Anoxic Encephalopathy - Cerebral Palsy Medical Malpractice Lawyers
Anoxic encephalopathy is also called Hypoxic-ischemic encephalopathy or HIE and represents an episode in which the fetus does not get the kind of blood supply and oxygenation it needs either in utero or in the Intrapartum (during delivery) state. There is subsequent brain injury and, in some cases, cerebral palsy is the result.
A cerebral palsy lawyer is a specialist personal injury advocate with expertise in medical malpractice compensation claims for cerebral palsy victims and their families. Most cases of cerebral palsy are not as a result of errors caused by healthcare professionals and it is a cerebral palsy lawyer’s job to distinguish between those cases that occur naturally and the 10% of cases that are the result of clinical negligence. Our cerebral palsy lawyers offer a wealth of experience and give free advice with no further obligation on liability and the potential value of a claim. Payment for services is based on a contingency fee basis which means that we get paid when you get paid. If the case is lost there is nothing whatsoever to pay. There are time limits in all personal injury compensation claims and failure to take legal action within the limitation period can mean that the opportunity to claim compensation is lost forever. If you have the slightest suspicion that your child’s condition has been caused by medical malpractice you should take legal advice from a cerebral palsy compensation claim lawyer as soon as your child’s diagnosis is confirmed by a doctor.
Anoxic encephalopathy can occur in up to 8 cases per 1000 births. The rate is higher in other countries that have limited resources for labor and delivery such as no ability to have a cesarean section. Birth asphyxia worldwide is the cause of 23 percent of all deaths in the neonatal period. It is one of the top twenty leading causes of burden of disease throughout all age groups because the disability can be lifelong. It causes 920,000 neonatal deaths and more than one million still births per year. Cerebral palsy, learning problems, mental retardation and other permanent disabilities can result from this kind of phenomenon. Up to fifty percent of cases of anoxic encephalopathy are fatal, while the remainder results in the various disabilities previously mentioned. Thirty percent of those who survive develop cerebral palsy that is documentable by the age of 18 months.
While adults maintain their cerebral blood flow at all costs, infants maintain their blood flow to the brain at varying rates, depending on the pulse and blood pressure. This puts them at a uniquely increased risk of developing anoxia if the pulse or blood pressure is diminished in the womb or when the mother is in labor. After the insult, the brain remains damaged for up to two days before recovery begins to occur and the infant’s level of consciousness increases to normal by day four. Besides a decreased level of consciousness, seizures can occur as a sign that a neurological insult has occurred. These seizures tend not to be long lasting.
Doctors can test for hypoxic-ischemic encephalopathy by checking the Apgar scores of the infant, which are decreased to three or less after five minutes, by checking for metabolic acidosis in the umbilical cord blood (a pH of less than 7 at the time of birth), by checking whether there is hypotonia, coma or seizures at or after birth, and by checking whether or not there is end organ damage besides the brain, such as the liver, kidneys, heart or intestines.
The causes of anoxic encephalopathy can include having a breech vaginal delivery that results in the head getting stuck, a difficult delivery of a large infant, an inadequate placenta that does not tolerate labor and delivering a preterm infant that does not tolerate labor.
In mild anoxic encephalopathy, there is often a decreased muscle tone along with increased deep tendon reflexes and poor feeding, irritability, excessive crying or sleepiness. This abnormal neurological exam usually resolves itself by day 3-4 of life. In moderate anoxic encephalopathy, the infant is often lethargic and has severe hypotonia and decreased deep tendon reflexes. The infant reflexes such as the Moro reflex may be absent. The infant may have periods of apnea and seizures within the first day of life. The infant often recovers within a couple of weeks of life. In severe anoxia, the infant may be in a coma or can be stuporous during the first hours or days of life. The breathing is poor, often requiring a ventilator. Reflexes and muscle tone are decreased and infant reflexes are poor. Pupils can be dilated or can react poorly to light. Seizures are common and blood pressure/heart rate can fluctuate wildly. It may take weeks to months for this to resolve itself.LAWYER HELPLINE: ☎ 855 804 7142