Hernia is when an organ or tissue protrudes through a weak area in the surrounding muscle or connective tissue. There are different types of hernias that generally vary by location. Congenital diaphragmatic hernia (CDH) is a developmental defect of the diaphragm that permits the abdominal viscera to herniate into the chest. The amount of herniated contents may be small or large and it generally contains parts of the intestine, spleen, or liver. CDH occurs during a critical period of lung development when bronchial and pulmonary artery branching occurs so lung compression by herniated bowel can lead to pulmonary hypoplasia, which is underdevelopment of the lungs. CDH occurs in 1 out of 2200 births and in 50% of CDH cases, there are other associated anomalies such as chromosomal abnormalities, congenital heart disease, and neural tube defects.

Within the first few hours of life, infants with CDH may present with mild or severe respiratory distress that may be incompatible with life. Symptoms include bluish skin due to lack of oxygen, rapid breathing, and fast heart rate. On physical exam, patients may have a barrel-shaped chest, scaphoid appearing abdomen due to loss of abdominal contents into the chest, and absence of breath sounds on the affected side. In the majority of patients with CDH, herniation occurs on the left; therefore, the heartbeat is displaced to the right due to a shift in the mediastinum. Right sided diaphragmatic hernias occur in 11% of cases and bilateral herniation only in 2%.

The level of respiratory distress depends on the severity of lung hypoplasia. In the prenatal period, lung hypoplasia can be determined using ultrasound to evaluate herniated contents and to measure the lung area to head circumference ratio. Postpartum, there is no specific test to quantify the amount of hypoplasia. The diagnosis of CDH is generally made prenatally by ultrasound; however, in those where CDH is not diagnosed in utero, it should be suspected in any full term infant presenting with respiratory distress and the diagnosis is made by chest x-ray showing herniation of abdominal contents into the hemithorax.

For neonates diagnosed by prenatal ultrasound, the following steps for monitoring and intervention are recommended: twice weekly nonstress testing or biophysical profile testing at 33-34 weeks in addition to ultrasound examinations at 28, 30, 32, and 34-35 weeks to assess fetal growth and amniotic fluid volume. If the fetus experiences growth restriction or oligohydramnios, which is a deficiency of amniotic fluid, the baby should deliver early and betamethasone (a steroid medication that assists in preterm fetal lung development) should be given prior to delivery if the fetus is less than 34 weeks.  The best mode and gestational age for delivery of a fetus with CDH is undetermined; however, the suggested time for planned induction of labor is between 38-39 weeks.

In the delivery room, infants with problematic CDH should be immediately intubated and ventilated with low peak pressure to minimize lung injury. A nasogastric tube on continuous suction is placed in the stomach for decompression of the abdominal contents, which can help expand available lung tissue. In addition, the infant should have an umbilicial artery line for monitoring of blood gases and blood pressure and possibly an umbilical vein catheter for administration of fluids and medications. Blood pressure support should be given and an echo should be done to determine cardiac abnormalities in addition to the extent of pulmonary hypertension and shunting.

Extracorporeal membrane oxygenation (ECMO) has been used as part of  the treatment in some hospitals. ECMO operates as a heart-lung bypass system; thus, it does the job the heart and lungs would be doing. ECMO can be used temporarily while the infant’s condition stabilizes and improves.  Once the infant is stable, he or she can undergo surgical repair of the diaphragmatic hernia, where the stomach, intestines, and other abdominal organs are returned to the abdominal cavity. The hole in the diaphragm is also repaired. If the diaphragm is absent, an artificial diaphragm will be constructed and placed. Following the operation, the infant will require breathing support due to underdevelopment of the lungs. Once the infant is taken off ventilation (breathing machine), he or she may need oxygen and medications to assist with breathing for weeks to years. Thus, CDH requires long term follow up to monitor the infant’s condition to ensure no future complications such as lung infections or other associated congenital problems. The prognosis is generally good for infants with CDH and survival is greater than 80%.

Cerebrospinal fluid (CSF) is a clear fluid that surrounds the brain and spinal cord. This fluid is continually produced and stored in ventricles, which are cavities of the brain. CSF cushions the brain, supplies the brain with nutrients, and removes wastes.  Excess fluid drained from the brain is absorbed by other tissues.

Hydrocephalus is a condition in which there is an abundance of CSF in the ventricles due to interference in proper drainage and absorption. To accommodate the extra fluid, the ventricles enlarge causing compression of  different parts of the brain.

