. The symptoms of Biliary Atresia are signs of an ongoing, destructive process within the liver, and any delay in seeking care can lead to irreversible damage. The primary goal is to get the infant into the care of a pediatric specialist, typically a gastroenterologist or hepatologist, as quickly as possible.

Is it necessary to see a doctor immediately for these symptoms?

Yes, it is absolutely necessary to see a doctor immediately if a newborn exhibits symptoms suggestive of Biliary Atresia, especially the combination of persistent jaundice (beyond two weeks) and pale, clay-colored stools. The urgency cannot be overstated because the success of the primary surgical intervention, the Kasai procedure (hepatoportoenterostomy), is highly dependent on the infant’s age at the time of surgery. The mantra among pediatric liver specialists is “time is liver.” Every day that passes without treatment allows the inflammatory and fibrotic process to cause more permanent damage to the liver.

The Kasai procedure involves removing the blocked extrahepatic bile ducts and attaching a loop of the small intestine directly to the liver at the spot where the bile ducts exit. This creates a new drainage path for the bile. Medical research and clinical data overwhelmingly show that the likelihood of re-establishing bile flow and delaying the need for a liver transplant is greatest when the surgery is performed before 60 days of age. Success rates, defined by the restoration of bile flow and clearance of jaundice, can be as high as 70-80% when performed within this critical window.

However, this success rate drops significantly to below 25-40% for infants who undergo the procedure after 90 days of age. An early and successful Kasai procedure can allow a child to live with their native liver for many years, sometimes even into adulthood. A delayed diagnosis almost guarantees the rapid progression to end-stage cirrhosis and the need for a liver transplant in early childhood.

What information should you prepare for the pediatrician’s appointment?

When preparing for a pediatrician’s appointment where Biliary Atresia is suspected, parents should gather specific, objective information that will help the doctor quickly and accurately assess the situation. This organized preparation can streamline the diagnostic process and underscore the urgency of the symptoms. Being able to provide clear evidence helps move beyond subjective descriptions and gives the healthcare provider tangible data to work with.

A comprehensive preparation checklist should include the following items:

Photos of Stool Color: This is arguably the most important piece of evidence. Take clear, well-lit photos of the baby’s stool in their diaper. Capture several examples over different days if possible, especially if the color varies. Comparing these photos to a standard infant stool color card can be extremely helpful.

Feeding and Weight Records: Keep a detailed log of the infant’s feeding habits. Note the type (breast milk or formula), amount, and frequency of feedings. Also, record any issues like spitting up, vomiting, or apparent disinterest in feeding. Bring all weight records from birth and any subsequent checkups to demonstrate the baby’s growth trajectory. A slowing or stagnant weight gain is a critical data point.

Symptom Diary: Create a timeline of the symptoms. Note when you first noticed the jaundice and whether it has improved, stayed the same, or worsened. Record the date of onset for other signs, such as changes in stool or urine color, abdominal swelling, or increased irritability.

Urine Observations: Be prepared to describe the color of the urine. Note if it is consistently dark, even when the baby appears well-hydrated. If possible, you can collect a sample on a white cotton ball inside the diaper to show the doctor the distinct brown or tea-like color.

List of Questions: Write down any questions or concerns you have ahead of time. During a stressful appointment, it can be easy to forget what you wanted to ask. This ensures you leave the office with a clear understanding of the next steps.

Medical Pathway for Diagnosing and Treating Biliary Atresia

The medical journey for an infant with Biliary Atresia is a highly structured, time-sensitive clinical pathway. Because the disease triggers rapid, continuous scarring of the liver, the entire medical team operates under a strict timeline to confirm the structural blockage, attempt a surgical bypass, and prepare for long-term hepatology management.

The Diagnostic Escalation Pathway

Definitively diagnosing biliary atresia requires a systematic escalation of testing, moving quickly from non-invasive blood work to microscopic and structural confirmation.

• Fractionated Bilirubin Panel: The frontline blood test. A conjugated (direct) bilirubin level greater than 20% of the total bilirubin establishes the presence of cholestasis (trapped bile). Liver function enzymes ($AST$ and $ALT$) will also be elevated, showing active liver cell injury.

• Abdominal Ultrasound: A high-resolution scan used to evaluate the biliary anatomy. In many affected infants, the gallbladder appears abnormally shrunken, structurally malformed, or entirely absent.

• HIDA Scan (Hepatobiliary Iminodiacetic Acid): A nuclear medicine transit test. A radioactive tracer is injected intravenously; if the liver absorbs the tracer but completely fails to excrete it into the small intestine over a 24-hour period, a physical mechanical blockage is highly suspected.