Normal pressure hydrocephalus (NPH) is a type of hydrocephalus that occurs commonly in older adults. NPH is different from other types of hydrocephalus because it develops gradually. The slow enlargement of the ventricles causes the fluid pressure in the brain to not be as high as in other types of hydrocephalus. However, the enlarged ventricles still press on normal brain tissue.

NPH often presents with the following clinical triad of findings: urinary incontinence, gait disturbance, and dementia, with urinary symptoms appearing later in the sequence.  Gait disturbance is often the initial and most prominent symptom of the triad. It may be progressive due to the expansion of the ventricular system. It generally presents as unsteadiness or impaired balance. Eventually, gait disturbances can lead to a need for canes or walkers. An increased tendency to fall backwards is also common. In the very late stages, the patient can progress to an inability to stand, sit, and rise from a chair.

Dementia presents as apathy, forgetfulness, and a dullness of thinking. Memory problems are often predominant, which can contribute to a misdiagnosis of Alzheimer’s disease. Although recall is severely impaired in NPH, recognition, a hallmark of Alzheimer’s, is either normal or slightly impaired.

Idiopathic NPH is normal pressure hydrocephalus occurring without a known cause; however, it can be attributed to any condition that blocks the flow of CSF such as bleeding from an abnormal blood vessel, an aneurysm, a closed head injury, meningitis or similar infections, and surgery on the skull.

The diagnosis of NPH is made by performing a lumbar puncture (spinal tap). If the initial pressure measurement is elevated, it points to a diagnosis of NPH. Clinical improvement after removal of CSF has a high predictive value for treatment success.  A CT scan of the brain will show enlarged ventricles, and an MRI may show certain technical findings consistent with enlarged ventricles and elevated cerebral pressures. Imaging alone cannot differentiate between NPH and other dementia causing conditions such as Alzheimer’s disease, Atherosclerotic vascular disease, and Parkinson’s disease.

Treatment for NPH is surgical diversion of the excess CSF. A shunt is implanted to drain CSF from the intracranial ventricular system to a different location such as the peritoneal space in the abdomen. The most common shunts utilized today are called the ventriculoperitoneal (VP) and ventriculoatrial (VA) shunts.  Placement of a shunt is a neurosurgical procedure performed under general anesthesia, and usually takes less than an hour to complete. Cognitive impairment associated with dementia has been reported to improve in more than fifty percent of cases. Successful treatment for NPH is available; therefore, it is medicaly negligent to misdiagnose NPH as Alzheimer’s dementia, where responses to the latest therapy innovations are only temporary.

Epilepsy is one of the most common neurologic diseases in the world and is present in 4% 
of the world’s population. The majority 
of patients with epilepsy can be managed medically. Intracranial surgery involves inherent 
risks; thus, surgery is only indicated if the benefits outweigh the risks of uncontrolled
 seizures. If surgery is indicated, the patient must undergo a pre-surgical evaluation that involves an extensive medical history focusing on
 seizure activity, type, frequency, and duration. In addition a physical exam must be performed to ensure 
there are no alternative causes for the seizures. The patient is considered a candidate for surgery for a variety of reasons such as inadequate response to medications; inability to tolerate medications due to side effects; seizures that significantly affect quality of life; seizures caused by a lesion such as scar tissue, brain tumor,arteriovenous malformation, or birth defect; partial seizures that always start in one area of the brain; and seizure discharges that spread to the whole brain (secondary generalization).

Once the patient meets the criteria for surgery, electrical brain mapping or electrocorticography is done to provide the surgeon with the necessary information about the brain
 to safely and accurately perform the surgery. Brain mapping is performed to localize the seizure focus, the area of the brain where the seizures begin. In addition, brain mapping identifies significant structures in the brain so the seizure focus may be removed without injuring vital brain structures relating to speech, comprehension, sight, movement, sensation, etc. Brain mapping is essential 
to determine whether the surgery is possible and the potential dangers to the surrounding 
brain regions.

Brain mapping determines the function of a particular area by providing direct stimulation via a current applied to a small area of the brain’s surface. Initially, the physician applies the lowest current and gradually the current is increased until a preset maximum is reached or a significant response is seen. The current interferes with how that area normally functions, but once the current is stopped that area of the brain resumes its usual activity. For example, if a current causes the patient to stop speaking, or to speak unclearly or incoherently, then that area is likely essential for language function. Once the function of an area is identified, a new location in that region is chosen and the physician starts over with the lowest current. Thus, a map is created that illustrates individual functions of different brain areas.