• Percutaneous Liver Biopsy: The pathological gold standard. A small tissue sample is extracted via a specialized needle. Pathologists look for the signature microscopic footprint of biliary atresia: bile duct proliferation (the liver desperately multiplying useless, tiny internal ducts) and bridging fibrosis (scar tissue).

• Intraoperative Cholangiogram: The absolute structural confirmation. Performed under anesthesia directly in the operating room, the surgeon injects a radiopaque dye directly into the gallbladder remnant. If fluoroscopic X-rays show the dye is trapped and cannot flow into the small intestine, the diagnosis of biliary atresia is officially confirmed, and the surgeon immediately transitions into the corrective open surgery.

Surgical Intervention: The Kasai Procedure

The primary surgical treatment for biliary atresia is the Kasai Procedure (technically termed a hepatoportoenterostomy). It is crucial to understand that the Kasai procedure is a palliative bypass, not a permanent cure. Its goal is to delay or eliminate the immediate need for an infant liver transplant by restoring bile drainage.

The Surgical Mechanism

1. Excision: The pediatric surgeon meticulously dissects and removes the entirely blocked, fibrous remnants of the extrahepatic (outside the liver) bile ducts and gallbladder.

2. Exposing the Porta Hepatis: The surgeon exposes the porta hepatis—the structural doorway on the underside of the liver. While the large main drainage tubes are destroyed, microscopic bile channels terminating at the liver’s raw edge may still be open.

3. Roux-en-Y Anastomosis: A loop of the infant’s own small intestine is surgically severed, brought upward into the upper abdomen, and sewn directly over the exposed porta hepatis. This creates a direct conduit (Roux-en-Y limb), allowing seeping microscopic bile to drain directly out of the liver and into the digestive tract.

Differential Diagnosis: Biliary Atresia vs. Neonatal Cholestasis

Biliary atresia is the most common reason an infant will require urgent liver surgery, but it must be clearly differentiated from other diseases that mimic its symptoms (jaundice and high direct bilirubin).

Unlike biliary atresia, these related conditions are genetic, metabolic, or inflammatory, meaning they do not possess a mechanical extrahepatic blockage and must never be operated on with a Kasai procedure.

Condition	Underlying Pathology	Primary Diagnostic Method	Key Histological / Clinical Difference
Biliary Atresia	Mechanical, progressive scarring and total obliteration of extrahepatic bile ducts.	Liver biopsy; Intraoperative cholangiogram.	Ductular proliferation, bile plugs, and rapid fibrosis on biopsy.
Neonatal Hepatitis	Diffuse, non-obstructive inflammation of hepatocytes caused by viruses (e.g., CMV) or metabolic errors.	Serum viral PCRs; Liver biopsy.	Large extrahepatic bile ducts are open and functional; biopsy reveals cellular giant-cell transformation without ductal proliferation.
Alpha-1 Antitrypsin Deficiency (AATD)	Genetic metabolic error where misfolded AAT proteins abnormally accumulate inside and damage liver cells.	Quantitative serum $AAT$ levels; Proteotype ($Pi$) genetic testing.	Diagnosed via low circulating AAT blood levels; biopsy shows PAS-positive, diastase-resistant protein globules inside liver cells.
Alagille Syndrome	Complex autosomal dominant genetic disorder affecting multiple organ systems (heart, skeleton, eyes).	Target genetic sequencing for JAG1 or NOTCH2 mutations.	Biopsy reveals a paucity (profound lack) of intrahepatic bile ducts inside the liver, the opposite of biliary atresia’s over-proliferation.

Long-Term Prognosis & Lifelong Management

The long-term outlook for a child born with biliary atresia is highly dependent on two main variables: the infant’s age at the time of the Kasai surgery and the success of postoperative medical management.

⏱️ The 60-to-90 Day Surgical Window

Timing is the single most critical prognostic factor. If the Kasai procedure is performed before 60 days of life, the success rate of restoring adequate bile flow is roughly 70–80%. If the surgery is delayed until after 90 days of life, the microscopic ducts inside the liver have usually scarred over permanently, dropping the success rate of restoring bile flow to less than 20–30%.

The Reality of Transplantation

Even when a Kasai surgery is highly successful and clears the infant’s jaundice, the underlying inflammatory disease often continues to cause quiet, slow, progressive liver injury.

• Roughly one-third (33%) of all infants diagnosed with biliary atresia will experience Kasai failure and require a liver transplant before their second birthday.