Electrode mapping can be performed in two ways: in a two-stage procedure (the most common way) or directly during the surgery itself. Generally, the current utilized is neither painful nor felt by the patient. However, an electrode occasionally makes contact with the membranes surrounding the brain and at these locations, the patient may experience pain or a tingling sensation when the current is applied. These contacts are easily identified and avoided because physicians always start at a low current.

In the two stage procedure, the surgeon creates an opening in the cranium that exposes the surface of the brain. Electrodes (small electrical contacts) are placed, the scalp is closed, and the patient is then closely monitored in a hospital bed. The electrodes then record the patient’s seizures identifying the seizure focus and map the areas of the brain under electrodes. The two stage procedure utilizes extra-operative brain mapping because it happens outside of an operating room. The patient is always awake, conscious, and able to fully participate during the mapping. The second stage of the procedure is the surgery itself, which removes the abnormal brain tissue using the information gathered from the electrical recordings and brain mapping.

Electrical brain mapping can also be performed during any surgery that exposes part of the brain. Therefore, it is an intraoperative procedure because it occurs during an operation. The surgeon tests locations on the brain’s surface using small electrical probes to create a map of functions. Even if the patient is under anesthesia, areas involved with movement can still be identified electrically; however, the patient must actively participate to map areas involving language, sensation, or vision. The patient is awakened from anesthesia and is given the necessary medications to eliminate pain. Intraoperative mapping is generally done when prior extraoperative mapping discovered important functions adjacent to the area targeted for removal.

Every neurosurgical procedure involves risks such as infection, bleeding, and cerebral edema (accumulation of water in the brain). The major risk for this procedure, specifically for individuals with epilepsy, is that a seizure may be triggered because mapped areas are in close proximity to where the seizures usually begin. Applying electrical currents to areas near the seizure focus can set off a seizure so physicians must closely monitor the patient’s brainwaves during the stimulation. If electrical discharges are noted that could evolve into a seizure, the stimulation is immediately stopped. If a patient suffers from a seizure, the mapping is stopped until the patient fully recovers. If the area being mapped is very sensitive, the patient is often given a powerful anti-seizure medication before receiving any further electrical stimulation.

If the surgeon collects incorrect data during electrical brain mapping and/or excises excessive brain tissue during surgery, the patient may be left with permanent neurological impairment. It is in these scenarios, among others, that a medical malpractice claim could arise.

An infant’s skull is comprised of boney plates separated by sutures.  Cranial sutures are strong, fibrous tissues that hold the bones together and they intersect in large soft spots known as fontanelles. The infant’s skull does not completely fuse until the age of two thereby granting the brain time to grow. Once the bones fuse, the sutures no longer remain flexible.

Craniosynostosis is due to premature fusion of one or more cranial sutures.  It affects 1 in every 2000 to 2500 births worldwide. Premature closure of sutures restricts the growth of the skull perpendicular to the affected suture. To accommodate, the growing brain, the skull grows parallel to the affected suture resulting in a skull deformity. Craniosynostosis can involve one or multiple sutures; however, the sagittal suture is the most common. There is an increased incidence of craniosynostosis in multiple pregnancies and in presence of uterine abnormalities; however, craniosynostosis involving multiple sutures is often a product of a genetic syndrome such as Apert’s and Crouzon syndrome.

The different types of craniosynostosis are sagittal synostosis, frontal plagiocephaly, and metopic synostosis. Symptoms depend on the type of craniosynostosis but they may include no “soft spot” on the newborn skull, a raised hard ridge along the affected sutures, unusual head shape, and slow or no increase in head size over time as the infant grows. The diagnosis of craniosynostosis is based upon physical exam and radiographic studies such as X-ray and CT which can further illustrate structural abnormalities. Complications associated with craniosynostosis include increased intracranial pressure; inhibition of brain growth; impairment in cognition and neurodevelopment such as global development delay and poor feeding; and poor self-esteem and social isolation due to aesthetic abnormalities.

Management for this condition begins with a primary care provider recognizing an abnormal head shape and referring to a craniofacial team for evaluation, preferably within the first few weeks of life.  The craniofacial team develops a treatment plan, coordinates future care, and monitors the patient’s progress. Intervention involves surgical repair of craniosynostosis to prevent intracranial hypertension.  Signs of intracranial hypertension include papilledema, a beaten copper appearance on skull radiograph, or increased measured ICP requiring urgent decompression.

The timing of surgery depends upon the severity of the condition and the child’s health.  Sometimes, surgery is performed at 8-12 months of age because intracranial volume is sufficiently large and the child may better endure the stress of surgery. Also, the calvarium is thicker allowing more stable fixation. The different classifications of craniosynostosis require different surgical plans. Prognosis depends on how many sutures are involved and the child’s overall health.  Individuals with this condition who undergo surgery generally improve and do well, especially when it is not associated with a genetic syndrome.

Child neglect is the most prevalent form of child maltreatment in the US. According to the National Child Abuse and Neglect Data System (NCANDS), approximately 899,000 children in the US who were victims of abuse and neglect in 2005, 62.8% suffered from neglect alone. Child neglect is a failure by parents or caregivers to provide for a child’s basic physical, educational, and emotional needs. It is difficult to define because it varies with the age and development of the child; therefore, it is problematic to determine the extent of the problem. Risk factors for abuse include: preexisting mental or physical illness, poverty, familial stress, substance abuse by parents or caregives. Physicians, nurses, day care personnel, relatives, and neighbors are generally the ones to suspect and report neglect; however, they may be the culprits too. Often times, signs of child neglect may include inadequate medical or custodial care.

Physical neglect encompasses the majority of neglect cases and it involves the parent/caretaker not granting the child basic necessities such as food, clothing, medical care, and shelter. By depriving the child of these essential things, his or her physical health, well being, psychological growth and development is jeopardized. Failure to thrive, malnutrition, serious illness, physical injury due to lack of supervision, and low self-esteem are a some of the byproducts of physical neglect. As an unfortunate example, infants are sometimes mistakenly left behind in cars or vans by their caregivers when the outside temperature is very hot, resulting in heat stroke or death to these infants.

Regarding child abuse, medical neglect is the failure to deliver necessary healthcare for a child thereby endangering the child’s well being. Situations involving medical neglect include when a parent refuses medical care for a child in an emergency or when a parents does not follow recommendations for a child with a treatable chronic disease or disability. Medical neglect often correlates with poverty; however, there is a difference between an inability to provide the appropriate care due to finances or cultural norms and being purposefully neglectful.

If one suspects child neglect, the first step is to report the incident to local child protective services agency in the county or state. The majority of states have a child abuse hotline or you can use the Childhelp National Child Abuse Hotline (1-800-4-A-CHILD). Professionals involved with children have a duty to report reasonable suspicion of abuse and neglect. Reasonable suspicion is based on objective evidence which includes firsthand observation or statements made by a parent or child. Symptoms of negelect include: difficulties in school, eating disorders, low self esteem, depression, anxiety, signs of physical injury, rebellious behavior, sleep disorders, and other vague physical complaints.

An outbreak of fungal meningitis due to contaminated epidural methylpredinsolone (steroid) injections, made by the New England Compounding Center, has been ongoing throughout the United States. Meningitis is a disease caused by inflammation of the meninges, the membranes that cover the brain and spinal cord. It can be caused by bacteria, viruses, fungus, physical injury, cancer, and certain medications. Fungal meningitis is generally rare and non-contagious. In the recent outbreak of fungal meningitis, the contaminant was an environmental mold known as Exerohilum rostratum, a plant pathogen that rarely causes human disease. It was identified by polymerase chain reaction assay from CSF in at least 25 patients and it has been detected in at least one unopened vial from the implicated batch of methylprednisolone . A quarter of the steroid vials in a bin at the England Compounding center contained “greenish black foreign matter” and several rooms utilized to produce sterile products demonstrated mold or bacterial overgrowth according to the FDA.

All locations that received contaminated injections were notified and individuals who received injections from these locations were informed of the possibility of fungal infection. It is likely that not every individual who underwent an injection will contract fungal meningitis. However, individuals with underlying health conditions, circumstances surrounding the injection, and the level of contamination of a particular vial may increase susceptibility. The New England compounding center, where the injections were produced, was closed and all their products were recalled. The CDC currently reports over 300 infected and 25 deaths in patients who received contaminated injections.

Patients should inform physicians of any symptoms such as new-onset headache, neck stiffness, photophobia, fever, or a stroke-like presentation. The incubation period is 1-4 weeks after receiving the contaminated injection. Any individual can contract fungal meningitis; however, it is often seen in individuals with weakened immune systems, such as AIDs or cancer, or individuals taking immune-suppressants, like steroids or anti-TNF medications.