• By the time these children reach early young adulthood, up to 80% will ultimately require a liver transplant to manage complications from biliary cirrhosis or portal hypertension.

Lifelong Care Protocol

For children living with their native liver post-Kasai, a highly specialized pediatric hepatology regimen is mandatory to maintain systemic health:

• Aggressive Nutritional Intervention: Because a lack of optimal bile flow impairs the breakdown of dietary fats, these infants suffer from severe malabsorption. They require special formulas fortified with Medium-Chain Triglycerides (MCT oil), which can be absorbed by the gut without needing bile, alongside highly concentrated, lifelong daily doses of fat-soluble vitamins ($A$, $D$, $E$, and $K$).

• Choleretic Medication Therapy: Children are placed on daily Ursodeoxycholic Acid (Ursodiol). This medication chemically alters the bile pool, making the bile fluid more watery and less toxic, which encourages it to flow more easily through the remaining microscopic ducts.

• Rigorous Clinical Surveillance: The child must be routinely monitored by a pediatric hepatologist via blood panels, abdominal ultrasounds, and upper endoscopies to watch for signs of worsening liver cirrhosis, bacterial bile duct infections (cholangitis), or bleeding from swollen esophageal veins (esophageal varices) caused by portal hypertension.

Conclusion

Biliary atresia is a rare condition, but recognizing the warning signs early can make a major difference in a baby’s health. Persistent jaundice, especially when combined with pale stools, dark urine, poor feeding, or slow growth, should be evaluated by a healthcare provider as soon as possible. The main treatment, the Kasai procedure, works best when performed early and may help restore bile flow and delay liver damage. Some children may still require a liver transplant later in life, but timely diagnosis and specialized care can improve outcomes and support healthier development.

Read more: Placenta Accreta Warning Signs and What Happens During Pregnancy Care

Frequently Asked Questions

1. What is biliary atresia?

Biliary atresia is a rare condition in newborns where the bile ducts inside or outside the liver become blocked or damaged. Because bile cannot flow normally into the intestine, it builds up in the liver and causes ongoing inflammation and scarring. The condition usually appears within the first weeks after birth and requires early medical attention. Without treatment, it can progress to serious liver disease.

2. How is biliary atresia different from normal newborn jaundice?

Newborn jaundice is common and often happens because a baby’s liver is still developing and cannot process bilirubin efficiently. Biliary atresia, however, causes a type of jaundice that usually persists or worsens because bile cannot leave the liver properly. Babies with biliary atresia often have pale or clay-colored stools and dark urine, which are warning signs that need medical evaluation. Early testing helps doctors distinguish between normal jaundice and more serious conditions.

3. What are the symptoms of biliary atresia?

The most common symptoms of biliary atresia include yellow skin and eyes, dark urine, pale or gray stools, poor weight gain, irritability, and an enlarged liver or abdomen. Symptoms usually appear within the first few weeks after birth. Some babies may initially seem healthy before signs become noticeable. Because liver damage can progress quickly, persistent symptoms should not be ignored.

4. What causes biliary atresia?

The exact cause of biliary atresia is unknown. Researchers believe it may involve a combination of genetic factors, abnormal immune responses, and possible environmental influences during pregnancy or early infancy. It is not caused by anything a parent did during pregnancy and is not considered a condition that can be prevented. Ongoing research continues to investigate why the bile ducts fail to develop or become damaged.

5. How is biliary atresia diagnosed?

Doctors diagnose biliary atresia through a combination of physical examination, blood tests, imaging studies, and specialized procedures. Blood tests can show abnormal liver function and elevated bilirubin levels. Ultrasound and other imaging tests may examine the liver and bile ducts, while a liver biopsy or surgical evaluation may confirm the diagnosis. Early diagnosis is important because treatment is most effective when started quickly.

6. How is biliary atresia treated?

The main treatment for biliary atresia is the Kasai procedure, a surgery that connects the intestine directly to the liver to help bile drain. The procedure is most successful when performed early, ideally within the first few months of life. Some babies experience improved bile flow after surgery, while others may continue to develop liver damage. Children with advanced liver disease may eventually need a liver transplant.

Sources

National Institute of Diabetes and Digestive and Kidney Diseases. Biliary Atresia. 
Mayo Clinic. Biliary Atresia. 
Cleveland Clinic. Biliary Atresia. 
Children’s Hospital of Philadelphia. Biliary Atresia.
National Organization for Rare Disorders. Biliary Atresia. 
MedlinePlus. Biliary Atresia. 
American Liver Foundation. Biliary Atresia.