Blood cultures, imaging (Xray or CT), and lumbar puncture are used to diagnose meningitis. A definitive diagnosis is generally made by evaluating cerebrospinal fluid collected from a lumber puncture, also known as a spinal tap. CSF findings in fungal meningitis are increased pressure, increased protein, decreased glucose, and increased lymphocytes. It is essential to diagnose the specific cause of meningitis to determine treatment and severity of illness.  Fungal meningitis is generally treated with long courses of high dose intravenous antifungal medications, such as amphotericin B or flucytosine. The length of treatment depends on the patient’s immune status and type of fungus. Individuals with weakened immune systems need to remain on treatment for longer.

Stryker Rejuvenate and ABG II Modular-Neck Stems– In July 2012, Stryker issued a voluntary recall of these hip implants after reports of fretting, corrosion, and early failure among patients. Typically hip implants last on average about 15 years; however, a greater percentage of these Stryker hip implants were failing within the first 5 years causing patients to have to undergo complex revision surgeries.

Typically, these Stryker hip implants are comprised of four component parts- the stem, neck, ball, and socket.  Due to corrosive breakdown of the chromium/cobalt metal neck and the titanium coated metal stem, patients are at risk for developing a high level of heavy metals such as cobalt and chromium in the surrounding tissue and bloodstream. Heavy metals in the tissue and blood can cause adverse side effects that include metallosis (a build-up of metallic debris), necrosis (the cell death of affected tissues), and osteolysis (the death of bone) – any of which can necessitate revision surgery.

After these Stryker implant are surgically placed, postoperative x-rays may appear normal and show the implant as being properly fitted and aligned. Within a few weeks, patients may encounter pain in the groin and surrounding area and limited mobility.  With longer exposure to heavy metals from these implants, patients may be at an increased risk of bone fractures and the formation of pseudo-tumors. Revision surgery to remove the Stryker implants may be complicated due to the difficulty in removing the stem component that is deeply embedded into the femur bone.

Unfortunately, the FDA approved these devices in 2008 and 2009 under their fast-track 510K approval process which meant that Stryker did not have to provide clinical studies on safety and efficacy.  These hip implants were basically grandfathered in as the FDA reasoned that the two implant systems were similar to the Wright Medical Profemur Hip Implant that was already on the market.  Unfortunately, later reports indicated that a high number of patients with the Wright Medical Profemur Hip Implant were forced to under revision surgeries to remove the failing implants.

Today, many patients are considering legal action for the damages they incurred as a result of these implants.  Patients need to identify what type of implant they received.  This information is best obtained from the product identification stickers that are attached to the patient’s surgical chart.  With these Stryker hip implants, the important components are generally the neck and stem.  Patients may still have a good case if the implanted neck and stem are Stryker Rejuvenate or ABG II components, even if the ball and socket components are from a different product line.

Moreover, patients may be incorrectly told by their doctors that they did not receive a Stryker Rejuvenate or ABG II Hip Implant in circumstances where the ball and socket are ADM or another product line.  These patients may still have a case if they still received a Stryker Rejuvenate or ABG II neck and stem, regardless of the product line of the ball and socket.  Remember, with the Stryker Rejuvenate or ABG II hip implant, it is typically the neck and stem that starts to corrode and cause complications.

Pheochromocytoma is an adrenal gland tumor comprised of chromaffin cells that produce and release excess epinephrine and norepinephrine, which are hormones that effect heart rate, metabolism, and blood pressure. Pheochromocytomas are generally benign and can appear at any age; however, they commonly occur during middle age.

If left untreated or unrecognized, this tumor can be life threatening. Researchers have yet to discover the underlying cause of pheochromocytoma. However, certain disorders such as Multiple Endocrine Neoplasia type II (MEN II), Von Hippel Lindau disease, Neurofibromatosis 1, and Familial Paraganglioma are associated with pheochromocytoma.

Isolated, paroxysmal episodes of hypertension occur in fewer than half of individuals with pheochromocytoma. Episodes of hypertension can occur at unpredictable intervals and usually last 15-20 minutes. During these episodes, the patient experiences hypertension, tachycardia, and fever; however, the patient’s vital signs can be normal at other times. As the tumor grows, episodes increase in frequency, length, and severity. Additional symptoms include abdominal pain, chest pain, irritability, pallor, and weight loss.

However, two thirds of patients experience chronic sustained hypertension. Whether sustained or episodic, the patient’s hypertension is associated with an increased risk of myocardial ischemia, heart failure, renal injury, and cerebrovascular accidents. Sudden cardiac death may occur secondary to catecholamaine-induced myocardial irritability and ventricular arrhythmias.

Diagnosis of pheochromocytoma is based on elevated levels of free catecholamines and metabolites, such as vanillymandelic acid and metanephrines, in the patient’s urine.  The following additional tests can be used to diagnose pheochromocytoma: abdominal CT scan, adrenal biopsy, catecholamines blood test, glucose blood test, metanephrine blood test, MIBG scintiscan, and MRI of the abdomen.

The current treatment for pheochromocytoma is surgery to excise the tumor. It is essential to stabilize the patient’s blood pressure and pulse with adrenergic blocking medication prior to surgery. When the tumor cannot be removed, medication is required to manage it. The majority of patients have benign tumors that are excisable; however, 10% of tumors recur and 25% of patients still have high blood pressure after surgery.

A medical malpractice lawsuit may arise when a patient presents with typical signs and symptoms of pheochromocytoma but the doctor fails to make the diagnosis thereby causing bodily injury, disability or death to the patient usually as a result of uncontrolled hypertension.

Wilson’s disease is a rare autosomal recessive disorder, where copper accumulates in the body’s tissues and organs, specifically the liver, brain, and eyes. The body acquires and stores too much copper. Copper deposition causes damage, death, and scarring of tissues leading to dysfunction of organs.

The incidence of Wilson’s disease is 1:300,000. If both parents possess an abnormal gene for Wilson’s disease, there is a 25% chance their child will have the disorder. The gene responsible for Wilson’s disease is ATP7B. DNA testing is available for this gene; however, testing is complicated because different ethnic groups may have different mutations in this gene.

It is commonly seen in eastern Europeans, Sicilians, and southern Italians. Symptoms begin to present at age 4. Symptoms include abnormal posture of arms and legs, confusion or delirium, dementia, difficulty moving arms/legs, difficulty walking, emotional or behavioral changes, abdominal distention, personality changes, speech impairment, tremors of arms or hands, uncontrollable movements, hemoptysis, jaundice, etc.

Specific signs and tests are used to verify the diagnosis of Wilson’s disease. A slit lamp examination may demonstrate limited eye movement and Kayser-Fleischer rings, brown-colored rings around the iris. Physical examination may illustrate injury to the central nervous system such as loss of muscle control, coordination, memory, thinking and IQ. Other neurological signs may include muscle tremors and confusion.

In addition, the presence of liver or spleen disorders may be an indication for Wilson’s disease. Lab tests that assist in the evaluation for Wilson’s disease include: CBC, serum ceruloplasmin, serum copper, serum uric acid, and urine copper. If the patient possesses liver problems, one would expect to see the following picture: high liver enzymes (AST and ALT), high bilirubin, high PT and PTT, and low albumin. There are a myriad of other tests such as 24-hour urine copper test as well as abdominal and neurological imaging that can provide further evidence for or against the diagnosis.

Lifelong treatment is required to control Wilson’s disease because it may cause fatal effects, such as loss of liver function and damage to the nervous system. In patients where the disorder is not fatal, symptoms may be disabling. The aim of treatment is to decrease the amount of copper in the body causing toxic effects.  Thus, medications known as chelators, which bind copper and remove it via the kidneys and guts, are utilized to treat this disorder. Unfortunately, certain medications that chelate copper, like penicillamine, can sometimes affect neurological function while others may not interfere with neurological function.

Also, a low-copper diet is recommended so individuals should avoid the following foods: chocolate, dried fruit, liver, mushrooms, nuts, and shellfish.  Individuals may want to drink distilled water because the majority of tap water flows through copper pipes. A liver transplant may be necessary in cases where the liver is severely damaged. In addition, people with severe neurological dysfunction may need special protective measures.

If left untreated, a variety of complications can result from Wilson’s disease including anemia, CNS damage, cirrhosis, liver necrosis, fatty liver, hepatitis, increased number of bone fractures and infections, jaundice, muscle atrophy, loss of ability to care for self and function independently, along with a number of other things. However, liver failure and injury to the central nervous system are the most common and dangerous effects. Wilson’s disease is fatal if it goes undiagnosed and untreated.